The neurologist facing pain in dementia

Abstract

IntroductionAgeing, which commonly underlies dementia, is usually associated with painful conditions. Nevertheless, utility analgesics are underused in dementia patients due to their difficulty communicating. Dementia lesions are also situated on the nociceptive pathways. For this reason, the pain experienced is different and distinctive for every lesion type. DevelopmentThe lateral pain pathway (lateral thalamus and primary parietal cortex), which is in charge of primary pain perception, is preserved in dementia. Overall pain perception, including pain intensity and threshold, thus remains unmodified. The medial pain pathway includes the intralaminar thalamic nuclei, the pons (locus coeruleus: LC), the mesencephalon (periaqueductal grey: PG), the hypothalamus (paraventricular nuclei, mammillary bodies) and different areas of the parietal (primary, secondary, operculum), temporal (amygdala, hippocampus) and frontal (anterior cingulate cortex: ACC). Since these locations are affected by dementia lesions, pain features controlled by these areas will be compromised: the cognitive-evaluative and affective dimensions, pain memory, and autonomic responses. Alzheimer disease (AD) manifests with reduced anticipatory and avoidance responses and flattening of the autonomic responses. These alterations are essentially secondary to degenerative changes in the medial temporal lobe (pain memory) and ACC (cognitive and affective dimensions) areas. Vascular dementias feature a cortico-subcortical deafferentation secondary to white matter lesions, resulting in a state of hyperpathy and hyperalgesia. In frontotemporal dementias, there is a reduction in pain expression linked to lesions in the orbitofrontal and anterior temporal areas, which are responsible for the emotional component of pain. In Parkinson's disease, painful conditions are common. They are attributed to early damage to the LC, which reduces its antinociceptive activity. Finally, dementia patients expect nothing from analgesic treatments. This negates the placebo effect, which in addition to the drug's pharmacokinetic action is an inherent part of the analgesic response. The placebo response is related to activity in the ACC and PG, but because these areas are commonly affected by dementia, higher doses of analgesics will be necessary. ConclusionsAssessing pain in dementia is complex, which is why scarcity of the analgesic treatment is underprescribed in dementias. Assessments must be specific and pain scales are useful for examining expressive, motor, emotional, functional, and social interaction capacities. For communicative patients, simple visual scales are helpful, whereas multidimensional scales are the most suitable for non-communicative patients. Pain may be responsible for progression and cognitive deterioration in dementia. Since this aetiology is treatable and reversible, doctors should not hesitate to start analgesic treatment. In order to minimise the risk of adverse events, treatment must be both intensive and also closely monitored.