Abnormalities of Cranial Nerve Function
The normal functions of the cranial nerves were described earlier, in the discussion of the neurologic examination. Cranial nerve dysfunction may be central or peripheral in type, depending on whether the neurologic lesion lies within the central components of the cranial nerves within the brain or in the peripheral portions of the nerves.
Clinical signs of cranial nerve dysfunction are ipsilateral to the lesions that cause them.BLINDNESS, STRABISMUS, OCULAR PARESIS OR PARALYSIS, ABNORMALITIES OF PUPIL SIZE OR PUPILLARY LIGHT REFLEXES. Lesions involving cranial nerves II, III, IV, and VI were described earlier, in the discussion of blindness and other visual dysfunctions.
FACIAL HYPALGESIA OR ANALGESIA, DEVIATED OR DROPPED JAW. Loss of or reduced sensory perception on the face, including the inside of the mouth, the nasal planum, the nasal septum, the cornea, and the lower jaw area, occurs with lesions of the trigeminal nerve. It is important to distinguish this from the signs of contralateral forebrain disease. Unilateral loss of facial sensation may result from damage to the peripheral portion of the trigeminal nerve or the trigeminal ganglion in the petrosal bone of the skull, or its connections in the pons, or from contralateral forebrain disease. Bilateral facial hypalgesia is most likely caused by diffuse forebrain dysfunction rather than trigeminal nerve disease. The mandibular branch of the trigeminal nerve also carries motor innervation to the muscles of mastication from the pontine motor nucleus of the trigeminal nerve. Bilateral involvement of the motor component of the nerve results in a dropped jaw and inability to prehend and chew food, together with drooling saliva. The muscles of mastication atrophy rapidly over a few weeks, most obviously in the masseter and temporalis muscles. Unilateral disease causes atrophy of the denervated muscles, and mild jaw weakness may be appreciated, but the animal can still eat and close the jaw.
Usually the mandible is deviated away from the side of the trigeminal nerve lesion. Central lesions in the trigeminal nerve may also involve adjacent structures in the brainstem, such as the facial nerve, the vestibular system, and the long motor and sensory tracts to and from the limbs.FACIAL PARESIS OR PARALYSIS. Lesions of the facial nerve result in ipsilateral atonia or hypotonia of the facial muscles. The clinical signs of facial nerve paralysis in all large animals include ptosis, dropped ear, and absence of the menace response and palpebral reflex. There is accumulation of food in the cheek pouch and commissure of the lips on the ipsilateral side. Affected animals frequently drool saliva from the lip commissure on the affected side. The animal is unable to open the nostril on the affected side during inspiration. The muzzle of the horse, goat, and sheep deviates away from the direction of the neurologic lesion. Deviation of the muzzle is not seen in cattle because of the normal rigidity of the planum nasale. If the neurologic lesion is located between the medulla oblongata and the stylomastoid foramen, the ipsilateral eye may be dry because of loss of innervation from the parasympathetic nucleus of cranial nerve VII. Lesions of the central components of the facial nerve in the medulla oblongata also destroy upper motor neurons, proprioceptive tracts, and reticular activating system (RAS) neurons, resulting in limb weakness, ataxia, and sometimes obtundation. Lesions of the peripheral component of cranial nerve VII cause facial atonia or hypotonia but do not produce obtundation or ataxia.
HEAD TILT, SPONTANEOUS NYSTAGMUS, DEAFNESS. Lesions involving cranial nerve VIII, the vestibulocochlear nerve, produce signs of vestibular dysfunction, as described previously. Deafness may also be a consequence of vestibulocochlear nerve disease. Bilateral deafness has been reported in Paint horses,51 where it may be a heritable defect associated with the gene for white coat color, similar to the situation that exists in a number of breeds of dogs with white or merle coat color.
Deafness can also result from severe aural disease. Although bilateral deafness■ TABLE 8.9
Diseases of Spasticity or Tremors in Horses and Ruminants
| Disease | Clinical Manifestations | Affected Species |
| Cerebellar hypoplasia | Intentional head tremor, basewide stance, hypermetria, hypertonia, | Cattle, sheep, goats |
| Bovine viral diarrhea Bluetongue Akabane Border disease Wesselsbron disease Hereditary | hyperreflexia, truncal ataxia, menace deficit, opisthotonos | |
| Cerebellar abiotrophy | Intentional head tremor, basewide stance, hypermetria, hypertonia, hyperreflexia, truncal ataxia, menace deficit, opisthotonos | Cattle, horses, goats |
| Grass staggers | Hypermetria, hyperreflexia, truncal ataxia, head tremors, basewide stance, recumbency, ptyalism, hyperexcitability, hyperesthesia | |
| Bermuda staggers | Cattle, horses | |
| Paspalum staggers | Horses | |
| Perennial ryegrass staggers | All species | |
| Other fungal tremorgens | All species | |
| Annual ryegrass toxicity | All species | |
| Kikuyu grass | Cattle, sheep | |
| Phalaris (canarygrass) | Sheep | |
| Hypomagnesemia | Hypermetria, hyperreflexia, truncal ataxia, recumbency, hyperesthesia, menace deficit, opisthotonos, aggressiveness, hypertonia | Cattle, horses |
| Lysosomal storage disease | Intentional head tremor, basewide stance, hypermetria, hypertonia, hyperreflexia, truncal ataxia, menace deficit, opisthotonos, blindness, aggressiveness | Cattle, goats |
| Locoism and Swainsona | Ataxia, obtundation, intentional head tremor, loss of herd instinct, | All species |
| poisoning | maniacal behavior, flaccidity of the nose and lips, basewide stance | |
| Aspergillus clavatus toxicosis | Ataxia, weakness, muscle tremors, hypersalivation, altered behavior, recumbency, opisthotonos, death | Cattle, sheep |
| Hereditary neuraxial edema | Recumbency, head tremor, good appetite, hyperesthesia, nystagmus, strabismus, muscular fasciculations | Cattle |
| Bovine familial convulsions | Tetaniform seizures, ataxia, hypermetria, hyperreflexia, head tremors, | Cattle |
| and ataxia | truncal ataxia | |
| Maple syrup urine disease | Obtundation, recumbency, opisthotonos, stimulus-induced tetanic spasms, convulsions, generalized decrease of spinal reflexes | Cattle |
| Solanum spp. storage disease | Head tremors, hypermetria, hypertonia, hyperesthesia, weight loss, opisthotonos, recumbency, and convulsions | Cattle, goats |
is fairly easy to recognize clinically, unilateral deafness may be less obvious. Inability to localize sound occurs when animals have unilateral deafness and may be suspected when animals alert to sound but do not turn toward the sound. Auditory evoked potentials can be used to determine the integrity of the auditory pathway in the inner ear and medulla oblongata.51,52
DYSPHAGIA, DYSPHONIA, STRIDOR. Lesions in the nuclei of cranial nerves IX, X, and XI in the medulla oblongata produce dysphonia, inspiratory dyspnea, dysphagia, and neurogenic atrophy of the trapezius, sternocephalicus, and brachiocephalicus muscles. The inspiratory dyspnea is characterized by roaring and stridor. Roaring is a stridor that is made during peak inspiratory flow in horses with idiopathic left recurrent laryngeal neuropathy. It is caused by paralysis of the left cricoarytenoideus dorsalis muscle, resulting in failure to abduct the arytenoid cartilages during inspiration. Additional evidence of paralysis of cranial nerves IX and X may be obtained by endoscopic examination of the pharynx. Other signs of paralysis of cranial nerves IX and X include failure to abduct the vocal folds, collapse of the pharynx, dorsal displacement of the soft palate, and inability to swallow a nasogastric tube. Animals with peripheral nerve deficits remain alert and appetent and do not show conscious proprioceptive deficits, whereas animals with centrally located lesions may be depressed and inappetent and may have ataxia and limb weakness. Animals with bilateral lesions in the peripheral nerves are unable to open the glottis during inspiration and display extreme respiratory distress. Peripheral lesions of the accessory nerve that have been present for longer than 1 month may produce neurogenic atrophy of the trapezius, brachiocephalicus, and sternocephalicus muscles.
This is frequently accompanied by aspiration pneumonia. Lesions of the visceral efferent component of cranial nerve X in ruminants produce vagal indigestion, which is characterized by ruminal distention with fluid, ruminal tympany, abomasal stasis, and sometimes a hypochloremic, hypokalemic metabolic alkalosis.Hypoglossal nerve lesions produce a weak or flaccid tongue. In animals with unilateral lesions, the tongue deviates away from the side with the lesion and is flaccid when it is manually extended from the mouth. After prolonged denervation (2 weeks or more) the ipsilateral side of the tongue atrophies and the tongue deviates toward the affected side. Horses with lesions in the forebrain may also fail to retract the tongue normally; however, the lingual musculature is normal, the tone is variable, and the animal can retract the tongue if it receives sufficient stimulation. In comparison, the tongue tone is consistently weak in cases of hypoglossal paralysis.
Signs of cranial nerve dysfunction, together with the central origins or projections of the nerves, are summarized in Table 8.10. Diseases that involve the brainstem and cranial nerves are summarized in Table 8.11.
Lesions of the medulla oblongata can produce severe obtundation, somnolence, or coma as a result of ARAS dysfunction in
■ TABLE 8.10
Clinical Signs of Cranial Nerve Dysfunction
| Cranial Nerve | Central Origin or Projection | Clinical Signs of Dysfunction | Comments |
| I—Olfactory | Olfactory bulb, limbic system (behavior and emotion centers), cerebral cortex | Loss of sense of smell (anosmia) | Olfactory nerve lesions are rare and difficult to detect clinically. |
| II—Optic | Optic chiasm, optic tract, lateral geniculate nucleus, optic radiation, occipital cortex | Blindness | See text for additional comments (blindness). |
| III—Oculomotor | Midbrain somatic and parasympathetic nuclei | Ventrolateral strabismus, ptosis (somatic component); dilated, nonresponsive pupil (parasympathetic component) | |
| IV—Trochlear | Midbrain | Dorsomedial strabismus | Trochlear nerve lesions are rare and usually accompanied by other signs of midbrain dysfunction. |
| V—Trigeminal | Pons (motor nucleus), | Dropped jaw in bilateral motor | Rabies is an important differential |
| medulla, and rostral | paralysis; deviated jaw in | diagnosis in animals with a | |
| cervical spinal cord (sensory tract) | unilateral paralysis; decrease or loss of sensation to most of the structures of the head and face in sensory nerve disease | dropped jaw. | |
| VI—Abducent | Rostral medulla oblongata | Medial strabismus (paralysis of the lateral rectus muscle) | |
| VII—Facial | Medulla oblongata | Facial paralysis (motor component); | The facial nerve is particularly |
| (rostral to middle); | loss of sense of taste to rostral | susceptible to damage in its | |
| motor, sensory, and parasympathetic | two thirds of the tongue; | peripheral course because of its | |
| decreased tear production (dry | proximity to the middle ear and to | ||
| components | eye) and decreased salivation (parasympathetic components) | the guttural pouch in horses and its superficial location on the face. | |
| VIII— | Medulla oblongata | Decreased hearing or deafness; | See description of vestibular disease |
| Vestibulocochlear | (middle) | vestibular signs (head tilt, nystagmus, falling, rolling) | in text. |
| IX, X, XI— | Medulla oblongata | Dysphagia (IX and X), laryngeal | Rabies is an important differential |
| Glossopharyngeal, | (nucleus ambiguus in | paresis to paralysis (X), atrophy | diagnosis in animals with |
| vagus, accessory | middle to caudal medulla and rostral cervical spinal cord) | of sternocephalicus, brachiocephalicus, and trapezius muscles (XI) | dysphagia or choke. |
| XII—Hypoglossal | Medulla oblongata (caudal) | Paralysis of the tongue | Acute unilateral lesions result in the tongue being deviated away from the side of the lesion. In chronic disease, atrophy and contracture of the affected side of the tongue result in deviation toward the affected side. |
addition to signs of vestibular dysfunction and functional deficits in cranial nerves V to XII. Other clinical signs of medullary lesions include ipsilateral paresis and proprioceptive deficits. The spinal reflexes of the ipsilateral limbs are exaggerated, and the extensor muscle tone is increased. Further details are given later in the discussion of quadriparesis and hemiparesis.