Deep Brain Stimulation and Swimming Performance: A Randomized Within-Person Crossover Study.

OBJECTIVE: To determine whether deep brain stimulation (DBS) causes swimming impairment, we systematically compared swimming ability between DBS on vs off in 18 patients. METHODS: We conducted a randomized blinded crossover study, comparing swimming ability between DBS on vs off, within participants. Participants swam 3 laps of front crawl and 3 laps of breaststroke. Prespecifed primary outcomes were proportion of lap completed, lap time, and Aquatic Skills Proficiency Assessment (ASPA) score. Prespecified secondary outcomes were a qualitative description of marked changes observed. RESULTS: Eighteen participants with Parkinson disease (n = 13), essential tremor (n = 3), Tourette syndrome (n = 1), or posttraumatic brain injury proximal tremor (n = 1), treated with posterior subthalamic area (n = 15) or globus pallidus interna (n = 3) DBS were assessed. There was no significant effect of DBS on/off status on any outcome measure for front crawl or breaststroke. Three participants showed changes in both qualitative and quantitative assessments. Of these, 1 participant displayed reduction in swimming ability: impairment in all outcomes with DBS on, normalizing with DBS off (the same individual as previously reported). The participant displayed difficulty coordinating limb movement as well as postural control. Two participants showed improvements in lap time and ASPA scores with DBS on. CONCLUSION: Overall DBS did not impair swimming performance, although 1 patient demonstrated a stimulation-induced drowning hazard. There were no anatomic or clinical features unique to the individual with swimming impairment. Patients should be warned about the possibility of DBS-induced drowning hazard and should swim with capable supervision after DBS. CLASSIFICATION OF EVIDENCE: This study provides Class IV evidence that for patients with implanted DBS electrodes, the stimulation on condition, compared with stimulation off, did not significantly impair swimming performance. A formal assessment of unblinding would have been helpful.

Modulation of saccades in humans by electrical stimulation of the posterior subthalamic area.

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.

Dystonic tics induced by deep brain stimulation of the posterior subthalamic area for essential tremor.

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.

Drowning hazard with deep brain stimulation: case report.

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.

Effect of graded fructose coingestion with maltodextrin on exogenous 14C-fructose and 13C-glucose oxidation efficiency and high-intensity cycling performance.

The ingestion of solutions containing carbohydrates with different intestinal transport mechanisms (e.g., fructose and glucose) produce greater carbohydrate and water absorption compared with single-carbohydrate solutions. However, the fructose-ingestion rate that results in the most efficient use of exogenous carbohydrate when glucose is ingested below absorption-oxidation saturation rates is unknown. Ten cyclists rode 2 h at 50% of peak power then performed 10 maximal sprints while ingesting solutions containing (13)C-maltodextrin at 0.6 g/min combined with (14)C-fructose at 0.0 (No-Fructose), 0.3 (Low-Fructose), 0.5 (Medium-Fructose), or 0.7 (High-Fructose) g/min, giving fructose:maltodextrin ratios of 0.5, 0. 8, and 1.2. Mean (percent coefficient of variation) exogenous-fructose oxidation rates during the 2-h rides were 0.18 (19), 0.27 (27), 0.36 (27) g/min in Low-Fructose, Medium-Fructose, and High-Fructose, respectively, with oxidation efficiencies (=oxidation/ingestion rate) of 62-52%. Exogenous-glucose oxidation was highest in Medium-Fructose at 0.57 (28) g/min (98% efficiency) compared with 0.54 (28), 0.48 (29), and 0.49 (19) in Low-Fructose, High-Fructose, No-Fructose, respectively; relative to No-Fructose, only the substantial 16% increase (95% confidence limits +/-16%) in Medium-Fructose was clear. Total exogenous-carbohydrate oxidation was highest in Medium-Fructose at 0.84 (26) g/min. Although the effect of fructose quantity on overall sprint power was unclear, the metabolic responses were associated with lower perceptions of muscle tiredness and physical exertion, and attenuated fatigue (power slope) in the Medium-Fructose and High-Fructose conditions. With the present solutions, low-medium fructose-ingestion rates produced the most efficient use of exogenous carbohydrate, but fatigue and the perception of exercise stress and nausea are reduced with moderate-high fructose doses.

Exercise can be pyrogenic in humans.

Exercise increases mean body temperature (T(body)) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE(2) can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T(body) in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), Vo(2 max): 53 ml x kg(-1) x min(-1) (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running ( approximately 75% Vo(2 max)) followed by 45-min cycling and 60-min seated recovery (28 degrees C, 50% relative humidity). Plasma cytokine (TNF-alpha, IL-10) concentrations were measured at rest and 30-min recovery. T(body) was similar at rest in PLAC (35.59 degrees C) and NSAID (35.53 degrees C) and increased similarly during running, but became 0.33 degrees C (SD 0.26) lower in NSAID during cycling (37.39 degrees C vs. 37.07 degrees C; P = 0.03), and remained lower throughout recovery. Sweating was initiated at T(body) of approximately 35.6 degrees C in both conditions but ceased at higher T(body) in PLAC than NSAID during recovery [36.66 degrees C (SD 0.36) vs. 36.39 degrees C (SD 0.27); P = 0.03]. Cardiac frequency averaged 6 x min(-1) higher in PLAC (P < 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W x m(-2); P = 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.

Attenuated gastric distress but no benefit to performance with adaptation to octanoate-rich esterified oils in well-trained male cyclists.

We investigated the effects of modifying a normal dietary fatty acid composition and ingestion of high-fat exercise supplements on gastrointestinal distress, substrate oxidation, and endurance cycling performance. Nine well-trained male cyclists completed a randomized triple-crossover comprising a 2-wk diet high in octanoate-rich esterified oil (MCFA) or twice long-chain fatty acids (LCFA). Following the diets, participants performed 3-h of cycling at 50% of peak power followed by 10 maximal sprints while ingesting either 1) a carbohydrate (CHO)+MCFA-rich oil emulsion after the 2-wk MCFA-rich dietary condition (MC-MC, Intervention) and 2) after one of the LCFA-rich dietary conditions (LC-MC, Placebo) or 3) CHO only following a LCFA-rich diet (LC-CHO, Control). During the 3-h ride MCFA-adaptation decreased octanoic-acid oxidation by 24% (90% confidence interval: 14-34%). The CHO+MCFA-rich oil emulsion reduced endogenous fat oxidation by 61% (33-89%) and 110% (89-131%) in the MC-MC and LC-MC conditions, respectively, and MCFA-adaptation reduced endogenous-carbohydrate oxidation by 10% (-3-23%). MCFA-adaptation attenuated gastrointestinal distress and nausea during the sprints, but the effect of the oil emulsion was to lower sprint power by 10.9% (7.7-14.1%) in the LC-MC condition and by 7.1% (5.7-8.5%) in the MC-MC condition, relative to the LC-CHO control; every one unit increase in nausea decreased mean power by 6.0 W (3.2-8.8 W). We conclude that despite some attenuation of endogenous-carbohydrate oxidation and gastric distress following adaptation to a MCFA-rich diet, repeat sprint performance was substantially impaired in response to the ingestion of a CHO+MCFA-rich oil emulsion.