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Objective: To test whether sensory temporal discrimination and
mental rotation can reveal differences between patients with earlyonset
parkinsonism, positive or negative for mutations in the parkin
gene compared to healthy controls.
Background: Abnormalities in temporal discrimination and mental
rotation have been described in various studies in primary dystonia
and Parkinson’s disease (PD) supporting the hypothesis of impaired
sensory processing and sensorimotor integration in those disorders.
So far these methods have not been applied to patients with earlyonset
parkinsonism and mutations in the parkin gene.
Methods: 6 parkin positive and 6 parkin negative patients with
early-onset parkinsonism, and 6 age matched controls were asked to
discriminate whether pairs of unimodal (visual, tactile) and crossmodal
(visuo-tactile) stimuli were simultaneous or sequential (temporal
discrimination threshold, TDT) and which stimulus preceded the
other (temporal order judgement, TOJ). In the mental rotation task
subjects had to judge the laterality of hands, feet, and a patch in a
face which covered the left or right eye. Reaction times (RT) and accuracy
were measured.
Results: Patients with mutations in the parkin gene showed significantly
higher thresholds for cross-modal TDT and TOJ, whereas parkin
negative patients were only impaired in cross-modal
TOJ. Accuracy in mentally rotating feet was significantly lower in
parkin positive patients than in controls, whereas RT revealed no differences
between the groups.
Conclusions: Since temporal discrimination of cross-modal stimuli
in contrast to unimodal stimuli requires the integrity of multisensory
integration in addition to temporal processing our results rather point
to a dysfunction of the former than to defective timing per se. Parkin
positive patients were less accurate in rotating feet and interestingly
there is a higher frequency of foot dystonia in these patients. However,
we did not find significant differences between patients with
and without mutations in the parkin gene, thus rather pointing to a
more general deficit of sensory processing and sensorimotor integration
in PD than to an association between the deficits and specific
genes or pathological processes.