Large Animal Neurology. Joe Mayhew

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СКАЧАТЬ in all positions of the head. Such examples of true strabismus are not often encountered in large animals. Mydriasis is seen with oculomotor nerve disease, and a tendency for lateral eyeball deviation has been observed in horses with midbrain lesions presumably involving the oculomotor nuclei. The dorsomedial, rotational positioning of the eyeball seen in many diffuse brain diseases in ruminants such as polioencephalomalacia and meningitis has been ascribed to the involvement of the trochlear cranial nerve IV. This may not however be due to a true trochlear paralysis as the eyeballs can be moved from this position by moving the head, suggesting that the dorsal oblique muscle and CN IV are functional. What is most frequently seen in large animals is a deviation of the eyeballs resulting from a disturbance of the vestibular system that alters the normal tonic mechanism controlling eye position. This strabismus is usually ipsilateral to the vestibular lesion and most often is ventral, but may be medial. The important difference is that the eyeballs can be moved out of this position. Periorbital lesions, particularly those of trauma and neoplasia, often result in mechanical eye deviations. The eyeball position of newborn foals often is rotated ventromedially relative to that of adult horses.¹⁸ Also, animals that are congenitally blind may have abnormal eyeball positioning and movement.

      By observing the corneal reflex, one can assess sensation from the cornea in the ophthalmic branch of the trigeminal nerve (see below) and the ability to retract the eyeball. The latter is purportedly mediated by just the retractor oculi muscle innervated by the abducens nerve CN VI. However, full eyeball retraction in large animals may require full function of all extraocular muscles innervated by CNs III, IV and VI to be effective. This reflex can be usefully tested by pressing on the closed eyelids while palpating for reflex eyeball retraction, thereby avoiding potential corneal damage.

       Trigeminal nerve—CN V

      This large, well‐protected cranial nerve contains motor nerve fibers that innervate the muscles of mastication in the mandibular branch, as well as sensory nerve fibers from most parts of the head in mandibular, maxillary, and ophthalmic branches.

      The total loss of motor function of the mandibular nerve bilaterally results in a relaxed, flaccid, and lowered jaw and an inability to chew; it is quite rarely seen, but occurs in large animals. The tongue protrudes because it drops forward in the mouth. Drooling results because of the lack of jaw movement. After 1–2 weeks, atrophy of the temporal, masseter, and pterygoid muscles results. Asymmetric lesions cause asymmetric muscle atrophy and a slightly deviated lower jaw without dysphagia that can become prominent with major dental problems due to irregular dental ware.

Normal horses frequently have visible asymmetry of the temporalis musculature (Figure 2.3). Most often this would appear to be a difference in the attachment of the origin of the muscle at the dorsal crests of the temporal fossae of the parietal bones and is often associated with marked, asymmetric dental problems with some asymmetry in muscle bulk. Any loss or gain in tissue bulk in, around, or behind one orbit results in asymmetric supraorbital fossae, and this can be used as a barometer for such abnormalities, including modest atrophy of chewing muscles resulting from a trigeminal lesion. Marked, asymmetric dental disease does cause asymmetry to the depth of the supraorbital fossae

      Function of the sensory branches of this cranial nerve is tested reflexly and directly by assessing sensation to the head. Movement of the ear, eyelids, and lower lips, in response to blunt stimulation of the face, is mediated via the sensory branches of the trigeminal nerve and the motor branches of the facial nerve. Thus, these reflexes require an intact brainstem and trigeminal CN V sensory and facial CN VII motor nuclei and nerves, but do not require the animal to feel the stimuli. Perception of sensation from the head should be assessed in the distribution of each of the major branches of the trigeminal nerve by observing a behavioral response such as head shaking in response to mild noxious stimuli applied to the facial regions innervated by the mandibular, maxillary, and ophthalmic branches of CN V. The mandibular branch certainly supplies sensory innervation for the major part of the rostral tongue in horses. In most patients, especially stoic or obtunded animals, general cerebral perception of such stimuli may be best assessed from lightly probing the internal nares and particularly the nasal septum. Lesions of the sensory nucleus of the trigeminal nerve in the lateral medulla oblongata can cause hypalgesia and hyporeflexia of the face, without weakness of the muscles of mastication. This may result in feed impacting in the rostral cheek pouch. In distinction to this, and especially in horses, prominent cerebral and thalamic lesions can produce contralateral facial hypalgesia without facial hyporeflexia, being most evident in the nasal septum. This is due to the involvement of the sensory pathways in the rostral brainstem and thalamus or to the parietal, sensory cerebral cortex, while sparing the trigeminal nuclei and reflex pathways in the brainstem.

      Detection of nasal hypalgesia in the form of slight asymmetry in the behavioral or avoidance response to a stimulus applied to the nasal septum can take considerable patience and should be confirmed by repeated testing. However, confirmation of this clue, along with the presence of asymmetric menace responses and an asymmetric hopping response in the thoracic limbs, may be the only subtle evidence needed to help confirm the presence of asymmetric forebrain disease.

       Facial nerve—CN VII

      This is predominantly a motor nerve innervating the muscles of facial expression, as well as the lachrymal and certain salivary glands. It contains the final motor neurons for movement of the ears, eyelids, lips, and nostrils, including the motor pathways of the menace, palpebral and corneal reflexes. Unilateral facial paralysis is generally seen as drooping of an ear, ptosis of an upper eyelid, drooping of the upper lip, and pulling of the affected nostril toward the unaffected side. General inspection of the symmetry of facial expression is useful. Some normal horses have an asymmetric contour of the external nares and slight deviation of the nostrils to one side. Very close inspection is required in production animals to detect a partial facial paresis because of the presence of collagenous facial structures compared to horses. Comparison of tone in the ears, eyelids, and lips on each side helps to detect facial weakness, especially when the patient is relaxed. Occasionally, a small amount of food may remain in the cheeks on an affected side. This must not be confused with difficulties with swallowing that result from sensory and/or motor trigeminal paralysis and from pharyngeal dysfunction. Because of a lack of muscle tone in cheek and lips, saliva may drool from the commissure of the lips with facial paralysis. If only weakness of the lips and a deviated nasal philtrum without a drooped ear and ptosis occur, probably only the buccal branches along the side of the face are involved. Mild weakness of facial muscles can often be felt rather than seen and will also become more evident when the patient is resting quietly or has been tranquilized. Involvement of one or two, but not all three branches of the facial nerve more commonly occurs with peripheral facial nerve diseases such as polyneuritis or head trauma. However, central lesions can selectively involve individual regions of the facial nucleus thus mimicking peripheral nerve disease, at least in diseases such as equine protozoal myeloencephalitis and listeriosis.

As with other cranial nerves, a diagnosis of CNS disease, compared to peripheral nerve involvement, can be made by identifying involvement of adjacent structures in the medulla oblongata when signs such as lethargy, limb weakness and ataxia, and a head tilt will often result. With lesions of the inner ear, which cause vestibular signs, there is often accompanying facial nerve paralysis because of concurrent middle ear involvement, and the facial nerve is only separated from the tympanic cavity by a thin membrane. Lack of any involvement of other central pathways is used to differentiate signs of such peripheral facial and vestibular nerve disease from involvement of their nuclei and their pathways in the medulla oblongata. Exquisitely focal lesions resulting from agents such as Sarcosystis neurona and Listeria monocytogenes can exceptionally destroy single and multiple central nuclear regions causing signs of selective cranial nerve dysfunction without producing clinical evidence of adjacent brainstem involvement, thereby mimicking peripheral cranial nerve disease.

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