03/30/2022
🔈 MYOGENIC & NEUROGENIC MUSCLE CRAMPS
What Is a Muscle Cramp?
A muscle cramp is a hyperexcitable neurologic phenomena of excessive, involuntary muscle contractions. It is important to distinguish between myogenic and neurogenic muscle cramps, because each has unique pathophysiology and management. The conventional definition of a muscle cramp is a painful contraction of a muscle or muscle group, relieved by contraction of antagonist muscles.
Care must be taken to avoid confusing muscle cramps with other phenomena including central hyperexcitability (eg, dystonia, spasticity, seizures, and stiff person/stiff limb syndromes) and peripheral processes, including tetany, myokymia, myotonia, neuromyotonia (focal muscle stiffness), or myalgia.
🔎 NEUROGENIC MUSCLE CRAMPS
The origin and propagation of neurogenic muscle cramps localizes to peripheral and central targets, including the neuromuscular junction, where mechanical disruption and electrolyte disturbances can influence hyperexcitability and cramp generation. Injury to peripheral nerve components including the motor neuron cell bodies or the motor axons can result in ephaptic transmission and development of muscle cramps.
Dysfunctional intramuscular small fiber sensory afferents (eg, mechanoreceptors and spindles) are also proposed to be involved in cramp generation. Centrally, persistent inward currents mediated by GABAergic transmitters at the spinal level can amplify incoming sensory input and lead to the propagation and amplification of cramp potentials. Disruption of chloride, sodium, and potassium channels and inadequate amino acids concentrations (eg, taurine) disrupt membrane currents to generate muscle cramps.
🔎 MYOGENIC MUSCLE CRAMPS
The pathophysiology of myogenic muscle cramps, in contrast, is usually the result of disrupted energy production in muscle cells and occurs most commonly in metabolic myopathies associated with disorders of glycogen, lipid, or mitochondrial metabolism. Metabolic myopathies cause deficient ATP levels. Because muscle relaxation is an adenosine triphosphate (ATP)-dependent active process, actin and myosin chains do not disengage, causing an electrically silent cramp (ie, contracture). The metabolic defect may also cause accumulation of potentially toxic metabolites that further aggravate ATP deficientcy. Myopathic cramps are also a potential symptom of myopathies linked to muscle membrane or intramuscular structural dysfunction in acquired and hereditary myopathies (eg, muscular dystrophy, congenital myopathies, and inflammatory myopathy).
CAUSES
Physiologic stressors are a common precipitant to muscle cramps. The most common is dehydration, in which electrolyte loss disrupts neuromuscular junction function and membrane stability. Other physiologic stressors include unusually prolonged or strenuous exercise, particularly in a deconditioned state in which muscle tendon shortening is common.
TREATMENT
Infrequent cramps that do not interfere in someone’s life rarely need investigation or treatment. There is no evidence that recurrent muscle cramps lead to significant long-lasting damage to muscles, and serious harm from muscle cramps (eg, tendon ruptures) is rare. If treatment is needed, the avoidance of the offending agent or appropriate electrolyte and vitamin replacement to treat the root cause are warranted. There is level B evidence that vitamin B-complex supplementation can reduce cramp frequency in people who experience at least 6 cramps per week.
In individuals with prominent dehydration (eg, athletes, malnourished individuals, or members of vulnerable populations), care must be taken to ensure adequate electrolyte-rich solutions, particularly high-salt formulations. In pregnant women, there is ample evidence that magnesium replacement is helpful in managing muscle cramps.
Reference: Practical Neurology
