Background: Pain continues to be underrecognized and undertreated in Alzheimer's disease (AD) while existing guidance about pain assessment and management in dementia is not widespread. Brain regions involved in pain processing and modulation are damaged during AD, and the pain experience in AD is not well understood. Experimental pain studies using psychophysics can further our understanding of the pain experience in AD, which may lead to improved assessment and management of pain in people living with AD. Objective: A systematic review was conducted to explicate the current understanding of experimentally evoked pain in AD from primary research using psychophysical methods. Data Sources: Peer-reviewed publications were found via PubMed, CINAHL, and PsycINFO. A total of 18 primary research, peer-reviewed full articles that met inclusion criteria were included, representing 929 total participants. Conclusions: Experimentally evoked pain in people with AD demonstrates that despite cognitive impairment and a reduced ability to effectively communicate, individuals with AD experience pain similar to or more unpleasant than cognitively intact older adults. This may mean amplified pain unpleasantness in people with AD. Implications for practice: Our current best practices need to be widely disseminated and put into clinical practice. Self-report of pain continues to be the gold standard, but it is ineffective for noncommunicative patients and those unable to understand pain scales or instructions because of memory/cognitive impairment. Instead, pain treatment should be ethically initiated based on patient reports and behaviors, caregiver/surrogate reports, review of the medical record for painful conditions, analgesic trials, and regular reassessments.
The purpose of this discursive manuscript is to review three distinct studies that used very similar research methods, allowing the results to be critically compared. Following a series of three fictional vignettes describing various clinical scenarios managing pain, we introduce the reader to the research method of pain psychophysics.Next, we discuss how the three research studies described compliment and contrast one another. The discursive review format offers nurses an overview of a research method seldom used by nursing scientists. Psychophysical experiments allow a unique opportunity to examine the neurobiology and psychology of the pain experience in people with dementia.
BackgroundPain continues to be underrecognized and undertreated in people with Alzheimer's disease (AD). The periaqueductal gray (PAG) is essential to pain processing and modulation yet is damaged by AD. While evidence exists of altered neural processing of pain in AD, there has not been a focused investigation of the PAG during pain in people with AD.PurposeTo investigate the role of the PAG in sensory and affective pain processing for people living with AD.MethodsParticipants from a larger study completed pain psychophysics assessments and then a perceptually-matched heat pain task (warmth, mild, and moderate pain) during a functional MRI scan. In this cross-sectional study, we examined blood oxygenation level-dependent (BOLD) responses in the PAG and other pain-related regions in participants with AD (n = 18) and cognitively intact older adults (age- and sex-matched, n = 18). Associations of BOLD percent signal change and psychophysics were also examined.ResultsThere were significant main effects of AD status on the temperature needed to reach each perception of warmth or pain, where people with AD reached higher temperatures. Furthermore, participants with AD rated mild and moderate pain as more unpleasant than controls. PAG BOLD activation was greater in AD relative to controls during warmth and mild pain percepts. No significant differences were found for moderate pain or in other regions of interest. Greater PAG activation during mild pain was associated with higher affective/unpleasantness ratings of mild pain in participants with AD but not in controls.ConclusionResults suggest a role for the PAG in altered pain responses in people with AD. The PAG is the primary source of endogenous opioid pain inhibition in the neuroaxis, thus, altered PAG function in AD suggests possible changes in descending pain inhibitory circuits. People with AD may have a greater risk of suffering from pain compared to cognitively intact older adults.
Pain is a multidimensional sensory and affective experience. People with Vascular Dementia (VaD) experience pain more intensely and have negative emotional responses. Further investigation is needed to understand the neurobiology of pain in VaD. We used experimental thermal pain in a cross-sectional design to determine if adults (age>64) with probable VaD experience increased pain intensity and increased pain unpleasantness during “mild” and “moderate” thermal pain. The final sample included 46 sex- and age-matched adults (23 VaD; 12 female) and controls (23 cognitively intact; 12 female) with an average age of 76.5 years (SD=7.5). Participants reported no daily analgesic use. We used a thermode placed on the thenar eminence to assess temperatures perceived as mild and moderate pain (°C) followed by unpleasantness ratings (0-20 scale). We assessed cognition and depression with the Mini-Mental State Exam (MMSE) and the Geriatric Depression Scale. After controlling for depression, and relative to controls, there was no statistically significant difference in the temperature at which people with VaD perceived mild or moderate pain (p = .086; Cohen’s d: mild=0.55, moderate=0.27). However, there was a statistically significant effect of VaD status on pain unpleasantness (p = .003). People with VaD reported mild and moderate pain as more unpleasant than controls (Cohen’s d = 0.79 and 0.60, respectively). Findings support previous work that people with VaD are at risk of experiencing more pain. Assessing pain intensity and affect can avoid under-treated pain in those with VaD.
Background: Pain consists of both sensory and affective networks. Literature exploring the effect of Alzheimer's disease (AD) on pain is limited. Some evidence suggests that the affective networks are impacted earlier while the sensory networks are preserved until late in the course of disease (Cole 2006). To examine the preservation
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