Neurologic Evaluation of the Equine Head and Neurogenic Dysphagia

THE EQUINE HEAD

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NEUROLOGIC EVALUATION OF THE EQUINE HEAD AND NEUROGENIC DYSPHAGIA Noah D. Cohen, VMD, PhD

Neurologic evaluation of horses with disease of the head is important because much of the central nervous system an.cl the cranial nerves are in this region. Neurologic evaluation should be preceded by signalment and anam­ nesis, evaluation of the horse's environment, and routine physical examination. A horse's age, breed, and gender may provide important diagnostic and prognostic information. Information sought from the client should include history of previous illness, initial clinical signs of disease, contacts with other animals, and whether other horses on the premises are similarly affected. The onset and progression of illness should be determined, because these data may indicate the general process of the disease. When physical examination suggests a neurologic disorder in a horse with disease of the head, further neurologic evaluation should be performed. Detailed descriptions of neurologic evaluation of the horse have been pub­ lished.3• 5• 6 Neurologic evaluation of the head should include assessment of behavior, mental status, posture and coordination of the head, and function of the cranial nerves. With practice, accurate assessment of these factors can be accomplished expeditiously. Although not discussed here, the gait, posture, tone of the tail and anus, cutaneous sensation, and neurologic function of the limbs should be assessed, because multifocal neurologic diseases, such as equine protozoal myelitis and encephalomyelitis caused by equine herpes virus type 1, concurrently affecting the head and other regions of the body, are not uncommon. The owner and others familiar with the horse (e.g., trainer, groom, rider) should be queried about the horse's normal behavior and whether changes in behavior have occurred. Stereotypic behavior (e.g., head-nodding, flank-suck­ ing, wood-chewing, persistent aggression) should be distinguished from abFrom the Department of Large Animal Medicine and Surgery, Texas A&M University College of Veterinary Medicine, College Station, Texas VETERINARY CLINICS OF NORTH AMERICA: EQUINE PRACTICE VOLUME 9 • NUMBER 1 • APRIL 1993

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normal behavior associated with neurologic disease (e.g., seizures, circling, head-pressing, and continuous yawning). Disorders involving the cerebrum and brainstem can cause abnormal behavior. Consciousness and awareness reflect mental status. Comatose horses are unresponsive to noxious stimuli and generally have lesions of the brainstem and a poor prognosis for survival; less profound states of altered awareness include semicoma, stupor, obtundation, somnolence, deliriousness, lethargy, and depression.6 In contrast, horses recumbent from disease of the spinal cord are usually alert and responsive early in the course of disease. Depression may occur with various systemic illnesses; depression associated with disease of the cerebrum or brainstem, however, is usually more severe than that observed with systemic illnesses. Head tilt associated with vestibular disease causes the poll to deviate from midline, but the caudal neck and the muzzle are generally on the midline. Horses with pain of the neck may have a head tilt, but the muzzle deviates from the midline toward the affected side. Cerebral disease may cause the horse to circle and the head and neck to deviate to one side of midline. Distinguishing head tilt from deviation of the head and neck in a horse with vestibular disease may be difficult if the horse is circling or stumbling (usually toward the side of the lesion). Horses with skeletal malformations or horses that are blind may also have abnormal posture of the head. CRANIAL NERVE EXAMINATION

Function of all cranial nerves (CNs) can be assessed most practically by examining regions of the head rather than evaluating function of each individual CN. A list of the major function, signs of dysfunction, and method of assessment for each cranial nerve is provided (Table 1). Sense of smell (CN I) is difficult to assess, because stimuli such as feed in the hand of the examiner or smoke may also stimulate sensory innervation (CN V) of the nasal mucosa. Eyes

The eyes (CNs II, III, IV, VI, VII, VIII) should be assessed for vision and motor function of the eyeball. The retinae should always be examined with an ophthalmoscope. Vision can be assessed by the menace response, a maze test, and pupillary light reflexes. Rapid movement of one's hand toward the horse's eye should normally result in closing of the eyelids and occasionally in retraction of the head. Care should be taken to avoid excessive motion of the hand that would create air currents, which stimulate the tarsal cilia and result in reflex closure of the eye. To detect visual deficit in one field, the menace gesture is directed toward the nasal and then the temporal visual fields.5 Partial visual deficit can be difficult to detect. The afferent portion of the menace response is carried by CN II, and the efferent portion is carried by a branch of CN VII and results in closure of the palpebral orifice from contraction of the orbicularis oculi muscle. Horses that are not blind may not have a normal menace response. Stoic, depressed, or frightened horses may not show a menace response. Although visually competent shortly after birth, foals generally do not have a menace response until they are several days old. Cerebellar disease can cause bilateral deficiency in the menace response in the absence of blindness or facial nerve

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(CN VII) paralysis. Lack of the menace response with cerebellar disease is thought to occur from loss of cerebellar modulation of cerebral visual function. If visual deficiency is in doubt, the horse can be subjected to a maze test to evaluate its ability to maneuver through an area with objects. Horses with intact vision that are depressed, ataxic, paretic, or suffering vestibular disease may stumble over objects in their path. The eyes should be examined for pupillary size and symmetry and for evidence of ocular disease that might affect pupillary response to light (e.g., synechiae). Pupillary light reflexes simultaneously evaluate function of CNs II and III. Light shined into one eye should result in constriction of that eye (direct response) and the contralateral eye (consensual response). Stimulation of the optic nerve (CN II) transmitted to the midbrain is integrated in the pretectal region and results in bilateral excitation of the parasympathetic component of the oculomotor nerve (CN III), causing constriction of both pupils. If, after stimulation, pupillary constriction is absent in both the stimu­ lated and contralateral eyes, the optic nerve of the stimulated eye is likely to be affected. Presence of a direct response in the contralateral eye and a consensual response in the affected eye confirms involvement of the optic nerve on the affected side (Table 2). If pupillary response is absent in the stimulated eye but a consensual response is seen in the contralateral eye, dysfunction of the oculomotor nerve of the stimulated eye should be suspected. If the horse has vision, and direct responses are present in both eyes, assessing consensual responses is unnecessary. Consensual responses can be difficult to assess, because they tend to be weaker than direct responses and because they can be awkward for an examiner to determine alone. A swinging light technique has been recommended to obviate these difficulties and to avoid the blinking response to bright light.6 Dilation of pupils and other motor functions of the eyes and face are under sympathetic nervous control. Sympathetic visceral efferent nerves originate in the first three to four thoracic segments, course through the thorax and cervical region, and eventually synapse in the cranial cervical ganglion, which lies beneath the atlas in the wall of the guttural pouch. Postganglionic fibers proceed rostrally between the tympanic bulla and petrous temporal bone. Damage to sympathetic nervous innervation to the head may result in Homer's syndrome (miosis, slight ptosis, and slight enophthalmus, as well as increased sweating on the face and ear of the affected side, ipsilateral distention of facial blood vessels, and ipsilateral hyperemia of the ocular conjunctiva). Disorders of CNs III, IV, and VI, which innervate the extraocular muscles, result in abnormal position of the eye. Characteristic forms of strabismus described for each of these nerves (see Table 1) should be present when the head is held in various positions. Strabismus associated with vestibular diseases or cerebral diseases is altered by changing position of the head. A ventromedial position of the eye in a healthy foal at rest is a normal finding. Normal vestibular nystagmus as the head is moved from side to side requires intact CNs III, IV, and VI as well as a normal vestibular system. Spontaneous nystagmus when the head is in a normal position or positional nystagmus when the head is moved to another position indicates vestibular disease. The character of the nystagmus can help distinguish peripheral from central vestibular disease involving CN VIII. With peripheral vestibular disor­ ders, the direction of the fast ocular movement (directed away from the side of the lesion) remains constant despite changing the position of the head. Nystagmus associated with peripheral disorders is horizontal or rotary. With central lesions, the direction of the fast phase of the nystagmus is not consistent

Table 1. FUNCTION AND ASSESSMENT OF INDIVIDUAL CRANIAL NERVES (CN) Name

CN No. I

Olfactory

II

Optic

Ill

Oculomotor

IV

Trochlear

V

Trigeminal

Function Olfaction (Sensory) Vision (Sensory) Eye muscles (Motor) Pupillary sphincter (Motor) Levator palpebrae muscles (Motor) Lateral oblique muscles of eye (Motor) Muscles of mastication (Motor) Skin of face, nasal mucosa (Sensory)

VI

Abducens

VII

Facial

Lateral rectus and retractor bulbi muscles (Motor) Facial muscles of expression (Motor) Mandibular, sublingual, and lacrimal glands (Motor) Taste rostral 2/3 of tongue (Sensory)

Dysfunction Loss of sense of smell

Assessment

Mydriasis

Reaction to odors, difficult to assess Menace response, pupillary light responses Move head and watch eye position Pupillary light responses

Ptosis

Observation

Dorsomedial strabismus

Move head and watch eye position Observation, electromyogram

Blindness Lateral strabismus

Asymmetric chewing Masseter atrophy Bilateral: dropped jaw and apparent dysphagia Hypoalgesia or hyperalgesia of face Medial strabismus

Decreased or excess response to touch, palpebral reflex Move head and watch eye position

Asymmetry of face, drooped ear and eye, deviated muzzle, food packed in cheek Partial dry mouth and dry eye (may see keratitis)

Observation, palpebral reflex

Loss of taste in affected region

Difficult to assess

Observation

N 0 \,J

VIII

Vestibulocochlear

IX

Glossopharyngeal

X

Vagus

XI

Accessory

XII

Hypoglossal

Equilibrium (Sensory) Hearing Some pharyngeal muscles (Motor) Parotid and zygomatic salivary glands (Motor) Taste caudal 1/3 of tongue (Sensory) Muscles and mucosa of pharynx & larynx (Motor & Sensory) Trapezius, omotransversarius, sternocephalicus, brachiocephalicus (Motor) Tongue muscles (Motor)

Dysequilibrium, head tilt, spontaneous nystagmus, circling, ataxia Deafness Dysphagia, pharyngeal paralysis

Observation

Dry mouth

Observation

Loss of taste and pain in affected region Dysphagia, dysphonia, aspiration pneumonia

Difficult to assess

Atrophy of neck muscles, inability to pull shoulder forward

Observation, electromyogram

Acute: deviation of tongue to ipsilateral Chronic: deviation of tongue to contralateral Paralysis-of tongue

Observation, failure to retract tongue

Difficult to assess Observation, endoscopy

Endoscopic examination, slap test, auscult thorax

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Table 2. PUPILLARY LIGHT REFLEXES Affected Eye Location of Lesion No lesion Retina or optic nerve Oculomotor nerve

Contralateral Eye

Direct Response

Consensual Response

Direct Response

Consensual Response

Present Absent Absent

Present Present Absent

Present Present Present

Present Absent Present

in presence or direction; the nystagmus may be horizontal, rotary, or vertical. Often, spontaneous nystagmus is short-lived and dissipates during the first few days of illness. Keratitis sicca may result from loss of the parasympathetic innervation in CN VII to the lacrimal glands, and exposure keratitis may result from facial nerve paralysis because of loss of ability to close the eyelids. Face and Head The face (CNs V, VII) should be examined from the front and sides to evaluate symmetry and movement of the eyes, ears, muzzle, nares, and facial musculature. The trigeminal nerve (CN V) contains motor fibers to the muscles of mastication and sensory fibers from most parts of the head. Unilateral atrophy of these muscles suggests unilateral, motor involvement of CN V; bilateral disease of motor branches of CN V causes a dropped jaw and inability to chew. The muscles of facial expression are innervated by motor branches of CN VII. The face should be examined for drooping of the ear and upper eyelid and deviation of the nostrils to one side (Fig. 1); paralysis of the lips may result in drooling. Distinguishing between central and peripheral origin of facial nerve paralysis can usually be accomplished by clinical observation (Table 3).4 The muzzle, nares, and temporalis muscles of some clinically normal horses may be asymmetric.7 Facial reflexes involving sensory innervation from CN V and motor inner­ vation from CN VII can be tested rapidly. Touching the ear, eyelids, and commissure of the mouth should result in movement of these structures. Touching the nasal mucosa is useful to evaluate sensory function of CN V in stoic or depressed horses. The sensory component of CN V should be evaluated, because sensory deficits can occur in the absence of motor involvement of this CN. Head tilt suggests a vestibular disorder (CN VIII). Visual accommodation that masks signs of head tilt can occur within days to weeks, particularly with acute vestibular disease. Blindfolding the horse may exacerbate clinical signs compensated by vision, and blindness may interfere with visual compensation of nystagmus. Tongue The hypoglossal nerve (CN XII) provides motor innervation to the muscles of the tongue. The tongue should be evaluated for symmetry, size, and movement. A clinically normal horse resists withdrawal of its tongue from the mouth. Acute unilateral disease of CN XII (central or peripheral) causes

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Figure 1. Characteristic facial expression of horse with uni­ lateral facial nerve paralysis. The drooped ear and eyelid on the affected side and deviation of the muzzle away from the affected side can be observed. These find­ ings suggest a lesion of the facial nerve proximal to (more central than) the level of emergence of the auriculopalpebral branch of this nerve. (Courtesy of G. Kent Carter, DVM, MS.)

contralateral deviation of the tongue from paralysis of the ipsilateral glossal muscles. Chronic lesions may result in cicatrization and contraction of affected muscles and deviation of the tongue toward the ipsilateral side. Bilateral lesions of CN XII result in inability to retract the tongue into the mouth and interfere with prehension and swallowing. A supranuclear palsy can occur that results in a weak, protruding tongue that can be reflexly stimulated to retract into the mouth. Such a palsy results from a cerebral lesion that affects motor pathways from the forebrain to the hypoglossal nucleus in the caudal brainstem.6• 7 Clinical signs of a fractured hyoid bone or a painful lingual lesion can be confused with clinical signs of dysfunction of CN XII. A weak tongue and reluctance to retract the tongue may be seen in a horse that chews or sucks its tongue or in a horse that is depressed. Failure to retract the tongue and loss of glossal tone are among the earliest signs of botulism. 12

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Table 3. LOCALIZING LESIONS CAUSING FACIAL NERVE (CN VII) PARALYSIS Affected Branches of CN VII

Location of Lesion Rostral to ramus of the mandible Between mandible and stylomastoid foramen Facial canal

Brainstem

Buccal branches Buccal branches Auriculopalpebral branches Buccal branches Auriculopalpebral branches Parasympathetic nerves All of the above, nucleus of CN VII

Clinical Signs A= Muzzle and nares droop, deviate to side of the lesion B= A+ Ear droop, eyelid droop, exposure keratitis C= B+ Dry eye + ( / - Dysequilibrium from peripheral involvement of CN VIII) D= C+ Signs of involvement of adjacent tissue (other cranial nerves involved, depression, weakness, ataxia)

Pharynx and Larynx

Sensory and motor innervation of the pharynx and larynx is supplied by CNs IX, X, and XL Swallowing can be observed by offering feed or water and by passage of a nasogastric tube. Listening to the horse at rest or during exercise may reveal abnormal sounds associated with laryngeal or pharyngeal dysfunction. The larynx can be palpated percutaneously to detect muscular asymmetry. Laryngeal motor function can be evaluated with an endoscope. In addition to passively inspecting voluntary laryngeal movements, the laryngeal adductor reflex (slap test) can be evaluated. The efferent pathway of this reflex is tl)rough CN X. Impulses travel caudally to the level of the cranial thorax, then back rostrally in the recurrent laryngeal nerve to the larynx. Slapping the withers just caudal to the scapula during expiration should result in momentary adduction of the contralateral arytenoid cartilage. This response can be evalu­ ated through an endoscope or palpated percutaneously as a slight muscular contraction in the dorsal, cranial laryngeal region. NEUROGENIC DYSPHAGIA

Dysphagia refers to difficulty in swallowing. Clinical signs occurring with difficulty in prehending or masticating can be similar to those seen with difficulty in swallowing. The numerous causes of dysphagia can be classified as obstructive, painful, or neurogenic (Table 4). 1• 2• 10 The purpose of this discussion is to provide a practical approach to diagnosis and management of common causes of neurogenic dysphagia in the horse. Causes

Diseases of the forebrain may result in difficulty in swallowing. Voluntary swallowing, but not involuntary swallowing, is generally lost, because these diseases usually occur above the level of the nuclei involved with involuntary

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Table 4. SOME CAUSES OF DYSPHAGIA IN THE HORSE Painful Causes Tooth root abscess Broken tooth Retained deciduous teeth, enamel points Periodontal disease Oral ulcerations or erosions Glossitis, lingual foreign body Pharyngeal or facial cellulitis Strangles Retropharyngeal lymphadenopathy Snake bite Fracture of mandibular, maxillary, or hyoid bones Masseter myonecrosis Trauma or excessive traction on tongue Mandibular, maxillary, or oral neoplasia, phycomycosis, or granuloma Obstructive Causes Pharyngeal abscess, neoplasia, or foreign body Esophageal choke Rostral displacement of the palatopharyngeal arch Dorsal displacement of the soft palate Cleft palate Epiglottic cyst Esophageal stricture, diverticulum Megaesophagus Follicular pharyngitis Neurologic Causes Guttural pouch empyema, mycosis, or tympany Lead toxicity Botulism Yellow star thistle Rabies Equine viral encephalitides (EEE, WEE, VEE) Hepatoencephalopathy Encephalitis or meningitis Verminous encephalitis or encephalomyelitis Equine leukoencephalomalacia (moldy corn toxicity) Otitis media-interna Grass sickness (western Europe) Trauma, neoplasia, or abscess of brainstem Equine rhinopneumonitis (rarely causes dysphagia) Equine protozoa! myelitis (rarely causes dysphagia)

swallowing reflexes. Lead poisoning, nigropallidal encephalomalacia (yellow star thistle or Russian knapweed intoxication), equine viral encephalitides, hepatoencephalopathy, and neonatal maladjustment syndrome are common examples. The nucleus ambiguus and nucleus solitarus in the caudal brainstem are the principal centers for control of laryngeal and pharyngeal function by CNs IX, X, and XI. Lesions involving these nuclei are rarely focal and usually involve adjacent or distant tissues as part of multifocal diseases such as equine protozoal myelitis (EPM) or equine rhinopneumonitis (ER). Equine diseases commonly associated with disease of the brainstem such as EPM, ER, or

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verminous encephalitis seldom involve CNs IX, X, and XI. Listeriosis affects the brainstem and may involve these nerves, but listeriosis of horses is rare. Peripheral disease of cranial nerves IX, X, and XI can cause dysphagia. Common causes of peripheral disease of these nerves include empyema and mycosis of the guttural pouch, trauma associated with surgery of the guttural pouch, botulism (in endemic areas), fracture of the stylohyoid bone, and extension of otitis media-interna. Rupture of the rectus capitis ventralis muscles in a horse caused damage of CNs IX, X, and XI, resulting in dysphagia.10 Clinical Signs Clinical signs of dysphagia include salivation, discharge of food or water from the nares, impaction of food in the mouth, quidding, coughing, and an anxious attitude when food is offered. Other accompanying clinical signs vary with the location and extent of neural tissue involved, and these accompanying findings are diagnostically and prognostically important. Horses with diffuse brain disease (e.g., hepatoencephalitis, viral encephalitides) generally show signs of altered behavior and mentation, as discussed in the section on neurologic examination. Such horses may lose voluntary swallowing but gen­ erally retain the swallowing reflex and have no deficits of cranial nerves. Horses with nigropallidal encephalomalacia have difficulty in prehension and in mov­ ing food toward the pharynx for deglutition but can swallow and have hypertonicity of the muscles of the lips and jaw (Fig. 2). These horses may

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Figure 2. Dysphagic horse with nigropallidal encephalomalacia. Taught facial muscles and presence of yellow star thistle retained in the horse's mouth can be observed. (Courtesy of Steven E. Wikse, DVM.)

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walk aimlessly or in circles. Horses with chronic intoxication of lead may have weight loss, proprioceptive deficits, and anemia. Dysphagia associated with a lesion of the brainstem is often accompanied by ataxia and signs of central involvement of the cranial nerves unless associated nuclei are focally affected. Dysphagia with evidence of central vestibular or facial nervous disease, with or without ataxia, should suggest a lesion of the caudal brainstem alone (e.g., trauma, verminous encephalitis) or multifocal disease involving the brainstem (e.g., EPM). Signs of ataxia and central involvement of cranial nerves are not seen with dysphagia caused by peripheral neuropathy (unless peripheral vestibular dis­ ease causes ataxia). The extent of accompanying signs and involvement of CNs other than IX, X, and XI depends on the location of the lesion. Empyema of a guttural pouch may cause chronic, mucopurulent nasal discharge, and mycosis of a guttural pouch may cause epistaxis. Botulism is characterized by progres­ sive, diffuse, symmetric muscular weakness. Progressive muscular weakness without dysphagia has occurred in horses in California with type C botulism.12 Horses with recent fractures of the stylohyoid bone may have pain, interman­ dibular swelling, and epistaxis. Facial nerve paralysis can cause difficulty in prehension and chewing and impaction of food in the mouth. Horses with dysphagia caused by otitis media-interna have signs of peripheral vestibular disease and, occasionally, concurrent facial nerve paralysis. Diagnostic Plan A history should be taken, and physical and endoscopic examinations should be conducted to exclude painful or obstructive causes of dysphagia. When the cause of dysphagia is not obvious and the clinical signs are of less than 2 weeks' duration, gloves should be worn during oral examination because of the risk of rabies. Anamnesis may be of particular importance in assessing the cause of neurologic disease. As previously discussed, the onset and progression of disease may indicate the general disease process involved. Exposure to lead or plants associated with nigropallidal encephalomalacia (yellow star thistle, Rus­ sian knapweed) should be determined when clinical signs are indicative of these toxicoses. When neurogenic dysphagia is considered possible, neurologic evaluation of the head should be performed. Altered behavior and mental status are suggestive of diffuse disease of the brain. Serum should be evaluated for evidence of hepatopathy by biochemical analysis that includes determination of bile acid concentration. Blood may be evaluated for concentration of lead and evidence of anemia. Measurements of concentration of free erythrocytic porphyrins and erythrocytic concentration of delta-aminolevulinic acid are preferred methods of diagnosing chronic intoxication of lead. The prognosis for horses with hepatoencephalopathy, nigropallidal encephalomalacia, and other diffuse cerebral disease is generally poor. Horses with lead toxicity have a guarded prognosis for survival. Signs of ataxia and central disorders of cranial nerves indicate involvement of the brainstem. Further neurologic evaluation is indicated to assess locomo­ tion, tone of the tail and anus, and sensation and reflexes of the limbs. Horses with trauma, neoplasia, or verminous infection of the brainstem have a guarded to poor prognosis for survival. Horses with EPM or ER may recover with appropriate care.

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If signs suggest peripheral neuropathy, the guttural pouches should be endoscopically examined. Radiography of the head may provide evidence of diseases of the guttural pouch, retropharyngeal lymphadenopathy, or fracture of a stylohyoid bone. The reversibility and extent of CN involvement and the severity of underlying disease dictate prognosis. Management Management of horses with neurogenic dysphagia may be unrewarding because of the poor prognosis associated with many causes of the disorder. Management should be directed toward maintaining adequate nutrition, treat­ ing or preventing aspiration pneumonia, and instituting specific therapy for the underlying cause of neurogenic dysphagia. A dysphagic horse can be fed with tubes inserted into the stomach through the nose or through a pharyngostomy or esophagostomy. Because of difficulties in managing a horse with a pharyngostomy or esophagostomy, a nasogastric tube is most practical and usually sufficient. Nasogastric intubation may be performed at each feeding; an indwelling tube, however, may prevent pharyn­ geal and esophageal trauma caused by repeated, difficult intubation of a horse with dysphagia. An indwelling nasogastric tube can be secured in position to the horse's halter with adhesive tape and the external end should be capped (a 3-mL syringe or its case generally works well). Keeping the nasogastric tube lubricated with a small amount of warm water applied to the exterior of the tube at the nostril may diminish irritation to the nares and nasal mucosa. Effects of maintaining an indwelling nasogastric tube for days or weeks on equine gastric motility are, to the author's knowledge, unknown. A muzzle should be used to prevent the horse from ingesting feed, bedding, or other materials. Nutritional and fluid requirements must be met. Dysphagia can result in catabolism of protein of muscle, decreased immunocompetence, and abnor­ malities of metabolism of lipids and bilirubin. 11 A nutritionally balanced diet that meets caloric requirements for maintenance must be provided.8• 9• 1 1 Caloric requirements for maintenance of the horse have been estimated as DE = 155(BW)0 75, where BW = body weight in kg and DE = digestible energy requirement in kilocalories.9 Thus, a 500-kg horse requires approximately 16,400 kcal/day. Caloric intake often must be increased because of increased catabolism in horses with severe metabolic disease. An appropriate balance of calcium and phosphorous must be provided, particularly to foals and young, growing horses. A calcium:phosphorous ratio of 1:1 to 2:1 in the diet should be achieved. Various methods of administering enteral nutrition by intubation are available. A gruel of a complete pelleted feed dissolved in water can be prepared. For a 500-kg horse requiring 16,400 kcal, 7 kgs of a commercially available, complete pelleted feed containing 14% protein must be fed daily. Because of volume, 1. 1 or 1. 75 kg of this diet dissolved in warm water should be fed every 4 or 6 hours, respectively. To decrease the volume of feed and increase caloric intake, the content of fat in the diet can be increased by adding corn oil (approximately 100 g/day). A liquid diet of dehydrated cottage cheese, electrolytes, and glucose has been fed to hypophagic horses.• Osmolite (Ross Laboratories, Columbus, OH), a commercially available liquid diet developed for human use, has been fed to dysphagic horses. 11 Although more costly than the aforementioned diets, the product is commercially available, and its low volume facilitates administration by nasogastric tube. Loose, low-volume feces

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are often produced when Osmolite is fed to horses. 11 Recently, a liquid diet formulated for horses (Equical, Ross Laboratories, Columbus, OH) became commercially available. Nutritional status of horses receiving total or partial enteral nutrition should be monitored. Body weight should be measured or estimated with a weight tape at least every several days. If dysphagic horses are hyperbilirubinemic from anorexia (but not hepatic disease), serum concentration of bilirubin also can be monitored to assess nutritional status. 11 In the author's experience, a lag of a few days occurs between correction of hypoalimentation and resolution of hyperbilirubinemia. Because intragastric administration of carbohydrate can cause laminitis, horses receiving enteral nutrition should be monitored for clinical signs of the condition. The feet should be examined for heat in the hooves, edema of the coronary band, sensitivity to hoof testers, and increased digital pulsation. The horse should be evaluated for pain while walking and for increased digital pulses at least daily. The daily carbohydrate intake for each of the recommended diets does not approach the amount used to induce laminitis. 8• 11 If a horse has been dysphagic for several days, however, it is advisable to increase enteral nutrition as follows: 25% of caloric requirements on day 1; 50% on day 2; 75% on day 3, and 100% on day 4 and thereaft�r. Abrupt termination of enteral nutrition with Osmolite once a horse regains the ability to swallow has been demonstrated to be safe. 11 A gradual change in diet is recommended, however, to avoid disrupting normal intestinal flora and motility. Regardless of the diet used, sufficient water should be added to provide approximately 50 mL/kg/day. For a 500-kg horse, at least 25 L (approximately 6 gallons) should be administered daily. Total volume administered intragastr­ ically to an adult horse at one time should not exceed 8 to 12 L (2 to 3 gal). Frequency of intragastric administration of fluid is determined by the type of diet fed. Generally, fluid should be provided every 6 to 8 hours. Because aspiration pneumonia can result from dysphagia, broad-spectrum antimicrobial drugs should be administered. Examples include a combination of trimethoprim-sulfonamide (15-30 mg/kg, per nasogastric tube, q 12 hrs), and a combination of procaine penicillin G (16-20 x 106 IU/kg, IM, q 12 hrs) and gentamicin (2.5 mg/kg, IV, q 8 hrs). Body temperature, coughing and nasal discharge, and the character of lung sounds should be monitored for all dysphagic horses. If aspiration pneumonia is suspected at the time of exami­ nation, a transtracheal wash for microbial culture and cytologic examination may be performed and empiric treatment with broad-spectrum antimicrobial drugs initiated, pending specific laboratory findings. Generally, aspiration pneumonia is a polymicrobial process, and broad-spectrum antimicrobial treat­ ment is required. Metronidazole may be added to the antimicrobial regimen to combat anaerobic bacteria. Additional, specific therapy is often needed for an underlying disease that has resulted in dysphagia (e. g., lead toxicity or botulism). If needed, information about treatment of specific disorders should be sought through written refer­ ences or consultation with a veterinary internist. SUMMARY

Neurologic evaluation should be performed in horses with diseases of the head. Although neurologic examination should focus on assessing behavior, mental status, and cranial nerve evaluation, evaluation of neurologic function

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of other body regions should be performed. Neurologic evaluation of the head can be performed expediently by practitioners to provide useful diagnostic and prognostic information. The numerous causes of dysphagia can be classified as obstructive, painful, or neurogenic. Common causes of neurogenic dysphagia are summarized, and methods for initial diagnosis and management are described. Maintaining adequate nutrition and preventing aspiration pneumonia are principal concerns in managing horses with neurogenic dysphagia. ACKNOWLEDGMENT The author wishes to thank Drs. G.K. Carter, M.K. Chaffin, J.F. Hawkins, and J.S. Schumacher for reviewing the manuscript.

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Noah D. Cohen, VMD, PhD Department of Large Animal Medicine and Surgery Texas A&M University College of Veterinary Medicine College Station, TX 77843-4475