Abstracts
Abdominal cramps
Assessed whether the interindividual differences in the development of flatulence and cramps in patients with lactose malabsorption are due to the quantity of malabsorbed lactose or gas accumulation, or if accelerated intestinal transit, or increased perception of gas might play a role.
[Hydrogen breath tests were performed.]
The unabsorbed amount of lactose, small bowel transit time and volume and rate of colonic hydrogen accumulation were the same in patients who did or did not have symptoms after lactose.
Patients with flatulence and cramps had a significantly longer time interval between the onset of the increase and peak breath hydrogen concentration and a significant correlation between the time of occurrence of peak symptoms and the time of peak breath hydrogen concentration.
Data suggest that subjective symptoms of lactose intolerance are not due to the amount of malabsorbed lactose or to the volume or rate of gas accumulation per se, but are related to increased perception of gas.
Hammer HF et al., Evaluation of the pathogenesis of flatulence and abdominal cramps in patients with lactose malabsorption. Wien Klin Wochenschr, 1996, 108:6, 175-9.
Botulinum & cramps
Contents:
Botulinum toxin (3)
Botulinum toxin (1)
Botulinum toxin is now widely used in the treatment of several hyperkinetic movement disorders. Evaluated its efficacy in treating muscle cramping syndromes.
Injected calf muscles and small flexor muscles of the foot in patients with an inherited benign cramp-fasciculation syndrome.
Botulinum toxin injection significantly lowered our patients' clinical cramp severity scores (mean +/- SD: before, 3.80 +/- 0.44; after, 1.40 +/- 0.54), left muscle strength unchanged and significantly increased their cramp threshold frequencies (before, 4.22 +/- 2.26 Hz; after, 10.0 +/- 3.74 Hz).
The clinical benefit induced by botulinum toxin lasted about 3 months. Botulinum toxin injections also significantly reduced fasciculation potentials in relaxed muscles (before, 0.86 +/- 0.19 fasciculations/sec; after, 0.45 +/- 0.11 fasciculations/sec).
Efficascy possibly from reducing presynaptic cholinergic stimulation of motor nerve terminals and impairing the input/output function of intrafusal and extrafusal motor end plates.
Bertolasi L et al., Botulinum toxin treatment of muscle cramps: a clinical and neurophysiological study. Ann Neurol, 1997 Feb, 41:2, 181-6.
Botulinum toxin (2)
Over a 5-year period, 40 patients, 11 with musician's and 29 with writer's cramp, were treated with botulinum toxin A using a precise injection technique.
Moderate to complete improvement in dystonia occurred in 28 patients (70%) after the first injection and in 34 patients (85%) after the second injection with better outcome in nonmusicians than in musicians.
Of note, weakness of uninjected muscles, immediately adjacent to those injected, was found in 25/40 patients (63%).
The most common patterns of toxin spread were from flexor digitorum sublimis to profundus, extensor carpi radialis to extensor digitorum communis, and extensor indicis proprius to extensor pollicis brevis. Spread to, and weakness of, adjacent uninjected muscles was a major factor contributing to suboptimal outcome in 6/39 (15%) such patients.
Ross MH et al., Treatment of occupational cramp with botulinum toxin: diffusion of toxin to adjacent noninjected muscles. Muscle Nerve, 1997 May, 20:5, 593-8.
Botulinum toxin (3)
Patients with disabling writer's cramp (WC # 43 plus 1 with a musician's cramp) were treated with botulinum toxin (BT) injections for a mean period of 12 months.
The forearm muscles causing the dystonic position were identified by inspection while writing; BT was then administered under electromyographic (EMG) guidance.
Patients reported significant improvement in writing after 56% treatment sessions (TS) and in pain after 62% TS. Mild weakness occurred after 32% TS.
29 patients discontinued treatment, generally after the initial BT injection. In 16 patients who remained on treatment with a mean follow-up of 21 (range, 3-48) months, the improvement in writing and pain was present after 76 and 79% of the TS, respectively.
BT injections offered a worthwhile and sustained functional improvement to 36% of our patients with WC.
Turjanski N et al., Botulinum toxin in the treatment of writer's cramp. Clin Neuropharmacol, 1996 Aug, 19:4, 314-20.
Dialysis & cramps
Determined the frequency and severity of leg cramps in 40 patients on dialysis with a history of leg cramps. [Quinine 325 mg at bedtime versus vitamin E 400 IU.]
During placebo washout, the vitamin E group had a mean of 10 leg cramps per month, and the quinine group had a mean of 11. The vitamin E and quinine groups had a 1 month reduction in leg cramps to 3.3 and 3.6, respectively which was sustained at 2 months.
A severity of pain index showed a statistically significant decrease for both groups.
Quinine and vitamin E were effective treatments for leg cramps in these patients. Considering the potential toxicity of quinine, vitamin E is recommended as the initial treatment of choice for patients on dialysis with leg cramps.
Roca AO et al., Dialysis leg cramps. Efficacy of quinine versus vitamin E. ASAIO J, 1992 Jul-Sep, 38:3, M481-5.
Cirrhosis cramps
Cirrhosis (1)
Patients (# 12) with liver cirrhosis complaining of painful muscle cramps were treated with Niuche-Shen-Qi-Wan (TJ-107).
Muscle cramps disappeared in 4 weeks on the average after oral administration of TJ-107 in all patients. During the period of TJ-107 administration, there was no significant improvement of hepatic function.
Results indicate that TJ-107 is useful for treatment of painful muscle cramps in cirrhotic patients.
Motoo Y et al., Effect of niuche-shen-qi-wan on painful muscle cramps in patients with liver cirrhosis: a preliminary report. Am J Chin Med, 1997, 25:1, 97-102.
Cirrhosis (2)
Defined the features, prevalence, and pathophysiology of therapy for muscle cramps in cirrhotic patients.
The following parameters were evaluated: mean arterial pressure (MAP), nutritional status, liver function tests, plasma volume (PV), plasma renin activity (PRA), and electrolyte, mineral, and acid-base status.
The prevalence of cramps was higher in cirrhotic patients than in controls, and it was related to the duration of recognized cirrhosis and to the severity of liver function impairment.
IV infusion of human albumin reduced the cramp frequency.
An increased prevalence of true muscle cramps occurs in patients with cirrhosis. Data indicate that the pathophysiological link between cirrhosis and cramps may be represented by the reduction of the effective circulating volume. Weekly infusion of human albumin may be an effective treatment for cramps in cirrhosis.
Angeli P et al., Cirrhosis and muscle cramps: evidence of a causal relationship. Hepatology, 1996 Feb, 23:2, 264-73.
Beta-blockers & cramps
Assessed the propensity of beta-adrenoceptor blockers to cause muscle cramps and to raise the serum creatine phosphokinase (CPK) level in patients with essential hypertension (#78).
[ISA; propranolol, metoprolol or arotinolol was administered for 3 months.] Thereafter, the patients were randomised to receive a beta-adrenoceptor blocker with ISA (pindolol or carteolol) for 3 months or a beta-adrenoceptor blocker without ISA for a further 3 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 or carteolol while the levels during treatment with propranolol, arotinolol and metoprolol did not change from those in the control period.
Imai Y et al., Muscle cramps and elevated serum creatine phosphokinase levels induced by beta-adrenoceptor blockers. Eur J Clin Pharmacol, 1995, 48:1, 29-34.
Children & cramps
Most leg cramps are benign and self-limited. Idiopathic nocturnal leg cramp is the most common from of cramps. Occasionally, leg cramps may signify a significant systemic disorder. Investigations are usually not necessary unless indicated by the history or physical examination.
Symptomatic treatment consists of stretching the affected calf muscle by forcible dorsiflexion of the foot.
Leung AK et al., Leg cramps in children. Clin Pediatr (Phila), 1997 Feb, 36:2, 69-73.
Brain tumor & cramps
Writer's cramp is frequently associated with hand tremor and with other focal dystonias. Sometimes brain infarction, haemorrhage, arterio-venous malformations or tumors are found to cause symptomatic focal dystonias.
A 44-year-old man came to our attention due to writer's cramp of his right hand and postural 6-8 Hz tremor. About three months after the onset of the disease the tremor and dystonia disappeared, while a right hemiparesis gradually appeared.
Cranial computed tomography showed a hypodense nonhomogeneous lesion in the left cerebral hemisphere parietally, that was assumed to represent a cystic tumor. The patient underwent craniotomy and the histological diagnosis revealed an astrocytoma (Grade II-III).
Findings confirm the common anatomical basis of symptomatic focal dystonia and tremor. Both can appear after disruption of the pathways within and adjacent to the basal ganglia.
Milanov I & Georgiev D: Writer's cramp and tremor due to brain tumor. Can J Neurol Sci, 1995 Feb, 22:1, 59-61.
Neuromuscular cramps
Case reports (#5 ) of neuromuscular disorders, presenting with frequent muscle cramps.
Clinical diagnosis and pathophysiologic concepts are highlighted.
Jansen PH et al., Muscle cramp as a feature of neuromuscular disease. Five neuromuscular disorders, accompanied by frequent muscle cramps. Acta Neurol Belg, 1992, 92:3, 138-47.
Leg cramps
Contents:
Leg cramps
Nocturnal Leg Cramps
Leg cramps - differential diagnosis and management
Leg cramps are a common problem, especially in the elderly.
The differential diagnosis is extensive and includes the following conditions: true cramps, such as those related to heat, hemodialysis and electrolyte disturbances, as well as idiopathic cramps (the most common type); contractures occurring in conditions such as metabolic myopathies and thyroid disease; tetany, which is usually related to electrolyte disturbances, and dystonias, such as occupational cramps and those related to antipsychotic medications.
Other leg problems that are not cramps, such as restless legs syndrome and periodic leg movements, also must be distinguished.
The etiology of idiopathic leg cramps is not clear. Treatments for leg cramps include stretching exercises, quinine sulfate and vitamin E, but no treatment is conclusively effective. Nonetheless, in many patients relief of symptoms is achieved with one or more of these treatments.
Riley JD & Antony SJ: Leg cramps: differential diagnosis and management [see comments]. Am Fam Physician, 1995 Nov 1, 52:6, 1794-8.
Nocturnal Leg Cramps Without Medication
This is an observation by a physician who, before using pharmacologic therapy for muscle cramps, recommends massaging each leg 10 to 15 minutes before bed, while keeping them elevated on blankets which rest on pillows at the foot of the bed. Before considering drug therapy he evaluates patients again after 4 to 6 weeks. The author believes that this will reduce polypharmacy in the elderly.
"Working Out Leg Cramps Without Medication", Osborne, Robert M., MD, Cortlandt Forum, May 1991;71.
Magnesium & cramps
Contents:
Magnesium deficiency
Magnesium - leg cramps
Magnesium - pregnancy
Magnesium deficiency
Magnesium deficiency is more common than is believed.
Discussed florid magnesium deficiency in 2 patients and the results of treatment.
While neither case was difficult to diagnose, the severity of symptoms was unusual.
Magnesium deficiency should always be included in the differential diagnosis of patients who present with persistent or severe muscle pain.
Bilbey DL & Prabhakaran VM: Muscle cramps and magnesium deficiency: case reports. Can Fam Physician, 1996 Jul, 42:, 1348-51.
Magnesium (2) - leg cramps
A clinical observation by a physician notes low serum magnesium levels should be assessed as a possible cause of nocturnal leg cramps. Malnutrition, short bowel syndrome, malabsorption and chronic alcohol abuse may lead to magnesium deficiency.
"Low Magnesium as a Cause of Leg Cramps", Friedman, M. Cortlandt Forum, June 1990;37:28-2.
Magnesium (3) - pregnancy
Determined whether women with pregnancy-related leg cramps would benefit from oral magnesium supplementation.
Oral magnesium, or placebo, was given for 3 weeks, after which new interviews and laboratory analyses were performed.
Serum magnesium levels in these patients were at, or below, the lower reference limit, as is also often the case in healthy pregnant patients. Oral magnesium substitution decreased leg cramp distress compared with initial complaints but did not significantly increase serum magnesium levels, excess magnesium being excreted as measured by an increase in urinary magnesium levels.
Oral magnesium supplementation seems to be a valuable therapeutic tool in the treatment of pregnancy-related leg cramps.
Dahle LO et al., The effect of oral magnesium substitution on pregnancy-induced leg cramps [see comments]. Am J Obstet Gynecol, 1995 Jul, 173:1, 175-80.
Vitamin E & cramps
Vitamin E & Cirrhosis
Evaluated cirrhosis patients for the role of vitamin E in their muscle cramps. 80% reported muscle cramps. Those with muscle cramps had lower serum vitamin E levels and vitamin E/total lipid ratios than those without cramps. Some patients with muscle cramps were given 200 mgs t.i.d. of vitamin E (tocopherol acetate). Cramping pain, frequency and duration were significantly lower in the vitamin E group after treatment. Vitamin E levels increased during treatment. No side effects were noted. Those who had subnormal vitamin E levels (less than 5 ug/ml) before the intervention trial seemed to receive the most benefit.
"Vitamin E and Cirrhotic Muscle Cramps." Anonymous. Israeli Journal of Medicine, 1991;27:221-223.
Vitamin A & cramps
Vitamin A & Nocturnal Leg Cramps
Recommends vitamin A 400 mg by mouth each evening for recurrent idiopathic nocturnal leg cramps.
"More Help For Nocturnal Leg Cramps", Hass, Frederick J., MD, Cortlandt Forum, August 1990;104.
Golfer's cramps
Described golfers' cramp or the "yips".
The typical description is that of a middle-aged golfer who has played competitive golf since his teens and develops the problem during a tournament in the form of a jerk, spasm, or freezing of movement while putting or chipping, with the rest of the game being relatively unaffected. The problem generally takes a chronic fluctuating course, and a number of 'trick' strategies are partially or fully successful.
The more severely affected golfers also did not differ significantly from the mildly affected ones, except on the subjective report of anxiety.
Data support the argument that golfers' cramp is not an anxiety disorder or a neurosis. The important role of anxiety and arousal in its manifestation is, nevertheless, recognized and its pathophysiology speculated upon.
Sachdev P: Golfers' cramp: clinical characteristics and evidence against it being an anxiety disorder. Mov Disord, 1992 Oct, 7:4, 326-32.
Heat cramps
A 17-year-old, nationally ranked, male tennis player (AH) had been experiencing heat cramps during tennis match play. His medical history and previous physical exams were unremarkable, and his in-office blood chemistry profiles were normal.
On-court evaluation and an analysis of a 3-day dietary record revealed that AH's sweat rate was extensive (2.5 L.hr-1) and that his potential daily on-court sweat sodium losses (89.8 mmol.hr of play-1) could readily exceed his average daily intake of sodium (87.0-174.0 mmol.day-1).
The combined effects of excessive and repeated fluid and sodium losses likely predisposed AH to heat cramps during play. AH was ultimately able to eliminate heat cramps during competition and training by increasing his daily dietary intake of sodium.
Bergeron MF: Heat cramps during tennis: a case report. Int J Sport Nutr, 1996 Mar, 6:1, 62-8.
Exercise & cramps
Exercise (1)
The 3 types of pain related to exercise are:
1. pain experienced during or immediately following exercise,
2. delayed onset muscle soreness, and
3. pain induced by muscle cramps.
Each is characterized by a different time course and etiology.
Pain perceived during exercise is considered to result from a combination of factors including: acids, ions, proteins, and hormones. Although it is commonly believed that lactic acid is responsible for this pain, evidence suggests that it is not the only factor. However, no single factor has ever been identified.
Delayed onset muscle soreness develops 24-48 hours after strenuous exercise biased toward eccentric (muscle lengthening) muscle actions, or strenuous endurance events like a marathon. Soreness is accompanied by a prolonged strength loss, a reduced range of motion, and elevated levels of creatine kinase in the blood.
These are taken as indirect indicators of muscle damage, and biopsy analysis has documented damage to the contractile elements. The exact cause of the soreness response is not known but thought to involve an inflammatory reaction to the damage.
Muscle cramps are sudden, intense, electrically active contractions elicited by motor neuron hyperexcitability. Although it is commonly assumed that cramps during exercise are the result of fluid electrolyte imbalance induced by sweating, 2 studies have not supported this. Moreover, participants in occupations that require chronic use of a muscle but do not elicit profuse sweating, such as musicians, often experience cramps. Fluid electrolyte imbalance may cause cramps if there is profuse prolonged sweating such as that found in working in a hot environment.
Thus, despite the common occurrence of pain associated with exercise, the exact cause of these pains remains a mystery.
Miles MP & Clarkson PM: Exercise-induced muscle pain, soreness, and cramps. J Sports Med Phys Fitness, 1994 Sep, 34:3, 203-16.
Exercise (2)
The etiology of exercise-associated muscle cramps (EAMC), defined as 'painful, spasmodic, involuntary contractions of skeletal muscle during or immediately after physical exercise', has not been well investigated and is therefore not well understood.
Historically, the causes of EAMC have been proposed as:
1. inherited abnormalities of substrate metabolism ('metabolic theory')
2. abnormalities of fluid balance ('dehydration theory'),
3. abnormalities of serum electrolyte concentrations ('electrolyte theory') and
4. extreme environmental conditions of heat or cold ('environmental theory').
The available scientific literature does not support these hypotheses for the causes of EAMC.
Electromyographic (EMG) data obtained from runners during EAMC revealed that baseline activity is increased (between spasms of cramping) and that a reduction in the baseline EMG activity correlates well with clinical recovery. Furthermore, during acute EAMC the EMG activity is high, and passive stretching is effective in reducing EMG activity. This relieves the cramp probably by invoking the inverse stretch reflex.
EAMC is possibly caused by sustained abnormal spinal reflex activity secondary to muscle fatigue. Local muscle fatigue is, therefore, responsible for increased muscle spindle afferent and decreased Golgi tendon organ afferent activity.
Muscles which cross 2 joints can more easily be placed in shortened positions during exercise and would therefore decrease the Golgi tendon organ afferent activity. In addition, sustained abnormal reflex activity would explain increased baseline EMG activity between acute bouts of cramping.
Finally, passive stretching invokes afferent activity from the Golgi tendon organ, thereby relieving the cramp and decreasing EMG activity.
Schwellnus MP et al., Aetiology of skeletal muscle 'cramps' during exercise: a novel hypothesis. J Sports Sci, 1997 Jun, 15:3, 277-85.
Menstrual cramps
Described how menstrual cramps vary from cycle to cycle within a woman over time. Examined the influence of weight and lifestyle factors on occurrence, duration, and severity of menstrual pain.
Menstrual pain occurred during 72% of observed menstrual bleeds, most commonly beginning the first day of menses. The median duration was two days. 60% of women reported at least one episode of severe pain, while 13% reported severe pain more than half the time.
Earlier age at menarche and long menstrual periods increased the occurrence, duration and severity of pain. In smokers, cramps tended to last longer.
Being overweight was an important risk factor for menstrual cramps and doubled the odds of having a long pain episode.
Frequent alcohol consumption decreased the probability of having menstrual cramps, but in women who had pain it increased duration and severity.
Physical activity was not associated with any pain parameter.
Women who have pain lasting 3 days are an important target group for prophylactic therapy. The occurrence and severity of menstrual cramps is influenced by potentially modifiable characteristics including weight, smoking, and alcohol consumption. Doctors may wish to counsel women presenting with dysmenorrhoea about the importance of healthy lifestyles and about the inefficacy of alcohol consumption as a treatment for dysmenorrhoea.
Harlow SD & Park M: A longitudinal study of risk factors for the occurrence, duration and severity of menstrual cramps in a cohort of college women. Br J Obstet Gynaecol, 1996 Nov, 103:11, 1134-42.
Muscle cramping
Muscle cramp - neurophysiology
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.
Reviewed 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.
Bentley S: Exercise-induced muscle cramp. Proposed mechanisms and management. Sports Med, 1996 Jun, 21:6, 409-20.
Muscle lengthening
Muscular lengthening
Verified that cramps can be evoked by electrical stimulation of peripheral nerve and clarified the physiological mechanism responsible by analyzing the effect of muscular stretching on cramps.
Muscle cramps induced by voluntary contraction and by electrical stimulation of the peripheral nerve were studied electrophysiologically in 10 healthy subjects.
Results showed:
1. Cramps can be induced even after peripheral nerve block by electrical stimulation distal to the block.
2. No cramps were recorded during or following maximal voluntary contraction without muscular shortening, while 7 of 10 subjects showed a true cramp following maximal effort with shortening of the muscle.
3. Muscle stretching caused a sudden interruption of cramps induced by either voluntary contraction or electrical stimulation of the peripheral nerve, even after the induction of nerve block.
4. The lengthening state of the muscle can strongly influence the possibility of evoking cramps by electrical stimulation of nerve.
Verifies the experimental model proposed by Lambert in 1969, emphasizing the relevance of frequency of stimulation and confirming the hypothesis that cramps are of peripheral origin. The effects of muscle stretch and lengthening on cramp interruption and development also have a peripheral mechanism.
Bertolasi L et al., The influence of muscular lengthening on cramps. Ann Neurol, 1993 Feb, 33:2, 176-80.
Pain & cramps
Painful muscle cramps
A sporadic Japanese case of myotonia congenita with painful muscle cramps is reported.
Electromyographic examinations disclosed myotonic discharge with dive bomber sounds at insertion, and high-amplitude, high-frequency motor unit potentials during the muscle cramps. Biopsied muscle specimens and EMG findings showed non-specific mild myopathic changes.
There was no abnormal expansion of CTG repeat within the myotonic dystrophy gene.
Sunohara N et al., Myotonia congenita with painful muscle cramps. Intern Med, 1996 Jun, 35:6, 507-11.
Quinine & cramps
Contents:
Quinine (4)
Quinine/hydroquinine (1)
Although quinine and hydroquinine are commonly prescribed for muscle cramps, controlled clinical trials of these drugs have reported mixed findings about efficacy.
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.
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 fewer cramps and median of 3 fewer cramp-days, whereas those on placebo reported only 3 fewer cramps and 1 fewer cramp-days. 32 (65%) of participants in the hydroquinine group had a 50% or greater reduction in the number of muscle cramps.
Also found a sustained effect after treatment had stopped. Hydroquinine was well tolerated, and resulted in only mild side-effects.
Jansen PH et al., Randomised controlled trial of hydroquinine in muscle cramps. Lancet, 1997 Feb 22, 349:9051, 528-32.
Quinine (2)
Studied the efficacy of quinine in the prevention of nocturnal leg muscle cramps.
Outpatients experienced an estimated two or more typical nocturnal leg cramps per week.
200 mg of quinine taken at bedtime.
During the 2 weeks patients used quinine, there was no statistically significant reduction in mean leg cramp number (quinine 3.5 vs placebo 4.2), mean leg cramp duration (quinine 152 seconds vs placebo 163 seconds), or patient ratings of severity using a 1 (low) to 10 (high) scale (quinine = 4.2 vs placebo = 4.0, P = 0.83).
No significant reduction in nocturnal leg cramp frequency, intensity, or duration could be found using nightly quinine in this study. Since quinine is not without the potential for side effects and drug interactions, clinicians need to carefully consider the likelihood of modest benefit associated with quinine against the potential for side effects and drug-drug interactions.
Sidorov J: Quinine sulfate for leg cramps: does it work? J Am Geriatr Soc, 1993 May, 41:5, 498-500.
Quinine (3)
Benign nocturnal leg cramps are a relatively common and bothersome complaint, particularly among the elderly.
Careful history taking and physical examination can exclude the majority of disorders in the differential diagnosis.
Mechanical treatment of an acute muscle cramp involves stretching of the affected muscle.
Prophylaxis includes both mechanical and pharmacologic measures. The efficacy of quinine sulfate has been supported in the majority of well-designed studies, but its use is controversial, and the FDA has banned over-the-counter quinine-based products used for leg cramps.
Potentially fatal hypersensitivity reactions and thrombocytopenia can occur with use of quinine.
Leclerc KM & Landry FJ: Benign nocturnal leg cramps. Current controversies over use of quinine. Postgrad Med, 1996 Feb, 99:2, 177-8, 181-4.
Quinine (4) - Veterans
Compared the efficacy and safety of quinine sulfate, vitamin E, and placebo in the treatment of nocturnal leg cramps.
Subjects received, in random order, quinine sulfate (200 mg at supper and 300 mg at bedtime), vitamin E (800 U at bedtime), or placebo for 4-week periods. These periods were separated by 4-week washout intervals.
Compared with treatment with placebo, quinine reduced the frequency of cramps and sleep disturbance, but not the average cramp severity.
13 of 27 patients had at least a 50% reduction in the number of cramps while receiving quinine; the response was usually seen within 3 days.
There was evidence of a mild increase in side effects while subjects received quinine.
Vitamin E was not effective in reducing leg cramp frequency, severity, or sleep disturbance.
Quinine sulfate, but not vitamin E, is superior to placebo in the treatment of nocturnal leg cramps.
Connolly PS et al., Treatment of nocturnal leg cramps. A crossover trial of quinine vs vitamin E [see comments]. Arch Intern Med, 1992 Sep, 152:9, 1877-80.
Rest cramps
The overall prevalence of rest cramps in the survey population (# 218) was 37%. The symptom was more prevalent in older subjects.
Rest cramps were most commonly experienced in the muscles of the leg, in 83% of the 86 cramp sufferers. Symptoms were usually present at night (73%). On average cramp episodes lasted for 9 min.
Most cramps sufferers experienced symptoms infrequently, but 40% had cramp episodes more than 3 times per week and 6% complained of daily episodes.
20% of cramp sufferers described their symptoms as very distressing.
A minority, 32% of the 86 cramp sufferers, had reported the symptoms to a general practitioner although the 86 subjects self-rated their health more negatively than the individuals without muscle cramps.
Peripheral vascular disease may play a relevant but limited role in the aetiology of rest cramps.
Naylor JR & Young JB: A general population survey of rest cramps. Age Ageing, 1994 Sep, 23:5, 418-20.
Veterans & cramps
Described patients with nocturnal leg cramps concerning their age, medical problems, and medications, and reviewed any medical evaluation performed for the complaint of nocturnal leg cramps.
Patients took quinine sulfate for nocturnal leg cramps.
Patients with nocturnal leg cramps had a significantly higher median number of medical problems than controls. Cardiovascular diseases and neurological diseases were significantly more common in patients with nocturnal leg cramps (cases) than in those without (controls) (82% versus 64% and 36% versus 18%, respectively). The most striking differences between patients with cramps and controls were peripheral vascular disease (34% versus 12%) and peripheral neurological deficit (12% versus 0%).
Patients with nocturnal leg cramps were prescribed significantly more medications than were controls, but no specific medication or type of medication was prescribed more frequently to patients with cramps (other than quinine).
Haskell SG & Fiebach NH: Clinical epidemiology of nocturnal leg cramps in male veterans. Am J Med Sci, 1997 Apr, 313:4, 210-4.
Writer's cramps
Contents:
Writer's cramp (4)
Writer's cramp (1)
Evaluated sensorimotor processing in patients with writer's cramp.
[PET and H2(15)O blood flow scans at rest and during vibration.]
Vibration produced a consistent peak response in primary sensorimotor area (PSA) and supplementary motor area (SMA), both contralateral to the vibrated hand. Both responses were significantly reduced approximately 25% in patients with writer's cramps whether vibrating the affected, or unaffected, hand. This indicates that patients with unilateral writer's cramp have bilateral brain dysfunction.
Tempel LW & Perlmutter JS: Abnormal cortical responses in patients with writer's cramp [published erratum appears in Neurology 1994 Dec;44(12):2411]. Neurology, 1993 Nov, 43:11, 2252-7.
Writer's cramp (2)
An 11-year-old girl was evaluated for walking difficulties and fatigue at the end of the day in the last 2 years. Handwriting was also difficult with 'cramps' after a short time of writing.
Neurological examination was normal most of the time but in the evening and after exercise, an abnormal walking posture and rare dystonic movements of the foot could sometimes be seen. The mother was found to have mild parkinsonism and is asymptomatic on L-dopa. In the daughter, all symptoms and signs disappeared on L-dopa, but returned when the drug was withdrawn. The changes on- and off-treatment were documented with videofilms and computerized analysis of writing samples. The situation has been stable during a 5-year follow-up.
Highlight this 'forme fruste' of dopa-sensitive childhood dystonia which becomes manifest with exercise and which can easily go unrecognized.
Also discuss and illustrate the methods used for the analysis of writing.
Deonna T et al., Dopa-responsive childhood dystonia: a forme fruste with writer's cramp, triggered by exercise. Dev Med Child Neurol, 1997 Jan, 39:1, 49-53.
Writer's cramp (3)
Studied the inhibition of median H-reflexes by conditioning stimuli on the radial nerve in 13 patients with writer's cramp (8 of the simple type and 5 of the dystonic type) and in 14 normal volunteers.
Results indicate that the attenuation of reciprocal inhibition was present not only in symptomatic arms but also in asymptomatic arms of patients with writer's cramp. The defect of reciprocal inhibition in the asymptomatic hand has never been documented.
Suggest that the preexistent electrophysiological abnormality may provide an explanation for the development of hand cramp after shifted writing.
Chen RS et al., Reciprocal inhibition in writer's cramp. Mov Disord, 1995 Sep, 10:5, 556-61.
Writer's cramp (4)
Patients with writer's cramp have 2 well-recognized neurophysiological abnormalities:
reduced reciprocal inhibition of the wrist flexor motoneurons at rest, and
increased cocontraction of antagonist muscles of the forearm during voluntary activity.
Demonstrate an impaired integration of sensory inputs into the voluntary motor activity during performance of a force-related task in patients with writer's cramp.
[Normal (control) subjects and patients activated wrist flexor and extensor muscles to maintain a predetermined level of force. Electrical stimuli were applied to median and radial nerve afferents and the modulatory effects induced in the electromyographic (EMG) activity were measured.]
In the agonist wrist flexors, patients had reduced homonymous and reciprocal inhibition. In the agonist wrist extensors, patients had reduced reciprocal excitation and reciprocal inhibition.
Results are compatible with an abnormal CNS processing of the inputs generated by external stimuli during voluntary contraction of wrist flexor and extensor muscles. Defective integration of inputs from peripheral nerve afferents into the command for voluntary movement may partly underlie the pathophysiology of the motor dysfunction in patients with writer's cramp.
Valls-Solé J & Hallett M: Modulation of electromyographic activity of wrist flexor and extensor muscles in patients with writer's cramp. Mov Disord, 1995 Nov, 10:6, 741-8.
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