Health Articles

Treatment of Nocturnal Leg Cramps

To relieve an established cramp, one must passively stretch the contracting muscle and gradually contract the apposing one. In some cases, this can be accomplished by simply walking around, which produces a relative dorsiflexion of the foot. Consciously dorsiflexing at the first sign of a leg or foot cramp might abort it. Prophylactic stretching can also prevent attacks, as might positions in bed that prevent foot dorsiflexion.

Patients who suffer from repeated attacks of nocturnal leg cramps seek a reduction in the frequency and severity of episodes. Quinine sulfate has been prescribed for decades for this purpose, but only recently have randomized, double-blind, controlled clinical trials been performed to assess its efficacy, and the number of patients studied remains small. Studies using low to moderate dose regimens (200-300 mg qhs) show less benefit than do those using higher doses (200 mg at supper, 300 qhs). This pattern suggests that response rates are related to serum level attained, which can vary greatly with age and preparation used. Risk of serious side effects is quite small but increases with dose and serum level. Cinchonism (nausea, vomiting, tinnitus, hearing loss), visual impairment, and ventricular arrhythmias are the most important of these adverse effects, appearing when serum levels exceed two to five times average serum concentration. An immune thrombocytopenia, occasionally fatal, has also been reported. The small, but real, risk of serious toxicity and the modest drug efficacy should temper one’s uncritical use of quinine for this otherwise benign condition. The drug is available without prescription in low-dose formulations. For those who suffer disabling nocturnal cramps unresponsive to nonpharmacologic measures, a careful trial of quinine may be useful after reviewing risks and benefits with the patient. Starting with small doses (200-300 mg qhs) is best, and platelet count should be monitored periodically. Only if meaningful benefit is obtained should quinine prophylaxis be continued.

Other drugs shown to be of some benefit include methocarbamol and chloroquine. Vitamin E is promoted in health food stores for treatment of nocturnal cramps, but it has been found to be no better than placebo when tested in double-blind, placebo-controlled fashion. It may be found in combination with quinine. The calcium channel blocker verapamil has shown promise in preliminary study.

If hypoglycemia is responsible, then adjustment of insulin regimen is needed . Altering the medication program may be necessary in cases in which beta-agonists or calcium channel blockers are thought to be responsible.
Epithelial cell abnormality

Nocturnal leg cramps are caused by unopposed foot flexion while in bed, placing the muscles of the calves and feet in their most shortened and therefore most vulnerable position. Without modulation by opposing muscles, the sustained contraction produces the painful cramp, which is experienced as sudden severe calf pain, often with a palpable or visibly hardened muscle. In many instances, a voluntary contraction triggers the cramp. Passive stretching relieves it.

Clinical Evaluation
History.

A detailed description of the cramping is essential and should include the setting in which the episodes occur. Those that develop at night or in the context of hemodialysis, hypoglycemia, or heavy sweating from prolonged exertion are likely to be true cramps, as are those coincident with use of calcium channel blockers or beta-agonists. Dystonic cramping is suggested by onset with occupation-related fine motor activity, and contracture by a lifelong onset with exercise. Associated symptoms should be reviewed for the paresthesias and carpopedal spasm of tetany, the weakness and fasciculations of lower motor neuron disease, and the cold or heat intolerance, skin changes, and related symptoms of thyroid disease. Location of the cramping is a less specific finding, but if calf pain is reported, one should include intermittent claudication in the differential diagnosis, particularly if pain is brought on by walking. Review of medications is always useful, but use of a potassium-wasting diuretic is not tantamount to an etiologic diagnosis, because hypokalemia is rarely responsible for true cramps (although it should be considered in the differential diagnosis of tetany). Also potentially pertinent in suspected tetany is any distant history of thyroidectomy (with coincident removal of the parathyroid glands).

Physical Examination.

The skin is examined for signs of thyroid disease, the neck for evidence of thyroidectomy, the lower extremities for diminished or absent pulses, muscle wasting, and fasciculations, and the nervous system for focal weakness and absent or abnormal deep tendon reflexes. If tetany is a consideration, one can try to elicit the facial spasm of Trousseau’s sign by tapping the facial nerve or the carpal spasm of Chvostek’s sign by inflating the arm cuff above systolic pressure.

Laboratory

For the majority of people who present with a clinical story of nocturnal muscle cramps, laboratory testing is unlikely to provide additional information. Other situations do require a few simple tests. If the patient with ordinary cramps is diabetic and taking insulin, then testing for hypoglycemia is indicated. If severe dehydration and hyponatremia are suspected, then determinations of serum sodium, blood urea nitrogen (BUN), and creatinine can guide assessment and treatment. The patient with possible tetany needs a check of sodium, potassium, calcium, albumin (to interpret the calcium level), and magnesium. Consideration of thyroid disease is best pursued by obtaining a serum thyrotropin (TSH) determination. The patient with fasciculations and possible lower motor neuron disease may need a nerve conduction study.