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Arjun S. Chandran, Stuti Joshi, Megan Thorburn, Rick Stell and Christopher R. P. Lind

OBJECTIVE

The posterior subthalamic area (PSA) is a promising target of deep brain stimulation (DBS) for medication-refractory essential tremor (ET). This case series describes a novel adverse effect manifesting as dystonic tics in patients with ET undergoing DBS of the PSA.

METHODS

Six patients with ET received electrode implants for DBS of the dorsal and caudal zona incerta subregions of the PSA.

RESULTS

Five of the 6 patients developed dystonic tics soon after clinical programming. These tics were of varying severity and required reduction of the electrical stimulation amplitude. This reduction resolved tic occurrence without significantly affecting ET control. Dystonic tics were not observed in 39 additional patients who underwent DBS of the same brain regions for controlling non-ET movement disorders.

CONCLUSIONS

The pathophysiology of tic disorders is poorly understood and may involve the basal ganglia and related cortico-striato-thalamo-cortical circuits. This series is the first report of DBS-induced tics after stimulation of any brain target. Although the PSA has not previously been implicated in tic pathophysiology, it may be a candidate region for future studies.

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Omar K. Bangash, Megan Thorburn, Jimena Garcia-Vega, Susan Walters, Rick Stell, Sergio E. Starkstein and Christopher R. P. Lind

The caudal zona incerta target within the posterior subthalamic area is an investigational site for deep brain stimulation (DBS) in Parkinson disease (PD) and tremor. The authors report on a patient with tremor-predominant PD who, despite excellent tremor control and an otherwise normal neurological examination, exhibited profound difficulty swimming during stimulation. Over the last 20 years, anecdotal reports have been received of 3 other patients with PD who underwent thalamic or pallidal lesioning or DBS surgery performed at the authors’ center and subsequently drowned. It may be that DBS puts patients at risk for drowning by specifically impairing their ability to swim. Until this finding can be further examined in larger cohorts, patients should be warned to swim under close supervision soon after DBS surgery.

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Omar K. Bangash, Arosha S. Dissanayake, Shirley Knight, John Murray, Megan Thorburn, Nova Thani, Arul Bala, Rick Stell and Christopher R. P. Lind

OBJECTIVE

Posterior subthalamic area (PSA) deep brain stimulation (DBS) targeting the zona incerta (ZI) is an emerging treatment for tremor syndromes, including Parkinson’s disease (PD) and essential tremor (ET). Evidence from animal studies has indicated that the ZI may play a role in saccadic eye movements via pathways between the ZI and superior colliculus (incerto-collicular pathways). PSA DBS permitted testing this hypothesis in humans.

METHODS

Sixteen patients (12 with PD and 4 with ET) underwent DBS using the MRI-directed implantable guide tube technique. Active electrode positions were confirmed at the caudal ZI. Eye movements were tested using direct current electrooculography (EOG) in the medicated state pre- and postoperatively on a horizontal predictive task subtending 30°. Postoperative assessments consisted of stimulation-off, constituting a microlesion (ML) condition, and high-frequency stimulation (HFS; frequency = 130 Hz) up to 3 V.

RESULTS

With PSA HFS, the first saccade amplitude was significantly reduced by 10.4% (95% CI 8.68%–12.2%) and 12.6% (95% CI 10.0%–15.9%) in the PD and ET groups, respectively. With HFS, peak velocity was reduced by 14.7% (95% CI 11.7%–17.6%) in the PD group and 27.7% (95% CI 23.7%–31.7%) in the ET group. HFS led to PD patients performing 21% (95% CI 16%–26%) and ET patients 31% (95% CI 19%–38%) more saccadic steps to reach the target.

CONCLUSIONS

PSA DBS in patients with PD and ET leads to hypometric, slowed saccades with an increase in the number of steps taken to reach the target. These effects contrast with the saccadometric findings observed with subthalamic nucleus DBS. Given the location of the active contacts, incerto-collicular pathways are likely responsible. Whether the acute finding of saccadic impairment persists with chronic PSA stimulation is unknown.