Approach

The first challenge in evaluating a patient with spasms, muscle pain, or both is to determine whether the patient is experiencing true cramps or some other symptom.[16] The second challenge is to determine, if possible, the aetiology of the cramping.[16] A targeted medical history and physical examination can narrow down potential aetiologies. Laboratory investigations can then be used to confirm or refute clinically suspected aetiologies. Sophisticated diagnostic studies (e.g., electromyogram [EMG], muscle biopsy, muscle enzymes, genetic studies) are generally needed by specialists only when symptoms are particularly difficult to diagnose.

History

Patient description of the cramp helps distinguish true cramps from myalgia (generalised or focal muscle pain without contractions), myokymia, and myopathy (contracture not associated with electrical activity on EMG). Symptom pattern helps to distinguish idiopathic (ordinary) cramp from cramp associated with underlying organic disease.

Patient history should elicit:

  • Duration (determines acute or chronic)

  • Which muscles are involved: of key importance because muscle involvement other than the gastrocnemius (with or without foot involvement) is more likely due to an organic cause

  • When and in what context the cramps occur (e.g., nocturnal, during dialysis, during exercise, during home parenteral nutrition)[3][77]

  • Specific precipitating or aggravating factors (e.g., exercise, hypoglycaemia in people with diabetes)

  • Any treatment used: may identify potentially dangerous self-treatments, such as tonic water (which contains quinine).

Idiopathic cramps:

  • Usually involve single muscles or part of a muscle, especially the gastrocnemius (with or without foot involvement)[3]​​[13][16]​​

  • After an explosive onset will last from seconds to minutes​[1][9][10][13][16]​​

  • Can be precipitated by both trivial movements and forceful contractions (particularly in an already shortened muscle)[16]

  • Frequently demonstrate visible or palpable knotting and abnormal posturing of the affected joint[1]

  • Frequently have a nocturnal onset[3]

  • Respond well to passive/active stretching[3]

  • Can result in persistent tenderness (particularly in children) and swelling.[13]​​[15][16]​​​

Organic cramps:

  • Local cramps in muscles other than the gastrocnemius or foot are frequently noted in the context of neuromuscular disease[1]

  • Widespread cramps, especially when associated with muscle weakness, suggest lower motor neuron disease

  • Cramps associated with myopathies generally last longer than true cramps and are not resolved by muscle stretching.

History should seek specific risk factors for cramps. These include strenuous exercise, pregnancy, cirrhosis, haemodialysis, hypoglycaemic episodes in people with diabetes mellitus, and the presence of other chronic medical conditions (e.g., thyroid disease, peripheral vascular disease, cardiovascular disease, hypokalaemia, neurological disease or deficit, arthritis, and gastritis).

It is important to elicit a full drug history because selected medications may be associated with cramping (e.g., imatinib, statins, and beta-blockers with intrinsic sympathomimetic activity, among others). See Risk factors.

Consumption of alcohol is associated with nocturnal leg cramps in people aged 60 years and older.[72]

Exercise-associated muscle cramps (EAMC) are usually found in people in training or in competition. Cramps occur only in fatigued, exercised muscles.

In patients with diabetes mellitus, cramps are seen most frequently during periods of hypoglycaemia (particularly 3 to 5 hours after going to bed and several hours after meals).[74] The degree of glycaemic control may be assessed using a blood glucose diary review. The timing of cramps is analysed in respect of any risk factors for hypoglycaemia (meal timing, excessive activity without compensatory dietary changes, alcohol consumption, prolonged abstinence from food).

Cramps in patients undergoing renal replacement therapy with haemodialysis occur most frequently during dialysis sessions, particularly when ultrafiltration rates are high in order to remove excess fluid.​[18][19][78]​​[79]

In patients with thyroid disease, symptoms of hyper- or hypothyroidism may be present.

Family history of illness is important, as many of the rarer muscle contraction syndromes are familial in nature.

Physical examination

A general physical examination, primarily targeting the neurological and musculoskeletal systems, is performed to rule out associated or differential conditions.

Neurological abnormalities (e.g., sensory loss, hyperreflexia, and spasticity) and musculoskeletal signs (e.g., weakness, loss of muscle bulk, and continuous fasciculations) point to organic aetiologies of cramping disease. Fasciculations are a common finding before and/or after a true cramp, but prominent fasciculations or continuous fasciculations are not commonly found in association with true cramp.[1]

Lower motor neuron diseases are associated with cramps and are characterised by muscle weakness, muscle atrophy, hyporeflexia, and muscle hypotonicity or flaccidity.[80] They include diseases such as poliomyelitis, multifocal motor neuropathy, benign focal amyotrophy, spinal muscular atrophy, Kennedy's disease (X-linked spinal and bulbar muscular atrophy), progressive muscular atrophy, and amyotrophic lateral sclerosis.

In patients with EAMC, normal diuresis and body temperature are the rule.

If cramps are severe and the patient has altered consciousness, is anuric, has non-exercise cramps (generalised cramps), or is hyperpyrexic or hypopyrexic, one or more systemic disorders (e.g., volume depletion, severe electrolyte imbalance, acute renal failure, or intracranial disorder) may be present, and immediate admission to the hospital is necessary.[42]

Laboratory evaluation

No tests are initially required if idiopathic cramps are strongly suspected.

Laboratory evaluation is most useful to verify suspected organic causes of cramps. Initial tests performed in people who have features on history and physical examination suggestive of an organic cause or associated condition include the following.

  • Serum or urine human chorionic gonadotrophin (hCG) to verify pregnancy.

  • Serum creatinine to verify any renal impairment.

  • Serum electrolyte panel, including magnesium and calcium, to verify type and severity of electrolyte disturbances.

  • Serum phosphate is measured in patients maintained on renal replacement therapy.

  • Serum creatine kinase (CK) in people taking a statin.

  • HbA1c may be obtained in patients with known diabetes. A lower than expected value relative to degree of observed control via fingerstick blood glucose may suggest, but not confirm, hypoglycaemia.

  • Thyroid stimulating hormone to verify hypo- or hyperthyroidism. Further thyroid function tests may be warranted.

  • Liver function panel (bilirubin, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, LDH) to assess any hepatic impairment.

  • Clotting studies (prothrombin time and INR) may also be performed if severe hepatic disease is suspected.

Further investigations

Additional tests performed by a specialist may include the following.

  • EMG: performed only in difficult-to-diagnose cases or if lower motor neuron disease is suspected.

  • Serum CK-MM: performed only if history or physical examination suggest a potential primary muscle disease or the patient is taking a statin. Serum aldolase is also measured if primary muscle disease is suspected. High levels in severe EAMC. In simple idiopathic cramps they should be within normal limits.

  • Serum alpha tocopherol (vitamin E) and zinc: in cirrhosis, low values may suggest potential therapeutic interventions.

  • Muscle biopsies: performed only if primary muscle disease or lower motor neuron disease is suspected.

  • Nerve conduction studies may be performed if lower motor neuron disease is suspected.

  • Genetic studies are generally requested only when a patient's symptoms are particularly difficult to diagnose or a familial cramping syndrome is suspected (e.g., muscular dystrophy, congenital myotonia, glycogen storage disease, continuous muscle fibre activity syndrome, Satoyoshi's syndrome, Schwartz-Jampel syndrome, or Brody's disease).

Considerations in children

The younger the child, the more likely that an organic cause will be found.[81] Nocturnal leg cramps were reported in about 7% of healthy children in one study, beginning only after 8 years of age and peaking in prevalence at 16 to 18 years of age.[15]

Cramps lasting longer than 10 minutes suggest an organic cause.

Idiopathic cramps are always unilateral, whereas organic causes produce unilateral or bilateral symptoms).[74][82]

Poor growth, as determined by standard developmental milestone measurements, suggests the presence of chronic disease, which may or may not be causative.

As with adults, a review of the medical history and a targeted physical examination for signs and symptoms of the organic diseases most frequently associated with cramps should allow idiopathic cramps to be ruled in or out with reasonable certainty. It is particularly important to consider the following.

  • Pregnancy in adolescents.

  • Nervous system disease, especially muscular dystrophy.

  • Myoglobinuria, presenting with prominent muscle pain. The urine may be pink or red, and serum should be checked for myoglobin. This test is considered only when primary muscle disease is a consideration.

  • Strenuous exercise in child athletes. Cramps should occur only during heavy exercise.

  • Growing pains are not associated with palpable/visible hardening of muscle usually seen with cramps.

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