Head Tilt and Nystagmus
The presence of a head tilt, wherein the head is rotated so that one ear is held closer to the ground than the other, indicates dysfunction of the vestibular system. Head tilt is usually accompanied by spontaneous or positional (abnormal) nystagmus and a variety of other clinical signs.
Vestibular disease can be classified as peripheral or central. Peripheral vestibular disease occurs with lesions of the vestibular apparatus of the inner ear (utricle, saccule, semicircular canals) or vestibulocochlear nerve (cranial nerve VIII) or, theoretically, when there is involvement of vestibular afferents from the proximal part of the neck. Animals with peripheral vestibular lesions have normal mentation but may be extremely disoriented, making assessment of mentation difficult. The head tilt (i.e., the lower ear) in animals with peripheral vestibular disease is toward the side of the lesion. Unilateral peripheral vestibular dysfunction causes decreased extensor tone in the limbs ipsilateral to the lesion and increased extensor tone in the contralateral limbs, resulting in the clinical signs of leaning, falling, curling, and rolling toward the affected side. Asymmetric peripheral vestibular lesions produce horizontal or rotatory conjugate nystagmus, with the fast phase directed away from the side of the lesion. The direction of the nystagmus in relation to the head is unchanged no matter what the position of the head. Physiologic nystagmus may be absent or decreased, particularly when the head is moved in a horizontal plane toward the side of the lesion. The facial nerve is closely associated with the vestibulocochlear nerve within the skull, and there may be facial paralysis along with peripheral vestibular disease when the facial nerve is also damaged by the underlying cause such as may occur in skull trauma, temporohyoid osteoarthropathy of horses, or severe otitis media or interna. Rarely, involvement of the postganglionic sympathetic nerve to the eye as it courses through the petrous temporal bone results in ipsilateral Horner's syndrome (ptosis, miosis, facial sweating in horses, reduced sweating on the nasal planum in cattle).Lesions within the vestibular centers in the medulla oblongata and cerebellum also cause signs of vestibular dysfunction. Head tilt in central vestibular disease is usually toward the side of the lesion but may be in the opposite direction when the underlying disease involves the cerebellum (i.e., paradoxical vestibular syndrome). Similarly, nystagmus may be horizontal or rotatory as in peripheral vestibular disease but also may be vertical, diagonal, or different in each eye (disconjugate nystagmus); may change in direction when the position of the head is changed (positional nystagmus); or may be horizontal or rotatory with the fast phase toward the side of the lesion (paradoxical vestibular syndrome). Signs of involvement of the motor and sensory tracts to and from the limbs as they course through the medulla usually accompany central vestibular disease. Proprioceptive and postural reaction deficits are present in the ipsilateral limbs, together with mild hyperreflexia. Obtundation and signs of other cranial nerve dysfunctions may accompany central vestibular disease and can be used diagnostically to distinguish central from peripheral lesions.
Animals with either peripheral or central vestibular lesions tend to lean against walls and may fall when forced to perform a complex motor maneuver. They may adopt recumbency with the lesion side directed down and have poor righting responses, particularly from lesion-side-down recumbency. When positioned so that the lesion side is directed up, they often will roll to a lesion-down position. Blindfolding the patient eliminates visual compensatory mechanisms and therefore increases the severity of the clinical signs (Romberg's test). Blindfolding may help reveal subtle dysfunction but should be done with caution. Animals with vestibular disease occasionally may have slight ventral strabismus in the ipsilateral eye and slight dorsal strabismus in the contralateral eye. These deviations are exaggerated when the head is held in the median plane and the chin is lifted. This vestibular strabismus can be differentiated from the ventrolateral true strabismus seen with lesions of the oculomotor nerve because the former changes when the head is rotated, whereas the latter does not.
Animals with bilateral vestibular lesions do not have strabismus, head tilt, or nystagmus. The animal stands with the legs basewide and may fall to either side when head position is rapidly altered. Affected animals may show a coarse side- to-side head tremor. Bilateral vestibular lesions are usually peripheral and are rarely encountered in clinical practice. Central lesions extensive enough to cause bilateral vestibular disease are likely to be fatal.