Muscle Spasms and Myoclonus
Richard Andrew LeCouteur
Muscle spasms are sudden, transient, and involuntary contractions of a single muscle or group of muscles, attended by pain and loss of function. Often all the muscles affected by a spasm are supplied by a single nerve.
A painful, tonic, spasmodic muscular contraction is often referred to as a cramp.Myoclonus may be defined as a disturbance of neuromuscular activity characterized by abrupt, brief, rapid, jerky, arrhythmic, asynergic, involuntary contractions involving portions of muscles, entire muscles, or groups of muscles, regardless of their functional association. The movements may be single or repetitive (10 to 50 per minute) and are similar to those that follow stimulation of a muscle. Myoclonus is seen primarily in muscles of the limbs, where involvement is often diffuse or widespread. Myoclonus may also be present in facial or masticatory muscles and muscles of the tongue, larynx, and pharynx. Myoclonus usually disappears during sleep.
This section describes muscle spasm and myoclonus as specific clinical signs associated with dysfunction of the musculoskeletal system.
Mechanisms of Muscle Spasms and Myoclonus
Spasms are usually of reflex origin and may result from irritation or stimulation at any level of the nervous system from the cerebral cortex to the muscle fibers. In most cases, however, spasms are caused by peripheral irritation affecting either muscles or nerves. Pain may cause either tonic or clonic spasms of muscles, especially if the painful stimulus is focal or discrete. Mechanical irritation may cause a localized spasm. There may be prolonged and characteristic muscle spasm associated with hyperirritability of nerves and muscles in tetany or tetanus. Spasms may follow injury or irritation of peripheral nerves, particularly during the process of regeneration. Spasms may also result from irritation or diseases affecting cortical centers in the brain, motor nuclei in the brainstem, or descending motor pathways in the spinal cord.
There has been much discussion regarding the pathologic process underlying myoclonic movements. Although it was originally thought that the neural discharge that excites the muscular contraction of myoclonus was confined to the motor unit, it is now known that myoclonus may also result from dysfunction of the brain (e.g., cerebral cortex, brainstem, basal nuclei, thalamus), spinal cord, peripheral nerve, neuromuscular junction, or the muscle itself, alone or in combination. A variety of processes evidently lead to hyperexcitability of the cerebral cortex, subcortical structures, or even the lower motor neurons alone. Myoclonic movements or muscle spasms may occur in a variety of conditions. They have been observed in association with encephalitis, meningitis, toxic and postanoxic states, metabolic disorders, degenerative diseases, and vascular and neoplastic conditions. Myoclonus has also been reported in association with lesions of peripheral nerves, nerve roots, and spinal cord.
Specifically, disturbances in plasma electrolyte concentrations, certain drugs, and toxins may elicit involuntary muscle activity. In general, the mechanism that is common to all causes of spasm or myoclonus involves inappropriate stimulation of a nerve or muscle cell, causing the cell to fire a series of action potentials, resulting in muscle contraction. For example, toxins may act directly on the muscle cell membrane to stimulate the release of calcium into the cell from the sarcoplasmic reticulum, thereby causing involuntary muscle contraction. Alternatively, some toxins may cause efferent neurons to release
■ BOX 13.10
■ TABLE 13.5
Causes of Muscle Spasms and Myoclonus in Horses
Anomalous or Congenital
Myotonia congenita
Metabolic
Hyperkalemic periodic paralysis
Hypocalcemia
Hypoglycemia
Hypothermia
Exhaustion
Shivering
Neoplastic
Insulinoma
Infectious or Inflammatory
Tetanus
Rabies
Equine influenza
Tick-borne encephalitis
Meningitis
Muscle cramps associated with ear ticks (Otobius megnini)
Idiopathic
Neonatal maladjustment syndrome
Toxic
Strychnine Organochlorines
Chlorinated hydrocarbons
neurotransmitter across the neuromuscular junctions, thereby stimulating receptors on the muscle cell membrane.
Approach to Diagnosis of Muscle Spasms and Myoclonus in Horses
A broad spectrum of diseases may be associated with muscle spasms or myoclonus in horses (Box 13.10). A thorough investigation is necessary to achieve an accurate diagnosis.
1. History. A comprehensive history should include evaluation of the environment and stablemates, description of any traumatic episodes, and any potential drug or toxin exposure.
2. Physical examination. Complete lameness and neurologic examinations should be done as extensions of a thorough physical examination.
3. Minimum database. Complete blood count, serum biochemistry panel (including muscle enzyme determinations), and cerebrospinal fluid analysis should be considered. In the case of muscle spasm and myoclonus, elevation in muscle enzymes may indicate secondary muscle damage rather than a primary muscle disease. A tetany panel, including serum calcium, phosphorus, and magnesium determinations, may be completed. Hypocalcemia may be a cause of muscle spasms in lactating horses, exhausted endurance horses, or horses transported long distances.
4. Specific diagnostic tests: Electrodiagnostic testing. A systematic study of individual muscles using EMG permits an accurate determination of the distribution of muscles affected by a pathologic process.
5. Nerve and muscle biopsy examination. This procedure evaluates the morphology of portions of the motor unit and may differentiate neuropathies, junctionopathies, and myopathies.
Causes and Pathogenesis of Muscle Spasms in Ruminants
| Sign | Pathogenesis |
| Posterior paralysis of | Single Mendelian recessive factor |
| Danish Red calves | from 1 bull |
| Inherited congenital | Decrease in inhibitory glycine |
| myoclonus of polled | receptors |
| Herefords and their crossbreeds | |
| Maple syrup urine | Deficiency of activity of |
| disease in polled | mitochondrial enzyme branched- |
| Herefords and their | chain alpha-keto acid |
| cross breeds | dehydrogenase |
| Lethal spasms in Jersey | Autosomal recessive gene from 1 |
| and Hereford calves | bull |
| Congenital brain | Autosomal recessive gene |
| edema in Herefords | |
| Hypomagnesemia | Stress; transport; dietary deficiency |
| (lactation tetany; | (lush pasture, high potassium and |
| grass tetany; grass | nitrogen); inclement weather; |
| staggers; wheat | lactation and pregnancy; individual |
| pasture poisoning) | susceptibility |
| Hypocalcemia | Onset of lactation, vitamin D |
| Hypoglycemia | deficiency, starvation, metabolic alkalosis, stress (sheep and goats), prepartum diets high in calcium, individual and breed susceptibility, IV oxytetracycline administration Failure to nurse, sepsis, bacterial |
| Tetanus | meningitis, enterotoxigenic colibacillosis, cold exposure, twin or triplet lambs Disinhibition of gamma motor |
| Rabies | neurons Encephalitis |
| Pseudorabies | Encephalitis |
| Meningitis | Bacterial infections, viral |
| Coccidiosis | encephalitides Possible labile neurotoxin |
| Chlorinated | Cause repetitive discharge of motor |
| hydrocarbons | and sensory neurons |
| Strychnine | Antagonist of glycine and |
| Organophosphates | acetylcholine and mainly affects the motor nerves in the spine Inactivation of cholinesterase |
| Cocklebur | Carboxyatractyloside (CAT) |
| Buckeye | Glycoside saponin (aesculin) |
Approach to Diagnosis of Muscle Spasms and Myoclonus in Ruminants
The approach to diagnosis of muscle spasms and myoclonus in ruminants is essentially the same as that described for horses. The cause and pathogenesis of muscle spasms in ruminants are outlined in Table 13.5).
In ruminants a tetany panel (consisting of serum calcium, phosphorus, and magnesium determinations) should be completed in any animal exhibiting these signs. In lactating cattle on grass pasture and in sheep transported long distances, hypomagnesemia and hypocalcemia are likely. Several infectious (e.g., rabies, pseudorabies), toxic, and inherited causes of muscle spasms and myoclonus should be suspected in ruminants. In postparturient animals and animals with wounds or bites, or animals recently castrated or tail docked, tetanus should be considered as a possible cause of muscle spasms and myoclonus.BIBLIOGRAPHY
The bibliography list can be found on the companion website at www.expertconsult.com.
BIBLIOGRAPHY
Auer JA, Stick JA: Equine surgery, ed 2, Philadelphia, PA, 1999, Saunders.
Auer JA, Stick JA: Equine surgery, ed 3, St Louis, MO, 2006, Saunders.
Auer JA, Stick JA: Equine surgery, ed 4, St Louis, MO, 2012, Saunders.
Greenough PR, Weaver AD: Lameness in cattle, ed 3, Philadelphia, PA, 1997, Saunders.
Hinchcliff K, Kaneps A, Geor R: Equine sports medicine and surgery, St Louis, MO, 2005, Saunders.
McIlwraith CW, Trotter GW: Joint disease in the horse, Philadelphia, PA, 1996, Saunders.
Nixon AJ: Equine fracture repair, Philadelphia, PA, 1996, Saunders.
Ross MW, Dyson SJ: Diagnosis and management of lameness in the horse, St Louis, MO, 2006, Saunders.
Ross MW, Dyson SJ: Diagnosis and management of lameness in the horse, ed 2, St Louis, MO, 2011, Saunders.
Stashack TS: Diagnosis of lameness. In Stashack TS, editor: Adams’ lameness in horses, ed 4, Philadelphia, PA, 1987, Lea & Febiger, p 100.
Stashack TS: Adams’ lameness in horses, ed 5, Philadelphia, PA, 2002, Lippincott Williams & Wilkins.
White NA, Moore JN: Current techniques in equine surgery and lameness, ed 2, Philadelphia, PA, 1998, Saunders.
Anderson DE, Desrochers A, St Jean G: Management of tendon disorders in cattle, Vet Clin North Am Food Anim Pract 24:551, 2008.
Desrochers A, Anderson DE, St. Jean G: Surgical treatment of lameness, Vet Clin North Am Food Anim Pract 17:143, 2001.
Greenough PR: Bovine laminitis and lameness, a hands-on approach, Toronto, Ontario, 2007, Elsevier Limited.
Kofler J: Ultrasonography as a diagnostic aid in bovine musculoskeletal disorders. Vet Clin North Am Food Anim Pract 25:687, 2009.
Smith-Maxie L: Peripheral nerve diseases. In Greenough PR, editor: Lameness in cattle, Philadelphia, PA, 1997, WB Saunders, pp 203-218.
Shearer JK, Van Amstel SR 2010. Pathophysiology and differentiation of toe lesions in dairy cattle, pp 253-255. Proceedings of the American College of Veterinary Internal Medicine, June 9-10, Anaheim, CA.
Van Amstel SR, Shearer JK: Review of pododermatitis circumscripta (ulceration of the sole) in dairy cows, J Vet Intern Med 20:805, 2006.
Van Amstel SR, Shearer JK: Clinical report—characterization of toe ulcers associated with thin soles in dairy cows, Bovine Practitioner 42:189, 2008.
Weaver AD: Spastic paresis and Downer cows. In Greenough PR, editor: Lameness in cattle, Philadelphia, PA, 1997, WB Saunders, pp 203-218.