Abnormal oscillatory synchronisation in the motor system leads to impaired movement

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Converging data suggest that abnormal synchronised oscillatory activity in the basal ganglia may contribute to bradykinesia in patients with Parkinson's disease. This synchrony preferentially occurs over 10–30 Hz, the so-called beta band. Correlative evidence has been supplemented by experiments in which direct stimulation of the basal ganglia in the beta band slows movement. Yet questions remain regarding the small scale of the latter effects and whether synchrony is an early or even obligatory feature of parkinsonism. Nevertheless, the principle that abnormally synchronised activity in the beta band can disrupt the function finds a precedent in the syndrome of cortical myoclonus. Here, pathologically synchronised discharges of pyramidal neurons are transmitted to the healthy spinal cord. The result is the synchronous discharge of motor units leading to rhythmic jerking.

Section snippets

Parkinson's disease

Parkinson's disease is a progressive age-related neurodegenerative disorder, affecting tens of millions of people worldwide. The disease is characterised by bradykinesia, rigidity and tremor. Tremor is most commonly present at rest and is of low frequency (4–5 Hz), but a faster tremor of around 8–10 Hz may appear on action or during postural contraction. The core, but not exclusive, pathology is the degeneration of the dopaminergic neurons in the substantia nigra pars compacta of the midbrain

Cortical myoclonus and the cerebellum

Despite the above issues, the principle that abnormally synchronised motor activity can disrupt function in otherwise normal targets seems reasonable and, indeed, finds precedent in the relatively obscure syndrome of cortical myoclonus (jerks). In this condition, various cerebral pathologies, such as neurodegenerative and auto-immune disease, lead to abnormally synchronised activity across pyramidal neurons in the motor cortex. In many instances, this synchronisation is rhythmic and assumes the

Conclusion

The evidence suggests that both basal ganglia and cerebellum may engage in abnormally synchronised oscillatory activity in the beta band in some motor disorders. The consequences of such synchronisation are dictated by several factors. First, is anatomy: the basal ganglia have widespread connectivity with cerebral cortex so that pathological beta synchrony leads to a strikingly multifaceted disease associated with bradykinesia and rigidity, but also impairments of complex movements and

References and recommended reading

Papers of particular interest, published over the period of the review, have been highlighted as:

  • • of special interest

  • •• of outstanding interest

Acknowledgements

Peter Brown is supported by the Medical Research Council. I am grateful to Peter Magill and Andrea Kühn for their helpful comments on this manuscript.

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