![]() The deficit of pursuit initiation, its correlation with the intensity of intention tremor, and the pathological VOR dumping provide additional evidence of a cerebellar dysfunction in the advanced stage of ET, when intention tremor becomes part of the clinical symptoms, and point to a common pathomechanism. Saccades and gaze‐holding function were not impaired. ![]() Gain and time constant (τ) of horizontal VOR were normal, but suppression of the VOR time constant by head tilt (‘otolith dumping’) was pathological in 41% of ET patients, particularly in ET IT patients. ET IT patients were significantly more affected than ET PT patients. The intention tremor score correlated with the pursuit deficit, e.g. 0.4 Hz: 0.90 versus 0.78) were also significantly decreased in ET patients, whereas pursuit latency was unaffected. Subsequent steady‐state pursuit velocity and sinusoidal pursuit gain (e.g. In the step ramp smooth pursuit paradigm, the initial eye acceleration in the first 60 ms of pursuit generation was significantly reduced in ET patients, particularly in ET IT patients, by ∼ 44% (mean 23.4°/s 2) compared with that of control subjects (mean 41.3°/s 2). ET patients showed two major deficits that may indicate cerebellar dysfunction: (i) an impaired smooth pursuit initiation and (ii) pathological suppression of the vestibulo‐ocular reflex (VOR) time constant by head tilts (‘otolith dumping’). Eight ET patients had clinical evidence of intention tremor (ET IT) six had a predominantly postural tremor (ET PT) without intention tremor. Vestibular function was assessed by electro‐oculography. ![]() ![]() Eye movements of 14 patients with ET and 11 age‐matched control subjects were recorded using the scleral search‐coil technique. The aim of this study was to determine whether a dysfunction also affects cerebellar structures involved in eye movement control. Experimental and clinical data indicate that the cerebellum is involved in the pathophysiology of advanced stages of essential tremor (ET). ![]()
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