Crumpy: causes, symptoms, diagnosis

In the literature, one can find indications that approximately one third of the population experiences spontaneous cramps at least once a year - a sudden, involuntary and painful tonic muscle contraction that occurs spontaneously or is provoked by movement and manifests itself as a visible muscle ridge (cord, "knot") that is dense upon palpation. Cramps usually affect one muscle or part of it.

I. Healthy people.

1. Excessive physical exertion.
2. Fluid loss through heavy sweating or diarrhea.
3. Idiopathic.

II. Neurological diseases.

1. Family crumpets.
2. Amyotrophic lateral sclerosis (cramps as a manifestation of pyramidal insufficiency and damage to the cells of the anterior horns of the spinal cord).
3. Other diseases of the anterior horn (progressive spinal muscular atrophies).
4. Irritation of a root or nerve (peripheral neuropathy: malignant tumors; trauma; compression lesions; polyneuropathies; multifocal motor neuropathy; late effects of poliomyelitis;).
5. Generalized motor unit hyperactivity (with or without peripheral neuropathy): Isaacs syndrome; paraneoplastic syndrome; inherited forms of persistent motor unit hyperactivity).
6. Mainly myogenic cramps (glycogen metabolism disorders; lipid metabolism disorders; local or diffuse myositis; endocrine myopathies; Becker muscular dystrophy).
7. Myotonic disorders.
8. Rigid person syndrome.
9. Satoyoshi syndrome.

III. Metabolic causes.

1. Pregnancy.
2. Tetany.
3. Other electrolyte disturbances.
4. Hypothyroidism (myxedema).
5. Hyperparathyroidism.
6. Uremia.
7. Cirrhosis.
8. Gastrectomy.
9. Alcohol.

IV. Iatrogenic causes.

1. Diuretic therapy.
2. Hemodialysis.
3. Vincristine.
4. Lithium.
5. Salbutamol.
6. Nifedipine.
7. Other drugs (penicillamine, aminocaproic acid, etc.).

V. Other reasons.

1. Intermittent claudication.
2. Crumpy when overheated.
3. Eosinophilia-myalgia syndrome.
4. Toxins (insecticides, strychnine, etc.).
5. Tetanus.

I. Healthy people

Excessive physical activity in a healthy person (especially in a deconditioned person) can cause an episode(s) of cramps. Prolonged and intense sweating or diarrhea, regardless of the cause of the latter, can also provoke cramps. Occasional cramps occur, the cause of which remains unclear (idiopathic). Most often, such cramps are observed in the calf muscles and can briefly fix the foot in an altered position.

II. Neurological diseases

Familial cramps have the same manifestations, but are more persistent, often develop spontaneously and are more easily provoked (physical activity, use of diuretics or laxatives). The course of the disease is undulating; during exacerbations, generalization of cramps is possible with their periodic and alternating occurrence not only in the gastrocnemius muscles, but also in the thigh muscles (posterior muscle group, sartorius muscle), anterior abdominal wall. Intercostal, pectoral muscles, and back muscles may be involved. In the facial area, the mylohyoid muscle is involved: after intense yawning, a unilateral spasm of this muscle usually develops with a characteristic painful compaction, palpable from the side of the diaphragm of the mouth. In some individuals, cramps develop against the background of constant more or less generalized fasciculations (syndrome of benign fasciculations and cramps); sometimes fasciculations are observed before the onset and at the end of cramping spasms. Passive stretching of the muscle or its active work (walking, etc.), as well as muscle massage, leads to the cessation of the cramp.

Night cramps are very common, especially when changing body or limb position, and are prevalent in the elderly population. Diseases of the peripheral nerves, muscles, veins, and arteries contribute to their occurrence.

Resting cramps may be the earliest manifestation of amyotrophic lateral sclerosis; clinical symptoms of progressive upper and lower motor neuron involvement occur later. Cramps in ALS may be seen in the muscles of the lower leg, thigh, abdomen, back, arms, neck, lower jaw, and even the tongue. Fasciculations and cramps alone without EMG signs of denervation cannot serve as a basis for diagnosing amyotrophic lateral sclerosis. Progressive spinal amyotrophies may be accompanied by fasciculations and cramps, but the main manifestation of this group of diseases is symmetrical amyotrophies with a benign course. Progressive spinal amyotrophies, as a rule, have neither clinical nor electromyographic signs of upper motor neuron involvement.

Cramps may be observed in radiculopathies and polyneuropathies (as well as plexopathies) of various origins. Patients who have had poliomyelitis in the past sometimes note the appearance of cramps and fasciculations.

A number of diseases of the nervous system that have a common neurophysiological basis in the form of so-called hyperactivity of motor units, manifest themselves, in addition to other clinical manifestations, as cramping syndrome: idiopathic (autoimmune) syndrome of constant muscle fiber activity (Isaacs syndrome); paraneoplastic syndrome (clinically similar to idiopathic Isaacs syndrome) can be observed in bronchogenic carcinoma, lymphoma and other malignant neoplasms with or without peripheral neuropathy; cramping-fasciculation syndrome (muscle pain-fasciculation syndrome); some hereditary diseases: hereditary myokymia with cramping, myokymia in paroxysmal dyskinesias. In most of the mentioned forms of neurological diseases, cramps are not the leading clinical syndrome and are observed most often in the context of progressive muscle stiffness, and electromyography reveals constant spontaneous activity in the affected muscles.

Cramps are found in some myotonic disorders. Lambert-Brodie syndrome (Lambert-strongrody) develops in the first or second decade of life and is manifested by progressive muscle pain induced by physical activity; muscle stiffness and cramps. Another rare disease is congenital myotonia with painful cramps. Some researchers consider this variant of myotonia to be a variant of Thomsen's myotonia. Cramps are observed in the picture of chondrodystrophic myotonia (Schwartz-Jampel syndrome). The latter is characterized by an autosomal dominant type of inheritance and begins to manifest in infants with myotonia, osteochondroplasia, growth retardation, hypertrophic muscles and a characteristic face with blepharophimosis, micrognathia and low-set ears. Muscle tightness and osteochondrodysplasia often limit joint mobility and result in a rigid gait.

Stiff-Person syndrome is characterized by the gradual onset of symmetrical tension of the proximal and especially axial muscles of the trunk (characterized by a fixed lumbar hyperlordosis that does not disappear in the supine position) with a rocky density of the muscles and painful spasms that are provoked by many factors and are sometimes accompanied by vegetative reactions. Sometimes this picture is superimposed by spontaneous or reflex ("stimulus-sensitive") myoclonus, provoked by various sensory stimuli. The EMG shows constant increased activity at rest. With progression, dysbasia develops. Hypertonicity disappears or decreases during sleep (especially in the REM phase), during the sedative effect of diazepam, general anesthesia, root or nerve block, and with the introduction of curare.

Satoyoshi syndrome begins in childhood or adolescence with recurrent, painful muscle spasms that often cause the limbs and trunk to assume abnormal postures (myospasm gravis). The spasms are triggered by voluntary movements and are usually not observed at rest or during sleep. Many patients subsequently develop alopecia, diarrhea with malabsorption, endocrinopathy with amenorrhea, and multiple secondary skeletal deformities. The pathogenesis of this syndrome is not fully understood; autoimmune mechanisms are suspected.

Mainly myogenic cramps are typical for such hereditary diseases as glycogenoses (glycogenoses types V, VII, VIII, IX, X and XI); deficiency of carnitine palmitoyltransferase I (autosomal recessive type of inheritance; early onset, often neonatal; episodes of non-ketonemic hypoglycemic coma; hepatomegaly; hypertriglyceridemia and moderate hyperammonemia; decreased activity of carnitine palmitoyltransferase I in fibroblasts and liver cells) and deficiency of carnitine palmitoyl transferase II (age of disease manifestations is variable; the most frequent complaint is muscle pain (myalgia) and spontaneous cramps; myoglobulinuria is characteristic; deficiency of the above enzyme is revealed in skeletal muscle biopsy). Local or diffuse myositis may be accompanied by cramps, as well as endocrine myopathies; the appearance of cramps has been described in Becker muscular dystrophy (it differs from Duchenne muscular dystrophy by its later onset and benign course). Severe myalgia in the legs, often in combination with cramps, are the earliest symptoms of this disease in about a third of patients.

III. Metabolic causes

Cramps during pregnancy are usually associated with a hypocalcemic state. Cramps are characteristic of tetany, which can be endocrinopathic (insufficiency of the parathyroid glands) and neurogenic (in the picture of hyperventilation syndrome). Mild forms of tetany without hyperventilation disorders are quite common. Latent tetany in children is sometimes called spasmophilia.

Tetany manifests itself in distal paresthesia, carpopedal spasms, typical cramps and attacks of laryngeal stridor. Tetanic syndrome in the picture of psychovegetative disorders usually serves as an indicator of the presence of hyperventilation disorders, which is often accompanied by symptoms of increased neuromuscular excitability (symptom of Chvostek, Trousseau, etc.).

Cramps can also be caused by other electrolyte disturbances. These include: hypokalemia (most common causes: diuretics, diarrhea, hyperaldosteronism, metabolic acidosis), acute hyponatremia (accompanied by fasciculations and cramps), decreased blood magnesium (weakness, cramps, fasciculations, and tetany). Blood electrolyte tests can easily detect these disturbances.

Hypothyroidism in infants and children often leads to hypothyroid myopathy with generalized muscle stiffness, hypertrophy of the calf muscles (Kocher-Debre-Semelaigne syndrome). In adults, hypothyroid myopathy is accompanied by moderate weakness of the muscles of the shoulder and pelvic girdle; 75% of patients complain of muscle pain, cramps, or muscle stiffness. If muscle hypertrophy joins these symptoms, the entire symptom complex in adults is called Hoffman syndrome. All forms of hypothyroid myopathy are characterized by slow muscle contraction and relaxation. Serum creatine kinase levels may be elevated.

Muscle pain and cramps are often observed in hyperparathyroidism; they are also observed in the picture of various manifestations of uremia. Metabolic causes underlie cramps in such diseases as liver cirrhosis, the state after gastrectomy, nutritional disorders in alcoholism.

IV. Iatrogenic causes

Typical causes of iatrogenic cramps include: diuretic therapy, hemodialysis, treatment with vincristine, lithium, salbutamol, nifedipine and some other drugs (penicillamine, aminocaproic acid, isoniazid, drugs that lower blood cholesterol levels, hypervitaminosis E, azathiaprine, withdrawal of corticosteroids, interferon and others).

V. Other reasons

Among other causes of cramps, it is worth mentioning intermittent claudication (claudicatio intermittens), in which ischemia of the soft tissues of the leg can manifest itself, in addition to the typical symptoms of intermittent claudication, as characteristic periodic cramping cramps.

High ambient temperatures, especially during prolonged physical work, can trigger cramping.

Eosinophilia-myalgia syndrome has been described in the United States as an epidemic outbreak in individuals taking L-tryptophan (eosinophilia, pneumonia, edema, alopecia, skin manifestations, myopathy, arthralgia, and neuropathy; severe, painful cramps, especially in the axial muscles, are characteristic of the late stages of this syndrome).

Some toxins (scorpion, black widow and some fish poisons; insecticides, etc.) cause intoxication, in the clinical manifestations of which cramps play an important role.

Tetanus is an infectious disease, the cardinal manifestations of which are progressive trismus, dysphagia, rigidity of the muscles of the back, abdomen and the whole body (generalized form). In the first three days, severe painful muscle spasms develop, provoked by sensory and emotional stimuli, as well as movements. Patients almost always retain consciousness.

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