Small-Amplitude cortical myoclonus in Parkinson's disease: Physiology and clinical observations

✍ Scribed by John N. Caviness; Charles H. Adler; Thomas G. Beach; Kristi L. Wetjen; Richard J. Caselli

• Publisher: John Wiley and Sons
• Year: 2002
• Tongue: English
• Weight: 88 KB
• Volume: 17
• Category: Article
• ISSN: 0885-3185
• DOI: 10.1002/mds.10177

✦ Synopsis

We studied the occurrence of small-amplitude myo- clonus in 20 idiopathic Parkinson's disease patients who had no evidence of dementia as defined by criteria in the Diagnostic and Statistical Manual of Mental Disorders, fourth edition. Parkinson's disease was diagnosed by United Kingdom Brain Bank criteria, and clinical assessment was performed with the Unified Parkinson's Disease Rating Scale motor score, Hoehn and Yahr staging, and the Mini-Mental State Examination. Clinical assessment showed a range of mild-to-moderate disease severity. All patients underwent polygraphic electro-encephalographic-electromyographic (EMG) recording with back-averaging, somatosensory evoked potential testing, and attempted elicitation of long-latency EMG responses. Multichannel surface EMG recording during muscle activation showed irregular, multifocal, brief (<50 msec) myoclonus EMG discharges. Back-averaging consistently showed a focal, short-latency, electroencephalographic transient prior to the myoclonus EMG discharge. Cortical somatosensory evoked potential waves were not enlarged, and long-latency EMG responses at rest were not present. The small-amplitude myoclonus in such cases arises from an abnormal discharge from the sensorimotor cortex. The mechanism of this cortical myoclonus in Parkinson's disease has differences from the more common "cortical reflex myoclonus" physiology. Advanced parkinsonism is not a requirement for manifestation of this myoclonus type. Although the myoclonus occurred without dementia in these cases, its relationship to the subsequent development of cognitive impairment remains to be defined.