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The Diagnosis of Neurological Disease in Horses

Description
Introduction


Neurologic disease in horses is a diagnostic and therapeutic challenge. Solving behavioral and gait problems in neurologic disease requires a thorough understanding of the functional regions of the nervous system. This article will help practitioners to define problems seen in equine neurologic disease, neuroanatomically localize neurologic lesions, and generate a list of common differential diagnoses. Once a list of differential diagnoses is generated an appropriate diagnostic and therapeutic regime can be planned.




Defining the Problems


The nervous system is a group of separate, integrated regions. Dementia, ataxia, weakness, spasticity, and hypermetria are major problems occurring from damage to the nervous system. 1, 2 The goal of problem solving in neurologic disease is the anatomic localization of lesions to major regions of the nervous system, such as the cerebrum, brainstem, cerebellum, spinal cord segments, or peripheral nerves. 2 It is only through anatomic localization that a list of differential diagnoses can be generated and a rational therapy planned.
A wide range of normal behaviors and gaits are seen in horses. Differences exist between individuals, sexes, breeds, and ages. Behavioral changes may be seen at the onset of estrus in mares, aggressive behavior may be seen in stallions, and changes in tack may lead to behavior changes (head shaking, chewing) in the performance of race horses.

Gait changes may be seen as a result of unusual conformation or shoeing. Some horses can show excessive flexion, pronounced external rotation (winging out), circumduction, or decreased action at normal gaits. The owner, trainer, or handler may help provide valuable information to help distinguish between normal and abnormal behavior and gait for that individual horse. Once a behavioral or gait problem is recognized, regardless of its severity, it must be defined in its simplest form and a problem list must be generated.


  • Aimless wandering, depression, semicoma, seizure, delirium, and blindness define the behavioral problem of dementia.

  • Increased swaying of the trunk, prolonged pelvic limb stride, waving of the limb in the air before placement, abduction of the limb during forward movement, crossing the limb under the body, and stepping on the opposite limb defines the proprioceptive problem of ataxia.

  • Knuckling, stumbling, dragging of the limb, and dipping of trunk during weight bearing defines the motor problem of weakness or paresis.

  • A stiff- stilted, short- strided (tin-soldier) gait, with a lack of joint flexion, defines the motor problem of spasticity.

  • Increased or exaggerated joint flexion defines the motor problem of hypermetria.

    These problems may occur together, which may make distinguishing them difficult. In addition, horses with musculoskeletal disease can show signs of weakness when painful limbs are passively lifted off the ground or spasticity when they use painful joints (reluctance to flex). However, when dementia and two gait problems are seen together, they are probably the result of a neurologic rather than a behavioral or musculoskeletal problem.




    Neuroanatomic Localization of Problems


    Many lesions affecting the nervous system can be localized to a single focus. When such localization is not possible, a diffuse or multifocal disease of the nervous system should be considered. A problem-oriented flow sheet may be helpful in systematically localizing problems of the nervous system.

  • Dementia can be localized to the cerebrum, brainstem, and cerebellum.

  • Mild depression, aimless wandering, mild paresis, seizure, delirium, and blindness with a normal pupillary light response (PLR) can be localized to the cerebrum.

  • Severe depression, obtunded profound weakness, and semicoma can be localized to the reticular activating system of the brainstem.

  • Ataxia, weakness, spasticity in four limbs turning in narrow circles, and cranial nerve signs (strabismus, absent PLR, absent palpebral reflex, ptosis, ear droop, deviated muzzle, head tilt, and facial muscle atrophy) can be localized to the brainstem.

  • Intention tremors, absent or decreased menace reflex, hypermetria, and muscle hypertonicity in all four limbs can be localized to the cerebellum.




    Cerebral Diseases




  • Liver Disease

    The most common metabolic cause of cerebral disease in horses is hepatoencephalopathy. Horses with hepatoencephalopathy present with dementia, head pressing, aimless wandering, star gazing, and in some cases, icterus. Frequently, these problems are most pronounced following feeding, especially after a high protein meal. 2 Increased serum ammonia and aromatic amino acids are thought to diffuse across the blood-brain barrier and act as false neurotransmitters, leading to the typical clinical problems. 5 Hepatoencephalopathy in young horses can be secondary to portacaval shunts; though rare, portacaval shunts should be considered in stunted foals with hepatoencephalopathy. 6



  • Electrolyte Disturbances

    Electrolyte imbalances causing neurologic problems occur sporadically in horses. One electrolyte abnormality that has gained attention recently is hyperkalemic periodic paralysis. Ataxia, weakness, muscle tremors, and seizure-like activity are problems seen in Quarter Horses postprandially, during exercise, or during stress or excitement. 7-9 However, sporadic occurrences not related to eating, exercise, or stress do occur. 8

    Hypomagnesemia and hypocalcemia can lead to signs of cerebral disease. These conditions can occur following stress, severe exercise, or secondary to diseases that cause intestinal stasis, decreased feed intake or decreased absorption, such as anterior enteritis, colic, and granulomatous enteritis.



  • Infections

    Infectious cerebral disease can result from viruses, such as eastern , western, and Venezuelan Equine Encephalomyelitis (EEE, WEE, VEE), rabies, EHV 1, from protozoa, such as Sarcocystis and Toxoplasma, and from bacteria, such as Streptococcus equi and Corynebacterium spp. Streptococcus cerebral abscesses are rare and can follow outbreaks of strangles on farms. 10, 11

    Rabies is of great importance because of its sporadic occurrence and potential zoonosis. Rabies should be considered in any horse with acutely developing local hyperesthesia, lameness, ataxia, and dementia of less than 10 days duration. Death usually occurs in these horses within 5 days after the onset of clinical signs. 12 A diagnostic or state health laboratory should be consulted if rabies is suspected, and a full necropsy should be delayed until negative results of brain-tissue analysis are received.

    Eastern and Western equine encephalomyelitides occur sporadically throughout the world. These togaviruses are transmitted by biting insects and cause extensive inflammation of the cerebrum. 2 Horses so affected are lethargic, unresponsive, aimlessly wander, circle, and in some cases are blind. The clinical signs may worsen acutely and progress to recumbency and death. Equine herpes virus 1 encephalomyelitis and equine protozoal myelitis (EPM) can also cause diffuse cerebral disease and will be discussed under diffuse or multifocal diseases.

    Bacterial meningitis is diagnosed uncommonly in older foals and horses, because of the vague clinical presentation. The cause of meningitis in horses is often unknown, but etiologic agents such as Streptococcus equi (Bastard Strangles), Klebsiella pneumoniae, and actinomyces have been isolated from cerebrospinal fluid of affected horses. Vague neurologic signs may be seen, such as depression, anorexia, and weakness. Signs often progress to involve the cranial nerves and lead to cervical stiffness, ataxia, hypermetra, intention tremors, recumbency, opisthotomus, convulsions, and coma. Signs may progress over several days in adult horses.



  • Other Agents

    Noninfectious agents that cause cerebral disease include toxicants, neoplasia, and malformations. Organophosphates, lead, arsenic, and strychnine toxicosis can cause cerebral lesions. Careful historical information and a farm visit may be helpful in determining these conditions. Brain neoplasia is rare and usually occurs in aged horses. Common tumors are pituitary adenoma, lymphosarcoma, and cholesteatoma. Seizures, blindness, delirium, and weakness may be present, depending on the location of the tumor.

    Ingestion of Russian knapweed or yellow star thistle causes nigropallidal encephalomalacia. This disease occurs in late summer and fall in horses on overgrazed pastures. Impaired prehension and mastication, facial muscle hypertonicity, and dysphagia are commonly seen in horses with acute toxicosis. These horses may be able to swallow but cannot prehend or chew feed. Seizures, head pressing, incoordination, and falling down may also be seen.

    Pituitary adenoma is the most common tumor in the horse. Polydypsia, polyuria, hirsutism, a pot-bellied appearance, hyperglycemia, and glucosuria may be seen. 18, 19 Pituitary tumors may rarely induce blindness and depression as a result of pressure on the optic nerve and brain stem. 2 In addition, meningiomas and ependymomas have been identified in horses showing signs of circling, blindness, and depression. Furthermore, a massive choroid plexus cholestol granuloma has been associated with intermittent circling, blindness, and depression in a horse. 2 However, cholesteatomas are usually found as an incidental finding at necropsy.

    Congenital malformations such as hydrocephalus rarely occur in young horses. A foal with an open fontanelle who shows progressive depression, ataxia, and weakness can have congenital hydrocephalus.

    Cranial trauma can occur from horses falling over backward and striking the poll, colliding with obstacles, and being kicked by other horses. Skull fractures involving the mandible, maxilla, incisive, frontal, parietal, and basisphenoid bones can lead to cerebral, brain stem, and cerebellar signs.Trauma usually results in cerebral edema, which causes a redistribution of brain tissue in the rigid calvarium. Death can occur from depression of the respiratory and cardiac centers in the brain stem. Cerebral trauma may result in mild weakness but does not usually cause ataxia unless severe. ( a common manifestation of head trauma is blindness which may be acute or progressive in onset.)



  • Brainstem Disease

    Brainstem disease can be secondary to trauma, toxicity, and infectious causes. Infectious brainstem disease will be discussed under diffuse and multifocal nervous system disease. Brainstem trauma occurs frequently in horses. Trauma without evidence of fractures is not uncommon. Basisphenoid basioccipital bone fractures occur when horses fall over backward and strike their poll, causing damage to the medulla and pons. Head tilt, ptosis, hemorrhage from the external ear canal, and leakage of cerebrospinal fluid from the nostril and ear may be seen. Intention tremors may be seen if the cerebellum is involved. Prognosis is guarded; horses may progress to recumbency and death, probably from respiratory failure. Horses that recover may have a residual head tilt and circling but may be salvaged for breeding.


  • Cerebellar Diseases

    Cerebellar diseases may be secondary to inflammatory, noninflammatory, or traumatic causes and may be associated with cranial nerve signs.
    The most common cerebellar disease is congenital cerebellar abiotrophy, which occurs in young Arabian foals. Intention tremors, decreased or absent menace response, normal vision, hypermetria, normal strength, and a base wide stance at rest are commonly seen in these horses.




  • Spinal Cord Disease

    Ataxia, paresis, and spasticity in all four limbs, with the rear limbs appearing worse than the front limbs, can be localized to the cervical spinal cord. Causes of cervical spinal cord lesions include malformations, trauma, and infections. Other conditions such as injection-site abscesses can occur, but less frequently. A history of previous cervical injection can be helpful in making the diagnosis.
    Cervical vertebral malformations include atlanto-occipital malformation and cervical stenotic myelopathy. Spinal compression results in the clinical signs. Atlanto- occipital malformation is rare and occurs in Arabian and Arabian-cross foals. The occipital bone, atlas, and axis are malformed and exhibit different anatomic features. 26 Problems characteristic of cranial cervical spinal cord compression from atlanto-occipital malformation can occur within the first few months of life. However, in some cases, no neurologic signs are seen, just restricted movement of the neck. 27

    Cervical stenotic myelopathy (CSM) (spinal ataxia, cervical vertebral instability, wobbler syndrome) can lead to cervical spinal cord compression. Problems usually develop between 6 and 30 months of age and can progress very rapidly or remain static. Large, rapidly growing Thoroughbred, Quarter Horse, and warmblood youngsters seem predisposed to CSM, whereas other breeds such as Standardbreds, Tennessee Walking Horses, and Arabians may be less predisposed. Frequently these horses present with some history of trauma and symmetric gait deficits, but they may present with asymmetric gait deficits. For example, a young racehorse may present initially for a unilateral hindlimb lameness, but the signs may progress to be a more symmetric presentation of obvious neurologic origin.

    Spinal cord trauma most commonly occurs when horses fall or collide with a relatively immovable object. Foals appear to be more susceptible to vertebral trauma than adult horses and frequently suffer fractures of the cranial cervical (C 1-C 5) and caudal thoracic vertebrae. 14 Hyperflexion injuries result in fracture and luxation of the dens, and hyperextention injuries result in vertebral epiphyseal fractures. Adult horses are more susceptible to injury of the caudal cervical (C 5-C 7) and caudal thoracic vertebrae.

    Profound weakness and hyporeflexia in the front limbs with hyperreflexia to normoreflexia in the rear limbs can be localized to the cranial intumescence (C 6-T 2). Lesions in this region are usually traumatic, although malformations of the thoracic vertebrae, fibrocartilaginous infarcts, and inflammatory diseases also occur. Normal front limb signs with mild ataxia and weakness in the rear limbs can be localized to the thoracolumbar spinal cord (T 3-L 3).

    Progressive symmetric ataxia, weakness, and spasticity of the pelvic limbs suggest equine degenerative myelopathy (EDM). 29, 30 However, EDM occurs most commonly in younger (adolescent) horses and is clinically indistinguishable from CSM. Only a positive myelogram may distinguish between the two conditions in any single case. In addition, horses with EDM eventually progress to recumbency, whereas the horse with CSM may stabilize without severe progression. Unfortunately, definitive diagnosis of EDM can only be made on histopathologic evaluation of the spinal cord. Although this condition has been reported in all equine species and several breeds, some reports indicate that Morgans, Standardbreds, and Quarter Horses are more often affected. 29-31



  • Peripheral Nerve Diseases

    Weakness, limb hyporeflexia, muscle hypotonicity, rapid muscle atrophy, and decreased pain sensation in any or all four limbs can be anatomically localized to the peripheral nerve or lower motor unit. Diseases of the peripheral nerves can be divided into several categories, depending on their anatomic location along the motor unit (ventral horn cells of the spinal cord, ventral root, peripheral nerve, neuromuscular junction, and muscle).

  • Diseases that affect the ventral horn cells of the spinal cord and internuncial neurons include EPM, aberrant parasite migration, and tetanus.

  • Diseases that affect the ventral roots include polyneuritis equi (neuritis of the cauda equina) and neoplasia.

  • Diseases of the peripheral nerve include suprascapular nerve paralysis (sweeny), radial nerve paralysis, and cranial gluteal nerve paralysis and occur following trauma or general anesthesia.

    Neuromuscular junction diseases include equine botulism (forage poisoning, shaker foal syndrome) and myasthenia-like syndrome. Dysphagia, decreased eyelid tone, delayed palpebral response, delayed PLR, and weakness in all four limbs suggest equine botulism. Normally horses displaying these symptoms respond to the examiner but appear depressed, weak, and listless. Horses with botulism usually progress to recumbency and may die of respiratory failure. Ileus, constipation, and urinary incontinence can occur in horses with botulism. The prognosis is guarded to poor, especially after recumbency has occurred.

    Unclassified disorders of the peripheral nerves include equine motor neuron disease (EMND), shivers, tics, and string halt. The exact cause of these conditions is not known, but abnormal sensory impulses may cause these disorders. 2 Also, EPM has been implicated in causing shivers in horses. 2 EMND (amyotrophic lateral sclerosis) is a degenerative neuropathy that affects the motor neurons and ventral roots in the spinal cord. Horses with this disease present with progressive trembling, weakness, and muscle wasting. Horses have a very short anterior stride without loss of proprioception. The disease stabilizes after 1-2 months and may remain static for up to 3 years. 33 The cause of EMND is unknown.




    Multifocal Diseases

    Dementia, cranial nerve signs, ataxia, and weakness in one or several limbs in an unequal distribution are problems that cannot be localized to a single focus and thus are considered diffuse or multifocal. Polyneuritis equi (the newer term for cauda equina neuritis), equine herpesvirus (EHV) 1 encephalomyelitis, EPM, and nonsuppurative myelitis are examples of multifocal or diffuse neurologic conditions. Subtle differences in the clinical problems exist between these conditions, which may help in their differentiation.
    Progressive symmetric weakness of the rear limbs, analgesia of the tail, anus, and perineum, and cranial nerve signs may suggest polyneuritis equi. 34 Fecal incontinence, paraphimosis, urine scalding, and bacterial cystitis may also be observed. The owner may mistake bilateral gluteal muscle atrophy and facial muscle atrophy for weight loss. The cause of polyneuritis equi is unknown, but bacterial, viral, and immune-mediated mechanisms have been proposed. Antimyelin antibodies have been detected in some cases. 34, 35
    Acute onset and rapidly stabilizing (within 24-48 hours) symmetric ataxia, bladder atony, urinary incontinence, and hypotonus of the tail and anus with or without cranial nerve signs suggest EHV 1 encephalomyelitis. 36 This condition may occur 7-10 days after an outbreakof respiratory disease or abortion. EHV 1 causes vasculitis and thrombosis, which lead to infarction and necrosis of the nervous tissue. The vasculitis is thought to be an immunocomplex disease. 37
    Progressive asymmetric ataxia, weakness, muscle atrophy, and cranial nerve signs suggest EPM. 29 This disease usually occurs in horses of racing and performance age. 29 Obscure hindlimb lameness, lateral digital extensor tenectomy, and medial patellar desmotomy are often part of the history. Sarcocystis neurona is thought to be the causative agent. 38-40 These protozoal organisms randomly invade the gray and white matter of the spinal cord, resulting in multifocal upper- and lower-motor neuron disease. S. neurona has recently been cultured from the spinal cord of infected horses. 40 Currently, serum and cerebrospinal fluid titers are available on an experimental basis from the University of Kentucky Equine Research Facility. a This test may provide an antemortem diagnosis for EPM, so that an effective treatment can be initiated early in the course of disease.




    Conclusion

    Defining problems of the neurologic system can be difficult and frustrating. However, with neuroanatomic localization of these problems to the major regions of the nervous system, a list of differential diagnoses can be generated. This list will help in planning a rational therapy.

    References
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