Neural substrate of emotion in man : a study in methodology

Emotional behaviour has several components, which include emotional perception, emotional expression, autonomic reactivity, and inner subjective experience. It is hypothesised that these different processes can be selectively disturbed after brain damage. However, emotional and cognitive deficits usually co-exist in a particular patient, and the relationship between cognition and emotion is discussed. Animal data indicate that, following an initial sensory analysis in primary and association cortex, a stimulus acquires emotional significance by interfacing with "limbic" processes through multimodal cortex. Emotional expressions also develop in the course of similar multistage integrations between motor and limbic processes. This suggests three possible relationships between cognitive and emotional deficit. First, an inability to either perceive or express emotion may be directly due to various primary "non-emotional" perceptuo-motor deficits. Secondly, damage to neural sites where limbic and sensori-motor systems interface may produce deficits which are simultaneously cognitive and emotional. For example, perseverative behaviour in the Wisconsin Card Sorting Test and inability to control emotional impulses may be different aspects of a single deficit, which is indissociably cognitive and emotional. Thirdly, there may be a class of "pure" emotional deficits, which are not associated with perceptuo-motor or cognitive deficit. Tests based on the above classification approach were used to assess the effect of lesion site on emotional functioning. Cognitive function, emotional perception, emotional expression, subjective response, and autonomic reactivity were assessed in 48 patients with focal brain lesions, and 10 matched non-brain injured controls. Patients with anterior lesions were impaired relative to posteriors and controls in emotional perception and expression. These frontal deficits remained after statistical control of lesion variables (size, aetiology, and degree of bilateral involvement), and non-emotional perceptual, motor or cognitive impairments. Though such statistical controls provide suggestive evidence of a specific emotional deficit, they cannot completely eliminate the possibility that the frontal deficit is secondary to perceptuo-motor or cognitive impairment. Experimental strategies designed to provide more positive evidence of a specific emotional disorder were employed, and met with partial success. Dysphasia affected performance on tests of emotional perception and expression after left brain damage. Following right hemisphere damage, visual perceptual deficit contributed to impairment in emotional perception. There were indications that hemispheric perceptual-cognitive asymmetries may not account for all right-left differences on the emotional subtests. However no current model of hemispheric emotional asymmetries could fully explain the present findings. For example, the data on emotional perception supported the view that the right hemisphere is specialised for attentional/emotional processes (Heilman et al, 1983), but neglect and emotional expression were not correlated. Also, the present data generally contradicted the hypothesis that positive and negative emotions are lateralised in the left and right hemispheres, respectively. The final chapter assesses the extent to which the data fit the proposed system for categorising emotional disorder. Limitations to the methods used in making this evaluation were discussed, and possible ways of overcoming these restrictions were briefly considered