Pain in Dementia Subtypes
If pain and its intensity can be accurately measured in dementia clients by considering the obstacles of communication and cognitive difficulties, do different dementias respond the same way to pain? The answer is probably not. According to neurologists, these variances in pain perception, response, tolerance, and threshold (the point at which pain is first sensed) are most likely due to neurological changes inherent to dementia subtypes.
In AD, the most studied dementia for pain research, neurologists believe loss of grey matter is the primary reason for differences in the effects of pain (Van Kooten et al, 2016). The structures of the pain network that assign meaning to pain are disrupted (Husebo et al, 2016), and there is a delay in the brain’s transmission and processing of sensory input and interpretation of pain (Gonzalez, 2015). Doctors also know autonomic responses (external signs of pain such as heart rate, respiration, pupil response, etc.) are blunted in Alzheimer’s patients (Gonzalez, 2015).
How does this information translate into pain for Alzheimer’s patients? In a nutshell, most studies show AD patients have a reduced pain experience when compared to controls (Binnekade et al, 2017). Their tolerance for pain increases, and they need more intense pain stimuli to elicit the same response as controls (those without AD). They perceive pain at the same starting point as those without AD, but their pain tolerance is much greater. And they rate their pain as lower than their CNAs or caregivers do. A friend’s wife provides us with an example of this phenomenon. She suddenly developed a pressure sore on her back that, although treated quickly, resulted in a silver dollar-sized wound that was half an inch deep. The pressure sore had to be suctioned, drained, and packed twice daily. Not once did she complain that it hurt or that procedures were uncomfortable. A patient without AD would require much local anesthesia for similar treatment. One other interesting aspect to pain perception in AD is a reduced placebo component to treatment (Achterberg and Lautenbacher, 2017). In the normal brain, a patient’s impression that an intervention will be effective can result in a beneficial outcome despite no treatment at all. The belief that a treatment will work is enough to produce a positive effect. This affective component is not typically seen in AD experiments.
In VaD, neurologists point to white matter lesions as the reason for changes in pain perception. Damage to white matter results in cells differentiating or taking over the function of others (Van Kooten et al, 2016). New infarcts may even cause the headaches which are so prevalent in this subtype: stroke victims also frequently report headaches (Scherder and Plooij, 2012). As a result of these changes in the brain, those with VaD have an increase or magnification in their perceived levels of pain (Gonzalez, 2015 and Van Kooten et al, 2016). They feel pain differently. When asked to self-report pain, those with VaD reported higher pain levels than their caregivers. Caregivers of these same clients reported pain in more locations than the client did. (Binnekade et al, 2017). Doctors attribute this finding to central neuropathic pain, which is common in VaD. This type of pain is thought to be the most undertreated type of pain in dementia (Scherder and Plooij, 2012).
Central neuropathic pain or central sensitization is a type of chronic pain syndrome caused by injury, change, or dysfunction to nerve pathways. The central nervous system does not properly process pain signals (www.arthritis.org, ret. 2019). Pain can be provoked by a benign stimulus (one that does not normally cause pain) or a higher level of pain than expected can be reported. Pain that starts in the body is amplified by the brain, causing heightened sensitivity to things that are not normally painful or making existing pain worse (Rath, 2017). It is unknown why this happens, but scientists hypothesize nerve cells “may become more efficient messengers” (Rath, 2017). Other symptoms may occur as a result of central sensitivity including anxiety, sleep problems, and depression.
In FTD (Frontotemporal Dementia), neurologists find atrophy, the loss and degeneration of brain cells, predominantly in the frontal cortex (Van Kooten et al, 2016). This area of the brain is related to emotional states and motivation. Since FTD is more prevalent in younger populations and pain is more prevalent in older populations, the limited number of FTD studies do not specifically address pain in isolation. Some studies measuring pain in conjunction with results do report a slower response to pain (Guerriero et al, 2016), a decrease in awareness of pain (Van Kooten et al, 2016), diminished expression of pain (Gonzalez, 2015), or an elevated pain threshold (Guerriero et al, 2016). Could these factors be related to the risk-taking and impulsivity frequently associated with FTD? Would a lack of awareness and decreased sensation of pain increase the incidence of such behaviors?
DLB (Dementia with Lewy Bodies) studies often occur in combination with trials assessing pain in PD as both diseases have Lewy body pathology. The percentage of patients with pain in PD (Parkinson’s Disease) is estimated to be between 40-60% (Van Kooten et al, 2016). It is believed that pain perception in DLB is changed, and that pain is common (Gonzalez, 2015). It is unknown how pain or its perception is altered.
Sources:
Achterberg W, Lautenbacher S. Editorial: Pain in dementia: A distressing combination of several factors. Current Alzheimer Research, 2017:14(5):468-470.
Binnekade T, Van Kooten J, Lobbezoo F, Rhebergen D, Van der Wouden C, Smallbrugge M, Sherder E. Pain experience in dementia subtypes: A systematic review. Current Alzheimer Research, 2017;14(5):471-485.
Gonzalez LCA. The neurologist facing pain in dementia. Neuralgia, 2015;30:574-585.
Guerriero F, Sgarlata C, Maurizi N, Francis M, Rollone M, Carbone M, Rondanelli M, Perna S, Ricevuti G. Pain management in dementia: so far, not so good. Journal of Gerontology-Geriatrics, 2016;64:31-39.
Husebo B, Achterberg W, Flo E. Identifying and managing pain in people with Alzheimer’s disease and other types of dementia: A systematic review. CNS Drugs, 2016;30:481-497.
Rath L. Your brain on pain: Changes in the central nervous system may explain why some pain becomes chronic. Arthritis Today, 2017;Nov/Dec:40.
Scherder E, Plooij B. Assessment and management of pain, with particular emphasis on central neuropathic pain, in moderate to severe dementia. Drugs & Aging, 2012;29(9):701-706.
Van Kooten J, Binnekade T, van der Wouden J, Stek M, Scherder E, Husebo B, Smallbrugge M, Hertogh C. A review of pain prevalence in Alzheimer’s, vascular, frontotemporal and lewy body dementias, Dement Geriatr Cogn Disord, 2016;41:220-232.