Question: What can visceral pain be accompanied by?

Answer: nausea and vomiting

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. <hl> It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. <hl> Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by <hl> nausea and vomiting <hl> and may be described as sickening, deep, squeezing, and dull. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.


Question: What type of pain are first degree burns classified as causing?

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.

Answer: Superficial

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. <hl> Superficial pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. <hl> Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.

Nociceptive pain may also be divided into "visceral", "deep somatic" and "superficial somatic" pain. Visceral structures are highly sensitive to stretch, ischemia and inflammation, but relatively insensitive to other stimuli that normally evoke pain in other structures, such as burning and cutting. Visceral pain is diffuse, difficult to locate and often referred to a distant, usually superficial, structure. It may be accompanied by nausea and vomiting and may be described as sickening, deep, squeezing, and dull. Deep somatic pain is initiated by stimulation of nociceptors in ligaments, tendons, bones, blood vessels, fasciae and muscles, and is dull, aching, poorly-localized pain. Examples include sprains and broken bones. <hl> Superficial <hl> pain is initiated by activation of nociceptors in the skin or other superficial tissue, and is sharp, well-defined and clearly located. Examples of injuries that produce superficial somatic pain include minor wounds and minor (first degree) burns.


Question: What percentage of people who've had upper limbs amputated feel phantom pain?

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

Answer: nearly 82%

<hl> The prevalence of phantom pain in upper limb amputees is nearly 82% , and in lower limb amputees is 54%. <hl> One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is <hl> nearly 82% <hl>, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is <hl> nearly 82% <hl> , and in lower limb amputees is 54%.


Question: What is the percentage of of phantom pain felt by lower limb amputees?

Answer: 54%

<hl> The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54% . <hl> One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is <hl> 54% <hl>. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is <hl> 54% <hl> .


Question: What may accompany urination for amputees?

Answer: phantom limb pain

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. <hl> One study found that eight days after amputation, 72 percent of patients had phantom limb pain , and six months later, 65 percent reported it. <hl> Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had <hl> phantom limb pain <hl>, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

One study found that eight days after amputation, 72 percent of patients had <hl> phantom limb pain <hl> , and six months later, 65 percent reported it.


Question: What may happen with intact body parts if there is continuous pain for a long period?

Answer: become sensitized

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. <hl> If the pain is continuous for a long period, parts of the intact body may become sensitized , so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation. <hl>

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may <hl> become sensitized <hl>, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

If the pain is continuous for a long period, parts of the intact body may <hl> become sensitized <hl> , so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.


Question: After six months, what percentage of people who had limbs amputated still felt pain in those limbs?

Answer: 65 percent

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. <hl> One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, 65 percent reported it. <hl> Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.

The prevalence of phantom pain in upper limb amputees is nearly 82%, and in lower limb amputees is 54%. One study found that eight days after amputation, 72 percent of patients had phantom limb pain, and six months later, <hl> 65 percent <hl> reported it. Some amputees experience continuous pain that varies in intensity or quality; others experience several bouts a day, or it may occur only once every week or two. It is often described as shooting, crushing, burning or cramping. If the pain is continuous for a long period, parts of the intact body may become sensitized, so that touching them evokes pain in the phantom limb, or phantom limb pain may accompany urination or defecation.


Question: What happens when an anesthetic injection is directed into the nerves a limb stump?

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Answer: may relieve pain

<hl> Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. <hl> Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Local anesthetic injections into the nerves or sensitive areas of the stump <hl> may relieve pain <hl> for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.


Question: How long can an anesthetic, at max, relieve pain for, despite wearing off in only hours?

Answer: permanently

<hl> Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently , despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. <hl> Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes <hl> permanently <hl>, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes <hl> permanently <hl> , despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain.


Question: What is injected in small amounts into the soft tissue between vertebrae to produce local pain?

Answer: hypertonic saline

<hl> Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. <hl> Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of <hl> hypertonic saline <hl> into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.


Question: Vibrating the stump of an amputee's limb can produce what in some patients?

Answer: relief

<hl> Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total relief from phantom pain. <hl> Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.

Local anesthetic injections into the nerves or sensitive areas of the stump may relieve pain for days, weeks, or sometimes permanently, despite the drug wearing off in a matter of hours; and small injections of hypertonic saline into the soft tissue between vertebrae produces local pain that radiates into the phantom limb for ten minutes or so and may be followed by hours, weeks or even longer of partial or total <hl> relief <hl> from phantom pain. Vigorous vibration or electrical stimulation of the stump, or current from electrodes surgically implanted onto the spinal cord, all produce relief in some patients.


Question: What is paraplegia?

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Answer: loss of sensation and voluntary motor control

<hl> Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. <hl> This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Paraplegia, the <hl> loss of sensation and voluntary motor control <hl> after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.


Question: What is the initial phantom body pain sensation experienced by people with spinal cord damage?

Answer: burning or tingling

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. <hl> This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. <hl> Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as <hl> burning or tingling <hl> but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.


Question: What can cause paraplegia?

Answer: serious spinal cord damage,

<hl> Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. <hl> This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Paraplegia, the loss of sensation and voluntary motor control after <hl> serious spinal cord damage, <hl> may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.


Question: What is an inefficient treatment for chronic pain which rarely provides any sort of true relief?

Answer: Surgical

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. <hl> Surgical treatment rarely provides lasting relief. <hl>

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. <hl> Surgical <hl> treatment rarely provides lasting relief.


Question: The sensation of a knife twisting in the flesh is an example of what type of pain?

Answer: phantom body

<hl> Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, phantom body pain in areas of complete sensory loss. <hl> This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.

Paraplegia, the loss of sensation and voluntary motor control after serious spinal cord damage, may be accompanied by girdle pain at the level of the spinal cord damage, visceral pain evoked by a filling bladder or bowel, or, in five to ten per cent of paraplegics, <hl> phantom body <hl> pain in areas of complete sensory loss. This phantom body pain is initially described as burning or tingling but may evolve into severe crushing or pinching pain, or the sensation of fire running down the legs or of a knife twisting in the flesh. Onset may be immediate or may not occur until years after the disabling injury. Surgical treatment rarely provides lasting relief.


Question: What triad are the inventory scales of hysteria, depression and hypochondriasis classified as?

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

Answer: neurotic

<hl> People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the " neurotic triad"). <hl> Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "<hl> neurotic <hl> triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the " <hl> neurotic <hl> triad").


Question: When people have long-term pain, what do they frequently display?

Answer: psychological disturbance

<hl> People with long-term pain frequently display psychological disturbance , with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). <hl> Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display <hl> psychological disturbance <hl>, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display <hl> psychological disturbance <hl> , with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad").


Question: Clinical evidence indicates that neuroticism is caused by what?

Answer: chronic pain

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). <hl> Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. <hl> When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to <hl> chronic pain <hl> causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.


Question: If long-term pain can be relieved by therapy, what does a person's neurotic triad score do?

Answer: fall

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. <hl> When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall , often to normal levels. <hl> Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety <hl> fall <hl>, often to normal levels. Self-esteem, often low in chronic pain patients, also shows improvement once pain has resolved.

When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety <hl> fall <hl> , often to normal levels.


Question: What shows improvement in many patients once their pain has been resolved?

Answer: Self-esteem

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. <hl> Self-esteem , often low in chronic pain patients, also shows improvement once pain has resolved. <hl>

People with long-term pain frequently display psychological disturbance, with elevated scores on the Minnesota Multiphasic Personality Inventory scales of hysteria, depression and hypochondriasis (the "neurotic triad"). Some investigators have argued that it is this neuroticism that causes acute pain to turn chronic, but clinical evidence points the other way, to chronic pain causing neuroticism. When long-term pain is relieved by therapeutic intervention, scores on the neurotic triad and anxiety fall, often to normal levels. <hl> Self-esteem <hl>, often low in chronic pain patients, also shows improvement once pain has resolved.

<hl> Self-esteem <hl> , often low in chronic pain patients, also shows improvement once pain has resolved.


Question: What is the term for pain which is acute and note alleviated by normal pain management?

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

Answer: Breakthrough

<hl> Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. <hl> It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

<hl> Breakthrough <hl> pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.


Question: How do cancer patients usually control their background pain?

Answer: medications

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. <hl> It is common in cancer patients who often have background pain that is generally well-controlled by medications , but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. <hl> The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by <hl> medications <hl>, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

It is common in cancer patients who often have background pain that is generally well-controlled by <hl> medications <hl> , but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication.


Question: Who is breakthrough pain common among?

Answer: cancer patients

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. <hl> It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. <hl> The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in <hl> cancer patients <hl> who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of opioids, including fentanyl.


Question: What class of medication is fentanyl an example of?

Answer: opioids

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. <hl> Management of breakthrough pain can entail intensive use of opioids , including fentanyl. <hl>

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. Management of breakthrough pain can entail intensive use of <hl> opioids <hl>, including fentanyl.

Management of breakthrough pain can entail intensive use of <hl> opioids <hl> , including fentanyl.


Question: What activity in relation to breakthrough pain requires heavy use of opiods?

Answer: Management

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. <hl> Management of breakthrough pain can entail intensive use of opioids, including fentanyl. <hl>

Breakthrough pain is transitory acute pain that comes on suddenly and is not alleviated by the patient's normal pain management. It is common in cancer patients who often have background pain that is generally well-controlled by medications, but who also sometimes experience bouts of severe pain that from time to time "breaks through" the medication. The characteristics of breakthrough cancer pain vary from person to person and according to the cause. <hl> Management <hl> of breakthrough pain can entail intensive use of opioids, including fentanyl.


Question: Which type of injection has caused patients to report they have pain but aren't bothered by it?

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Answer: morphine

<hl> Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. <hl> Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with <hl> morphine <hl> injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.


Question: How much do some patients going through psychosurgery suffer from the sensation of pain?

Answer: little, or not at all

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. <hl> Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all . <hl> Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer <hl> little, or not at all <hl>. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer <hl> little, or not at all <hl> .


Question: IASP's definition of pain includes what aspect as an essential part?

Answer: unpleasantness

<hl> Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. <hl> Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Although <hl> unpleasantness <hl> is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.


Question: What is it possible to induce which is, contrary to expectations, devoid of unpleasantness?

Answer: a state described as intense pain

<hl> Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. <hl> Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce <hl> a state described as intense pain <hl> devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.


Question: What perspective towards pain are some people with perfectly normal nerves born with?

Answer: Indifference

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. <hl> Indifference to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus. <hl>

Although unpleasantness is an essential part of the IASP definition of pain, it is possible to induce a state described as intense pain devoid of unpleasantness in some patients, with morphine injection or psychosurgery. Such patients report that they have pain but are not bothered by it; they recognize the sensation of pain but suffer little, or not at all. <hl> Indifference <hl> to pain can also rarely be present from birth; these people have normal nerves on medical investigations, and find pain unpleasant, but do not avoid repetition of the pain stimulus.


Question: An abnormality of the nervous system can render a small number of people insensitive to what?

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

Answer: pain

<hl> A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". <hl> Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

A much smaller number of people are insensitive to <hl> pain <hl> due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.


Question: What is it known as when someone is born without being able to feel pain because of their nervous system?

Answer: congenital insensitivity to pain

<hl> A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as " congenital insensitivity to pain ". <hl> Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "<hl> congenital insensitivity to pain <hl>". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as " <hl> congenital insensitivity to pain <hl> ".


Question: What happens to children with congenital insensitivity to pain?

Answer: repeated damage to their tongues, eyes, joints, skin, and muscles

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". <hl> Children with this condition incur carelessly- repeated damage to their tongues, eyes, joints, skin, and muscles . <hl> Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-<hl> repeated damage to their tongues, eyes, joints, skin, and muscles <hl>. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

Children with this condition incur carelessly- <hl> repeated damage to their tongues, eyes, joints, skin, and muscles <hl> .


Question: What is the life expectancy for people who can't feel pain?

Answer: reduced

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. <hl> Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). <hl> These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a <hl> reduced <hl> life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.


Question: What gene is responsible for coding for a sodium channel necessary for conducting pain nerve stimuli?

Answer: SCN9A

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. <hl> A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the SCN9A gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli. <hl>

A much smaller number of people are insensitive to pain due to an inborn abnormality of the nervous system, known as "congenital insensitivity to pain". Children with this condition incur carelessly-repeated damage to their tongues, eyes, joints, skin, and muscles. Some die before adulthood, and others have a reduced life expectancy.[citation needed] Most people with congenital insensitivity to pain have one of five hereditary sensory and autonomic neuropathies (which includes familial dysautonomia and congenital insensitivity to pain with anhidrosis). These conditions feature decreased sensitivity to pain together with other neurological abnormalities, particularly of the autonomic nervous system. A very rare syndrome with isolated congenital insensitivity to pain has been linked with mutations in the <hl> SCN9A <hl> gene, which codes for a sodium channel (Nav1.7) necessary in conducting pain nerve stimuli.


Question: When was Descartes pontificating about his theories regarding pain?

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

Answer: 1644

<hl> In 1644 , René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. <hl> Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In <hl> 1644 <hl>, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In <hl> 1644 <hl> , René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed].


Question: What did Descartes think pain was?

Answer: a disturbance

<hl> In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. <hl> Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In 1644, René Descartes theorized that pain was <hl> a disturbance <hl> that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.


Question: What state does the intensive theory conceive pain as being?

Answer: emotional

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". <hl> Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. <hl> By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an <hl> emotional <hl> state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.


Question: What theory perceives pain as being a specific sensation?

Answer: Specificity

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. <hl> Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". <hl> Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. <hl> Specificity <hl> theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.


Question: Who migrated to the theory of specificity en mass?

Answer: psychologists

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. <hl> By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by psychologists . <hl> However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

In 1644, René Descartes theorized that pain was a disturbance that passed down along nerve fibers until the disturbance reached the brain, a development that transformed the perception of pain from a spiritual, mystical experience to a physical, mechanical sensation[citation needed]. Descartes's work, along with Avicenna's, prefigured the 19th-century development of specificity theory. Specificity theory saw pain as "a specific sensation, with its own sensory apparatus independent of touch and other senses". Another theory that came to prominence in the 18th and 19th centuries was intensive theory, which conceived of pain not as a unique sensory modality, but an emotional state produced by stronger than normal stimuli such as intense light, pressure or temperature. By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by <hl> psychologists <hl>. However, after a series of clinical observations by Henry Head and experiments by Max von Frey, the psychologists migrated to specificity almost en masse, and by century's end, most textbooks on physiology and psychology were presenting pain specificity as fact.

By the mid-1890s, specificity was backed mostly by physiologists and physicians, and the intensive theory was mostly backed by <hl> psychologists <hl> .


Question: What year was peripheral pattern theory developed?

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

Answer: 1955

<hl> In 1955 , DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. <hl> They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In <hl> 1955 <hl>, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In <hl> 1955 <hl> , DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe.


Question: Whose suggestion prompted the development of peripheral pattern theory?

Answer: John Paul Nafe

<hl> In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe . <hl> They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by <hl> John Paul Nafe <hl>. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by <hl> John Paul Nafe <hl> .


Question: What does the gate control theory specify the diameter of which is responsible for the amount of pain sensation?

Answer: nerve fibers

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". <hl> The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. <hl> Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) <hl> nerve fibers <hl> carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].


Question: What did DC Sinclair and G Weddell propose a property of all skin fiber endings is?

Answer: identical

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. <hl> They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical , and that pain is produced by intense stimulation of these fibers. <hl> Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are <hl> identical <hl>, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain[citation needed].

They proposed that all skin fiber endings (with the exception of those innervating hair cells) are <hl> identical <hl> , and that pain is produced by intense stimulation of these fibers.


Question: Why were peripheral pattern theory and gate control theory left behind?

Answer: superseded by more modern theories of pain

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. <hl> Both peripheral pattern theory and gate control theory have been superseded by more modern theories of pain [citation needed]. <hl>

In 1955, DC Sinclair and G Weddell developed peripheral pattern theory, based on a 1934 suggestion by John Paul Nafe. They proposed that all skin fiber endings (with the exception of those innervating hair cells) are identical, and that pain is produced by intense stimulation of these fibers. Another 20th-century theory was gate control theory, introduced by Ronald Melzack and Patrick Wall in the 1965 Science article "Pain Mechanisms: A New Theory". The authors proposed that both thin (pain) and large diameter (touch, pressure, vibration) nerve fibers carry information from the site of injury to two destinations in the dorsal horn of the spinal cord, and that the more large fiber activity relative to thin fiber activity at the inhibitory cell, the less pain is felt. Both peripheral pattern theory and gate control theory have been <hl> superseded by more modern theories of pain <hl>[citation needed].

Both peripheral pattern theory and gate control theory have been <hl> superseded by more modern theories of pain <hl> [citation needed].


Question: How many dimensions did Melzack and Casey describe pain in terms of?

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

Answer: three

<hl> In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). <hl> They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its <hl> three <hl> dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)


Question: The affective-motivational dimension of pain is characterized by what urge?

Answer: urge to escape the unpleasantness

<hl> In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness ), and "cognitive-evaluative" <hl> (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and <hl> urge to escape the unpleasantness <hl>), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and <hl> urge to escape the unpleasantness <hl> ), and "cognitive-evaluative"


Question: What did Melzack and Casey theorize could influence the perception of the magnitude of pain?

Answer: cognitive activities

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). <hl> They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. <hl> Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" <hl> cognitive activities <hl> can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)


Question: War game excitement appears to block what aspect of pain?

Answer: dimensions

<hl> In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three dimensions : "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). <hl> They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three <hl> dimensions <hl>: "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion). They theorized that pain intensity (the sensory discriminative dimension) and unpleasantness (the affective-motivational dimension) are not simply determined by the magnitude of the painful stimulus, but "higher" cognitive activities can influence perceived intensity and unpleasantness. Cognitive activities "may affect both sensory and affective experience or they may modify primarily the affective-motivational dimension. Thus, excitement in games or war appears to block both dimensions of pain, while suggestion and placebos may modulate the affective-motivational dimension and leave the sensory-discriminative dimension relatively undisturbed." (p. 432) The paper ends with a call to action: "Pain can be treated not only by trying to cut down the sensory input by anesthetic block, surgical intervention and the like, but also by influencing the motivational-affective and cognitive factors as well." (p. 435)

In 1968 Ronald Melzack and Kenneth Casey described pain in terms of its three <hl> dimensions <hl> : "sensory-discriminative" (sense of the intensity, location, quality and duration of the pain), "affective-motivational" (unpleasantness and urge to escape the unpleasantness), and "cognitive-evaluative" (cognitions such as appraisal, cultural values, distraction and hypnotic suggestion).