Diseases of the Brainstem and Cranial Nerves of the Horse: Relevant Examination Techniques and Illustrative Video Segments

1. Introduction

This lecture focuses on the functions of the portions of the brainstem caudal to the diencephalon. In addition to regulation of many of the homeostatic mechanisms of the body, this part of the brainstem controls consciousness, pupillary diameter, eye movement, facial expression, balance, prehension, mastication and swallowing of food, and movement and coordination of the trunk and limbs. Dysfunction of the brainstem and/or cranial nerves therefore manifests in a great variety of ways including reduced consciousness, ataxia, limb weakness, dysphagia, facial paralysis, jaw weakness, nystagmus, and strabismus. Careful neurologic examination in the field can provide accurate localization of brainstem and cranial nerve lesions. Recognition of brainstem/cranial nerve dysfunction is an important step in the processes of diagnosis and treatment.

2. Anatomy and Nomenclature

The brainstem includes the diencephalon, mesencephalon (midbrain), and rhombencephalon (hindbrain).¹  With the exception of the olfactory nerves (I), all cranial nerves are arrayed along the brainstem. The hindbrain is divided into metencephalon (pons and cerebellum) and myelencephalon (medulla oblongata). Because the diencephalon was discussed in the previous lecture under Forebrain Diseases, it will not be covered here. 

3 Functions (Location)

Pupillary Light Response, Pupil Size (Midbrain, Cranial Nerves II, III)

In the normal horse, pupil size reflects the balance of sympathetic (dilator) and parasympathetic (constrictor) influences on the smooth muscle of the iris.^2-4 Preganglionic neurons for sympathetic supply to the head arise in the gray matter of the first four thoracic segments of the spinal cord and subsequently course rostrally in the cervical sympathetic nerve within the vagosympathetic trunk. After synapse in the cranial cervical ganglion adjacent to the guttural pouch, the post-ganglionic sympathetic neurons continue to the smooth muscle of the orbit and act to cause pupillary dilation. Emotional and other influences on sympathetic pupillary tone are governed by hypothalamic centers that act through upper motor neuron (UMN) tracts descending from the midbrain. Interruption of pre- or post-ganglionic sympathetic nerves to the eye causes Horner’s syndrome, with miosis of the pupil, ptosis (reflecting hypotonia of the dorsal tarsal (Mueller’s) muscle), and spontaneous sweating and vasodilatation over the side of the face. Parasympathetic preganglionic neurons arise in the midbrain and exit the skull in the oculomotor nerve (III). These neurons synapse behind the eye in the ciliary ganglion. Post-ganglionic neurons pass along the optic nerve to innervate the ciliary muscle and constrictor of the pupil. The afferent part of the pupillary light reflex passes via the optic nerves and optic tracts, past the thalamus, to terminate in the midbrain. There is extensive decussation of these tracts both in the chiasm and midbrain.

Eye Position (Midbrain, Pons, Cranial Nerves III, IV, VI)

From nuclei in the midbrain and pons, the oculomotor, trochlear, and abducens nerves exit the cranial cavity through the orbital fissure and ramify in the periorbital tissues to innervate the muscles of the eye. The oculomotor nerve also supplies the levator palpebrae and pupillary constrictor muscles, and the abducens nerve innervates the retractor bulbi muscle. Lesions in these nerves (or nuclei) cause true strabismus.

Mastication (Pons, Cranial Nerve V)

The lower motor neurons of the trigeminal nerve arise in the pons and pass through the petrous temporal bone in the foramen ovale adjacent to sensory trigeminal neurons and are distributed to the muscles of mastication: masseters, pterygoids, temporals, and rostral digastricus. With unilateral damage to the trigeminal nucleus (or nerve), there is deviation of the lower jaw toward the normal side. By 2 weeks after injury, there is obvious muscular atrophy. Bilateral severe involvement of the trigeminal nuclei (or nerves) causes a dropped jaw, weak jaw tone, slight tongue protrusion, and inability to prehend or chew feed.

Facial Expression and Movement (Medulla, Cranial Nerve VII)

The facial nerves arise from nuclei in the rostral medulla and exit the calvarium with CN VIII via the internal acoustic meatus. The nerve courses through the facial canal in the petrous temporal bone adjacent to the middle ear and emerges through the stylomyastoid foramen. The facial nerve is distributed to the muscles of facial expression including those of the ear, eyelid, nose, and lips and the caudal belly of the digastric muscle. With involvement of the nucleus or proximal nerve, there is drooping of the ear and lip, ptosis, collapse of the nostril, and the muzzle is pulled toward the normal side. Saliva often drools from the affected side of the mouth, and the horse has difficulty prehending food, especially grain. There may be exposure keratitis. The facial nerve also contributes parasympathetic neurons to lacrimal glands. The sensory component of the facial nerve contains fibers from the tongue (taste) and middle ear.

Balance and Equilibrium (Medulla, Cranial Nerve VIII), Hearing (Medulla, Cranial Nerve VIII, Forebrain)

The vestibular system is responsible for orientation of the horse relative to gravity. The receptor is in the bony labyrinth of the inner ear. The membranous labyrinth includes 3 semicircular ducts containing endolymph that connect to vestibular nerve endings at the cristae ampullares. Vestibular neurons pass centrally through the internal acoustic meatus to penetrate the rostral medulla and terminate in 4 vestibular nuclei. These nuclei have numerous projections to the nuclei controlling extraocular muscles, the cerebellum, and the spinal cord. The vestibular system controls the conjugate movements of the eyes during movement of the head through extensive connections with the nuclei of cranial nerves III, IV, and VI. Vestibular-cerebellar pathways pass through the caudal cerebellar peduncle. These pathways function to smoothly co-ordinate the movements of the eyeballs, trunk, and limbs with those of the head. Vestibulospinal tracts descend ipsilaterally to synapse on LMN and facilitate extensor muscles of the limbs while inhibiting flexor muscles. Some vestibulospinal tracts cross and reduce extensor tonus in contralateral limbs.

Unilateral disease involving the peripheral part of the vestibular system causes asymmetric ataxia with preservation of strength. The poll rotates toward the side of the lesion, and the head and neck may be turned toward the lesion. The body leans, falls, or rolls toward the side of the lesion, and the horse may stagger in tight circles. Because there is some visual compensation for vestibular ataxia, blindfolding exacerbates the signs. In horses with central vestibular disease, head tilt may be either toward or away from the side of the lesion. The latter presentation is known as paradoxical central vestibular disease and usually follows involvement of vestibular connections within the cerebellum. Unilateral vestibular disease often causes spontaneous or positional nystagmus, and physiological (vestibular) nystagmus may be absent or abnormal when the head is moved toward the side of the lesion. In peripheral disease, the nystagmus is always horizontal, rotatory, or arc-shaped, with the fast phase away from the lesion. With central involvement of the vestibular system, nystagmus also may be vertical. Typically, the eye on the affected side rotates ventrally in the orbit, whereas the eye on the normal side rotates dorsally (especially when the head is extended). This abnormal eye position is termed vestibular strabismus. Bilateral vestibular disease is characterized by severe symmetric ataxia and wide, sweeping movements of the head from side to side. [...]