What causes muscle spasms?
Normal voluntary muscle contraction begins when electrical signals are sent from the brain through the spinal cord along nerve cells called motor neurons. These include both the upper motor neurons within the brain and the lower motor neurons within the spinal cord and leading out to the muscle. At the muscle, chemicals released by the motor neuron stimulate the internal release of calcium ions from stores within the muscle cell. These calcium ions then interact with
muscle proteins within the cell, causing the proteins (actin and myosin) to slide past one another. This motion pulls their fixed ends closer, thereby shortening the cell and, ultimately, the muscle itself. Recapture of calcium and unlinking of actin and myosin allows the muscle fiber to relax.
Abnormal contraction may be caused by abnormal activity at any stage in this process. Certain mechanisms within the brain and the rest of the central nervous system help regulate contraction. Interruption of these mechanisms can cause spasm. Motor neurons that are overly sensitive may fire below their normal thresholds. The muscle membrane itself may be over sensitive, causing contraction without stimulation. Calcium ions may not be recaptured quickly enough, causing prolonged contraction.
Interuption of brain mechanisms and overly sensitive motor neurons may result from damage to the nerve pathways. Possible causes include stroke, multiple sclerosis, cerebral palsy, neurodegenerative diseases, trauma, spinal cord injury, and nervous system poisons such as strychnine, tetanus, and certain insecticides. Nerve damage may lead to a prolonged or permanent muscle shortening called contracture.
Changes in muscle responsiveness may be due to or associated with:
Prolonged exercise. Curiously, relaxation of a muscle actually requires energy to be expended. The energy is used to recapture calcium and to unlink actin and myosin. Normally, sensations of pain and fatigue signal that it is time to rest. Ignoring or overriding those warning signals can lead to such severe energy depletion that the muscle cannot be relaxed, causing a cramp. The familiar advice about not swimming after a heavy meal, when blood flow is directed away from the muscles, is intended to avoid this type of cramp. Rigor mortis, the stiffness of a corpse within the first 24 hours after death, is also due to this phenomenon.
Dehydration and salt depletion. This may be brought on by protracted vomiting or diarrhea, or by copious sweating during prolonged exercise, especially in high temperatures. Loss of fluids and salts--especially sodium, potassium, magnesium, and calcium--can disrupt ion balances in both muscle and nerves. This can prevent them from responding and recovering normally, and can lead to cramp.
Metabolic disorders that affect the energy supply in muscle. These are inherited diseases in which particular muscle enzymes are deficient. They include deficiencies of myophosphorylase (McArdle's disease), phosphorylase b kinase, phosphofructokinase, phosphoglycerate kinase, and lactate dehydrogenase.
Myotonia. This causes stiffness due to delayed relaxation of the muscle, but does not cause the spontaneous contraction usually associated with cramps. However, many patients with myotonia do experience cramping from exercise. Symptoms of myotonia are often worse in the cold. Myotonias include myotonic dystrophy, myotonia congenita, paramyotonia congenita, and neuromyotonia.
Fasciculations may be due to fatigue, cold, medications, metabolic disorders, nerve damage, or neurodegenerative disease, including amyotrophic lateral sclerosis. Most people experience brief, mild fasciculations from time to time, usually in the calves.