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Changes in the Purkinje cells (PCs) and climbing fibers (CFs) have been postulated to be involved in essential tremor (ET) disease pathogenesis.1 PCs receive 2 excitatory inputs: CFs and parallel fibers (PFs). CFs form synapses predominantly on the thick, proximal PC dendrites, whereas PFs form synapses on the thin, distal PC dendritic branchlets. CF-PC and PF-PC innervation territories on PC dendritic arbors are tightly regulated for proper PC function. We recently reported more CF-PC synapses on the thin, distal PC dendritic branchlets in ET cases than controls,2 and this pathologic feature was associated with tremor severity in a small sample of 8 ET cases. We now expand the ET case sample nearly fivefold (37 cases) and assess the association between abnormal CF-PC connections and a wider range of clinical features. The overarching goal was to begin to mark out clinical characteristics that track with pathologic features in ET.
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Louis et al. (2015) studied this question.
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