PHYSICAL EXAMINATION

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ASSESSMENT OF THE NERVOUS SYSTEM Todd C. Holbrook, DVM, and Susan L. White, DVM, MS

The goal of the neurologic examination is to localize the lesion(s) as accurately as possible to aid in forming the list of differential diagnoses, devising appropriate therapy, and evaluating the prognosis. To diagnose neurologic disease accurately, it is essential that the examiner is well versed in neuroanatomy and is familiar with the specific diseases that can affect various sites in the neurologic system of the species being examined. Clinicians should be systematic and should carefully examine the entire animal when possible. If an obvious primary lesion is present and this problem is concentrated on first, other important abnormalities in the neurologic system may be overlooked. Cattle are sometimes difficult to examine because of their size and lack of cooperation (especially beef breeds), whereas in small ruminants, certain portions of the examination such as proprioception assessment can be performed with greater accuracy owing to their smaller size. This article describes our approach to the ruminant neurologic examination. Specific diseases affecting the nervous system of ruminants are discussed elsewhere and are not addressed in this article. Selected references for further reading are listed at the end of the article. SIGNALMENT AND HISTORY

An accurate history along with the animal's signalment, including gestational and lactational stage when appropriate, are invaluable in assisting the clinician's examination. Many neurologic manifestations of disease in ruminants vary in incidence and clinical signs among the different species, ages, and gender affected. The signalment alone may allow the clinician to form an initial list of differential diagnoses. For example, nervous ketosis and polioencephalomalacia are two neurologic diseases with very different and, usually, specific signalments. Historical information that should be obtained includes the time and nature of

From the Department of Large Animal Medicine, University of Georgia College of Veterinary Medicine, Athens, Georgia

VETERINARY CLINICS OF NORTH AMERICA: FOOD ANIMAL PRACTICE VOLUME 8 • NUMBER 2 • JULY 1992

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onset of neurologic signs and the clinical progression. Often, the owner has given some type of therapy to the animal prior to veterinary examination, and the progression of clinical signs in relation to therapy may assist in your evaluation. Congenital neurologic disease usually is apparent at birth, and signs may progress over time. Infectious causes can be acute or chronic in onset but usually are progressive. Traumatic lesions typically are acute in onset and may stabilize or improve over time. It is also important to note if signs indicative of multifocal disease were present historically and their progression over time. Signs of depression that are followed by a head tilt and ear droop suggest a single lesion in the brainstem. By contrast, an animal with a head tilt and no depression that subsequently develops hindlimb dysfunction has a multifocal disease affecting peripheral cranial nerve eight and the spinal cord. Information on general management practices, including nutrition, vaccination, deworming programs and stocking rate, is obtained. It is important to ascertain the condition of the animal's environment by direct inspection or from the history. Specific questions should be tailored to relevant cases, such as access to crank-case oil, old batteries, linoleum, or lead-based paint in suspected cases of lead toxicity. The number of animals affected in the group and history of any other herd problems may be beneficial in forming the differential diagnoses. An example that exemplifies the importance of herd history is the occurrence of cerebellar disease in calves infected in utero with bovine viral diarrhea virus. Members of the herd may have shown signs of bovine viral diarrhea, such as respiratory disease, diarrhea, oral ulceration, and laminitis, several months previously. The animal's intended use and economic value also are important in devising economical treatment options and evaluating the prognosis. After obtaining the history and performing a thorough physical examination, the neurologic examination is initiated.

THE NEUROLOGIC EXAMINATION

The precise manner in which the neurologic system is examined varies with the clinician's personal preferences. Initially, the animal's general appearance and any obvious neurologic abnormalities are noted from a distance. This is followed by a thorough systematic neurologic evaluation of the animal. Starting at the head of the animal, the entire animal is examined. After evaluating the head and ocular structures, the animal's trunk and limbs are briefly assessed, followed by gait evaluation. In addition, spinal reflexes and postural reactions are assessed when possible.

Observation

The neurologic examination should begin from a distance as the clinician initially evaluates the animal's general mental status, behavior, body symmetry, and gait. By evaluating the animal's mental awareness and responsiveness to stimuli, the lesion is first localized as being intracranial (cerebral, brainstem, cerebellar, and ophthalmic), or extracranial (spinal cord or peripheral nerve). Animals with only extracranial neurologic disease have normal mentation. Gait abnormalities can be caused by disease affecting the cerebellum, brainstem, spinal cord, or peripheral motor nerves. The clinical signs characterizing the gait abnormality are used to localize the lesion to one of these areas.

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Brain

Intracranial lesions usually cause an abnormal mental status if the cerebral cortex or brainstem is affected. Difficulty arises in this classification when secondary disease processes such as dehydration cause depression. Animals recumbent from spinal cord disease alone are usually bright and alert and continue to eat and drink. The intracranial lesions can be divided into those affecting the cerebrum, brainstem, and cerebellum. Depending on the nature and location of intracranial lesions, a variety of clinical signs can result, including, but not limited to depression, stupor, coma, seizures, abnormal behavior, blindness, nystagmus, strabismus, facial asymmetry, head tilt, circling, intention tremors, and ataxia. Cerebral Disease

Cerebral disease is common in ruminants, especially in the young. Cerebral disease of any significant degree invariably causes some change in mental status. It often is prudent to ask the owner his or her interpretation of the animal's behavior, because subtle changes may be more apparent to them. The degree of depression (Fig. 1) caused by cerebral disease can vary; however, coma should not occur with cerebral disease alone. Lesions affecting the cerebrum can result from a variety of causes including metabolic, toxic, infectious, traumatic, congenital, and neoplastic. The signs may be caused by diffuse, localized, or space-occupying lesions in the cerebrum. Lesions affecting only one cerebral hemisphere may cause aimless circling or leaning toward the abnormal side, without signs of vestibular disease. Other signs of cerebral disease include blindness, head pressing, hyperexcitability, aggressiveness, abnormal vocalization, and seizures. The animal's gait is not affected by cerebral disease alone. Abnormal postural reactions are present in these cases, but unfortunately can only be assessed in calves and small ruminants. Seizures result from the sudden uncontrolled firing of nerve cells in the cerebral cortex and may be manifested by localized or generalized signs. Seizures should be

Figure 1. This cow is exhibiting depression due to diffuse cortical disease.

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suspected when the animal has repetitive episodes of unusual activity, including changes in muscular tone or movement, consciousness, or behavior. With this in mind, it should be noted that localized seizures can occur involving muscle groups of the face or body, during which the animal remains standing. In comparison, generalized seizures usually cause involuntary bouts of muscular activity in which the animal is recumbent, has exaggerated paddling limb movements, or thrashes. Cerebellar Disease

The cerebellum simplistically has the regulatory function of coordinating various portions of the nervous system, including the vestibular apparatus, the nerves controlling skeletal muscles of the body, and the cerebrum. By doing so, it affects muscle tone, gait, head and body posture, ocular position and movement, and balance. Abnormalities of this portion of the brain alone do not cause depression. Clinical signs (Fig. 2) seen with diffuse involvement include wide based stance and ataxia without weakness or deficits in conscious proprioception (position sense). Ataxia simply means uncoordinated gait and can be caused by other problems in addition to those discussed in this section, including vestibular and spinal cord disease. An ataxic gait caused by cerebellar disease usually is represented by hypermetria. Hypermetria is most easily recognized in the forelimbs as an accentuated upward phase of movement as the limb is voluntarily advanced. Truncal ataxia results in pronounced swaying of the body as the animal walks. Nystagmus (involuntary rhythmical eye movements) may result from the loss of cerebellar influence on the vestibular system and extraocular muscles. The abnormal ocular motion of cerebellar disease is usually not as rhythmic and consistent as that seen with vestibular disease. Intention tremors, often recognized as jerking movements of the head as the animal voluntarily moves its head toward an object such as food, may be present. Loss of the menace response can occur bilaterally or

Figure 2. This calf had diffuse cerebellar disease. Note the head position and wide-based

stance.

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ipsilaterally with diffuse or localized cerebellar disease, respectively. The abnormal menace response in this instance occurs in the absence of other nerve deficits (i.e. vision), and may be due to altered influence on the cerebrum. Opisthotonus can be seen with severe lesions of the rostral cerebellum. These animals are recumbent with the head and neck in hyperextension, the forelimbs rigid, and the hindlimbs flexed. Brainstem Disease Depression

Depression caused by brainstem disease can vary from moderate to marked, and includes stupor and coma. The degree of depression is most severe with damage to the reticular activating system (RAS) in the rostral brainstem. Depression of brainstem origin often is accompanied by neurologic deficits of one or more cranial nerves (eNs), ataxia, and, sometimes, abnormal respiratory patterns due to damage to the respiratory centers in the medulla oblongata. Ataxia resulting from brains tern and spinal cord lesions and their differentiation are discussed in the section on assessment of gait. Cranial Nerves

Each pair of eNs has their respective nuclei in the brainstem, and the function of each nerve should be evaluated when possible. The eNs are numbered from I to XII, and these numbers roughly correspond to the locations of the nerves as they exit the brains tern from rostral to caudal. Practically speaking, as long as your examination routinely evaluates eNs II to X and XII, (not necessarily in this order), the majority of eN deficits will be noted. In the authors' experience, deficits of eNs I and XI are extremely rare, and these nerves are difficult to evaluate. The eN examination is important to further localize the lesion within the brainstem. It also is important to ascertain if the disease is unilateral, bilateral, or multifocal to aid in the differential diagnosis. Peripheral eN disease is discussed later. The function of the nerves are examined in a logical manner, not in order of their numbering. See Table 1 for a summary of the eNs and signs of their respective dysfunction.

Table 1. CRANIAL NERVES (CN) Number

Nerve

CNI CN II CN III CNIV CN V

Olfactory OptiC Oculomotor Trochlear Trigeminal

CN VI

Abducens

CN VII CN VIII CNIX CN X CN XI CN XII

Facial Vestibulocochlear Glossopharyngeal Vagus Accessory Hypoglossal

Results of Nerve Dysfunction Loss of smell Loss of vision Mydriasis, ventrolateral strabismus Dorsomedial strabismus Loss of facial sensation, and function of the muscles of mastication Medial strabismus, inability to retract the eyeball within the orbit Loss of motor function to muscles of facial expression Hearing loss (cochlear), nystagmus, head tilt (vestibular) Dysphagia Dysphagia Dysphagia Tongue paresis, tongue atrophy

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Facial Symmetry and Position of the Head and Eyes (Cranial Nerve 111- VIII)

First the animal's facial symmetry, ear position, head posture, and ocular position are assessed. With these observations, CNs III through VIII can be briefly evaluated. Facial symmetry and ear position can be altered by disease of CN V and VII, respectively. The facial nerve (CN VII) supplies innervation to the muscles of facial expression; deficits usually can be noted by ear drooping or paresis on the ipsilateral side (Fig. 3). This obviously can be influenced by ear conformation. Brahman cattle, their cross-breeds, and Nubian goats naturally have drooping ears, and CN VII deficits in these breeds may be subtle and more easily noted by assessing voluntary ear movement and ear muscle tone, in addition to symmetry. Other signs of CN VII dysfunction in ruminants are deviation of the muzzle (toward the normal side), lip droop on the ipsilateral side, and eyelid paresis or paralysis on the affected side. Muzzle deviation and lip drooping are more obvious in small ruminants owing to their facial anatomy; cattle tend to have a more flattened, firm muzzle. Retention of food in the cheek can indicate CN VII dysfunction. Often, exposure keratitis is present in the eye on the affected side owing to loss of palpebral function and subsequent corneal epithelial damage from exposure and desiccation. Facial asymmetry from atrophy of the masseter muscles may occur with long-standing trigeminal nerve damage. Cranial nerve V is responsible for the motor function of the muscles of mastication. Bilateral dysfunction of this nerve causes the lower jaw to be dropped. These animals may have difficulty prehend-

Figure 3. This goat has unilateral cranial nerve deficits secondary to listeriosis. Note the ear droop and muzzle deviation.

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ing food and may drool saliva. Bilateral facial atrophy may not be visually appreciated if the atrophy is symmetrical. Palpation of the area, however, will reveal the muscle loss as the underlying bony structures are easily defined. Unilateral dysfunction may be difficult to appreciate until atrophy occurs, because motor function is adequate for mastication. By placing several fingers on the animal's dental pad and lower incisors and attempting to open the mouth, the tone of the masseter muscles can be assessed. Because the trigeminal nerve (eN V) also supplies sensory innervation to the face, a blunt instrument can be used to touch the face, inside the nasal cavity, and ear canals (bilaterally) to test this nerve function. If not severely depressed, most animals will shake their head and attempt to move away from such stimuli. The more stoic or depressed cow may react to more vigorous pinching of these areas with a hemostat. Head and Ocular Position

The animal's general posture and head position may reveal evidence of neurologic disease. Sick ruminants, especially cattle, may lie recumbent with the neck curved laterally and caudally, laying their head against their sides. This tends to be a nonspecific sign of disease and does not necessarily imply neurologic dysfunction. Abnormal head positioning can result from disease of the cerebrum, cerebellum, and vestibular system (Fig. 4). With few exceptions, regardless of intracranial or extracranial damage, the head tilt is toward the side of the lesion and can vary from barely noticeable to severe head tilt and inability to lie stemally. The head tilt and abnormal posture tend to be worse with vestibular disturbances as compared to cerebral causes. Some severely affected animals, especially small ruminants, may lie in various positions, including dorsal recumbency, with their entire body twisted and curved toward the side of the lesion. It is important to remember the normal ocular position in ruminants and the response to head movement. As the nose is forced dorsally, the normal response is for the eyes to remain in a constant horizontal plane; thus, the animal appears to

Figure 4. This goat has peripheral vestibular disease secondary to otitis. Note the marked head tilt.

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look downward. This response is most marked in cattle and sheep. Goats tend to have transient eye movement downward as the nose is raised, followed by the eye being returned to the normal position. When the head is moved laterally, the eyes lag behind head movement, and normal horizontal vestibular nystagmus is created. The fast phase of ocular movement is always toward the direction of head movement. Normal vertical nystagmus can be created in small ruminants; however, it is more difficult to evaluate, especially if the animal resists head movement. Normal nystagmus requires function of all three CNs responsible for ocular positioning (III, IV, and VI), the vestibular system, and connections between their nuclei. Vestibular Disease

Other signs that can be seen in vestibular disease are a wide-based stance, deficits in proprioception, circling toward the side of the lesion, and nystagmus. Cranial nerve VIII is an integral part of the vestibular apparatus, and vestibular disease results in an abnormal head and ocular position. It is very clinically important (in regard to prognosis) to determine if the cause of vestibular disease is due to damage within the cranium, (CN VIII nucleus in the brainstem) or to CN VIII damage outside the cranial vault. The presence of a wide-based stance, circling, and nystagmus only indicates vestibular disease; it does not allow differentiation of central and peripheral lesions. The character of the nystagmus and evidence of brainstem disease will assist in differentiation. As central vestibular disease by definition affects the brainstem, signs of depression or other CN deficits with vestibular disease suggest an intracranial cause. In animals that remain ambulatory, abnormal proprioception (position sense), and abnormal postural reactions can be noted in central vestibular disease. These abnormalities occur in central vestibular disease in both the fore- and hindlimbs and are caused by brainstem damage resulting in the loss of nerve tracts carrying sensory information of limb position. Abnormal nystagmus is a rhythmic back-and-forth movement of the eye(s) within the socket that usually is present in diseases of the vestibular system. Usually, both eyes move in the same direction and there tends to be a fast and slow phase to the movement, although they can be equal in timing. There can be horizontal, vertical, or rotary nystagmus. Horizontal nystagmus is most commonly noted. Horizontal and rotary nystagmus can be present with either central or peripheral lesions. Vertical nystagmus, however, is very suggestive of central vestibular disease. As the eye movement is examined, the animal's head should be moved slowly in all directions, including flexion and extension. With central vestibular disease, the nystagmus may change direction as the orientation of the head is changed. The direction of the fast phase of ocular movement is always away from the side. with the vestibular lesion in peripheral disease and does not change direction as the head position is manipulated. Animals tend to adjust to vestibular disturbances; therefore, the clinical signs may be more severe in acute disease, and nystagmus may improve or disappear over time. Signs of vestibular disease may be worsened in these instances if the animal is blindfolded or placed in a stall with no natural horizons. Ocular deviation also can occur with vestibular disease; however, no extraocular muscle de nervation exists, and changing the head position reveals that the ocular deviation is not constant. Strabismus

Persistent ocular deviation within the orbit indicates cranial nerve dysfunction. Cranial nerves involved in ocular positioning and movement are the oculo-

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motor nerve (CN III), trochlear nerve (CN IV), and abducens nerve (CN VI). These three nerves are influenced by connections with the cerebellum and vestibular system. True strabismus or ocular malposition is constant in its relation to the bony orbit regardless of head position. Cerebellar or vestibular disease can result in ventrolateral strabismus, but the eyeball position may be changed by movement of the head. The oculomotor nerve innervates the dorsal, ventral, and medial rectus muscles and the ventral oblique muscles of the eye. Lesions of this nucleus should lead to ipsilateral stable ventrolateral strabismus. Parasympathetic fibers from this nerve also innervate the constrictor muscles of the pupil; thus, lesions here should also produce mydriasis. The troclear nerve innervates the dorsal oblique ocular muscles, and this lesion causes constant dorsomedial strabismus. As the trochlear nerve crosses midline before exiting the brains tern, the lesion can cause ipsilateral, contralateral, or bilateral dorsomedial strabismus depending on its location. Bilateral dorsomedial strabismus is commonly present in ruminants with polioencephalomalacia (Fig. 5). Lesions of the abducens nerve (CN VI) result in constant medial strabismus, and loss of the ability to retract the eyeball on the ipsilateral side as this nerve innervates the retractor bulbi and lateral rectus muscles. To test for eyeball retraction, simply apply gentle pressure on the eyeball over the closed eyelid. Visual Assessment and Ocular Examination

The next component of the CN examination is more efficient if performed in conjunction with the ophthalmic examination. This portion of the examination evaluates the function of CN II (optic n.) and the visual pathway, the sensory branch of CN V (trigeminal n.), and again evaluates the function of the facial nerve (CN VII). The three basic tests used are the palpebral reflex, menace response, and evaluation of pupillary light reflexes. Figures 6 and 7 depict the neuroanatomy of the visual and pupillary light pathways. Palpebral Reflex

The facial nerve (CN VII) supplies innervation to the muscles of facial expression and the trigeminal supplies sensation to the face as well as motor function to

Figure 5. This ewe has dorsomedial strabismus, indicating a trochlear nerve lesion. Her condition responded favorably to thiamine treatment (polioencephalomalacia).

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Figure 6. Anatomic pathway of

the menace response. 1 = retina; 2 = optic nerve; 3 = optic chiasm; 4 = optic tract; 5 = lateral geniculate nucleus; 6 = optic radiation; 7 = visual cortex; 8 = internal capsule, association fiber; 9 = motor cortex; 10 = internal capsule, projection fiber; 11 = crus cerebri; 12 = longitudinal fibers of pons; 13 = pontine nucleus; 14 = transverse fibers of pons and middle cerebellar peduncle; 15 = cerebellar cortex; 16 = efferent cerebellar pathway; 17 = facial nuclei; 18 = facial muscles - orbicularis oculi.

Figure 7. Anatomic pathway of the pupillary light

reflex. 1 = retina; 2 = optic nerve; 3 = optic chiasm; 4 = optic tract; 5 = pretectal nucleus; 6 = oculomotor nucleus; 7 = oculomotor nerve; 8 = ciliary ganglion; 9 = constrictor muscles of pupil.

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the muscles of mastication. When the periocular area is touched, the normal animal will close the palpebral fissure. If the palpebral reflex is performed and no response is seen, the animal may have a lesion in either the facial nerve or nucleus, in the trigeminal nerve or nucleus, or both (on the affected side). To rule out eN v sensory dysfunction, additional testing of facial sensation should be performed. If the animal exhibits a pain response to pinching the face with hemostats but does not have a palpebral reflex, the lesion is in the facial nerve or nucleus. In addition to having generalized decreased reactions to stimuli, very depressed ruminants may have an abnormal palpebral reflex and menace response without specific damage to the neurologic pathways involved. Menace Response

The optic nerve (eN II) and visual pathway are evaluated along with eN VII (facial n.) by the menace response. The afferent (ingoing) visual pathway evaluated by the menace response includes the ipsilateral retina, optic nerve, optic chiasm, optic tract, lateral geniculate nucleus in the thalamus, optic radiation, and contralateral occipital visual cortex. The efferent (outgoing) pathway responsible for closure of the eyelid is the contralateral occiptal visual cortex and the ipsilateral facial nucleus and nerve. The hand is moved quickly toward the animal's eye and the response is noted. Care should be taken not to touch the periocular structures or create air currents that would cause the animal to react to the tactile stimulation received by the sensory branches of the trigeminal nerve (palpebral reflex). The normal animal will react by blinking or moving the head and neck away from the gesture. It should be noted that the menace response is a learned condition and may be absent in neonates up to 2 to 3 weeks of age. A bright light will often elicit a blink response in normal neonates when shone directly in the eye. Normal neonates often close the palpebral fissure or move the head away in response to the light. The menace response must be interpreted with respect to the palpebral response, which evaluates the facial and trigeminal nerves. An animal with adequate vision may be unable to respond to the menace by closure of the eyelid if the function of CN VII is abnormal. In this situation, if the animal has normal abducens nerve function, the eyeball usually is retracted as the menace is performed (especially noted in cattle). Vision also should be assessed by making the animal walk through an obstacle course. If the animal has been blind for a duration of time, it may ambulate well in its normal environment; however, such animals usually have a slow, cautious gait, appear very alert to noises around them, and stumble over objects placed in their path. Pupillary Light Reflex

The pupillary light reflex (PLR) does not evaluate visual ability, as the visual occipital cortex is not required (hence it is a true reflex). The afferent pathway for the PLR, however, does have in common several of the same structures as those used in vision, and used together, the PLR and menace response allow further lesion localization. The afferent pathway for the PLR involves the retina, optic nerve, optic chiasm, optic tract, and pretectal and oculomotor nuclei in the brain stem. The efferent pathway is the oculomotor nerve and ciliary ganglion (behind the eye), which innervate the pupillary constrictor muscle. Both a direct and consensual PLR should be evaluated, although the consensual often is more difficult to assess. It should be noted that ruminants tend to have a relatively slow PLR normally. This part of the examination optimally is performed after the animal has adjusted to a dark environment for several minutes. This is more applicable to examination of small ruminants, which can be taken to a dark area

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easily. A bright, focused light source is shone directly into the tapetal retina, and the PLR is assessed. Owing to crossover at the optic chiasm and connections between the pretectal and oculomotor nuclei bilaterally, shining the light in one eye results in a consensual PLR in the opposite eye. Unilateral mydriasis (pupil dilation) is termed anisocoria, and it usually is associated with a lesion of the oculomotor nucleus (on the same side as the mydriasis). In this instance, there is no direct PLR in the mydriatic eye, but a consensual PLR is present along with a normal menace (vision) in both eyes if no other lesions are present. Cerebral swelling from edema or space-occupying lesions can increase pressure on the brainstem, leading to dysfunction of the oculomotor nuclei resulting in anisocoria if the pressure is unequal. The most common cause of bilateral blindness in runlinants is diffuse disease of the cerebral cortex. As the lesion involves the occipital visual cortex, affected animals are blind but have normal direct and consensual PLRs. If an animal is blind and has dilated pupils that are nonresponsive to light, the lesion is likely in the optic chiasm, or alternatively, lesions are present bilaterally in the retina or optic nerves. Animals with blindness in one eye and normal PLRs may have a lesion in the opposite lateral geniculate nucleus, optic radiation, or visual cortex. Horner's Syndrome

Horner's syndrome is a rare condition that is characterized by a combination of the following neurologic deficits. The clinical signs of Homer's syndrome include miosis (constricted pupil), ptosis (narrowing of the palpebral fissure), and enophthalmia (recession of the eyeball within the orbit), all on the same side as the lesion. Cattle with this syndrome also exhibit loss of sweating on the half of the nose ipsilateral to the lesion. Lesions can occur in several locations that affect the sympathetic innervation to the pupil and extraocular smooth muscles, and result in these clinical signs. The pathway of thi3 innervation travels from the midbrain down the spinal cord to the thoracic segments Tl to T3. These nerves then exit the spinal cord through the ventral root and travel up the vagosympathetic trunk (cranially in the neck) until they reach the base of the ear, where they synapse near the tympanic bulla at the cranial cervical ganglion. The nerve fibers then continue rostrally to innervate the smooth muscles of the pupil and periorbital area. Any lesion along this pathway can result in Horner's syndrome. Ophthalmic Examination

Examination of the eye is an important aspect of the neurologic examination. In addition to changes in ocular position, movement, and pupil size, other abnormalities can be manifestations of neurologic or systemic disease. To perform an ocular examination in ruminants, a hand-held direct ophthalmoscope and bright focusing light source are all that are needed. Knowledge of normal ruminant ocular anatomy is a must for accurate interpretation of findings. The structures that can be examined include the adnexa, sclera, cornea, anterior chamber, iris, lens, vitreous, retina, and optic disc. Begin by examining the ocular size and symmetry, noting if either globe is excessively prominent (exophthalmic) or is smaller than normal (enophthalmic). The first two fingers can be placed on the closed lids of both eyes and gentle pressure intermittently applied to grossly characterize the ocular pressures and evaluate the retrobulbar area for enlargement. The periocular adnexa should not be overlooked. Third eyelid protrusion can be a sign of neurologic disease. The third eyelid or nictitating membrane can be evaluated with greater accuracy if the

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globe is gently pushed on to cause its protrusion. Next, observe the sclera, cornea, and extraocular structures with a penlight. Taking advantage of normal ocular positioning, the sclera can be examined by forcing the upper eyelid upward with a finger or thumb as the animal's head is tilted to the side, causing the animal to look downward. The scleral vasculature can be evaluated in this way, giving the clinician an indication of the animal's systemic condition. Cornea

The cornea should be transparent and free of vessels. If the cornea and lens are clear, three separate spots of light should be seen as a bright penlight is shone into the eye. These correspond to the surface of the cornea and the anterior and posterior surfaces of the lens, respectively. If abnormalities in the cornea are suspected, fluorescein staining should be performed to rule out corneal ulceration. The easiest method to stain the eye is to place a small portion of the dye strip in a 10 mL syringe, aspirate an adequate volume of sterile saline, remove the needle, and quickly squirt the solution over the cornea. After the animal is allowed to blink to disperse the dye, the excess stain should be rinsed from the cornea with sterile saline before interpretation. Any area that stains green after rinsing has a defect in the corneal epithelium. Neurologic causes of corneal disease can occur secondary to dysfunction of the ophthalmic branch of eN v or eN VII. Damage to this branch of eN V leads to neurotrophic keratitis owing to sensory loss, whereas loss of eN VII causes exposure keratitis, resulting from the inability to close the eyelid. The corneal reflex will help rule out eN V sensory abnormalities. If the cornea is touched (and eN VII is intact) the normal animal will close the lid. After examination of the cornea, the ophthalmoscope can be used to inspect the internal ocular structures. Set the diopter dial and aperture on the ophthalmoscope appropriately prior to starting this part of the examination. The aperture setting changes the diameter of light emitted from the instrument. In general, the wider settings are best for examining the external ocular structures, whereas the smaller aperture allows better examination of internal structures. The diopter setting changes the depth of focus and can be used to view ocular structures from shallow to deep or vice versa depending on the direction the dial is turned. Another option is to keep the diopter constant and move toward or away from the eye to focus at different depths. One should remember to brace the hand holding the ophthalmoscope on the animal's head so the hand and instrument move with the animal, decreasing the chance of ocular trauma if the animal throws its head quickly. If the animal is in a head catch, securely tying the head obviously decreases the risk of injury to both the animal and examiner during ocular examination of unruly cattle. Anterior Chamber

The clarity and depth of the anterior chamber are noted. To evaluate clarity, use a small focused beam of light such as that obtainable with the small aperture of the ophthalmoscope and hold the light perpendicular to the animal's cornea at a distance of 1 inch. By viewing the beam of light being transmitted through the anterior chamber from a 45° angle, a spot of light should be present on the cornea and iris. If the light seen in the anterior chamber is hazy, as in a smoke-filled room, aqueous flare is present (protein leakage from uveal blood vessels), indicating inflammation. Anterior uveitis can occur with infectious and traumatic neurologic disease. Other signs of anterior uveitis include hypopyon (the presence of white blood cells in the anterior chamber) and the presence of fibrin and red blood cells (hyphema).

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Iris and Lens

The iris should be inspected for any irregularities in its margins or adherence to adjacent ocular structures (synechia), which can occur with inflammation. Lens clarity and location are noted, and both the anterior and posterior lens capsules are inspected. Most ruminants normally have remnants of the hyaloid artery. These can be seen as punctate dots on the posterior lens capsule or complete vascular ghosts extending from the lens to the retina. Sometimes, only the retinal portion of the remnant is present. In calves and lambs, blood may be seen in this structure until approximately 2 months of age.

Fundus

The retina is examined for evidence of hemorrhage, retinal detachment, or degeneration. Retinal hemorrhage can occur in neonatal sepsis and other diseases characterized by vasculitis or coagulopathy and is indicative of systemic inflammation. The hemorrhages usually appear as small red to brown dots or streaks with hazy margins. In these instances, bleeding in other tissues usually is present, and acute death can result from brainstem hemorrhage. Just after death while the cornea remains clear, a panoramic view of the retina can be obtained with the aid of a glass microscope slide and a bright light source. The glass slide is pressed against the cornea, changing its shape and optical properties, and the light is able to illuminate a large portion of the retina. Retinal detachment may be identified by a veil of retinal tissue that is out of focus when viewed at the same depth as the surrounding normal retina. The retina usually remains attached at the optic disc. The optic disc size, shape, color, and edge definition are noted. Papilloedema or swelling of the optic disc may occur with inflammation of the optic disc or concurrently with edema of the cerebral cortex and causes the edge of the disc to appear out of focus. Tongue and Larynx

The eN examination is not complete until the tongue and larynx are evaluated. The hypoglossal nerve (eN XII) is necessary for normal tongue tone and movement, whereas swallowing and normal laryngeal function require the glossopharyngeal nerve (eN IX) and the vagus nerve (eN X). It is important at this point to examine the oral cavity, remembering gloves should be worn if rabies is even remotely suspected. The tongue should be grasped with the examiner's hand and manipulated to determine its strength and coordination. Normal cattle have a very strong tongue and can usually pull it from the examiner's hand. Goats and sheep also have surprisingly strong tongue muscles. The tongue may have evidence of atrophy if the lesion is longstanding. With unilateral damage to eN XII, the tongue may be hanging out of the mouth on the side of the lesion. With partial eN XII paralysis, it may be noted that although the tongue is not hanging out of the mouth, the animal consistently licks only one side of the face when using its tongue. Animals that have difficulty swallowing (dysphagia), usually have excess saliva and food material at the muzzle, and frequently cough. Dysphagia can occur from damage to cranial nerves IX and X. To examine the larynx in adult cattle, the cow is restrained by wrapping the arm over the cow's head, grasping the opposite upper cheek firmly, and pulling her head against the examiner's body. The hand used for the examination is placed in the corner of the cow's mouth just behind the lower incisors, then the fingers are held together and oriented vertically as the hand is carefully guided between the cheek teeth back to the larynx. Once the hand reaches the larynx, it can be maneuvered more easily and the structures in

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the area palpated. As the laryngeal structures are touched, the normal animal will swallow and may cough. In goats, sheep, and calves, swallowing can be evaluated by manipulating the larynx externally or watching the animal eat and drink. Dysphagia from only partial dysfunction of CNs IX or X may be difficult to definitively diagnose clinically. The only clinical signs may be frequent cough and aspiration pneumonia. Peripheral Cranial Nerve Dysfunction

Cranial nerve deficits caused by lesions in the peripheral portion of the nerves outside the brainstem are not accompanied by other signs of brainstem disease such as ataxia and depression. The differentiation of central from peripheral lesions is very important in respect to the prognosis. The most common peripheral CNs to be affected by disease are CNs V, VII, and VIII. Peripheral CN lesions of VII and VIII can be caused by inner ear infections, as these two nerves are in close proximity as they exit the brainstem in the petrosal bone. These two nuclei are also in close proximity in the brainstem, and thus, both are also commonly affected when central lesions occur in the area of their nuclei. Cranial nerve VII can be damaged by trauma and result in facial paralysis that varies depending on the exact location of the lesion. Cattle that struggle in a head chute can injure a branch of the facial nerve as it crosses the zygomatic arch. A lesion in this location causes ipsilateral eyelid paralysis, but ear position is normal.

Evaluation of Gait

The animal's gait initially should be observed from a distance. If the animal is broken to halter, it should be walked in a straight line, circled, and backed if possible as its gait is analyzed. Even the uncooperative ruminant usually can be evaluated by observing the animal walk in an enclosed area. Particular attention should be paid to the consistency of the flight of each limb and if the limb is adducted or abducted as the animal walks in a straight line and a circle. The animal can also be led over objects such as curbs to test conscious limb placement. In some instances, ataxia may be more evident if the animal is blindfolded. Walking up and down a hill also can lead to greater manifestation of the ataxia. This part of the examination is followed by palpation of the musculature and further testing of strength, postural reactions, and reflexes to allow greater lesion localiza tion. Upper Motor Neuron versus Lower Motor Neuron

Lesions of the brainstem, spinal cord, and peripheral motor nerves affect the gait. The signs caused by lesions in these areas are better understood when categorized as upper (UMN) and lower (LMN) motor neuron disorders. The UMNs are control neurons of the brain and brainstem that modify the initiation of motor movements and the maintenance of movement and muscular tone to counteract gravity. The UMNs accomplish this by influencing the LMNs. The cell bodies of LMNs are present in the ventral horn gray matter of the spinal cord and CN nuclei in the brainstem. Their peripheral processes (axons) serve simply as the connection of the central nervous system to the musculature. Loss of UMNs and LMNs cause typical signs that can be used to localize the neurologic lesion. The LMNs of the forelimbs pass through the brachial plexus; those of the hindlimbs pass through the lumbosacral plexus.

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Lesions of UMNs cause a loss of the animal's spatial sense of limb position (proprioception), weakness or paralysis, increased extensor tone, and exaggerated or normal reflexes. LMN lesions directly affect muscle innervation and therefore lead to loss of muscle power (paralysis) and tone and decreased or absent reflexes. Abnormal gait can be manifested as ataxia, with and without weakness. Cerebellar and peripheral vestibular disorders cause ataxia without concurrent weakness or conscious proprioceptive deficits. These disorders may cause circling toward the side of the lesion due to increased tone of the muscles on the opposite side of the body. Consequently, reflexes such as the patellar reflex may be exaggerated on the side opposite the lesion. Hypermetria may be present with cerebellar disorders, and is also a manifestation caused by loss of inhibition of extensor tonus (UMN deficit) to the contralateral limb muscles. Although these animals may have a wide-based stance at rest and are ataxic when walked, it is important to note they do not have loss of their sense of proprioception, nor muscle strength.

Spinal Reflexes

Spinal reflexes can be examined in recumbent mature cattle and in calves and small ruminants of all ages. The normal reflex requires function of the spinal cord segment where the LMN is located for that reflex and the peripheral nerve connecting the LMN to the muscle. Cows that have been recumbent for any period of time usually develop myositis, and therefore may have decreased or absent reflexes due to muscle damage from pressure-induced ischemia and necrosis. When performing the spinal reflex examination the animal is placed in lateral recumbency and the upper forelimb and hindlimb are evaluated. The animal is then rolled over and the examination is repeated on the opposite upper limbs.

Flexor Reflex

The flexor reflex is the most consistent reflex in ruminants. It is assessed by pinching the skin between the digits or a dew claw with a pair of pliers or large hemostats. The normal response is flexion and withdrawal of the limb. The reflex in the front leg requires the spinal cord segments C6 to T2, the sensory and motor fibers of the median and ulnar nerves, and motor fibers of the musculocutaneous and axillary nerves. The hindlimb flexor reflex uses the sciatic nerve and spinal cord segments L5 to 53. More caution obviously should be taken when performing the reflex on the hindlegs of adult cattle. Here, application of an electric shock to the coronary band with an extended prod is safest.

Patel/ar and Triceps Reflexes

Other reflexes that should be assessed but are less consistently inducible include the patellar and triceps reflex. The patellar reflex is performed by holding the hindleg partially flexed and tapping on the patellar ligaments. A pair of pliers or hoof testers work well for testing this reflex in adult cattle. The reflex requires spinal cord segments L4 to L5 and the femoral nerve. Normally, the response is brisk extension of the stifle. The triceps reflex is performed by holding the forelimb in mild flexion and tapping on the triceps tendon located just proximal and caudal to the elbow. Though inconsistent in the normal animal, the reflex should result in contraction of the triceps muscle and extension of the elbow. The reflex pathway involves the spinal cord segments C7, C8, and TI plus the radial nerve.

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Neonates

The young calf, kid, and lamb normally exhibit a crossed extensor reflex when the opposing flexor is assessed owing to immaturity of the UMN pathways in the first several weeks of life. As the stimulus is applied to the leg being tested, the animal flexes the upper limb and simultaneously extends the opposite down limb. Similarly, in older animals, severe UMN disease above the limb being tested may cause a crossed extensor reflex. Neonates also tend to have stronger, more easily elicited spinal reflexes. Postural Reactions

Tests of proprioception to define abnormalities of UMN pathways are difficult to perform in adult cattle. Evidence of UMN dysfunction includes alterations of normal foot flight and placement. Abnormalities due to sensory loss noted during walking include stumbling, circumduction of the outside rear limbs when circled, scuffing the toe when advancing the leg, exaggerated foot placement noted as the foot slaps the ground, and exaggerated limb flexion. Affected cattle may stand with the limbs in abnormal positions, such as a very wide- or narrow-based stance. Calves and small ruminants can be evaluated more accurately because postural reactions can be performed. Placement

The easiest postural test of proprioception is to evaluate placement of the limb as a foot is knuckled or placed in an abnormally wide or narrow position under the body. The normal animal will either not allow such maneuvers or quickly replace the foot to the normal position. Very young calves, kids, and lambs have a wide-based stance normally; therefore, the response to induced knuckling is more reliable. Hopping

The hopping test of proprioception is performed by lifting a limb and pushing the animal to force it to hop laterally on the opposite, weight-bearing limb. If examining the animal alone, it is easiest to straddle the animal facing the limbs to be evaluated while using your legs for restraint of the animal. In this manner, the animal is held in a position with the examiner's legs, as the opposite end of the animal is pivoted, forcing the animal to hop laterally in a small circle. The opposite limb can next be assessed by pivoting the animal in the opposite direction. The forelimbs of larger calves can be evaluated by standing at the shoulder and picking up a front leg as the examiner's shoulder is used to force the animal to hop laterally. If the animal has UMN deficits, it may not initiate hopping normally or may not follow through once the movement is initiated. This test allows the clinician to lateralize the neurologic lesion. Although other postural reactions can be assessed, placement and hopping are the most consistent and simplest to evaluate. Lesion Localization

To localize a lesion resulting in gait abnormalities, both UMNs and LMNs must be assessed. Lesions resulting only in UMN deficits to the fore- and hindlimbs may be located above the sixth cervical segment, including the brain. Lesions in the brainstem resulting in ataxia from UMN dysfunction usually are accompa-

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nied by other signs of brains tern disease, such as depression and CN deficits. Lesions between C6 and T2 affect the brachial plexus (LMNs to forelimbs) and UMNs to the rear limbs. This results in weakness or paralysis of the forelimbs with concurrent poor or absent reflexes; the hindlimbs are less weak and have normal or exaggerated reflexes. An animal with normal strength, proprioception, and reflexes of the forelimbs that has weakness or paralysis in the hindlimbs with normal or exaggerated reflexes has a lesion between T3 and L3. Because animals with spinal cord disease distal to T3 have normal forelimb function, they may bear weight in the front limbs, leading to a "dog sitting" posture (Fig. 8). Less severely affected animals may be able to rise in the hindlimbs but are noticeably weak. Lesions of the L4 to S2 area lead to weakness or paralysis in the rear limbs with decreased or absent rear limb reflexes (LMN deficits), but the forelimbs are normal. Bladder paralysis, decreased anal tone, and decreased perineal sensation can occur with lesions in this area. Animals affected below the third sacral spinal cord segment only may have normal hindlimbs with abnormal anal tone, bladder paralysis, and decreased perineal sensation. Loss of tail and anal tone from trauma to the coccygeal nerves can occur in cattle from excessive manipulation of the tail during restraint or assisting the animal to stand by lifting the tail. Peripheral Nerve Dysfunction

Disorders of peripheral nerves are common in ruminants, especially adult cattle. By definition, peripheral nerve dysfunction is LMN disease. Signs include weakness, paralysis, poor muscle tone, and decreased to absent reflexes. Muscle atrophy also occurs in muscles affected more chronically. Evaluation of hindlimb motor dysfunction should include evaluation of the sacroiliac area and pelvis per rectum, or by radiology in smaller ruminants.

Figure 8. This lamb has a spinal cord lesion distal to T3, as normal thoracic limb function is

present. Note the "dog Sitting" posture.

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Hindlimbs

Obturator nerve and sciatic nerve paralyses most commonly occur in cows with dystocias which result in pressure on the nerve(s) during parturition. These nerves are commonly affected bilaterally, whereas other peripheral nerve deficits usually are unilateral. Trauma to these nerves also can occur from pelvic fractures. The obturator nerve innervates the adductor muscles of the hindlimbs, and abnormalities result in wide-based stance and gait in the hindlimbs or recumbency in a "frog-legged" position. In dairy cows that slip on concrete floors or ice, causing severe abduction of the hindlimbs, traumatic rupture of adductor muscles can cause signs similar to obturator paralysis. Sciatic nerve injury can result from intramuscular injections. The sciatic nerve is responsible for stifle flexion and extension and hip extension. Deficits of the sciatic nerve can cause recumbency, or the animal may stand with the foot knuckled over and the hock dropped. Affected animals may not be able to flex the stifle and flex or extend the hock and fetlock. Femoral nerve paralysis results in the inability to bear weight owing to loss of function to the extensors of the stifle. This neurologic abnormality can be seen in calves resulting from dystocias caused by "hiplock". Peroneal and tibial nerve paralyses can occur from prolonged recumbency. Animals with peroneal nerve damage have a flexed fetlock and extended hock. Tibial nerve damage results in hyperflexion of the hock and partial knuckling at the fetlock.

Forelimbs

Suprascapular nerve paralysis results in a short-strided gait in the affected limb and abduction of the leg and shoulder during weight-bearing. With more chronic injuries, atrophy of the supraspinatus and infraspinatus muscles (sweeny) occurs. Radial nerve paralysis can be caused by trauma from struggling in cattle chutes or from prolonged recumbency on a hard surface. Because this nerve innervates the extensors of the elbow, carpus, and fetlock, injury can result in the inability to bear weight with high lesions or a dropped elbow and flexed fetlock with lower lesions. Brachial plexus damage can result in a combination of clinical signs, depending on the specific nerve(s) affected. Severe brachial plexus injury results in complete loss of motor and sensory function of the forelimb.

Suggested Readings 1. Brewer BD: Neurologic disease of sheep and goats. Vet Clin North Am Large Anim Pract 6:677, 1983 2. de Lahunta A: Veterinary Neuroanatomy and Clinical Neurology, ed 2. Philadelphia, WB Saunders, 1983 3. George LW: Localization and differentiation of neurologic diseases. In Smith BP (ed): Large Animal Internal Medicine. St Louis, CV Mosby, 1990, p 145 4. George LW: Diseases of the nervous system. In Smith BP (ed): Large Animal Internal Medicine. St Louis, CV Mosby, 1990, P 901 5. Howard JL (ed): Current Veterinary Therapy 2: Food Animal Practice. Philadelphia, WB Saunders, 1986

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6. Mayhew IG: Large Animal Neurology: A Handbook For Clinicians. Philadelphia, Lea & Febiger, 1989

Address reprint requests to Todd C. Holbrook, DVM Department of Large Animal Medicine University of Georgia College of Veterinary Medicine Athens, GA 30602