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At least 19 recordsLinked to original sources
PubMed1994

[Three siblings of painful muscle cramps (generalized muscle cramp disease) with alopecia and endocrinological disorders].

Three siblings with generalized painful muscle cramps, generalized alopecia, and endocrinological abnormalities are presented. Their clinical features are very similar to those in sporadic cases reported as having generalized muscle cramp disease. Autosomal recessive inheritance was suggested in our patients. Abnormal laboratory tests include hypersecretion of insulin after glucose loading, elevated levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH), and hypersecretion of LH in the LH-RH test. An elevation of IgG and IgG index in the cerebrospinal fluid (CSF) of two patients suggests IgG production in the CSF. Oral administration of 75 to 150 mg of dantrolene sodium decreased the frequency, intensity, and duration of cramps in all cases. Autoimmune mechanisms based upon hereditary abnormalities are suggested as a cause of their disease.

Adult↗
PubMed1995

Human motor unit activity during induced muscle cramp.

Muscle cramp was induced in the medial head of the gastrocnemius muscle in four of seven subjects using unloaded maximal voluntary contraction of the triceps surae in the shortened position. Surface electromyography over the medial and lateral heads of gastrocnemius and the soleus muscles demonstrated that the muscle activity during cramp was localized to part or all of the medial head of the gastrocnemii. In the same muscle, a tungsten electrode was used to record from 200 motor units during 16 episodes of cramp and 871 units during 26 voluntary contractions. For the first 30 s, significantly higher motor unit firing rates were recorded during cramp compared with unloaded voluntary contractions. Motor unit firing rates were also more variable during cramp. When the cramped muscle was stretched forcibly to break the cramp, motor unit activity increased in all the triceps surae muscles. In some experiments, the Achilles tendon of five subjects was vibrated for 50 s before and after voluntary contraction or cramp. The tonic vibration reflex (TVR) was depressed or absent after four episodes of cramp but it was unchanged after voluntary contraction. These data are interpreted to indicate that motor units are involved in ordinary muscle cramp. A positive feedback loop between peripheral afferents and alpha motor neurons, mediated by changes in presynaptic input, is a possible mechanism underlying muscle cramp.

Adolescent↗
PubMed1983

A double-blind comparison of quinine sulphate and placebo in muscle cramps.

Muscle cramps are painful and common in elderly patients but have largely escaped medical investigation. Quinine sulphate is usually the sole drug prescribed, even though firm evidence for its efficacy is not available. The results of the present double-blind cross-over study show that quinine was significantly superior to placebo in decreasing the number, severity and duration of nocturnal cramps. Since quinine is not a primary drug in any other condition, further studies of drugs with similar pharmacological actions may thus improve our management of this painful complaint.

Clinical Trials as Topic↗
PubMed1989

Is this really a muscle cramp?

Most muscle cramps are benign, but cramps that occur on exertion or in a patient with abnormal findings on physical examination or electromyography are usually caused by significant systemic disease. The most common systemic causes are metabolic diseases; central or peripheral nervous system diseases are less often responsible. Most systemic diseases that cause muscle cramps are amenable to specific treatment. If symptomatic treatment is desired, the first choice would appear to be stretching. If that is ineffective, carisoprodol (Rela, Soma, Soprodol), vitamin E, or verapamil hydrochloride (Calan, Isoptin) may be used. Quinine sulfate (Quine, Quinamm) is potentially toxic and may not be effective.

Carisoprodol↗
PubMed1983

[Clinical aspects and treatment of calf muscle cramps during pregnancy].

Of 8204 gravidae, 486 (5,9%) complained at least once of muscle cramps during pregnancy. Muscle cramps were noticed most often in the second half of pregnancy. Gravidae with muscle cramps were on the average older and of higher parity; there was no relationship between muscle cramps and complications during pregnancy or unfavorable fetal outcome. In an uncontrolled therapeutic trial 21 women with muscle cramps received 1,8 g monomagnesium-aspartate twice daily per mouth for 4 weeks. 21 women with muscle cramps had no therapy. 4 weeks after the initiation of magnesium therapy 19/21 women were free of symptoms, compared to only 7/21 patients in the control group. Muscle cramps during pregnancy do not have to be considered a risk factor; they can be significantly improved by the administration of oral magnesium.

Adult↗
PubMed1985

Physiotherapy and electromyography in muscle cramp.

Four cases of muscle cramps, at a sports institute, are presented. Electric activity was increased in cramp due to overload. The influence of stretching, electro- and compression therapies on these increased Electromyographic (EMG) activities was studied. The registration was performed with an EMG-analyser combined with a recorder, using surface electrodes.

Adult↗
PubMed1991

Tocainide therapy in muscle cramps and spasms due to neuromuscular disease.

Significant improvement in symptoms of disabling cramps and muscle spasms was obtained in 9 patients with motor neuron diseases, tetany, and myotonic disorders who were treated with tocainide, a lidocaine analog. No significant side effects were observed except for light-headedness and fatigue in 1 patient, who also showed slight prolongation of intraventricular conduction time. Tocainide is useful in treating disabling muscle spasms and cramps associated with conditions characterized by neuromuscular irritability. This effect is probably based on stabilization of the membrane potential at various levels (motor neurons, peripheral nerve, or muscle fiber membrane).

Adult↗
PubMed1980

[Action of quinine sulphate on the incidence of muscle cramps during hemodialysis (author's transl)].

Muscle cramps are a complication occurring during hemodialysis or in the periods between dialysis in 26% of patients. Out of a group of 21 patients undergoing hemodialysis three times a week for terminal renal failure, eight patients (38%) were selected with and special tendency to develop muscular cramps. Quinine was chosen because of its action upon the neuromuscular end motor plate. A double-blind study was carried out for 16 weeks, divided in two periods of 8 weeks, administering in each one of them either quinine sulphate (300 mg capsule) or placebo at the beginning of hemodialysis. The frequency of muscle cramps was significantly reduced (p < 0.005) by quinine sulphate when compared to placebo. Before and during the study blood tests, liver function, ECG, and EMG were monitored, and ophthalmological and audiometric evaluations were performed. No secondary effects of the administration of quinine sulphate could be found.

Acute Kidney Injury↗
PubMed1978

Analysis of tonic muscle activity and muscle cramps during hemodialysis.

A problem associated with some patients undergoing hemodialysis is the presence of muscle cramps. As the etiology of these cramps is still unknown, the purpose of this study was to evaluate tonic muscle activity and muscle cramps during hemodialysis. Forty-six complete dialysis treatment sessions were studied. Electromyographic (EMG) activity was recorded from a leg muscle in patients who cramped and control patients who did not cramp. EMG was analyzed via a minicomputer for each minute of recording time. Results indicated the mean muscle cramp latency from start of dialysis was 248 minutes. Average muscle cramp was 10 minutes in duration and took three minutes to develop and seven minutes to fully dissipate. Tonic EMG activity in patients with muscle cramps showed a continued increase throughout the latter part of dialysis whereas the control patients showed a continual decline. The results suggest that the latent increase in EMG activity may be causally related to muscle cramps and may be a useful predictor as to the onset of muscle cramps during hemodialysis.

Electromyography↗
PubMed1989

Muscle cramps in cancer patients.

We prospectively evaluated 50 cancer patients with new complaints of muscle cramps. Neurologic examination and laboratory evaluation identified disorders related to neural, muscular, or biochemical abnormalities in 41 (82%) patients. Abnormalities were confined mainly to the peripheral nervous system and included peripheral neuropathy in 22 patients, root and plexus pathology in 17 patients (six with leptomeningeal metastases), and polymyositis in two patients. Hypomagnesemia accounted for muscle cramps in only one patient. Identifiable causes of muscle cramps were related mostly either to metastatic or nonmetastatic complications of the underlying malignancy (14 patients) or to complications of its treatment (21 patients). Cramps, or rather complaints of cramps, were the presenting symptom of recognizable and previously unsuspected neurologic dysfunction in 64% (27 of 42) of the identified causes. Therefore, we conclude that muscle cramps in cancer patients may not be a benign complaint and that they usually mark the presence of an identifiable neurologic disorder. The use of simple clinical and laboratory measures is rewarding in the evaluation of these patients and leads to diagnosis in the majority of them.

Adolescent↗
PubMed1986

Painful muscle cramps. A symptom of liver cirrhosis?

We found an 88% incidence of painful muscle cramps in 33 patients with cirrhosis, as compared to 21% in a matched population without liver disease. The cramps were characterized by severe pain, occurred in calf muscles several times a week (mainly at rest or during sleep), and lasted for a few minutes. No definite etiological factor could be found and the underlying pathophysiology remains obscure, as in most other types of muscle cramps. However, the strikingly high incidence and uniformity of the phenomenon may justify the inclusion of painful muscle cramps among the recognized symptoms of cirrhosis.

Female↗
PubMed1995

Muscle cramps and elevated serum creatine phosphokinase levels induced by beta-adrenoceptor blockers.

We have assessed the propensity of beta-adrenoceptor blockers to cause muscle cramps and to raise the serum creatine phosphokinase (CPK) level in 78 patients with essential hypertension. After a control period, a beta-adrenoceptor blocker without intrinsic sympathomimetic activity (ISA; propranolol, metoprolol or arotinolol) was administered for three months. Thereafter, the patients were randomised to receive a beta-adrenoceptor blocker with ISA (pindolol or carteolol) for three months or a beta-adrenoceptor blocker without ISA for a further three months. This pattern was continued until all beta-adrenoceptor blockers had been given. At the end of each period, CPK and CPK-MB levels were measured. Of the 78 subjects, muscle cramps occurred in 27 during treatment with pindolol and 32 during treatment with carteolol. No complaints were made by subjects treated with propranolol and arotinolol, but muscle cramps were reported in 2 treated with metoprolol. While muscle cramps were caused both by pindolol and carteolol in 16 subjects, they were caused by either of these drugs in the remainder of the subjects. Muscle cramp occurred mainly in the calves when the patients were in bed at night. Serum CPK and CPK-MB levels increased significantly during treatment with pindolol (control period vs pindolol, CPK = 96 vs 133 IU.ml-1, CPK-MB = 14 vs 18 IU.ml-1) or carteolol (CPK = 117 IU.ml-1, CPK-MB = 18 IU.ml-1) while the levels during treatment with propranolol, arotinolol and metoprolol did not change from those in the control period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1986

Exercise-induced muscle cramp: a prospective biochemical study in marathon runners.

Exercise-induced muscle cramp has been considered to result from disturbances of fluid and electrolyte balance resulting from excessive sweat loss. Serum biochemical and haematological measurements were made on 82 male marathon runners before and after a 42.2-km race. Fifteen (18%) of the runners reported an attack of muscle cramp which occurred after 35 +/- 6 km (mean +/- S.D.) had been covered. These subjects were not different from the others in terms of racing performance or training status. Serum electrolyte concentrations, including sodium and potassium, were not different between those suffering from cramp and those not so affected either before or after the race, although a significant (P less than 0.001) increase in serum sodium concentrations occurred in both groups. Serum bicarbonate concentrations fell to the same extent (from 28 to 24 mmol l-1) in both groups. Significant decreases in plasma volume, calculated from the changes in circulating haemoglobin and haematocrit, occurred in both groups of subjects, but there was no difference in the extent of the haemoconcentration. The results suggest that exercise-induced muscle cramp may not be associated with gross disturbances of fluid and electrolyte balance.

Adult↗
PubMed1989

Phenytoin-induced improvement in muscle cramping and insulin action in three patients with the syndrome of insulin resistance, acanthosis nigricans, and acral hypertrophy.

Phenytoin sodium has been used to treat muscle cramps of diverse causes, and is known to increase insulin sensitivity during long-term use. We have previously described a syndrome of insulin resistance, acanthosis nigricans, and acral hypertrophy with continual muscle cramping. The effect of 300 mg/d of phenytoin (Dilantin) on muscle cramping and carbohydrate economy was studied in three affected patients and four control subjects. Oral glucose tolerance tests, euglycemic insulin infusion studies, and monocyte insulin binding tests were conducted before and after phenytoin administration. All three patients had notable improvement in muscle cramps. In response to phenytoin, metabolic improvements were variable, with improvement characteristically better in patients with less severe baseline metabolic abnormalities. Patient 1, with the mildest degree of glucose intolerance, had decreased fasting insulin and blood glucose levels, improved glucose tolerance, and insulin-mediated glucose disposal, associated with an increase in monocyte insulin receptors. Patient 2 had reduced fasting plasma glucose and insulin levels and improved oral glucose tolerance, suggesting a beneficial effect on carbohydrate metabolism. Patient 3, with the most severely impaired carbohydrate economy, showed no metabolic improvement despite marked lessening of muscle pain. These clinical characteristics were unaffected in control subjects. We conclude that phenytoin is of value in the therapy of muscle cramps and glucose intolerance in patients with this syndrome.

Acanthosis Nigricans↗
PubMed1991

Muscle cramps in the cancer patient: causes and treatment.

Muscle cramps may occur in healthy individuals without any apparent cause; these are regarded as benign cramps. Cramps may also develop as a symptom of a systemic disease, such as uremia. Cramps probably originate in the distal portion of the motor nerve. It is unclear whether the nerve terminals are hyperexcitable or prone to repetitive activity in the various related conditions. In the cancer patient, muscle cramps may not be a benign complaint because they often represent an unsuspected underlying pathologic condition associated either with the neoplastic process or the undesirable side effects of therapy. Initial evaluation with a detailed neurologic examination, a complete biochemical profile with magnesium levels and muscle enzymes, and electrodiagnostic examination will lead to the diagnosis in the majority of these patients. Recognized etiologies of cramps may be related to neurologic abnormalities or to nonneurologic causes. Treatment decisions should be oriented according to the following classification: (1) reversible causes; (2) potentially reversible causes and (3) irreversible causes. Whereas the remedy in the first category is to attack the underlying process, if possible, pharmacologic suppression of cramps is the primary approach in the others. Membrane-stabilizing agents, such as quinine, phenytoin or carbamazepine, may be selected according to either nocturnal or daytime predominant occurrence of cramps.

Clinical Protocols↗
PubMed1991

A randomized controlled trial of quinidine in the treatment of cirrhotic patients with muscle cramps.

In an attempt to evaluate the effect of quinidine in the treatment of patients with cirrhosis and muscle cramps, 31 cirrhotic patients with muscle cramps were randomly divided into two groups and given orally 400 mg of quinidine sulfate per day or placebo, respectively. Baseline clinical and laboratory data for these two groups were similar. Four weeks after oral administration of quinidine, the number of cramps significantly decreased from 14.4 +/- 1.7 (mean +/- S.E.) to 4.4 +/- 1.1 episodes (p less than 0.0001), but it remained unchanged in the placebo group (from 11.8 +/- 1.0 to 11.5 +/- 1.5 episodes, p greater than 0.05). In addition, 88% of the 16 patients on quinidine and 13% of the 15 patients on a placebo showed a greater than 50% reduction in the number of cramps during a 4-week treatment period (p less than 0.0001). The peak and trough serum levels of quinidine in patients having received quinidine for 2 weeks were 1.3 +/- 0.1 and 0.7 +/- 0.1 mg/l, respectively. There was a significant relationship between serum quinidine concentrations and attenuation of cramps. No significant adverse effect was observed during the study, except for five (31%) patients who developed mild diarrhea after quinidine therapy. Diarrhea subsided spontaneously or was controlled by medications without the interruption of quinidine therapy. It was concluded that quinidine is a safe and effective drug for the treatment of cirrhotic patients with muscle cramps.

Aged↗