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Surgery_Schwartz_12202 | Surgery_Schwartz | evaluate the spine. A patient with a spine injury at one level has a significant risk for additional injuries at other levels.Cervical The cervical spine is more mobile than the thoraco-lumbar spine. Stability comes primarily from the multiple liga-mentous connections of adjacent vertebral levels. Disruption of the cervical ligaments can lead to instability in the absence of fracture. The mass of the head transmits significant forces to the cervical spine during abrupt acceleration or deceleration, increasing risk for injury.Jefferson Fracture A Jefferson fracture is a bursting fracture of the ring of C1 (the atlas) due to compression forces. There are usually two or more fractures through the ring of C1. The open-mouth odontoid view may show lateral dislocation of the lateral masses of C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures | Surgery_Schwartz. evaluate the spine. A patient with a spine injury at one level has a significant risk for additional injuries at other levels.Cervical The cervical spine is more mobile than the thoraco-lumbar spine. Stability comes primarily from the multiple liga-mentous connections of adjacent vertebral levels. Disruption of the cervical ligaments can lead to instability in the absence of fracture. The mass of the head transmits significant forces to the cervical spine during abrupt acceleration or deceleration, increasing risk for injury.Jefferson Fracture A Jefferson fracture is a bursting fracture of the ring of C1 (the atlas) due to compression forces. There are usually two or more fractures through the ring of C1. The open-mouth odontoid view may show lateral dislocation of the lateral masses of C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures |
Surgery_Schwartz_12203 | Surgery_Schwartz | C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures dislocated <7 mm usually are treated with a rigid collar, while those dislocated 7 mm or greater usually are treated with a halo vest. Surgical intervention is not indicated.Odontoid Fractures The odontoid process, or dens, is the large ellipse of bone arising anteriorly from C2 (the axis) and projecting up through the ring of C1 (the atlas). Several strong ligaments connect the dens to C1 and to the base of the skull. Odontoid fractures usually result from flexion forces. Odontoid fractures are classified as type I, II, or III. A type I fracture involves the tip only. A type II fracture passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. | Surgery_Schwartz. C1. The rule of Spence states that 7 mm or greater combined dislocation indicates disruption of the transverse liga-ment. The transverse ligament stabilizes C1 with respect to C2. Jefferson fractures dislocated <7 mm usually are treated with a rigid collar, while those dislocated 7 mm or greater usually are treated with a halo vest. Surgical intervention is not indicated.Odontoid Fractures The odontoid process, or dens, is the large ellipse of bone arising anteriorly from C2 (the axis) and projecting up through the ring of C1 (the atlas). Several strong ligaments connect the dens to C1 and to the base of the skull. Odontoid fractures usually result from flexion forces. Odontoid fractures are classified as type I, II, or III. A type I fracture involves the tip only. A type II fracture passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. |
Surgery_Schwartz_12204 | Surgery_Schwartz | passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. Surgery often is undertaken for widely displaced fractures (poor chance of fus-ing) and for those that fail external immobilization. Type I frac-tures usually fuse with external immobilization only.Hangman’s Fracture Traditionally considered a hyperexten-sion/distraction injury from placement of the noose under the angle of the jaw, hangman’s fractures also may occur with hyperextension/compression, as with diving accidents, or hyper-flexion. The injury is defined by bilateral C2 pars interarticularis fractures. The pars interarticularis is the bone between superior and inferior facet joints. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of | Surgery_Schwartz. passes through the base of the odontoid process. A type III fracture passes through the body of C2. Types II and III are considered unstable and should be externally immobilized or fused surgically. Surgery often is undertaken for widely displaced fractures (poor chance of fus-ing) and for those that fail external immobilization. Type I frac-tures usually fuse with external immobilization only.Hangman’s Fracture Traditionally considered a hyperexten-sion/distraction injury from placement of the noose under the angle of the jaw, hangman’s fractures also may occur with hyperextension/compression, as with diving accidents, or hyper-flexion. The injury is defined by bilateral C2 pars interarticularis fractures. The pars interarticularis is the bone between superior and inferior facet joints. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of |
Surgery_Schwartz_12205 | Surgery_Schwartz | Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of external immobilization.Jumped Facets—Hyperflexion Injury The facet joints of the cervical spine slope forward. In a hyperflexion injury, the supe-rior facet can “jump” over the inferior facet of the level above if the joint capsule is torn. Hyperflexion/rotation can cause a unilateral jumped facet, whereas hyperflexion/distraction leads to bilateral jumped facets. Patients with unilateral injury usually are neurologically intact. Those with bilateral injury, however, typically suffer from spinal cord damage, since the anteropos-terior diameter of the spinal canal is compromised by bilateral injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the | Surgery_Schwartz. Thus, the posterior bony connection between C1 and C3 is lost. Hangman’s fractures heal well with external immobilization. Surgery is indicated if there is spinal cord compression or after failure of external immobilization.Jumped Facets—Hyperflexion Injury The facet joints of the cervical spine slope forward. In a hyperflexion injury, the supe-rior facet can “jump” over the inferior facet of the level above if the joint capsule is torn. Hyperflexion/rotation can cause a unilateral jumped facet, whereas hyperflexion/distraction leads to bilateral jumped facets. Patients with unilateral injury usually are neurologically intact. Those with bilateral injury, however, typically suffer from spinal cord damage, since the anteropos-terior diameter of the spinal canal is compromised by bilateral injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the |
Surgery_Schwartz_12206 | Surgery_Schwartz | injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the thoracolumbar spine has a higher thresh-old for injury than the cervical spine. A three-column model is useful for categorizing thoracolumbar injuries.39 The anterior longitudinal ligament and the anterior half of the vertebral body constitute the anterior column. The posterior half of the ver-tebral body and the posterior longitudinal ligament constitute the middle column. The pedicles, facet joints, laminae, spinous processes, and interspinous ligaments constitute the posterior column.Compression Fracture Compression fracture is a compression/flexion injury causing failure of the anterior column only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury | Surgery_Schwartz. injury, leading to spinal cord compression (Fig. 42-11).Thoracolumbar The thoracic spine is stabilized significantly by the rib cage. The lumbar spine has comparatively large vertebrae. Thus, the thoracolumbar spine has a higher thresh-old for injury than the cervical spine. A three-column model is useful for categorizing thoracolumbar injuries.39 The anterior longitudinal ligament and the anterior half of the vertebral body constitute the anterior column. The posterior half of the ver-tebral body and the posterior longitudinal ligament constitute the middle column. The pedicles, facet joints, laminae, spinous processes, and interspinous ligaments constitute the posterior column.Compression Fracture Compression fracture is a compression/flexion injury causing failure of the anterior column only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury |
Surgery_Schwartz_12207 | Surgery_Schwartz | only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury causing failure of the anterior and middle columns. It is unstable, and perhaps half of patients have neurologic deficit due to compression of the cord or cauda equina from bone frag-ments retropulsed into the spinal canal.Chance Fracture Chance fracture is a flexion-distraction injury causing failure of the middle and posterior columns, sometimes with anterior wedging. Typical injury is from a lap seat-belt hyperflexion with associated abdominal injury. It often is unsta-ble and associated with neurologic deficit.Fracture-Dislocation Fracture-dislocation is failure of the anterior, middle, and posterior columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation | Surgery_Schwartz. only. It is stable and not associated with neurologic deficit, although the patient may still have significant pain (Fig. 42-12).Burst Fracture Burst fracture is a pure axial compression injury causing failure of the anterior and middle columns. It is unstable, and perhaps half of patients have neurologic deficit due to compression of the cord or cauda equina from bone frag-ments retropulsed into the spinal canal.Chance Fracture Chance fracture is a flexion-distraction injury causing failure of the middle and posterior columns, sometimes with anterior wedging. Typical injury is from a lap seat-belt hyperflexion with associated abdominal injury. It often is unsta-ble and associated with neurologic deficit.Fracture-Dislocation Fracture-dislocation is failure of the anterior, middle, and posterior columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation |
Surgery_Schwartz_12208 | Surgery_Schwartz | columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation causing decreased canal diameter (Fig. 42-13).Initial Assessment and Management. The possibility of a spine injury must be considered in all trauma patients. A patient with no symptoms referable to neurologic injury, a normal neu-rologic examination, no neck or back pain, and a known mecha-nism of injury unlikely to cause spine injury is at minimal risk for significant injury to the spine. Victims of moderate or severe trauma, especially those with injuries to other organ systems, usually fail to meet these criteria or cannot be assessed ade-quately. The latter often is due to impaired sensorium or signifi-cant pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient | Surgery_Schwartz. columns caused by flexion/dis-traction, shear, or compression forces. Neurologic deficit can result from retropulsion of middle column bone fragments into the spinal canal, or from subluxation causing decreased canal diameter (Fig. 42-13).Initial Assessment and Management. The possibility of a spine injury must be considered in all trauma patients. A patient with no symptoms referable to neurologic injury, a normal neu-rologic examination, no neck or back pain, and a known mecha-nism of injury unlikely to cause spine injury is at minimal risk for significant injury to the spine. Victims of moderate or severe trauma, especially those with injuries to other organ systems, usually fail to meet these criteria or cannot be assessed ade-quately. The latter often is due to impaired sensorium or signifi-cant pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient |
Surgery_Schwartz_12209 | Surgery_Schwartz | pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient care until completion of clinical and radiographic evaluation.The trauma patient should be kept on a hard, flat board with straps and pads used for immobilization. A hard cervical collar is kept in place. These steps minimize forces transferred through the spine and therefore decrease the chance of causing dislocation, subluxation, or neural compression during transport to the trauma bay. The patient is then moved from the board to a flat stretcher. The primary survey and resuscitation are com-pleted. Physical examination and initial X-rays follow.For the examination, approach the patient as described in “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature | Surgery_Schwartz. pain. Because of the potentially catastrophic consequences of missing occult spine instability in a neurologically intact patient, a high level of clinical suspicion should govern patient care until completion of clinical and radiographic evaluation.The trauma patient should be kept on a hard, flat board with straps and pads used for immobilization. A hard cervical collar is kept in place. These steps minimize forces transferred through the spine and therefore decrease the chance of causing dislocation, subluxation, or neural compression during transport to the trauma bay. The patient is then moved from the board to a flat stretcher. The primary survey and resuscitation are com-pleted. Physical examination and initial X-rays follow.For the examination, approach the patient as described in “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature |
Surgery_Schwartz_12210 | Surgery_Schwartz | “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature of the trauma, and if there was loss of consciousness, numbness, or inability to move any or all limbs. Assess motor function by response to commands or pain, as appropriate. Assess pinprick, light touch, and joint position, if possible. Determining the ana-tomically lowest level of intact sensation can pinpoint the level of the lesion along the spine. Testing sensation in an ascending fashion will allow the patient to better discern the true stimulus Brunicardi_Ch42_p1827-p1878.indd 184301/03/19 7:16 PM 1844SPECIFIC CONSIDERATIONSPART IIas opposed to determine when it is extinguished. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association | Surgery_Schwartz. “Neurologic Examination” earlier in this chapter. Evaluation for spine or SCI is easier and more informative in awake patients. If the patient is awake, ask if he or she recalls details of the nature of the trauma, and if there was loss of consciousness, numbness, or inability to move any or all limbs. Assess motor function by response to commands or pain, as appropriate. Assess pinprick, light touch, and joint position, if possible. Determining the ana-tomically lowest level of intact sensation can pinpoint the level of the lesion along the spine. Testing sensation in an ascending fashion will allow the patient to better discern the true stimulus Brunicardi_Ch42_p1827-p1878.indd 184301/03/19 7:16 PM 1844SPECIFIC CONSIDERATIONSPART IIas opposed to determine when it is extinguished. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association |
Surgery_Schwartz_12211 | Surgery_Schwartz | Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association provides a method of clas-sifying patients with spine injuries. The classification indicates completeness and level of the injury and the associated deficit. A form similar to that shown in Fig. 42-14 should be available in the trauma bay and completed for any spine injury patient. The association also has worked to develop recommendations and guidelines to standardize the care of SCI patients in an effort to improve the quality of care.Neurologic Syndromes. Penetrating, compressive, or isch-emic cord injury can lead to several characteristic presentations Figure 42-11. A. Lateral cervical spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B. | Surgery_Schwartz. Document muscle stretch reflexes, lower sacral reflexes (i.e., anal wink and bulbocavernosus), and rectal tone.American Spinal Injury Association Classification The American Spinal Injury Association provides a method of clas-sifying patients with spine injuries. The classification indicates completeness and level of the injury and the associated deficit. A form similar to that shown in Fig. 42-14 should be available in the trauma bay and completed for any spine injury patient. The association also has worked to develop recommendations and guidelines to standardize the care of SCI patients in an effort to improve the quality of care.Neurologic Syndromes. Penetrating, compressive, or isch-emic cord injury can lead to several characteristic presentations Figure 42-11. A. Lateral cervical spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B. |
Surgery_Schwartz_12212 | Surgery_Schwartz | spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B. Sagittal T2-weighted magnetic resonance imaging of the same patient, revealing compromise of the spinal canal and compression of the cord. Note the bright signal within the cord at the level of compression, indicating spinal cord injury. C. Lateral cervical spine X-ray of same patient after application of cervical trac-tion and manual reduction. Note restoration of normal alignment. D. Lateral cervical spine X-ray after posterior cervical fusion to restabilize the C5–C6 segment of the spine.ABCDBrunicardi_Ch42_p1827-p1878.indd 184401/03/19 7:16 PM 1845NEUROSURGERYCHAPTER 42Figure 42-12. A. Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. | Surgery_Schwartz. spine X-ray of an elderly woman who struck her head during a backward fall. Arrowhead points to jumped facets at C5–C6. Note the anterior displace-ment of the C5 body with respect to the C6 body. B. Sagittal T2-weighted magnetic resonance imaging of the same patient, revealing compromise of the spinal canal and compression of the cord. Note the bright signal within the cord at the level of compression, indicating spinal cord injury. C. Lateral cervical spine X-ray of same patient after application of cervical trac-tion and manual reduction. Note restoration of normal alignment. D. Lateral cervical spine X-ray after posterior cervical fusion to restabilize the C5–C6 segment of the spine.ABCDBrunicardi_Ch42_p1827-p1878.indd 184401/03/19 7:16 PM 1845NEUROSURGERYCHAPTER 42Figure 42-12. A. Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. |
Surgery_Schwartz_12213 | Surgery_Schwartz | Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. B. Axial computed tomography scan through the same fracture. Arrowhead demonstrates a transverse discontinu-ity in the superior endplate of the L2 body.ABFigure 42-13. Sagittal reconstruction of an axial fine-slice com-puted tomography scan through the lumbar spine demonstrating a severe fracture-dislocation through the body of L2.based on the anatomy of injury. The neurologic deficits may be deduced from the anatomy of the long sensory and motor tracts and understanding of their decussations (Fig. 42-15). Four pat-terns are discussed. First, injury to the entire cord at a given level results in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal | Surgery_Schwartz. Lateral lumbar spine X-ray showing a compres-sion fracture of L2. Arrowhead points to anterior wedge deformity. Note the posterior wall of the vertebral body has retained normal height and alignment. B. Axial computed tomography scan through the same fracture. Arrowhead demonstrates a transverse discontinu-ity in the superior endplate of the L2 body.ABFigure 42-13. Sagittal reconstruction of an axial fine-slice com-puted tomography scan through the lumbar spine demonstrating a severe fracture-dislocation through the body of L2.based on the anatomy of injury. The neurologic deficits may be deduced from the anatomy of the long sensory and motor tracts and understanding of their decussations (Fig. 42-15). Four pat-terns are discussed. First, injury to the entire cord at a given level results in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal |
Surgery_Schwartz_12214 | Surgery_Schwartz | in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal canal diameter and crushing the cord. Second, injury to half the cord at a given level results in Brown-Séquard syndrome, with loss of motor control and proprioception ipsilat-erally and loss of nociception and thermoception contralaterally. The typical mechanism is a stab or gunshot wound. Third, injury to the interior gray matter of the cord in the cervical spine results in a central cord syndrome, with upper extremity worse than lower extremity weakness and various degrees of numbness. The typical mechanism is transient compression of the cervical cord by the ligamentum flavum buckling during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with | Surgery_Schwartz. in anatomic or functional cord transection with total loss of motor and sensory function below the level of the lesion. The typical mechanism is severe traumatic vertebral subluxation reducing spinal canal diameter and crushing the cord. Second, injury to half the cord at a given level results in Brown-Séquard syndrome, with loss of motor control and proprioception ipsilat-erally and loss of nociception and thermoception contralaterally. The typical mechanism is a stab or gunshot wound. Third, injury to the interior gray matter of the cord in the cervical spine results in a central cord syndrome, with upper extremity worse than lower extremity weakness and various degrees of numbness. The typical mechanism is transient compression of the cervical cord by the ligamentum flavum buckling during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with |
Surgery_Schwartz_12215 | Surgery_Schwartz | during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with paralysis and loss of nociception and thermoception bilaterally. The typical mechanism is an acute disc herniation or ischemia from anterior spinal artery occlusion.Studies. Anteroposterior and lateral plain films provide a rapid survey of the bony spine. Plain films detect fractures and dislo-cations well. Adequate visualization of the lower cervical and upper thoracic spine often is impossible because of the shoul-der girdle. Complete plain film imaging of the cervical spine includes an open-mouth view to assess the odontoid process and the lateral masses of C1. Fine-slice CT scan with sagittal and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI | Surgery_Schwartz. during traumatic neck hyperextension. This syndrome occurs in patients with preex-isting cervical stenosis. Fourth, injury to the ventral half of the cord results in the anterior cord syndrome, with paralysis and loss of nociception and thermoception bilaterally. The typical mechanism is an acute disc herniation or ischemia from anterior spinal artery occlusion.Studies. Anteroposterior and lateral plain films provide a rapid survey of the bony spine. Plain films detect fractures and dislo-cations well. Adequate visualization of the lower cervical and upper thoracic spine often is impossible because of the shoul-der girdle. Complete plain film imaging of the cervical spine includes an open-mouth view to assess the odontoid process and the lateral masses of C1. Fine-slice CT scan with sagittal and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI |
Surgery_Schwartz_12216 | Surgery_Schwartz | and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI provides the best soft tissue imaging. Canal compromise from subluxation, acute disc herniations, or ligamentous disrup-tion is clearly seen. MRI also may detect EDHs or damage to the spinal cord itself, including contusions or areas of ischemia.Brunicardi_Ch42_p1827-p1878.indd 184501/03/19 7:16 PM 1846SPECIFIC CONSIDERATIONSPART IIIndications for Screening for Vascular Injury With Cer-vical Spine Trauma It is important to consider the pres-ence of blunt cerebrovascular injury in patents with cervical spine trauma; however, the specific indications for obtaining a screening CT angiography study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture, | Surgery_Schwartz. and coronal reconstructions provides good detail of bony anatomy and is good for characterizing fractures seen on plain films, as well as visualizing C7–T1 when not well seen on plain films. MRI provides the best soft tissue imaging. Canal compromise from subluxation, acute disc herniations, or ligamentous disrup-tion is clearly seen. MRI also may detect EDHs or damage to the spinal cord itself, including contusions or areas of ischemia.Brunicardi_Ch42_p1827-p1878.indd 184501/03/19 7:16 PM 1846SPECIFIC CONSIDERATIONSPART IIIndications for Screening for Vascular Injury With Cer-vical Spine Trauma It is important to consider the pres-ence of blunt cerebrovascular injury in patents with cervical spine trauma; however, the specific indications for obtaining a screening CT angiography study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture, |
Surgery_Schwartz_12217 | Surgery_Schwartz | study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level, or any fracture at the level of C1–C3, among other indications such as concerning mecha-nism, Lefort mid-face fractures, or basilar fractures through the carotid canal. A recent single-center retrospective study41 (n = 1717 cervical spine fractures) found a higher risk of ver-tebral artery injury only in the setting of fractures of C1 and C2 (combined), those that involve the transverse foramen, or had significant subluxation. They did not find that “high-risk” cervical spine fractures as defined by the Denver Criteria were associated with an increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and | Surgery_Schwartz. study are controversial. Many trauma centers rely on the Denver Criteria.40 These criteria indicate that screening should be employed for a cervical ver-tebral body or transverse foramen fracture, subluxation, or ligamentous injury at any level, or any fracture at the level of C1–C3, among other indications such as concerning mecha-nism, Lefort mid-face fractures, or basilar fractures through the carotid canal. A recent single-center retrospective study41 (n = 1717 cervical spine fractures) found a higher risk of ver-tebral artery injury only in the setting of fractures of C1 and C2 (combined), those that involve the transverse foramen, or had significant subluxation. They did not find that “high-risk” cervical spine fractures as defined by the Denver Criteria were associated with an increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and |
Surgery_Schwartz_12218 | Surgery_Schwartz | increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and contrast-exposure in patients with cervical spine fractures.Figure 42-14. The American Spinal Injury Association system for categorizing spinal cord injury patients according to level and degree of neurologic deficit.Dorsal column(touch, vibration)Corticospinal tract(upper motor)Anterior horn(lower motor)Spinothalmic tract(pain, temperature)TransectionCentral cordBrown-SequardAnterior spinal a.Figure 42-15. Spinal cord injury patterns. a. = artery. (Adapted with permission from Hoff J, Boland M: Neurosurgery, in Schwartz SI: Principles of Surgery, 7th ed., New York, NY: McGraw-Hill Education; 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in | Surgery_Schwartz. increased risk of blunt cerebrovascular injury. Based on these data, we feel that it is appropriate to use a more defined set of screening criteria as outlined by Lock-wood et al to reduce cost and contrast-exposure in patients with cervical spine fractures.Figure 42-14. The American Spinal Injury Association system for categorizing spinal cord injury patients according to level and degree of neurologic deficit.Dorsal column(touch, vibration)Corticospinal tract(upper motor)Anterior horn(lower motor)Spinothalmic tract(pain, temperature)TransectionCentral cordBrown-SequardAnterior spinal a.Figure 42-15. Spinal cord injury patterns. a. = artery. (Adapted with permission from Hoff J, Boland M: Neurosurgery, in Schwartz SI: Principles of Surgery, 7th ed., New York, NY: McGraw-Hill Education; 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in |
Surgery_Schwartz_12219 | Surgery_Schwartz | 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in acute spinal cord injury. The National Acute Spinal Cord Injury studies (NASCIS I, II, and III) provided some support for the view that administration of high-dose methylprednilosone in acute spinal cord injury results in improved neurologic outcomes. A post-hoc analy-sis performed as part of NASCIS II demonstrated improved neurologic outcomes if methylprednilosone was administered within 8 hours of injury. A post-hoc analysis in NASCIS III showed improved outcomes at 6 weeks and 6 months, but not 1 year when methylprednilosone was administered within 3 and 8 hours of injury.42,43,44 However, these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid | Surgery_Schwartz. 1999.)Brunicardi_Ch42_p1827-p1878.indd 184601/03/19 7:16 PM 1847NEUROSURGERYCHAPTER 42Definitive Management Spinal-Dose Steroids Several studies have investigated the use of methylprednilosone in acute spinal cord injury. The National Acute Spinal Cord Injury studies (NASCIS I, II, and III) provided some support for the view that administration of high-dose methylprednilosone in acute spinal cord injury results in improved neurologic outcomes. A post-hoc analy-sis performed as part of NASCIS II demonstrated improved neurologic outcomes if methylprednilosone was administered within 8 hours of injury. A post-hoc analysis in NASCIS III showed improved outcomes at 6 weeks and 6 months, but not 1 year when methylprednilosone was administered within 3 and 8 hours of injury.42,43,44 However, these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid |
Surgery_Schwartz_12220 | Surgery_Schwartz | these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid administration. All three NASCIS trials showed that methylprednilosone was associated with a higher rate of complications such as pneumonia, severe sepsis, and poor wound healing. A recent Cochrane review did not observe a significant increase in complications or mortal-ity associated with methylprednilosone administration in acute spinal cord injury, but did observe a trend towards this effect.45 Despite the lack of clear evidence on this issue, the most recent acute spinal cord injury guidelines provide a controversial level I recommendation against the use of corticosteroids in acute spinal cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical | Surgery_Schwartz. these findings are tempered by the fact that these benefits were modest and only demonstrated in post-hoc analyses, and by the high rate of medical compli-cations associated with corticosteroid administration. All three NASCIS trials showed that methylprednilosone was associated with a higher rate of complications such as pneumonia, severe sepsis, and poor wound healing. A recent Cochrane review did not observe a significant increase in complications or mortal-ity associated with methylprednilosone administration in acute spinal cord injury, but did observe a trend towards this effect.45 Despite the lack of clear evidence on this issue, the most recent acute spinal cord injury guidelines provide a controversial level I recommendation against the use of corticosteroids in acute spinal cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical |
Surgery_Schwartz_12221 | Surgery_Schwartz | cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical complications associated with corticosteroids47). Thus, clear consensus on the use of spinal-dose steroids does not exist.48 A decision to use or not use spinal-dose steroids may be dictated by local or regional practice patterns, especially given the legal liability issues surrounding SCI. Patients with gunshot or nerve root (cauda equina) injuries, or those who are pregnant, <14 years old, or on chronic steroids were excluded from the NASCIS studies and should not receive spinal-dose steroids. In addition to steroids, hypothermia for SCI has also received attention. There is even less evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and | Surgery_Schwartz. cord injury.46 Some authors have argued for the use of methylprednilosone within 8 hours of acute spinal cord injury in carefully selected patients (e.g., young males that are less prone to medical complications associated with corticosteroids47). Thus, clear consensus on the use of spinal-dose steroids does not exist.48 A decision to use or not use spinal-dose steroids may be dictated by local or regional practice patterns, especially given the legal liability issues surrounding SCI. Patients with gunshot or nerve root (cauda equina) injuries, or those who are pregnant, <14 years old, or on chronic steroids were excluded from the NASCIS studies and should not receive spinal-dose steroids. In addition to steroids, hypothermia for SCI has also received attention. There is even less evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and |
Surgery_Schwartz_12222 | Surgery_Schwartz | evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and minimizing stress transmitted through the spine. Commonly used rigid cervical orthoses include Philadelphia and Miami-J collars. Cervical collars are inadequate for C1, C2, or cervicothoracic instability. Cervicothoracic orthoses brace the upper thorax and the neck, improving stabilization over the cervicothoracic region. Minerva braces improve high cervical stabilization by brac-ing from the upper thorax to the chin and occiput. Halo vest assemblies provide the most external cervical stabilization. Four pins are driven into the skull to lock the halo ring in position. Four posts arising from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A | Surgery_Schwartz. evidence supporting the use of this treatment, and thus, it is not currently recommended.49Orthotic Devices Rigid external orthotic devices can stabilize the spine by decreasing range of motion and minimizing stress transmitted through the spine. Commonly used rigid cervical orthoses include Philadelphia and Miami-J collars. Cervical collars are inadequate for C1, C2, or cervicothoracic instability. Cervicothoracic orthoses brace the upper thorax and the neck, improving stabilization over the cervicothoracic region. Minerva braces improve high cervical stabilization by brac-ing from the upper thorax to the chin and occiput. Halo vest assemblies provide the most external cervical stabilization. Four pins are driven into the skull to lock the halo ring in position. Four posts arising from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A |
Surgery_Schwartz_12223 | Surgery_Schwartz | from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A physician familiar with the technique should fit a halo vest. Assistance from a trained orthotics technician improves fitting and adjustment of the other devices.Surgery Neurosurgical intervention has two goals: decompres-sion of the spinal cord and nerve roots, and stabilization of the spine. When spinal cord injury is caused by a hyperflexiondistraction injury that results in cord compression and an unstable spine, both surgical decompression and fusion are typically required. However, in cases of a hyperextension injury causing central cord syndrome due to chronic cervical stenosis, surgi-cal decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be | Surgery_Schwartz. from a tight-fitting rigid plastic vest immobilize the halo ring. Lumbar stabilization may be provided by thoracolumbosacral orthoses. A variety of compa-nies manufacture lines of spinal orthotics. A physician familiar with the technique should fit a halo vest. Assistance from a trained orthotics technician improves fitting and adjustment of the other devices.Surgery Neurosurgical intervention has two goals: decompres-sion of the spinal cord and nerve roots, and stabilization of the spine. When spinal cord injury is caused by a hyperflexiondistraction injury that results in cord compression and an unstable spine, both surgical decompression and fusion are typically required. However, in cases of a hyperextension injury causing central cord syndrome due to chronic cervical stenosis, surgi-cal decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be |
Surgery_Schwartz_12224 | Surgery_Schwartz | decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be important for both decompression and stabili-zation. However, in some cases, reduction of the fracture may not be sufficient for decompression, and further decompressive surgery may still be needed.50Several controversial topics require consideration here. First, the timing of surgery has been a controversial topic. In the past, it has been suggested that patients with incomplete injury, or a deteriorating exam warrant emergent decompres-sion, whereas patients with complete injuries can undergo sur-gery in a nonemergent manner. It is important to appreciate the risks of taking a medically unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical | Surgery_Schwartz. decompression may be needed without the need for inter-nal fixation. In cases where there significant anterolisthesis (subaxial cervical jumped or perched facets), reduction of the fracture may be important for both decompression and stabili-zation. However, in some cases, reduction of the fracture may not be sufficient for decompression, and further decompressive surgery may still be needed.50Several controversial topics require consideration here. First, the timing of surgery has been a controversial topic. In the past, it has been suggested that patients with incomplete injury, or a deteriorating exam warrant emergent decompres-sion, whereas patients with complete injuries can undergo sur-gery in a nonemergent manner. It is important to appreciate the risks of taking a medically unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical |
Surgery_Schwartz_12225 | Surgery_Schwartz | unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical decompression: it can allow early mobilization, aggressive nursing care, and physical ther-apy. Furthermore, a recent prospective cohort study found that the odds of observing a two-point increase in ASIA grade at 6 months was higher in patients that underwent surgery within 24 hours, as compared to those that underwent surgery after 24 hours.51 These data suggest that a subpopulation of patients may significantly benefit from early surgery; however, the char-acteristics of these patients were not described, suggesting a het-erogeneous population in terms of preoperative ASIA grade and imaging.In general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation, | Surgery_Schwartz. unstable patient to surgery, such as a polytrauma patient with hemorrhagic shock or a complete spinal cord injury patient in neurogenic shock. However, there are clear benefits to early surgical decompression: it can allow early mobilization, aggressive nursing care, and physical ther-apy. Furthermore, a recent prospective cohort study found that the odds of observing a two-point increase in ASIA grade at 6 months was higher in patients that underwent surgery within 24 hours, as compared to those that underwent surgery after 24 hours.51 These data suggest that a subpopulation of patients may significantly benefit from early surgery; however, the char-acteristics of these patients were not described, suggesting a het-erogeneous population in terms of preoperative ASIA grade and imaging.In general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation, |
Surgery_Schwartz_12226 | Surgery_Schwartz | general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation, may be medically stabilized before undergoing surgery. Surgical stabilization may be indicated for some inju-ries that would eventually heal with conservative treatment. Solid surgical stabilization may also allow a patient to be man-aged with a rigid cervical collar who would otherwise require halo-vest immobilization.Continued Care. Regional SCI centers with nurses, respira-tory therapists, pulmonologists, physical therapists, physiat-rists, and neurosurgeons specifically trained in caring for these patients may improve outcomes. Frequently encountered ICU issues include hypotension due to neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of | Surgery_Schwartz. general, spine trauma patients with complete neurologic deficit, without any signs of recovery, or those without any neu-rologic deficits who have bony or ligamentous injury requiring open fixation, may be medically stabilized before undergoing surgery. Surgical stabilization may be indicated for some inju-ries that would eventually heal with conservative treatment. Solid surgical stabilization may also allow a patient to be man-aged with a rigid cervical collar who would otherwise require halo-vest immobilization.Continued Care. Regional SCI centers with nurses, respira-tory therapists, pulmonologists, physical therapists, physiat-rists, and neurosurgeons specifically trained in caring for these patients may improve outcomes. Frequently encountered ICU issues include hypotension due to neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of |
Surgery_Schwartz_12227 | Surgery_Schwartz | neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of deep venous thrombosis, autonomic hyperreflexia, and decubitus ulcer for-mation are important. Many patients with cervical or high tho-racic cord injuries require prolonged ventilatory support until the chest wall becomes stiff enough to provide resistance for diaphragmatic breathing. Patients with high cervical cord inju-ries (C4 or above) will often require permanent ventilatory sup-port. Patients should be transferred to SCI rehabilitation centers after stabilization of medical and surgical issues.Peripheral Nerve TraumaThe peripheral nervous system extends throughout the body and is subject to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and | Surgery_Schwartz. neurogenic shock (due to loss of sympathetic tone) and aspiration pneumonia. The recent guidelines recommend maintaining MAPs >85 for 7 days after injury.46 Chronically, prevention and treatment of deep venous thrombosis, autonomic hyperreflexia, and decubitus ulcer for-mation are important. Many patients with cervical or high tho-racic cord injuries require prolonged ventilatory support until the chest wall becomes stiff enough to provide resistance for diaphragmatic breathing. Patients with high cervical cord inju-ries (C4 or above) will often require permanent ventilatory sup-port. Patients should be transferred to SCI rehabilitation centers after stabilization of medical and surgical issues.Peripheral Nerve TraumaThe peripheral nervous system extends throughout the body and is subject to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and |
Surgery_Schwartz_12228 | Surgery_Schwartz | to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and sensory functions. The key Brunicardi_Ch42_p1827-p1878.indd 184701/03/19 7:16 PM 1848SPECIFIC CONSIDERATIONSPART IIinformation-carrying structure of the nerve is the axon. The axon transmits information from the neuronal cell body and may measure from <1 mm to >1 m in length. Axons that travel a significant distance are often covered with myelin, which is a lipid-rich, electrically insulating sheath formed by Schwann cells. Myelinated axons transmit signals much more rapidly than unmyelinated axons because the voltage shifts and currents that define action potentials effectively jump from gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium | Surgery_Schwartz. to injury from a wide variety of trauma. Periph-eral nerves transmit motor and sensory information from the CNS to the body. An individual nerve may have pure motor, pure sensory, or mixed motor and sensory functions. The key Brunicardi_Ch42_p1827-p1878.indd 184701/03/19 7:16 PM 1848SPECIFIC CONSIDERATIONSPART IIinformation-carrying structure of the nerve is the axon. The axon transmits information from the neuronal cell body and may measure from <1 mm to >1 m in length. Axons that travel a significant distance are often covered with myelin, which is a lipid-rich, electrically insulating sheath formed by Schwann cells. Myelinated axons transmit signals much more rapidly than unmyelinated axons because the voltage shifts and currents that define action potentials effectively jump from gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium |
Surgery_Schwartz_12229 | Surgery_Schwartz | gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium form bundles known as fascicles. Fascicles run through a tubular collagenous tissue known as perineurium. Groups of fascicles are suspended in mesoneurium. Fascicles and their mesoneurium run through another tubular collagenous tissue known as epineurium. The epineurium and its contents form the nerve.There are four major mechanisms of injury to peripheral nerves. Nerves may be lacerated, stretched, compressed, or contused. Knives, passing bullets, or jagged bone fractures may lacerate nerves. Adjacent expanding hematomas or dislocated fractures may stretch nerves. Expanding hematomas, external orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause | Surgery_Schwartz. gap to gap over the insulated lengths of the axon.Axons, whether myelinated or unmyelinated, travel through a collagenous connective tissue known as endoneurium. Groups of axons and their endoneurium form bundles known as fascicles. Fascicles run through a tubular collagenous tissue known as perineurium. Groups of fascicles are suspended in mesoneurium. Fascicles and their mesoneurium run through another tubular collagenous tissue known as epineurium. The epineurium and its contents form the nerve.There are four major mechanisms of injury to peripheral nerves. Nerves may be lacerated, stretched, compressed, or contused. Knives, passing bullets, or jagged bone fractures may lacerate nerves. Adjacent expanding hematomas or dislocated fractures may stretch nerves. Expanding hematomas, external orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause |
Surgery_Schwartz_12230 | Surgery_Schwartz | orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause damage to the various anatomic components of the nerve. The patterns of damage are categorized in “Types of Injury.”Certain nerve segments are particularly vulnerable to injury. The following four characteristics make a nerve seg-ment more vulnerable: proximity to a joint, superficial course, passage through a confined space, and being fixed in position.Types of Injury. The traditional classification system for peripheral nerve injury is the Seddon classification. Seddon described three injury patterns as defined in the “Neurapraxia,” “Axonotmesis,” and “Neurotmesis” sections. The Seddon clas-sification provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. | Surgery_Schwartz. orthoses such as casts or braces, or blunt trauma over a super-ficial nerve may compress or crush nerves. Shock waves from high-velocity bullets may contuse nerves. These mechanisms of injury cause damage to the various anatomic components of the nerve. The patterns of damage are categorized in “Types of Injury.”Certain nerve segments are particularly vulnerable to injury. The following four characteristics make a nerve seg-ment more vulnerable: proximity to a joint, superficial course, passage through a confined space, and being fixed in position.Types of Injury. The traditional classification system for peripheral nerve injury is the Seddon classification. Seddon described three injury patterns as defined in the “Neurapraxia,” “Axonotmesis,” and “Neurotmesis” sections. The Seddon clas-sification provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. |
Surgery_Schwartz_12231 | Surgery_Schwartz | provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. Axon degeneration does not occur. Return of normal axonal function occurs over hours to months, often in the 2to 4-week range.Axonotmesis Axonotmesis is the disruption of axons and myelin. The surrounding connective tissues, including endo-neurium, are intact. The axons degenerate proximally and dis-tally from the area of injury. Distal degeneration is known as Wallerian degeneration. Axon regeneration within the con-nective tissue pathways can occur, leading to restoration of function. Axons regenerate at a rate of 1 mm per day. Significant functional recovery may occur for up to 18 months. Scarring at the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous | Surgery_Schwartz. provides a simple, anatomically based approach to peripheral nerve injury.52Neurapraxia Neurapraxia is defined as the temporary failure of nerve function without physical axonal disruption. Axon degeneration does not occur. Return of normal axonal function occurs over hours to months, often in the 2to 4-week range.Axonotmesis Axonotmesis is the disruption of axons and myelin. The surrounding connective tissues, including endo-neurium, are intact. The axons degenerate proximally and dis-tally from the area of injury. Distal degeneration is known as Wallerian degeneration. Axon regeneration within the con-nective tissue pathways can occur, leading to restoration of function. Axons regenerate at a rate of 1 mm per day. Significant functional recovery may occur for up to 18 months. Scarring at the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous |
Surgery_Schwartz_12232 | Surgery_Schwartz | the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous components, such as the epineurium, may or may not be intact. Proximal and distal axonal degeneration occurs. The likelihood of effective axonal regeneration across the site of injury depends on the extent of neuroma formation and on the degree of persisting anatomic alignment of the connective tissue structures. For instance, an injury may damage axons, myelin, and endoneurium, but leave perineurium intact. In this case, the fascicle sheath is intact, and appropriate axonal regeneration is more likely to occur than if the sheath is interrupted.Management of Peripheral Nerve Injury. The sensory and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration. | Surgery_Schwartz. the site of injury from connective tissue reaction can form a neuroma and interfere with regeneration.Neurotmesis Neurotmesis is the disruption of axons and endoneurial tubes. Peripheral collagenous components, such as the epineurium, may or may not be intact. Proximal and distal axonal degeneration occurs. The likelihood of effective axonal regeneration across the site of injury depends on the extent of neuroma formation and on the degree of persisting anatomic alignment of the connective tissue structures. For instance, an injury may damage axons, myelin, and endoneurium, but leave perineurium intact. In this case, the fascicle sheath is intact, and appropriate axonal regeneration is more likely to occur than if the sheath is interrupted.Management of Peripheral Nerve Injury. The sensory and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration. |
Surgery_Schwartz_12233 | Surgery_Schwartz | and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration. Clean, sharp injuries may also benefit from early exploration and reanastomosis. Most other peripheral nerve injuries should be observed. EMG/NCS studies should be done 3-6 to weeks postinjury if deficits persist. Axon seg-ments distal to the site of injury will conduct action potentials normally until Wallerian degeneration occurs, rendering EMG/NCS before 3 weeks uninformative. Continued observation is indicated if function improves. Surgical exploration of the nerve may be undertaken if no functional improvement occurs over 3 months. If intraoperative electrical testing reveals conduction across the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not | Surgery_Schwartz. and motor deficits should be accurately documented. Deficits are usually immediate. Progressive deficit suggests a process such as an expanding hematoma and may warrant early sur-gical exploration. Clean, sharp injuries may also benefit from early exploration and reanastomosis. Most other peripheral nerve injuries should be observed. EMG/NCS studies should be done 3-6 to weeks postinjury if deficits persist. Axon seg-ments distal to the site of injury will conduct action potentials normally until Wallerian degeneration occurs, rendering EMG/NCS before 3 weeks uninformative. Continued observation is indicated if function improves. Surgical exploration of the nerve may be undertaken if no functional improvement occurs over 3 months. If intraoperative electrical testing reveals conduction across the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not |
Surgery_Schwartz_12234 | Surgery_Schwartz | the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not heal. A nerve graft may be needed to bridge the gap between the proximal and distal nerve ends. The sural nerve often is harvested, as it carries only sensory fibers and leaves a minor deficit when resected. The connective tissue structures of the nerve graft may provide a pathway for effective axonal regrowth across the injury.Patterns of Injury Brachial Plexus The brachial plexus may be injured in a variety of ways. Parturition or a motorcycle accident can lead to plexus injury due to dislocation of the glenohumeral joint. Attempting to arrest a fall with one’s hands can lead to a stretch injury of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with | Surgery_Schwartz. the injury, continue observation. In the absence of con-duction, the injured segment should be resected and end-to-end primary anastomosis attempted. However, anastomoses under tension will not heal. A nerve graft may be needed to bridge the gap between the proximal and distal nerve ends. The sural nerve often is harvested, as it carries only sensory fibers and leaves a minor deficit when resected. The connective tissue structures of the nerve graft may provide a pathway for effective axonal regrowth across the injury.Patterns of Injury Brachial Plexus The brachial plexus may be injured in a variety of ways. Parturition or a motorcycle accident can lead to plexus injury due to dislocation of the glenohumeral joint. Attempting to arrest a fall with one’s hands can lead to a stretch injury of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with |
Surgery_Schwartz_12235 | Surgery_Schwartz | of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with injury to the various components of the brachial plexus, and understanding them all would require extensive neuroana-tomic discussion. Two well-known eponymous syndromes are Erb’s palsy and Klumpke’s palsy. Injury high in the plexus to the C5 and C6 roots resulting from glenohumeral dislocation causes Erb’s palsy with the characteristic “bellhop’s tip” posi-tion. The arm hangs at the side, internally rotated. Hand move-ments are not affected. Injury low in the plexus, to the C8 and T1 roots, resulting from stretch or compression injury, causes Klumpke’s palsy with the characteristic “claw hand” deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in | Surgery_Schwartz. of the plexus due to abrupt movement of the shoulder girdle. An api-cal lung (Pancoast) tumor can cause compression injury to the plexus. There are many patterns of neurologic deficits possible with injury to the various components of the brachial plexus, and understanding them all would require extensive neuroana-tomic discussion. Two well-known eponymous syndromes are Erb’s palsy and Klumpke’s palsy. Injury high in the plexus to the C5 and C6 roots resulting from glenohumeral dislocation causes Erb’s palsy with the characteristic “bellhop’s tip” posi-tion. The arm hangs at the side, internally rotated. Hand move-ments are not affected. Injury low in the plexus, to the C8 and T1 roots, resulting from stretch or compression injury, causes Klumpke’s palsy with the characteristic “claw hand” deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in |
Surgery_Schwartz_12236 | Surgery_Schwartz | deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in the spiral groove of the humerus. Improper crutch use can cause damage to the axillary portion. The section of the nerve traversing the spiral groove can be damaged by humerus fractures or pressure from improper posi-tioning during sleep. This classically occurs when the patient is intoxicated and is called “Saturday night palsy.” The key find-ing is wrist drop (i.e., weakness of hand and finger extensors). Axillary (proximal) injury causes triceps weakness in addition to wrist drop.Common Peroneal Neuropathy The common peroneal nerve forms the lateral half of the sciatic nerve (the medial half being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to | Surgery_Schwartz. deformity. There is weakness of the intrinsic hand muscles, similar to that seen with ulnar nerve injury.Radial Nerve The radial nerve courses through the axilla, then laterally and posteriorly in the spiral groove of the humerus. Improper crutch use can cause damage to the axillary portion. The section of the nerve traversing the spiral groove can be damaged by humerus fractures or pressure from improper posi-tioning during sleep. This classically occurs when the patient is intoxicated and is called “Saturday night palsy.” The key find-ing is wrist drop (i.e., weakness of hand and finger extensors). Axillary (proximal) injury causes triceps weakness in addition to wrist drop.Common Peroneal Neuropathy The common peroneal nerve forms the lateral half of the sciatic nerve (the medial half being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to |
Surgery_Schwartz_12237 | Surgery_Schwartz | being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to Brunicardi_Ch42_p1827-p1878.indd 184801/03/19 7:16 PM 1849NEUROSURGERYCHAPTER 42form the deep and superficial peroneal nerves. The superficial, fixed location at the fibular neck makes the common peroneal nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg at the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior), eversion weakness, and numbness over the anterolat-eral surface of the lower leg and dorsum of the foot. In contrast, a foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to | Surgery_Schwartz. being the tibial nerve). It receives contributions from L4, L5, S1, and S2. It emerges as a separate nerve in the popliteal fossa and laterally wraps around the fibular neck, after which it splits to Brunicardi_Ch42_p1827-p1878.indd 184801/03/19 7:16 PM 1849NEUROSURGERYCHAPTER 42form the deep and superficial peroneal nerves. The superficial, fixed location at the fibular neck makes the common peroneal nerve susceptible to compression. The classic cause of traumatic peroneal neuropathy is crush injury from a car bumper striking the lateral aspect of the leg at the knee. Symptoms of common peroneal neuropathy include foot drop (weakness of the tibialis anterior), eversion weakness, and numbness over the anterolat-eral surface of the lower leg and dorsum of the foot. In contrast, a foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to |
Surgery_Schwartz_12238 | Surgery_Schwartz | foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to compressive fibers or adhesions that may be lysed, with the possibility of return of function.CEREBROVASCULAR DISEASECerebrovascular disease is the most frequent cause of new, rapid-onset, nontraumatic neurologic deficit. It is far more common than seizures or tumors. Vascular structures are subject to a vari-ety of chronic pathologic processes that compromise vessel wall integrity. Diabetes, high cholesterol, high blood pressure, and smoking – common comorbidities in the general population – are important risk factors for vascular disease. These conditions can lead to vascular damage by such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These | Surgery_Schwartz. foot drop due to L5 radiculopathy spares eversion because the S1 fibers are intact. Surgical exploration of a common peroneal crush lesion is typically a low yield endeavor. Rare cases may be due to compressive fibers or adhesions that may be lysed, with the possibility of return of function.CEREBROVASCULAR DISEASECerebrovascular disease is the most frequent cause of new, rapid-onset, nontraumatic neurologic deficit. It is far more common than seizures or tumors. Vascular structures are subject to a vari-ety of chronic pathologic processes that compromise vessel wall integrity. Diabetes, high cholesterol, high blood pressure, and smoking – common comorbidities in the general population – are important risk factors for vascular disease. These conditions can lead to vascular damage by such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These |
Surgery_Schwartz_12239 | Surgery_Schwartz | such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These processes may coexist. For instance, a vessel containing an atheromatous plaque will have a decreased luminal diameter. The plaque also may have compromised endothelium, providing the opportunity for thrombus formation, which can lead to acute total occlusion of the remaining lumen. Aneurysms and dissection often occur in atheromatous vessels. Specific patterns of disease relevant to the cerebrovascular system include atheromatous and thrombotic carotid occlusion, brain ischemia from proximal embolic disease, vessel wall rupture leading to hemorrhage, and rupture of abnor-mal, thin-walled structures, specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of | Surgery_Schwartz. such mechanisms as atheroma deposition causing luminal stenosis, endothelial damage promot-ing thrombogenesis, and weakening of the vessel wall result-ing in aneurysm formation or dissection. These processes may coexist. For instance, a vessel containing an atheromatous plaque will have a decreased luminal diameter. The plaque also may have compromised endothelium, providing the opportunity for thrombus formation, which can lead to acute total occlusion of the remaining lumen. Aneurysms and dissection often occur in atheromatous vessels. Specific patterns of disease relevant to the cerebrovascular system include atheromatous and thrombotic carotid occlusion, brain ischemia from proximal embolic disease, vessel wall rupture leading to hemorrhage, and rupture of abnor-mal, thin-walled structures, specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of |
Surgery_Schwartz_12240 | Surgery_Schwartz | specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of the neural tissues supplied by the occluded vessel, and the presence or absence of collateral circulation. The circle of Willis provides extensive collateral circulation, as it connects the right and left carotid arteries to each other and each to the vertebrobasilar system. Patients with complete occlusion of the carotid artery proximal to the circle of Willis may be asymptomatic if the blood flow patterns can shift and provide sufficient circulation to the ipsilateral cerebral hemisphere from the contralateral carotid and the basilar artery. However, the anatomy of the circle of Willis is highly variable. Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than | Surgery_Schwartz. specifically aneurysms and AVMs.Ischemic DiseasesIschemic stroke accounts for approximately 85% of acute cerebrovascular events. Symptoms of acute ischemic stroke vary based on the functions of the neural tissues supplied by the occluded vessel, and the presence or absence of collateral circulation. The circle of Willis provides extensive collateral circulation, as it connects the right and left carotid arteries to each other and each to the vertebrobasilar system. Patients with complete occlusion of the carotid artery proximal to the circle of Willis may be asymptomatic if the blood flow patterns can shift and provide sufficient circulation to the ipsilateral cerebral hemisphere from the contralateral carotid and the basilar artery. However, the anatomy of the circle of Willis is highly variable. Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than |
Surgery_Schwartz_12241 | Surgery_Schwartz | Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than the basilar. Similarly, one vertebral artery is often domi-nant and the other is hypoplastic. These variations may make disease in a particular vessel more neurologically devastating than in a patient with full collateral circulation. Occlusion distal to the circle of Willis generally results in a stroke in the territory supplied by that particular artery.Neurologic deficit from occlusive disease may be tempo-rary or permanent. A patient with sudden-onset focal neurologic deficit that resolves within 24 hours has had a transient ischemic attack (TIA). A patient with permanent deficit has had a com-pleted stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid | Surgery_Schwartz. Patients may have a congenitally hypoplastic or missing com-municating artery with resultant bilateral ACA supply by one carotid, or the PCA may be supplied by the carotid artery rather than the basilar. Similarly, one vertebral artery is often domi-nant and the other is hypoplastic. These variations may make disease in a particular vessel more neurologically devastating than in a patient with full collateral circulation. Occlusion distal to the circle of Willis generally results in a stroke in the territory supplied by that particular artery.Neurologic deficit from occlusive disease may be tempo-rary or permanent. A patient with sudden-onset focal neurologic deficit that resolves within 24 hours has had a transient ischemic attack (TIA). A patient with permanent deficit has had a com-pleted stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid |
Surgery_Schwartz_12242 | Surgery_Schwartz | stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid artery chronically narrowed by atheroma can lead to acute carotid occlusion. As discussed previously, this can be asymptomatic due to sufficient collateralization. The more common concern is thromboem-bolus. Intracranial arterial occlusion by local thrombus formation may occur, but it is rare compared to embolic occlusion.Management. Complete occlusion of the carotid artery with-out referable neurologic deficit requires no treatment. A patient with new neurologic deficit and an angiographically confirmed complete carotid occlusion contralateral to the symptoms should be considered for emergent carotid endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of | Surgery_Schwartz. stroke.Thrombotic DiseaseThe most common area of neurologically significant vessel thrombosis is the carotid artery in the neck. Disease occurs at the carotid bifurcation. Thrombosis of a carotid artery chronically narrowed by atheroma can lead to acute carotid occlusion. As discussed previously, this can be asymptomatic due to sufficient collateralization. The more common concern is thromboem-bolus. Intracranial arterial occlusion by local thrombus formation may occur, but it is rare compared to embolic occlusion.Management. Complete occlusion of the carotid artery with-out referable neurologic deficit requires no treatment. A patient with new neurologic deficit and an angiographically confirmed complete carotid occlusion contralateral to the symptoms should be considered for emergent carotid endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of |
Surgery_Schwartz_12243 | Surgery_Schwartz | endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of opera-tive candidates. In nonemergent cases, the results of the large-scale North American Symptomatic Carotid Stenosis Trial (NASCET) demonstrated a stroke reduction benefit to surgical revascularization in patients with severe stenosis, defined as occlusion of 70% to 99% of the carotid.54 Practice guidelines recommend revascularization at this level of stenosis even if asymptomatic. Surgical options for these patients include both carotid endarterectomy and carotid stenting, which have been shown to produce equal outcomes over long-term follow-up.55Embolic DiseaseEmboli causing strokes may originate from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous | Surgery_Schwartz. endarterectomy.53 Surgery should be performed within 2 hours of symptom onset and should not be performed on obtunded or comatose patients. These restrictions significantly reduce the number of opera-tive candidates. In nonemergent cases, the results of the large-scale North American Symptomatic Carotid Stenosis Trial (NASCET) demonstrated a stroke reduction benefit to surgical revascularization in patients with severe stenosis, defined as occlusion of 70% to 99% of the carotid.54 Practice guidelines recommend revascularization at this level of stenosis even if asymptomatic. Surgical options for these patients include both carotid endarterectomy and carotid stenting, which have been shown to produce equal outcomes over long-term follow-up.55Embolic DiseaseEmboli causing strokes may originate from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous |
Surgery_Schwartz_12244 | Surgery_Schwartz | from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous carotid bifurcations, or from the systemic venous system in the presence of a right-to-left shunt, such as a patent foramen ovale. The majority of emboli enter the anterior (carotid) circulation rather than the posterior (vertebro-basilar) circulation. Characteristic clinical syndromes result from embolic occlusion of various vessels within these circulations.Common Types of Strokes Anterior Cerebral Artery Stroke The ACA supplies the medial frontal and parietal lobes as it courses into the inter-hemispheric fissure. Due to its vascular supply of the motor cortex, ACA stroke characteristically results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm | Surgery_Schwartz. from a number of sources, including: the left atrium in atrial fibrillation, a hypokinetic left ventricular wall segment, valvular vegetations, an atheromatous aortic arch, stenotic/atheromatous carotid bifurcations, or from the systemic venous system in the presence of a right-to-left shunt, such as a patent foramen ovale. The majority of emboli enter the anterior (carotid) circulation rather than the posterior (vertebro-basilar) circulation. Characteristic clinical syndromes result from embolic occlusion of various vessels within these circulations.Common Types of Strokes Anterior Cerebral Artery Stroke The ACA supplies the medial frontal and parietal lobes as it courses into the inter-hemispheric fissure. Due to its vascular supply of the motor cortex, ACA stroke characteristically results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm |
Surgery_Schwartz_12245 | Surgery_Schwartz | results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm weakness. Dominant-hemisphere MCA stroke causes language deficits due to its sup-ply of Broca’s area, Wernicke’s area, and the white matter tracts that connect the two. Proximal MCA occlusion with ischemia and swelling in the entire MCA territory can lead to significant intracranial mass effect and midline shift (see Fig. 42-6), termed malignant MCA stroke.Posterior Cerebral Artery Stroke The PCA supplies the occipital lobe. PCA stroke results in a contralateral homony-mous hemianopsia (see Fig. 42-6).Posterior Inferior Cerebellar Artery Stroke The PICA sup-plies the lateral medulla and the inferior half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia, | Surgery_Schwartz. results in contralateral leg weakness.Middle Cerebral Artery Stroke The MCA supplies the lateral frontal and parietal lobes and the temporal lobe. MCA stroke results in contralateral face and arm weakness. Dominant-hemisphere MCA stroke causes language deficits due to its sup-ply of Broca’s area, Wernicke’s area, and the white matter tracts that connect the two. Proximal MCA occlusion with ischemia and swelling in the entire MCA territory can lead to significant intracranial mass effect and midline shift (see Fig. 42-6), termed malignant MCA stroke.Posterior Cerebral Artery Stroke The PCA supplies the occipital lobe. PCA stroke results in a contralateral homony-mous hemianopsia (see Fig. 42-6).Posterior Inferior Cerebellar Artery Stroke The PICA sup-plies the lateral medulla and the inferior half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia, |
Surgery_Schwartz_12246 | Surgery_Schwartz | half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia, ipsilateral Horner’s syndrome, and ipsilateral limb ataxia. The constellation of symptoms resulting from PICA occlusion is referred to as the lateral medullary or Wallenberg’s syndrome.Management. Ischemic stroke management has two goals: reopen the occluded vessel and maintain blood flow to ischemic “penumbra” tissues bordering the vascular territory. Reopen-ing the vessel has historically been attempted with recombinant tPA.56 tPA administration within 3 hours of the onset of neu-rologic deficit improves outcome at 3 months. In the setting of suspected ischemic stroke, a head CT must be performed immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet | Surgery_Schwartz. half of the cerebellar Brunicardi_Ch42_p1827-p1878.indd 184901/03/19 7:16 PM 1850SPECIFIC CONSIDERATIONSPART IIhemispheres. PICA stroke results in nausea, vomiting, nystag-mus, dysphagia, ipsilateral Horner’s syndrome, and ipsilateral limb ataxia. The constellation of symptoms resulting from PICA occlusion is referred to as the lateral medullary or Wallenberg’s syndrome.Management. Ischemic stroke management has two goals: reopen the occluded vessel and maintain blood flow to ischemic “penumbra” tissues bordering the vascular territory. Reopen-ing the vessel has historically been attempted with recombinant tPA.56 tPA administration within 3 hours of the onset of neu-rologic deficit improves outcome at 3 months. In the setting of suspected ischemic stroke, a head CT must be performed immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet |
Surgery_Schwartz_12247 | Surgery_Schwartz | immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet count less than 100,000/µL, and systolic blood pressure >185 mmHg are among the contraindications to tPA therapy.In recent years, a paradigm shift in ischemic stroke man-agement has occurred with the advent of endovascular mechani-cal thrombectomy. Though tPA can be effective for strokes of smaller vessels, it produces recanalization in only 20% of large vessel ischemic strokes, and even less for internal carotid artery occlusion.57 In mechanical thrombectomy, the intracra-nial circulation is accessed endovascularly, and stent-retriever devices can be deployed to definitively remove clot and stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating | Surgery_Schwartz. immediately to differentiate ischemic from hemorrhagic stroke. Intracranial hemorrhage, major surgery within the previous 2 weeks, GI or genitourinary hemorrhage in the previous 3 weeks, platelet count less than 100,000/µL, and systolic blood pressure >185 mmHg are among the contraindications to tPA therapy.In recent years, a paradigm shift in ischemic stroke man-agement has occurred with the advent of endovascular mechani-cal thrombectomy. Though tPA can be effective for strokes of smaller vessels, it produces recanalization in only 20% of large vessel ischemic strokes, and even less for internal carotid artery occlusion.57 In mechanical thrombectomy, the intracra-nial circulation is accessed endovascularly, and stent-retriever devices can be deployed to definitively remove clot and stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating |
Surgery_Schwartz_12248 | Surgery_Schwartz | stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating mechanical thrombectomy for large vessel occlusion were pub-lished. The MR-CLEAN trial was one of these. In this trial, 500 patients were randomized to tPA and medical therapy vs. mechanical thrombectomy. The latter group had a significantly better 90-day outcome. A domino effect ensued in which four other similarly large-scale trials (e.g., REVASCAT)58 were ter-minated early.Benefits to mechanical thrombectomy include less strin-gent criteria than tPA administration, focused therapy, and time windows between 6 and 12 hours in trials. Currently, mechani-cal thrombectomy is being used for large vessel occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve. | Surgery_Schwartz. stent open involved vessels. Initial investigations into the technol-ogy began in 1999 with varied success. Technological advances proceeded, and in 2015, large-scale clinical trials investigating mechanical thrombectomy for large vessel occlusion were pub-lished. The MR-CLEAN trial was one of these. In this trial, 500 patients were randomized to tPA and medical therapy vs. mechanical thrombectomy. The latter group had a significantly better 90-day outcome. A domino effect ensued in which four other similarly large-scale trials (e.g., REVASCAT)58 were ter-minated early.Benefits to mechanical thrombectomy include less strin-gent criteria than tPA administration, focused therapy, and time windows between 6 and 12 hours in trials. Currently, mechani-cal thrombectomy is being used for large vessel occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve. |
Surgery_Schwartz_12249 | Surgery_Schwartz | occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve. It should be noted that current guidelines still support tPA as first-line therapy even for those eligible for mechanical thrombectomy.Patients not eligible for tPA or mechanical thrombectomy require hemodynamic optimization and neurologic monitoring. Admit such patients to the ICU stroke service for blood pres-sure management and frequent neurologic checks. Permissive hypertension allows for maximal cerebral perfusion. Systolic blood pressure >180 mmHg may require treatment, but the opti-mal mean arterial pressure goal is between 100 and 140 mmHg. Give normal saline solution without glucose (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or | Surgery_Schwartz. occlusion within 6 hours of symptom onset for those patients not eligible for tPA, which accounts for about 10% of ischemic stroke. Its indica-tions and associated technology continue to evolve. It should be noted that current guidelines still support tPA as first-line therapy even for those eligible for mechanical thrombectomy.Patients not eligible for tPA or mechanical thrombectomy require hemodynamic optimization and neurologic monitoring. Admit such patients to the ICU stroke service for blood pres-sure management and frequent neurologic checks. Permissive hypertension allows for maximal cerebral perfusion. Systolic blood pressure >180 mmHg may require treatment, but the opti-mal mean arterial pressure goal is between 100 and 140 mmHg. Give normal saline solution without glucose (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or |
Surgery_Schwartz_12250 | Surgery_Schwartz | (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or increas-ing mass effect from swelling, which typically peaks 3 to 5 days after the stroke. Significant swelling from an MCA or cerebellar stroke may cause herniation and brain stem injury. A decom-pressive hemicraniectomy or suboccipital craniectomy can be a life-saving intervention for these select stroke patients. In stud-ies of malignant MCA syndrome, decompressive hemicraniec-tomy showed favorable mortality and functional outcomes.59 This treatment option, however, should be considered with the understanding of potentially poor functional recovery regardless of therapy. One study showed that less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic | Surgery_Schwartz. (which could injure neurons in the penumbra due to osmotic fluid shift), and aim for normovolemia. A stroke patient who worsens clinically should undergo repeat head CT to evaluate for hemorrhage or increas-ing mass effect from swelling, which typically peaks 3 to 5 days after the stroke. Significant swelling from an MCA or cerebellar stroke may cause herniation and brain stem injury. A decom-pressive hemicraniectomy or suboccipital craniectomy can be a life-saving intervention for these select stroke patients. In stud-ies of malignant MCA syndrome, decompressive hemicraniec-tomy showed favorable mortality and functional outcomes.59 This treatment option, however, should be considered with the understanding of potentially poor functional recovery regardless of therapy. One study showed that less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic |
Surgery_Schwartz_12251 | Surgery_Schwartz | less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic DiseasesIntracranial hemorrhage from abnormal or diseased vascular structures accounts for approximately 15% of acute cerebrovas-cular events. Hypertension and amyloid angiopathy account for most intraparenchymal hemorrhages, although AVMs, aneu-rysms, venous thrombosis, tumors, hemorrhagic conversion of ischemic infarct, and fungal infections also may be the cause. The term intracranial hemorrhage is frequently used to signify intraparenchymal hemorrhage and will be used here. Intracra-nial hemorrhage causes local neuronal injury and dysfunction and also may cause global dysfunction due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of | Surgery_Schwartz. less than half of malignant MCA patients who underwent decompressive hemicraniectomy returned home following rehabilitation, which is even fewer for those undergoing medical therapy.60Hemorrhagic DiseasesIntracranial hemorrhage from abnormal or diseased vascular structures accounts for approximately 15% of acute cerebrovas-cular events. Hypertension and amyloid angiopathy account for most intraparenchymal hemorrhages, although AVMs, aneu-rysms, venous thrombosis, tumors, hemorrhagic conversion of ischemic infarct, and fungal infections also may be the cause. The term intracranial hemorrhage is frequently used to signify intraparenchymal hemorrhage and will be used here. Intracra-nial hemorrhage causes local neuronal injury and dysfunction and also may cause global dysfunction due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of |
Surgery_Schwartz_12252 | Surgery_Schwartz | due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of intraven-tricular hemorrhage, and location to predict mortality. AVM or aneurysm rupture (along with trauma, discussed previously in this chapter) result in subarachnoid hemorrhage (SAH) because the major cerebral and cortical blood vessels travel in the sub-arachnoid space, between the pia and the arachnoid membranes. SAH can cause immediate concussive-like neuronal dysfunc-tion by exposure of the brain to intra-arterial pressure pulsa-tions during the hemorrhage. Moreover, it can cause delayed ischemia from cerebral arterial vasospasm, which can present as acute worsening of the patient’s neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for | Surgery_Schwartz. due to mass effect if sufficiently large. The Intracerebral Hemorrhage (ICH Score) is commonly used to risk-stratify these patients, and it takes into account GCS, age, hemorrhage volume, presence of intraven-tricular hemorrhage, and location to predict mortality. AVM or aneurysm rupture (along with trauma, discussed previously in this chapter) result in subarachnoid hemorrhage (SAH) because the major cerebral and cortical blood vessels travel in the sub-arachnoid space, between the pia and the arachnoid membranes. SAH can cause immediate concussive-like neuronal dysfunc-tion by exposure of the brain to intra-arterial pressure pulsa-tions during the hemorrhage. Moreover, it can cause delayed ischemia from cerebral arterial vasospasm, which can present as acute worsening of the patient’s neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for |
Surgery_Schwartz_12253 | Surgery_Schwartz | neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for possible underlying lesions, such as AVM or tumor.Hemorrhagic stroke most commonly occurs within the basal ganglia or cerebellum. The patient is usually hypertensive on admission and has a history of poorly controlled hyperten-sion. Such patients are more likely to present with lethargy or obtundation compared to those who suffer an ischemic stroke. Depressed mental status results from mass effect from the hema-toma in deep structures, which can produce midline shift or herniation. Ischemic stroke does not cause mass effect acutely. Therefore, patients are more likely to present with normal con-sciousness and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal | Surgery_Schwartz. neurological status days to weeks after the injury. Patients presenting with intracranial hemorrhages that do not follow typical patterns should undergo cerebral angiography or MRI to evaluate for possible underlying lesions, such as AVM or tumor.Hemorrhagic stroke most commonly occurs within the basal ganglia or cerebellum. The patient is usually hypertensive on admission and has a history of poorly controlled hyperten-sion. Such patients are more likely to present with lethargy or obtundation compared to those who suffer an ischemic stroke. Depressed mental status results from mass effect from the hema-toma in deep structures, which can produce midline shift or herniation. Ischemic stroke does not cause mass effect acutely. Therefore, patients are more likely to present with normal con-sciousness and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal |
Surgery_Schwartz_12254 | Surgery_Schwartz | and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal symptoms caused by ischemic stroke. Table 42-3 pro-vides a listing of relative incidences of intracranial hemorrhage by anatomic distribution.Hypertension. Hypertension increases the relative risk of intracranial hemorrhage by approximately fourfold, likely due to chronic degenerative vasculopathy. Hypertensive hemor-rhages often present in the basal ganglia, thalamus, or pons, and result from breakage of small perforating arteries that branch off of much larger parent vessels (Fig. 42-16).Most hypertensive hemorrhages should be medically man-aged. The hematoma often contains intact, salvageable axons because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age, | Surgery_Schwartz. and a focal neurologic deficit. Hemorrhagic strokes tend to present with a relatively gradual decline in neurologic function as the hematoma expands, rather than the immediately maximal symptoms caused by ischemic stroke. Table 42-3 pro-vides a listing of relative incidences of intracranial hemorrhage by anatomic distribution.Hypertension. Hypertension increases the relative risk of intracranial hemorrhage by approximately fourfold, likely due to chronic degenerative vasculopathy. Hypertensive hemor-rhages often present in the basal ganglia, thalamus, or pons, and result from breakage of small perforating arteries that branch off of much larger parent vessels (Fig. 42-16).Most hypertensive hemorrhages should be medically man-aged. The hematoma often contains intact, salvageable axons because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age, |
Surgery_Schwartz_12255 | Surgery_Schwartz | because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age, nondominant hemisphere, rapid deterioration, and significant Brunicardi_Ch42_p1827-p1878.indd 185001/03/19 7:16 PM 1851NEUROSURGERYCHAPTER 42Table 42-3Anatomic distribution of intracranial hemorrhages and correlated symptoms% OF INTRACRANIAL HEMORRHAGESLOCATIONCLASSIC SYMPTOMS50Basal ganglia (putamen, globus pallidus), internal capsuleContralateral hemiparesis15ThalamusContralateral hemisensory loss10–20Cerebral white matter (lobar)Depends on location (weakness, numbness, partial loss of visual field)10–15PonsHemiparesis; may be devastating10CerebellumLethargy or coma due to brain stem compression and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right | Surgery_Schwartz. because the blood dissects through and along neural tracts, and surgical clot evacuation destroys these axons. Factors potentially favoring surgery include: superficial clot location, young age, nondominant hemisphere, rapid deterioration, and significant Brunicardi_Ch42_p1827-p1878.indd 185001/03/19 7:16 PM 1851NEUROSURGERYCHAPTER 42Table 42-3Anatomic distribution of intracranial hemorrhages and correlated symptoms% OF INTRACRANIAL HEMORRHAGESLOCATIONCLASSIC SYMPTOMS50Basal ganglia (putamen, globus pallidus), internal capsuleContralateral hemiparesis15ThalamusContralateral hemisensory loss10–20Cerebral white matter (lobar)Depends on location (weakness, numbness, partial loss of visual field)10–15PonsHemiparesis; may be devastating10CerebellumLethargy or coma due to brain stem compression and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right |
Surgery_Schwartz_12256 | Surgery_Schwartz | and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right basal ganglia hemorrhage (arrowhead). The blood clot is bright white. Hypodensity around the clot represents cerebral edema. There is blood within the ventricular system. B. Another patient with intraventricular extension of a basal ganglia hemorrhage. The patient developed right-sided weak-ness and then lethargy. Head computed tomography indicated hydrocephalus. A ventriculostomy was placed for cerebrospinal fluid drainage (arrowhead indicates cross-sectional view of the catheter entering the anterior horn of the right lateral ventricle).mass effect. However, the most comprehensive randomized clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More | Surgery_Schwartz. and/or hydrocephalus1–6Brain stem (excluding pons)Often devastatingFigure 42-16. A. Head computed tomography scan of a patient with left-sided weakness and progressive lethargy reveals a right basal ganglia hemorrhage (arrowhead). The blood clot is bright white. Hypodensity around the clot represents cerebral edema. There is blood within the ventricular system. B. Another patient with intraventricular extension of a basal ganglia hemorrhage. The patient developed right-sided weak-ness and then lethargy. Head computed tomography indicated hydrocephalus. A ventriculostomy was placed for cerebrospinal fluid drainage (arrowhead indicates cross-sectional view of the catheter entering the anterior horn of the right lateral ventricle).mass effect. However, the most comprehensive randomized clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More |
Surgery_Schwartz_12257 | Surgery_Schwartz | clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More recent studies have assessed the role of minimally-invasive catheter evacuation of clot; these investigations are ongoing.62 Medical management remains the gold standard, however, and includes moderate blood pressure control, normalizing platelet and clotting function, phenytoin or levetiracetam for seizure prophylaxis, and electrolyte management. Intubate patients who cannot clearly follow commands to prevent aspiration and hypercarbia. Follow and document the neurologic examination and communicate with the family regarding appropriateness for rehabilitation vs. withdrawal of care.Amyloid Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive | Surgery_Schwartz. clinical trials to date did not show an overall improved outcome in surgically evacuated intracranial hemorrhage, except for the subgroup of patients with clot <1 cm from the cortical surface.61 More recent studies have assessed the role of minimally-invasive catheter evacuation of clot; these investigations are ongoing.62 Medical management remains the gold standard, however, and includes moderate blood pressure control, normalizing platelet and clotting function, phenytoin or levetiracetam for seizure prophylaxis, and electrolyte management. Intubate patients who cannot clearly follow commands to prevent aspiration and hypercarbia. Follow and document the neurologic examination and communicate with the family regarding appropriateness for rehabilitation vs. withdrawal of care.Amyloid Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive |
Surgery_Schwartz_12258 | Surgery_Schwartz | Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive intracranial hemorrhage. Amy-loid laden vessels may hemorrhage multiple times. The super-ficial location of amyloid hemorrhages may make surgical evacuation less morbid compared to typical deep hypertensive hemorrhages. Nonetheless, medical management and family counseling should be approached similarly to patients with hypertensive hemorrhages.Brunicardi_Ch42_p1827-p1878.indd 185101/03/19 7:16 PM 1852SPECIFIC CONSIDERATIONSPART IITable 42-5The Hunt-Hess clinical grading system for subarachnoid hemorrhageHUNT-HESS GRADECLINICAL PRESENTATION0Asymptomatic; unruptured aneurysm1Awake; asymptomatic or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g., | Surgery_Schwartz. Angiopathy. The presence of pathologic amyloid deposition in the media of small cortical vessels compromises vessel integrity and tends to cause more superficial (lobar) hemorrhages than hypertensive intracranial hemorrhage. Amy-loid laden vessels may hemorrhage multiple times. The super-ficial location of amyloid hemorrhages may make surgical evacuation less morbid compared to typical deep hypertensive hemorrhages. Nonetheless, medical management and family counseling should be approached similarly to patients with hypertensive hemorrhages.Brunicardi_Ch42_p1827-p1878.indd 185101/03/19 7:16 PM 1852SPECIFIC CONSIDERATIONSPART IITable 42-5The Hunt-Hess clinical grading system for subarachnoid hemorrhageHUNT-HESS GRADECLINICAL PRESENTATION0Asymptomatic; unruptured aneurysm1Awake; asymptomatic or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g., |
Surgery_Schwartz_12259 | Surgery_Schwartz | or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g., pronator drift)4Stuporous; significant neurologic deficit (e.g., hemiplegia)5Comatose; posturingTable 42-4Prevalence of cerebral aneurysm by locationPREVALENCEANEURYSM LOCATION (VERNACULAR NAME)Anterior circulation 85% 30% Anterior communicating artery (A-Comm)25% Posterior communicating artery (P-Comm)20% Middle cerebral artery bifurcation10% OtherPosterior circulation 15% 10% Basilar artery, most frequently at the basilar tip5% Vertebral artery, usually at the posterior inferior cerebellar arteryCerebral Aneurysm. An aneurysm is a focal dilatation of the vessel wall and is most often a balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g., | Surgery_Schwartz. or mild headache; mild nuchal rigidity2Awake; moderate to severe headache, cranial nerve palsy (e.g., cranial nerve III or IV), nuchal rigidity3Lethargic; mild focal neurologic deficit (e.g., pronator drift)4Stuporous; significant neurologic deficit (e.g., hemiplegia)5Comatose; posturingTable 42-4Prevalence of cerebral aneurysm by locationPREVALENCEANEURYSM LOCATION (VERNACULAR NAME)Anterior circulation 85% 30% Anterior communicating artery (A-Comm)25% Posterior communicating artery (P-Comm)20% Middle cerebral artery bifurcation10% OtherPosterior circulation 15% 10% Basilar artery, most frequently at the basilar tip5% Vertebral artery, usually at the posterior inferior cerebellar arteryCerebral Aneurysm. An aneurysm is a focal dilatation of the vessel wall and is most often a balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g., |
Surgery_Schwartz_12260 | Surgery_Schwartz | balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g., posterior com-municating artery or ophthalmic artery). Approximately 85% of aneurysms arise from the anterior circulation (carotid) and 15% from the posterior circulation (vertebrobasilar). Table 42-4 shows the percentage distribution of cerebral aneurysms by location. Aneurysms are thin walled and at risk for rupture. The major cerebral vessels, and therefore aneurysms, lie in the subarachnoid space. Rupture results in SAH. The aneurys-mal tear may be small and seal quickly, or it may not. SAH may consist of a thin layer of blood in the CSF spaces, or thick layers of blood around the brain and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe | Surgery_Schwartz. balloon-like outpouching, but may also be fusiform. Aneurysms usually occur at branch points of major vessels (e.g., internal carotid artery bifurca-tion), or at the origin of smaller vessels (e.g., posterior com-municating artery or ophthalmic artery). Approximately 85% of aneurysms arise from the anterior circulation (carotid) and 15% from the posterior circulation (vertebrobasilar). Table 42-4 shows the percentage distribution of cerebral aneurysms by location. Aneurysms are thin walled and at risk for rupture. The major cerebral vessels, and therefore aneurysms, lie in the subarachnoid space. Rupture results in SAH. The aneurys-mal tear may be small and seal quickly, or it may not. SAH may consist of a thin layer of blood in the CSF spaces, or thick layers of blood around the brain and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe |
Surgery_Schwartz_12261 | Surgery_Schwartz | and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe “thunderclap” headache. A patient will classically describe “the worst head-ache of my life.” Presenting neurologic symptoms may range from mild headache to coma to sudden death. The Hunt-Hess grading system categorizes patients clinically (Table 42-5). The World Federation of Neurological Surgery (WFNS) SAH Grading Scale is also used for this purpose. The Fisher Scale and a more recent modified form use head CT characteristics, described in the following section, to stratify patients based on risk of vasospasm-induced delayed cerebral ischemia. Both scales are used in conjunction as a quick way to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the | Surgery_Schwartz. and extending into brain parenchyma, resulting in a clot with mass effect. Because the meningeal linings of the brain are sensitive with free nerve endings, SAH usually results in a sudden, severe “thunderclap” headache. A patient will classically describe “the worst head-ache of my life.” Presenting neurologic symptoms may range from mild headache to coma to sudden death. The Hunt-Hess grading system categorizes patients clinically (Table 42-5). The World Federation of Neurological Surgery (WFNS) SAH Grading Scale is also used for this purpose. The Fisher Scale and a more recent modified form use head CT characteristics, described in the following section, to stratify patients based on risk of vasospasm-induced delayed cerebral ischemia. Both scales are used in conjunction as a quick way to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the |
Surgery_Schwartz_12262 | Surgery_Schwartz | to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the base of the brain, as shown in Fig. 42-17. CT is rapid, noninvasive, and approxi-mately 95% sensitive. In patients with suspicious symptoms but negative head CT, a lumbar puncture (LP) should be per-formed. An LP with xanthochromia and high red blood cell counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH. Negative CT and LP essentially rules out SAH. Patients diagnosed with SAH require four-vessel cerebral angiography within 24 hours to assess for aneurysm or other vascular malformation. Cathe-ter angiography remains the gold standard for assessing the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction | Surgery_Schwartz. to communicate severity of aneurysmal SAH.Patients with symptoms suspicious for SAH should have a head CT immediately. Acute SAH appears as a bright signal in the fissures and CSF cisterns around the base of the brain, as shown in Fig. 42-17. CT is rapid, noninvasive, and approxi-mately 95% sensitive. In patients with suspicious symptoms but negative head CT, a lumbar puncture (LP) should be per-formed. An LP with xanthochromia and high red blood cell counts (usually 100,000/mL), which do not decrease between tubes 1 and 4, is consistent with SAH. Negative CT and LP essentially rules out SAH. Patients diagnosed with SAH require four-vessel cerebral angiography within 24 hours to assess for aneurysm or other vascular malformation. Cathe-ter angiography remains the gold standard for assessing the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction |
Surgery_Schwartz_12263 | Surgery_Schwartz | the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction angiographic view of a cerebral aneurysm. Figure 42-18B shows the anatomy of the circle of Willis in a simplified graphic representation to assist in visualizing the locations of various cerebral aneurysms.SAH patients should be admitted to the neurologic ICU. Hunt-Hess grade 4 and 5 patients require intubation and hemo-dynamic monitoring and stabilization. The current standard of care for ruptured aneurysms requires early aneurysmal occlu-sion. There are two options for occlusion. The patient may undergo craniotomy with microsurgical dissection and place-ment of a titanium clip across the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally | Surgery_Schwartz. the patient’s cerebral vasculature, relevant anomalies, and pres-ence, location, and morphology of the cerebral aneurysms. Figure 42-18A demonstrates the typical anteroposterior digital subtraction angiographic view of a cerebral aneurysm. Figure 42-18B shows the anatomy of the circle of Willis in a simplified graphic representation to assist in visualizing the locations of various cerebral aneurysms.SAH patients should be admitted to the neurologic ICU. Hunt-Hess grade 4 and 5 patients require intubation and hemo-dynamic monitoring and stabilization. The current standard of care for ruptured aneurysms requires early aneurysmal occlu-sion. There are two options for occlusion. The patient may undergo craniotomy with microsurgical dissection and place-ment of a titanium clip across the aneurysm neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally |
Surgery_Schwartz_12264 | Surgery_Schwartz | neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally taken the form of “coiling.” The patient is taken to the interventional neuro-radiology suite for placement of looped titanium coils inside the aneurysm dome. The coils support thrombosis and prevent Figure 42-17. Non contrast CT scan on the left shows diffuse subarachnoid blood in the cisterns with some concentration in the region of the anterior cerebral arteries. This is confirmed by the image on the right, a CT angiogram, where the arrow indicates an anterior communicating artery aneurysm.Brunicardi_Ch42_p1827-p1878.indd 185201/03/19 7:16 PM 1853NEUROSURGERYCHAPTER 42Figure 42-18. A. Anteroposterior view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle | Surgery_Schwartz. neck to exclude the aneurysm from the circulation and reconstitute the lumen of the parent vessel. The second option is to utilize an endovascular approach for treatment, which has traditionally taken the form of “coiling.” The patient is taken to the interventional neuro-radiology suite for placement of looped titanium coils inside the aneurysm dome. The coils support thrombosis and prevent Figure 42-17. Non contrast CT scan on the left shows diffuse subarachnoid blood in the cisterns with some concentration in the region of the anterior cerebral arteries. This is confirmed by the image on the right, a CT angiogram, where the arrow indicates an anterior communicating artery aneurysm.Brunicardi_Ch42_p1827-p1878.indd 185201/03/19 7:16 PM 1853NEUROSURGERYCHAPTER 42Figure 42-18. A. Anteroposterior view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle |
Surgery_Schwartz_12265 | Surgery_Schwartz | view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle of Willis and the common sites for aneu-rysms. ICA = internal cerebral artery; MCA = middle cerebral artery. (Reproduced with permission from Osborn AG: Handbook of Neuroradiology: Brain and Skull. St. Louis, MO: Mosby-Year Book, Inc; 1991.)AIntracranial aneurysumsAnteriorcommunicating artery30% – 35%MCA bifurcation20%Basilar5%Posterior fossaMiscellaneous sites distalto circle of Willis1% – 3%ICA/posteriorcommunicating30% – 35%Bblood flow into the aneurysm. Newer endovascular options include flow diversion and stent-assisted coiling. Factors favor-ing craniotomy and clipping include young age, good medical condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is | Surgery_Schwartz. view after injection of contrast dye in the right internal carotid artery demonstrates an aneurysm of the middle cerebral artery bifurcation. B. Figure depicting the anatomy of the circle of Willis and the common sites for aneu-rysms. ICA = internal cerebral artery; MCA = middle cerebral artery. (Reproduced with permission from Osborn AG: Handbook of Neuroradiology: Brain and Skull. St. Louis, MO: Mosby-Year Book, Inc; 1991.)AIntracranial aneurysumsAnteriorcommunicating artery30% – 35%MCA bifurcation20%Basilar5%Posterior fossaMiscellaneous sites distalto circle of Willis1% – 3%ICA/posteriorcommunicating30% – 35%Bblood flow into the aneurysm. Newer endovascular options include flow diversion and stent-assisted coiling. Factors favor-ing craniotomy and clipping include young age, good medical condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is |
Surgery_Schwartz_12266 | Surgery_Schwartz | condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is believed to result in a more definitive cure. The decision to clip or coil is complex and should be fully explored. Practice standards have changed in recent years with the advent of more nuanced endovascular techniques and treatment options, as described earlier. Current guidelines favor endovas-cular therapy as the preferred first-line approach. The Interna-tional Subarachnoid Aneurysm Trial researchers suggested that endovascular occlusion resulted in better mortality outcomes for certain types of cerebral aneurysms, although this trial was marred by poor selection and randomization techniques, and the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64 | Surgery_Schwartz. condition, and broad aneurysm necks. Factors favoring coil-ing include age, medical comorbidities, and narrow aneurysm necks. Due to coil migration or compaction over time, surgical clipping is believed to result in a more definitive cure. The decision to clip or coil is complex and should be fully explored. Practice standards have changed in recent years with the advent of more nuanced endovascular techniques and treatment options, as described earlier. Current guidelines favor endovas-cular therapy as the preferred first-line approach. The Interna-tional Subarachnoid Aneurysm Trial researchers suggested that endovascular occlusion resulted in better mortality outcomes for certain types of cerebral aneurysms, although this trial was marred by poor selection and randomization techniques, and the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64 |
Surgery_Schwartz_12267 | Surgery_Schwartz | the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64 However, this trial has a number of similar criticisms as well. Debate also continues regarding optimal care for unruptured intracranial aneurysms, with a recent large-scale study showing no clear benefit to open surgical vs. endovascu-lar approaches.65SAH patients often require 1 to 3 weeks of ICU care after aneurysm occlusion for medical complications that accompany neurologic injury. In addition to routine ICU concerns, SAH patients are also at risk for cerebral vasospasm. In vasospasm, cerebral arteries constrict pathologically and can cause isch-emia or stroke from 4 to 21 days after SAH. Current vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the | Surgery_Schwartz. the validity of its conclusions have been questioned.63 Long-term outcomes may be better in younger patients with clipped aneurysms, as demonstrated in the Barrow Ruptured Aneurysm Trial (BRAT).64 However, this trial has a number of similar criticisms as well. Debate also continues regarding optimal care for unruptured intracranial aneurysms, with a recent large-scale study showing no clear benefit to open surgical vs. endovascu-lar approaches.65SAH patients often require 1 to 3 weeks of ICU care after aneurysm occlusion for medical complications that accompany neurologic injury. In addition to routine ICU concerns, SAH patients are also at risk for cerebral vasospasm. In vasospasm, cerebral arteries constrict pathologically and can cause isch-emia or stroke from 4 to 21 days after SAH. Current vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the |
Surgery_Schwartz_12268 | Surgery_Schwartz | vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the incidence and degree of spasm, though its mechanism is debated. Neurointerventional options for treating symptomatic vasospasm include intra-arterial papaverine or nicardipine, and balloon angioplasty for larger caliber vessels.Aneurysmal SAH has an approximate mortality rate of 50% in the first month. Approximately one-third of survivors return to pre-SAH function, and the remaining two-thirds have mild to severe disability. Most require rehabilitation after hospitalization.Arteriovenous Malformations. AVMs are abnormal, dilated arteries and veins without an intervening capillary bed. The nidus of the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often | Surgery_Schwartz. vasospasm prophylaxis includes maintenance of optimal perfusion with hypertension and mild hypervolemia, as well as administration of nimodipine, a calcium channel blocker that may decrease the incidence and degree of spasm, though its mechanism is debated. Neurointerventional options for treating symptomatic vasospasm include intra-arterial papaverine or nicardipine, and balloon angioplasty for larger caliber vessels.Aneurysmal SAH has an approximate mortality rate of 50% in the first month. Approximately one-third of survivors return to pre-SAH function, and the remaining two-thirds have mild to severe disability. Most require rehabilitation after hospitalization.Arteriovenous Malformations. AVMs are abnormal, dilated arteries and veins without an intervening capillary bed. The nidus of the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often |
Surgery_Schwartz_12269 | Surgery_Schwartz | the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often than large AVMs, which tend to present with seizures. Headache, bruit, or focal neurologic deficits are less common symptoms. AVMs hemorrhage at an average rate of 2% to 4% a year. Figure 42-19 demonstrates the angiographic appearance of an AVM in arterial and venous phases.For unruptured AVMs, recent evidence from over two hundred patients supports medical management alone rather than intervention due to risk of stroke.66 Because AVM rupture can present radiographically as SAH, it is important to consider several management differences as compared to aneurysmal SAH. Definitive therapy for the AVM usually is delayed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs, and vasospasm is much less common. Three | Surgery_Schwartz. the AVM contains a tangled mass of vessels but no neural tissue. AVMs may be asymptomatic or present with SAH, intra-parenchymal hemorrhage, or seizures. Small AVMs present with hemorrhage more often than large AVMs, which tend to present with seizures. Headache, bruit, or focal neurologic deficits are less common symptoms. AVMs hemorrhage at an average rate of 2% to 4% a year. Figure 42-19 demonstrates the angiographic appearance of an AVM in arterial and venous phases.For unruptured AVMs, recent evidence from over two hundred patients supports medical management alone rather than intervention due to risk of stroke.66 Because AVM rupture can present radiographically as SAH, it is important to consider several management differences as compared to aneurysmal SAH. Definitive therapy for the AVM usually is delayed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs, and vasospasm is much less common. Three |
Surgery_Schwartz_12270 | Surgery_Schwartz | for the AVM usually is delayed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs, and vasospasm is much less common. Three therapeutic modalities for AVMs are currently in common use: microsurgical exci-sion, interventional radiology or endovascular embolization, and stereotactic radiosurgery (SRS). AVMs that are large, near eloquent cortex, or that drain to deep venous structures are con-sidered high grade and more difficult to surgically resect with-out causing a significant neurologic deficit. Radiosurgery can treat these lesions, although it is limited to lesions <3 cm in diameter and has a 2-year lag time (i.e., the AVM may bleed in the interval). Embolization reduces flow through the AVM. It is usually considered adjunctive therapy, but it may serve as the sole treatment for deep, inaccessible lesions.4Brunicardi_Ch42_p1827-p1878.indd 185301/03/19 7:16 PM 1854SPECIFIC CONSIDERATIONSPART IITUMORS OF THE | Surgery_Schwartz. for the AVM usually is delayed 3 to 4 weeks to allow the brain to recover from acute injury. There is less risk of devastating early rebleeding from AVMs, and vasospasm is much less common. Three therapeutic modalities for AVMs are currently in common use: microsurgical exci-sion, interventional radiology or endovascular embolization, and stereotactic radiosurgery (SRS). AVMs that are large, near eloquent cortex, or that drain to deep venous structures are con-sidered high grade and more difficult to surgically resect with-out causing a significant neurologic deficit. Radiosurgery can treat these lesions, although it is limited to lesions <3 cm in diameter and has a 2-year lag time (i.e., the AVM may bleed in the interval). Embolization reduces flow through the AVM. It is usually considered adjunctive therapy, but it may serve as the sole treatment for deep, inaccessible lesions.4Brunicardi_Ch42_p1827-p1878.indd 185301/03/19 7:16 PM 1854SPECIFIC CONSIDERATIONSPART IITUMORS OF THE |
Surgery_Schwartz_12271 | Surgery_Schwartz | adjunctive therapy, but it may serve as the sole treatment for deep, inaccessible lesions.4Brunicardi_Ch42_p1827-p1878.indd 185301/03/19 7:16 PM 1854SPECIFIC CONSIDERATIONSPART IITUMORS OF THE CENTRAL NERVOUS SYSTEMA wide variety of tumors affect the brain and spine. Primary benign and malignant tumors arise from the various elements of the CNS, including neurons, glia, and meninges. Tumors metas-tasize to the CNS from many primary sources. Presenta-tion varies widely depending on relevant neuroanatomy. Prognosis depends on histology and anatomy. Modern brain tumor centers use team approaches to CNS tumors, as patients may require a combination of surgery (including newer, more minimally invasive approaches), radiation therapy, chemother-apy, SRS, and research protocol enrollment for studies assessing the efficacy of newer approaches such as immunotherapy. Tumors affecting the peripheral nervous system are discussed in the “Peripheral Nerve” section.Intracranial TumorsIntracranial | Surgery_Schwartz. adjunctive therapy, but it may serve as the sole treatment for deep, inaccessible lesions.4Brunicardi_Ch42_p1827-p1878.indd 185301/03/19 7:16 PM 1854SPECIFIC CONSIDERATIONSPART IITUMORS OF THE CENTRAL NERVOUS SYSTEMA wide variety of tumors affect the brain and spine. Primary benign and malignant tumors arise from the various elements of the CNS, including neurons, glia, and meninges. Tumors metas-tasize to the CNS from many primary sources. Presenta-tion varies widely depending on relevant neuroanatomy. Prognosis depends on histology and anatomy. Modern brain tumor centers use team approaches to CNS tumors, as patients may require a combination of surgery (including newer, more minimally invasive approaches), radiation therapy, chemother-apy, SRS, and research protocol enrollment for studies assessing the efficacy of newer approaches such as immunotherapy. Tumors affecting the peripheral nervous system are discussed in the “Peripheral Nerve” section.Intracranial TumorsIntracranial |
Surgery_Schwartz_12272 | Surgery_Schwartz | assessing the efficacy of newer approaches such as immunotherapy. Tumors affecting the peripheral nervous system are discussed in the “Peripheral Nerve” section.Intracranial TumorsIntracranial tumors can cause brain injury from mass effect, dys-function or destruction of adjacent neural structures, swelling, or abnormal electrical activity (seizures). Supratentorial tumors commonly present with focal neurologic deficit, such as contra-lateral limb weakness, visual field deficit, headache, or seizure. Infratentorial tumors often cause increased ICP due to hydro-cephalus from compression of the fourth ventricle, leading to headache, nausea, vomiting, or diplopia. Cerebellar hemisphere or brain stem dysfunction can result in ataxia, nystagmus, or cranial nerve palsies. Infratentorial tumors rarely cause seizures.All patients with symptoms concerning for brain tumor should undergo MRI with and without gadolinium. Gadolinium-based contrast can identify locations of blood-brain barrier | Surgery_Schwartz. assessing the efficacy of newer approaches such as immunotherapy. Tumors affecting the peripheral nervous system are discussed in the “Peripheral Nerve” section.Intracranial TumorsIntracranial tumors can cause brain injury from mass effect, dys-function or destruction of adjacent neural structures, swelling, or abnormal electrical activity (seizures). Supratentorial tumors commonly present with focal neurologic deficit, such as contra-lateral limb weakness, visual field deficit, headache, or seizure. Infratentorial tumors often cause increased ICP due to hydro-cephalus from compression of the fourth ventricle, leading to headache, nausea, vomiting, or diplopia. Cerebellar hemisphere or brain stem dysfunction can result in ataxia, nystagmus, or cranial nerve palsies. Infratentorial tumors rarely cause seizures.All patients with symptoms concerning for brain tumor should undergo MRI with and without gadolinium. Gadolinium-based contrast can identify locations of blood-brain barrier |
Surgery_Schwartz_12273 | Surgery_Schwartz | rarely cause seizures.All patients with symptoms concerning for brain tumor should undergo MRI with and without gadolinium. Gadolinium-based contrast can identify locations of blood-brain barrier break-down of tumors and, when used in conjunction with other MRI sequences, is essential in narrowing the differential diagnosis. Ini-tial management of a patient with a symptomatic brain tumor gen-erally includes dexamethasone for reduction of vasogenic edema, and phenytoin or levetiracetam if the patient has seized. Patients with significant weakness, lethargy, or hydrocephalus should be admitted for observation until definitive care is administered.Metastatic TumorsCerebral metastases are the most common type of intracranial tumor. Prolonged cancer patient survival and improved CNS imaging have increased the likelihood of diagnosing cerebral metastases. The sources of most cerebral metastases are (in decreasing frequency): lung, breast, kidney, GI tract, and mela-noma. Lung and breast | Surgery_Schwartz. rarely cause seizures.All patients with symptoms concerning for brain tumor should undergo MRI with and without gadolinium. Gadolinium-based contrast can identify locations of blood-brain barrier break-down of tumors and, when used in conjunction with other MRI sequences, is essential in narrowing the differential diagnosis. Ini-tial management of a patient with a symptomatic brain tumor gen-erally includes dexamethasone for reduction of vasogenic edema, and phenytoin or levetiracetam if the patient has seized. Patients with significant weakness, lethargy, or hydrocephalus should be admitted for observation until definitive care is administered.Metastatic TumorsCerebral metastases are the most common type of intracranial tumor. Prolonged cancer patient survival and improved CNS imaging have increased the likelihood of diagnosing cerebral metastases. The sources of most cerebral metastases are (in decreasing frequency): lung, breast, kidney, GI tract, and mela-noma. Lung and breast |
Surgery_Schwartz_12274 | Surgery_Schwartz | have increased the likelihood of diagnosing cerebral metastases. The sources of most cerebral metastases are (in decreasing frequency): lung, breast, kidney, GI tract, and mela-noma. Lung and breast cancers account for more than half of cerebral metastases. Metastatic cells usually travel to the brain hematogenously and frequently seed the gray-white junction due to characteristic blood vessel caliber change. Other com-mon locations are the cerebellum and the meninges. Menin-geal involvement may result in carcinomatous meningitis, also known as leptomeningeal carcinomatosis. MRI preand post-contrast administration is the study of choice for evaluation. Figure 42-20 demonstrates bilateral cerebellar metastases. These lesions are typically well circumscribed, round, and multiple. Such findings should prompt a metastatic work-up, including CT scan of the chest, abdomen, and pelvis, and a bone scan.Management largely depends upon the primary tumor, overall tumor burden, patient’s medical | Surgery_Schwartz. have increased the likelihood of diagnosing cerebral metastases. The sources of most cerebral metastases are (in decreasing frequency): lung, breast, kidney, GI tract, and mela-noma. Lung and breast cancers account for more than half of cerebral metastases. Metastatic cells usually travel to the brain hematogenously and frequently seed the gray-white junction due to characteristic blood vessel caliber change. Other com-mon locations are the cerebellum and the meninges. Menin-geal involvement may result in carcinomatous meningitis, also known as leptomeningeal carcinomatosis. MRI preand post-contrast administration is the study of choice for evaluation. Figure 42-20 demonstrates bilateral cerebellar metastases. These lesions are typically well circumscribed, round, and multiple. Such findings should prompt a metastatic work-up, including CT scan of the chest, abdomen, and pelvis, and a bone scan.Management largely depends upon the primary tumor, overall tumor burden, patient’s medical |
Surgery_Schwartz_12275 | Surgery_Schwartz | should prompt a metastatic work-up, including CT scan of the chest, abdomen, and pelvis, and a bone scan.Management largely depends upon the primary tumor, overall tumor burden, patient’s medical condition, and location and number of metastases. The beliefs of the patient and family regarding aggressive care must be considered, with the primary goal of optimizing survival time while maintaining or improv-ing neurological function. Neurosurgical intervention can be indicated for a number of reasons. Biopsy can be obtained to provide a tissue diagnosis and further direct therapy. Hydro-cephalus from increased intracranial pressure due to intracranial tumor burden can be temporized via placement of a ventricu-loperitoneal shunt. Craniotomy can be used for debulking of intracranial tumor burden or resection. Data from random-ized controlled trials have supported the use of craniotomy for tumor resection plus whole-brain radiation therapy (WBRT) or stereotactic radiosurgery (SRS) for | Surgery_Schwartz. should prompt a metastatic work-up, including CT scan of the chest, abdomen, and pelvis, and a bone scan.Management largely depends upon the primary tumor, overall tumor burden, patient’s medical condition, and location and number of metastases. The beliefs of the patient and family regarding aggressive care must be considered, with the primary goal of optimizing survival time while maintaining or improv-ing neurological function. Neurosurgical intervention can be indicated for a number of reasons. Biopsy can be obtained to provide a tissue diagnosis and further direct therapy. Hydro-cephalus from increased intracranial pressure due to intracranial tumor burden can be temporized via placement of a ventricu-loperitoneal shunt. Craniotomy can be used for debulking of intracranial tumor burden or resection. Data from random-ized controlled trials have supported the use of craniotomy for tumor resection plus whole-brain radiation therapy (WBRT) or stereotactic radiosurgery (SRS) for |
Surgery_Schwartz_12276 | Surgery_Schwartz | burden or resection. Data from random-ized controlled trials have supported the use of craniotomy for tumor resection plus whole-brain radiation therapy (WBRT) or stereotactic radiosurgery (SRS) for patients with a single surgically accessible metastatic lesion, compared to radiation therapy alone. In one randomized trial assessing surgery and WBRT vs. WBRT alone, local recurrence decreased and median 5ABFigure 42-19. A. Lateral view after injection of contrast dye in the left internal carotid artery demonstrates a 3 × 4 cm left frontal arteriove-nous malformation indicated by arrowheads. This image was taken 1.06 seconds after dye injection, and is referred to as an arterial phase image. B. Same view taken 4.10 seconds after dye injection, providing a venous phase image. The arrow points to the arteriovenous malfor-mation nidus. The arrowheads indicate two pathologically enlarged draining veins. ACA = anterior cerebral artery; ICA = internal carotid artery; MCA = middle cerebral | Surgery_Schwartz. burden or resection. Data from random-ized controlled trials have supported the use of craniotomy for tumor resection plus whole-brain radiation therapy (WBRT) or stereotactic radiosurgery (SRS) for patients with a single surgically accessible metastatic lesion, compared to radiation therapy alone. In one randomized trial assessing surgery and WBRT vs. WBRT alone, local recurrence decreased and median 5ABFigure 42-19. A. Lateral view after injection of contrast dye in the left internal carotid artery demonstrates a 3 × 4 cm left frontal arteriove-nous malformation indicated by arrowheads. This image was taken 1.06 seconds after dye injection, and is referred to as an arterial phase image. B. Same view taken 4.10 seconds after dye injection, providing a venous phase image. The arrow points to the arteriovenous malfor-mation nidus. The arrowheads indicate two pathologically enlarged draining veins. ACA = anterior cerebral artery; ICA = internal carotid artery; MCA = middle cerebral |
Surgery_Schwartz_12277 | Surgery_Schwartz | to the arteriovenous malfor-mation nidus. The arrowheads indicate two pathologically enlarged draining veins. ACA = anterior cerebral artery; ICA = internal carotid artery; MCA = middle cerebral artery.Brunicardi_Ch42_p1827-p1878.indd 185401/03/19 7:16 PM 1855NEUROSURGERYCHAPTER 42survival increased from 15 to 40 weeks.67 For multiple metas-tases, it should be noted that craniotomy primarily for resec-tion is typically not indicated unless all detectable metastases can be resected. It may however still be useful for symptomatic relief from a primary lesion. Recent data suggest that SRS (e.g. Gamma Knife) may be applied to multiple metastases in one session with improved outcome.68Glial TumorsGlial cells provide the anatomic and physiologic support for neurons and their processes in the brain. Tumors arising from glial cells are termed gliomas, and they represent the most com-mon primary brain tumor. The several types of glial cells give rise to distinct primary CNS | Surgery_Schwartz. to the arteriovenous malfor-mation nidus. The arrowheads indicate two pathologically enlarged draining veins. ACA = anterior cerebral artery; ICA = internal carotid artery; MCA = middle cerebral artery.Brunicardi_Ch42_p1827-p1878.indd 185401/03/19 7:16 PM 1855NEUROSURGERYCHAPTER 42survival increased from 15 to 40 weeks.67 For multiple metas-tases, it should be noted that craniotomy primarily for resec-tion is typically not indicated unless all detectable metastases can be resected. It may however still be useful for symptomatic relief from a primary lesion. Recent data suggest that SRS (e.g. Gamma Knife) may be applied to multiple metastases in one session with improved outcome.68Glial TumorsGlial cells provide the anatomic and physiologic support for neurons and their processes in the brain. Tumors arising from glial cells are termed gliomas, and they represent the most com-mon primary brain tumor. The several types of glial cells give rise to distinct primary CNS |
Surgery_Schwartz_12278 | Surgery_Schwartz | processes in the brain. Tumors arising from glial cells are termed gliomas, and they represent the most com-mon primary brain tumor. The several types of glial cells give rise to distinct primary CNS neoplasms.Astrocytoma. Astrocytoma is the most common primary CNS neoplasm. The term glioma often is used to refer to astrocyto-mas specifically, excluding other glial tumors. Astrocytomas are graded from I to IV. Grades I and II are referred to as low-grade astrocytoma or low grade glioma, grade III as anaplastic astro-cytoma, and grade IV as glioblastoma multiforme (GBM). Prog-nosis varies significantly between grades I/II, III, and IV, but not between I and II. Median survival is 8 years after diagnosis with a low-grade tumor, 2 to 3 years with an anaplastic astrocytoma, and roughly 1 year with a GBM. GBMs account for almost two-thirds of all astrocytomas, anaplastic astrocytomas account for two-thirds of the rest, and low-grade astrocytomas the remainder. Fig. 42-21 demonstrates the | Surgery_Schwartz. processes in the brain. Tumors arising from glial cells are termed gliomas, and they represent the most com-mon primary brain tumor. The several types of glial cells give rise to distinct primary CNS neoplasms.Astrocytoma. Astrocytoma is the most common primary CNS neoplasm. The term glioma often is used to refer to astrocyto-mas specifically, excluding other glial tumors. Astrocytomas are graded from I to IV. Grades I and II are referred to as low-grade astrocytoma or low grade glioma, grade III as anaplastic astro-cytoma, and grade IV as glioblastoma multiforme (GBM). Prog-nosis varies significantly between grades I/II, III, and IV, but not between I and II. Median survival is 8 years after diagnosis with a low-grade tumor, 2 to 3 years with an anaplastic astrocytoma, and roughly 1 year with a GBM. GBMs account for almost two-thirds of all astrocytomas, anaplastic astrocytomas account for two-thirds of the rest, and low-grade astrocytomas the remainder. Fig. 42-21 demonstrates the |
Surgery_Schwartz_12279 | Surgery_Schwartz | with a GBM. GBMs account for almost two-thirds of all astrocytomas, anaplastic astrocytomas account for two-thirds of the rest, and low-grade astrocytomas the remainder. Fig. 42-21 demonstrates the typical appearance of a GBM.The great majority of astrocytomas infiltrate adjacent brain. Juvenile pilocytic astrocytomas and pleomorphic xantho-astrocytomas are exceptions. These tumors are circumscribed, low grade, and associated with a good prognosis. Histologic features associated with higher grade include hypercellularity, nuclear atypia, and endovascular hyperplasia. Necrosis is pres-ent only with GBMs; it is required for the diagnosis.Gross total resection should be attempted for suspected astrocytomas. Motor cortex, language centers, deep or midline structures, or brainstem location may make this impossible without unacceptable, devastating neurologic deficit. Advanced imaging, such as diffusion tensor imaging (DTI) and functional MRI (fMRI), are seeing increased use as means of | Surgery_Schwartz. with a GBM. GBMs account for almost two-thirds of all astrocytomas, anaplastic astrocytomas account for two-thirds of the rest, and low-grade astrocytomas the remainder. Fig. 42-21 demonstrates the typical appearance of a GBM.The great majority of astrocytomas infiltrate adjacent brain. Juvenile pilocytic astrocytomas and pleomorphic xantho-astrocytomas are exceptions. These tumors are circumscribed, low grade, and associated with a good prognosis. Histologic features associated with higher grade include hypercellularity, nuclear atypia, and endovascular hyperplasia. Necrosis is pres-ent only with GBMs; it is required for the diagnosis.Gross total resection should be attempted for suspected astrocytomas. Motor cortex, language centers, deep or midline structures, or brainstem location may make this impossible without unacceptable, devastating neurologic deficit. Advanced imaging, such as diffusion tensor imaging (DTI) and functional MRI (fMRI), are seeing increased use as means of |
Surgery_Schwartz_12280 | Surgery_Schwartz | may make this impossible without unacceptable, devastating neurologic deficit. Advanced imaging, such as diffusion tensor imaging (DTI) and functional MRI (fMRI), are seeing increased use as means of assessing peritumoral structure and function to guide surgical decision-making. However, some lesions may be in such precarious regions as to be limited to stereotactic needle biopsy specimen. Gross total resection followed by fractioned radiotherapy (FRT) improves survival for all grades, although radiation therapy may be delayed until recurrence in low-grade tumors. Alongside FRT, adjuvant chemotherapy with temozolomide was demon-strated in a randomized controlled trial to increase short-term survival rate.69 Bevacizumab, an anti-VEGF antibody, is another treatment option under investigation. There are various ongoing research studies for GBM adjuvant therapy; these should be dis-cussed with the patient and family. Other options include Iotrex-containing balloons for conformal radiation | Surgery_Schwartz. may make this impossible without unacceptable, devastating neurologic deficit. Advanced imaging, such as diffusion tensor imaging (DTI) and functional MRI (fMRI), are seeing increased use as means of assessing peritumoral structure and function to guide surgical decision-making. However, some lesions may be in such precarious regions as to be limited to stereotactic needle biopsy specimen. Gross total resection followed by fractioned radiotherapy (FRT) improves survival for all grades, although radiation therapy may be delayed until recurrence in low-grade tumors. Alongside FRT, adjuvant chemotherapy with temozolomide was demon-strated in a randomized controlled trial to increase short-term survival rate.69 Bevacizumab, an anti-VEGF antibody, is another treatment option under investigation. There are various ongoing research studies for GBM adjuvant therapy; these should be dis-cussed with the patient and family. Other options include Iotrex-containing balloons for conformal radiation |
Surgery_Schwartz_12281 | Surgery_Schwartz | There are various ongoing research studies for GBM adjuvant therapy; these should be dis-cussed with the patient and family. Other options include Iotrex-containing balloons for conformal radiation brachytherapy (Glia-Site), placed in the resection cavity at the time of surgery ABFigure 42-20. A. Precontrast T1-weighted axial magnetic resonance imaging demonstrating bilateral hemorrhagic cerebellar metastases. Patient presented with ataxia and then lethargy progressing to deep coma. This patient has total effacement of the fourth ventricle and severe brain stem compression. The fourth ventricle cerebrospinal fluid space should be at the tip of the arrowhead. Patient recovered to normal mental status after emergent posterior fossa craniotomy. B. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a ring-enhancing lesion in the lateral left temporal lobe with moderate edema. The uncus (U) is compressing the left cerebral peduncle (CP) and displacing the brain stem to | Surgery_Schwartz. There are various ongoing research studies for GBM adjuvant therapy; these should be dis-cussed with the patient and family. Other options include Iotrex-containing balloons for conformal radiation brachytherapy (Glia-Site), placed in the resection cavity at the time of surgery ABFigure 42-20. A. Precontrast T1-weighted axial magnetic resonance imaging demonstrating bilateral hemorrhagic cerebellar metastases. Patient presented with ataxia and then lethargy progressing to deep coma. This patient has total effacement of the fourth ventricle and severe brain stem compression. The fourth ventricle cerebrospinal fluid space should be at the tip of the arrowhead. Patient recovered to normal mental status after emergent posterior fossa craniotomy. B. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a ring-enhancing lesion in the lateral left temporal lobe with moderate edema. The uncus (U) is compressing the left cerebral peduncle (CP) and displacing the brain stem to |
Surgery_Schwartz_12282 | Surgery_Schwartz | imaging demonstrating a ring-enhancing lesion in the lateral left temporal lobe with moderate edema. The uncus (U) is compressing the left cerebral peduncle (CP) and displacing the brain stem to the right.Brunicardi_Ch42_p1827-p1878.indd 185501/03/19 7:17 PM 1856SPECIFIC CONSIDERATIONSPART IIfor recurrence. Adjuvant therapy remains marginally effective; survival has changed little over the last several decades.Oligodendroglioma. Oligodendroglioma accounts for approx-imately 10% of gliomas, arising from the oligodendrocytes that create myelin in the CNS. They often present with seizures. Calcifications and hemorrhage on CT or MRI suggest the diag-nosis. Oligodendrogliomas are also graded from I to IV; grade portends prognosis. Prognosis is better overall than for astro-cytomas. Median survival ranges from 2 to 7 years for high-est and lowest grade tumors, respectively. Aggressive resection improves survival. Many oligodendrogliomas will respond to procarbazine, lomustine (CCNU), | Surgery_Schwartz. imaging demonstrating a ring-enhancing lesion in the lateral left temporal lobe with moderate edema. The uncus (U) is compressing the left cerebral peduncle (CP) and displacing the brain stem to the right.Brunicardi_Ch42_p1827-p1878.indd 185501/03/19 7:17 PM 1856SPECIFIC CONSIDERATIONSPART IIfor recurrence. Adjuvant therapy remains marginally effective; survival has changed little over the last several decades.Oligodendroglioma. Oligodendroglioma accounts for approx-imately 10% of gliomas, arising from the oligodendrocytes that create myelin in the CNS. They often present with seizures. Calcifications and hemorrhage on CT or MRI suggest the diag-nosis. Oligodendrogliomas are also graded from I to IV; grade portends prognosis. Prognosis is better overall than for astro-cytomas. Median survival ranges from 2 to 7 years for high-est and lowest grade tumors, respectively. Aggressive resection improves survival. Many oligodendrogliomas will respond to procarbazine, lomustine (CCNU), |
Surgery_Schwartz_12283 | Surgery_Schwartz | survival ranges from 2 to 7 years for high-est and lowest grade tumors, respectively. Aggressive resection improves survival. Many oligodendrogliomas will respond to procarbazine, lomustine (CCNU), and vincristine (PCV) che-motherapy. A particular chromosomal deletion, 1p19q, has been associated with robust response to the chemotherapeutic agent temozolomide. Radiation has not been clearly shown to prolong survival.Recent updates to brain tumor classification by the WHO (discussed in the following section) note that high-grade (at least II or III) oligodendrogliomas and astrocytomas are classi-fied together as diffuse gliomas. In fact, more similarity is seen between high-grade astrocytomas and oligodendrolgiomas than between high-grade astrocytomas and low-grade astrocytomas. Further discussion of this nosology is beyond the scope of this chapter, but implications for the future of neuro-oncology are discussed here.Ependymoma. The lining of the ventricular system consists of | Surgery_Schwartz. survival ranges from 2 to 7 years for high-est and lowest grade tumors, respectively. Aggressive resection improves survival. Many oligodendrogliomas will respond to procarbazine, lomustine (CCNU), and vincristine (PCV) che-motherapy. A particular chromosomal deletion, 1p19q, has been associated with robust response to the chemotherapeutic agent temozolomide. Radiation has not been clearly shown to prolong survival.Recent updates to brain tumor classification by the WHO (discussed in the following section) note that high-grade (at least II or III) oligodendrogliomas and astrocytomas are classi-fied together as diffuse gliomas. In fact, more similarity is seen between high-grade astrocytomas and oligodendrolgiomas than between high-grade astrocytomas and low-grade astrocytomas. Further discussion of this nosology is beyond the scope of this chapter, but implications for the future of neuro-oncology are discussed here.Ependymoma. The lining of the ventricular system consists of |
Surgery_Schwartz_12284 | Surgery_Schwartz | discussion of this nosology is beyond the scope of this chapter, but implications for the future of neuro-oncology are discussed here.Ependymoma. The lining of the ventricular system consists of cuboidal/columnar ependymal cells from which ependy-momas may arise. Although most pediatric ependymomas are supratentorial, two-thirds of adult ependymomas are infratento-rial. Supratentorial ependymomas arise from the lateral or third ventricles. The infratentorial tumors arise from the floor of the fourth ventricle (i.e., off the posterior brainstem). The most com-mon symptoms are headache, nausea, vomiting, or vertigo, sec-ondary to increased ICP from obstruction of CSF flow through the fourth ventricle. The tumors may grow out the foramina of Luschka to form a cerebellopontine angle mass. They may also spread through the CSF to form “drop mets” in the spinal canal. The two main histologic subtypes are papillary and anaplastic, the latter characterized by increased mitotic activity and | Surgery_Schwartz. discussion of this nosology is beyond the scope of this chapter, but implications for the future of neuro-oncology are discussed here.Ependymoma. The lining of the ventricular system consists of cuboidal/columnar ependymal cells from which ependy-momas may arise. Although most pediatric ependymomas are supratentorial, two-thirds of adult ependymomas are infratento-rial. Supratentorial ependymomas arise from the lateral or third ventricles. The infratentorial tumors arise from the floor of the fourth ventricle (i.e., off the posterior brainstem). The most com-mon symptoms are headache, nausea, vomiting, or vertigo, sec-ondary to increased ICP from obstruction of CSF flow through the fourth ventricle. The tumors may grow out the foramina of Luschka to form a cerebellopontine angle mass. They may also spread through the CSF to form “drop mets” in the spinal canal. The two main histologic subtypes are papillary and anaplastic, the latter characterized by increased mitotic activity and |
Surgery_Schwartz_12285 | Surgery_Schwartz | They may also spread through the CSF to form “drop mets” in the spinal canal. The two main histologic subtypes are papillary and anaplastic, the latter characterized by increased mitotic activity and areas of necrosis. Gross total resection often is impossible because the tumor arises from the brain stem. The goal of surgery is to achieve maximal resection without injuring the very delicate brainstem. Suboccipital craniotomy and midline separation of the cerebellar hemispheres allows access to tumors in the fourth ventricle. Postoperative radiation therapy significantly improves survival. Patients with CSF spread documented by LP or con-trast MRI should also have whole-spine radiation plus focused doses to visualized metastases.Choroid Plexus Papilloma. The choroid plexus is composed of many small vascular tufts covered with cuboidal epithelium. It represents part of the interface between blood and brain. The choroid cells create CSF from blood via ultrafiltration and release it into | Surgery_Schwartz. They may also spread through the CSF to form “drop mets” in the spinal canal. The two main histologic subtypes are papillary and anaplastic, the latter characterized by increased mitotic activity and areas of necrosis. Gross total resection often is impossible because the tumor arises from the brain stem. The goal of surgery is to achieve maximal resection without injuring the very delicate brainstem. Suboccipital craniotomy and midline separation of the cerebellar hemispheres allows access to tumors in the fourth ventricle. Postoperative radiation therapy significantly improves survival. Patients with CSF spread documented by LP or con-trast MRI should also have whole-spine radiation plus focused doses to visualized metastases.Choroid Plexus Papilloma. The choroid plexus is composed of many small vascular tufts covered with cuboidal epithelium. It represents part of the interface between blood and brain. The choroid cells create CSF from blood via ultrafiltration and release it into |
Surgery_Schwartz_12286 | Surgery_Schwartz | small vascular tufts covered with cuboidal epithelium. It represents part of the interface between blood and brain. The choroid cells create CSF from blood via ultrafiltration and release it into the ventricular system. Choroid plexus papil-lomas and choroid plexus carcinomas (rare, mostly pediatric) may arise from these cells. Papillomas usually occur in infants (typically supratentorial in the lateral ventricle) but also occur in adults (usually infratentorial in the fourth ventricle). Papillomas ABFigure 42-21. A. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a ring-enhancing lesion in the anteromedial right temporal lobe with central necrosis (dark area) consistent with glioblastoma multiforme. B. T2-weighted axial magnetic resonance imaging with extensive bright signal signifying peritumoral edema seen with glioblastoma multiformes.Brunicardi_Ch42_p1827-p1878.indd 185601/03/19 7:17 PM 1857NEUROSURGERYCHAPTER 42are well circumscribed and vividly | Surgery_Schwartz. small vascular tufts covered with cuboidal epithelium. It represents part of the interface between blood and brain. The choroid cells create CSF from blood via ultrafiltration and release it into the ventricular system. Choroid plexus papil-lomas and choroid plexus carcinomas (rare, mostly pediatric) may arise from these cells. Papillomas usually occur in infants (typically supratentorial in the lateral ventricle) but also occur in adults (usually infratentorial in the fourth ventricle). Papillomas ABFigure 42-21. A. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a ring-enhancing lesion in the anteromedial right temporal lobe with central necrosis (dark area) consistent with glioblastoma multiforme. B. T2-weighted axial magnetic resonance imaging with extensive bright signal signifying peritumoral edema seen with glioblastoma multiformes.Brunicardi_Ch42_p1827-p1878.indd 185601/03/19 7:17 PM 1857NEUROSURGERYCHAPTER 42are well circumscribed and vividly |
Surgery_Schwartz_12287 | Surgery_Schwartz | bright signal signifying peritumoral edema seen with glioblastoma multiformes.Brunicardi_Ch42_p1827-p1878.indd 185601/03/19 7:17 PM 1857NEUROSURGERYCHAPTER 42are well circumscribed and vividly enhance due to extensive vasculature. Like ependymomas, adult choroid plexus papillo-mas usually present with symptoms of increased ICP. Treatment is surgical excision. Total surgical excision is curative; recurrent papillomas should be re-resected. Radiation and chemotherapy are not indicated for papillomas. Radiation is adjunctive to aggressive surgery for carcinomas, but the results are generally poor.Neural Tumors and Mixed TumorsNeural and mixed tumors are a diverse group that includes tumors variously containing normal or abnormal neurons and/or normal or abnormal glial cells. Primitive neuroectodermal tumors arise from bipotential cells, capable of differentiating into neurons or glial cells.Medulloblastoma. Medulloblastoma is classically described as the most common type of primitive | Surgery_Schwartz. bright signal signifying peritumoral edema seen with glioblastoma multiformes.Brunicardi_Ch42_p1827-p1878.indd 185601/03/19 7:17 PM 1857NEUROSURGERYCHAPTER 42are well circumscribed and vividly enhance due to extensive vasculature. Like ependymomas, adult choroid plexus papillo-mas usually present with symptoms of increased ICP. Treatment is surgical excision. Total surgical excision is curative; recurrent papillomas should be re-resected. Radiation and chemotherapy are not indicated for papillomas. Radiation is adjunctive to aggressive surgery for carcinomas, but the results are generally poor.Neural Tumors and Mixed TumorsNeural and mixed tumors are a diverse group that includes tumors variously containing normal or abnormal neurons and/or normal or abnormal glial cells. Primitive neuroectodermal tumors arise from bipotential cells, capable of differentiating into neurons or glial cells.Medulloblastoma. Medulloblastoma is classically described as the most common type of primitive |
Surgery_Schwartz_12288 | Surgery_Schwartz | tumors arise from bipotential cells, capable of differentiating into neurons or glial cells.Medulloblastoma. Medulloblastoma is classically described as the most common type of primitive neuroectodermal tumor (PNET), although this term has been removed in the latest WHO classification of central nervous system tumors. Most occur in the first decade of life, but there is a second peak around age 30. Medulloblastoma is the most common malignant pediatric brain tumor. They are usually midline. Most occur in the cerebellum and present with symptoms of increased ICP. Histologic char-acteristics include densely packed small round cells with large nuclei and scant cytoplasm. They are generally not encapsulated, frequently disseminate within the CNS, and should undergo sur-gical resection followed by radiation therapy and chemotherapy.Ganglioglioma. Ganglioglioma is a mixed tumor in which both neurons and glial cells are neoplastic. They occur in the first three decades of life, often in the | Surgery_Schwartz. tumors arise from bipotential cells, capable of differentiating into neurons or glial cells.Medulloblastoma. Medulloblastoma is classically described as the most common type of primitive neuroectodermal tumor (PNET), although this term has been removed in the latest WHO classification of central nervous system tumors. Most occur in the first decade of life, but there is a second peak around age 30. Medulloblastoma is the most common malignant pediatric brain tumor. They are usually midline. Most occur in the cerebellum and present with symptoms of increased ICP. Histologic char-acteristics include densely packed small round cells with large nuclei and scant cytoplasm. They are generally not encapsulated, frequently disseminate within the CNS, and should undergo sur-gical resection followed by radiation therapy and chemotherapy.Ganglioglioma. Ganglioglioma is a mixed tumor in which both neurons and glial cells are neoplastic. They occur in the first three decades of life, often in the |
Surgery_Schwartz_12289 | Surgery_Schwartz | by radiation therapy and chemotherapy.Ganglioglioma. Ganglioglioma is a mixed tumor in which both neurons and glial cells are neoplastic. They occur in the first three decades of life, often in the medial temporal lobe, as circumscribed masses that may contain cysts or calcium and may enhance. The presenting symptom is usually a seizure, due to the medial temporal location. Patients have a good prognosis after complete surgical resection.Neural Crest TumorsMultipotent neural crest cells develop into a variety of dispa-rate cell types, including smooth muscle cells, sympathetic and parasympathetic neurons, melanocytes, Schwann cells, and arachnoid cap cells. They migrate in early development from the primitive neural tube throughout the body.Miscellaneous TumorsMeningioma. Meningiomas are derived from arachnoid cap cells of the arachnoid mater. They appear to arise from the dura mater grossly and on MRI and are commonly referred to as dural-based tumors. The most common intracranial | Surgery_Schwartz. by radiation therapy and chemotherapy.Ganglioglioma. Ganglioglioma is a mixed tumor in which both neurons and glial cells are neoplastic. They occur in the first three decades of life, often in the medial temporal lobe, as circumscribed masses that may contain cysts or calcium and may enhance. The presenting symptom is usually a seizure, due to the medial temporal location. Patients have a good prognosis after complete surgical resection.Neural Crest TumorsMultipotent neural crest cells develop into a variety of dispa-rate cell types, including smooth muscle cells, sympathetic and parasympathetic neurons, melanocytes, Schwann cells, and arachnoid cap cells. They migrate in early development from the primitive neural tube throughout the body.Miscellaneous TumorsMeningioma. Meningiomas are derived from arachnoid cap cells of the arachnoid mater. They appear to arise from the dura mater grossly and on MRI and are commonly referred to as dural-based tumors. The most common intracranial |
Surgery_Schwartz_12290 | Surgery_Schwartz | derived from arachnoid cap cells of the arachnoid mater. They appear to arise from the dura mater grossly and on MRI and are commonly referred to as dural-based tumors. The most common intracranial locations are along the falx (Fig. 42-22), the convexities (i.e., over the cerebral hemispheres), and the sphenoid wing. Less common locations include the foramen magnum, olfactory groove, and inside the lateral ventricle. Most are slow growing, encapsu-lated, benign tumors. Aggressive atypical or malignant menin-giomas may invade adjacent bone or cerebral cortex. Previous cranial irradiation increases the incidence of meningiomas. Approximately 10% of patients with a meningioma have multiple meningiomas. Total resection is curative, although involvement with small perforating arteries or cranial nerves may make total resection of skull base tumors impossible with-out significant neurologic deficit. The Simpson grading scale is used to characterize the extent of resection. Small, | Surgery_Schwartz. derived from arachnoid cap cells of the arachnoid mater. They appear to arise from the dura mater grossly and on MRI and are commonly referred to as dural-based tumors. The most common intracranial locations are along the falx (Fig. 42-22), the convexities (i.e., over the cerebral hemispheres), and the sphenoid wing. Less common locations include the foramen magnum, olfactory groove, and inside the lateral ventricle. Most are slow growing, encapsu-lated, benign tumors. Aggressive atypical or malignant menin-giomas may invade adjacent bone or cerebral cortex. Previous cranial irradiation increases the incidence of meningiomas. Approximately 10% of patients with a meningioma have multiple meningiomas. Total resection is curative, although involvement with small perforating arteries or cranial nerves may make total resection of skull base tumors impossible with-out significant neurologic deficit. The Simpson grading scale is used to characterize the extent of resection. Small, |
Surgery_Schwartz_12291 | Surgery_Schwartz | or cranial nerves may make total resection of skull base tumors impossible with-out significant neurologic deficit. The Simpson grading scale is used to characterize the extent of resection. Small, asymptom-atic meningiomas can be followed until symptomatic or until significant growth is documented on serial imaging studies. Atypical and malignant meningiomas may require postoperative radiation. Patients may develop recurrences from the surgical bed or distant de novo tumors.Vestibular Schwannoma (Acoustic Neuroma). Vestibular schwannomas predominantly arise from the superior half of the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII) (Fig. 42-23). Commonly, patients present with progressive hearing loss, tinnitus, or balance difficulty. Large tumors may cause brain stem compression and obstructive hydrocephalus. Bilateral acoustic neuromas are pathognomonic for neurofibro-matosis type 2 (NF2), a syndrome resulting from mutation of chromosome 22. NF2 patients | Surgery_Schwartz. or cranial nerves may make total resection of skull base tumors impossible with-out significant neurologic deficit. The Simpson grading scale is used to characterize the extent of resection. Small, asymptom-atic meningiomas can be followed until symptomatic or until significant growth is documented on serial imaging studies. Atypical and malignant meningiomas may require postoperative radiation. Patients may develop recurrences from the surgical bed or distant de novo tumors.Vestibular Schwannoma (Acoustic Neuroma). Vestibular schwannomas predominantly arise from the superior half of the vestibular portion of the vestibulocochlear nerve (cranial nerve VIII) (Fig. 42-23). Commonly, patients present with progressive hearing loss, tinnitus, or balance difficulty. Large tumors may cause brain stem compression and obstructive hydrocephalus. Bilateral acoustic neuromas are pathognomonic for neurofibro-matosis type 2 (NF2), a syndrome resulting from mutation of chromosome 22. NF2 patients |
Surgery_Schwartz_12292 | Surgery_Schwartz | stem compression and obstructive hydrocephalus. Bilateral acoustic neuromas are pathognomonic for neurofibro-matosis type 2 (NF2), a syndrome resulting from mutation of chromosome 22. NF2 patients have an increased incidence of spinal and cranial meningiomas and gliomas.Vestibular schwannomas may be treated with microsur-gical resection or SRS (Gamma Knife radiosurgery or linear accelerator technology). The main complication with treatment is damage to the facial nerve (cranial nerve VII), which runs through the internal auditory canal with the vestibulocochlear nerve. Risk of facial nerve dysfunction increases with increasing tumor diameter. SRS is preferred for tumors <3 cm, and micro-surgical resection for those >3 cm (SRS can be supplemented for any residual tumor following resection).Pituitary Adenoma. Pituitary adenomas arise from the anterior pituitary gland (adenohypophysis). Tumors <1 cm diameter are considered microadenomas; larger tumors are macroadenomas. Figure | Surgery_Schwartz. stem compression and obstructive hydrocephalus. Bilateral acoustic neuromas are pathognomonic for neurofibro-matosis type 2 (NF2), a syndrome resulting from mutation of chromosome 22. NF2 patients have an increased incidence of spinal and cranial meningiomas and gliomas.Vestibular schwannomas may be treated with microsur-gical resection or SRS (Gamma Knife radiosurgery or linear accelerator technology). The main complication with treatment is damage to the facial nerve (cranial nerve VII), which runs through the internal auditory canal with the vestibulocochlear nerve. Risk of facial nerve dysfunction increases with increasing tumor diameter. SRS is preferred for tumors <3 cm, and micro-surgical resection for those >3 cm (SRS can be supplemented for any residual tumor following resection).Pituitary Adenoma. Pituitary adenomas arise from the anterior pituitary gland (adenohypophysis). Tumors <1 cm diameter are considered microadenomas; larger tumors are macroadenomas. Figure |
Surgery_Schwartz_12293 | Surgery_Schwartz | resection).Pituitary Adenoma. Pituitary adenomas arise from the anterior pituitary gland (adenohypophysis). Tumors <1 cm diameter are considered microadenomas; larger tumors are macroadenomas. Figure 42-22. Postcontrast T1-weighted coronal magnetic reso-nance imaging demonstrating a brightly enhancing lesion arising from the falx cerebri with moderate edema and mass effect on the right lateral ventricle. This is a falcine meningioma. Note also the small separate meningioma arising from the dura over the cerebral convexity.Brunicardi_Ch42_p1827-p1878.indd 185701/03/19 7:17 PM 1858SPECIFIC CONSIDERATIONSPART IIPituitary tumors may be functional (i.e., secrete endocrinologi-cally active compounds at pathologic levels) or nonfunctional (i.e., secrete nothing or inactive compounds). Functional tumors are often diagnosed when quite small, due to endocrine dysfunc-tion. The most common endocrine syndromes are Cushing’s disease, due to adrenocorticotropic hormone secretion, ForbesAlbright | Surgery_Schwartz. resection).Pituitary Adenoma. Pituitary adenomas arise from the anterior pituitary gland (adenohypophysis). Tumors <1 cm diameter are considered microadenomas; larger tumors are macroadenomas. Figure 42-22. Postcontrast T1-weighted coronal magnetic reso-nance imaging demonstrating a brightly enhancing lesion arising from the falx cerebri with moderate edema and mass effect on the right lateral ventricle. This is a falcine meningioma. Note also the small separate meningioma arising from the dura over the cerebral convexity.Brunicardi_Ch42_p1827-p1878.indd 185701/03/19 7:17 PM 1858SPECIFIC CONSIDERATIONSPART IIPituitary tumors may be functional (i.e., secrete endocrinologi-cally active compounds at pathologic levels) or nonfunctional (i.e., secrete nothing or inactive compounds). Functional tumors are often diagnosed when quite small, due to endocrine dysfunc-tion. The most common endocrine syndromes are Cushing’s disease, due to adrenocorticotropic hormone secretion, ForbesAlbright |
Surgery_Schwartz_12294 | Surgery_Schwartz | tumors are often diagnosed when quite small, due to endocrine dysfunc-tion. The most common endocrine syndromes are Cushing’s disease, due to adrenocorticotropic hormone secretion, ForbesAlbright syndrome, due to prolactin secretion, and acromegaly, due to growth hormone secretion. Nonfunctional tumors are typically diagnosed as larger lesions causing mass effects such as visual field deficits due to compression of the optic chiasm or panhypopituita-rism due to compression of the gland. Figure 42-24 demonstrates a large pituitary adenoma. Hemorrhage into a pituitary tumor causes abrupt symptoms of headache, visual disturbance, decreased men-tal status, and endocrine dysfunction. This is known as pituitary apoplexy.Symptomatic pituitary tumors should be decompressed surgically to eliminate mass effect and/or to attempt an endo-crine cure. However, prolactin-secreting tumors (prolactinomas) usually shrink with dopaminergic therapy alone. First-line phar-macotherapy for small | Surgery_Schwartz. tumors are often diagnosed when quite small, due to endocrine dysfunc-tion. The most common endocrine syndromes are Cushing’s disease, due to adrenocorticotropic hormone secretion, ForbesAlbright syndrome, due to prolactin secretion, and acromegaly, due to growth hormone secretion. Nonfunctional tumors are typically diagnosed as larger lesions causing mass effects such as visual field deficits due to compression of the optic chiasm or panhypopituita-rism due to compression of the gland. Figure 42-24 demonstrates a large pituitary adenoma. Hemorrhage into a pituitary tumor causes abrupt symptoms of headache, visual disturbance, decreased men-tal status, and endocrine dysfunction. This is known as pituitary apoplexy.Symptomatic pituitary tumors should be decompressed surgically to eliminate mass effect and/or to attempt an endo-crine cure. However, prolactin-secreting tumors (prolactinomas) usually shrink with dopaminergic therapy alone. First-line phar-macotherapy for small |
Surgery_Schwartz_12295 | Surgery_Schwartz | eliminate mass effect and/or to attempt an endo-crine cure. However, prolactin-secreting tumors (prolactinomas) usually shrink with dopaminergic therapy alone. First-line phar-macotherapy for small prolactinomas is cabergoline, a dopamine agonist that inhibits production and secretion of prolactin, and is preferred over bromocriptine for its superior side effect profile. Consider surgery for prolactinomas with persistent mass effect or endocrinologic dysfunction in spite of adequate dopamine agonist therapy. Most pituitary tumors are approached transna-sally via the transsphenoidal approach, and minimally invasive, endoscopic surgical techniques are being used increasingly.Hemangioblastoma. Hemangioblastomas occur almost exclusively in the posterior fossa, with about 20% occurring in patients with von Hippel-Lindau (VHL) disease, a multisys-tem neoplastic disorder. Other tumors associated with VHL are renal cell carcinoma, pheochromocytoma, and retinal angio-mas. Many appear as cystic | Surgery_Schwartz. eliminate mass effect and/or to attempt an endo-crine cure. However, prolactin-secreting tumors (prolactinomas) usually shrink with dopaminergic therapy alone. First-line phar-macotherapy for small prolactinomas is cabergoline, a dopamine agonist that inhibits production and secretion of prolactin, and is preferred over bromocriptine for its superior side effect profile. Consider surgery for prolactinomas with persistent mass effect or endocrinologic dysfunction in spite of adequate dopamine agonist therapy. Most pituitary tumors are approached transna-sally via the transsphenoidal approach, and minimally invasive, endoscopic surgical techniques are being used increasingly.Hemangioblastoma. Hemangioblastomas occur almost exclusively in the posterior fossa, with about 20% occurring in patients with von Hippel-Lindau (VHL) disease, a multisys-tem neoplastic disorder. Other tumors associated with VHL are renal cell carcinoma, pheochromocytoma, and retinal angio-mas. Many appear as cystic |
Surgery_Schwartz_12296 | Surgery_Schwartz | with von Hippel-Lindau (VHL) disease, a multisys-tem neoplastic disorder. Other tumors associated with VHL are renal cell carcinoma, pheochromocytoma, and retinal angio-mas. Many appear as cystic tumors with an enhancing tumor on the cyst wall known as the mural nodule. Surgical resection is curative for sporadic (non-VHL associated) tumors. Pathology reveals abundant thin-walled vascular channels; internal debulk-ing may be bloody. En bloc resection of the mural nodule alone, leaving the cyst wall, is sufficient.Lymphoma. CNS lymphoma may arise either primarily in the CNS or secondarily from systemic disease. Recent rising inci-dence may be due to growing transplant and AIDS populations. Presenting symptoms include mental status changes, headache due to increased ICP, and cranial nerve palsy due to lymphoma-tous meningitis (analogous to carcinomatous meningitis). Often, lymphoma appears hyperdense on CT due to dense cellularity. Most lesions typically enhance with contrast on MRI, | Surgery_Schwartz. with von Hippel-Lindau (VHL) disease, a multisys-tem neoplastic disorder. Other tumors associated with VHL are renal cell carcinoma, pheochromocytoma, and retinal angio-mas. Many appear as cystic tumors with an enhancing tumor on the cyst wall known as the mural nodule. Surgical resection is curative for sporadic (non-VHL associated) tumors. Pathology reveals abundant thin-walled vascular channels; internal debulk-ing may be bloody. En bloc resection of the mural nodule alone, leaving the cyst wall, is sufficient.Lymphoma. CNS lymphoma may arise either primarily in the CNS or secondarily from systemic disease. Recent rising inci-dence may be due to growing transplant and AIDS populations. Presenting symptoms include mental status changes, headache due to increased ICP, and cranial nerve palsy due to lymphoma-tous meningitis (analogous to carcinomatous meningitis). Often, lymphoma appears hyperdense on CT due to dense cellularity. Most lesions typically enhance with contrast on MRI, |
Surgery_Schwartz_12297 | Surgery_Schwartz | palsy due to lymphoma-tous meningitis (analogous to carcinomatous meningitis). Often, lymphoma appears hyperdense on CT due to dense cellularity. Most lesions typically enhance with contrast on MRI, and can be differentiated by diffusion restriction on diffusion-weighted sequences. Surgical excision is not indicated. A stereotactic needle biopsy specimen usually confirms the diagnosis. Sub-sequent treatment includes steroids, whole-brain radiation, and chemotherapy. Intrathecal methotrexate is an additional treat-ment option.Embryologic TumorsEmbryologic tumors result from embryonal remnants that fail to involute completely or differentiate properly during development.Craniopharyngioma. Craniopharyngiomas are benign cystic lesions that occur in the sellar region that occur most frequently in children. A second peak of incidence also exists around 50 years of age. Craniopharyngiomas arise from remnant embry-onic tissue in the pituitary stalk. Calcification occurs in all pedi-atric and | Surgery_Schwartz. palsy due to lymphoma-tous meningitis (analogous to carcinomatous meningitis). Often, lymphoma appears hyperdense on CT due to dense cellularity. Most lesions typically enhance with contrast on MRI, and can be differentiated by diffusion restriction on diffusion-weighted sequences. Surgical excision is not indicated. A stereotactic needle biopsy specimen usually confirms the diagnosis. Sub-sequent treatment includes steroids, whole-brain radiation, and chemotherapy. Intrathecal methotrexate is an additional treat-ment option.Embryologic TumorsEmbryologic tumors result from embryonal remnants that fail to involute completely or differentiate properly during development.Craniopharyngioma. Craniopharyngiomas are benign cystic lesions that occur in the sellar region that occur most frequently in children. A second peak of incidence also exists around 50 years of age. Craniopharyngiomas arise from remnant embry-onic tissue in the pituitary stalk. Calcification occurs in all pedi-atric and |
Surgery_Schwartz_12298 | Surgery_Schwartz | in children. A second peak of incidence also exists around 50 years of age. Craniopharyngiomas arise from remnant embry-onic tissue in the pituitary stalk. Calcification occurs in all pedi-atric and roughly half of adult craniopharyngiomas. Symptoms result from compression of adjacent structures, especially the optic chiasm. Pituitary or hypothalamic dysfunction or hydro-cephalus may develop. Treatment is primarily surgical. Excision ABFigure 42-23. A. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a brightly enhancing mass on the right ves-tibular nerve with an enhancing tail going into the internal auditory canal (arrowhead). Pathology demonstrated vestibular schwannoma. B. Postcontrast T1-weighted sagittal magnetic resonance imaging of the same lesion, indicated by the arrowhead. Note small incidental meningioma at the top of the scan.Brunicardi_Ch42_p1827-p1878.indd 185801/03/19 7:17 PM 1859NEUROSURGERYCHAPTER 42is somewhat easier in children, as the | Surgery_Schwartz. in children. A second peak of incidence also exists around 50 years of age. Craniopharyngiomas arise from remnant embry-onic tissue in the pituitary stalk. Calcification occurs in all pedi-atric and roughly half of adult craniopharyngiomas. Symptoms result from compression of adjacent structures, especially the optic chiasm. Pituitary or hypothalamic dysfunction or hydro-cephalus may develop. Treatment is primarily surgical. Excision ABFigure 42-23. A. Postcontrast T1-weighted axial magnetic resonance imaging demonstrating a brightly enhancing mass on the right ves-tibular nerve with an enhancing tail going into the internal auditory canal (arrowhead). Pathology demonstrated vestibular schwannoma. B. Postcontrast T1-weighted sagittal magnetic resonance imaging of the same lesion, indicated by the arrowhead. Note small incidental meningioma at the top of the scan.Brunicardi_Ch42_p1827-p1878.indd 185801/03/19 7:17 PM 1859NEUROSURGERYCHAPTER 42is somewhat easier in children, as the |
Surgery_Schwartz_12299 | Surgery_Schwartz | by the arrowhead. Note small incidental meningioma at the top of the scan.Brunicardi_Ch42_p1827-p1878.indd 185801/03/19 7:17 PM 1859NEUROSURGERYCHAPTER 42is somewhat easier in children, as the tumor is often soft and easily suctioned. Adult tumors are often firm and adherent to adjacent vital structures. Visual loss, pituitary endocrine hypo-function, diabetes insipidus, and cognitive impairment from basal frontal injury are common complications.Epidermoid. Epidermoid tumors are cystic lesions with strati-fied squamous epithelial walls from trapped ectodermal cell rests that grow slowly and linearly by desquamation into the cyst cavity. The cysts contain keratin, cholesterol, and cellu-lar debris (Fig. 42-25). They occur most frequently in the cer-ebellopontine angle and may cause symptoms due to brainstem compression. Recurrent bouts of aseptic meningitis may occur due to release of irritative cyst contents into the subarachnoid space (Mollaret’s meningitis). Treatment is | Surgery_Schwartz. by the arrowhead. Note small incidental meningioma at the top of the scan.Brunicardi_Ch42_p1827-p1878.indd 185801/03/19 7:17 PM 1859NEUROSURGERYCHAPTER 42is somewhat easier in children, as the tumor is often soft and easily suctioned. Adult tumors are often firm and adherent to adjacent vital structures. Visual loss, pituitary endocrine hypo-function, diabetes insipidus, and cognitive impairment from basal frontal injury are common complications.Epidermoid. Epidermoid tumors are cystic lesions with strati-fied squamous epithelial walls from trapped ectodermal cell rests that grow slowly and linearly by desquamation into the cyst cavity. The cysts contain keratin, cholesterol, and cellu-lar debris (Fig. 42-25). They occur most frequently in the cer-ebellopontine angle and may cause symptoms due to brainstem compression. Recurrent bouts of aseptic meningitis may occur due to release of irritative cyst contents into the subarachnoid space (Mollaret’s meningitis). Treatment is |
Surgery_Schwartz_12300 | Surgery_Schwartz | symptoms due to brainstem compression. Recurrent bouts of aseptic meningitis may occur due to release of irritative cyst contents into the subarachnoid space (Mollaret’s meningitis). Treatment is surgical drainage and removal of the cyst wall. Intraoperative spillage of cyst contents may lead to severe chemical meningitis and must be avoided by containment and aspiration.Dermoid. Dermoids are less common than epidermoid tumors. They contain hair follicles and sebaceous glands in addition to a squamous epithelium. Dermoids may be found anywhere along the craniospinal axis. They are more commonly midline structures and are associated with more anomalies than epidermoids. They may be associated with trauma, as from a lumbar puncture that drags skin structures into the spine. Bacterial meningitis may occur when dermoids are associated with a dermal sinus tract. Treatment of symptomatic lesions is surgical resection, again with care to control cyst contents.Teratoma. Teratomas are germ | Surgery_Schwartz. symptoms due to brainstem compression. Recurrent bouts of aseptic meningitis may occur due to release of irritative cyst contents into the subarachnoid space (Mollaret’s meningitis). Treatment is surgical drainage and removal of the cyst wall. Intraoperative spillage of cyst contents may lead to severe chemical meningitis and must be avoided by containment and aspiration.Dermoid. Dermoids are less common than epidermoid tumors. They contain hair follicles and sebaceous glands in addition to a squamous epithelium. Dermoids may be found anywhere along the craniospinal axis. They are more commonly midline structures and are associated with more anomalies than epidermoids. They may be associated with trauma, as from a lumbar puncture that drags skin structures into the spine. Bacterial meningitis may occur when dermoids are associated with a dermal sinus tract. Treatment of symptomatic lesions is surgical resection, again with care to control cyst contents.Teratoma. Teratomas are germ |
Surgery_Schwartz_12301 | Surgery_Schwartz | may occur when dermoids are associated with a dermal sinus tract. Treatment of symptomatic lesions is surgical resection, again with care to control cyst contents.Teratoma. Teratomas are germ cell tumors that arise in the midline, often in the pineal region (the area behind the third ventricle, above the midbrain and cerebellum). They contain elements from all three embryonal layers: ectoderm, meso-derm, and endoderm. Teratomas may contain skin, cartilage, GI glands, and teeth. Teratomas with more primitive features are more malignant, while those with more differentiated tissues are more benign. Surgical excision may be attempted. However, the prognosis for malignant teratomas is very poor.Spinal TumorsApproximately 20% of CNS tumors occur in the spine, and a wide variety of spinal tumors exist. Unlike cranial tumors, the majority of spinal tumors are histologically benign. Under-standing two major spinal concepts—stability and neural com-pression—facilitates an understanding of the | Surgery_Schwartz. may occur when dermoids are associated with a dermal sinus tract. Treatment of symptomatic lesions is surgical resection, again with care to control cyst contents.Teratoma. Teratomas are germ cell tumors that arise in the midline, often in the pineal region (the area behind the third ventricle, above the midbrain and cerebellum). They contain elements from all three embryonal layers: ectoderm, meso-derm, and endoderm. Teratomas may contain skin, cartilage, GI glands, and teeth. Teratomas with more primitive features are more malignant, while those with more differentiated tissues are more benign. Surgical excision may be attempted. However, the prognosis for malignant teratomas is very poor.Spinal TumorsApproximately 20% of CNS tumors occur in the spine, and a wide variety of spinal tumors exist. Unlike cranial tumors, the majority of spinal tumors are histologically benign. Under-standing two major spinal concepts—stability and neural com-pression—facilitates an understanding of the |
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