Hemifacial spasm is defined as unilateral, involuntary, irregular clonic or tonic movement of muscles innervated by the seventh cranial nerve. Most frequently attributed to vascular loop compression at the root exit zone of the facial nerve, there are many other etiologies of unilateral facial movements that must be considered in the differential diagnosis of hemifacial spasm. The primary purpose of this review is to draw attention to the marked heterogeneity of unilateral facial spasms and to focus on clinical characteristics of mimickers of hemifacial spasm and on atypical presentations of nonvascular cases. In addition to a comprehensive review of the literature on hemifacial spasm, medical records and videos of consecutive patients referred to the Movement Disorders Clinic at Baylor College of Medicine for hemifacial spasm between 2000 and 2010 were reviewed, and videos of illustrative cases were edited. Among 215 patients referred for evaluation of hemifacial spasm, 133 (62%) were classified as primary or idiopathic hemifacial spasm (presumably caused by vascular compression of the ipsilateral facial nerve), and 4 (2%) had hereditary hemifacial spasm. Secondary causes were found in 40 patients (19%) and included Bell's palsy (n=23, 11%), facial nerve injury (n=13, 6%), demyelination (n=2), and brain vascular insults (n=2). There were an additional 38 patients (18%) with hemifacial spasm mimickers classified as psychogenic, tics, dystonia, myoclonus, and hemimasticatory spasm. We concluded that although most cases of hemifacial spasm are idiopathic and probably caused by vascular compression of the facial nerve, other etiologies should be considered in the differential diagnosis, particularly if there are atypical features.

The objective of this report is to draw attention to tardive dyskinesia (TD) caused by aripiprazole, a third generation antipsychotic. TD has been traditionally attributed to typical (first-generation) antipsychotics, but other dopamine receptor blocking drugs and atypical (second- and third-generation) neuroleptics are emerging as an important cause of TD. We reviewed the medical records of patients with TD seen at the Baylor College of Medicine Movement Disorders Clinic between 2002 and 2010 to identify patients with TD associated with aripiprazole. Among 236 patients with TD seen over the specified period, 8 (3.4%) were found to have aripiprazole-associated TD. In 5 patients, TD occurred after exclusive exposure to aripiprazole. The mean age at onset was 55.8 ± 14.8 years with a female predominance. The average duration of treatment with aripiprazole was 18.4 ± 26.4 months. Oro-bucco-lingual stereotypy was seen in all patients. In most patients, TD did not spontaneously improve after stopping aripiprazole. Of the 5 patients treated with tetrabenazine, 4 improved during follow-up. Although aripiprazole, a third generation antipsychotic, has been promoted to have a low risk of TD, the drug accounts for about 3.5% of patients with TD evaluated in a movement disorders clinic. This largest reported series draws attention to the growing incidence of TD and other drug-induced movement disorders associated with "atypical antipsychotics."

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Treatments to slow the progression are a major unmet need in Parkinson's disease. Detailed assessment of randomized trials testing putative neuroprotective drugs was undertaken to inform the design, reporting, and interpretation of future studies. This study is a systematic review of trials testing neuroprotective drugs. Data were extracted independently by two coauthors. Fifteen completed, published trials involving 4,087 participants tested 13 different drugs in 18 double-blind comparisons with placebo. Seven comparisons involving 2,000 subjects assessed MAO-B inhibitors. The primary outcome was change in the Unified Parkinson's Disease Rating Scale score in eight trials and time to need for dopaminergic therapy in seven. Mean participant age was 62 years, 35% were women, the interval from diagnosis to entry averaged 11 months, and the number of participants averaged 272 (largest = 806). Follow-up averaged <16 months in all but two trials. Detailed randomization methods and success of double-blinding were reported in 20% and 13%, respectively. Based on the investigators' conclusions, six trials were interpreted as consistent with a neuroprotective effect, three as negative, and five as either confounded or not meeting criteria for futility. Neuroprotection trials have involved relatively uniform groups of participants early in the clinical disease course, with outcomes weighted heavily toward motor deterioration. Future trials should include participants with wider ranges of disease stages and assess broader neurological outcomes.

Background: Orthostatic tremor is an uncommon disorder manifest by high frequency, low amplitude leg tremor upon weight bearing. Treatment with oral tremor agents is inconsistent and usually not satisfactory.Methods: We implanted bilateral ventralis intermedius nuclei deep brain stimulators into an 82-year-old male with refractory orthostatic tremor. Results:The patient had a marked subjective and objective improvement in leg and arm tremor, mainly manifested by an improved ability to stand.Discussion: Bilateral thalamic deep brain stimulation may be considered in refractory cases of orthostatic tremor.