Spinal Cord Stimulation - Orthostatic Tremor

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Spinal Cord Stimulation - Orthostatic Tremor

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Chronic spinal cord stimulation in medically intractable orthostatic tremor
J K Krauss, R Weigel, C Blahak, H Bäzner, H‐H Capelle, E Grips, M Rittmann, and J C Wöhrle
The pathophysiological mechanisms underlying the development and manifestation of orthostatic tremor are unclear. Although the primary cause of orthostatic tremor remains unidentified, evidence suggests that various neuronal systems are affected, including the cerebellum, brain stem, striatum and thalamus, corticosubcortical pathways, and, in particular, the corticocerebellothalamic loop.3,5 The concept that orthostatic tremor is driven by a primary central generator has been accepted most widely, but it has also been suggested that the spinal cord may generate the 16‐Hz tremor.16 Furthermore, orthostatic tremor has been thought to be the product of exaggerated activity of a physiological generator oscillating at approximately 16 Hz.17 Presumably, the generator of orthostatic tremor projects through the reticulospinal tract.5 Recently, a “double lesion” model has been suggested for orthostatic tremor to be manifested.3 According to this hypothesis, an abnormally active oscillator would have the key role, but orthostatic tremor would develop only if coupled with additional dysfunction at the level of the basal ganglia or the cerebellum, resulting in deficient control of the oscillator.

The therapeutic effect of SCS on orthostatic tremor in our study is presumably modulation of sensory input to the neuronal network subserving orthostatic tremor. The finding that the 16‐Hz motor activity in the legs is still present indicates that SCS may have a more indirect modulatory influence on the activity of the primary oscillatory generator. The improvement in unsteadiness along with reduction in the EMG amplitude, however, concurs with the hypothesis that the exaggerated sense of imbalance when standing still could be the actual core abnormality in patients with orthostatic tremor.17 Interestingly, in a previous study that showed small improvements in clinical parameters on blinded video rating after levodopa challenges in a group of patients with orthostatic tremor, the mean EMG frequency of tremor was also unchanged despite power analysis showing a clear reduction in the area under the curve.6 It is important to note, that there is a discrepancy between subjective and objective unsteadiness in orthostatic tremor, and that it has been postulated that the sense of instability in orthostatic tremor is related to “tremulous disruption” of proprioceptive afferent activity from the legs.18 Thus, SCS could also act by masking the pathological disruption to a certain extent and de‐escalate activity in a reverberating vicious cycle. An alternative mechanism could be its effect on interneurones mediating either spinocerebellar input or projections to motor pathways and the reticulospinal tract.

Link to Research Report
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