Recent developments in pain in dementia
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《英国医生杂志》
1 Centre of Human Movement Sciences, Rijksuniversiteit Groningen, A Deusinglaan 1, 9713 AV Groningen, Netherlands, 2 Department of Clinical Neuropsychology, Vrije Universiteit, Van der Boechorststraat 1, 1081 BT Amsterdam, Netherlands, 3 Netherlands Institute of Brain Research, 1105 AZ Amsterdam, 4 College of Nursing, University of Iowa, Iowa City, IA 52333, USA, 5 Department of Nursing Home Medicine and EMGO-Institute, VU Medical Centre, 1081 BT Amsterdam, 6 Clinical Pharmacology Centre, University Hospital, 63000 Clermont-Ferrand, France, 7 Department of Neuroscience, University of Turin Medical School, 10125 Turin, Italy
Correspondence to: E Scherder eja.scherder@psy.vu.nl
Introduction
Several observational studies indicate that pain is undertreated among cognitively impaired elderly people. Fewer analgesics are prescribed for the oldest category of cancer patients (> 75 years) than for younger patients, and low cognitive performance was one of the independent predictors of this finding.5 In addition, people in advanced stages of dementia who have had hip fractures receive significantly less opioid analgesics than do those who are cognitively intact.6 Another remarkable finding is that the prevalence of use of analgesic is considerably lower among patients with Alzheimer's disease than in those with vascular dementia.7 One possible explanation for this finding is that an impairment in language, which limits patients' ability to communicate about their pain, is more common in Alzheimer's disease than in vascular dementia.8 These observations stress the importance of increasing our knowledge of pain recognition in this population.3
Assessment of the sensory-discriminative and motivational-affective aspects of pain
The processing of sensory-discriminative aspects occurs in the lateral pain system, whereas motivational-affective aspects are processed by the medial pain system.4 Although the distinction between these aspects of pain, and subsequently between the two pain systems, has so far received too little attention in clinical studies on pain in dementia, experimental pain studies have shown its importance. Registration of pain related somato-sensory evoked potentials in patients with severe dementia showed that the processing of pain that involves areas of the medial pain system (such as the anterior cingulate gyrus) was impaired, although the pain stimulus itself was perceived adequately (lateral pain system).18 Benedetti et al observed that the pain thresholds (a sensory-discriminative aspect) of patients with Alzheimer's disease did not differ from those of elderly people without dementia, whereas pain tolerance (a motivational-affective aspect) was significantly increased in the Alzheimer's disease group.19
The explanation of these findings is that areas that belong to the medial pain system (such as the thalamic intralaminar nuclei) and that play an important role in the motivational-affective processing of pain are severely affected in Alzheimer's disease.20 In contrast, the primary sensory areas (the lateral pain system) are relatively preserved in Alzheimer's disease,21 which explains the unchanged pain threshold (table 2). The lateral pain system does show some functional decline, however, as the sensory threshold was elevated in patients with Alzheimer's disease, compared with elderly people without dementia,22 and patients with Alzheimer's disease indicated that the pain they experienced was less intense.23 In other words, although patients with Alzheimer's disease may still perceive the presence of pain, they may experience its intensity and affective aspects to a lesser extent. Consequently, people with dementia may have difficulty understanding the meaning of the sensation and placing it in context. This could potentially explain the atypical behavioural responses observed in this population (such as frowning or fearful expressions, combativeness, withdrawal, and agitation).
Table 2 Relation between neuropathology and results of experimental and clinical studies with respect to influence of subtypes of dementia, and the influence of Parkinson's disease and multiple sclerosis without cognitive impairment, on motivational-affective aspects and presence or intensity of pain
In summary, with respect to Alzheimer's disease, the change in the processing of the affective components of experimental pain (higher tolerance) resembles the decrease in the motivational-affective components of clinical pain.23 This is noteworthy, as experimental studies often use acute pain stimuli (such as electrical stimuli),19 although most elderly people in nursing homes have persistent pain.24 Interestingly, the incidence, severity, and duration of post-lumbar puncture headache (an acute painful condition) were found to be low in patients with dementia,25 supporting the role of the medial pain system in processing the initial motivational-affective aspects of experimental acute pain.26 Persistent pain is characterised by "secondary" motivational-affective aspects of pain, however, in which the cognitive appraisal of the pain (for example, the future consequences of and behavioural responses to pain) plays a very important role.27 Instruments that assess pain in dementia should therefore focus on pain related cognitive processes as well.
To date, no experimental pain studies have been conducted in other subtypes of dementia, such as vascular dementia and frontotemporal dementia. A recent review of the neuropathology of these disorders indicates that atrophy in the prefrontal cortex in frontotemporal dementia and white matter lesions in vascular dementia, in which areas become disconnected (de-afferentiation), could be responsible for the clinically observed respective decrease and increase in the motivational-affective aspects of pain (table 2).28 The difference in pain experience between subtypes of dementia underscores that studies on pain should not focus solely on the general definitions of "cognitively impaired elderly people" or "elderly people with dementia." A systematic key word search of PubMed, however, shows that such broad diagnoses were still used in most pain studies in the past decade (1994-2004) (figure).
Number of clinical and experimental publications on pain in dementia, Alzheimer's disease, frontotemporal dementia, and vascular dementia between 1994 and 2004. Note that most of the papers do not distinguish the subtype of dementia
Future
Skoog I. Psychiatric epidemiology of old age: the H70 study—the NAPE lecture 2003. Acta Psychiatr Scand 2004;109: 4-18.
Horgas AL, Elliott AF. Pain assessment and management in persons with dementia. Nurs Clin North Am 2004;39: 593-606.
Herr K, Decker S. Assessment of pain in older adults with severe cognitive impairment. Ann Long Term Care 2004;12: 46-52.
Sewards TV, Sewards MA. The medial pain system: neural representations of the motivational aspect of pain. Brain Res Bull 2002;59: 163-80.
Bernabei R, Gambassi G, Lapane K, Landi F, Gatsoni C, Dunlop R, et al. Management of pain in elderly patients with cancer. JAMA 1998;279: 1877-82.
Morrison RS, Siu AL. A comparison of pain and its treatment in advanced dementia and cognitively intact patients with a hip fracture. J Pain Symptom Manage 2000;19: 240-8.
Semla TP, Cohen D, Paveza G, Eisdorfer C, Gorelick P, Luchins D, et al. Drug use patterns of persons with Alzheimer's disease and related disorders living in the community. J Am Geriatr Soc 1993;41: 408-13.
Lindeboom J, Weinstein HC. Neuropsychology of cognitive ageing, minimal cognitive impairment, Alzheimer's disease, and vascular cognitive impairment. Eur J Pharmacol 2004;490: 83-6.
Ferrell BA, Ferrell BR, Rivera L. Pain in cognitively impaired nursing home patients. J Pain Symptom Manage 1995;10: 591-8.
Scherder EJA, Bouma A. Visual analogue scales for pain assessment in Alzheimer's disease. Gerontology 2000;46: 47-53.
Closs SJ, Barr B, Briggs M, Cash K, Seers K. A comparison of five pain assessment scales for nursing home residents with varying degrees of cognitive impairment. J Pain Symptom Manage 2004;27: 196-205.
Herr KA, Spratt K, Mobily PR, Richardson G. Pain intensity assessment in older adults: use of experimental pain to compare psychometric properties and usability of selected pain scales with younger adults. Clin J Pain 2004;20: 207-19.
Hadjistavropoulos T, LaChapele DL, Hadjistavropoulos HD, Green S, Asmundson GJG. Using facial expressions to assess musculoskeletal pain in older persons. Eur J Pain 2002;6: 179-87.
Kovach CR, Weissman DE, Griffie J, Matson S, Muchka S. Assessment and treatment of discomfort for people with late-stage dementia. J Pain Symptom Manage 1999;18: 412-9.
Caligiuri MP, Peavy G, Galasko DR. Extrapyramidal signs and cognitive abilities in Alzheimer's disease. Int J Geriatr Psychiatry 2001;16: 907-11.
Rainero I, Vighetti S, Bergamasco B, Pinessi L, Benedetti F. Autonomic responses and pain perception in Alzheimer's disease. Eur J Pain 2000;4: 267-74.
Benedetti F, Arduino C, Vighetti S, Asteggiano G, Tarenzi L, Rainero I. Pain reactivity in Alzheimer patients with different degrees of cognitive impairment and brain electrical activity deterioration. Pain 2004;111: 22-9.
Yamamoto M, Kachi T, Igata A. Pain-related somatosensory evoked potentials in dementia. J Neurol Sci 1996;137: 117-9.
Benedetti F, Vighetti S, Ricco C, Lagna E, Bergamasco B, Pinessi L, et al. Pain threshold and pain tolerance in Alzheimer's disease. Pain 1999;80: 377-82.
Rüb U, Del Tredici K, Del Turco D, Braak H. The intralaminar nuclei assigned to the medial pain system and other components of this system are early and progressively affected by Alzheimer's disease-related cytoskeletal pathology. J Chem Neuroanat 2002;23: 279-90.
Dickson DW. Neuropathology of Alzheimer's disease and other dementias. Clin Geriatr Med 2001;17: 209-28.
Gibson SJ, Voukelatos X, Ames D, Flicker L, Helme RD. An examination of pain perception and cerebral event-related potentials following carbon dioxide laser stimulation in patients with Alzheimer's disease and age-matched control volunteers. Pain Res Manage 2001;6: 126-32.
Scherder EJA, Bouma A. Visual analogue scales for pain assessment in Alzheimer's disease. Gerontology 2000;46: 47-53.
Helme RD, Gibson SJ. The epidemiology of pain in elderly people. Clin Geriatr Med 2001;17: 417-31.
Blennow K, Wallin A, H?ger O. Low frequency of post-lumbar puncture headache in demented patients. Acta Neurol Scand 1993;88: 221-3.
Créac'h C, Henry P, Caillé J-M, Allard M. Functional MR imaging analysis of pain-related brain activation after acute mechanical stimulation. Am J Neuroradiol 2000;21: 1402-6.
Price DD. Psychological and neural mechanisms of the affective dimension of pain. Science 2000;288: 1769-72.
Scherder EJA, Sergeant JA, Swaab DF. Pain processing in dementia and its relation to neuropathology. Lancet Neurol 2003;2: 677-86.
Bacher Svendsen K, Staehelin Jensen T, Overvad K, Hansen HJ, Koch-Henriksen N, Bach FW. Pain in patients with multiple sclerosis: a population-based study. Arch Neurol 2003;60: 1089-94.
Waseem S, Gwinn-Hardy K. Pain in Parkinson's disease: common yet seldom recognized symptom is treatable. Postgrad Med 2001;110: 33-46.
Braak H, Rüb U, Sandmann-Keil D, Gai WP, de Vos RAI, Jansen Steur ENH, et al. Parkinson's disease: affection of brain stem nuclei controlling premotor and motor neurons of the somatomotor system. Acta Neuropathol 2000;99: 489-95.
Kakigi R, Kuroda Y, Neshige R, Endo C, Shibasaki H. Physiological study of the spinothalamic tract conduction in multiple sclerosis. J Neurol Sci 1992;107: 205-9.
Snider SR, Fahn S, Isgreen WP, Cote LJ. Primary sensory symptoms in parkinsonism. Neurology 1976;34: 957-9.(Erik Scherder, professor in movement sci)
Correspondence to: E Scherder eja.scherder@psy.vu.nl
Introduction
Several observational studies indicate that pain is undertreated among cognitively impaired elderly people. Fewer analgesics are prescribed for the oldest category of cancer patients (> 75 years) than for younger patients, and low cognitive performance was one of the independent predictors of this finding.5 In addition, people in advanced stages of dementia who have had hip fractures receive significantly less opioid analgesics than do those who are cognitively intact.6 Another remarkable finding is that the prevalence of use of analgesic is considerably lower among patients with Alzheimer's disease than in those with vascular dementia.7 One possible explanation for this finding is that an impairment in language, which limits patients' ability to communicate about their pain, is more common in Alzheimer's disease than in vascular dementia.8 These observations stress the importance of increasing our knowledge of pain recognition in this population.3
Assessment of the sensory-discriminative and motivational-affective aspects of pain
The processing of sensory-discriminative aspects occurs in the lateral pain system, whereas motivational-affective aspects are processed by the medial pain system.4 Although the distinction between these aspects of pain, and subsequently between the two pain systems, has so far received too little attention in clinical studies on pain in dementia, experimental pain studies have shown its importance. Registration of pain related somato-sensory evoked potentials in patients with severe dementia showed that the processing of pain that involves areas of the medial pain system (such as the anterior cingulate gyrus) was impaired, although the pain stimulus itself was perceived adequately (lateral pain system).18 Benedetti et al observed that the pain thresholds (a sensory-discriminative aspect) of patients with Alzheimer's disease did not differ from those of elderly people without dementia, whereas pain tolerance (a motivational-affective aspect) was significantly increased in the Alzheimer's disease group.19
The explanation of these findings is that areas that belong to the medial pain system (such as the thalamic intralaminar nuclei) and that play an important role in the motivational-affective processing of pain are severely affected in Alzheimer's disease.20 In contrast, the primary sensory areas (the lateral pain system) are relatively preserved in Alzheimer's disease,21 which explains the unchanged pain threshold (table 2). The lateral pain system does show some functional decline, however, as the sensory threshold was elevated in patients with Alzheimer's disease, compared with elderly people without dementia,22 and patients with Alzheimer's disease indicated that the pain they experienced was less intense.23 In other words, although patients with Alzheimer's disease may still perceive the presence of pain, they may experience its intensity and affective aspects to a lesser extent. Consequently, people with dementia may have difficulty understanding the meaning of the sensation and placing it in context. This could potentially explain the atypical behavioural responses observed in this population (such as frowning or fearful expressions, combativeness, withdrawal, and agitation).
Table 2 Relation between neuropathology and results of experimental and clinical studies with respect to influence of subtypes of dementia, and the influence of Parkinson's disease and multiple sclerosis without cognitive impairment, on motivational-affective aspects and presence or intensity of pain
In summary, with respect to Alzheimer's disease, the change in the processing of the affective components of experimental pain (higher tolerance) resembles the decrease in the motivational-affective components of clinical pain.23 This is noteworthy, as experimental studies often use acute pain stimuli (such as electrical stimuli),19 although most elderly people in nursing homes have persistent pain.24 Interestingly, the incidence, severity, and duration of post-lumbar puncture headache (an acute painful condition) were found to be low in patients with dementia,25 supporting the role of the medial pain system in processing the initial motivational-affective aspects of experimental acute pain.26 Persistent pain is characterised by "secondary" motivational-affective aspects of pain, however, in which the cognitive appraisal of the pain (for example, the future consequences of and behavioural responses to pain) plays a very important role.27 Instruments that assess pain in dementia should therefore focus on pain related cognitive processes as well.
To date, no experimental pain studies have been conducted in other subtypes of dementia, such as vascular dementia and frontotemporal dementia. A recent review of the neuropathology of these disorders indicates that atrophy in the prefrontal cortex in frontotemporal dementia and white matter lesions in vascular dementia, in which areas become disconnected (de-afferentiation), could be responsible for the clinically observed respective decrease and increase in the motivational-affective aspects of pain (table 2).28 The difference in pain experience between subtypes of dementia underscores that studies on pain should not focus solely on the general definitions of "cognitively impaired elderly people" or "elderly people with dementia." A systematic key word search of PubMed, however, shows that such broad diagnoses were still used in most pain studies in the past decade (1994-2004) (figure).
Number of clinical and experimental publications on pain in dementia, Alzheimer's disease, frontotemporal dementia, and vascular dementia between 1994 and 2004. Note that most of the papers do not distinguish the subtype of dementia
Future
Skoog I. Psychiatric epidemiology of old age: the H70 study—the NAPE lecture 2003. Acta Psychiatr Scand 2004;109: 4-18.
Horgas AL, Elliott AF. Pain assessment and management in persons with dementia. Nurs Clin North Am 2004;39: 593-606.
Herr K, Decker S. Assessment of pain in older adults with severe cognitive impairment. Ann Long Term Care 2004;12: 46-52.
Sewards TV, Sewards MA. The medial pain system: neural representations of the motivational aspect of pain. Brain Res Bull 2002;59: 163-80.
Bernabei R, Gambassi G, Lapane K, Landi F, Gatsoni C, Dunlop R, et al. Management of pain in elderly patients with cancer. JAMA 1998;279: 1877-82.
Morrison RS, Siu AL. A comparison of pain and its treatment in advanced dementia and cognitively intact patients with a hip fracture. J Pain Symptom Manage 2000;19: 240-8.
Semla TP, Cohen D, Paveza G, Eisdorfer C, Gorelick P, Luchins D, et al. Drug use patterns of persons with Alzheimer's disease and related disorders living in the community. J Am Geriatr Soc 1993;41: 408-13.
Lindeboom J, Weinstein HC. Neuropsychology of cognitive ageing, minimal cognitive impairment, Alzheimer's disease, and vascular cognitive impairment. Eur J Pharmacol 2004;490: 83-6.
Ferrell BA, Ferrell BR, Rivera L. Pain in cognitively impaired nursing home patients. J Pain Symptom Manage 1995;10: 591-8.
Scherder EJA, Bouma A. Visual analogue scales for pain assessment in Alzheimer's disease. Gerontology 2000;46: 47-53.
Closs SJ, Barr B, Briggs M, Cash K, Seers K. A comparison of five pain assessment scales for nursing home residents with varying degrees of cognitive impairment. J Pain Symptom Manage 2004;27: 196-205.
Herr KA, Spratt K, Mobily PR, Richardson G. Pain intensity assessment in older adults: use of experimental pain to compare psychometric properties and usability of selected pain scales with younger adults. Clin J Pain 2004;20: 207-19.
Hadjistavropoulos T, LaChapele DL, Hadjistavropoulos HD, Green S, Asmundson GJG. Using facial expressions to assess musculoskeletal pain in older persons. Eur J Pain 2002;6: 179-87.
Kovach CR, Weissman DE, Griffie J, Matson S, Muchka S. Assessment and treatment of discomfort for people with late-stage dementia. J Pain Symptom Manage 1999;18: 412-9.
Caligiuri MP, Peavy G, Galasko DR. Extrapyramidal signs and cognitive abilities in Alzheimer's disease. Int J Geriatr Psychiatry 2001;16: 907-11.
Rainero I, Vighetti S, Bergamasco B, Pinessi L, Benedetti F. Autonomic responses and pain perception in Alzheimer's disease. Eur J Pain 2000;4: 267-74.
Benedetti F, Arduino C, Vighetti S, Asteggiano G, Tarenzi L, Rainero I. Pain reactivity in Alzheimer patients with different degrees of cognitive impairment and brain electrical activity deterioration. Pain 2004;111: 22-9.
Yamamoto M, Kachi T, Igata A. Pain-related somatosensory evoked potentials in dementia. J Neurol Sci 1996;137: 117-9.
Benedetti F, Vighetti S, Ricco C, Lagna E, Bergamasco B, Pinessi L, et al. Pain threshold and pain tolerance in Alzheimer's disease. Pain 1999;80: 377-82.
Rüb U, Del Tredici K, Del Turco D, Braak H. The intralaminar nuclei assigned to the medial pain system and other components of this system are early and progressively affected by Alzheimer's disease-related cytoskeletal pathology. J Chem Neuroanat 2002;23: 279-90.
Dickson DW. Neuropathology of Alzheimer's disease and other dementias. Clin Geriatr Med 2001;17: 209-28.
Gibson SJ, Voukelatos X, Ames D, Flicker L, Helme RD. An examination of pain perception and cerebral event-related potentials following carbon dioxide laser stimulation in patients with Alzheimer's disease and age-matched control volunteers. Pain Res Manage 2001;6: 126-32.
Scherder EJA, Bouma A. Visual analogue scales for pain assessment in Alzheimer's disease. Gerontology 2000;46: 47-53.
Helme RD, Gibson SJ. The epidemiology of pain in elderly people. Clin Geriatr Med 2001;17: 417-31.
Blennow K, Wallin A, H?ger O. Low frequency of post-lumbar puncture headache in demented patients. Acta Neurol Scand 1993;88: 221-3.
Créac'h C, Henry P, Caillé J-M, Allard M. Functional MR imaging analysis of pain-related brain activation after acute mechanical stimulation. Am J Neuroradiol 2000;21: 1402-6.
Price DD. Psychological and neural mechanisms of the affective dimension of pain. Science 2000;288: 1769-72.
Scherder EJA, Sergeant JA, Swaab DF. Pain processing in dementia and its relation to neuropathology. Lancet Neurol 2003;2: 677-86.
Bacher Svendsen K, Staehelin Jensen T, Overvad K, Hansen HJ, Koch-Henriksen N, Bach FW. Pain in patients with multiple sclerosis: a population-based study. Arch Neurol 2003;60: 1089-94.
Waseem S, Gwinn-Hardy K. Pain in Parkinson's disease: common yet seldom recognized symptom is treatable. Postgrad Med 2001;110: 33-46.
Braak H, Rüb U, Sandmann-Keil D, Gai WP, de Vos RAI, Jansen Steur ENH, et al. Parkinson's disease: affection of brain stem nuclei controlling premotor and motor neurons of the somatomotor system. Acta Neuropathol 2000;99: 489-95.
Kakigi R, Kuroda Y, Neshige R, Endo C, Shibasaki H. Physiological study of the spinothalamic tract conduction in multiple sclerosis. J Neurol Sci 1992;107: 205-9.
Snider SR, Fahn S, Isgreen WP, Cote LJ. Primary sensory symptoms in parkinsonism. Neurology 1976;34: 957-9.(Erik Scherder, professor in movement sci)