Klinische Neurophysiologie 2012; 43 - V063
DOI: 10.1055/s-0032-1301466

Compensatory premotor activity during affective face processing in subclinical carriers of a single mutant Parkin allele

S Anders 1, B Sack 1, A Pohl 2, T Münte 1, C Klein 1, F Binkofski 2
  • 1Klinik für Neurologie, Universität zu Lübeck, Lübeck
  • 2Klinik für Neurologie, RWTH Aachen, Universitätsklinik, Aachen

Aims: Parkinson`s Disease (PD) has a long presymptomatic stage, which indicates a substantial capacity of the human brain to compensate for dopaminergic nerve degeneration before clinical manifestation of the disease. Neuroimaging studies in subclinical carriers of a single mutation in the Parkin or PINK1 gene provide evidence that increased motor-related cortical activity can compensate for progressive dopaminergic nerve degeneration in the presymptomatic stage of PD. However, it is currently unknown whether similar compensatory mechanisms are effective in non-motor basal ganglia-cortical gating loops. Here, we ask whether asymptomatic Parkin mutation carriers show altered patterns of brain activity during processing of affective facial gestures, and whether this might compensate for latent facial emotion recognition deficits.

Methods: Eight asymptomatic heterozygous Parkin mutation carriers and eight matched controls underwent fMRI and a subsequent facial emotion recognition task.

Results: Parkin mutation carriers showed stronger activity in the right IFGop (inferior frontal gyrus pars opercularis) during execution and perception of affective facial gestures than healthy controls. They also showed a slightly reduced ability to recognize facial emotions that was least severe in individuals who showed the strongest increase of IFGop activity. Additionally, Parkin mutation carriers showed a weaker-than-normal increase of activity in the left lateral orbitofrontal cortex (BA47), which was unrelated to facial emotion recognition ability.

Conclusion: Our findings are consistent with the hypothesis that compensatory activity in the ventral premotor cortex, a key area of the putative mirror neuron system, can reduce impairments in facial emotion recognition in subclinical Parkin mutation carriers. A break-down of this compensatory mechanism might lead to the impairment of facial expressivity and facial emotion recognition observed in manifest Parkinson’s disease.