The amygdala of patients with Parkinson's disease is silent in response to fearful facial expressions.

We previously found that patients with Parkinson's disease (PD) were impaired with respect to recognition of fear and disgust in facial expressions. To investigate the neural mechanisms that underlie this impairment, we recorded visual event-related potentials (ERPs) in response to the viewing of fearful facial expressions. Ten normal elderly volunteers and nine patients with PD were studied. Fearful, surprised, and neutral facial expressions were presented randomly for 500 ms each, with a probability of 0.1, 0.1, and 0.8, respectively. The locations of the components of the ERPs were analyzed using a scalp-skull-brain/dipole tracing method. The ERPs elicited in response to the facial stimuli consisted of a negative peak (N1), two positive peaks, and a subsequent slow negative shift. For N1, the equivalent current dipoles were concentrated in the fusiform gyrus, right superior temporal gyrus, parahippocampal gyrus, cingulate cortex, and cerebellum, in normal subjects. In response to the fearful stimulus, dipoles were also generated from the amygdala in seven out of 10 normal subjects. In contrast, in patients with PD, N1 was centered bilaterally in the angular gyrus and supramarginal gyrus, and there was no neuronal activity in the amygdala. After N1, dipoles moved toward the frontal region in normal subjects, whereas they remained in the parietal lobes in patients with PD. These results suggest that neither the amygdala nor the temporal visual-associated cortices are involved in responding to fearful expressions in patients with PD. Corticostriatal connections may be variably affected by a lack of dopamine or by pathological changes in the amygdala. Thus, somatosensory recruitment may overcome the mild cognitive emotional deficits that are present in patients with PD owing to a dysfunction of the amygdala.