Disturbed Cerebellar Functions in Patients with Essential Tremor
February 1, 2002 2 minutes read
Disturbed Cerebellar Functions in Patients with Essential Tremor
Abstract & Commentary
Source: Stolze H, et al. The gait disorder of advanced essential tremor. Brain. 2001;124:2278-2286.
There have been anecdotal reports of a gait disorder characterized by an abnormal tandem gait in almost 50% of patients with essential tremor (ET) (Singer C, et al. Mov Disord. 1994;9:193-196). Stolze and colleagues assessed cerebellar-like abnormalities in 25 patients with ET, 8 patients with cerebellar diseases (CD) and 21 age-matched healthy controls. Tremor was rated according to the clinical scale of Fahn and associates (Fahn S, Tolosa E, Marin C. In: Jankovic J, Tolosa E, eds. Parkinson’s Disease and Movement Disorders. 3rd ed. Baltimore, Md: Urban and Schwarzenberg; 1998:225-234.) Normal and tandem gait were studied both on a walkway and on a treadmill using a three-dimensional infrared movement analysis system.
During normal walking, ET and CD subjects showed only slight abnormalities on tandem gait. However, ET patients exhibited a broad-based ataxic and dysmetric gait that was indistinguishable from the gait in CD. The gait disorder was much more pronounced in the 15 ET patients (60% of the total) who had intention tremor of the hands. Patients with gait disorder due to CD or ET were more severely disturbed in their activities of daily living than those without gait disorder.
Stolze et al conclude that their results are strong evidence for a CD in ET causing both a gait abnormality and the tremor itself.
Commentary
Stolze et al found that ET patients who have a cerebellar-like intention tremor rather than predominantly postural tremor of the upper extremities are also likely to have a cerebellar-like disorder of tandem gait. At first glance this conclusion seems to be tautological, but that is not the case. The association between ET and a gait disorder has been noted by clinicians but thought to be coincidental. Since ET is hypothesized to be caused by oscillatory activity in the olivo-cerebello-rubral pathways, it seems plausible that other cerebellar motor functions could be disturbed in ET patients (Deuschl G, et al. Brain. 2000;123:1568-1580). In support of a cerebellar connection are case reports of the disappearance of ET after cerebellar and pontine strokes (Nagaratnam N, Kalasagail G. J Neurol Sci. 1997;149:195-196) and PET studies demonstrating cerebellar hyperactivity in ET (Hallett M, Dubinsky RM. J Neurol Sci. 1993;114:45-48).
Further clinical studies of ET patients before and after medical and surgical treatment should take an integrative approach that seeks to understand the genesis of both tremor and ataxia. —John J. Caronna, MD. Dr. Caronna, Vice-Chairman, Department of Neurology, Cornell University Medical Center; Professor of Clinical Neurology, New York Hospital, is Associate Editor of Neurology Alert.
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