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At least 19 recordsLinked to original sources

[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↗

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↗

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↗

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↗

Creatine monohydrate treatment alleviates muscle cramps associated with haemodialysis.

BACKGROUND: Muscle cramp is a common complication of haemodialysis. The exact mechanism of this complication is still unknown. Many approaches have been used to relieve the muscle cramping but have had variable effects. One of the possible mechanisms of haemodialysis-associated muscle cramps (HAMC) is the disturbance of muscle energy metabolism. Creatine monohydrate can enhance muscle metabolism. We evaluated the clinical effect of creatine monohydrate on HAMC. METHODS: Ten patients with frequent muscle cramps during haemodialysis were randomly selected into two groups, control and placebo. In a double-blind manner, 12 mg of creatine monohydrate or placebo was given to each patient before each dialysis session for 4 weeks. The incidence of muscle cramp during haemodialysis was compared between the two groups. Dialysis adequacy, haemodynamic status, and side-effects were also evaluated. We continued to observe and compare the patients during a 4-week washout period to verify the effect of creatine monohydrate. RESULTS: The frequency of symptomatic muscle cramps decreased by 60% in the creatine monohydrate treatment group (6.2+/-0.8 vs 2.6+/-1.8 times/4 weeks, P<0.05) during the treatment period. This decreasing incidence of muscle cramps disappeared in the washout period in the creatine group (6.6+/-1.1 times/4 weeks). There was no difference in the incidence of muscle cramps in the placebo group. The haematocrit, Kt/V, serum albumin, and haemodynamics remained unchanged in both groups during the treatment and washout periods. Serum creatinine increased slightly after creatine monohydrate treatment (10.7+/-3.2 vs 12.4+/-3.2 mg/dl, P<0.05). No adverse effect was found in either group during the treatment and washout periods. CONCLUSION: These data suggest that creatine monohydrate can reduce the incidence of HAMC and that it may be a safe agent.

Adult↗

Exercise-induced muscle cramp. Proposed mechanisms and management.

Muscle cramp is a common, painful, physiological disturbance of skeletal muscle. Many athletes are regularly frustrated by exercise-induced muscle cramp yet the pathogenesis remains speculative with little scientific research on the subject. This has resulted in a perpetuation of myths as to the cause and treatment of it. There is a need for scientifically based protocols for the management of athletes who suffer exercise-related muscle cramp. This article reviews the literature and neurophysiology of muscle cramp occurring during exercise. Disturbances at various levels of the central and peripheral nervous system and skeletal muscle are likely to be involved in the mechanism of cramp and may explain the diverse range of conditions in which cramp occurs. The activity of the motor neuron is subject to a multitude of influences including peripheral receptor sensory input, spinal reflexes, inhibitory interneurons in the spinal cord, synaptic and neurotransmitter modulation and descending CNS input. The muscle spindle and golgi tendon organ proprioceptors are fundamental to the control of muscle length and tone and the maintenance of posture. Disturbance in the activity of these receptors may occur through faulty posture, shortened muscle length, intense exercise and exercise to fatigue, resulting in increased motor neuron activity and motor unit recruitment. The relaxation phase of muscle contraction is prolonged in a fatigued muscle, raising the likelihood of fused summation of action potentials if motor neuron activity delivers a sustained high firing frequency. Treatment of cramp is directed at reducing muscle spindle and motor neuron activity by reflex inhibition and afferent stimulation. There are no proven strategies for the prevention of exercise-induced muscle cramp but regular muscle stretching using post-isometric relaxation techniques, correction of muscle balance and posture, adequate conditioning for the activity, mental preparation for competition and avoiding provocative drugs may be beneficial. Other strategies such as incorporating plyometrics or eccentric muscle strengthening into training programmes, maintaining adequate carbohydrate reserves during competition or treating myofascial trigger points are speculative and require investigation.

Central Nervous System↗

Muscle cramps: a 'complication' of cirrhosis.

Muscle cramps are a common complaint in clinical practice. They are associated with various metabolic, endocrine, neurological and electrolyte abnormalities. A variety of hypotheses have been generated to explain the cause of muscle cramping, yet none has been able to support a consistent pathophysiological mechanism. Muscle cramps are painful, involuntary contractions of skeletal muscle. They occur frequently in individuals with cirrhosis, regardless of the etiology, and are thought to be a symptom of cirrhotic-stage liver disease. The pathophysiology of these cramps remains elusive; hence, a specific therapy has not been identified. Many therapeutic approaches have been offered, yet their efficacy, safety and mechanism of action remain poorly defined. This review defines muscle cramps and illuminates its prevalence in the cirrhotic individual. Current theories relating to the pathogenesis of muscle cramps are reviewed, and an overview of the various pharmacological agents that have had therapeutic success for this distressing and frustrating symptom is provided.

Humans↗

[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↗

Degeneration of skeletal muscle fibers in the rat administrated carbon tetrachloride: similar histological findings of the muscle in a 64-year-old patient of LC with muscle cramp.

It is well known that painful muscle cramps occur frequently in patients with advanced liver cirrhosis (LC). Although many studies discuss the pathophysiological causes of these muscle cramps in various conditions, the results are not clear as far as the cause associated to LC is concerned. In order to investigate the cause of muscle cramps in LC, we examined the histological findings of skeletal muscle fibers in LC rat model and in a patient with LC. LC (n=9) was induced in rats by chronic carbon tetrachloride administration. The histological findings of skeletal muscle tissues from the lower leg in LC rats and those of the upper arm in a patient with LC were compared. The degenerated muscle fibers and centronucleus in LC rats were similar to the opaque fibers frequently observed in myotonic dystrophy with severe muscle rigidity in patients with LC. In conclusion, results of this study suggest that one of the causes for muscle cramps in patients with LC is due to skeletal muscle fiber degeneration. Therefore, histological observation of skeletal muscle fibers should be considered in the treatment of painful muscle cramps.

Journal Article↗

Effect of orally administered shao-yao-gan-cao-tang (Shakuyaku-kanzo-to) on muscle cramps in maintenance hemodialysis patients: a preliminary study.

Muscle cramps are one of the most common complications of hemodialysis (HD), and often are a source of great pain in spite of various clinical measures. The traditional herbal medicine, shao-yao-gan-cao-tang (Japanese name: Shakuyaku-kanzo-to), consists of equal amounts of paeony and licorice roots, and has been used in Japan and China for muscle pain or skeletal muscle tremors. To determine whether this medicine is able to prevent frequent and unendurable muscle cramps in patients undergoing HD, Shakuyaku-kanzo-to at 6 g per day was prospectively administered for 4 weeks to five patients on HD who were suffering from frequent muscle cramps. The frequency and severity of cramping before and after the treatment treatment were carefully observed and compared. Skeletal muscle cramps completely disappeared in two of the treated patients after the start of oral administration of Shakuyaku-kanzo-to. Moreover, the frequency of cramping was significantly decreased in two of the remaining three patients after persistent administration. The severity of muscle cramps was also decreased by this treatment in the responsive patients. No serious side effects were detected during the treatment period. The inhibitory effect of Shakuyaku-kanzo-to on muscle contraction was also experimentally examined by using phrenic nerve-diaphragm preparations from male Wistar rats. Differences between the twitch responses were determined when the diaphragms and the nerves were stimulated in the presence and absence of the extract of Shakuyaku-kanzo-to. The results demonstrated that extracts of paeony and licorice roots inhibit contraction of skeletal muscles in rats. Taken together, we suggest that administration of Shakuyaku-kanzo-to is a safe, effective treatment for preventing muscle cramps in patients undergoing HD.

Administration, Oral↗

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↗

Randomised controlled trial of hydroquinine in muscle cramps.

BACKGROUND: Although quinine and hydroquinine are commonly prescribed for muscle cramps, controlled clinical trials of these drugs have reported mixed findings about efficacy. We investigated hydroquinine therapy in otherwise healthy adults who had frequent, ordinary muscle cramps. METHODS: This randomised, double-blind, placebo-controlled, parallel-group trial consisted of three consecutive 2-week periods: qualification, treatment, and washout, 68 women and 44 men who had at least three muscle cramps per week were enrolled. During the treatment period, participants were randomly assigned 300 mg daily dose of hydroquinine hydrobromide dihydrate (54 participants) or placebo (58). The frequency, severity (1-10), duration, and location of muscle cramps, as well as any side-effects, were recorded by participant in daily diaries. The primary outcome measures were the number of muscle cramps and the number of days during which the participants had muscle cramps (cramp-days). FINDINGS: We excluded five participants from both groups from the analysis. Thus, data from 49 hydroquinine-group participants and 53 placebo-group participants were analysed. In both groups the total number of muscle cramps and the number of cramp-days decreased during the treatment period compared with the qualification period. However, these improvements were greater in the hydroquinine group than in the placebo group. The hydroquinine-group participants reported a median of 8 (95% CI 7-12) fewer cramps and median of 3 (1-4) fewer cramp-days, whereas those on placebo reported only 3 (0-5) fewer cramps and 1 (0-5) fewer cramp-days. 32 (65%) of participants in the hydroquinine group had a 50% or greater reduction in the number of muscle cramps. After the onset of cramps, hydroquinine did not reduce the severity or duration of cramps. We also found a sustained effect after treatment had stopped. Hydroquinine was well tolerated, and resulted in only mild side-effects. INTERPRETATION: In our study, 300 mg hydroquinine was safe to take in the short-term and significantly more effective than placebo in the prevention of frequent, ordinary muscle cramps. This therapeutic effect outlasted the duration of treatment.

Administration, Oral↗

Preliminary observation: oral zinc sulfate replacement is effective in treating muscle cramps in cirrhotic patients.

BACKGROUND: While not life threatening, muscle cramps severely affect the quality of life of patients with cirrhosis. AIM: To determine whether oral zinc sulfate therapy decreases the frequency and severity of muscle cramps in cirrhotic patients. METHODS: 12 patients with cirrhosis (5 Child's A, 3 Child's B, and 4 Child's C), hypozincemia and muscle cramps at least thrice weekly received oral zinc sulfate 220 mg BID for 12 weeks. Patients answered a questionnaire regarding their muscle cramps symptoms at the beginning and end of the study. RESULTS: Muscle cramps occurred in all patients at rest, mainly while sleeping (8/12), and in two patients also during exercise. Cramps were located in calves (10/12), feet (4/12) and hands (4/12) more commonly. Zinc supplementation improved cramps in 10/12 patients, and in seven of these patients the cramps completely resolved. One patient experienced mild watery diarrhea that resolved upon discontinuation of the zinc sulfate. No other complication of zinc supplementation was noted. CONCLUSION: A potential relationship between zinc deficiency and muscle cramps in the setting of cirrhosis has not been suggested before. Zinc supplementation may lead to improvement in symptoms associated with muscle cramps in cirrhosis.

Dietary Supplements↗

[A case of isolated ACTH deficiency accompanied by generalized painful muscle cramp].

We report a patient who had generalized painful muscle cramps associated with isolated ACTH deficiency. A 68-year-old woman was hospitalized because of painful muscle cramps present for one year. Neurological examination revealed no abnormalities except for generalized painful muscle cramps. Serum electrolyte and CPK levels were normal. Serum ACTH and cortisol levels as well as urine 17-OHCS were low. An ACTH loading test employing insulin, TRH and LH-RH indicated isolated ACTH deficiency. Just after the muscle cramp, EMG revealed a low amplitude in the biceps muscle. Colon biopsy showed mild fibrosis and inflammatory cell infiltration in the lamina propria. Her muscle cramps improved markedly after two weeks of hydrocortisone replacement therapy and resolved after three weeks, suggesting that this symptom was closely related to isolated ACTH deficiency. Our case suggests that isolated ACTH deficiency may present with very similar clinical symptoms to Satoyoshi disease.

Adrenocorticotropic Hormone↗

Axillary injection of botulinum A toxin in a patient with muscle cramps associated with severe axillary hyperhidrosis.

Muscle cramps may be caused by fluid and salt loss induced by diffuse or focal hyperhidrosis. Recent reports have described the efficacy of botulinum, toxin in the treatment of primary focal hyperhidrosis. Botulinum toxin inhibits sweating by blocking exocytosis of acetylcholine from presynaptic cholinergic nerve terminals. We report the case of a patient who complained of frequent muscle cramps associated with unusually severe axillary hyperhidrosis. We used botulinum toxin to treat the excessive focal sweating presuming that it would also reduce the muscle cramps. A total dose of 200 MU of botulinum A toxin (Dysport) per axilla markedly reduced sweating and cramps. The beneficial effect started four days after the injection and it was still present five months later. Treatment was repeated in the sixth month with analogous results. No side-effects were observed and no compensatory sweating occurred.

Axilla↗