IBEC Seminar: Richard Reilly

All a question of Timing: Sensory processing in Dystonia and Parkinson’s Disease

There are many challenges in the diagnosis and management of neurological disorders. Neural Engineering can help address some of these by the development of novel engineering, computational and experimental methods to help understand the pathogenesis of neurological disorders. This talk will detail results from recent neural engineering studies into understanding cervical dystonia and Parkinson’s disease.

While the pathogenesis of cervical dystonia remains unknown, recent animal and clinical experimental studies have indicated its probable mechanisms. Human movement involves a complex series of coordinated musculoskeletal but also neural processes. A breakdown in any of these processes can result in irregular movement. The temporal discrimination threshold is the shortest time interval at which two sensory stimuli presented sequentially are detected as asynchronous by the observer. Studies in our group and that of others have shown that abnormal temporal discrimination is a mediational endophenotype of cervical dystonia and informs new concepts of disease pathogenesis. Our hypothesis is that both abnormal temporal discrimination and cervical dystonia are due to a disorder of the midbrain network for covert attentional orienting caused by reduced gamma-aminobutyric acid inhibition, resulting from, in turn, from as yet undetermined, genetic mutations. Such disinhibition is a) subclinically manifested by abnormal temporal discrimination due to prolonged duration firing of the visual sensory neurons in the superficial laminae of the superior colliculus, b) clinically manifested by cervical dystonia due to disinhibited burst activity of the cephalomotor neurons of the intermediate and deep laminae of the superior colliculus. Abnormal temporal discrimination in unaffected first-degree relatives of patients with cervical dystonia represents a subclinical manifestation of defective gamma-aminobutyric acid activity both within the superior colliculus and from the substantia nigra pars reticulata. This talk will review some our recent experiments addressing this hypothesis.

Sensory and perceptual disturbances are common in Parkinson’s disease. Subtle deficits of the sensory system, often not detected by routine examination, occur in people with Parkinson’s disease. From simple anosmia and impaired kinesthetic perception, to more complex visual hallucinations and spatiotemporal perceptual abnormalities, altered sensory processing is found across multiple modalities. Of note, integration of multiple environmental sensory inputs is crucial for a refined but complex goal-directed motor output (e.g. locomotion through a crowded environment). There is increasing evidence that these sensory deficits contribute to the pathophysiology of some of the abnormal motor features of Parkinson’s disease. This talk will review some of our recent experiments to probe multisensory deficits in Parkinson’s disease and introduce one intervention developed around sensory and cognitive processing.

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