The use of intravenous propofol may represent a new, rapid, and highly effective form of abortive headache treatment in the headache clinic or emergency room setting and may offer an alternative to other treatment modalities for acute migraine and other severe intractable headaches. The effectiveness of propofol raises many new questions about the pathophysiology of migraine and other headaches.

Many non-pharmacological treatments have been implicated in the treatment of primary headache, with exercise being a common recommendation. In this review we first provide an overview of the relationship between exercise and primary headaches. We then review the physiology of pain modulation, with focus on the endogenous opioids, endocannabinoids, and neuropeptides calcitonin gene-related peptide (CGRP) and brain-derived neurotrophic factor (BDNF), and their associations with primary headache and exercise. Finally, we summarize current literature evaluating effects of exercise on primary headache in an effort to understand the benefits and disadvantages of exercise in primary headaches.

Parkinsonism can result from numerous causes (1). Postinfectious etiologies are rare today but were common in the past. Postencephalitic parkinsonism was one of the most dramatic sequelae of encephalitis lethargica (von Economo's disease). This epidemic began in 1916-1917 in Austria, and cases had been reported throughout the world by 1919 (2). The two sexes were affected equally, and all races and occupations could be affected. The peak incidence in the United States was in 1923 with about 2,000 reported deaths. No major outbreaks of epidemic encephalitis occurred after 1926 and by 1935 the disease had virtually disappeared. Sporadic cases were reported, however, as late as the 1950s (3). Epidemics highly suggestive of a condition similar to encephalitis lethargica has been described in the 17th and 18th centuries. The disease occurred at all ages, but young adults appeared particularly susceptible. The onset was acute or subacute, and symptoms progressed over several weeks. Overall mortality rate approached 40%. Only a small percentage of patients made a complete recovery. Although a viral agent was never identified, the clinical and pathological features were typical of viral infection. Lymphocytic pleocytosis in the cerebrospinal fluid occurred in over half of the patients.The symptoms of encephalitis lethargica were variable (45). Acute manifestations usually lasting several weeks frequently included fever, lethargy, somnolence, ocular nerve palsy, nervousness, delirium, hallucinations, parkinsonism, and dyskinesias. Severe disturbances of the sleep cycle were common. The somnolent state usually persisted for weeks or months and in some instances for several years. Delirium and increased psychomotor activity occurred in other pal A videotape segment accompanies this article.

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