The degenerative diseases of the brain are grouped together under the name encephalomalacia. By definition encephalomalacia means softening of the brain. It is used here to include all degenerative changes. Leukoencephalomalacia and polioencephalomalacia refer to softening of the white and gray matter respectively. Abiotrophy is the premature degeneration of neurons due to an inborn metabolic error of development and excludes exogenous insults of neurons. The underlying cellular defect in most abiotrophies is inherited. The syndrome produced in most degenerative diseases of the nervous system is essentially one of loss of function.
Some indication of the diversity of causes of encephalomalacia and degenerative diseases of the nervous system can be appreciated from the examples which follow but many sporadic cases occur in which the cause cannot be defined.
• Hepatic encephalopathy thought to be due to high blood levels of ammonia associated with advanced liver disease.1 This is recorded in experimental pyrrolizidine alkaloid poisoning in sheep, in hepatic arteriovenous anomaly and thrombosis of the portal vein in the horse. Congenital portocaval shunts are also a cause
• Abiotrophy involving multisystem degenerations in the nervous system as focal or diffuse lesions involving the axons and myelin of neuronal processes.2 These include a multifocal encephalopathy in the Simmental breed of cattle in New Zealand and Australia,2 and progressive myeloencephalopathy in Brown Swiss cattle, known as ‘weavers’ because of their ataxic gait (see below and Chapter on Inherited Defects)
• Poisoning by organic mercurials and, in some instances, lead; possibly also selenium poisoning; a bilateral multifocal cerebrospinal poliomalacia of sheep in Ghana
• Cerebrovascular disorders corresponding to the main categories in humans are observed in animals, but their occurrence is chiefly in pigs and their clinical importance is minor
• Congenital hypomyelinogenesis and dysmyelinogenesis are recorded in lambs (hairy shakers), piglets (myoclonia congenita) and calves (hypomyelinogenesis congenita). All are associated with viral infections in utero. Equine herpesvirus-1 infections in horses cause ischemic infarcts
• Bovine spongiform encephalopathy
• Plant poisons, e.g. Astragalus spp., Oxytropis spp., Swainsona spp., Vicia spp., Kochia scoparia
• Focal symmetrical encephalomalacia of sheep, thought to be a residual lesion after intoxication with Clostridium perfringens type D toxin
• Polioencephalomalacia caused by thiamin inadequacy in cattle and sheep and sulfur toxicosis in cattle; poliomalacia of sheep caused possibly by an antimetabolite of nicotinic acid
• Progressive spinal myelopathy of Murray Grey cattle in Australia2
• Spongiform encephalopathy in newborn polled Hereford calves similar to maple syrup urine disease2
• Neuronal dystrophy in Suffolk sheep2
• Shakers in horned Hereford calves associated with neuronal cell body chromatolysis2
• The abiotrophic lysosomal storage diseases – progressive ataxia of Charolais cattle, mannosidosis, gangliosidosis, globoid cell leukodystrophy of sheep
• The inherited defect of Brown Swiss cattle known as ‘weavers’, and presented elsewhere, is a degenerative myeloencephalopathy5
• Swayback and enzootic ataxia due to nutritional deficiency of copper in lambs
• Prolonged parturition of calves causing cerebral hypoxia and the weak calf syndrome
• Idiopathic brainstem neuronal chromatolysis in cattle6
• Bovine bonkers due to the consumption of ammoniated forages
• Inherited neuronal degeneration in Angora goats.2
• Leukoencephalomalacia caused by feeding moldy corn infested with Fusarium moniliforme, which produces primarily fumonisin B1 and, to a lesser extent, fumonisin B27-10
• Nigropallidal encephalomalacia caused by feeding on yellow star thistle (Centaurea solstitialis)
• Poisoning by bracken and horsetail causing a conditioned deficiency of thiamin
• Ischemic encephalopathy of neonatal maladjustment syndrome of foals
• Equine degenerative myeloencephalopathy;11 may be associated with a vitamin E deficiency.
Swainsonine and slaframine produced by Rhizoctonia leguminicola cause mannose accumulation and parasympathomimetic effects. Lolitrems from Acremonium lolii and paspalitrems from Claviceps paspali are tremorgens found in grasses.7
The pathogenesis of the degenerative diseases can be subdivided into:
• Metabolic and circulatory disorders
• Intoxications and toxic–infectious diseases
• Hereditary, familial, and idiopathic degenerative diseases.12
Hepatic encephalopathy is associated with acquired liver disease and the resultant hyperammonemia and other toxic factors are considered to be neurotoxic. Disorders of intermediary metabolism result in the accumulation of neurotoxic substances such as in maple syrup urine disease of calves. Lysosomal storage diseases are caused by a lack of lysosomal enzymes which results in an accumulation of cellular substrates and affecting cell function. Central nervous system hypoxia and ischemia impair the most sensitive elements in brain tissue especially neurons. Severe ischemia results in necrosis of neurons and glial elements and areas of infarcts. Gas-anesthesia-related neurological disease occurs in animals that have been deprived of oxygen for more than 5 minutes.
The hypoxia is lethal to neurons and upon recovery from the anesthetic affected animals are blind and seizures may occur. The typical lesion consists of widespread neuronal damage. Postanesthetic hemorrhagic myelopathy and postanesthetic cerebral necrosis in horses are typical examples. Hypoglycemia occurs in neonates deprived of milk and in acetonemia and pregnancy toxemia and clinical signs of lethargy, dullness progressing to weakness, seizures and coma have been attributed to hypoglycemia. However, there are no studies of the central nervous system in farm animals with hypoglycemia and the effects, if any, on the nervous tissue are unknown.
A large number of poisonous substances including poisonous plants, heavy metals (lead, arsenic, mercury), salt poisoning, farm chemicals, antifreeze, herbicides and insecticides can directly affect the nervous system when ingested by animals. They result in varying degrees of edema of the brain, degeneration of white and gray matter and hemorrhage of both the central and peripheral nervous system. Toxic-infectious diseases such as edema disease of swine and focal symmetrical encephalomalacia of sheep are examples of endotoxins and exotoxins produced by bacterial infections which have a direct effect on the nervous system resulting in encephalomalacia.
Several nutritional deficiencies of farm animals can result in neurological disease:
• Vitamin A deficiency affects bone growth, particularly remodeling of the optic nerve tracts, and CSF absorption. The elevated CSF pressure and constriction of the optic nerve tracts results in edema of the optic disc and wallerian-type degeneration of the optic nerve resulting in blindness
• Copper deficiency in pregnant ewes can result in swayback and enzootic ataxia of the lambs. Copper is an integral element in several enzyme systems such as ceruloplasmin and lysyl oxidase, and copper deficiency affects several organ systems. The principal defect in swayback appears to be one of defective myelination probably caused by interference with phospholipid formation. However, some lesions in the newborn are more extensive, and show cavitation with loss of axons and neurons rather than simply demyelination. In the brain, there is a progressive gelatinous transformation of the white matter, ending in cavitation that resembles porencephaly or hydranencephaly. In the spinal cord the lesions are bilateral and it is suggested that the copper deficiency has a primary axonopathic effect
• Thiamine deficiency in ruminants can result in polioencephalomalacia or cerebrocortical necrosis. Thiamine, mainly as thiamine diphosphate (pyrophosphate), has an important role as a coenzyme in carbohydrate metabolism especially the pentose pathway. Diffuse encephalopathy may occur characterized by brain edema and swelling, resulting in flattening of the gyri, tentorial herniation and coning of the cerebellar vermis. Bilateral areas of cerebral cortical laminar necrosis are widespread.
A large number of neurological diseases of farm animals are characterized by abnormalities of central myelinogenesis. In most instances the underlying abnormality directly or indirectly affects the oligodendrocyte and is reflected in the production of central nervous system myelin of diminished quantity or quality or both. Many of these are inherited and are manifest from or shortly after birth. They include leukodystrophies, hypomyelinogenesis, spongy degeneration, and related disorders.12 Neuronal abiotrophy, motor neuron diseases, neuronal dystrophy and degenerative encephalomyelopathy of horses and cattle are included in this group.
Polioencephalomalacia appears to be, in some cases at least, a consequence of acute edematous swelling of the brain and cortical ischemia. The pathogenesis of leukoencephalomalacia appears to be related to vasogenic edema as a result of cardiovascular dysfunction and an inability to regulate cerebral blood flow. Whether the lesion is in the gray matter (polioencephalomalacia) or in the white matter (leukoencephalomalacia) the syndrome is largely one of loss of function although as might be expected irritation signs are more likely to occur when the gray matter is damaged.
Weakness of all four limbs is accompanied by:
In the early stages, particularly in ruminant polioencephalomalacia, there are involuntary signs including muscle tremor, opisthotonos, nystagmus, and convulsions.
In equine leukoencephalomalacia, which may occur in outbreaks, initial signs include anorexia and depression.3 In the neurotoxic form, which is most common, the anorexia and depression progresses to ataxia, circling, apparent blindness, head-pressing, hyperesthesia, agitation, delirium, recumbency, seizures, and death. An early and consistent sign in affected horses is reduced proprioception of the tongue, manifest as delayed retraction of the tongue to the buccal cavity after the tongue has been extended.10 In the hepatotoxicosis form, clinical findings include icterus, swelling of the lips and nose, petechiation, abdominal breathing and cyanosis. Horses with either syndrome may be found dead without any premonitory signs.
In many of the leukoencephalomalacias, the course may be one of gradual progression of signs, or more commonly a level of abnormality is reached and maintained for a long period, often necessitating euthanasia of the animal. For example, equine degenerative myeloencephalopathy is a diffuse degenerative disease of the equine spinal cords and caudal portion of the brainstem and primarily affects young horses. There is an insidious onset of symmetrical spasticity, ataxia, and paresis. Clinical signs may progress slowly to stabilize for long periods. All four limbs are affected, but the pelvic limbs are commonly more severely affected than the thoracic limbs. There is no treatment for the disease, no spontaneous recovery and, once affected, horses remain atactic and useless for any athletic function.
There are no clinicopathological tests specific for encephalomalacia but various tests may aid in the diagnosis of some of the specific diseases mentioned above under Etiology.
Gross lesions including areas of softening, cavitation and laminar necrosis of the cortex may be visible. The important lesions are described under each of the specific diseases.
The prognosis depends on the nature of the lesion. Early cases of thiamine-deficiency-induced polioencephalomalacia can recover completely if treated with adequate levels of thiamin. Encephalomalacia due to sulfur-induced polioencephalomalacia and lead poisoning is more difficult to treat. Young calves with acquired in utero hypomyelinogenesis and horses with myelitis associated with equine herpesvirus-1 infection can make complete recoveries.
The syndromes produced by encephalomalacia resemble very closely those caused by most lesions that elevate intracranial pressure. The onset is quite sudden and there is depression of consciousness and loss of motor function. One major difference is that the lesions tend to be nonprogressive and affected animals may continue to survive in an impaired state for long periods.
De Lahunta A. Abiotrophy in domestic animals: a review. Can J Vet Res. 1990;54:65-76.
Summers BA, Cummings JF, de Lahunta A. Veterinary neuropathology. St Louis: Mosby, 1995.
Cebra CK, Cebra ML. Altered mentation caused by polioencephalomalacia, hypernatremia, and lead poisoning. Vet Clin North Am Food Anim Pract. 2004;20:287-302.
1 Maddison JE. J Vet Intern Med. 1992;6:341.
2 De Lahunta A, et al. Can J Vet Res. 1990;54:65.
3 Wilkins PA, et al. Cornell Vet. 1994;84:53.
4 Woodman MP, et al. Vet Rec. 1993;132:586.
5 Toenniessen JG, Morin DE. Compend Contin Educ Pract Vet. 1995;17:271.
6 Stewart WB. Vet Rec. 1997;140:260.
7 Plumlee KH, Galey FD. J Vet Intern Med. 1994;8:49.
8 Uhlinger C. J Am Vet Med Assoc. 1991;198:126.
9 Smith GW, et al. Am J Vet Res. 2002;63:538.
10 Foreman JH, et al. J Vet Intern Med. 2004;18:223.
11 Dill SG, et al. Am J Vet Res. 1990;51:1300.
12 Summers BA, et al. Veterinary neuropathology. St Louis: Mosby, 1995.
The effects of trauma to the brain vary with the site and extent of the injury but initially nervous shock is likely to occur followed by death, recovery, or the persistence of residual nervous signs.
Traumatic injury to the brain may result from direct trauma applied externally, by violent stretching or flexing of the head and neck or by migration of parasitic larvae internally. Recorded causes include the following:
• Direct trauma, an uncommon cause because of the force required to damage the cranium. Accidental collisions, rearing forwards, falling over backwards after rearing are the usual reasons
• Periorbital skull fractures in horses caused by direct traumatic injury commonly from collision with gate posts1
• Cerebral injury and cranial nerve injury, accounted for in a large percentage of neurological disease in horses.2 Young horses under 2 years of age seem most susceptible to injuries of the head
• Injury by heat in goat kids achieved with prolonged application of a hot iron used for debudding
• Pulling back violently when tethered causing problems at the atlanto-occipital junction
• Animals trapped in bogs, sumps, cellars, and waterholes and dragged out by the head; recumbent animals pulled on to trailers suffering dire consequences to the medulla and cervical cord, although the great majority of them come to surprisingly little harm
• The violent reaction of animals to lightning stroke and electrocution causing damage to central nervous tissue; the traumatic effect of the electrical current itself also causing neuronal destruction
• Spontaneous hemorrhage into the brain – rare but sometimes occurring in cows at parturition, causing multiple small hemorrhages in the medulla and brainstem
• Brain injury at parturition, recorded in lambs, calves, and foals and possibly a significant cause of mortality in the former.
The initial reaction in severe trauma or hemorrhage is nervous shock. Slowly developing subdural hematoma, a common development in humans, is accompanied by the gradual onset of signs of a space-occupying lesion of the cranial cavity but this seems to be a rare occurrence in animals. In some cases of trauma to the head, clinical evidence of injury to the brain may be delayed for a few days until sufficient swelling, callus formation or displacement of the fracture fragments has occurred. Trauma to the cranial vault may be classified, from least to most severe, as concussion, contusion, laceration, and hemorrhage.
Concussion is usually a brief loss of consciousness which results from an abrupt head injury which produces an episode of rapid acceleration/deceleration of the brain.
With a more violent force, the brain is contused. There is maintenance of structure but loss of vascular integrity, resulting in hemorrhage into the parenchyma and meninges relative to the point of impact. Bony deformation or fracture of the calvaria result in two different kinds of focal lesions:
The most severe contusion is laceration where the central nervous system tissue is physically torn or disrupted by bony structures lining the cranium or by penetrating objects such as bone fragments. Focal meningeal hemorrhage is a common sequel to severe head injury. Subdural hematomas usually follow disruption of bridging cerebral veins that drain into the dural venous sinuses but subarachnoid hemorrhages are more common. The importance of these hemorrhages is that they develop into space-occupying masses that indent and compress the underlying brain. Progressive enlargement of the hematoma can result in secondary effects such as severe, widespread brain edema, areas of ischemia, herniations, midline shift, and lethal brainstem compression.
In birth injuries the lesion is principally one of hemorrhage subdurally and under the arachnoid.
Traumatic insult of the brains of sheep with a .22 caliber firearm results in a primary hemorrhagic wound track with indriven bone fragments and portions of muscle and skin.3 There is crushing and laceration of tissues during missile penetration, secondary tracks due to bone and bullet fragments, widely distributed stretch injuries to blood vessels, nerve fibers and neurons as a consequence of the radial forces of the temporary cavity that develops as a bullet penetrates tissue, marked subarachnoid and intraventricular hemorrhage, and distortion and displacement of the brain. The lesions are consistently severe and rapidly fatal.
The syndrome usually follows the pattern of greatest severity initially with recovery occurring quickly but incompletely to a point where a residual defect is evident, this defect persisting unchanged for a long period and often permanently. This failure to improve or worsen after the initial phase is a characteristic of traumatic injury.
With severe injury there is cerebral shock in which the animal falls unconscious with or without a transient clonic convulsion. Consciousness may never be regained but in animals that recover it returns in from a few minutes up to several hours. During the period of unconsciousness, clinical examination reveals dilatation of the pupils, absence of the eye preservation and pupillary light reflexes, and a slow, irregular respiration, the irregularity being phasic in many cases. There may be evidence of bleeding from the nose and ears and palpation of the cranium may reveal a site of injury. Residual signs vary a great deal, blindness is present if the optic cortex is damaged; hemiplegia may be associated with lesions in the midbrain; traumatic epilepsy may occur with lesions in the motor cortex.
Fracture of the petrous temporal bone is a classic injury in horses caused by rearing and falling over backwards. Both the facial and the vestibular nerves are likely to be damaged so that at first the animal may be unable to stand and there may be blood from the ear and nostril of the affected side. When the animal does stand the head is rotated with the damaged side down. There may be nystagmus, especially early in the course of the disease. The ear, eyelid, and lip on the affected side are also paralyzed and sag. Ataxia with a tendency to fall is common. Some improvement occurs in the subsequent 2 or 3 weeks as the horse compensates for the deficit, but there is rarely permanent recovery. An identical syndrome is recorded in horses in which there has been a stress fracture of the petrous temporal bone resulting from a pre-existing inflammation of the bone. The onset of signs is acute but unassociated with trauma.
Fracture of the basisphenoid and/or basioccipital bones is also common. These fractures can seriously damage the jugular vein, carotid artery and glossopharyngeal, hypoglossal and vagus nerves. The cavernous sinus and the basilar artery may also be damaged and lead to massive hemorrhage within the cranium. Large vessels in the area are easily damaged by fragments of the fractured bones, causing fatal hemorrhage. A midline fracture of the frontal bones can also have this effect.
Other signs of severe trauma to the brain include opisthotonos with blindness and nystagmus and, if the brainstem has been damaged, quadriplegia. There may also be localizing signs, including head rotation, circling and falling backwards. Less common manifestations of resulting hemorrhage include bleeding into the retropharyngeal area, which may cause pressure on guttural pouches and the airways and lead to asphyxia. Bleeding may take place into the guttural pouches themselves.
Newborn lambs affected by birth injury to the brain are mostly dead at birth, or die soon afterwards. Surviving lambs drink poorly and are very susceptible to cold stress. In some flocks it may be the principal mechanism causing perinatal mortality.
Radiography of the skull is important to detect the presence and severity of fractures, which may have lacerated nervous tissue. CSF should be sampled from the cerebellomedullary cistern and examined for evidence of red blood cells. Extreme care must be taken to ensure that blood vessels are not punctured during the sampling procedure as this would confound the interpretation of the presence of red blood cells. The presence of heme pigments in the CSF suggests the presence of pre-existing hemorrhage; the presence of eosinophils or hypersegmented neutrophils suggests parasitic invasion.
In most cases a gross hemorrhagic lesion will be evident but in concussion and nematodiasis the lesions may be detectable only on histological examination.
In those animals that recover consciousness within a few hours or earlier, the prognosis is favorable and little or no specific treatment may be necessary other than nursing care. When coma lasts for more than 3–6 hours the prognosis is unfavorable and slaughter for salvage or euthanasia is recommended. Treatment for edema of the brain as previously outlined may be indicated when treatment for valuable animals is requested by the owner. Animals that are still in a coma 6–12 hours following treatment are unlikely to improve and continued treatment is not warranted.
Focal diseases of the brain
Abscesses of the brain occur most commonly in young farm animals under 1 year of age and rarely in older animals. Brain abscesses produce a variety of clinical signs depending on their location and size. Basically the syndrome produced is one of a space-occupying lesion of the cranial cavity with some motor irritation signs. Localized or diffuse meningitis is also common, along with the effects of the abscess.
Abscesses in the brain originate in a number of ways. Hematogenous infections are common, but direct spread from injury to the cranium or via the nasopharynx may also occur.
The lesions may be single, but are often multiple, and are usually accompanied by meningitis. The infection usually originates elsewhere.
• Actinobacillus mallei from glanders lesions in lung
• Streptococcus zooepidemicus var. equi as a complication of strangles in horses
• Corynebacterium pseudotuberculosis in a goat causing an encapsulated abscess in the left cerebellar peduncles1
• Actinomyces bovis and Mycobacterium bovis from visceral lesions in cattle
• Fusobacterium necrophorum from lesions in the oropharynx of calves
• Pseudomonas pseudomallei in melioidosis in sheep
• Staphylococcus aureus in tick pyemia of lambs
• Systemic fungal infections such as cryptococcosis may include granulomatous lesions in brain.2
• Via peripheral nerves from oropharynx, the one specific disease is listeriosis in ruminants and New World camelids
• Multifocal meningoencephalitis associated with lingual arteritis induced by barley spikelet clusters3
• Space-occupying lesions of facial and vestibulocochlear nerves and geniculate ganglion secondary to otitis media in calves4
• Abscesses of rete mirabile of pituitary gland secondary to nasal septal infection after nose-ringing in cattle.5 Arcanobacterium (Actinomyces or Corynebacterium) pyogenes is the most common isolate and several other species of bacteria that cause chronic suppurative lesions have been recovered.5 Similar abscesses, usually containing A. pyogenes, occur in the pituitary gland itself
• Extensions from local suppurative processes in cranial signs after dehorning, from otitis media. The lesions are single, most commonly contain A. pyogenes and are accompanied by meningitis.
Infectious agents can invade the central nervous system by four routes:
Single abscesses cause local pressure effects on nervous tissue and may produce some signs of irritation, including head-pressing and mania, but the predominant effect is one of loss of function due to destruction of nerve cells. Multiple abscesses have much the same effect but whereas in single abscesses the signs usually make it possible to define the location of the lesion, multiple lesions present a confusing multiplicity of signs and variation in their severity from day to day, suggesting that damage has occurred at a number of widely distributed points and at different times.
The pituitary abscess syndrome has an uncertain pathogenesis. The pituitary gland is surrounded by a complex mesh of intertwined arteries and capillary beds known as the rete mirabile, which has been identified in cattle, sheep, goats, and pigs but not horses. This extensive capillary network surrounding the pituitary gland makes it susceptible to localization by bacteria that originate from other sources of infection. Nose-ringing of cattle may result in septic rhinitis, which could result in infection of the dural venous sinus system, which communicates with the subcutaneous veins of the head. Bacteria may also reach the rete mirabile by way of lymphatics of the nasal mucosa and cribriform plate. Cranial nerve deficits occur as a result of the extension of the abscess into the adjacent brainstem.
General signs include mental depression, clumsiness, head-pressing, and blindness, often preceded or interrupted by transient attacks of motor irritation including excitement, uncontrolled activity, and convulsions. A mild fever is usually present but the temperature may be normal in some cases.
The degree of blindness varies depending on the location of the abscess and the extent of adjacent edema and meningoencephalitis. The animal may be blind in one eye and have normal eyesight in the other eye or have normal eyesight in both eyes. Unequal pupils and abnormalities in the pupillary light reflex, both direct and consensual, are common. Uveitis, iris bombé, and a collection of fibrin in the anterior chamber of an eye may be present in some cases of multiple meningoencephalitis in cattle.3 Nystagmus is common when the lesion is near the vestibular nucleus; strabismus may also occur.
Localizing signs depend on the location of lesions and may include cerebellar ataxia, deviation of the head with circling and falling, hemiplegia or paralysis of individual or groups of cranial nerves often in a unilateral pattern. In the later stages there may be papilledema. In calves with lesions of the facial and vestibulocochlear nerves and geniculate ganglion, clinical signs may include drooping of the ears and lips, lifting of the nose, slight unilateral tilting of the head and uncontrolled saliva flow. Inability to swallow may follow and affected calves become dehydrated.
These localizing signs may be intermittent, especially in the early stages, and may develop slowly or acutely.
Pituitary gland abscesses are most common in ruminants, primarily cattle 2–5 years of age,5 but are relatively rare. The most common history includes anorexia, ataxia, depression, and drooling from the mouth with inability to chew and swallow. The most common clinical findings are depression, dysphagia, dropped jaw, blindness, and absence of pupillary light reflexes. Terminally, opisthotonos, nystagmus, ataxia, and recumbency are common. Characteristically, the animal stands with a base-wide stance, with its head and neck extended and its mouth not quite closed; there is difficulty in chewing and swallowing, and drooling of saliva. Affected animals are usually nonresponsive to external stimuli. Cranial nerve deficits are common, usually asymmetrical, multifocal and progressive. These include reduced tone of the jaw, facial paralysis, strabismus, and a head tilt. There may also be ptosis and prolapse of the tongue. Bradycardia has been recorded in about 50% of cases.5 Terminally there is opisthotonos, nystagmus, and loss of balance, followed by recumbency.
Leukocytes, protein, and bacteria may be present in the CSF, but only when the abscess is not contained.
In pituitary gland abscessation there may be hematological evidence of chronic infection including neutrophilia, hyperproteinemia, and increased fibrinogen,5 although it is unlikely that a pituitary abscess itself is sufficiently large enough to induce these changes.
Radiographic examination will not detect brain abscesses unless they are calcified or cause erosion of bone. Computed tomography has been used to diagnose a brain abscess in the horse.6
Electroencephalographic assessment of central blindness due to brain abscess in cattle has been reported.7
The abscess or abscesses may be visible on gross examination and if superficial are usually accompanied by local meningitis.8 Large abscesses may penetrate to the ventricles and result in a diffuse ependymitis. Microabscesses may be visible only on histological examination. A general necropsy examination may reveal the primary lesion.
Brain abscess is manifested by signs of involuntary movements and loss of function, which can occur in many other diseases of the brain, especially when local lesions develop slowly. This occurs more frequently with tumors and parasitic cysts but it may occur in encephalitis. The characteristic clinical findings are those of a focal or multifocal lesion of the brain, which include:
• Localizing signs of hemiparesis and ataxia
• Vestibular signs, including head tilt and positional nystagmus
There may be evidence of the existence of a suppurative lesion in another organ, and a high cell count and detectable infection in the CSF to support the diagnosis of abscess. Fever may or may not be present. The only specific disease in which abscess occurs is listeriosis, in which the lesions are largely confined to the medulla oblongata and the characteristic signs include circling and unilateral facial paralysis. Occasional cases may be associated with fungal infections, including cryptococcosis. Toxoplasmosis is an uncommon cause of granulomatous lesions in the brain of most species.
Many cases of brain abscess are similar to otitis media but there is, in the latter, rotation of the head, a commonly associated facial paralysis and an absence of signs of cerebral depression.
The pituitary gland syndrome in cattle must be differentiated from listeriosis, polioencephalomalacia, lead poisoning, other brain abscesses and thrombomeningoencephalitis. In sheep and goats, Paraelaphostrongylus tenuis infection and caprine arthritis encephalomyelitis syndrome may resemble the pituitary gland abscess syndrome.
Parenteral treatment with antimicrobials is indicated but the results are generally unsatisfactory because of the inaccessibility of the lesion, with the clear exception being listeriosis. Treatment of pituitary gland abscess is not recommended, and an antemortem diagnosis is rarely obtained.
Perdrizet JA, Dinsmore P. Pituitary abscess syndrome. Compend Contin Educ Pract Vet. 1986;8:S311-S318.
Summers BA, Cummings JF, de Lahunta A. Veterinary neuropathology. St Louis, MO: Mosby, 1995.
Morin DE. Brainstem and cranial nerve abnormalities: Listeriosis, otitis media/interna, and pituitary abscess syndrome. Vet Clin North Am Food Anim Pract. 2004;20:243-274.
1 Glass EN, et al. Cornell Vet. 1993;83:275.
2 Teuscher E, et al. Zentralbl Vet Med A. 1984;31:132.
3 Sorden SD, Radostits OM. Aust Vet J. 1996;37:227.
4 Van der Lugt JJ, Jordaan P. Vet Rec. 1994;134:579.
5 Perdrizet JA, Dinsmore P. Compend Contin Educ Pract Vet. 1986;8:S311.
6 Allen JR, et al. Equine Vet J. 1987;19:552.
7 Strain GM, et al. Cornell Vet. 1987;77:374.
8 Summers BA, Cummings JF, de Lahunta A. Veterinary neuropathology. St Louis, MO: Mosby, 1995.
Infection of the middle ear (otitis media) occurs in young animals of all species but especially dairy calves and pigs, to a lesser extent feedlot cattle and lambs, and rarely foals. The infection may gain entrance from the external ear (e.g. caused by ear mite infestation) or hematogenously, but the spread is chiefly an ascending infection of the eustachian tubes in a young animal from a respiratory tract infection. Extension of infection into the inner ear leads to otitis interna.
Otitis media was present in 68% of 237 pigs that were slaughtered because of illness.1 It is suggested that otitis media in pigs develops first as an acute inflammation in the auditory tube and then extends to other parts of the ear and brain. When abscesses form at the ventrum of the brainstem, the vestibulocochlear nerve is usually involved in the lesion.1 Infection in the ear may extend into the brain by following the auditory nerve. Perilymph filling the scala vestibuli and scala tympani is also a possible tract for the extension of the infection because there is a communication between the perilymph-filled spaces of the bony labyrinth and the subarachnoid space.
The peak of occurrence in calves and lambs is 1–4 weeks of age. The highest prevalence is in suckling dairy calves and weaned cattle and sheep in feedlots, where the disease is probably secondary to respiratory tract infection. Outbreaks of otitis media/interna have occurred in beef calves from 6–10 weeks of age on pasture with their dams; mixed cultures of Escherichia coli, Pseudomonas spp., and Acinetobacter spp. were isolated.2 Otitis media/interna in suckling dairy calves can also occur in outbreaks, and Mycoplasma bovis is frequently isolated from the middle and inner ears of affected calves.3
The onset of clinical signs commonly includes dullness, fever, inappetence, tachypnea, and a purulent discharge from the affected ear accompanied by rotation of the head (in otitis interna) and drooping of the ear a few days later due to involvement of the facial nerve in the inflammation.2 Deep palpation at the base of the ears may elicit a pain response.3
Rotation of the head, with the affected side down and facial paralysis may occur on the same side, and walking in circles with a tendency to fall to the affected side is common. In most cases the animals are normal in other respects, although depression and inappetence can occur in advanced cases.
Otitis media/interna occurs in horses4,5 and two clinical syndromes have been described.
The first syndrome is primary otitis media characterized by abnormal behavior, including head tossing, head shaking, and ear rubbing.4 Violent, uncontrollable behavior includes throwing themselves on the ground, rolling, and thrashing. This may progress to involve the bony structures of the temporal and proximal stylohyoid bones, resulting in a degenerative arthritis and eventual fusion of the temporohyoid bone.
The second syndrome is characterized by an acute onset of neurologic deficits. Commonly, there is vestibulocochlear nerve and often facial nerve dysfunction characterized by head tilt to the side of the lesion, nystagmus with the slow component to the affected side and weakness of the extensor muscles on the affected side resulting in an ataxia or reluctance or refusal to stand. Horses that can stand often will lean on walls for support of the affected side.
Definitive diagnosis is dependent on either a positive tympanocentesis or, in the majority of cases, bony proliferation of the temporal bone and proximal part of the stylohyoid bone, or lysis of the tympanic bulla, as determined by radiography4 or computed tomography.3 This can be visualized using endoscopy of the auditory tube diverticula in horses with otitis media/interna.5 In some cases, the tympanic membrane is ruptured, which can be seen using an otoscope.5
Tympanocentesis is done under general anesthesia in horses or sedation in ruminants by directing a 15 cm needle through the tympanic membrane visualized with the aid of an otoscope. The technique is somewhat difficult because of the long and angled external auditory canal. Sterile 0.9% NaCl (0.5–1 mL) is injected into the tympanic cavity and then, after a few seconds, withdrawn. A positive tap consists of withdrawal of a cloudy or yellow fluid, which on analysis may contain evidence of pus and can be sampled for culture and antimicrobial susceptibility.
The disease needs to be differentiated from otitis externa, in which the head may be carried in a rotated position, but usually intermittently, and this is accompanied by head shaking and the presence of exudate and an offensive smell in the ear canal, and from cerebral injury or abscess, and similar lesions of the upper cervical cord. All of these are characterized by deviation of the head, not rotation. At necropsy the tympanic bulla contains pus, and a variety of organisms, such as staphylococci, streptococci, Pasteurella haemolytica, and Neisseria catarrhalis, may be isolated.
Treatment consists of broad-spectrum antimicrobials daily for 4 weeks, and anti-inflammatory agents. The prognosis with treatment with fluoroquinolones is very good in calves, although a 50% mortality rate has been reported in calves that were not treated with other antimicrobial agents.6 The use of lincomycin at 6.5 mg/kg BW combined with spectinomycin at 10 mg/kg BW intravenously twice daily for 5 days has been reported to be successful for the treatment of otitis media in beef calves.2 Anecdotal reports exist in cattle of the use of a knitting needle to rupture the tympanic membrane, with rapid resolution of the head tilt because of the decreased pressure in the middle ear. Bilateral tympanic bulla osteotomy has been performed in an affected calf, resulting in a rapid resolution of the head tilt.3
Primary tumors of the central nervous system are extremely rare in farm animals. They produce a syndrome indicative of a general increase in intracranial pressure and local destruction of nervous tissue. Tumors of the peripheral nervous system are more common.
The reader is referred to the review literature for a summary of available references on the tumors of the central nervous system of farm animals, which include:
The development of the disease parallels that of any space-occupying lesion, with the concurrent appearance of signs of increased intracranial pressure and local tissue destruction. Many lesions found incidentally at necropsy may not have had any related clinical findings.
The clinical findings are similar to those caused by a slowly developing abscess and localizing signs depend on the location, size, and speed of development of the tumor. Clinical signs are usually representative of increased intracranial pressure, including opisthotonos, convulsions, nystagmus, dullness, head-pressing, and hyperexcitability. Common localizing signs include circling, deviation of the head, disturbance of balance. Lesions close to the pituitary gland may cause diabetes insipidus and Cushing’s syndrome.3 A 17-year-old horse with an ependymoma had an 18-month history of slowly progressive ataxia culminating in a sudden loss of ability to control the pelvic limbs, with dog-sitting, spinning, and falling.4
There are no positive findings in clinicopathological examination which aid in diagnosis.
The pituitary gland (hypophysis) consists of the adenohypophysis (pars distalis, intermedia, tuberalis) and the neurohypophysis (pars nervosa). Tumors of the pituitary gland occur in the horse.1 Cushing’s syndrome in horses almost invariably originates from an adenoma of the pars intermedia of the pituitary gland.1 Initially, these animals exhibit only one remarkable sign, namely, hirsutism. Horses with Cushing’s disease only do not manifest polyuria and polydipsia. Major sequelae of an adenoma of the pars intermedia of the pituitary gland are type 2 diabetes mellitus and laminitis. Diagnosis of an adenoma of the pars intermedia of the pituitary gland in the horse mainly depends on dynamic endocrinological function tests. The sensitivity of the adrenocorticotropin (ACTH) test is about 80%.1
Many primary tumors of non-nervous tissue have the potential for metastasis to the central nervous system.
• Ocular squamous cell carcinoma of cattle may invade the cranium through the cribriform plate
• Lymphomas of cattle may metastasize to the central nervous system with either a multicentric distribution or occasionally as the only lesion. Most commonly bovine lymphoma occurs as an epidural mass in the vertebral canal. Intracranial lymphoma usually involves the leptomeninges or the choroid plexus. Clinical signs are related to the progressive compression of the nervous tissue at the site of the mass. Lymphoma in the horse has occurred in the epidural space with spinal cord compression.
Cholesterinic granulomas, also known as cholesteatomas may occur in up to 20% of older horses without any clinical effects.1 However, they can be associated with significant neurological disease. Affected horses are commonly obese.1 Cholesterinic granulomas occur in the choroid plexus of the fourth ventricle or in the lateral ventricles and mimic cerebrocortical disease. It has been suggested that cholesterol granulomas result from chronic hemorrhage into the plexus stroma but the underlying pathogenesis is unknown.
Brownish nodular thickening of the plexuses with glistening white crystals is a common incidental finding in mature and aged horses. Occasionally, deposits in the plexuses of the lateral ventricles are massive and fill the ventricular space and cause secondary hydrocephalus due to the build up of CSF behind the mass. CSF may be xanthochromic with an elevated total protein.1Clinical findings include episodes of abnormal behavior such as depression and bolting uncontrollably, running into fences and walls.2 Some horses exhibit profound depression, somnolence, and reluctance to move.1 Seizures have also been reported.1 Other clinical findings reported include decreased performance, aggression, head tilt, incoordination, intermittent convulsions, hindlimb ataxia progressing to recumbency, intermittent circling in one direction, and spontaneous twitching along the back and flank. There are often serious changes in temperament, with previously placid animals becoming violent and aggressive. In others there are outbursts of frenzied activity followed by coma. The horse may be normal between attacks and these may be precipitated by moving the head rapidly.
These signs are referable to cerebrocortical disease and the differential diagnosis of cholesterol granulomas must include diffuse cerebral encephalopathy due to abscess, tumor, toxicosis, metabolic disease, encephalomyelitis, trauma, and hydrocephalus. At necropsy, large cholesterol granulomas are present in the choroid plexus.
Coenurosis is the disease caused by invasion of the brain and spinal cord by the intermediate stage of Taenia multiceps. The syndrome produced is one of localized, space-occupying lesions of the central nervous system. In most countries the disease is much less common than it used to be and relatively few losses occur.
The disease is associated with Coenurus cerebralis, the intermediate stage of the tapeworm T. multiceps, which inhabits the intestine of dogs and wild Canidae. The embryos, which hatch from eggs ingested in feed contaminated by the feces of infested dogs, hatch in the intestine and pass into the bloodstream. Only those embryos that lodge in the brain or spinal cord survive and continue to grow to the coenurid stage. C. cerebralis can mature in the brain and spinal cords of sheep, goats, cattle, horses, and wild ruminants, and occasionally humans, but clinical coenurosis is primarily a disease of sheep and occasionally cattle. Infection in newborn calves, acquired prenatally, has occasionally been observed.
The early stages of migration through nervous tissue usually passes unnoticed, but in heavy infections an encephalitis may be produced. Most signs are caused by the mature coenurus, which may take 6–8 months to develop to its full size of about 5 cm. The cyst-like coenurus develops gradually and causes pressure on nervous tissue, resulting in its irritation and eventual destruction. It may cause sufficient pressure to rarefy and soften cranial bones.
In acute outbreaks due to migration of larval stages, sheep show varying degrees of blindness, ataxia, muscle tremors, nystagmus, excitability, and collapse. Sheep affected with the mature coenurus show an acute onset of irritation phenomena including a wild expression, salivation, frenzied running and convulsions. Deviation of the eyes and head may also occur. Some animals may die in this stage but the greater proportion go on to the second stage of loss of function phenomena, the only stage in most affected animals. The most obvious sign is slowly developing partial or complete blindness in one eye. Dullness, clumsiness, head-pressing, ataxia, incomplete mastication and periodic epileptiform convulsions are the usual signs. Papilledema may be present. Localizing signs comprise chiefly deviation of the head and circling; there is rotation of the head with the blind eye down, and deviation of the head with circling in the direction of the blind eye.1
In young animals local softening of the cranium may occur over a superficial cyst and rupture of the cyst to the exterior may follow, with final recovery. When the spinal cord is involved there is a gradual development of paresis and eventually inability to rise. Death usually occurs after a long course of several months.
Clinicopathological examinations are not generally used in diagnosis in animals and serological tests are not sufficiently specific to be of value. Radiological examinations are helpful in defining the location of the cyst, especially if there is a prospect of surgical intervention.1
Thin-walled cysts may be present anywhere in the brain but are most commonly found on the external surface of the cerebral hemispheres. In the spinal cord the lesions are most common in the lumbar region but can be present in the cervical area. Local pressure atrophy of nervous tissue is apparent and softening of the overlying bone may occur.
The condition needs to be differentiated from other local space-occupying lesions of the cranial cavity and spinal cord, including abscess, tumor, and hemorrhage. In the early stages the disease may be confused with encephalitis because of the signs of brain irritation. Clinically there is little difference between them and, while clinical signs and local knowledge may lead to a presumptive diagnosis, demonstration of the metacestode is essential.
Surgical drainage of the cyst may make it possible to fatten the animal for slaughter, and surgical removal with complete recovery is possible in a majority of cases. The life cycle can be broken most satisfactorily by control of mature tapeworm infestation in dogs. Periodic treatment of all farm dogs with a tenicide is essential for control of this and other more pathogenic tapeworms. Carcasses of livestock infested with the intermediate stages should not be available to dogs.
Diseases of the meninges
Inflammation of the meninges occurs most commonly as a complication of a pre-existing disease. Meningitis is usually associated with a bacterial infection and is manifested clinically by fever, cutaneous hyperesthesia, and rigidity of muscles. Although meningitis may affect the spinal cord or brain specifically, it commonly affects both and is dealt with here as a single entity. Meningoencephalitis is common in neonatal farm animals. Primary bacterial meningitis is extremely rare in adult farm animals, with the exception of listeriosis and Histophilus somni (formerly Haemophilus somnus) infection, although the latter is more a vasculitis than a primary meningitis. The possibility of immunodeficiency should be considered in adult horses with bacterial meningitis.1
Most significant meningitides are bacterial, although most viral encephalitides have some meningitic component.
• Viral diseases – bovine malignant catarrh, sporadic bovine encephalomyelitis
• Bacterial diseases – listeriosis, H. somni, chronic lesions elsewhere in the body possibly associated with meningitis in adult animals;2 rarely tuberculosis.
Streptococcal and coliform septicemias are probably the commonest causes of meningitis in neonatal farm animals. The infection may originate from an omphalophlebitis, bacteremia,3 or bacterial translocation across the gastrointestinal tract in neonates less than 24 h of age or with enteritis. Septicemia occurs in all species, especially calves, and may be accompanied by polysynovitis, endocarditis, and hypopyon. The causative bacteria are usually a mixed flora.4
Hematogenous infection occurs from other sites also. In neonatal animals, some of the common infections are:
Inflammation of the meninges causes local swelling and interference with blood supply to the brain and spinal cord but as a rule penetration of the inflammation along blood vessels and into nervous tissue is of minor importance and causes only superficial encephalitis. Failure to treat meningitis associated with pyogenic bacteria often permits the development of a fatal choroiditis, with exudation into CSF, and ependymitis. There is also inflammation around the nerve trunks as they pass across the subarachnoid space. The signs produced by meningitis are thus a combination of those resulting from irritation of both central and peripheral nervous systems. In spinal meningitis there is muscular spasm with rigidity of the limbs and neck, arching of the back and hyperesthesia with pain on light touching of the skin. When the cerebral meninges are affected, irritation signs, including muscle tremor and convulsions, are the common manifestations. Since meningitis is usually bacterial in origin, fever and toxemia can be expected if the lesion is sufficiently extensive.
Defects of drainage of CSF occur in both acute and chronic inflammation of the meninges and produce signs of increased intracranial pressure. The signs are general although the accumulation of fluid may be localized to particular sites such as the lateral ventricles.
Acute meningitis usually develops suddenly and is accompanied by fever and toxemia in addition to nervous signs. Vomiting is common in the early stages in pigs. There is trismus, opisthotonos, and rigidity of the neck and back. Motor irritation signs include tonic spasms of the muscles of the neck causing retraction of the head, muscle tremor and paddling movements. Cutaneous hyperesthesia is present in varying degrees, even light touching of the skin causing severe pain in some cases. There may be disturbance of consciousness manifested by excitement or mania in the early stages, followed by drowsiness and eventual coma.
Blindness is common in cerebral meningitis but not a constant clinical finding. In young animals, ophthalmitis with hypopyon may occur, which supports the diagnosis of meningitis. The pupillary light reflex is usually much slower than normal. Examination of the fundus of the eyes may reveal evidence of optic disk edema, congestion of the retinal vessels and exudation.
In uncomplicated meningitis the respiration is usually slow and deep, and often phasic in the form of Cheyne–Stokes breathing (a breathing pattern characterized by a period of apnea followed by a gradual increase in the depth and rate of respiration) or Biot’s breathing (a breathing pattern characterized by unpredictable irregularity). Terminally there is quadriplegia and clonic convulsions.
The major clinical finding of meningoencephalitis in calves under 2 weeks of age was depression which progressed rapidly to stupor but the mental state changed to hyperesthesia, opisthotonos and seizures in unresponsive terminal cases.3 Meningoencephalitis should be considered in calves that have been treated for the effects of diarrhea with fluid therapy but fail to respond and remain depressed.
In a series of 32 cases of meningitis in neonatal calves, the mean age at admission was 6 days (range, 11 hours– 30 days). The major clinical findings were lethargy (32/32), recumbency (32/32), anorexia and loss of the suck reflex (26/32), and stupor and coma (21/32).5 The frequency of other clinical findings were as follows: opisthotonos (9/32), convulsions (7/32), tremors (6/32), and hyperesthesia (6/32). The case fatality rate was 100%.
Although meningitis in farm animals is usually diffuse, affecting particularly the brainstem and upper cervical cord, it may be quite localized and produce localizing signs, including involvement of the cranial or spinal nerves. Localized muscle tremor, hyperesthesia and rigidity may result. Muscles in the affected area are firm and board-like on palpation. Anesthesia and paralysis usually develop caudal to the meningitic area. Spread of the inflammation along the cord is usual. Reference should be made to the specific diseases cited under Etiology for a more complete description of their clinical manifestations.
In newborn calves, undifferentiated diarrhea, septic arthritis, omphalophlebitis and uveitis are frequent concurrent clinical findings. Bacterial meningitis has been reproduced experimentally in calves, resulting in typical clinical signs consisting of convulsions, depression, circling and falling to one side, ataxia, propulsive walking, loss of saliva, tremors, recumbency, lethargy, and nystagmus.6
CSF collected from the lumbosacral space or cisterna magna in meningitis contains elevated protein concentrations, has a high cell count and usually contains bacteria.4,7 The collection of CSF from the lumbosacral space of calves has been described under the section on Special examination of the nervous system.7 Culture and determination of drug sensitivity of the bacteria is advisable because of the low concentrations of antimicrobial agents achieved in CSF. In a series of meningitis in neonatal calves, the CSF revealed pleocytosis (mean 4000 leukocytes/μL; range, 130–23 270 leukocytes/μL), xanthochromia, turbidity and a high total protein concentration.5
Hyperemia, the presence of hemorrhages, and thickening and opacity of the meninges, especially over the base of the brain, are the usual macroscopic findings. The CSF is often turbid and may contain fibrin. A local superficial encephalitis is commonly present. Additional morbid changes are described under the specific diseases and are often of importance in differential diagnosis. In neonatal calves with meningitis, lesions of septicemia are commonly present at necropsy and E. coli is the most commonly isolated organism.
Hyperesthesia, severe depression, muscle rigidity, and blindness are the common clinical findings in cerebral meningitis but it is often difficult to differentiate meningitis from encephalitis and acute cerebral edema. Examination of the CSF is the only means of confirming the diagnosis before death. Analysis of CSF is very useful in the differential diagnosis of diseases of the nervous system of ruminants.7.8 Details are presented under Examination of CSF in the section on Special examination of the nervous system. Subacute or chronic meningitis is difficult to recognize clinically. The clinical findings may be restricted to recumbency, apathy, anorexia, slight incoordination if forced to walk and some impairment of the eyesight. Spinal cord compression is usually more insidious in onset and is seldom accompanied by fever; hyperesthesia is less marked or absent and there is flaccidity rather than spasticity.
The infection is usually bacterial, and parenteral treatment with antimicrobial agents is necessary. Large doses daily for several days are required. The levels of antimicrobial agents that are achieved in the meninges and CSF following parenteral administration to farm animals are not known. Presumably, the blood–brain and blood–CSF barriers are not intact in meningitis and minimum inhibitory concentrations of some drugs may be achieved.
The injection of antimicrobial agents into the cerebromedullary cistern or into the lumbosacral space is not recommended. If parenteral treatment with the antimicrobial of choice, determined by a susceptibility test, does not result in a beneficial response in 3–5 days the prognosis is unfavorable.
The choice of antimicrobial agent will depend on the suspected cause of the meningitis. The common antibiotics, such as penicillin and oxytetracycline, are effective for the treatment of meningoencephalitis in cattle due to H. somni when treatment is begun early. Neonatal streptococcal infections also respond beneficially to penicillin when treated early before irreparable injury has occurred.
The response to therapy will depend on the causative pathogen and the severity of the inflammation present. Some cases of meningitis, such as that in swine associated with S. suis type 2, commonly do not respond to treatment when clinical signs are obvious. Conversely, the meningoencephalitis in cattle associated with H. somni will respond dramatically if treatment is begun as soon as clinical signs are apparent. The prognosis in meningitis associated with infection with E. coli is unfavorable. In a series of 32 cases admitted to a veterinary teaching hospital, even after intensive therapy the case fatality rate was 100%.5
Based on recent experiences in human medicine, the most promising antimicrobials for the treatment of meningitis in farm animals, particularly the neonates, may be the new third-generation cephalosporins, which resist hydrolysis by beta-lactamases, have enhanced penetration into the CSF and are bactericidal at very low concentrations.4 Clinical experience with these agents in the treatment of neonatal meningitis has been very encouraging. The aminoglycosides are also indicated in the treatment of meningitis in newborn animals.5 Moxalactam and cefotaxime are used widely for the treatment of Gram-negative bacillary meningitis in human and ceftazidime is equally effective.4 Trimethoprim–sulfonamide combinations, with or without gentamicin, which is synergistic with the former, are also recommended. The principles of the pharmacotherapeutics of bacterial meningitis in farm animals have been reviewed.4
1 Pellegrini-Masini A, et al. J Am Vet Med Assoc. 2005;227:114.
2 Scott PR, et al. Vet Rec. 1993;133:623.
3 Scott PR, Penny CD. Vet Rec. 1993;133:119.
4 Jamison JM, Prescott JF. Compend Contin Educ Pract Vet. 1988;10:225.
5 Green SL, Smith LL. J Am Vet Med Assoc. 1992;201:125.
6 Nazifi S, et al. J Vet Med A. 1997;44:55.
Toxic and metabolic encephalomyelopathies
A very large number of poisons, especially poisonous plants and farm chemicals, and some metabolic defects cause abnormalities of function of the nervous system. Those plants that cause degenerative nervous system disease are listed under encephalomalacia; those that cause no detectable degenerative change in tissue are listed here.
A partial list of toxins and metabolic errors or imbalances that can cause nervous system dysfunction are as follows.
• Hypoglycemia and ketonemia of pregnancy toxemia (with degenerative lesions in some) and acetonemia
• Depression due to strong ion (metabolic) acidosis associated with diarrhea and dehydration, particularly in neonatal animals
• Hypomagnesemia of lactation tetany
• Hyper-d-lactatemia in neonatal calves with diarrhea and adult ruminants with grain overload
• High blood levels of ammonia in hepatic insufficiency
• Unspecified toxic substances in uremic animals
• Exogenous toxins, including carbon tetrachloride, hexachloroethane, and trichloroethylene
• Plants causing anemic and histotoxic hypoxia, especially plants causing cyanide or nitrite poisoning
• Poison plants, including Helichrysum spp., tansy mustard, male fern, kikuyu grass (or a fungus, Myrothecium sp. on the grass).
• Metabolic deficits, including hypoglycemia (piglets, ewes with pregnancy toxemia), hypomagnesemia (of whole milk tetany of calves, lactation tetany, cows and mares)
• Nutritional deficiencies of vitamin A (brain compression in calves and pigs), pyridoxine (experimentally in calves)
• Inorganic poisons, including lead (calves), mercury (calves), farm chemicals such as organic arsenicals (pigs), organophosphates, chlorinated hydrocarbons, strychnine, urea, metaldehyde
• Bacterial toxins, including Clostridium tetani, Clostridium perfringens type D
• Fungal toxins, e.g. Claviceps purpurea
• Grasses, including Wimmera ryegrass (Lolium rigidum) or the nematode on it, Echinopogon ovatus
• Weeds – Oenanthe spp. (hemlock water dropwort), Indigophera spp. (in horses), Cicuta spp. (water hemlock), Albizia tanganyinicus, Sarcostemma spp. and Euphorbia spp.
• Grasses – Phalaris tuberosa (aquatica) (and other Phalaris spp.), Lolium rigidum, Echinopogon ovatus
• Weeds – Romulea bulbocidum, sneezeweed (Helenium spp.), Indigophera spp., Iceland poppy (Papaver nudicaule), Gomphrena spp., Malva spp., Stachys spp., Ipomoea spp., Solanum esuriale
• Trees – Kalmia spp., Erythrophloeum spp., Eupatorium rugosum
• Ferns – Xanthorrhea spp., Zamia spp. Induced thiamin deficiency caused by bracken and horsetail poisoning.
This includes, for example, Australian stringhalt caused by Arctotheca calendula (flatweed).
There is an additional long list of plants that cause diarrhea and nervous signs, especially ataxia, together, but whether the latter are due to the former or caused by neurotoxins is not identified.
The nervous signs include tremor, incoordination, and convulsions.
Many of the toxic substances and metabolic defects listed above cause paresis when their influence is mild and paralysis when it is severe. Some of the items appear in both lists. Because an agent appears in one list and not the other is not meant to suggest that it does not cause the other effect. It is more likely that it occurs in circumstances that are almost always conducive to the development of a mild syndrome (or a severe one, as the case may be).
• Disturbance of function at neuromuscular junctions e.g.: hypocalcemia, hypomagnesemia, hypokalemia (as in downer cows), tetanus, botulism and hypoglycemia of pregnancy toxemia in cows and ewes, and tick paralysis. Hypophosphatemia has not been demonstrated to be a definitive cause of weakness in cattle
• Nutritional deficiency, but including only experimentally induced deficiency of nicotinic and pantothenic acids: biotin and choline, cause posterior paresis and paralysis in pigs and calves
• Toxic diseases of the nervous system, including disease associated with many chemicals used in agriculture, e.g.: piperazine, rotenone, 2,4-d and 2,4,5-T, organophosphates, carbamates, chlorinated hydrocarbons, propylene glycol, metaldehyde, levamisole, toluene, carbon tetrachloride, strychnine, and nicotine sulfate.
Psychoses or neuroses are extremely rare in farm animals, although the vices of crib-biting and weaving in horses could be included in this category.
Crib-biting is an acquired habit in which the horse grasps an object, usually the feed box or any solid projection, with the incisor teeth, then arches the neck and, by depressing the tongue and elevating the larynx, pulls upwards and backwards and swallows air, emitting a loud grunt at the same time. This results in erosion of the incisor teeth, intermittent bouts of colic and flatulence. Crib-biting must be distinguished from chewing wood due to boredom and from pica due to a mineral deficiency. Some horses perform similarly but do not actually seize the object with their teeth; they just rest their teeth or their chin on it.
Wind sucking is the vice in which the horse flexes and arches the neck and swallows air and grunts but there is no grasping of objects.
Grasping is the seizing of an object with the teeth but without swallowing of air.
Persistent kicking of the stall, in the absence of pruritic lesions of the lower limbs, continuous circling of a stall, pawing of the floor with a forefoot and weaving, standing at the window looking out while rocking from one forefoot to the other and swinging the head and neck to the same side, are all neurotic vices caused by boredom in active horses. The extreme case is the animal that bites itself and causes cutaneous and subcutaneous mutilation.
Hysteria in sows at farrowing is a common occurrence. This syndrome occurs most commonly in gilts. Affected animals are hyperactive and restless and they attack and savage their piglets as they approach the head during the initial teat sucking activity after birth. Serious and often fatal injuries result. Cannibalism is not a feature.
When the syndrome occurs, the remaining piglets and freshly born piglets should be removed from the sow and placed in a warm environment until parturition is finished. The sow should then be tested to see if she will accept the piglets. If not, ataractic or neuroleptic drugs should be administered to allow initial sucking, after which the sow will usually continue to accept the piglets.
Azaperone (2 mg/kg BW) is usually satisfactory and pentobarbital sodium administered intravenously until the pedal reflex is lost has been recommended. Promazine derivatives are effective but subsequent incoordination may result in a higher crushing loss of piglets. The piglets’ teeth should be clipped.
Affected gilts should be culled subsequently as the syndrome may recur at subsequent farrowing. Where possible, gilts should be placed in their farrowing accommodation 4–6 days before parturition and the farrowing environment should be kept quiet at the time of parturition.
The incidence of cannibalism has increased with intensification of pig rearing and it is now a significant problem in many pig-rearing enterprises. Tail-biting is the most common and occurs in groups of pigs, especially males, from weaning to market age. Ear-chewing is less common and is generally restricted to pigs in the immediate postweaning and early growing period, although both syndromes may occur concurrently. The incidence of ear-chewing has increased with the practice of docking piglet tails at birth.
Tail-biting usually begins with one or two pigs sucking or chewing the tails of pen mates. Initially the practice causes no resentment but as the tail becomes raw and eroded, pain is shown. Rarely, if the offending agonists are removed at this stage, the problem will not progress. Generally the raw eroded tail becomes attractive to other individuals within the group and the vice spreads within the group to involve the majority of pigs. Most of the tail may eventually be removed, leaving a raw bleeding stump.
Productivity is affected by severe lesions and sequelae such as spinal abscessation with paralysis and abscessation or pyemia with partial or total carcass condemnation are not uncommon.
Ear-biting occurs in similar fashion. The lesions are usually bilateral and most commonly involve the ventral part of the ear. Lesions from bite wounds may also occur on the flanks of pigs. There is frequently an association with mange infestation with both of these vices.
A syndrome of snout-rubbing to produce eroded necrotic areas on the flanks of pigs has been described. Affected pigs were invariably colored, although both white and colored pigs acted as agonists.
The causes of these forms of cannibalism in pigs are poorly understood but they are undoubtedly related to an inadequate total environment. Affected groups are usually more restless and have heightened activity. Factors such as a high population density, both in terms of high pen density and large group size, limited food and competition for food, low protein and inadequate nutrition, boredom and inadequate environment in terms of temperature, draft and ventilation have been incriminated in precipitating the onset of these vices.
When a problem is encountered each of these factors should be examined and corrected or changed if necessary. Prevention is through the same measures. Chains or tires are frequently hung for displacement activity but are not particularly effective.
The problem may recur despite all attempts at prevention. Also for economic reasons it is not always possible to implement the radical changes in housing and management that may be necessary to avoid the occurrence of these vices. Because of this, the practice of tipping or docking the piglets’ tails at birth has become common as a method of circumventing the major manifestation of cannibalism.
Seizures occur most frequently in conjunction with other signs of brain disease. The syndrome of inherited, recurrent seizures, which continues through life with no underlying morphological disease process, is true epilepsy, which is extremely rare in farm animals. Familial epilepsy has been recorded in Brown Swiss cattle and is described under that heading in Chapter 12.
Residual lesions after encephalitis may cause symptomatic epileptiform seizures but there are usually other localizing signs. A generalized seizure is manifested by an initial period of alertness, the counterpart of the aura in human seizures, followed by falling in a state of tetany, which gives way after a few seconds to a clonic convulsion with paddling, opisthotonos and champing of the jaws. The clonic convulsions may last for some minutes and are followed by a period of relaxation. The animal is unconscious throughout the seizure, but appears normal shortly afterwards.
Some seizures may be preceded by a local motor phenomenon such as tetany or tremor of one limb or of the face. The convulsion may spread from this initial area to the rest of the body. This form is referred to as jacksonian epilepsy and the local sign may indicate the whereabouts of the local lesion or point of excitation. Such signs are recorded very rarely in dogs and not at all in farm animals. The seizures are recurrent and the animal is normal in the intervening periods.
Sudden severe trauma to the spinal cord causes a syndrome of immediate, complete, flaccid paralysis caudal to the injury because of spinal shock. This is so brief in animals as to be hardly recognizable clinically. Spinal shock is soon followed by flaccid paralysis in the area supplied by the injured segment and spastic paralysis caudal to it.
Trauma is the most common cause of monoplegia in large animals. There are varying degrees of loss of sensation, paresis, paralysis, and atrophy of muscle.
• Animals falling off vehicles, through barn floors
• Osteoporotic or osteodystrophic animals, especially aged brood mares and sows, spontaneously while jumping or leaning on fences
• Spondylosis and fracture of thoracolumbar vertebrae in old bulls in insemination centers
• Cervical vertebral fractures account for a large percentage of spinal cord injuries in horses1
• Trauma due to excessive mobility of upper cervical vertebrae may contribute to the spinal cord lesion in wobbles in horses
• Dislocations of the atlanto-occipital joint are being reported increasingly
• Stenosis of the cervical vertebral canal at C2–C4 in young rams, probably as a result of head-butting2
• Fracture of T1 vertebra in calves turning violently in an alleyway wide enough to admit cows
• Vertebral fractures in 7–10-month-old calves escaping under the head gate of chute and forcefully hitting their backs (just cranial to the tuber coxae) on the bottom rail of the gate3
• Vertebral fractures in neonatal calves associated with forced extraction during dystocia2,4
• Lightning strike may cause tissue destruction within the vertebral canal.
• Obstruction to blood flow to the cord by embolism, or of drainage by compression of the caudal vena cava, e.g. in horses during prolonged dorsal recumbency under general anesthesia;5 in pigs due to fibrocartilaginous emboli, probably originating in injury to the nucleus pulposus of an intervertebral disk.5
The lesion may consist of disruption of nervous tissue or its compression by displaced bone or hematoma. Minor degrees of damage may result in local edema or hyperemia or, in the absence of macroscopic lesions, transitory injury to nerve cells, classified as concussion. The initial response is that of spinal shock, which affects a variable number of segments on both sides of the injured segment and is manifested by complete flaccid paralysis. The lesion must affect at least the ventral third of the cord before spinal shock occurs. When the shock wears off the effects of the residual lesion remain. These may be temporary in themselves and completely normal function may return as the edema or the hemorrhage is resorbed. In sheep, extensive experimental damage to the cord may be followed by recovery to the point of being able to walk, but not sufficiently to be of any practical significance.
Traumatic lesions usually affect the whole cross-section of the cord and produce a syndrome typical of complete transection. Partial transection signs are more common in slowly developing lesions. Most of the motor and sensory functions can be maintained in 3-month-old calves with experimental left hemisection of the spinal cord.6
In a retrospective study of dystocia-related vertebral fractures in neonatal calves, all the fractures were located between the 11th thoracic vertebra and the fourth lumbar vertebra, with 77% occurring at the thoracolumbar junction.4 All but one case was associated with a forced extraction using unspecified (53%), mechanical (28%) or manual (17%) methods of extraction. Traction is most commonly applied after the fetus has entered the pelvic canal. Manual traction varies from 75 kg pressure applied by one man to 260 kg applied by three or more men. The forces applied in mechanical traction vary from 400 kg for a calf puller to over 500 kg for a tractor. The transfer of these forces to the vertebrae and to the physeal plates at the thoracolumbar junction could readily cause severe tissue damage. In a prospective study of vertebral fractures in newborn calves, all fractures were located at the thoracolumbar area, especially the posterior epiphysis of T13.2
Spinal shock develops immediately after severe injury and is manifested by flaccid paralysis (reflex loss) caudal to a severe spinal cord lesion. There is a concurrent fall in local blood pressure due to vasodilatation and there may be local sweating. Stretch and flexor reflexes and cutaneous sensitivity disappear but reappear within a half to several hours, although hypotonia may remain. The extremities are affected in most cases and the animal is unable to rise and may be in sternal or lateral recumbency. The muscles of respiration may also be affected, resulting in interference with respiration. The body area supplied by the affected segments will eventually show flaccid paralysis, disappearance of reflexes and muscle wasting – a lower motor neuron lesion.
When the injury is caused by invasion by parasitic larvae there is no stage of spinal shock but the onset is acute, although there may be subsequent increments of paralysis as the larva moves to a new site.
Neonatal calves with dystocia-related vertebral fractures are weak immediately after birth or remain recumbent and make no effort to rise.
Sensation may be reduced at and caudal to the lesion and hyperesthesia may be observed in a girdle-like zone at the cranial edge of the lesion as a result of irritation of sensory fibers by local inflammation and edema. Because of interference with the sacral autonomic nerve outflow there may be paralysis of the bladder and rectum, although this is not usually apparent in large animals. The vertebral column should be examined carefully for signs of injury. Excessive mobility, pain on pressure, and malalignment of spinous processes may indicate bone displacements or fractures. Rectal examination may also reveal damage or displacement particularly in fractures of vertebral bodies and in old bulls with spondylosis.
Residual signs may remain when the shock passes off. This usually consists of paralysis, which varies in extent and severity with the lesion. The paralysis is apparent caudal to and at the site of the lesion. The reflexes return except at the site of the lesion. There is usually no systemic disturbance but pain may be sufficiently severe to cause an increase in heart rate and prevent eating.
Recovery may occur in 1–3 weeks if nervous tissue is not destroyed but when extensive damage has been done to a significantly large section of the cord there is no recovery and disposal is advisable. In rare cases animals that suffer a severe injury continue to be ambulatory for up to 12 hours before paralysis occurs. In such instances it may be that a fracture occurs but displacement follows at a later stage during more active movement. Recovered animals may be left with residual nervous deficits or with postural changes such as torticollis.
In horses fracture/dislocation of cranial cervical vertebrae occurs fairly commonly. Affected animals are recumbent and unable to lift the head from the ground. However, they may be fully conscious and able to eat and drink. It may be possible to palpate the lesion, but a radiograph is usually necessary. Lesions of the caudal cervical vertebrae may permit lifting of the head but the limbs are not moved voluntarily. In all cases the tendon and withdrawal reflexes in the limbs are normal to supernormal.
Old bulls in artificial insemination centers develop calcification of the ventral vertebral ligaments and subsequent spondylosis or rigidity of the lumbar area of the vertebral column. When the bull ejaculates vigorously the calcified ligaments may fracture and this discontinuity may extend upward through the vertebral body. The ossification is extensive, usually from about T2–L3, but the fractures are restricted to the midlumbar region. There is partial displacement of the vertebral canal and compression of the cord. The bull is usually recumbent immediately after the fracture occurs but may rise and walk stiffly several days later. Arching of the back, slow movement, trunk rigidity and sometimes unilateral lameness are characteristic signs. Less severe degrees of spondylosis have been recorded in a high proportion of much younger (2–3-year old) bulls, but the lesions do not appear to cause clinical signs.
Radiologic examination may reveal the site and extent of the injury. CSF obtained from the lumbosacral space may reveal the presence of red blood cells, suggesting pre-existing hemorrhage.
The abnormality is always visible on macroscopic examination. In neonatal calves with dystocia-related vertebral fractures, hemorrhage around the kidneys, around the adrenal glands and in the perivertebral muscles is a common finding and a useful indicator that a thoracolumbar fracture is present. In addition to the vertebral fracture, subdural and epidural hemorrhage, myelomalacia, spinal cord compression, severed spinal cord, and fractured ribs are common findings.
Differentiation from other spinal cord diseases is not usually difficult because of the speed of onset and the history of trauma, although spinal myelitis and meningitis may also develop rapidly. Other causes of recumbency may be confused with trauma especially if the animal is not observed in the immediate preclinical period. In most diseases characterized by recumbency, such as azoturia, acute rumen impaction and acute coliform mastitis, there are other signs to indicate the existence of a lesion other than spinal cord trauma. White muscle disease in foals is characterized by weakness and the serum creatine kinase activity will be increased.
Treatment is expectant only, surgical treatment rarely being attempted. Large doses of corticosteroids or nonsteroidal anti-inflammatory agents are recommended to minimize the edema associated with the spinal cord injury. Careful nursing on deep bedding with turning at 3-hourly intervals, massage of bony prominences and periodic slinging may help to carry an animal with concussion or other minor lesion through a long period of recumbency. In cattle especially, recumbency beyond a period of about 48 hours is likely to result in widespread necrosis of the caudal muscles of the thigh and recovery in such cases is improbable. A definitive diagnosis of a vertebral fracture with paralysis usually warrants a recommendation for euthanasia.
The gradual development of a space-occupying lesion in the vertebral canal produces a syndrome of progressive weakness and paralysis. A pre-existing inflammatory or neoplastic lesion of the vertebral body may result in spontaneous fracture of the vertebral body and compression of the spinal cord.
Compression of the spinal cord occurs from space-occupying lesions in the vertebral canal, the common ones being as follows.
The most commonly occurring tumor in animals is lymphomatosis, which the nerve trunks and invades the vertebral canal, usually in the lumbosacral region and less commonly in the brachial and cervical areas This tumor is particularly common in adult cattle with multicentric lymphosarcoma due to bovine leukosis virus infection.
Rare tumors include: fibrosarcomas, metastases, plasma cell myeloma, angioma, melanoma in a horse,1 hemangiosarcoma in a horse,2 neurofibroma and lymphosarcoma, e.g. in horses, vascular hamartoma in a goat.3
Vertebral body abscesses (osteomyelitis) occur most commonly in neonatal farm animals generally in association with a chronic suppurative lesion elsewhere in the body.
• Docking wounds in lambs, bite wounds in pigs and chronic suppurative pneumonia in calves are common occurrences
• Polyarthritis and endocarditis may also be present
• Compression of the spinal cord is caused by enlargement of the vertebral body abscess into the vertebral canal and there may or may not be deviation of the vertebral canal and its contents
• The original site of infection may have resolved when the clinical signs referable to the spinal cord abscess appear
• Hematogenous spread may also occur from Arcanobacterium (Actinomyces or Corynebacterium) pyogenes in cattle, Actinomyces bovis in cattle with lumpy jaw, Corynebacterium pseudotuberculosis in sheep
• Epidural abscesses causing compression of the spinal cord and not associated with vertebral bodies also occur in lambs.4
• Exostoses over fractures with no displacement of vertebral bodies
• Similar exostoses on vertebral bodies of lambs grazing around old lead mines
• Hypovitaminosis A in young growing pigs causing compression of the nerve roots passing through the vertebral foramina
• Congenital deformity or fusion of the atlanto-occipital-axial joints in calves, foals and goats (see Congenital defects, below)
• Congenital spinal stenosis of calves.5
Rarely there is protrusion of an intervertebral disc, identifiable by myelogram, and progressive paresis and ataxia also occur rarely in diskospondylitis in horses. Cervical pain is a more common sign in the latter. The degenerative lesions in disks in the neck of the horse resemble the Hansen type 2 disk prolapses in dogs.
Adult sows and boars may have degeneration of intervertebral disks and surrounding vertebral osteophytes. Less commonly ankylosing spondylosis, arthrosis of articular facets, defects in annulus fibrosus and vertebral end plates, and vertebral osteomyelitis or fracture. These lesions of diskospondylitis cause lameness in boars and sows rather than compression of cord and paresis/paralysis.
These are not to be confused with the many extravertebral causes of posterior lameness or paralysis in adult pigs, which are discussed in Chapter 13 on the musculoskeletal system.
This is a major problem and is dealt with more extensively under the heading of enzootic incoordination of horses. For purposes of comparison the diseases involved are listed here:
• Nonfatal fractures of the skull (basisphenoid, basioccipital, and petrous temporal bones)
• Atlanto-occipital instability
• Stenosis of cranial vertebral orifice of C3–C7;7 this may be effective as a compression mechanism only if the vertebrae adopt exaggerated positions
• Abnormal growth of interarticular surfaces
• Dorsal enlargement of caudal vertebral epiphyses and bulging of intervertebral disks
• Formation and protrusion of false joint capsules and extrasynovial bursae
• Spinal myelitis due to parasitic invasion or equine herpesvirus-1 virus, even louping-ill virus and probably others
• Spinal abscess usually in a vertebral body
• Cerebellar hypoplasia – most commonly the inherited version in Arabian foals
• Degenerative myelomalacia/myelopathy – cause unknown
• Fusion of occipital bone with the atlas, which is fused with the axis
The development of any of the lesions listed above results in the gradual appearance of motor paralysis or hypoesthesia, depending on whether the lesion is ventrally or dorsally situated. In most cases there is involvement of all motor and sensory tracts but care is necessary in examination if the more bizarre lesions are to be accurately diagnosed. There may be hemiparesis or hemiplegia if the lesion is laterally situated. Paraparesis or paraplegia is caused by a bilateral lesion in the thoracic or lumbar cord and monoplegia by a unilateral lesion in the same area. Bilateral lesions in the cervical region cause tetraparesis to tetraplegia (quadriplegia).
In horses with chronic compressive myelopathy (wobbles), compression of the spinal cord results in necrosis of white matter, and some focal loss of neurons.8,9 With time, secondary wallerian-like neuron fiber degeneration in ascending white matter tracts cranial to the focal lesion and in descending white matter tracts caudal to the lesion occurs. Astrocytic gliosis is a prominent and persistent alteration of the spinal cord of horses with chronic cervical compressive myelopathy and is associated with nerve fiber degeneration at the level of the compression and in well-delineated areas of ascending and descending nerve fiber tracts. It is possible that the persistent astrocytic gliosis may prevent, or slow, recovery of neurological function in affected horses.
Vertebral osteomyelitis in young calves occurs most commonly in the thoracolumbar vertebrae and less commonly in the cervical vertebrae. The abscess of the vertebral body gradually enlarges and causes gradual compression of the spinal cord, which causes varying degrees of paresis of the pelvic limbs and ataxia.10 The abscess may extend into adjacent intervertebral spaces and result in vertebral arthritis with lysis of the articular facets. The onset of paresis and paralysis may be sudden in cases of abscessation or osteomyelitis of the vertebrae, which may fracture and cause displacement of bony fragments into the vertebral canal with compression and traumatic injury of the spinal cord. Vertebral body abscesses between T2 and the lumbar plexus will result in weakness of the pelvic limbs and normal flexor withdrawal reflexes of the pelvic limbs. Lesions at the site of the lumbar plexus will result in flaccid paralysis of the pelvic limbs.
Varying degrees of progressive weakness of the thoracic limbs or pelvic limbs may be the initial clinical findings. With most lesions causing gradual spinal cord compression, difficulty in rising is the first sign, then unsteadiness during walking due to weakness, which may be more marked in one of a pair of limbs. The toes are dragged along the ground while walking and the animal knuckles over on the fetlocks when standing. Finally the animal can rise only with assistance and then becomes permanently recumbent. These stages may be passed through in a period of 4–5 days.
The paralysis will be flaccid or spastic depending on the site of the lesion and reflexes will be absent or exaggerated in the respective states. The ‘dog-sitting’ position in large animals is compatible with a spinal lesion caudal to the second thoracic vertebral segment. Calves with vertebral osteomyelitis caudal to T2 are usually able to sit up in the ‘dog-sitting’ position, they are bright and alert and will suck the cow if held up to the teat. In some cases, extensor rigidity of the thoracic limbs resembles the Schiff–Sherrington syndrome and indicates a lesion of the thoracic vertebrae.
Lesions involving the lumbar plexus will result in flaccid paralysis of the pelvic limbs and an absence of the flexor withdrawal reflexes. Lesions involving the sacrococcygeal vertebrae will cause a decrease in tail tone, decreased or absent perineal reflex and urinary bladder distension.
Pain and hyperesthesia may be evident before motor paralysis appears. The pain may be constant or occur only with movement. In vertebral body osteomyelitis in the horse, vertebral column pain and a fever may be the earliest clinical abnormalities. With neoplasms of the epidural space, the weakness and motor paralysis gradually worsen as the tumor enlarges.
Considerable variation in signs occurs depending on the site of the lesion. There may be local hyperesthesia around the site of the lesion and straining to defecate may be pronounced. Retention of the urine and feces may occur. There is usually no detectable abnormality of the vertebrae on physical examination.
In the wobbler horse, circumduction of the limbs with ataxia is typical. The ataxia is usually pronounced in the pelvic limbs, and weakness is evident by toe dragging and the ease with which the horse can be pulled to one side while walking. Ataxia with hypometria is often evident in the thoracic limbs, especially while walking the horse on a slope and with the head elevated.
Calves with congenital spinal stenosis are usually unable to stand or can do so only if assisted. There are varying degrees of weakness and ataxia of the pelvic limbs. They are bright and alert and will suck the cow if assisted. Those that survive for several weeks will sometimes assume the ‘dog-sitting’ position.
Radiographic examination of the vertebral column should be carried out if the animal is of a suitable size. Myelography is necessary to demonstrate impingement on the spinal cord by a stenotic vertebral canal. Myelography using the contrast medium Iopamidol has been done in neonatal calves for the detection of spinal cord compression causing paresis.11 The contrast medium was introduced through the foramen magnum under general anesthesia.
The cerebrospinal fluid may show a cellular reaction if there is some invasion of the spinal canal.
Gross abnormalities of the vertebrae and the bony spinal canal are usually obvious. Those diseases of the spinal cord characterized by degeneration without gross changes require histological techniques for a diagnosis.
Differentiation between abscess, tumor and exostosis in the vertebral canal is usually not practicable without radiographic examination. Vertebral osteomyelitis is difficult to detect radiographically, particularly in large animals, because of the overlying tissue. In bovine lymphosarcoma there are frequently signs caused by lesions in other organs. A history of previous trauma may suggest exostosis. The history usually serves to differentiate the lesion from acute trauma.
• Spinal myelitis, myelomalacia and meningitis may resemble cord compression but are much less common. They are usually associated with encephalitis, encephalomalacia and cerebral meningitis respectively
• Meningitis is characterized by much more severe hyperesthesia and muscle rigidity
• Rabies in the dumb form may be characterized by a similar syndrome but ascends the cord and is fatal within a 6-day period.
In the newborn there are many congenital defects in which there is defective development of the spinal cord. Most of them are not characterized by compression of the cord, the diminished function being caused in most cases by an absence of tissue. Spina bifida, syringomyelia and dysraphism are characterized by hindquarter paralysis or, if the animal is able to stand, by a wide-based stance and overextension of the legs when walking. Some animals are clinically normal.
A generalized degeneration of peripheral nerves such as that described in pigs and cattle causes a similar clinical syndrome; so does polyradiculoneuritis. A nonsuppurative ependymitis, meningitis and encephalomyelitis, such as occurs in equine infectious anemia, may also cause an ataxia syndrome in horses.
Paresis or paralysis of one limb (monoplegia) is caused by lesions in the ventral gray matter, nerve roots, brachial and lumbosacral plexus, and peripheral nerves and muscles of the limbs.
1 Schott HC, et al. J Am Vet Med Assoc. 1990;196:1820.
2 Newton-Clarke MJ, et al. Vet Rec. 1994;135:182.
3 Middleton JR, et al. Vet Rec. 1999;144:264.
4 Scott PR, Will RG. Aust Vet J. 1991;147:582.
5 Doige CE, et al. Vet Pathol. 1990;27:16.
6 Hill BD, et al. Aust Vet J. 1993;70:156.
7 Tomizawa N, et al. J Vet Med Sci. 1994;56:227.
8 Yovich JV, et al. Aust Vet J. 1991;68:326.
9 Yovich JV, et al. Aust Vet J. 1991;68:334.
The subject of back pain, and its relationship to lameness, is a very important one in horses. There is often a lesion in the vertebral canal and by pressing on the cord or peripheral nerves it causes gait abnormalities that suggest the presence of pain, or they actually cause pain. Spondylosis, injury to dorsal spinous processes, and sprain of back muscles are common causes of the same pattern of signs. Because these problems are largely orthopedic ones, and therefore surgical, their exposition is left to other authorities.
It is necessary in horses to differentiate spinal cord lesions from acute nutritional myodystrophy, and subacute tying-up syndrome. Those diseases are characterized by high serum creatine kinase and aspartate aminotransferase activities.
Inflammation of the spinal cord is usually associated with viral encephalitis. The signs are referable to the loss of function, although there may be signs of irritation. For example, hyperesthesia or paresthesia may result if the dorsal root ganglia are involved. This is particularly noticeable in pseudorabies and to a lesser extent in rabies. Paralysis is the more usual result. There are no specific myelitides in farm animals. Listeriosis is sometimes confined in its lesion distribution to the spinal cord in sheep. Viral myelitis associated with equine herpesvirus-1 (the equine rhinopneumonitis virus) is now commonplace and equine infectious anemia and dourine include incoordination and paresis in their syndromes. In goats, caprine arthritis encephalitis is principally a myelitis, involving mostly the white matter.
Equine protozoal myeloencephalitis causes multifocal lesions of the central nervous system, mostly the spinal cord.1 The most accurate diagnosis is based on histological findings:
• Necrosis and mild to severe, nonsuppurative myeloencephalitis
• Infiltration of neural tissue by mononuclear cells
• Sometimes giant cells, neutrophils, and eosinophils
• Infiltration of perivascular tissue by mononuclear cells including lymphocytes and plasma cells.
Equine protozoal myeloencephalitis is caused primarily by Sarcocystis neurona, which has the opossum (Didelphis virginiana) as the definitive host, raccoons as the most likely intermediate host, with the horse acting as a dead end host.1 Occasional cases of protozoal myeloencephalitis in horses are associated with Neospora hughesi.
Myelitis associated with Neosporum caninum infection in newborn calves has been described.2 Affected calves were recumbent and unable to rise but were bright and alert. Histologically there was evidence of protozoal myelitis.
Myelomalacia occurs rarely as an entity separate from encephalomalacia. One recorded occurrence is focal spinal poliomalacia of sheep and in enzootic ataxia the lesions of degeneration are often restricted to the spinal cord. In both instances there is a gradual development of paralysis without signs of irritation and with no indication of brain involvement. Progressive paresis in young goats may be associated with the virus of caprine arthritis encephalitis and other unidentified, possibly inherited causes of myelomalacia.3
Degeneration of spinal cord tracts has also been recorded in poisoning by Phalaris aquatica in cattle and sheep, by sorghum in horses, by 3-nitro-4-hydroxyphenylarsonic acid in pigs and by selenium in ruminants; the lesion is a symmetrical spinal poliomalacia. Poisoning of cattle by plants of Zamia spp. produces a syndrome suggestive of injury to the spinal cord but no lesions have been reported. Pantothenic acid or pyridoxine deficiencies also cause degeneration of spinal cord tract in swine.
A disease of obscure etiology in sheep with spinal cord degeneration is Murrurrundi disease. A spinal myelinopathy, possibly of genetic origin is recorded in Murray Grey calves.4 Affected animals develop ataxia of the hindlegs, swaying of the hindquarters and collapse of one hindleg with falling to one side. Clinical signs become worse over an extended period.
Sporadic cases of degeneration of spinal tracts have been observed in pigs. One outbreak is recorded in the litters of sows on lush clover pasture. The piglets were unable to stand, struggled violently on their sides with rigid extension of the limbs and, although able to drink, usually died of starvation. Several other outbreaks in pigs have been attributed to selenium poisoning.
An inherited lower motor neuron disease of pigs has been recorded.5 Clinical findings of muscular tremors, paresis or ataxia developed at 12–59 days of age. There is widespread degeneration of myelinated axons in peripheral nerves and in the lateral and ventral columns of lumbar and cervical segments of the spinal cord. Axonal degeneration is present in ventral spinal nerve roots and absent in dorsal spinal nerve roots when sampled at the same lumbar levels.
Equine degenerative myeloencephalopathy of unknown etiology affects young horses and has been recorded in the USA, Canada, the UK, and Australia.6 The major clinical signs are referable to bilateral leukomyelopathy involving the cervical spinal cord. There is abnormal positioning and decreased strength and spasticity of the limbs as a result of upper motor neuron and general proprioceptive tract lesions. Hypalgesia, hypotonia, hyporeflexia, muscle atrophy, or vestibular signs are not present and there is no evidence of cranial nerve, cerebral or cerebellar involvement clinically. Abnormal gait and posture are evident, usually initially in the pelvic but eventually also in the thoracic limbs. There are no gross lesions but histologically there is degeneration of neuronal processes in the white matter of all spinal cord funiculi, especially the dorsal spinocerebellar and sulcomarginal tracts. The lesion is most severe in the thoracic segments. The disease is progressive and there is no known treatment.
Equine motor neuron disease affects horses from 15 months to 25 years of age of many different breeds.7,8 Progressive weakness, short-striding gait, trembling, long periods of recumbency, and trembling and sweating following exercise are characteristic clinical findings. The weakness is progressive and recumbency is permanent. Appetites remain normal or become excessive. At necropsy, degeneration and/or loss of somatic motor neurons in the spinal ventral horns and angular atrophy of skeletal muscle fibers are characteristic.7
Sporadic cases of spinal cord damage in horses include hemorrhagic myelomalacia following general anesthesia9 and acute spinal cord degeneration following general anesthesia and surgery.10 Following recovery from the anesthesia, the horse is able to assume sternal recumbency but not able to stand.10 A hemorrhagic infarct assumed to be due to cartilage emboli, and a venous malformation causing spinal cord destruction have also occurred in the horse. The disease must be differentiated from myelitis and spinal cord compression caused by space-occupying lesions of the vertebral canal, and cervical, vertebral malformation/malarticulation.
1 Fayer R, et al. J Vet Intern Med. 1990;4:54.
2 Parish SM, et al. J Am Vet Med Assoc. 1987;191:1599.
3 Lancaster MJ, et al. Aust Vet J. 1987;64:123.
4 Richards RB, Edwards JR. Vet Pathol. 1986;23:35.
5 O’Toole D, et al. J Vet Diagn Invest. 1994;6:230.
6 Mayhew IG, et al. J Vet Intern Med. 1987;1:45.
7 Step DL, et al. J Am Vet Med Assoc. 1993;202:26.
8 Cummings JF, et al. Cornell Vet. 1990;80:357.
Diseases of the peripheral nervous system
The peripheral nervous system consists of cranial and spinal nerve components. As such, the peripheral nervous system includes the dorsal and ventral nerve roots, spinal ganglia, spinal and specific peripheral nerves, cranial nerves and their sensory ganglia, and the peripheral components of the autonomic nervous system.1
There are several different causes of peripheral nervous system disease.
Polyneuritis equi, also known as neuritis of the cauda equina or cauda equina syndrome, is a rare and slowly progressive demyelinating granulomatous disease affecting peripheral nerves in the horse.2 Polyneuritis equi is characterized by signs of lower motor neuron lesions, primarily involving the perineal region but also affecting other peripheral nerves, especially the 5th and 7th cranial nerves. The 8th, 9th, 10th and 12th cranial nerves also may be involved. Clinical signs of perineal region paresis/paralysis predominate, manifest as varying degrees of hypotonia, hypalgesia and hyporeflexia of the tail, anus and perineal region. Degrees of urinary bladder paresis and rectal dilatation are also present. Differential diagnoses include sacral or coccygeal trauma, equine herpes myeloencephalopathy, equine protozoal myeloencephalitis, rabies and equine motor neuron disease.2
Cranial neuritis with guttural pouch mycosis and empyema in the horse may cause abnormalities of swallowing, laryngeal hemiplegia and Horner’s syndrome if the glossopharyngeal and vagal nerves are involved in the inflammatory process of the guttural pouch.1
Equine laryngeal hemiplegia, often called roaring, is a common disease of the horse in which there is paralysis of the left cricoarytenoid dorsalis muscle resulting in an inability to abduct the arytenoid cartilage and vocal fold, which causes an obstruction in the airway during inspiration. Endoscopic examination reveals asymmetry of the glottis. On exercise, inspiratory stridor develops as the airflow vibrates a slack and adducted vocal fold. The abnormality is due to idiopathic distal degeneration of axons in the left recurrent laryngeal nerve (see more details in Chapter 10).
Injection injuries to peripheral nerves may result from needle puncture, the drug deposited, pressure from an abscess or hematoma, or fibrous tissue around the nerve.1 The sciatic nerve has been most commonly affected in cattle because historically most intramuscular injections were given deep in the hamstring muscles. Young calves were particularly susceptible because of the small muscle masses. Current recommendations in cattle are that intramuscular injections should be administered cranial to the shoulder.
Femoral nerve paralysis in calves occurs in large calves born to heifers with dystocia. The injury occurs when calves in anterior presentation fail to enter the birth canal because their stifle joints become engaged at the brim of the pelvis. Traction used to deliver these calves causes hyperextension of the femur and stretching of the quadriceps muscle and its neural and vascular supplies. In most cases the right femoral nerve is affected. Such calves are unable to bear weight on the affected leg within days after birth, the quadriceps muscle is atrophied and the patella can be luxated easily. The patellar reflex is absent or markedly reduced in the affected limb because this reflex requires an intact femoral nerve and functional quadriceps muscle. Varying degrees of rear limb paresis result, accompanied by varying degrees of hind limb gait abnormality.3,4 Skin analgesia maybe present over the proximal lateral to cranial to medial aspect of the tibia.3 At rest, the affected leg is slightly flexed and the hip on the affected side is held slightly lower.4 During walking, the animal has difficulty in advancing the limb normally because the limb collapses when weight-bearing. In severe cases of muscle atrophy, the patella is easily luxated both medially and laterally. Injury to the femoral nerve is relatively easy to clinically identify, and there is usually no need to perform electromyographic studies of atrophied quadriceps muscle in order to document denervation.
Calving paralysis is common in heifers that have experienced a difficult calving. Affected animals are unable to stand without assistance; if they do stand, the hind limbs are weak and there is marked abduction and inability to adduct. It has always been erroneously thought that traumatic injury of the obturator nerves during passage of the calf in the pelvic cavity was the cause of the paresis; however, detailed pathological and experimental studies have demonstrated that most calving paresis/paralysis is due to damage to the sciatic nerve.5-8 Experimental transection of the obturator nerves does not result in paresis. The term obturator nerve paralysis should only be used for postparturient cattle with an inability to adduct one or both hindlimbs, and calving paralysis in the preferred descriptive term for hind limb paresis/paralysis occurring in the immediate postparturient period.
Damage to the sciatic nerve results in rear limb weakness and knuckling of the fetlocks; the latter clinical sign is an important means for differentiating sciatic nerve damage from obturator nerve damage. The patellar reflex in ruminants with sciatic nerve damage is normal or increased, because the reflex contraction of the quadriceps muscle group by the femoral nerve is unopposed by the muscles of the hindlimb innervated by the sciatic nerve.
The peroneal nerve is most frequently damaged by local trauma to the lateral stifle, where the peroneal nerve runs in a superficial location lateral to the head of the fibular bone. Damage to the peroneal nerve leads to knuckling over of the fetlock joint due to damage to the extensor muscles of the distal limb, resulting in the dorsal aspect of the hoof resting on the ground when the animal is standing. Full weight can be borne on the affected limb when the digit is placed in its normal position, but immediately upon walking the digit is dragged. There is a loss of skin sensation on the anterior aspect of the metatarsus and digit.
Damage to the tibial nerve causes mild hyperflexion of the hock and a forward knuckling of the fetlock joint. Tibial nerve damage is very rare, and most cases described as tibial nerve damage are actually sciatic nerve damage.
Pantothenic acid deficiency may occur in pigs fed diets based solely on corn (maize). Affected animals develop a goose-stepping gait due to degenerative changes in the primary sensory neurons of the peripheral nerves.
Heavy metal poisoning including lead and mercury poisoning in horses has been associated with clinical signs of degeneration of peripheral cranial nerves but these are not well documented.
A multicentric schwannoma causing chronic ruminal tympany and forelimb paresis has been recorded in an aged cow.9 Neoplastic masses were present throughout the body and both right and left brachial plexi were involved. The peripheral nerves of each brachial plexus were enlarged. Large tumor masses were present on the serosal surfaces of the esophagus, pericardial sac and epicardium, within the myocardium, endocardium and the ventral branches of the first four thoracic spinal nerves. A large mass was present in the anterior mediastinum near the thoracic inlet.
Grass sickness in the horse occurs exclusively in the UK and is characterized by a peracute to chronic alimentary tract disease of horses on pasture (hence the name). Gastrointestinal stasis is partial or complete. Peracute cases are in shock and in a state of collapse with gastric refluxing. Acute, subacute and chronic cases also occur. Degenerative changes occur in the autonomic ganglia, especially the celiac– mesenteric, stellate, thoracic sympathetic chain, ciliary, cranial and caudal cervical, the craniospinal sensory ganglia and selected nuclei in the central nervous system.9 The etiology is unknown.
Summers BA, Cummings BA, de Lahunta A. Veterinary neuropathology. St Louis, MO: Mosby, 1995.
Constable PD. Clinical examination of the ruminant nervous system. Vet Clin North Am Food Anim Pract. 2004;20:185-214.
Divers TJ. Acquired spinal cord and peripheral nerve disease. Vet Clin North Am Food Anim Pract. 2004;20:231-242.
1 Summers BA, Cummings BA, de Lahunta A. Veterinary neuropathology. St Louis, MO: Mosby, 1995.
2 Vatistas N, Mayhew J. J Pract. 1995;17:26.
3 Tryphonas L, et al. J Am Vet Med Assoc. 1974;164:801.
4 Paulsen DB, et al. Bovine Pract. 1981;2:14-26.
5 Vaughan LC. Vet Rec. 1964;76:1293.
6 Cox VS, et al. Am J Vet Res. 1975;36:427.
7 Cox VS, Breazile JE. Vet Rec. 1973;93:109.
Congenital defects of the central nervous system
The pathogenesis of congenital defects, including those of the central nervous system, has been dealt with in general terms in Chapter 3. Inheritance, nutrition, virus infection in early pregnancy and some toxins can all play a part in the genesis of these defects and the purpose of this section is to guide the diagnostician through the recognition of the defect to the possible causes. However, many such cases occur sporadically and a specific cause cannot be identified.
Although most developmental defects are present at birth there are a few that appear later in life, especially the abiotrophic diseases. in which an essential metabolic process (essential. that is. for cellular structure and function) is missing and the tissue undergoes degeneration.
The diseases to be identified are listed under the headings of the principal clinical signs and syndromes that they produce. Many affected neonates are weak and die either during birth or soon afterwards so that they tend to be diagnoses for pathologists rather than clinicians. There may be an unintentional bias toward more clinically conspicuous diseases in the following material. The reader is referred to the review literature for details of specific congenital defects.
• Hydrocephalus, sporadic or inherited, with obvious enlargement of the cranium
• Meningocele with protrusion of a fluid-filled sac through the open fontanelle in the cranial vault. The defect is inherited in some pigs
• Hydrocephalus with spina bifida combination – the Arnold–Chiari syndrome – in cattle
• Hydrocephalus with congenital achondroplasia (bulldog calf syndrome)
• Cranium bifidum (may include meningocele) of pigs
• Ventral meningomyelocele in a filly foal1
• Microphthalmia – in microcephaly the cranium is usually of normal size
• Some cases of failure of closure of neural tube, e.g. spina bifida in lambs.2 There is a defect in the skin and dorsal arch of the vertebra in the lumbosacral area in some cases
• Exophthalmos with or without strabismus, an inherited form in Jersey and Shorthorn cattle does not appear until the animal is more than 6 months of age
• Neurofibromas occurring as enlargements on peripheral nerves and seen as subcutaneous swellings. They are passed from cow to calf
• Persistent cloaca and caudal spinal agenesis in calves3
• Hydranencephaly, porencephaly and other structural defects due to intrauterine infection with Akabane, Bluetongue, Cache Valley and Wesselsbron viruses.
• Enzootic ataxia due to nutritional deficiency of copper. It may also develop later, within the first month of postnatal life
• Inherited congenital posterior paralysis of calves, and of pigs
• Congenital spinal stenosis of calves4
• Spina bifida, sometimes accompanied by flexion and contracture and atrophy of hindlegs; most are stillborn. In rare cases the affected calf is ambulatory5
• Spinal dysraphism in Charolais and Angus calves, syringomyelia and hydromyelia in calves
• Tetraparesis, tetraplegia, progressive ataxia with head deviation in foals with congenital occipitoatlanto-axial malformations. A familial tendency to the defects occurs in Arab and non-Arabian horses. Additional signs include stiffness of the neck, palpable abnormalities at the site and a clicking sound on passive movement. Foals may be affected at birth or develop signs later. The defect is identifiable radiographically
• A congenital dysplasia of the atlanto-occipital joint with excessive mobility is recorded in Angora goats and causes a compressive myelopathy. Devon calves may be affected by the same deformity6 and similar ones have been recorded in calves that were recumbent at birth5 and others in which ataxia developed subsequently7
• More widespread malacic changes have been recorded in the spinal cord of calves but without the specific etiology being determined.
• Inherited cerebellar hypoplasia of calves, Arabian foals, lambs
• Cerebellar hypoplasia and hypomyelinogenesis in calves from cows infected with BVD virus and possibly Akabane virus during pregnancy
• Cerebellar hypoplasia in piglets after hog cholera vaccination of dams
• Inherited cerebellar ataxia in pigs and foals
• Familial convulsions and ataxia of Angus cattle
• Intracranial hemorrhage in newborn foals, discussed in more detail under Neonatal maladjustment syndrome
• Spinal cord hypoplasia in Akabane virus infection in ruminants.
• Congenital paresis and tremor of piglets
• Inherited congenital spasms of cattle
• Inherited neonatal spasticity (Jersey and Hereford cattle) develops at 2–5 days old
• Border disease (hairy shakers) in lambs due to BVD virus
• Inherited neuraxial edema (now inherited congenital myoclonus) of polled Hereford cattle and congenital brain edema of Herefords
• Myoclonia congenita as a result of infection with hog cholera or Aujeszky’s disease viruses
• Tremor with rigidity due to hydranencephaly and porencephaly in calves infected in utero with BVD virus
• Brain injury during birth in calves and lambs
• Brain compression due to hypovitaminosis A in calves and pigs
• Neonatal maladjustment syndrome (barkers and wanderers) in Thoroughbred foals
• Congenital toxoplasmosis in calves, bluetongue virus infection in lambs
• Tetanic convulsion in inherited neuraxial edema (now inherited congenital myoclonus) of Hereford calves, but only when lifted to standing position
• Inherited idiopathic epilepsy of Brown Swiss cattle
• Familial convulsions and ataxia of Angus cattle
• Inherited narcolepsy/catalepsy in Shetland ponies and Suffolk horses (not really a convulsion)
• Microencephaly in calves, probably inherited, with no abnormality of the cranium, but the cerebral hemispheres, cerebellum and brainstem are reduced in size and the corpus callosum and fornix are absent
• Microcephaly recorded in sheep; many are dead at birth, viable ones are unable to stand, blind, incoordinate and have a constant tremor
• Anencephaly in calves with absence of cerebral hemispheres, rostral midbrain, occurs sporadically in calves
• Hydranencephaly associated with Akabane virus infection of calf, kid, and possibly lamb in utero
• Congenital porencephaly in lambs after intrauterine infection with bluetongue virus.
• Spontaneous microphthalmia and anophthalmia in calves, usually of unknown cause
• Congenital lenticular cataracts in cattle and lambs
• Blindness developing after birth in gangliosidosis of cattle and ceroid lipofuscinosis of sheep
• Constriction of optic nerve by vitamin A deficiency causing blindness in calves and pigs
• Constriction of optic nerve and blindness with BVD virus infection in calves in utero
• Cerebellar atrophy (abiotrophy) in calves and foals; a probably inherited cerebellar abiotrophy in sheep aged 3.5–6 years
• Inherited idiopathic epilepsy of Jerseys and Shorthorns
• Bovine generalized glycogenosis
• Multifocal symmetrical necrotizing encephalomyelopathy (Leigh’s disease) in Angus, Simmental, and Limousin cattle7
• Globoid cell leukodystrophy of sheep
• Ceroid lipofuscinosis of sheep
• Progressive ataxia of Charolais cattle
Done JT. Developmental disorders of the nervous system in animals. Adv Vet Sci. 1976;20:69.
Cho DY, Leipold HW. Congenital defects of the bovine central nervous system. Vet Bull. 1977;47:489.
Summers BA, Cummings JF, de Lahunta A. Veterinary neuropathology. St Louis, MO: Mosby, 1995.
Washburn KE, Streeter RN. Congenital defects of the ruminant nervous system. Vet Clin North Am Food Anim Pract. 2004;20:413-434.
* In the following discussion of diseases of the brain, the terms ‘irritation’, ‘release’, ‘paralysis’ and ‘nervous shock’ are used to describe groups of signs. These terms are used in accordance with their definitions under the principles of nervous dysfunction.