Muscle cramps are a common problem characterized by a sudden, painful, involuntary contraction of muscle. These true cramps, which originate from peripheral nerves, may be distinguished from other muscle pain or spasm. Medical history, physical examination, and a limited laboratory screen help to determine the various causes of muscle cramps. Despite the "benign" nature of cramps, many patients find the symptom very uncomfortable. Treatment options are guided both by experience and by a limited number of therapeutic trials. Quinine sulfate is an effective medication, but the side-effect profile is worrisome, and other membrane-stabilizing drugs are probably just as effective. Patients will benefit from further studies to better define the pathophysiology of muscle cramps and to find more effective medications with fewer side-effects.

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The MR scans in SS show a rather distinctive pattern of supratentorial white matter lesions that always involve the corpus callosum. There is often deep gray matter, posterior fossa involvement, and frequent parenchymal with occasional leptomeningeal enhancement. The central callosal lesions differ from those in demyelinating disease, and should support the diagnosis of SS in patients with at least two of the three features of the clinical triad.

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The anatomic site of origin of muscle fasciculations and cramps has been debated for many years. Many authors have argued for a central origin of the abnormal discharges in the anterior horn cells. However, most of the evidence favors a very distal origin in the intramuscular motor nerve terminals. The factors giving rise to these discharges are not well understood. Fasciculations may be related to chemical excitation of motor nerve terminals, whereas cramps may result from mechanical excitation of motor nerve terminals during muscle shortening.