Disgust in Neurological Disorders. In The Handbook of Disgust Research (pp. 209-223).

Abstract

Recognition of disgust-related stimuli, disgust-related emotional responses and disgust-related emotional experiences are affected in many neurological disorders. Here, we propose a model of the putative “disgust system” in the brain, that maps recognition, responses and experience onto specific neural systems—the superior temporal cortex, the striatum (and basal ganglia) and the insular cortex. That basic mapping is used to explain the disgust-related changes in a range of neurological disorders. Recognition of facial expressions of disgust is affected in temporal lobe epilepsy, amyotrophic lateral sclerosis, Parkinson’s disease, frontotemporal dementia, and Huntington’s disease. From the point of view of the tripartite model discussed above, deficits in the recognition of disgust may not be too unexpected in these disorders. There is evidence for insular dysfunction in medial temporal lobe epilepsy, amyotrophic lateral sclerosis, behavioural variant frontotemporal dementia, Parkinson’s disease, and Huntington’s disease. All five disorders also show evidence of dysfunction of the superior temporal sulcus. Deficits in the processing of disgust-related prosody have also been found in Parkinson’s disease, medial temporal lobe epilepsy, amyotrophic lateral sclerosis, and Huntington’s disease, which again probably relate to anatomical changes in the superior temporal cortex. A loss of the capacity to demonstrate disgust-related facial expressions has been reported in Parkinson’s disease and frontotemporal dementia, as has reduced physiological responses to disgust-inducing film clips in Alzheimer’s disease, probably all secondary to changes at the level of the striatum. In contrast, the emotional experience of disgust is largely unaffected in many neurological disorders, with the exception of dementia with Lewy bodies and behavioural variant frontotemporal dementia, which have both been associated with a reduction in disgust-related experiences, possibly reflecting damage to the insular cortex. When disgust is directed at the self (self-disgust), experienced levels are actually higher (vs. healthy controls) both at baseline and in response to self-disgust inducing manipulations in Parkinson’s disease. Although disgust-related changes are largely untouched by current pharmacotherapies aimed at the core features of many neurological disorders, identifying the neural substrate for those changes is an important first step in the development of treatments targeting those changes—changes that can have a severe negative impact on the quality of life for many neurological patients.