Assessment of Chief Complaint

Obtaining information on signalment and history and performing a thorough physical examination including assessment of the nervous system constitute the complete neurologic examination. Information on signalment is important, because disease susceptibility may be linked to age, species, breed, and sex. For example, Suffolk sheep older than 2 years of age are more likely to be affected by scrapie than younger animals, or animals of different breeds. The signalment often is ascertained by simple observation, but specific details such as production status and exact age are more accurately determined through client interview. Some diseases capable of causing neurologic signs are specific to sheep or goats, especially those diseases with an infectious or genetic basis. In general, young animals with neurologic problems are more likely to have congenital, inherited, or infectious disorders, whereas older animals are more likely to be affected by neoplastic and degenerative diseases. Knowledge of common neurologic diseases, in either individual animals or groups, related to gender or a particular breed or age can greatly assist the clinician in developing a list of entities to consider in the differential diagnosis. Many sheep and goats are production animals, so the expenses associated with evaluation and treatment must be weighed against the prognosis for future productivity. Because sheep and goats are flock and herd animals, the interests of the population also must be considered.

The clinical history is an important step in the diagnosis of neurologic disease. Information related to onset, duration, and progression of the chief complaint can assist with an etiologic diagnosis (What is the cause?) after the anatomic diagnosis (Where is the lesion?) has been made. In collecting historical information, it is important to determine the nature of the first clinical signs but also to define the relationship between the severity of clinical signs with respect to time (as on a sign-time graph). Some neurologic diseases occur acutely, with all clinical signs apparent within hours. Traumatic, toxic, infectious, and metabolic diseases can manifest with this pattern, whereas degenerative, neoplastic, or some viral disorders may develop more slowly, requiring days to weeks before the full complement of clinical signs becomes apparent. In addition to specific information related to the chief complaint, information on diet, housing, gestational status, and vaccination and deworming regimens should be part of the information gathered from the client. In interviewing clients for historical information, ambiguous or leading questions should be carefully avoided, because the information thus obtained may be inaccurate.

A thorough physical examination should be performed in conjunction with every neurologic examination. The nervous system is integrated within many other body systems, and diseases of the cardiovascular, respiratory, musculoskeletal, and endocrine and metabolic systems can manifest with clinical signs similar to those observed with nervous system disease. Before being subjected to the stress of handling, the animal should be observed in its normal surroundings to assess behavior, mental status, gait, tremors, and head, neck and limb postures.

Mentation

Evaluation of mentation can assist the clinician in differentiating intracranial from extracranial disease processes. As described previously, some systemic diseases will result in depression without nervous system pathology. During the period of initial observation, the animal’s mental status and behavior can be assessed, but this must be done when the animal is not stimulated. For animals to be alert and oriented, the cerebral cortex and the ascending reticular activating system must be functioning properly. The ascending reticular activating system makes up the major portion of the brain stem parenchyma and is responsible for arousal and sleep-wake transitions in animals. Consequently, disorders involving the ascending reticular activating system can cause somnolence. The ascending reticular activating system is composed of several neuronal circuits connecting the brain stem to the cortex. External stimuli, such as light, touch, sound, smell, and temperature, help to maintain consciousness. An animal should appear as sensitive to its environment as its herdmates. If removed from its usual environment, the normal animal will be alert and cautious of new situations and aware of the examiner. The animal should follow the examiner’s movement with its head, eyes, and ears. All animals should avoid painful stimuli. Abnormal mentation in ruminants can be placed into one of the following categories: (1) excitement, mania, or hyperesthesia; (2) seizures; (3) depression; (4) aimless circling, stupor, and coma; (5) abnormal vocalization; and (6) blindness.¹ Stupor is characterized as a condition of unresponsiveness to environmental stimulation such as light and sound, with rentention of response to painful stimuli. By contrast, a comatose animal is nonresponsive to either environmental or painful stimulation.

Behavioral changes may be difficult to assess if the animal’s environment has been changed. Alterations in behavior include aggression, vocalization, compulsive activities such as circling or walking or gazing, yawning, head pressing, and increased or abnormal sexual activity. The neuroanatomic localization of behavioral disorders may be difficult because the components of the limbic system—hypothalamus, hippocampus, amygdala, and portions of the cerebral cortex—all are associated with complex behavior.

Gait and Posture

To properly assess gait and posture, the goat or sheep should be allowed to move freely within an enclosed area. A pet or tame animal can be walked at a slow pace by the client using a halter. Observations on forelimb gait are made as the animal is walked toward the examiner, and observations on hindlimb gait should be made as the animal is walked away from the examiner. Gait is defined as a regularly repeating series of leg movements during walking or running. Goats and sheep walk by first flexing the hindlimb on one side and then the forelimb on the same side. This process is then repeated for the opposite side. Animals integrate multiple neural processes in order to walk. The cerebrum initiates voluntary locomotion and adjusts movements according to learned functions. The cerebellum contributes to the coordination of movement. The vestibular system maintains balance and helps anticipate alterations in the animal’s center of gravity so that it can compensate appropriately. Spinal cord reflexes are responsible for maintaining the limbs in extension, supporting the animal’s weight, and initiating stepping motion. The organization of stepping motion is performed at the brain stem in the reticular formation.

Diseases of the nervous system, muscles, bones, joints, and associated connective tissues can affect gait. When associated with conditions originating in the nervous system, gait abnormalities can result from lesions within the cerebellum, brain stem, spinal cord, or peripheral nerves. Ataxia is a term used to describe an abnormal gait characterized by incoordination, but without spasticity, weakness, or involuntary movements. Ataxia can be classified by the quality of signs observed and the pathway involved; the three types are vestibular ataxia, cerebellar ataxia, and proprioceptive ataxia. In general, vestibular ataxia is associated with a head tilt, while cerebellar ataxia is characterized by hypermetria and no proprioceptive deficits. Proprioceptive ataxia also is referred to as spinal ataxia because it is associated with spinal cord lesions and is characterized by abnormal proprioception, weakness, and lack of head tilt, circling, or other intracranial signs.

Posture typically is evaluated with the animal at rest in a comfortable position and unrestrained. Head, neck, trunk, and limb posture should be assessed and abnormalities identified. Head tilt, rotation of the neck and thoracic, and wide-based stance are examples of abnormal head, neck, trunk, and limb posture, respectively. A “base-wide” stance can be caused by lesions within the vestibular system, cerebellum, or spinal cord. The inverse posture, or “base-narrow” stance, can result from muscle weakness due to peripheral nerve disease, abnormalities of neuromuscular junctions, or disorders of the skeletal muscles. Spasticity is a condition of increased tone of skeletal muscles producing abnormal limb posture. Abnormal distribution of weight to one side should be noted, because this finding can indicate either weakness of ipsilateral extensor muscles from a peripheral nerve disorder or increased tone of contralateral extensor muscles, which would indicate a UMN lesion.²

Assessment of Cranial Nerves

Twelve pairs of cranial nerves, labeled I to XII, are described as follows: cranial nerve I (CN I), the olfactory nerve,; CN II, the optic nerve; CN III, the oculomotor nerve; CN IV, the trochlear nerve; CN V, the trigeminal nerve; CN VI, the abducent (or abducens) nerve; CN VII, the facial nerve; CN VIII, the vestibulocochlear nerve; CN XI, the glossopharyngeal nerve; CN X, the vagal nerve; CN XI, the spinal accessory nerve; and CN XII, the hypoglossal nerve. Clinical evaluation of CN I (olfactory nerve) and CN XI (spinal accessory nerve) cannot be reliably performed in sheep and goats. Because the intact sense of smell is important for nutritional intake, CN I is assumed to be intact in sheep and goats that are eating. CN XI (spinal accessory nerve) has axonal inputs from cervical spinal nerves and innervates specific muscles of the neck. Damage to CN XI is rare because the nerve is protected throughout much of its course by the muscles it innervates, and injury to the spinal canal or base of the skull is accompanied by neurologic deficits that can mask clinical signs of CN XI damage.

Abnormalities in the function of CNs result from localized lesions involving neuronal cell bodies within the brain or the specific nerves themselves. With the exception of CN I and CN II which are located within the cerebral cortex, all CNs arise from the brain stem. Knowledge of the location of CN nuclei assists the clinician in neuroanatomic localization of lesions. The presence of neurologic deficits involving CNs III to XII in a sheep or goat that is severely depressed or somnolent would indicate that the responsible lesion is most likely to be within the brain stem.

Cranial Nerve II (Optic Nerve): Menace Response

Vision is the function of CN II. The nerve transmits sensory information from electrochemical receptors in the retina to the visual cortex in the occipital lobe of the cerebrum. The visual pathway (Figure 13-1) is an afferent pathway and consists of an extraparenchymal portion (retinas, optic nerves, optic chiasm) and an intraparenchymal portion (optic tracts, lateral geniculate nucleus in the thalamus, optic radiations, visual cortices). In ruminants, 90% of optic nerve fibers cross at the chiasm to enter the contralateral optic tract; this arrangement has important implications in evaluating lesions of the visual pathways. During assessment of the chief complaint, the client may report that the animal appears blind, but an important consideration is that depressed or somnolent animals or animals with loss of balance due to cerebellar or vestibular disease can stumble and appear blind.

Figure 13-1 Schematic of the simplified pathways of vision and pupillary light reflex (see text for details).

The clinical assessments of visual ability include the menace response test and the obstacle test. Eliciting the menace response, which also is referred to as the blink response or eye preservation response, is the easiest method for evaluation of vision impairment; however, the obstacle test, if performed accurately, is superior for assessing vision in ruminants. For this test, objects are placed in the path of the animal, and then its ability to negotiate around the objects is assessed. Degrees of blindness can occur with ocular disease, and the simplest obstacle test is to determine if the blind animal moves toward the lighted opening when placed in a dark environment.

The menace response evaluates the entire visual pathway, CN VII, and the cerebellum. This test assesses a response, rather than a reflex, because the response involves the cerebrum and thus is a learned response. The presence of a response or its magnitude parallels the maturity of the cerebellum—thus a reduced response is detected in kids and lambs less than a week of age. A diminished or absent menace response also can be observed in animals that are severely depressed or have cerebellar disease or CN VII lesions. The normal response is characterized by an eyelid blink, ocular retraction, and head aversion as the examiner rapidly moves a finger toward the eye from a rostral direction. It is important to limit air movement toward the eye and not to touch the eye or adnexa, because such maneuvers may result in a response in animals with intact facial sensation (CN V). Alternatively, the examiner can drop an object into the animal’s visual field from above, which should elicit the menace response from the animal. This method is considered imprecise, with a stimulus that is too slow, for adequate evaluation of this reflex in ruminants. When a visual deficit is observed during the menace response or obstacle test, pupillary light reflexes are tested to assist in localizing the lesion and in characterizing the blindness as central or peripheral.

CN V (Trigeminal Nerve): Corneal and Palpebral Reflexes

The large CN V contains motor nerve fibers that innervate the muscles of mastication and acquires sensory information from most parts of the head. The nerve is divided into three branches: ophthalmic, maxillary, and mandibular. All three branches have sensory nerves, but only the mandibular branch contains motor nerve fibers. The mandibular nerve innervates the masseter, temporal, rostral digastric, pterygoid, and mylohyoid muscles. The masticatory muscles should be palpated for symmetry and atrophy. Bilateral loss of motor function of the mandibular nerve is rare but would result in muscle atrophy of the temporal and masseter muscles, a flaccid and lowered jaw, inability to chew, and excessive drooling, which can result in bicarbonate loss. The animal’s tongue may protrude from the mouth as a result of fatigue, but the tongue can be withdrawn to appropriate stimulation. Unilateral lesions can cause asymmetric muscle atrophy and a slightly lowered position of the jaw. This may not result in dysphagia, but abnormal wear of teeth and dental problems may be evident.

Function of the sensory branches is tested by corneal and palpebral reflexes (Figures 13-2 and 13-3) and assessing sensation across multiple areas of the face. In the palpebral and corneal reflexes, CN V is the afferent (sensory) portion, whereas CN VII is the efferent (motor) portion of the reflex. The corneal reflex is performed by slowly advancing a finger or cotton swab toward the animal’s eye and placing it directly on the cornea. The palpebral reflex is performed by touching a finger on periococular skin without the animal’s visualizing the finger. The corneal reflex and touching the medial canthus of the eye for the palpebral reflex assess the ophthalmic branch of CN V, which innervates the eye and surrounding skin and is responsible for the maintenance of corneal epithelium. The maxillary branch of CN V can be assessed by touching the lateral canthus of the eye during elicitation of the palpebral reflex. The normal reflex response with intact CN V, CN VI, and CN VII is closure of the lid, retraction of the eye, and aversion of the head, respectively. The mandibular branch of CN V can be assessed by touching the ear base and observing for closure of the lid. A deficient palpebral reflex with a normal menace response suggests a lesion in the trigeminal nerve or ganglion. Loss of CN V innervation to the corneal epithelium can result in neurotropic or exposure keratitis, because the affected animal cannot sense corneal dryness or the presence of ocular foreign bodies.

Figure 13-2 The corneal reflex is assessed by gently placing a finger or the loosened fibers of a cotton tip applicator directly on the cornea.

Figure 13-3 The palpebral reflex is tested by touching the periorbital skin with the examiner’s finger while keeping the animal from seeing the approaching finger.

Damage to any branch of the trigeminal nerve results in sensory losses to the areas it innervates. Deficits in CN V function will manifest as the ipsilateral loss of sensation over the face and affected animals will not reflexly blink or twitch the face. This is a subcortical reflex and does not require conscious input. The consciously mediated, coordinated movement of the head away from the noxious stimuli is assessed by stimulating the nasal septum. The examiner applies stimulation using a finger or cotton swab to the inner (medial) surface of the nasal septum (Figure 13-4). The response in a normal animal is blinking and facial twitching; the head is pulled away in response to a painful stimulus. This response requires conscious recognition of the noxious stimulus by way of CN V maxillary nerve to the contralateral parietal cortex. This determination is important, because an animal with a CN V maxillary branch abnormality will have neither sensation nor conscious recognition of pain, whereas a sheep or goat with a contralateral cerebral cortical lesion will have normal sensation but no conscious recognition of the painful stimuli.

Figure 13-4 Assessment of the conscious recognition of a noxious stimulus by way of the maxillary branch of cranial nerve V to the contralateral parietal cortex. The animal demonstrates the appropriate response of blinking and attempting to withdraw the head from the stimulus.

Postural Reactions

Postural reactions complement the evaluation of gait. Postural reactions are easily examined in sheep and goats and include the following: hopping, wheelbarrowing, hemi-standing, hemi-walking, placing, and proprioception. Testing for the hopping postural reaction is performed by lifting three limbs off the ground while walking the animal forward. Each of the front limbs should be evaluated for the hopping postural reaction; a normal animal will lift and place the limb as it would with normal locomotion. Wheelbarrowing is similar, but only the two hindlimbs are lifted off the ground as the animal is walked forward. Hemi-standing and hemi-walking are similar postural reactions that are assessed by lifting the ipsilateral front limbs and hindlimbs while the animal is observed at rest and during locomotion, respectively. Placing is assessed by lifting the goat or sheep and advancing it to the edge of a table; normal animals lift the front legs to place them on the table. Proprioception reflects the animal’s ability to consciously recognize an abnormal limb posture. To test for the proprioception reaction, the standing animal’s distal limb is flexed at the fetlock joint, resulting in weight-bearing at the dorsum of the digit. A normal proprioceptive reaction will quickly result in correction of the abnormal weight-bearing.

Spinal Reflexes

Five spinal reflexes should be evaluated in sheep and goats with suspected neurologic disease: the extensor reflex of the front limb, the panniculus reflex, the patellar reflex, the perineal reflex, and the withdrawal reflexes of the forelimbs and hindlimbs. The spinal reflexes are best examined with the animal in lateral recumbency, with the side to be evaluated in the upper position. Spinal reflexes involve a local reflex arc that includes a stretch or touch receptor, an afferent peripheral nerve that relays information to the spinal cord gray matter, spinal cord interneurons that can stimulate or inhibit other neurons, an efferent motor neuron that exits the spinal cord, and a muscle. Spinal reflexes do not require conscious or voluntary input for normal function.

Assessment of spinal reflexes tests the integrity of the lower motor neuron (LMN) but also can provide some information on influences of the upper motor neurons (UMNs) on the LMN (Table 13-1). The UMNs are a group of neurons that do not physically exit the nervous system and provide stimulatory or inhibitory influences to the LMN. The LMNs are composed of the peripheral nerves and the effector organs (primarily skeletal muscles). Several responses can be observed when spinal reflexes are tested. A normal response can be observed, which indicates normal sensory and motor components of the reflex arc. An exaggerated response often is observed with UMN pathway abnormalities. A diminished or absent response indicates LMN disease in either its sensory or motor components. In addition to diminished responses, animals with LMN disease exhibit muscle atrophy, hyporeflexia or areflexia, hypotonia or atonia, and paresis.

TABLE 13-1 Summary of Lower and Upper Motor Neuron Signs

Testing the extensor reflex of the front limb assesses the radial nerve. The radial nerve is responsible for weight-bearing of the front limb and innervates the triceps muscle group. With the animal in lateral recumbency, the extensor reflex is assessed by placing a hand under the foot of the animal and pushing the limb gently toward the animal until extensor tone is noted. The normal reflex is for the animal to “push back” with its leg. Animals with LMN disease display decreased or absent resistance, and those with UMN disease may exhibit increased tone of the triceps muscle.

Testing the patellar reflex evaluates motor and sensory components of the femoral nerve. The femoral nerve innervates the quadriceps muscles, which are responsible for extension of the stifle and weight-bearing in the hindlimb. The patellar reflex is a tendinous reflex and is elicited by lightly tapping the patellar tendon with a reflex hammer while observing an extension of the stifle. Patellar reflex testing is a subjective assessment, and clinicians should be as consistent as possible in technique. To begin, the limb should be in relaxed flexion with the patellar tendon just barely tightened. The tendon is palpated, and then, while the examiner’s fingers are kept on the tendon, the limb is flexed until the tendon feels tight. To raise tension in the tendon, the clinician can place a hand under the foot while extending the digits. The tapping on the tendon is done with a pendulum motion. The reflex cannot be elicited if the limb is tense, but by tapping the tendon rhythmically, the animal relaxes over time. The strength of the patellar reflex is proportional to the force applied to the tendon. The plexor (hammer) used for examination of large dogs is adequate for testing the reflex of small ruminants. The patellar reflex combined with the proprioceptive reaction is used to determine the integrity of the LMN. With LMN lesions, deficits exist in conscious proprioception and patellar reflexes, whereas deficits of conscious proprioception in animals with intact patellar reflexes indicate lesions in the UMN.

Withdrawal reflexes also are referred to as flexion reflexes, and testing is performed by applying a noxious stimulus to the medial or lateral digits of the front limbs and hindlimbs. A hemostat often is used to apply the stimulus. In the front limb, the withdrawal reflex evaluates the axillary, median, and ulnar nerves. In the hindlimb, the reflex evaluates the sciatic nerve on the lateral part of the limb and the femoral nerve on the medial part of the limb. A normal response is the flexion of the limb fully away from the stimulus.

Testing the perineal reflex is performed by pinching the skin around the anus. The perineal reflex tests the afferent pudendal nerve, whereas the efferent nerve fibers are part of the caudal nerves. The normal response is anal sphincter contraction and downward contraction of the tail. During the reflex test, the tail should not be manipulated, because this may cause contraction of the anus.

The panniculus reflex or cutaneous trunci reflex also relies on a reflex arc. This test is performed by applying stimuli to both sides of the body starting caudally at the wing of the ileum to the cranial thoracic area (at the T2 level). The stimulus usually is applied with the tip of a ballpoint pen or a hemostat. The sensory fibers from the skin enter the dorsal root of the spinal cord and then ascend to the C8 and T1 segments, where the efferent limb of the reflex is the motor neurons of the lateral thoracic nerve. A normal reflex is flinching of the skin. If twitching of the skin occurs at the level of the wing of the ileum, then the afferent limb is intact in its entirety. However, a transection of the spinal cord caudal to T1 may result in a decreased or absent cutaneous response in the area caudal to the transection.

Pain

Whereas spinal reflexes test the LMN, assessments of conscious proprioception, voluntary motor functions, superficial pain sensation, and deep pain sensation are used to test UMNs. With compromise to the spinal cord, conscious proprioception is the first deficit observed, followed in order by voluntary motor function, superficial pain sensation, and deep pain sensation. Superficial pain sensation can be assessed by applying a noxious stimulus over a dermatome or cutaneous zone, which is an area of skin on the animal’s body surface that is innervated by a single nerve. A two-step pinch technique is recommended to test superficial pain sensation. First, a small area of skin is lightly tented using a hemostat. After a slight pause, a second, sharp skin pinch is applied. Intact superficial pain sensation is present if a reflex withdrawal occurs, and the UMN is intact if the animal demonstrates conscious recognition of the pain through an aversion response, vocalization, or both. Deep pain sensation is determined by placing a large hemostat or needle-holders across the digit just above the coronary band, and progressively pinching to stimulate the periosteum. As with the superficial pain sensation, a positive response is conscious recognition of the stimulus as evidenced by aversion, vocalization, or both. The assessment of deep pain sensation is important for prognosis for the recumbent small ruminant with neurologic disease, because deep pain is the last function to be lost with a severe spinal cord lesion.

Cerebral Disease

Nervous system disorders involving the cerebrum can be variable in severity and frequently are characterized by alterations in mental acuity, behavioral changes, seizures, and blindness. Diffuse or symmetric cerebral disease often does not affect the gait on flat surfaces, but gait can appear abnormal on ascending or descending slopes. Likewise, postural and proprioceptive reflexes are normal with diffuse cerebral disorders unless the affected animal is moved across slopes. In most animals with diffuse cerebral disease, spinal reflexes are normal. Of note, metabolic abnormalities are considered the most common cause of symmetric cerebral disease in ruminants.¹ Dehydration and acid-base and electrolyte abnormalities often result in depression in small ruminants.

With unilateral lesions located within the cerebrum, a majority of clinical signs will be observed contralateral to the lesion, with the exception of circling and head turn, which usually are in the direction of the lesion. Specific examples of clinical signs associated with asymmetric cerebral disease are contralateral hemiparesis, circling with the head turned toward the side of the lesion, contralateral facial sensation deficits, and presence of a contralateral menace deficit with normal palpebral reflexes and normal pupillary light reflexes.

Cerebellar Disease

The cerebellum functions by providing input data to motor areas of the cerebral cortex and brain stem, thus clinical signs of cerebellar dysfunction reflect failure of smooth, coordinated movements of the head, body, and limbs. Clinical cerebellar disease with lack of coordinating input results in ataxia, truncal sway, dysmetria, intention tremors, pupillary abnormalities, and vestibular signs. Sheep and goats with clinical cerebellar disease are characterized by normal mentation and abnormal gait; however, depression and stupor can be observed in kids and lambs with congenital cerebellar disease as a result of failure to nurse with subsequent dehydration and hypoglycemia (metabolic disease). In sheep and goats with cerebellar ataxia, strength is preserved in the front limbs and hindlimbs, and proprioceptive deficits are not observed. Strength of the limbs is assessed by applying pressure on the withers and the pelvis. Although diffuse cerebellar disease, which is more common in large domestic animals/livestock, causes ataxia of all four limbs, unilateral cerebellar lesions result in ipsilateral ataxia of front and rear limbs.

Brain Stem and Cranial Nerve Diseases

Sheep and goats with brain stem lesions may have normal or abnormal mentation. Because the ascending reticular activating system in the rostral brain stem frequently is affected by diseases of the brain stem, profound depression and stupor are common. Cranial nerve deficits in a small ruminant with abnormal mentation characterized as depression and stupor suggest that the lesion is localized to the brain stem. During the complete neurologic examination, the evaluation of cranial nerve function should receive much attention. Clinical signs associated with brain stem disease include cranial nerve deficits (as described previously), ipsilateral hemiparesis, coma, and stupor (with abnormalities of the ascending reticular activating system). In addition, respiratory and cardiovascular abnormalities may be noted, because the respiratory center is located in the caudal brain stem.

Spinal Cord and Peripheral Nerve Diseases

Clinical signs of spinal cord disease depend on the location of the disease within the spinal cord. In examining a small ruminant with suspected spinal cord or peripheral nerve disease, differentiating LMN disease from UMN disease is useful. As described previously, the UMNs are a group of neurons that do not physically exit the nervous system and provide stimulatory or inhibitory influences to the LMNs. The LMNs are composed of the peripheral nerves and the effector organs (primarily skeletal muscles). Clinical signs of UMN disease include proprioceptive deficits, weakness, and paralysis, but exaggerated reflexes and increased extensor tone also are observed. Lesions of the LMN result in clinical signs consisting of paresis or paralysis combined with absent or diminished spinal reflexes.

Peripheral nerve injuries are uncommon in sheep and goats but result in clinical signs referable to LMN disease, including paresis, paralysis, diminished or absent spinal reflexes, and muscle atrophy. The radial nerve and brachial plexus can be traumatized in the forelimb. In the hindlimb, the sciatic, peroneal, femoral, or obturator nerve can become damaged.

Radial nerve paralysis can result from fractures of ribs or the humerus or from avulsion of the brachial plexus, and the severity of clinical signs often is dependent on the location of traumatic injury. Damage to the radial nerve causes a lack of innervations to the triceps muscle group and the inability to extend the elbow joint. The more distal the injury on the limb, the less the animal’s gait is affected. Trauma to the distal radial nerve results in paralysis of the extensor muscles of the carpus and digits, and knuckling of the lower limb. A loss of sensory innervation to the dorsum of the leg below the elbow also may be evident. The animals may have scuffed or abnormally shaped hooves, as well as abrasions on the front of the fetlocks.

The femoral nerve provides innervations to the quadriceps muscle group. Animals with femoral nerve paralysis drag or carry the affected rear limb while hopping on the unaffected leg. Injury to this nerve can occur as a result of extreme extension of the hind limb or as a result of injection sites that have become infected. Sensation of medial skin surfaces often is preserved through the saphenous branch of the femoral nerve, because this branch separates from the rest of the femoral nerve proximally at the level of the iliopsoas muscle.

Obturator nerve paralysis occurs as a result of extreme abduction of the rear limb or as a lambing or kidding injury. When the nerve is damaged, the animal is unable to adduct its rear limb. Unilateral involvement of the obturator nerve is associated with gait abnormalities less frequently than is bilateral involvement. Radiographs of the pelvis are warranted to rule out pelvic fracture.

Sciatic (ischiadic) nerve paralysis can occur after pelvic or lumbosacral fractures. The nerve arises from spinal cord segments L6 to S2 and travels in the vertebral canal before its fibers exit. The sciatic nerve innervates the muscles that extend the hip and flex the stifle before dividing into the peroneal and tibial branches. The tibial nerve provides motor innervations to the gastrocnemius muscle, whereas the peroneal provides motor innervations to the extensors of the digits. The tibial and peroneal nerves also collect sensory input from the distal portion of the hindlimb. Whereas lumbosacral fractures usually cause bilateral hindlimb paresis or paralysis, damage to the proximal sciatic nerve, which can be a consequence of acetabular and femoral fractures, results in dysfunction of flexor muscles only. The extensor muscles of the stifle remain functional, allowing the animal to bear weight but not flex the stifle. The animal will exhibit a dropped hock, and the limb will be knuckled over. On testing, the animal’s flexor response is greatly inhibited, and with pinching of the medial claw, the animal flexes its hip without flexing the rest of the limb. This differential response occurs because the medial side of the limb still has intact sensory innervation through the saphenous branch of the femoral nerve. Many of these injuries resolve over time, but a poor prognosis is associated with the complete loss of deep pain.

The peroneal nerve supplies the muscles that flex the hock and extend the digits and provides cutaneous sensory innervation to the dorsal aspect of the foot and cranial surface of the hock and tibia. Improperly administered injections may injure this nerve, resulting in knuckling onto the dorsum of the fetlock and overextension of the hock. Animals appear to be able to compensate fairly well with this type of injury by extenuated flexing of the hip and extension of the stifle at walk. The flexor response is depressed when the dorsum of the fetlock is stimulated; however, if the sole of the hoof is stimulated, the animal flexes its leg but keeps the hock fixed.

Complete Blood Count and Serum Biochemistry Panel

Because metabolic disorders are the most frequent cause of symmetric cerebral dysfunction, the complete blood count and serum biochemistry panel should be performed to evaluate for the presence of hypocalcemia, hypoglycemia, acid-base disorders, electrolyte abnormalities, and inflammatory conditions. Anomalies observed during routine blood workup may be primary or secondary to the nervous system disorder.⁶ (see Appendix 2)

Cerebrospinal Fluid Analysis

CSF is located within the subarachnoid space; therefore diseases involving the CNS can lead to alterations in the normal composition of the CSF. The CSF can be collected from the atlantooccipital space but is more easily obtained at the lumbosacral site. General anesthesia or heavy sedation is required for atlantooccipital CSF collection, and anesthesia for neurologically impaired animals often is contraindicated. Positioning and restraint are critically important for successful collection of CSF (Figure 13-5, A). Sampling can be performed in the standing sheep or goat provided that restraint is sufficient to prevent lateral motion, or the animal can be sedated. If recumbent, most sheep or goats can be manually restrained in sternal recumbency. Ideally, the animal is positioned such that the hips are flexed and the pelvic limbs extended alongside the abdomen, with the pelvis kept straight and level. The skin over the lumbosacral space should be clipped and aseptically prepared. A palpable indentation should be felt at the lumbosacral space, and this site should be infiltrated with 2% lidocaine (0.5 mL administered subcutaneously [SC]) (Figure 13-5, B). A final scrub should be applied, and the clinician should don sterile gloves.

Figure 13-5 Collection of cerebrospinal fluid. A, Correct positioning of an animal for collection of cerebrospinal fluid from the lumbosacral space. The animal is placed in sternal recumbency, and both pelvic limbs are pulled cranially to arch the spinal column. B, The lumbosacral space is identified at the intersection of a line connecting the caudal aspects of the tuber coxae with the vertebral midline (between L6 and S1). C, Cerebrospinal fluid is collected by free catch or aspiration using a 5- to 10-mL syringe and immediately placed into tubes for analysis.

For lambs and kids weighing less than 30 kg, a 20- or 21-gauge, 1-inch needle can be used; an 18- or 20-gauge, 1.5-inch needle can be used for adult sheep and goats. A disposable needle or a stylet-type spinal needle can be used. The needle should be inserted on midline halfway between the last palpable lumbar dorsal spinous process and the first palpable sacral dorsal spinous process. The needle should be placed perpendicular to the spine from the lateral view and straight up and down as viewed from the back of the animal. If bone is encountered, the needle should be redirected either cranially or caudally. The needle is advanced until a slight “pop” is felt as the needle passes through both the interarcuate ligament and the subarachnoid membrane. The animal may move or jump slightly when the needle punctures the dura mater, or the tail and anus may reflexively contract. The clinician can periodically remove the stylet to check for presence of CSF in the hub of the needle. Approximately 1 mL of fluid/5 kg of body weight can be safely removed, but only 1 to 2 mL is necessary for cytologic evaluation. Gently and slowly aspirating CSF or allowing it to flow freely from the needle prevents excessive movement and blood contamination (Figure 13-5, C). The CSF samples should be placed in ethylenediamine tetraacetic acid (EDTA) for cytologic analysis and in a serum separator tube for culture. For biochemical analysis, CSF should be placed in serum separator or lithium heparin tubes. Cytologic evaluation of CSF should be performed rapidly, ideally within 60 minutes of collection. If this is not possible, the CSF can be mixed with an equal volume of 40% ethanol to preserve the cells.

Once collected, CSF can be evaluated for gross appearance, cytology, protein concentration, biochemical composition, and presence of bacteria. Normal CSF is clear and colorless. Red discoloration indicates presence of blood in the CSF, and the hemorrhage may be iatrogenic (Figure 13-6, A) or the result of the collection or from previous hemorrhage within the CSF. In general, blood from a previous hemorrhage is evenly mixed with the CSF and often does not clot, as opposed to iatrogenic hemorrhage during collection, in which the red discoloration may lessen as additional fluid is collected and the CSF will clot. Xanthochromia is orange or yellow discoloration of the CSF, and this finding can be observed for up to 10 days after occurrence of bleeding within the CSF. Turbid CSF usually indicates a high white blood cell count, as can occur with bacterial meningitis. The total nucleated cell and differential counts should be performed to assist with an etiologic diagnosis. Normal CSF contains less than 10 nucleated cells/μL, with a majority of cells being mononuclear (see Appendix II , Table F). Bacterial infections of the nervous system usually are characterized by a neutrophilic pleocytosis (Figure 13-6, B), with the exception of listeriosis in small ruminants where mononuclear pleocytosis (Figure 13-6, C) is usually present. Mononuclear pleocytosis can also be observed with viral encephalitides and PEM. Cerebrospinal nematodiasis, secondary to aberrant migration of nematode parasites, often results in marked elevations of eosinophils, which may be the predominant CSF leukocyte in affected animals (Figure 13-6, D). Normal protein concentrations in CSF are considerably lower than in blood. CSF protein concentration of healthy sheep is less than 40 mg of protein/dL and that of healthy goats less than 15 mg of protein/dL. CSF glucose content generally is low compared with that in the peripheral blood. Glucose concentrations normally are 80% of the value in peripheral blood, and decreased concentrations are detected in animals with bacterial meningoencephalitis as a consequence of bacterial glucose consumption.

Figure 13-6 A, Iatrogenic blood contamination during collection of a cerebrospinal fluid (CSF) sample. This can be differentiated from histopathologic evidence of disease by the presence of red and white blood cells in ratios similar to those in blood samples and the presence of thrombocytes. Similar findings are detected in cases of traumatic injury occurring within 30 minutes of CSF collection. B-D, CSF cytology for different neurologic diseases. B, Findings in a goat with streptococcal meningitis. A majority of nucleated cells are neutrophils that show degenerative changes. The identification of many small cocci in pairs or short chains suggests streptococcal meningitis. C, Findings in a goat with listeriosis include a mixed-cell mononuclear pleocytosis, with a predominance of mononuclear cells, small lymphocytes, and presence of neutrophils. D, Findings in a goat with cerebrospinal nematodiasis include predominance of eosinophils, which is seen in cases of aberrant spinal migration by Parelaphostrongylus tenuis.

(Courtesy Dr. Elizabeth Spangler, Auburn, Alabama.)

Medical Imaging

After a lesion has been localized within the CNS, plain survey films may be helpful to identify luxations of the vertebral column, osteomyelitis, or fractures of the pelvis. Survey radiographs of the skull can be used to diagnose fractures or assess involvement of the tympanic bulla in cases of otitis. Radiographic techniques used in medium to large dogs are applicable in sheep and goats. For UMN disease of the forebrain, brain stem, or cerebellum, several diagnostic imaging procedures can be performed. The structural integrity of the UMN anatomy can be evaluated by the use of computed tomography (CT) and magnetic resonance imaging (MRI). Myelography can be used to identify compressive or expansive lesions in the spinal cord. Electromyography also can be used to determine whether specific neurons are responsible for neuromuscular disease by assessing the electrical activity of the muscle after a neuron is stimulated. Electroencephalography can be used to assess the electrical activity in various parts of the brain. It is used primarily in cases of presumed neurologic disease manifested by seizures, narcolepsy, and encephalopathy.

Etiology and Pathophysiology

In meningitis, one or more of the three layers (dura mater, arachnoid, and pia mater) covering the CNS are inflamed, and involvement of adjacent structures (CNS or spinal cord) is common. Meningitis and meningoencephalitis may result from many different disorders but principally follow extension of local processes or hematogenous dissemination.¹ Infections extending into meninges and nervous tissues may be caused by surgical procedures such as dehorning and tail docking, thermal osteonecrosis after cauterization for dehorning, sinusitis, otitis interna, and skull fractures. Bacteremia associated with pneumonia, omphalophlebitis, mastitis, endocarditis, or other septic processes also may cause meningoencephalitis. Hematogenous infection is especially common in neonatal septicemia arising with failure of passive transfer. Any of several bacterial pathogens may be involved in the disease. In neonatal meningoencephalitis, Escherichia coli, Pasteurella multocida, Streptococcus spp., Staphylococcus spp., and Arcanobacterium pyogenes have been reported and invasion of the CNS may depend on various virulence factors.¹ Goat kids affected by polyarthritis and pleuropneumonitis caused by Mycoplasma mycoides ssp. mycoides, may develop meningoencephalitis.² Pseudomonas aeruginosa may cause septicemia and meningitis in goats secondary to mastitis.³ In the CSF, host immune defense mechanisms provide only limited protection because antibody and complement concentrations of CSF are low.^1,3 Bacterial and inflammatory insults may potentially lead to congestion and infarction of arachnoidal or subependymal veins, decreased CSF absorption, intraventricular hypertension, and necrosis of nerve cells.^1,3

Clinical Signs

Affected animals often are severely lethargic and depressed but may be hyperexcitable. In cases associated with neonatal septicemia, diarrhea and dysthermia are common. Clinical examination reveals hyperesthesia, a stiff and extended neck, and pain induced by movement of the head and neck. Passive manipulation of the neck may result in sudden tonic extension and rigidity of the limbs.³ Loss of cranial nerve functions may be recognizable as nystagmus, strabismus, and facial palsy.^1,3 Progression of the disease leads to decreased sensory functions, propulsive walking, seizures, and coma.

Diagnosis

Meningitis should be suspected on the basis of clinical signs, especially in neonates with indications of failure of passive transfer and sepsis. To differentiate the disease from metabolic abnormalities, serum electrolytes and glucose should be evaluated. Confirmation of meningitis is based on CSF analysis or postmortem examination. Marked increases in protein concentration, total leukocyte count, and proportion of neutrophils in CSF samples are characteristic of bacterial meningitis. CSF glucose concentration is below that in serum, reflecting bacterial consumption of glucose in the CSF.¹ Xanthochromia and free or intracellular bacteria also may be present. Bacteriologic culture and sensitivity testing should be attempted if therapy is intended.

Treatment

Case-fatality rates in farm animals with bacterial meningitis are high, owing in part to late recognition of the disease. Therapy is based on aggressive and prolonged administration of antibiotics, supplemented with antiinflammatory drugs, and anticonvulsive therapy as needed. The choice of antibiotic should be guided by an initial Gram stain of CSF or by culture and sensitivity testing. Preferably, antibiotic therapy should be administered by the intravenous route to attain maximum peak blood and CSF concentrations.³ The use of a third-generation cephalosporin (e.g., ceftiofur, 1 to 5 mg/kg given intravenously [IV] one to three times daily) has been recommended, and a combination of antibiotics may be used (e.g., a β-lactam plus a trimethoprim-sulfonamide agent).¹ These recommended regimens are empirical, and other intravenous antibiotics may be used. The choice of antiinflammatory agent has not been evaluated in farm animals, but nonsteroidal antiinflammatory drugs are thought to be beneficial. Seizures should be controlled using diazepam (0.01 to 0.2 mg/kg every 30 minutes).¹ In neonates with failure of passive transfer, plasma should be administered (15 to 25 mL/kg IV).

Prevention

Timely administration of adequate colostrum is the most important method of preventing bacterial meningitis in neonates. Proper sanitation should be provided during surgical procedures, and dehorning of goats should be performed with attention to hygiene, analgesia, and limited thermal cauterization. When predisposing conditions are recognized, early therapy may prevent extension to the nervous system.

Etiology and Pathophysiology

Clostridium perfringens types C and D (and possibly type E) are important pathogens of sheep and goats that cause infection manifesting primarily as enteric disease and peracute death, with associated pathologic changes in the nervous system. The organisms are ubiquitous in the environment and feces of farm animals. C. perfringens type C produces α and β toxins, which are not degraded in young animals (less than 10 days of age), owing to low intestinal concentrations of proteolytic enzymes. The β toxin induces ion-conductive channels in membranes of excitable cells, leading to irreversible depolarization and neurologic disease.¹ Disease associated with C. perfringens type D usually is seen in young animals consuming overly plentiful diets, allowing clostridial overgrowth and production of α and ε toxins in the small intestine; however, neonatal lambs in unvaccinated flocks also may be affected.² Activation of ε toxin from its precursor is induced by enteric proteases. The active toxin causes disruption of tight junctions of vascular endothelial cells and vasogenic edema in different organs, including brain, lungs, and kidneys.³ The systemic effects of ε toxin may be facilitated by intestinal activity of β₂ toxins⁴ (see Chapters 12 and 16).

Clinical Signs

The duration of disease is limited to a few hours, and clinical signs preceding death may not be observed. Abdominal discomfort and signs of colic, such as teeth-grinding and vocalization, may be noted. Hemorrhagic diarrhea may be present in some cases and is regularly observed in goats with type D enterotoxemia.⁵ Neurologic signs include depression, tetany, opisthotonos, convulsions, and coma.^5,6 In type D enterotoxemia, focal encephalomalacia may develop, which is characterized by aimless wandering, blindness, and walking into inanimate objects.⁵

Diagnosis

The short duration of clinical disease precludes use of most antemortem diagnostic modalities. Identification of large numbers of clostridia in fecal smears may be suggestive. At postmortem examination, the presence of enteritis with numerous clostridia in the upper small intestine and, in cases of type D enterotoxemia, edematous tissues supports the diagnosis. Toxin assays may be performed using polymerase chain reaction (PCR) techniques, enzyme-linked immunoassay (ELISA), or mouse inoculation assays.

Treatment

Affected animals usually die before systemic antibiotics (affording coverage of the gram-positive spectrum) and fluid therapy could have any effect. Administration of C and D antitoxin probably is more beneficial to prevent disease in at-risk herdmates than as a treatment of moribund animals.⁶

Prevention

Routine vaccination of sheep and goats against C. perfringens C and D is paramount. Regular boosters should be administered to all breeding stock. Administration of C and D antitoxin shortly after birth should provide protection to lambs and kids of unvaccinated dams for approximately 2 weeks.⁶

Etiology and Pathophysiology

In small ruminants, lentiviral leukoencephalomyelitis is caused by caprine arthritis-encephalitis virus (CAEV) in goats and either maedi visna virus (MVV) or, less commonly, ovine progressive pneumonia virus (OPPV) in sheep. In North America, OPPV usually is associated with respiratory disease; however, neurologic disease in sheep also has been described.¹ Small ruminant lentiviruses (SLRVs) belong to the genus Lentivirus, family Retroviridae, and have a worldwide distribution, although prevalence varies widely among herds.² While differing in certain clinical aspects, SLRVs share many virologic, epidemiologic, and pathophysiologic features. The nomenclature may indicate SLRVs to be species-specific, but natural infection of sheep with CAEV and goats with MVV is possible, and crossing of species barriers is not uncommon.^3,4

The SRLVs are enveloped RNA viruses that, on infection of host cells, transcribe their genome into a double-stranded DNA that is inserted into the host’s genome, resulting in life-long infection.² Monocytes and macrophages are the primary cells infected by SRLVs, and invasion of target organs is believed to be in macrophages.^5,6 Transmission of SRLVs is primarily horizontal. Infection of lambs or kids by ingestion of colostrum and milk from infected dams is a main route of transmission. Horizontal transmission by the respiratory route may cause infections in older animals. In utero infections are possible, but their relative importance is unclear.^2,6 Inflammatory changes associated with SRLV infection may occur in the CNS, lungs, udder, joints, lymph nodes, and blood vessels, potentially resulting in progressive dysfunction of the affected organ(s).

Clinical Signs

Clinical signs associated with SLRV infection are slowly progressive and initially nonspecific. Neurologic disease (leukoencephalomyelitis) is a relatively rare form of infection in comparison with respiratory disease in adult sheep and arthritis in adult goats.^1,7 In sheep, clinical signs usually occur in animals older than 1 to 3 years of age; however, clinical disease has been reported in younger sheep.^2,7,8 Initial signs include weight loss, hindlimb weakness, and abnormal stance with progression to ascending paresis and paralysis. Death occurs several months after initial signs are noticed and may be preceded by neurologic signs localized to the head, such as lip twitching, nystagmus, and blindness.

The clinical course of neurologic disease is more rapid in goats than in sheep. Affected goats usually are 1 to 5 months of age; however, adult goats may be affected.⁶ Clinical signs include a short, choppy gait and unilateral or bilateral posterior paresis and ataxia. Initially, the mentation appears to be unaffected, and animals eat, drink, or nurse normally. Progression of the disease leads to tetraparesis, and head tilt, circling, torticollis, opisthotonos, and blindness may develop.

Diagnosis

Neurologic disorders associated with SRLV infection are relatively rare, and other conditions should be considered in the workup. Presence of interstitial pneumonia may suggest SRLV infection, but clinical signs of respiratory disease often are absent. CSF analysis may reveal increased protein concentrations and mononuclear pleocytosis. Identification of SRLV antibodies is performed by AGID or ELISA techniques. The presence of antibodies in serum implies infection but not disease causation. PCR techniques may be used to detect SLRV infections before antibodies are produced.⁹ Postmortem diagnosis is based on identification of a nonsuppurative demyelinating encephalomyelitis and lymphocytic infiltration of the CNS.

Treatment

Effective therapies to slow or halt the disease do not exist, and affected animals should be humanely euthanized (see Chapter 16).

Prevention

Successful vaccination strategies suitable for field conditions are not available.¹⁰ Eradication of SRLVs from a herd is possible with use of test-and-slaughter programs, which may not be feasible in herds with high prevalence rates. Control measures should be chosen according to herd prevalence of infection.¹⁰ In herds with mixed populations of sheep and goats, cross-specific transmission is possible, and measures for control of both CAEV and MVV-OPPV must be instituted.¹¹

Prevention is based on identification of seropositive animals and segregation of infected from uninfected animals, removal of infected animals, and continued serologic testing. Prevention of perinatal transmission is achieved by separation of lambs and kids from their dam immediately after birth, and by cleaning uterine and placental fluids off newborns.² Because consumption of colostrum and milk from infected dams is an important method of transmission, these products should be harvested only from uninfected dams. Alternatively, heating of colostrum to 56° C (130 F) for 60 minutes decreases the load of infectious virus and appears to decrease immunoglobin concentrations only minimally.^12,13 Use of pasteurized milk or milk replacers is recommended in kid- and lamb-raising protocols. Iatrogenic transmission by needles, tattooing equipment, and other surgical instruments must be prevented through use of disposable instruments or sterilization² (see Chapters 11 and 16).