Handbook of Atypical Parkinsonism by Wenning Gregor K. Riley David E. Colosimo Carlo. & David E. Riley & Gregor K. Wenning

Author:Wenning, Gregor K.,Riley, David E.,Colosimo, Carlo. & David E. Riley & Gregor K. Wenning
Language: eng
Format: epub
Publisher: Cambridge University Press
Published: 2011-04-01T04:00:00+00:00

Electrophysiology

In case reports of CBD where it is mentioned, electroencephalography (EEG) has been normal or has shown slow- and sharp wave activity, particularly over the more affected hemisphere, and/or diffuse bilateral slowing [1,4]. Studies of patients with CBS without pathological confirmation have demonstrated asymmetrical slowing including focal intermittent slow waves (typically contralateral to the dominantly affected limb), intermittent sharp waves, and less commonly, frontal intermittent rhythmic delta activity and slowing of background activity [114,123].

Electrophysiological studies have been used to assess myoclonus in CBS. No electrophysiological studies have been reported of patients with pathologically proven CBD. Electrophysiological testing of the myoclonus in CBS has found a pattern different from other syndromes with parkinsonism and suggestive of a cortical process, although distinct from classic cortical reflex myoclonus [65,124–126]. While most studies suspect a cortical source of the myoclonus, a subcortical origin has also been proposed [127]. Typically, the electromyography (EMG) pattern shows synchronous short duration bursts (20–50 ms) of upper limb muscle discharges (agonist and antagonist muscles) and a lack of associated large EEG potentials or giant somatosensory evoked potentials (SEPs) [65,124–126]. Short latencies (approximately 40 ms) are typically reported between stimulus and elicited jerk [65,124,125]. In addition, the long-latency responses (LLRs) are reported to be enhanced at rest in CBS patients and to have an abnormally increased amplitude during motor activation [125].

Somatosensory evoked potentials are typically but variably abnormal in CBS. Abnormal morphology of the parietal P25-N33 component [65], abnormal morphology of the parietal N20-P25 complex [126], and minimal abnormalities in parietal SEP responses but absent frontal SEP responses [125] have all been reported.

Transcranial magnetic stimulation (TMS) in CBS patients shows variable disruption of the ipsilateral silent period indicating callosal pathology [128]. A study of TMS in various syndromes with parkinsonism showed persistent callosal impairment in both CBS and PSP groups with intact ipsilateral silent periods in MSA and ideopathic PD patients [129]. Recently, normal TMS findings in a patient with CBS supported consideration of an alternate diagnosis, ultimately shown pathologically to be CJD [51].

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