Signalment

The species, breed, age, and pedigree of an animal are important considerations in the differential diagnosis of neurologic disease. Many diseases are species-specific, particularly in the case of infectious and genetic diseases. Equine protozoal myeloencephalitis, for example, would not be a differential diagnosis in the case of cattle with signs of neurologic disease. Other infectious diseases, such as rabies virus infection, can affect many species. In yet other instances, all species may be affected but may have varying susceptibility to the disease. Such is the case with tetanus caused by Clostridium tetani exotoxin; horses and small ruminants are significantly more susceptible to the disease than are cattle. Some diseases not only are species-specific but also have higher incidence in certain breeds of that species. An example of this is equine degenerative myeloencephalopathy, which has been reported in several breeds of horses but has an increased incidence in some breeds, such as the Appaloosa.¹ Examples of the numerous other breed-related neurologic diseases of large animals include cerebellar abiotrophy (Arabian foals), progressive ataxia (Charolais), demyelinating myelopathy (Limousins), neuraxial edema (polled Herefords), neuraxonal dystrophy (Morgans), hydrocephalus (horned Herefords and shorthorns), epileptic seizures and Weaver syndrome (Brown Swiss cattle), ceroid lipofuscinosis (Hampshire sheep), cerebellar abiotrophy, GM1 gangliosidosis (Holsteins), and many others.^2-11 Atlantoaxial malformations most commonly occur in Arabian foals and Holstein calves but are not seen exclusively in those breeds.^12,13

Disease susceptibility also may be linked to age. Acute lead poisoning, for example, occurs most commonly in calves, whereas adult cattle tend to develop the subacute form of the disease.¹⁴ Some diseases are found in the neonate at birth. A large number of congenital disorders of the central nervous system (CNS) can affect domestic livestock. These diseases have a variable clinical course, depending on the nature of the disorder. Inborn errors of myelin metabolism worsen with age, whereas other developmental conditions may remain stable throughout the animal’s life.^15-20 Examples of these disorders are listed in Chapters 51 and 52.

A knowledge of the most likely disease entities to occur within individual animals or groups of animals of particular species, breeds, and ages, therefore, can greatly assist the clinician in arriving at a list of likely differential diagnoses and formulating a rational diagnostic and therapeutic plan.

History

Many disorders of the CNS produce characteristic patterns of onset and progression that can have diagnostic importance. Some CNS diseases occur acutely, developing the full range of clinical signs within hours. If the disease is not fatal, the signs either stabilize by 24 hours and remain constant thereafter or improve. Diseases that may display this clinical course include traumatic injuries and some types of toxic, infectious, and metabolic diseases. Diseases with degenerative, neoplastic, and certain viral causes may develop more slowly, requiring days to weeks before the full extent of clinical signs is apparent.^2,21,22

Diet

The diet of patients with neurologic disease should be evaluated^23-29 (Table 8-2). Common deficiencies of livestock include vitamins A and E, copper, selenium, and magnesium. Vitamin A deficiency occurs in feedlot animals that have no access to green plants; affected cattle become blind and develop seizures. Equine motor neuron disease is seen mainly in horses that are housed without access to pasture and whose diet is deficient in vitamin E.³⁰ Copper deficiency occurs in ruminants pastured in areas with shale or volcanic soils, which either are deficient in copper or contain high concentrations of molybdenum and sulfur (secondary copper deficiency). The deficiency produces demyelination of the spinal cord in lambs and kids and pathologic fractures of the lumbar spine of rapidly growing calves. Dietary deficiency of calcium in rapidly growing weaned calves also results in vertebral and long bone fractures. Although dietary deficiencies of vital nutrients are commonly associated with the development of neurologic diseases, oversupplementation of certain nutrients also may produce neurologic disorders. Overfeeding of calcium, micronutrient imbalance, protein, and energy to horses, for instance, has been linked to the development of cervical vertebral instability and stenosis (wobbler syndrome) in horses.^31,32

Table 8-2 Dietary Deficiencies Associated with Neurologic Disorders of Livestock

Environment

Examination of the patient’s environment may provide valuable information about the cause of CNS disease. Outbreaks of botulism and listeriosis have been associated with ingestion of rotting vegetation around haystacks, silos, and feed bunks.^33,34 Plant poisonings are common in livestock, and identification of neurotoxic plants is important whenever multiple animals are affected simultaneously.^34-36 (Table 8-3). Clinical signs of plant poisonings are variable and may include ataxia, hypermetria, head tremors, convulsions, paralysis, coma, or sudden death. Nonplant neurointoxicants of livestock include lead, ethylene glycol, organic mercurials, chlorinated hydrocarbons, organophosphates, salt, sulfur, petroleum distillates, and many others. Dose of the neurointoxicant may be important, with different clinical signs appearing depending on the level of exposure. Ingestion of high concentrations of organophosphates or carbamates inhibits cholinesterase and produces signs of parasympathetic and neuromuscular activation, including marked ataxia, coma, muscle tremors, salivation, and miotic pupils. When low doses of organophosphates are ingested chronically, however, the result is an axonopathy of spinal cord and medullary neurons. The clinical signs that result are predominantly those of hindlimb paresis and ataxia, which may progress to tetraparesis and recumbency.³⁷ Ingestion of petroleum distillates (motor oil, gasoline, kerosene) by cattle can induce narcosis. Some petroleum distillates also may contain toxic concentrations of lead. Other sources of lead include paints, batteries, waste dumps, and smelters. Therapeutic and dietary interventions also may result in toxicoses when improperly administered. Overtreatment of cattle with propylene glycol produces profound ataxia, depression, and coma. Ingestion of ammonia or ammoniated feedstuff produces hyperesthesia, excitability, coma, and convulsions. High concentrations of salt in drinking water or, more commonly, lack of fresh water or interruption of the water supply followed by unlimited access to water, can result in laminar necrosis of the cerebral cortex or eosinophilic meningitis.³⁷ The clinical signs are those of cerebral dysfunction, including blindness, dullness, seizures, coma, and death. Although this syndrome has been reported in cattle and sheep,^38-40 pigs seem to be particularly susceptible.

Table 8-3 Poisonous Plants Producing Neurologic Signs (Also See Chapter 54)

Geographic area also may be important in the differential diagnosis of neurologic disease. Certain infectious diseases may be more common in particular areas of the country or even regions within a single state where the conditions for disease vectors are optimal.⁴¹ The travel history of the animal must be considered, as well as the animal’s location at the time clinical signs appeared. Travel also may result in increased contact with other animals and greater risk of exposure to infectious diseases. Recent movement of animals onto the premises may be important with respect to the likelihood of infectious diseases such as equine herpesvirus 1 and equine infectious anemia.

Vaccination and Disease History

When a neurologic problem is evaluated, the vaccination history and previous herd or individual disease problems should be noted. Some vaccines are highly protective, whereas others are less so. Examples of effective vaccines include those for focal symmetric encephalomalacia (enterotoxemia caused by Clostridium perfringens type D), rabies, and tetanus. Neurologic disease may be a secondary complication of disease in another organ system. Foals and calves with severe diarrhea, for example, may convulse secondary to hypokalemia, hypernatremia, or hypoglycemia. Preexisting diseases or clinical syndromes should be determined. For example, outbreaks of the CNS form of equine herpesvirus I are often preceded by respiratory disease or abortions in herdmates. Thromboembolic meningoencephalitis of cattle often follows an outbreak of respiratory disease within the herd. Historical evidence of limited colostral intake may be important in the diagnosis of bacterial meningitis of neonates. Bloody diarrhea often precedes the onset of nervous coccidiosis of calves.

Gestational Stage

Hypomagnesemia, eclampsia (hypocalcemia), hypokalemia syndrome, hypophosphatemia (postparturient hemoglobinuria) and nervous ketosis are common causes of recumbency, convulsions, and tremors in adult livestock. These diseases usually occur between the end of the last trimester and the first 2 months after parturition.

General Comments

A thorough physical examination should always precede or be performed concurrently with the neurologic examination. Physical examination may reveal evidence of systemic disease that underlies the neurologic problem—for example, icterus in animals with liver disease resulting in hepatic encephalopathy, unthriftiness in animals on poor diets, or traumatic injuries. In some instances disease of organ systems other than the nervous system may take precedence for diagnosis and treatment. Such may be the case with animals in shock or suffering from other life-threatening cardiovascular or respiratory disturbances. A common practice is to perform a general physical examination followed by a neurologic examination, but many aspects of nervous system function, such as assessment of mental status and cranial nerve examination, may be carried out during the physical examination.

The neurologic examination should be carried out in a systematic fashion. The exact order of the examination is not important in itself, but procedures that may cause discomfort or pain, such as palpation of the spine, should be left until last. A common system used by many neurologists is to start at the head and progress to the tail.⁴² This system is very useful in small animals but may be less so in large animals. Some clinicians prefer to examine the animal standing in the stall initially, then observe the gait. Because large animals are less amenable to handling than the typical cat or dog, another system for the neurologic examination is to begin with procedures that require minimal handling of the animal, such as observation of mental status, posture, and gait, and proceed to those that require greater manipulation: examination of the cranial nerves, assessment of spinal reflexes, and so on. The latter is the system that is described in the following sections. Each individual should develop a system that is effective for him or her, bearing in mind that one goal of the neurologic examination is to induce as little stress in the animal as possible because stress may alter the results of the examination.

Neurologic examination alone rarely leads to definitive diagnosis, but rather helps to answer the questions “Does the animal have neurologic disease?”and “What is the location of the neurologic lesion?” Once these questions are answered, a list of differential diagnoses can be made in light of other information such as the signalment of the animal and the history of the current problem. The diagnostic plan is based on the location of the lesion and the most likely differential diagnoses.

Mentation and Behavior

Initial examination should be done from a distance. The examiner observes the animal’s mental state and whether its responses to its surroundings are appropriate. This is done ideally in the animal’s usual environment, where it would be expected to be most calm. When this is not possible, the influence of factors such as the stress and excitement of previous travel and the animal’s natural fear of unfamiliar surroundings, sounds, and smells must be taken into account. The reports from the animal’s usual handler may be informative, if he or she is a good observer and has an understanding of normal behavior in animals. Compare the patient’s interaction with its environment to a summary of its previous behavior and to the activities of the herdmates. Normal animals respond to mild stimulation. Most normal animals actively seek food when offered but vigorously avoid needle pricks. All livestock should recognize and fear strangers and should show awareness of the examiner’s position. Normal animals change the posture of the head, ears, and eyes as the examiner moves. Depending on previous conditioning, normal behavior may include cautionary moves, avoidance, belligerence, or affection. Animals with decreased mental awareness (obtunded, dull, depressed) have reduced responses that may include lassitude, lack of recognition, unwillingness to rise or lift the head from the ground, head pressing, propulsive walking, lack of appetite, drooped ears, convulsions, stupor, or coma (Fig. 8-1). Systemic illness also may cause dull mentation; thorough physical examination and, perhaps, diagnostic tests including a complete blood count and serum chemistry are important in determining whether systemic disease is present. Furthermore, animals with primary CNS disease tend to have more profound dullness than do those with systemic disease alone. Hyperexcitability, rage, mania, or frantic motor activities are suggestive of a lesion of the limbic system, an assembly of connected groups of neurons (nuclei) and neuronal tracts in the cerebrum, thalamus, hypothalamus, and midbrain that is involved in emotional responses and patterns of behavior. Such animals may strike or kick at inappropriate times, demolish their stalls, bellow, show belligerence, or, if recumbent, struggle violently. The age, species, previous management system, and even the breed of animal are important considerations in the assessment of behavior. Bulls and stallions exhibit behavior that is very different from that of steers and geldings. Beef cattle behave differently than dairy cattle do. Animals that are handled regularly show fewer and milder fearful or aggressive responses than do animals that are handled rarely.

Fig. 8-1 Dull mentation in a horse with cerebral toxicosis caused by sage toxicity (Salvia species).

Changes in mental status are consequences of disease affecting either the cerebrum or the ascending reticular activating system (ARAS). The cerebral cortex is the “seat of consciousness”: conscious perception of both external stimuli (e.g., vision, hearing, touch) and internal stimuli (e.g., abdominal pain) depends on the integrity of the cerebral cortex. Both primary intracranial diseases (e.g., encephalitis, traumatic injury) and extracranial diseases (e.g., metabolic derangements, toxicities) can alter the functions of the cerebral cortex.

The ARAS is composed of a number of neuronal pathways that lie centrally within the brainstem (medulla oblongata, midbrain, and thalamus). The ARAS receives collateral input from all sensory information reaching the brain, which it conveys ultimately to the cerebral cortex, where it reaches the level of consciousness. The ARAS is important in maintaining the animal’s level of consciousness and arousal. The relationship between the cerebral cortex and the ARAS is sometimes described as follows: the cerebral cortex determines the content of consciousness, and the ARAS determines the level of consciousness. Diseases affecting the ARAS tend to produce more profound depression of consciousness, such as coma, than do those affecting the cerebral cortex alone, although this is not an absolute rule. Lesions of the ARAS occur commonly within the midbrain segment of this system, so that other signs of midbrain disease, such as pupillary dilation and loss of the oculocephalic reflexes (see below), often are observed in animals with lesions of the ARAS.

A seizure (convulsion, ictus) is a manifestation of cerebral cortex dysfunction characterized by loss of consciousness or involuntary motor activities. Seizures may be generalized or focal (partial). Generalized seizures are characterized by loss of consciousness and variable degrees of involuntary motor activity, which may include flailing of the limbs, elimination of feces and urine, and nystagmus. Localized involuntary movements with or without obvious alterations of consciousness characterize focal seizures. Alternatively, focal seizures may result in episodes of abnormal or bizarre behavior or momentary lapses of consciousness without collapse or significant motor activity. A third form of seizure is focal with secondary generalization. The onset of the seizure is focal, but seizure activity subsequently spreads throughout the cerebral cortex, resulting in a generalized seizure. Animals with this form of seizure activity exhibit initial focal signs, such as head turning, bellowing, focal tremors, and so on, followed by loss of consciousness and generalized signs of involuntary motor activity, as described previously. In most animals with focal seizures, with or without secondary generalization, the outward manifestation of the seizure is always the same. Rarely, seizures may be preceded by an aura, a period in which the animal exhibits anxiety or restless behavior shortly before the onset of the seizure itself. In most cases of seizures in animals, however, an aura is not observed. A postictal phase, a period of time subsequent to the seizure during which the animal exhibits abnormal behavior such as lethargy, restlessness, or anxiety, is usual after seizures in most animals. The postictal phase usually lasts a few minutes to hours but may last as long as several days. The postictal phase may be the only stage of the seizure observed by the animal’s handler. Thus, any animal with a history of episodes of abnormal behavior should be suspected of having seizures. The typical history is that the animal is found in a dull or excited state, without the handler observing the onset of this change of behavior. Additional supporting evidence includes physical injuries such as scrapes and cuts that may have been incurred during the seizure itself.

Abnormalities of cerebral cortex dysfunction are the ultimate cause of seizure activity. During a seizure, groups of neurons in the cerebral cortex exhibit spontaneous electrical activity resulting in the clinical manifestations of focal or generalized seizures. Whereas neurons in the cerebral cortex ultimately become involved, abnormal electrical activity can begin elsewhere in the brain, such as in the brainstem, with subsequent spread of this activity to the cerebrum. Causes of seizures are legion, including alterations in the neuronal environment resulting from metabolic disturbances or toxicities, and the effects of structural brain diseases such as congenital or developmental disorders, traumatic injuries, neoplasia, and inflammatory conditions. Diagnosis of seizures and other states of altered mentation must include a thorough physical examination and screening for metabolic diseases such as electrolyte imbalances and hepatic or renal failure.

Abnormalities in the neurologic examination found between seizures (interictal period) support a diagnosis of primary brain disease and are an indication for diagnostic procedures such as cerebrospinal fluid (CSF) tap. Some toxins cause systemic signs as well as seizures, such as neuromuscular involvement (tremors, weakness) or parenchymal organ failure (icterus, uremia). Such signs, combined with a good clinical history and complete examination of the animal’s environment, will help to direct specific toxicologic screening tests.

Narcolepsy is a condition wherein the normal mechanisms of sleep are disturbed. Although sudden onset of rapid eye movement (REM) sleep is one manifestation of narcolepsy, the acute onset of cataplexy—complete paralysis of striated muscles—usually is a more prominent clinical feature. Animals may be observed to suddenly collapse to the ground or to buckle at the knees. Cardiac and respiratory muscles are not affected. Narcoleptic attacks may be difficult to distinguish from seizures but are not accompanied by the involuntary motor activity that characterizes most generalized seizures. In some cases owners observe traumatic injuries to the head, face, and limbs without observing the cataplectic attacks that cause the trauma. Narcolepsy has been reported both in cattle and horses.^43-46

Gait

Gait should be evaluated by moving the animal in a straight line, moving it in a tight circle, backing up, and moving it over obstacles such as a curb. Having the patient walk up and down a slope with varying steepness and with the head elevated may reveal more subtle abnormalities. The examination may need to be modified depending on the species of the patient, amenability to handling, and consideration of safety concerns. In general, horses are more tolerant of handling than are ruminants.

Quadrupeds begin walking by protracting the rear limb, followed by the forelimb of the same side, then the opposite rear limb, and finally the opposite forelimb. Gait on a level surface requires integrity of the musculature, motor and sensory components of the peripheral nerves, local spinal reflexes, ascending and descending pathways in the spinal cord, and centers within the brainstem. Dysfunction of any of these areas results in an animal with mild to severe proprioceptive disturbances when standing or walking, which are exacerbated by turning the animal in a circle or stepping it on and off a curb. Animals with cerebral disease usually are able to perform simple motor activities such as walking along a straight path without obvious deficits but exhibit decreased proprioception when they are required to perform complex motor activities, such as walking on slopes or negotiating obstacles such as curbs or ground poles. Performance of such complex maneuvers requires coordination of proprioception and motor activities within the cerebral cortex, basal nuclei, and other CNS centers. Subtle deficits may be elicited by walking and then trotting the patient, or walking or trotting the patient briskly and then stopping suddenly. While a helper is walking the animal in a straight line on a level surface, the examiner should take hold of the tail and pull the animal sharply to one side. The normal animal will move toward the pull but should not stumble or fall. If the tension on the tail is maintained, strength can be assessed. Animals with lesions anywhere within the ascending or descending pathways controlling gait may show decreased proprioception in the form of stumbling, tripping, or crossing the limbs or may be weak. This maneuver also is useful for assessing the symmetry of a lesion. Circling the patient in a wide circle and then a tight circle also may elicit deficits, such as knuckling, stumbling, interference between feet, pivoting on one foot, or wide movements in the outside limb, that are not observed when the animal is walked in a straight line. Assessment of gait is facilitated when animals are halter-broken and can be lead. This is not the case in many ruminants, so the clinician must rely more on observing the animal in its usual environment or in a confined area such as a pen. A handler may drive animals that are not halter-broken, but this should be done with caution; safety of the animal and handler must be the top priority.

A grading system for gait deficits has been described elsewhere,⁴⁷ as follows:

Proprioception is the sense of position in space. Receptors lie in the skin, joints, and muscles. Ascending pathways run mainly in the dorsal funiculus of the spinal cord, relaying information to centers in the brainstem and cerebral cortex. Descending pathways involved in proprioception are largely similar to those that control gait. The vestibular system and pathways in the spinal cord to and from the vestibular centers in the medulla oblongata and cerebellum also help to control proprioception. Abnormalities of proprioception include knuckling, stumbling, adduction or abduction of the limbs, circumduction, and interference between limbs (Fig. 8-2). Animals with proprioceptive deficits often slap down the feet hard, rather like the gait of a person walking down stairs in the dark, unsure of where the next step is. Walking the animal off a curb or step exaggerates this appearance. When spun in a tight circle, normal animals lift the inside forefoot as the weight shifts. The outside rear leg is put down within a line demarcated by the lateral margin of the trunk. When spun in a tight circle, patients with abnormal proprioception may pivot on the inner forefoot rather than lifting it and replacing it into a normal position. The outside foot may circumduct widely, knuckle, or buckle, and the inside foot may step on the outside foot. Animals with abnormal proprioception worsen when they are required to climb hills or lift the foot over a curb or are walked with the head elevated. The gait of noncompliant cattle may be assessed by observation of maneuvers through corrals, alleys, or a squeeze chute.

Fig. 8-2 Examples of conscious proprioceptive deficits in a horse. The signs of proprioceptive deficits in ruminants are similar.

Having the animal walk backward tests strength and proprioceptive function further. The normal subject should be able to do so in a smooth, coordinated fashion. Animals with lesions of either the ascending or descending motor pathways may exhibit abnormalities such as foot dragging and weakness, sometimes to the point of “dog-sitting.” Otherwise cooperative animals may be reluctant to move straight backward and will try avoidance maneuvers such as circling to one side or the other in order to avoid it. Such tactics should raise the index of suspicion of a neurologic deficit. Care should be taken when backing an animal with severe neurologic deficits because some animals could fall backward during the procedure. Animals that are uncooperative or that have been little handled may exhibit reluctance to walk backward that is not caused by neurologic disease. Observing the patient’s general level of cooperation and having a good history will help the examiner determine whether the problem is caused by neurologic disease or is the result of the animal’s lack of compliance.

Cerebellar disease causes generalized ataxia with a rolling, drunken gait. Protraction of the limbs is delayed and limb movements are exaggerated, a condition known as hypermetria. This is often accompanied by opisthotonos, which is a hyperextension of the head and neck, and intention tremor, most easily observed in the head. Purposeful movements, such as reaching out to take food, exaggerate intention tremor, and muscular relaxation, as in a recumbent animal, eliminates it.

Spontaneous circling is seen in diseases of the vestibular system, midbrain, and cerebrum. Circling varies from a mild tendency to circle in one direction to tight and compulsive circling, seen particularly with midbrain disease. Circling occurs toward the side of the lesion, except in paradoxic vestibular disease (caused by lesions in the vestibular components of the cerebellum), in which the animal circles away from the side of the lesion. Localization of the neurologic lesion in animals that circle is made on the basis of other neurologic abnormalities, such as the state of consciousness, the presence of proprioceptive deficits, and the presence of signs such as head tilt, spontaneous nystagmus, seizures, or abnormal ocular function.

Conscious Proprioception and Postural Reactions

The integrity of conscious proprioceptive pathways may be tested by means of the postural reactions. Normal animals stand at rest with the limbs in line with the abaxial boundaries of the trunk. When the limbs are moved, normal animals do not permit the limbs to be placed outside of the body axis or across midline. After placement of the limbs in an abnormal position, the neurologically intact animal returns to a normal stance within a few seconds. Animals with conscious proprioceptive deficits allow the limb to remain in the abnormal position for longer than the usual period of time. This can vary from animals in which replacement of the limb into a normal position is slightly slowed to animals that do not try to replace the limb at all. The examiner should cross one of the animal’s limbs over the opposite limb, or abduct one limb; the normal response is for the limb to be placed back into the resting position. Normal animals often strongly resist attempts to place the limbs in abnormal positions. Animals with proprioceptive deficits may spontaneously place the limbs in abnormal positions: excessively adducted, abducted, or even crossed. Abnormalities of proprioception alone are poorly localizing signs, although a couple of generalities may be stated. Unilateral lesions rostral to the medulla oblongata produce mild to moderate proprioceptive and postural deficits in the contralateral limbs. Unilateral lesions in the medulla oblongata or spinal cord produce more severe proprioceptive and postural deficits in the ipsilateral limbs. Lesions of the cerebellum very rarely result in postural deficits.

Additional postural reactions, such as hopping and hemiwalking, can be tested in small ruminants, calves, and some foals. Hopping is tested in the forelimbs by lifting the rear limbs a few inches off the ground by means of a hand and arm placed around the abdomen, flexing one forelimb slightly, and moving the animal away from the side of the flexed forelimb, so that it has to hop laterally on the forelimb still in contact with the ground. It is easiest if the examiner stands in one place and turns clockwise when testing the animal’s right forelimb and counterclockwise when testing the left forelimb. Hopping in the rear limbs can be tested similarly, supporting both forelimbs off the ground with an arm around the chest. Hemiwalking is done by supporting both limbs on one side of the body in a slightly flexed position and pushing the animal toward the opposite side so that it must walk laterally on the two limbs still in contact with the ground. Both hopping and hemiwalking should be done with care not to push the patient over. Hopping and hemiwalking involve the same ascending and descending motor tracts involved in gait on a level surface but also require integrity of the cerebral cortex. These maneuvers are abnormal on the ipsilateral side in animals with lesions in the skeletal muscles, peripheral nerves, spinal cord, and medulla oblongata and on the contralateral side in animals with lesions in the midbrain, thalamus, or cerebrum. Animals with cerebral lesions have normal gait on a level surface, but marked deficits in hemiwalking and hopping.

Abnormalities of Posture and the Righting Response

Posture refers to the position of the body and head in space, in relationship to gravity and to each other. Animals adopt slightly different postures when on a sloped surface or an uneven surface compared with posture on a level surface. However, sustained postures such as head tilt (Fig. 8-3), in which one ear is closer to the ground than the other, and head turn (Fig. 8-4), in which the muzzle is turned back toward the trunk, are abnormal. Circling often accompanies head tilt and head turn, and all tend to be toward the direction of the lesion. The exception to this rule occurs in paradoxic vestibular syndrome as a result of involvement of the cerebellar components of the vestibular system, in which head tilt and circling occur in the direction away from the side of the lesion. When proprioceptive deficits accompany circling they are ipsilateral when the lesion is in the medulla oblongata and contralateral when the lesion lies in the cerebrum, thalamus, or midbrain. Head tilt, head turn, and circling reflect the presence of lesions that are unilateral within the neuraxis or are asymmetric.

Fig. 8-3 Head tilt caused by vestibular dysfunction in a horse that sustained head trauma.

Fig. 8-4 Head turn in a steer with polioencephalomalacia.

The righting response is most easily tested in small ruminants and in recumbent large animals (Fig. 8-5). The response is initiated by receptors in the eyes and vestibular labyrinths and by proprioceptive receptors in the joints, tendons, and muscles. Information regarding limb position and balance is relayed ultimately to the cerebral cortex. Descending impulses are initiated in the motor cortex and relayed via the brainstem and spinal cord to the appendicular musculature. The normal response to stimulation is to lift the head, assume sternal recumbency, and rise. The normal horse rises on the forelimbs first, whereas the normal ruminant rises on the rear limbs first. Animals that are reluctant to rise but do so normally after sufficient stimulation may have a disease of the cerebral cortex or the thalamus. Animals that are in lateral recumbency and unable to lift the head from the ground may have lesions in the peripheral or brainstem vestibular centers or in the cervical spinal cord proximal to the C4 spinal cord segment. Unilateral lesions in this area result in an inability to lift the head from the ground when the lesion side is up. When the lesion side is down, the animal can raise the head slightly. Animals with incomplete lesions of the cervicothoracic spinal cord (C7 to T1 spinal cord segments) are able to lift the head and neck but may remain recumbent. Animals with lesions of the thoracolumbar and lumbosacral spinal cord (T3 to S3 spinal cord segments) usually can lift the head and neck, arise on the forelimbs, and assume a dog-sitting position when stimulated.

Fig. 8-5 A, Afferent pathways responsible for providing proprioceptive information to the brainstem and higher centers. B, Efferent pathways responsible for providing motor activities to the motor neurons.

Spinal Reflexes

The spinal reflexes are stereotyped responses to specific stimuli. They include the myotactic or tendon reflexes, the panniculus or cutaneous trunci reflex, the perineal reflex, and several others. As their name implies, spinal reflexes depend on the integrity of local spinal cord segments, as well as the peripheral nerves, neuromuscular junctions, and muscles. Lesions in the spinal cord that are located rostral to the spinal origin of the peripheral nerves to the limbs being tested result in normal to increased spinal reflexes and are commonly referred to as upper motor neuron lesions. Lesions in the spinal cord segments at the level of the reflex arc or in the peripheral nerves, neuromuscular junctions, or muscles result in decreased spinal reflexes and are commonly referred to as lower motor neuron lesions.

It is appropriate at this point to define the terms upper motor neuron and lower motor neuron. Upper motor neurons are nerve cells whose cell bodies lie within the brain and whose axons terminate at synapses within the brain or in the spinal cord. Disease affecting upper motor neurons results in normal to increased spinal reflexes, as well as ataxia, variable severity of weakness, and sometimes increased muscle tone (spasticity). The nerve cell bodies of lower motor neurons lie in the nuclei of cranial nerves in the brainstem or within the ventral horn gray matter of the spinal cord. Their axons project beyond the CNS, course within the peripheral or cranial nerves, and terminate at neuromuscular junctions. Diseases affecting lower motor neurons result in decreased spinal reflexes, ataxia, moderate to severe weakness, decreased muscle tone, and rapid, pronounced atrophy of the denervated muscles.

Myotactic Reflexes

Myotactic or tendon reflexes are tested by sharply striking the tendon of a specific muscle (or sometimes the muscle itself) and evaluating the strength of the reflex contraction. The ascending component of the reflex arc involves the muscle spindles, which are stretch detectors, sensory fibers in the peripheral nerve, the dorsal nerve root and its ganglion, and the central projection of the sensory nerve fiber onto the ventral horn cell in the same spinal cord segment (Fig. 8-6). The descending component of the reflex arc involves the ventral horn cell (lower motor neuron), the ventral nerve root, the motor fibers in the peripheral nerve, the neuromuscular junction, and the myofibers in the muscle being tested. Lesions in either the ascending or descending components of the reflex arc result in a decreased to absent myotactic reflex. Lesions in the spinal cord above the level of the reflex arc and lesions of the brain result in a normal to increased myotactic reflex.

Fig. 8-6 Pathways governing patellar tendon reflex.

The myotactic reflexes can be tested only in the recumbent animal and thus are able to be examined only in a limited number of large animal patients. These reflexes should be tested only in the limbs that are uppermost when the animal is lying on one side. The animal must be turned over to test the limbs on the opposite side. These reflex responses are more subtle than in small animals and may not be elicited in some normal patients. The reflex responses are assigned a qualitative clinical score. One common classification is as follows:

Clonus is a phenomenon observed with severe upper motor neuron lesions: the response of the muscle being tested is rapid, repeated contractions rather than a single contraction. The innervation of the limbs is listed in Tables 8-4 and 8-5.

Table 8-4 Innervation of the Forelimbs of Large Animals

* Contributes innervation in the ruminant only.

† Contributes innervation in the horse only.

Table 8-5 Innervation of the Hindlimbs of Large Animals

* Contributes innervation in the horse only.

† Contributes innervation in the ruminant only.

Flexor Reflexes

The flexor reflexes are elicited in the recumbent large animal. A painful stimulus is applied to the uppermost foot. The normal reflex consists of two phases: (1) a rapid limb flexion, and (2) a slower conscious perception of the stimulus, characterized by attempts to assume sternal recumbency, vocalization, ear and eye movements, violent kicking, and so on. The forelimb flexor reflex tests the integrity of the axillary, median, and musculocutaneous nerves and spinal cord segments C5 through T2, as well as the flexor muscles of the limb. The hindlimb flexor reflex is mediated by means of the sciatic, peroneal, and tibial nerves and the hindlimb flexor muscles.

Spinal cord and peripheral nerve lesions may be localized further by testing the integrity of the sensory innervation of the skin of the limbs. Areas of decreased or absent cutaneous sensation reflect lesions of the peripheral nerves innervating those regions of the skin or of the spinal cord segments in which those sensory nerves terminate. The skin over the trunk and much of the limbs is innervated by more than one peripheral nerve. Some areas of the limbs derive sensory innervation from a single peripheral nerve. These areas are termed the autonomous zones for those peripheral nerves. Damage to a peripheral nerve innervating the skin of a limb therefore will result in decreased to absent cutaneous sensation in the autonomous zone for that nerve. This information can be used to localize lesions. Decrease or loss of sensation to an entire limb or to limbs on both sides of the body suggest a lesion affecting several local spinal cord segments, or a transverse spinal cord lesion rostral to the affected limbs.

Other Spinal Reflexes

Muscle Mass and Tone

Normal mass and tone of the musculature depends on an intact nerve supply. Primary diseases of muscle and loss of use of a limb secondary to orthopedic disease are often associated with mild to moderate muscle atrophy that develops over weeks to months. Atrophy caused by denervation, however, is more severe and rapid in onset. Visible loss of mass of specific muscles or groups of muscles is most likely caused by damage to the nerve supply to those muscles, either by direct injury to peripheral nerves or injury to the origins of those nerves in the ventral horn gray matter of the spinal cord (Fig. 8-7). Knowledge of the central origins of the nerves to the limbs and the course of those nerves in the periphery can be used to specifically localize neurologic lesions (see Tables 8-4 and 8-5). Electromyography and nerve conduction testing can further be used to help identify muscle denervation and peripheral neuropathies (see Chapter 35). Regeneration of peripheral nerves after an acute insult can occur. Regeneration is accomplished by outgrowths of axonal buds from the proximal stump. The buds either grow along previous peripheral nerve rootlets or generate new neural pathways in concert with proliferation of myelin precursor cells. The rate of growth of the axonal buds has been estimated to be approximately 1 to 4 mm/day.⁵¹

Fig. 8-7 Muscle atrophy in the gluteal muscles in a horse with equine protozoal myeloencephalitis.

Muscle tone can be evaluated in the recumbent animal by passively flexing the limbs. Evaluation is not accurate in the standing animal or in animals supported in slings because of resistance from taut bands of connective tissue. In normal animals repeated flexion is accompanied by an increase in the tone in the flexed limb. The limbs of animals with a lower motor neuron deficit remain flaccid. Small ruminants tend to show a greater relative amount of extensor tone in the limbs than do cattle or horses. Evaluation of the test must be conservative because some severely obtunded large animals display generalized hypotonia, even though the lower motor neurons are functional. The cause of the hypotonia is unknown.

The tone of the forelimbs is controlled through spinal cord segments C6 to T1 and the radial, musculocutaneous, median, ulnar, axillary, and long thoracic nerves. The motor tone of the rear limbs is controlled through spinal cord segments L3 to S2 and the femoral, cranial and caudal gluteal, and sciatic nerves. The lower motor neurons to the anus originate in spinal cord segments S1 to S5, via the pudendal nerve. The tail is innervated by the coccygeal segmental spinal nerves.

Examination of Cranial Nerves

Examination of the cranial nerves is most easily carried out by examining the functions of groups of nerves that innervate particular regions of the head rather than performing the examination in a strictly numeric order. For example, examination of vision and other ocular functions such as the menace response, pupillary light reflexes, and physiologic nystagmus reveals the integrity of several cranial nerves, not only II, III, IV, and VI, but also V (sensory to the cornea), VII (motor to the eyelids), and VIII (providing vestibular input to control the functions of III, IV, and VI), as well as centers within the brain.

CRANIAL NERVE II—OPTIC NERVE

Vision is the function of cranial nerve II, the optic nerve. Observing the animal’s response to its environment provides a good initial assessment. Does it respond to visual cues, such as movement, or does it walk into objects? Noise may cause the animal to turn its head toward the sound, so the observer must be careful to distinguish such responses from those made in response to visual cues. A maze can be set up using straw bales or other objects, and the animal gently driven through the maze. Normal animals will avoid colliding with objects. Animals that are severely obtunded, however, may walk into objects even when they can see. Thorough evaluation of the complete neurologic examination is necessary to distinguish this from true blindness.

The menace response measures the integrity of the entire visual pathway. The ascending pathway runs from the retina via the optic nerves, midbrain, and internal capsule to the visual areas in the occipital lobe of the cerebrum. Information from the visual cortex is processed and relayed to the motor cortex. The descending pathway of the menace response runs from the motor cortex via the pons to the nucleus of the facial nerve in the medulla oblongata and thence via the facial nerve to the orbicularis oculi muscle. Input to this motor pathway also arises from the cerebellum. The menace test is performed by rapidly advancing the hand toward the eye and observing a reflex closure of the eyelids. In addition to the closure of the eyelids, some animals display a generalized avoidance response characterized by coordinated movement of the head and neck away from the stimulus. The opposite eye may be covered to ensure that only one eye is being stimulated. Care must be taken not to touch the face or eyelashes. Many authors warn that air currents generated by rapid movement of the hand toward the face can elicit the response even in blind animals, but this has not been our experience. The menacing gesture is directed first at the nasal and then at the temporal parts of the visual field. Blindness in one visual field is termed hemianopsia. The menace response measures the integrity of the retina, optic nerve, optic chiasm, midbrain, internal capsule, and occipital cortex. There is approximately 90% crossing over of optic nerve fibers in the optic chiasm of livestock. Animals with a postchiasmal lesion in the internal capsule, midbrain, or occipital lobe will show hemianopsia in the contralateral visual field. In practical terms, lesions central to the optic chiasm cause loss of vision in the opposite eye, with apparently normal vision in the ipsilateral eye.

Menace deficit may be the result of facial nerve paralysis. In such cases the animal does not blink but shows avoidance of the stimulus by pulling the head away. Facial nerve deficits will be apparent in these animals by their inability to close the eyelids under any circumstances and by other signs such as facial drooping on the same side. Animals with cerebellar disease also may display a menace deficit, yet possess normal vision. The precise pathway by which the cerebellum influences the menace reflex is not known, but interruption of this pathway is thought to disrupt upper motor neuron control of the facial nerve, which becomes dysfunctional. Menace deficits resulting from facial nerve or cerebellar disease may be differentiated from deficits in other areas by maze testing. Animals with cerebellar or facial nerve disease retain visual acuity and maneuver through the course successfully. The maze test measures the patient’s ability to identify and avoid obstacles. In addition to the optic pathways, the test measures the integrative pathways in the frontal and parietal lobes of the brain, the motor neurons, and the proprioceptive pathways (Table 8-6). Myasthenic diseases (e.g., botulism, hypocalcemia, or hypomagnesemia) result in bilaterally decreased menace and palpebral responses but do not produce blindness.

Table 8-6 Guide to Neuroophthalmologic Lesion Location

The pupillary light reflex measures the integrity of the retina, optic nerves, optic chiasm, pretectal and oculomotor nuclei in the midbrain, oculomotor nerve, ciliary ganglia, and constrictor pupillae muscle. The test is performed by shining a bright light into each eye and observing constriction of the pupil in the ipsilateral eye (direct response) and the contralateral eye (indirect response). Reducing the ambient light level may facilitate this test by causing the pupils to dilate. The reflex in large animals is considerably slower than observed in cats and dogs. A “swinging light” test has been recommended in large animals to reduce the blink and startle responses elicited by suddenly shining a bright light into the eyes.⁴⁷ A strong light source is slowly shone from one eye to the other while bringing it closer and closer to the head and observing the responses in each pupil. The effects on the pupillary light reflex of lesions at various levels along the visual pathway are shown in Table 8-6.

Unilateral lesions of the cerebral cortex result in blindness of the opposite eye. The pupillary light reflexes usually are normal. If the cortical disease is accompanied by increased intracranial pressure, the oculomotor nerve or nucleus may become dysfunctional because of midbrain compression, resulting in ipsilateral mydriasis.

CRANIAL NERVE VII—FACIAL NERVE

The motor nucleus of cranial nerve VII originates in the middle and ventral part of the medulla oblongata. The motor fibers are distributed to muscles of facial expression. Just as the motor fibers are exiting from the lateral aspect of the brainstem they merge with axons from the parasympathetic facial nucleus. These fibers innervate the lacrimal and salivary glands. They separate from the motor component of the facial nerve as it traverses the petrous temporal bone. Lesions of CN VII located between the brainstem and the petrous temporal bone usually result in “dry eye.” More distal lesions, however, have no effect on tear production. The tone of the facial musculature is examined by palpation of the ears, lips, eyelids, and muzzle. Clinical signs of facial nerve dysfunction include drooped ear and lips, drooling saliva, and retention of food in the cheek pouch on the denervated side (Fig. 8-8). Closure of the eyelids is weak in partial facial nerve lesions and absent in severe lesions. Despite this, there is slight drooping of the upper eyelid (ptosis) because of paralysis of the frontalis muscle, which contributes to eyelid retraction. In species with a soft muzzle (e.g., horses, sheep, and goats), there is a marked deviation of the filtrum away from the side with the lesion after unilateral loss of facial nerve function. The filtrum of affected cattle is not deviated because of the large amount of fibrous tissue in the planum nasale. In chronic facial paralysis the face may be deviated toward the affected side because of atrophy and contracture of the denervated musculature of the face.

Fig. 8-8 Acute right facial paralysis in a horse with guttural pouch mycosis. Note the drooped right ear and deviation of the muzzle toward the left side.

OTHER ASPECTS OF PHYSICAL EXAMINATION OF THE PATIENT WITH NEUROLOGIC DISEASE

Diagnosis of a neurologic disease can often be facilitated by the observation of physical abnormalities in other systems. When one examines animals with chronic ataxia or tetraparesis, the head, neck, and back should be gently manipulated while the spine is palpated for crepitation or swelling. This finding could indicate the presence of a fracture, malformation, or luxation of one or more cervical vertebrae or vertebral osteomyelitis. Do not manipulate the neck whenever there is evidence of acute cervical vertebral trauma. Swelling, bruising, or hair loss on the skin around the head or bleeding from the ears or nose could signify cranial trauma. Hair loss and dermatitis around the perineum and medial thigh may indicate urinary incontinence. In neonates a hairless patch over the dorsum of the spine could indicate a meningomyelocele. Displacement of the sacrum could indicate sacroiliac luxation. Crepitation over coxofemoral or stifle joints of recumbent cattle could indicate a luxation or fracture. If luxation of the coxofemoral joint is suspected, the animal should be rolled on its back, and the length of the two pelvic limbs should be compared while the legs are held in extension. A pelvic examination should be performed in all large animals to detect displacement of the hip joint into the obturator foramen or fractures through the shaft of the ilium. All joints should be passively manipulated to detect dislocations or fractures. The heart should be auscultated for murmurs that could suggest left-sided endocarditis because such lesions can shower bacteria into the meninges. Odors on the breath such as ammonia, ketones, or petroleum distillates could provide clues about possible toxic causes. Identification of concurrent bronchopneumonia may indicate the possibility of thromboembolic meningoencephalitis in cattle or herpesvirus myelitis in horses. The ocular fundus should be examined ophthalmoscopically to detect retinal hemorrhages (trauma), papilledema (increased intracranial pressure), or vasculitis.

Examination of the Neonate

Most of the physical diagnostic techniques described in the preceding paragraph for the adult may be applied in examination of the neonate. Most spinal reflexes of livestock are well developed after birth. In the normal foal under 3 weeks of age, the limbs are hypertonic and hyperreflexic, with occasional myoclonus occurring after percussion of the patellar or triceps tendons. This hyperreflexia is most pronounced in the rear limbs. A lack of menace response for up to 2 weeks after delivery also has been observed. Nevertheless, foals are visual and aware of their surroundings almost immediately after birth. When restrained the newborn foal relaxes into a trancelike state, periodically awakening and struggling violently before becoming passive again.

The results of daily examinations of 10 normal calves indicated that the spinal reflexes were present by 24 hours after birth. Most cortical responses were developed by 3 weeks of age. Bottle-reared calves aggressively attempt to suck while being examined, including vigorously butting of the handler with the head. Beef calves attempt to escape restraint and do not attempt to suck. See Chapters 15 and 21 for more details on neonates.

ABNORMAL MENTATION AND BEHAVIOR AND SEIZURES

Decreased mental alertness (dullness, obtundation, stupor, coma) is the most common change of mental status in animals with neurologic disease, although increased responsiveness to external stimuli (anxiety, mania, aggression) sometimes occurs. Altered mentation results from changes in the cerebrum, thalamus, or ARAS. Diseases affecting the ARAS tend to produce severe changes in mentation (stupor, coma), whereas those affecting the cerebrum or thalamus tend to produce a wider range of clinical signs, from slight dullness to coma. In order of worsening severity, decreased mental status in animals can be categorized as follows.

Blindness and Ocular Abnormalities

Blindness may be the result of lesions in the eye, optic nerve, optic chiasm, or central projections of the visual pathways. Ophthalmic examination, including fundic examination, should be part of the routine physical examination. Animals presented with the complaint of blindness should receive a more detailed ophthalmic examination to determine whether primary ocular disease is the cause of the problem (see Chapter 39). Sophisticated diagnostics such as electroretinography (ERG) may be indicated in some animals. When no ocular disease can be found to account for blindness, a lesion in the nervous system is likely to be responsible. Observing the animal’s ability to negotiate its environment, particularly in unfamiliar surroundings, and eliciting the menace reflex are the primary methods of determining visual function. Further testing can be performed by setting up a maze of objects for the animal to negotiate, by using different light levels and assessing vision in bright versus dim light, and by blindfolding each eye in turn when unilateral deficits are suspected. Blindfolding should be used judiciously, because of the stress caused to the patient and the risks of worsening clinical signs in animals that do have visual deficits or other deficits such as vestibular dysfunction. Eighty percent to 90% of optic nerve fibers (axons of retinal ganglion cells) cross to the opposite side of the brain in the optic chiasm of ungulates; thus central representation of vision in these species is predominantly contralateral. Fibers that remain uncrossed originate from the temporal aspect of the retina. Lesions in the visual apparatus distal to the optic chiasm (i.e., lesions of the globe, the retina, or the optic nerve) produce ipsilateral visual deficits. Lesions proximal to the optic chiasm produce lesions in the opposite visual field (contralateral hemianopsia). The following discussion refers to severe or complete lesions, because these are most easily understood and described. Partial lesions will produce similar but milder signs, for example, reduced visual acuity rather than complete blindness. Absent or reduced menace reflex also can be caused by lesions of the facial nerve (cranial nerve VII), the cerebellum, or the cerebrum. Animals with facial nerve lesions can see but cannot blink even when the canthi of the eye are touched. Animals with cerebellar disease can see and can blink in response to the examiner touching the periorbital area. Cerebellar disease causes additional signs such as intention tremor, hypermetria, and ataxia. Animals with moderate to severe cerebral disease usually will blink in response to tactile stimulation of the face and periorbital area but appear to have decreased vision and may have a reduced to absent menace reflex (see earlier). Localization of lesions causing blindness is summarized in Table 8-6.

Pupil size and movement of the globes are mediated via cranial nerves II, III, IV, and VI and the sympathetic innervation of the eye. Clinical signs of diseases affecting these nerves are described earlier in the sections on cranial nerves and Horner’s syndrome.

Circling

Circling can be a manifestation of lateralized disease in several regions of the brain: the cerebrum and thalamus, the midbrain, or the medulla oblongata. Circling associated with cerebral disease is toward the side of the lesion (ipsiversive) and is thought to result from lesions affecting the deep structures of the cerebrum or thalamic components rather than the cerebral cortex. Animals that circle secondary to cerebral disease often have a head turn toward the side of the lesion in addition to the circling. Whereas gait may appear normal on a level surface, affected animals have proprioceptive and postural reaction deficits on the side of the body contralateral to the lesion. Head tilt and spontaneous nystagmus are not present. Physiologic nystagmus (the oculocephalic reflex) is normal when the examiner turns the animal’s head from side to side. The severity of circling seen with lateralized cerebral disease is variable, from a subtle tendency to marked circling.

Diseases affecting solely or predominantly one side of the midbrain also result in circling. The circling is ipsiversive, occurs without manifestations of head tilt or spontaneous nystagmus, and is accompanied by contralateral proprioceptive and postural reaction deficits. Circling in midbrain disease is compulsive, in contrast to that seen in cerebral disease or vestibular disease. In both cerebral and midbrain disease the animal’s level of consciousness usually is decreased, more severely with midbrain than cerebral disease. Midbrain lesions also may cause abnormalities of the oculocephalic and pupillary light reflexes because of the involvement of the somatic and parasympathetic nuclei of the oculomotor nerve (cranial nerve III) and the medial longitudinal fasciculus. The medial longitudinal fasciculus relays sensory information from vestibular centers in the medulla oblongata to the nuclei of cranial nerves III, IV, and VI.

Severe midbrain disease results in decerebrate posture: the animal is unconscious and in opisthotonus (extreme extension of the head and neck) with extensor rigidity of all four limbs. Severe midbrain disease may be the result of traumatic injuries or infectious diseases and particularly is a consequence of increased intracranial pressure from a variety of causes. When intracranial pressure is increased above normal there is a tendency for the occipital lobes of the cerebrum to be herniated caudally, under the tentorium cerebelli. This results in compression of the midbrain and is usually fatal. The presence of decerebrate rigidity warrants a very grave prognosis and the need for immediate and aggressive treatment with agents that decrease intracranial pressure (intravenous mannitol, dimethyl sulfoxide [DMSO], and other diuretics).

Head Tilt and Nystagmus

The presence of a head tilt, wherein one ear is held closer to the ground than the other, indicates disease of the vestibular system. Head tilt usually is accompanied by spontaneous (abnormal) nystagmus and a variety of other clinical signs. Vestibular disease can be classified as peripheral or central. Peripheral vestibular disease occurs when lesions of the vestibular apparatus of the inner ear (utricle, saccule, semicircular canals) are present or when there is abnormality of the peripheral portion of the vestibulocochlear nerve (cranial nerve VIII). Animals with peripheral vestibular lesions have normal mentation but may be extremely disoriented, making assessment of mentation difficult. The head tilt in peripheral vestibular disease is toward the side of the lesion. The vestibular system is involved in the maintenance of normal posture. Unilateral peripheral vestibular dysfunction causes decreased extensor tone in the limbs ipsilateral to the lesion and increased extensor tone in the contralateral limbs, resulting in the clinical signs of leaning, falling, and rolling toward the affected side. Proprioception and postural reactions are normal in peripheral vestibular disease, although they may be hard to evaluate in severe cases and in larger animals. Peripheral vestibular lesions produce a horizontal or rotatory nystagmus, with the fast phase directed away from the side of the lesion. The direction of the nystagmus in relation to the rest of the head is unchanged no matter what the position of the head. Physiologic nystagmus may be absent in severe cases, but more often it is decreased, particularly when the head is turned toward the side of the lesion. The facial nerve runs in proximity to the petrous temporal bone, and facial paralysis may be present in animals with peripheral vestibular disease when the facial nerve also is damaged by the underlying cause, such as may occur in traumatic injuries or severe otitis media or interna. Similarly, involvement of the postganglionic sympathetic nerve to the eye as it courses through the petrous temporal bone results in an ipsilateral Horner’s syndrome (ptosis, miosis, enophthalmos, facial sweating in horses, reduced sweating on the nasal planum in cattle).

Lesions within the vestibular centers in the medulla oblongata and cerebellum also cause vestibular dysfunction. Central vestibular disease may produce clinical signs similar to peripheral vestibular lesions but can be distinguished from the latter by a number of features. Head tilt in central vestibular disease usually is toward the side of the lesion but may be in the opposite direction when the underlying disease involves the cerebellum (paradoxic vestibular syndrome). Similarly, nystagmus may be identical to that seen in peripheral vestibular disease but also may be vertical, diagonal, or different in each eye (disconjugate nystagmus); may change in direction when the position of the head is changed (positional nystagmus); or may be horizontal or rotatory with the fast phase toward the side of the lesion (paradoxic vestibular syndrome). Signs of involvement of the motor and sensory tracts to the limbs as they course through the medulla usually accompany central vestibular disease. Proprioceptive and postural reaction deficits are present in the ipsilateral limbs, together with mild hyperreflexia. The nuclei of cranial nerves V to XII also may be affected by diseases that cause central vestibular lesions. Signs of cranial nerve dysfunction accompanying vestibular abnormalities, other than that of the facial nerve alone, indicate central vestibular disease. Horner’s syndrome, however, is not seen in conjunction with central vestibular disease. Decreased mentation often occurs in animals with central vestibular disease, in contrast to the normal mental status of animals with peripheral vestibular lesions.

Animals with either peripheral or central vestibular lesions tend to lean against the walls and may fall when forced to perform a complex motor maneuver. They may adopt recumbency with the lesion side directed down and have poor righting responses, particularly from lesion-side-down recumbency. When positioned so that the lesion side is directed up, they often will roll to a lesion-down position. Blindfolding the patient eliminates visual compensatory mechanisms and therefore increases the severity of the clinical signs (Romberg test). Blindfolding may help in the detection of subtle lesions but should be done with caution because it may result in falling. Animals with vestibular disease occasionally may have slight ventral strabismus in the ipsilateral eye and slight dorsal strabismus in the contralateral eye. This strabismus can be differentiated from the ventrolateral strabismus seen with lesions of the oculomotor nerve because the strabismus accompanying vestibular lesions is mild and changes or disappears when the head position is changed. The strabismus in animals with paralysis of the oculomotor nerve does not change as the head position is altered. In the cow and sheep, evaluation of globe position must be conducted with the head held in normal position because these animals rotate the globe downward when the head and neck are extended. Conversely, the globe is maintained in the center of the palpebral fissure at all head positions in the horse and the goat.

Animals with bilateral vestibular lesions do not have head tilt or nystagmus. The animal stands with the legs base-wide and may fall to either side when the head position is rapidly altered. Affected animals may show a coarse side-to-side head tremor. Bilateral vestibular lesions usually are peripheral in type and are rarely encountered in clinical practice. Central lesions extensive enough to cause bilateral vestibular disease are likely to be fatal.

Incoordination, Hypermetria, Dysmetria, and Intention Tremor

Clinical signs that occur in animals with cerebellar disorders include hypermetria, intention tremor, and truncal ataxia (excessive body sway during movement along a straight path). Conscious proprioceptive fibers do not pass through the cerebellum. Consequently, postural placement of the limbs is normal. Animals with cerebellar disease move the limbs with excessive rate, range, and force. There is a slight delay in lifting the limb from the ground. At the peak of protraction the limbs are lifted too high and too far anteriorly. The legs then hit the ground with excessive force. When the animal is turned, the legs circumduct. The animal may violently thrust the outside rear limb backward and laterally when turned. The forelimbs and the hindlimbs occasionally collide during the turn (interference). At rest the animal stands with the legs abducted, in a base-wide stance. This is not a conscious proprioceptive deficit, however, because the animal consciously returns the limbs to the base-wide posture if the leg position is manually corrected. There is intention tremor, most marked in the head. When the animal attempts to reposition the head, it overshoots the intended position, corrects, and then overshoots again. The sequence of overcompensation and overcorrection results in a coarse oscillation. The head tremor is most conspicuous when the animal is alert, especially when eating. Intention tremor disappears when the animal is recumbent and the musculature is relaxed. In animals with cerebellar disorders, the extensor muscles of the limbs may be hypertonic, and spinal reflexes occasionally are exaggerated. Foals with cerebellar disease fall backward. This does not usually occur in ruminants. Lesions of the rostral cerebellar vermis can result in opisthotonos. Animals with cerebellar cortical disease may lack a menace response but retain their vision and can negotiate around obstacles. The reason for the menace deficit is unclear, but it is thought to result from disruption of efferent pathways emanating from the occipital (visual) cortex and passing through the cerebellar cortex to the motor nucleus of the facial nerve. Animals with pure cerebellar dysfunction remain bright, alert, and responsive to external stimuli. Animals with very severe lesions of the cerebellum may be recumbent and unable to rise, with decerebellate posture. This posture is characterized by opisthotonos and forelimb extensor rigidity, with normal or flexed hindlimbs. Unlike decerebrate rigidity, animals in decerebellate rigidity have normal mentation and a good prognosis if the underlying disease is not progressive. Cerebellar disease is often bilaterally symmetric, but lateralized lesions cause signs on the ipsilateral side of the body. Diseases that cause spasticity or tremors in livestock are listed in Table 8-9.

Table 8-9 Diseases of Spasticity or Tremors in Horses and Ruminants

Involvement of the vestibular components of the cerebellum (caudal cerebellar peduncle, flocculonodular lobe, and fastigial nucleus) results in signs of paradoxic vestibular syndrome, described earlier.

Abnormalities of Cranial Nerve Function

The normal functions of the cranial nerves are described earlier, in the discussion of the neurologic examination. Cranial nerve dysfunction may be central or peripheral in type, depending on whether the neurologic lesion lies within the central components of the cranial nerves within the brain or in the peripheral portions of the nerves. Clinical signs of cranial nerve dysfunction are ipsilateral to the lesions that cause them.

DYSPHAGIA, DYSPHONIA, STERTOROUS BREATHING

Lesions in the nucleus ambiguus (cranial nerves IX, X, and XI) produce dysphonia, inspiratory dyspnea, dysphagia, and neurogenic atrophy of the trapezius, sternocephalicus, and brachiocephalicus muscles. The inspiratory dyspnea is characterized by roaring and snoring. Roaring is a stertor that is made during peak inspiratory flow. It is caused by paralysis of the cricoarytenoideus dorsalis muscle, resulting in a failure to abduct the arytenoid cartilages during inspiration. Additional evidence of paralysis of cranial nerves IX to XI may be obtained by endoscopic examination of the pharynx. Other signs of paralysis of cranial nerves IX to XI include failure to abduct the vocal folds, collapse of the pharynx, dorsal displacement of the soft palate, and inability to swallow a nasogastric tube. Lesions in the peripheral parts of the glossopharyngeal, vagus, and accessory spinal nerves produce similar laryngeal signs but may be differentiated from centrally located lesions by attitude, appetite, and conscious proprioceptive responses. Animals with peripheral nerve deficits remain alert and appetent and do not show conscious proprioceptive deficits, whereas animals with centrally located lesions may be depressed and inappetent and may have proprioceptive and postural deficits. Animals with bilateral lesions in the peripheral nerves are unable to open the glottis during inspiration and display extreme respiratory distress. Peripheral lesions of the accessory nerve that have been present for longer than 1 month may produce neurogenic atrophy of the trapezius, brachiocephalicus, and sternocephalicus muscles. This is frequently accompanied by aspiration pneumonia. Lesions of the visceral efferent component of cranial nerve X in ruminants produce vagal indigestion, which is characterized by ruminal distention with fluid, ruminal tympany, abomasal stasis, and sometimes a hypochloremic, hypokalemic metabolic alkalosis. This is an important disease of the ruminant gastrointestinal tract. Hypoglossal nerve lesions produce a weak or flaccid tongue. In animals with unilateral lesions, the tongue deviates away from the side with the lesion and is flaccid when it is manually extended from the mouth. After prolonged denervation (1 month or more) the ipsilateral side of the tongue atrophies and the tongues deviates toward the affected side. Horses with lesions in the sensorimotor cortex may also fail to retract the tongue normally; however, the tongue tone is variable, and the animal can retract it if it receives sufficient stimulation. In comparison, the tongue tone is consistently weak in cases of hypoglossal paralysis.

Signs of cranial nerve dysfunction, together with the central origins or projections of the nerves, are summarized in Table 8-10. Diseases that involve the brainstem and cranial nerves are summarized in Table 8-11.

Table 8-10 Clinical Signs of Cranial Nerve Dysfunction

Table 8-11 Diseases of the Brainstem and Cranial Nerves

Disease	Location	Clinical Signs and Laboratory Findings
Viral encephalomyelitis, rabies, malignant catarrhal fever (cattle only)	Multifocal brainstem, particularly medulla oblongata	Head tilt, nystagmus, circling, ataxia, proprioceptive deficit, tongue paralysis, anisocoria, dilated nonresponsive pupils, strabismus, paralyzed tongue, dysphonia, dysphagia, plus cortical signs (rage, fright, fear, convulsions); CSF may show pleocytosis (mainly mononuclear cells); high protein
Listeriosis (cattle)	Multifocal brainstem, particularly basal ganglia, metencephalon, and medulla oblongata	Circling, head tilt, facial paralysis, roaring, snoring, dysphagia, obtundation, coma, convulsions, ataxia, proprioceptive deficit; CSF shows pleocytosis (mainly mononuclear); increased protein
Thromboembolic meningoencephalomyelitis (cattle)	Multifocal brainstem and cortex	Circling, nystagmus, head tilt, strabismus, tongue paralysis, dysphagia, facial paralysis, coma, convulsions, obtundation, xanthochromic CSF with increased neutrophils
Peripheral vestibular disease	Petrous temporal bone, membranous labyrinths, vestibulocochlear nerve, also associated with facial nerve paralysis	Head tilt, circling, or leaning toward lesion side, ventrolateral strabismus on ipsilateral side, dorsomedial strabismus on contralateral side, nystagmus (usually horizontal and constant)
Verminous migration	Multifocal brainstem, most commonly thalamus, diencephalon	Circling, nystagmus, head tilt, strabismus, tongue paralysis, facial paralysis, obtundation, coma, convulsions, depression, proprioceptive deficit, bradycardia, salivation, head pressing, hemianopsia; high protein and increased WBCs in CSF
Space-occupying mass Tumor Abscess	Cerebellopontine angle; cranial nerves V, VII, and VIII	Head tilt, strabismus, proprioceptive deficit, facial analgesia, jaw drop, obtundation, coma, strabismus, nystagmus, hyperreflexia, hypertonia, falling or circling toward affected side, blindness on contralateral side, tongue paralysis, hemianopsia, bradycardia, coma, convulsion
Horner’s syndrome	C8 to T1 motor neurons (gray matter), spinal roots, vagosympathetic trunk, sympathetic tracts of spinal cord, periorbita	Miosis, enophthalmos, lack of nasal sweat (cattle only), ipsilateral facial swelling (horses only)
Guttural pouch mycosis (horses)	Guttural pouch	Dysphagia, head shyness, head shaking, roaring, dysphonia, protrusion of the tongue from the mouth, epistaxis, head tilt, nystagmus, facial sweating, shivering, Horner’s syndrome, colic, facial paralysis

CSF, Cerebrospinal fluid; WBCs, white blood cells.

Lesions of the medulla oblongata can produce severe obtundation, somnolence, or coma as a result of ARAS dysfunction in addition to signs of vestibular dysfunction and functional deficits in cranial nerves V to XII. Other clinical signs of medullary lesions include ipsilateral paresis and conscious proprioceptive deficits as a result of dysfunction in the rubrospinal, reticulospinal, spinothalamic, and spinocerebellar pathways. The spinal reflexes of the ipsilateral limbs are exaggerated, and the extensor muscle tone is increased. Further details are given in the discussion of quadriparesis and hemiparesis, later.

Measurement of Brainstem Function Using Auditory Evoked Potentials

The integrity of the vestibulocochlear apparatus can be examined using brainstem auditory evoked potentials.^53-55 This method examines the averaged waveform that is generated after an auditory click in the ear. The individual signals from a single click stimulus are small and therefore must be amplified by repeating the stimulus (30 to 100 dB, 10 Hz) between 30 and 1000 times and recording the voltage difference between two electrodes placed on the head. The recording electrode is usually placed over the petrous temporal bone, and the reference electrode at the vertex, or elsewhere on the head. The technique of signal averaging is used to eliminate background electrical activity and enhance the specific waveforms generated by the auditory impulse. The response usually is measured for 10 ms after the stimulus is applied. Ablation of the entire cochlear apparatus and vestibular nerve, as might occur with otitis interna, would result in a loss or attenuation of waveform activity after the click stimulus. Injury to the brainstem vestibular nuclei would result in a loss of waves II through VI. Damage to the trapezoid body (pons), lateral lemniscus, caudal colliculus, and medial geniculate body would result in a loss of waveforms III through VI, respectively. Increased latency between the peaks is usually associated with toxic or degenerative diseases of the CNS.

Paresis and Ataxia in Two or Four Limbs

Quadriparesis and hemiparesis are seen with lesions affecting the mid to caudal brainstem (midbrain, medulla oblongata) or the cervical spinal cord (C1 to T2 spinal cord segments). Quadriparesis also can be seen in generalized peripheral nerve or muscle disease, discussed later. Paraparesis results from disease affecting the spinal cord between segments T3 and L2 or the peripheral nerves to the hindlimbs. Disease of the cerebrum and thalamus does not produce appreciable paresis and ataxia when the animal is walking in a straight line on a level surface, but these signs become apparent in the limbs contralateral to the lesion when the animal is asked to circle, back, step over obstacles, or walk on a slope. Localization of the lesion when signs of paresis and ataxia are present depends on the assessment of muscle mass and tone, spinal reflexes, and evaluation of brainstem function, as determined by the presence or absence of signs such as altered mentation, cranial nerve deficits, or vestibular dysfunction.

Quadriparesis and ataxia with normal muscle mass and tone and normal to increased spinal reflexes indicate a lesion in the brainstem or in spinal cord segments C1 to C5. Presence of clinical signs of brain disease will facilitate localization of the lesion to an intracranial site, as described earlier. Lesions in the midbrain cause contralateral postural and proprioceptive deficits, whereas those in the medulla oblongata cause ipsilateral signs. Cerebellar disease causes a truncal ataxia, without significant loss of proprioceptive or postural functions, and with no or mild hyperreflexia of the limbs. Lesions of the thalamus and cerebrum cause minimal to no paresis or ataxia when the animal is gaited on a level surface, but contralateral proprioceptive and postural reaction deficits are present. Altered mentation and other signs of cerebral or thalamic disease are expected, such as circling or cortical blindness. Animals with spinal cord disease have normal mentation. The clinical signs shown by such patients depend on the location of the lesion and the relative amount of damage to gray (cell bodies) and white (myelinated spinal cord tracts) matter. Loss of white matter results in sensory loss, whereas gray matter damage produces lower motor neuron deficits. The sensory losses are either proprioceptive responses or cutaneous sensory deficits. White matter is usually more susceptible to pressure changes than gray matter, so proprioceptive deficits are consistently observed during the first stages of spinal cord disease. Spinal cord diseases may be localized to one of the following five regions: high cervical (C1 to C5), cervicothoracic (C6 to T2), thoracolumbar (T3 to L2), lumbosacral (L3 to S2), and sacrococcygeal (S3 to Cd5) regions. Tables 8-4 and 8-5 list the peripheral nerves and the spinal segments that innervate them.

Cervical Spinal Cord

Animals with incomplete section of the cervical region of the spinal cord display hemiparesis or tetraparesis. The clinical signs include knuckling, stumbling, failure to lift the inside feet when turned in a tight circle, interference, hypermetria, abnormal postural placement responses, crossing over midline when turned, and excessive truncal sway. Animals with more severe lesions of the cervical spinal cord become recumbent and are unable to lift the head from the ground. There is an asymmetric righting response in animals with unilateral lesions. They can raise the head and neck to a variable distance only when lying with the lesion side facing down. Muscle tone and spinal reflexes in the limbs of recumbent animals are exaggerated. The urinary bladder is distended. The animals have difficulty urinating, and afterward the bladder contains a large amount of urine. Animals with complete spinal cord transection anterior to C6 die suddenly as a result of paralysis of the intercostal muscles and the diaphragm.

Lesions between C6 and T2 spinal segments (brachial intumescence) result in conscious proprioceptive deficits in all four limbs and tetraparesis or tetraplegia. There is hypotonia and hyporeflexia of the forelimbs and hypertonia and hyperreflexia of the hindlimbs. Unilateral lesions result in ipsilateral signs. Lesions of C6 to T2 segments involving white but not gray matter do not produce forelimb hypotonia. Conscious perception of painful stimuli may be depressed in all limbs. Flexor reflexes in the forelimbs may be depressed but are normal in the hindlimbs. The righting responses of the head and neck are normal. Urination is difficult, and the urinary bladder is distended and has a large residual volume. After 1 month or more, lesions of the gray matter of the spinal cord or the peripheral nerves may result in neurogenic atrophy of one or more muscle groups of the forelimbs. Gray matter lesions of T1 to T3 spinal segments may result in Horner’s syndrome, which is characterized by miosis, enophthalmos, and ptosis in all species. Unilateral facial sweating occurs in horses; lack of sweating on the planum nasale occurs in cattle. Differentiation of high (C1 to C5) and low (C6 to T2) cervical spinal cord lesions may be difficult in horses, especially when signs are fairly mild.

Lesions of the thoracolumbar region (T3 to L3) result in normal activity of the forelimbs and proprioceptive deficits in the hindlimbs. These deficits are similar to those described previously for the cervical areas and include ataxia, knuckling, stumbling, abduction, adduction, interference, excessive truncal sway, and failure to lift the inside foot when pivoted in a tight turn. With complete lesions, the animal becomes recumbent but intermittently assumes a dog-sitting position, with the forelimbs extended and weight bearing and the hindlimbs flexed. Muscle tone and spinal reflexes are exaggerated in the hindlimbs. The urinary bladder is distended, and residual volume is large. The tone of the urethral sphincter is normal. Young animals with severe spinal cord lesions between T2 and L2 display transient hypertonia of the forelimbs (Schiff-Sherrington syndrome). This condition is caused by interference with inhibitory fibers ascending from the lumbar segments in the dorsal funiculi to the lower motor neurons of the forelimbs.⁵⁶ These fibers synapse on the neurons of the brachial intumescence. Hypertonia from this deficit may be differentiated from cervical cord lesions by the lack of conscious proprioceptive deficits in the forelimbs of animals with thoracolumbar lesions.

The lumbosacral region (L3 to S2) of the spinal cord contains lower motor neuron efferents to and general proprioceptive afferents from the pelvic limbs. Lesions in this area result in paraparesis or paraplegia. Affected animals are ataxic and have conscious proprioceptive deficits of the hindlimbs. Patients with complete spinal cord lesions of L3 to S2 exhibit flaccid paraplegia, which is accompanied by hyporeflexia or areflexia of the hindlimbs. With prolonged denervation, neurogenic atrophy of the hindlimb musculature occurs.

Lesions located between L3 and L6 spinal cord segments result in urinary bladder distention and maintenance of a large residual volume. The sphincter tone is intact, but urine is not voided unless the intravesicular pressure exceeds that of the sphincter. These animals usually have contact dermatitis of the perineum and preputial area because of urine scalding. Lesions located around S1 and S2 segments result in bladder distention and flaccidity. Urine may drip continuously from the urethral orifice. The rate of flow may be increased by manually pressing on the bladder during a rectal examination.

Lesions of the sacrococcygeal (S3 to Cd5) region (cauda equina) produce flaccidity of the tail and anus and, in males, paraphimosis. Lesions in this area also result in desensitization of the tail, penis, vulva, anus, and perineum. The urethral sphincter is dilated, and urine constantly drips from the urethral orifice. The animal does not evacuate the bladder and is unable to defecate, resulting in a large dilated urinary bladder and distention of the rectum with feces.

If the entire neurologic lesion is located caudal to S3, ataxia or conscious proprioceptive deficit is not present. The combination of flaccidity of the tail and anus and the constant urine leakage produces contact dermatitis of the perineum and hindlimbs. Perineal scalding is characteristic of lesions of the cauda equina. Specific diseases of the spinal cord, peripheral nerves, and motor end plate are listed in Table 8-12.

Table 8-12 Diseases of the Spinal Cord, Peripheral Nerve, and Motor End Plate of Large Animals

Muscle Atrophy, Reduced Muscle Tone, Flaccid Paresis, Focal Analgesia

Clinical signs of reduced muscle tone, muscle atrophy, and flaccid paresis indicate peripheral nerve, muscle, or neuromuscular diseases. Signs may be localized to a single limb, as in the case of traumatic peripheral nerve injury; generalized, as in botulism and many myopathies; or multifocal, as in equine protozoal myeloencephalitis and other diseases that attack multiple areas of the CNS, destroying the ventral horn gray matter of the spinal cord, or nuclei of cranial nerves in the brainstem. Details of neuromuscular diseases and the use of ancillary diagnostic testing to localize peripheral nerve, muscle, and neuromuscular disease are described in Chapter 35.

Peripheral nerve lesions, whether of the central components of the nerves in the spinal cord and brainstem or along their peripheral course in the limbs and head, also can result in focal hypalgesia or anesthesia. Knowledge of the autonomous zones for the peripheral nerves innervating the limbs can be used to localize such peripheral nerve lesions.

Urinary Incontinence and Urine Retention

The clinical signs of urinary bladder denervation are variable and depend on the lesion location. Lesions of the sacral segments of the spinal cord produce a flaccid bladder, which distends with a large residual volume. Spontaneous urine leakage occurs continuously from the urethra. Additional urine flow occurs when the abdominal pressure is increased. The urethral sphincter is dilated and atonic. Lesions of the brainstem or spinal cord anterior to S1 produce reflex dyssynergia, a disturbance in coordination of micturition, wherein the facilitatory influence of the bladder stretch receptor (afferents) maintains tonic activity on the efferents of the urethral sphincter. The lack of inhibition of these reflexes from the upper motor neuron pathways produces hypertonicity of the urethral sphincters and results in an impediment to urine flow. There is a high intravesicular pressure and a large postvoiding urine volume. The urine escapes paroxysmally only when the intravesicular pressure exceeds the sphincter pressure. After approximately 1 month of denervation, local spinal reflexes between the sacral afferent and efferent neurons develop in the S1 to S5 segments, and incomplete voiding occurs. In these cases the residual volume remains large, and the normal urination posture is not attained.