Transient and state modulation of beta power in human subthalamic nucleus during speech production and finger movement.

Signs of Parkinson's disease (PD) are augmented by speech and repetitive motor tasks. The neurophysiological basis for this phenomenon is unknown, but may involve augmentation of ß (13-30 Hz) oscillations within the subthalamic nucleus (STN). We hypothesized that speech and motor tasks increase ß power in STN and propose a mechanism for clinical observations of worsening motor state during such behaviors. Subjects undergoing deep brain stimulation (DBS) surgery performed tasks while STN local field potential (LFP) data were collected. Power in the ß frequency range was analyzed across the entire recording to observe slow shifts related to block design and during time epochs synchronized to behavior to evaluate immediate fluctuations related to task execution. Bilaterally symmetric ß event related desynchronization was observed in analysis time-locked to subject motor and speech tasks. We also observed slow shifts of ß power associated with blocks of tasks. Repetitive combined speech and motor, and isolated motor blocks were associated with the highest bilateral ß power state. Overt speech alone and imagined speech were associated with a low bilateral ß power state. Thus, changing behavioral tasks is associated with bilateral switching of ß power states. This offers a potential neurophysiologic correlate of worsened PD motor signs experienced during clinical examination with provocative tasks: switching into a high ß power state may be responsible for worsening motor states in PD patients when performing unilateral repetitive motor tasks and combined speech and motor tasks. Beta state changes could be chronically measured and potentially used to control closed loop neuromodulatory devices in the future.

Idiopathic normal pressure hydrocephalus: a systematic review of diagnosis and outcome.

OBJECTIVE: Patient selection for cerebrospinal fluid diversion is difficult, because idiopathic normal pressure hydrocephalus (INPH) mimics other neurodegenerative disorders and no findings reliably predict outcome. The literature was reviewed to identify diagnostic criteria that predict shunt response and to formulate prognostic expectations. METHODS: MEDLINE was searched, and 44 articles meeting predetermined criteria were included. RESULTS: Clinical series were frequently retrospective with small patient numbers and unstandardized outcome evaluation. Clinical findings suggestive of shunt responsiveness were the complete triad (gait disturbance, urinary incontinence, and dementia) with early gait disturbance. Degree of hydrocephalus was not correlated with clinical improvement. Reduction of the subcortical low-blood flow area was correlated with improvement in three small studies. Clinical response to prolonged cerebrospinal fluid drainage predicted shunt outcome in all cases in two small series. Overall, 59% (range, 24-100%) of patients improved after shunting, and 29% (range, 10-100%) of patients experienced prolonged improvement. Complications occurred in 38% (range, 5-100%) of patients, additional surgery was required in 22% (range, 0-47%) of patients, and there was a 6% (range, 0-35%) combined rate of permanent neurological deficit and death. CONCLUSION: Shunting INPH is associated with an approximately 29% rate of significant improvement and a 6% significant complication rate. Enlargement of the subcortical low-flow area and clinical improvement secondary to prolonged lumbar drainage may provide additive predictive value above clinical and computed tomographic criteria. A multicenter clinical trial that focuses on the value of ancillary tests, defines the clinical course of a patient with a ventriculoperitoneal shunt, and evaluates the cost effectiveness of shunting INPH is needed to better describe outcome from shunting in INPH.