History and exam
Key diagnostic factors
common
presence of risk factors
Risk factors strongly associated with muscle cramps include pregnancy, strenuous exercise, concurrent haemodialysis, and cirrhosis.
Other less strongly associated factors include age >60 years, female sex, family history of cramp, prescribed drugs, hypoglycaemia in diabetes mellitus, and the presence of various chronic medical conditions.
nocturnal onset (idiopathic cramp)
Cramps occurring only during sleep are usually idiopathic cramps (benign or ordinary).[3]
gastrocnemius muscle involvement, with or without foot involvement (idiopathic cramp)
Cramps involving only these muscles are more likely to be idiopathic cramps (benign or ordinary).[13]
duration <10 minutes (idiopathic cramp)
unilateral (idiopathic cramp)
Idiopathic cramps are always unilateral (organic causes produce unilateral or bilateral symptoms).
precipitation by both trivial movements and forceful contractions (idiopathic cramp)
Finding in idiopathic cramps.
visible or palpable muscular knotting
Finding in all cramps.
good response to passive/active stretching (idiopathic cramp)
If the cramp does not respond to passive/active stretching, organic associations or differential diagnoses need to be considered.
normal neurological examination (idiopathic cramp)
Common with idiopathic cramps.
normal general physical examination (idiopathic cramp)
Typically, no abnormal findings on examination in people with idiopathic cramp.
uncommon
other local muscle involvement (neuromuscular disease cramp)
Local cramps in muscles other than the gastrocnemius or foot are frequently noted in the context of neuromuscular disease.[1]
widespread muscle cramps (lower motor neuron disease)
Widespread cramps, particularly when associated with muscle weakness, suggest lower motor neuron disease (e.g., amyotrophic lateral sclerosis).
duration >10 minutes (organic cause)
Cramps lasting longer than 10 minutes (particularly in a child) suggest an organic cause.
abnormal neurological examination (organic cause)
Neurological abnormalities such as sensory loss, hyperreflexia, and spasticity point to organic aetiologies of cramping disease.
abnormal musculoskeletal examination (organic cause)
Signs such as weakness, loss of muscle bulk, and continuous fasciculations (by direct visualisation or palpation) point to organic aetiologies of cramping disease.
Other diagnostic factors
uncommon
signs of a chronic medical condition (organic cause)
True cramp may be associated with various chronic medical conditions, including peripheral vascular disease, cardiovascular disease, hypokalaemia, neurological disease or deficit, arthritis, and gastritis, and there may be associated signs or symptoms.
Hypothyroidism (and, much less frequently, hyperthyroidism) predisposes to cramps.
Various familial disorders may be suspected by their typical signs and symptoms.
Risk factors
strong
pregnancy
strenuous exercise
Particularly in endurance events such as triathlons, marathons, and ultramarathons.[28][29][30]
Team sports (e.g., rugby) also predispose to exercise-associated muscle cramps (EAMC).[28][30]
Various hypotheses for EAMC have been suggested but have not been proven.[39][40] There may be different types of EAMC that are initiated by different mechanisms.[30]
Risk factors for EAMC in marathon runners include older age, longer running history, higher body mass index, shorter daily stretching time, irregular stretching habits, and a positive family history of cramps.[40] Other risk factors in marathon runners and triathletes include high-intensity running, long-duration running (>30 km), subjective muscle fatigue, and hill running.[40][41]
For athletes in general, the most important risk factors include a past history of EAMC, increased exercise intensity by race pace or subjective assessment (intrinsic factors), and increased environmental temperature and humidity (extrinsic factors).[28] All lead to premature muscle fatigue.
Muscles most frequently affected include force-generating biarticular muscles (e.g., the triceps surae, hamstrings, and quadriceps).[42]
haemodialysis
Intradialytic cramps have been reported in 15% to 87% of patients undergoing haemodialysis support.[18][19][20][21][22]
Hyperphosphataemia enhances cramp risk in patients undergoing haemodialysis.[20]
Although data are scant, the frequency of cramps in patients undergoing peritoneal dialysis is said to be similar to that in haemodialysis recipients.[20]
There is some evidence to suggest a correlation between free serum leptin concentrations and frequency of intradialytic cramps.[43]
cirrhosis
Cramps have been reported in 22% to 88% of patients with cirrhosis.[23][24][25][26][27]
Clinically relevant cramps (defined as those occurring at least once weekly, negatively affecting the patient's quality of life, and requiring analgaesia) were reported in 12% to 42% of these patients.[24][25][26][27][44] Cramps are a major cause of the poor quality of life experienced by patients with cirrhosis.[45][46]
The prevalence of cramp is higher in patients with cirrhosis than in patients with non-cirrhotic liver disease.[27]
There is a significantly higher frequency of finger and thigh cramps compared with that reported by control subjects and people with chronic non-cirrhotic liver disease.[25]
Diuretic use has not been found to be a causative or a contributing factor to cramps in people with cirrhosis.[24][25][26][27]
use of imatinib
Tyrosine kinase inhibitors (TKIs), such as imatinib, are a class of medicine used for certain types of cancer. Imatinib was reported to cause cramps in up to 50% of patients, with the frequency increasing when doses of >750 mg/day were used.[47] Cramps usually occur in the hands, feet, calves, and thighs.[48] Skeletal muscle toxicity including muscle cramps has been associated with all TKIs.[49]
weak
age >60 years
Idiopathic (ordinary) cramps are most frequently seen in older people.[3]
The ageing process is a theoretical risk factor.[52] Ageing has mostly been reported to increase the incidence of cramps, although some studies have found no effect.[9][11][14]
A sedentary lifestyle has been associated with nocturnal leg cramps in patients over 60 years.[53]
female sex
family history of cramp
Certain genetic syndromes are associated with cramps.
Familial muscle contraction syndromes include Kocher-Debre-Semelaigne, muscular dystrophies (such as Becker's, limb-girdle type 1c, or Brody's disease), congenital myotonia, glycogen storage disease (such as McArdle's disease), Isaac's disease, Satoyoshi's syndrome, Schwartz-Jampel syndrome, and autosomal dominant cramps.
use of statins
Statins cause myopathy (a combination of myalgias, weakness, and cramping) in a small proportion of recipients (1% to 10%), especially when combined with fibrate therapy (e.g., gemfibrozil) or used in high doses.[54]
Cramps have been anecdotally related to statin use, but there are scant data linking statins to this effect.[55]
However, in one epidemiological trial, cramps were noted in 20/338 (6%) of statin recipients.[56]
Cramps alone occur in a vanishingly small proportion of cases of statin myopathy.
use of other agents that may cause muscle cramps
Numerous agents have been implicated in the development of cramps. However, most supportive data are weak, consisting of case reports or series.
Examples include antihypertensives (e.g., diuretics, ACE inhibitors, calcium-channel blockers), lipid-lowering agents (e.g., fibrates, nicotinic acid), beta-agonists (e.g., salbutamol, terbutaline) corticosteroids (e.g., prednisolone, beclometasone), non-corticosteroid hormonally active drugs (e.g., medroxyprogesterone, testosterone, oestrogens, progesterone, insulin, teriparatide, raloxifene), others (e.g., carbimazole, cisplatin, oxaliplatin, penicillamine, phenothiazines, pyrazinamide, zolmitriptan), opioid withdrawal or alcohol consumption, and bowel cleansing agents (e.g., sodium phosphate).[5][57][58][59][60][61][62][63][64][65][66][67][68][69][70][71][72][73]
hypoglycaemia in patients with diabetes mellitus
Case series have demonstrated a relationship between hypoglycaemia in patients with diabetes mellitus and the emergence of cramps.[64][74][75]
Cramps have been traced to the presence of risk factors for hypoglycaemia several hours before the episode (e.g., alcohol consumption, prolonged abstinence from food, excessive activity without compensatory dietary changes, excessive doses of antidiabetic medication). Thus, cramps are prominent 3 to 5 hours after going to bed and several hours after a meal.
Cramps occur together with other symptoms and signs of hypoglycaemia (intense hunger, tremor, profuse sweating, tachycardia, mental clouding). These all respond rapidly to correction of the hypoglycaemic state.
chronic diseases
Various chronic medical conditions have been found to be associated with muscle cramps (e.g., peripheral vascular disease, cardiovascular disease, hypokalaemia, neurological disease or deficit, arthritis, and gastritis).[8][10][11][76]
Hypothyroidism (and, much less frequently, hyperthyroidism) predisposes to cramps.
home parenteral nutrition
About one quarter of patients maintained on home parenteral nutrition report muscle cramps directly related to feedings and may require a slowing of the feeding rate, or pharmacological therapy.[77]
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