Chapter 104 Vestibular Disease
Dogs and cats have the ability to control posture and movements of the body and eyes relative to the external environment. The vestibular system mediates these activities through a network of receptors and neural elements. Disease leading to dysfunction of the vestibular system can lead to dramatic signs of disequilibrium. The investigation, treatment, and prognosis of the cause of the disequilibrium can differ depending on whether the peripheral or central components of the system are affected.
This chapter outlines the relevant anatomy of the vestibular system and how this influences the clinical signs of its dysfunction, in addition to the diseases that are most commonly responsible for the acute onset of clinical signs constituting an emergency.
The vestibular system can be divided into peripheral components located in the inner ear and central nervous system (CNS) components. Three major CNS areas receive projections from the peripheral sensory receptors of the vestibular system: the cerebral cortex, the spinal cord, and the cerebellum. The projection to the cerebral cortex incorporates extensions to the extraocular muscles.
From Platt S, Olby N, editors: Manual of canine and feline neurology, ed 3, Gloucester, 2004, British Small Animal Veterinary Association.
The cell location for the first neuron is within the vestibular ganglion of the eighth cranial or vestibulocochlear nerve, and the axon projects into the ipsilateral vestibular nuclei. These neurons receive input from the vestibular receptors in the membranous labyrinth contained within a bony labyrinth in the petrous temporal bone. The sensory neurons are incorporated into the vestibulocochlear nerve, which leaves the petrous temporal bone via the internal acoustic meatus, along with the facial nerve, and enters the medulla of the brain stem.1
The cell location for the second neuron is in the vestibular nuclei, which are situated in the medulla oblongata. From these nuclei, axons travel in the medial longitudinal fasciculus within the brain stem. The ascending axons within the fasciculus give off numerous side branches to the motor nuclei of cranial nerves III, IV, and VI, thereby providing coordinated conjugated eyeball movements associated with changes in position of the head. Some axons project from the nuclei into the reticular formation and go on to provide afferents to the vomiting center located there.1
The vestibulospinal tract descends from the vestibular nuclei and projects mainly onto α-neurons or extensor motor neurons throughout the length of the cord via interneurons in the ventral grey column.1 This pathway is strongly facilitatory to the ipsilateral alpha and gamma motor neurons to extensor muscles.
The vestibular nuclei project directly to the cortex of the ipsilateral flocculonodular lobe (the flocculus of the hemisphere and the nodulus of the caudal vermis), as well as the fastigial nucleus of the cerebellum.1 The return pathway from a cerebellar nucleus to the vestibular nuclei is also ipsilateral; this is an extremely large projection, providing the cerebellum with a strong influence over the activity of the vestibular nuclei. These pathways between the cerebellum and the vestibular nuclei travel in the caudal cerebellar peduncle.
Unilateral vestibular disease produces asymmetric signs, often on or toward the side of the disease. The most common clinical signs of vestibular disease are head tilt, nystagmus, and ataxia; these may be single entities or a combination of signs.2 The primary aim of the neurologic examination is to determine if these vestibular signs are due to a peripheral vestibular system (inner ear) disease or a central vestibular system (brain stem and cerebellum, or both) disease. Localization of the disease determines the most appropriate diagnostic tests, the differential diagnoses, and the prognosis.
The essential determination of whether these signs are due to a peripheral or central disease may be possible by the identification of associated neurologic signs that are present only with central disease.2 Signs of central vestibular syndrome suggest damage to the brain stem and are not present in patients with inner ear disease unless there has been extension of the inner ear disease into the brain stem, such as can be seen with otitis media, otitis interna, and neoplasia.3
|Clinical Signs||Peripheral Vestibular Disease||Central Vestibular Disease|
|Head tilt||Toward the lesion||Toward the lesion, or away from the lesion with paradoxical disease|
|Spontaneous nystagmus||Horizontal or rotatory with the fast phase away from the side of the lesion|
|Horizontal, rotatory, vertical and or positional with the fast phase toward or away from the lesion|
|Paresis and proprioceptive deficits||None||Commonly ipsilateral to the lesion|
|Mentation||Normal to disoriented||Depressed, stuporous, obtunded, or comatose|
|Cranial nerve deficits||Ipsilateral CN VII deficit||Ipsilateral CN V, VII, IX, X, and XII|
|Horner’s syndrome||Common ipsilateral to the lesion||Uncommon|
|Head tremors||None||Can occur with concurrent cerebellar dysfunction|
|Circling||Infrequent but can be seen toward the side of the lesion||Usually toward the side of the lesion|
CN, Cranial nerve.
Loss of equilibrium is most commonly represented clinically as a head tilt that may be present with either central or peripheral vestibular disease. The head tilt is always toward the side of the lesion with peripheral disease but may be toward either side with central disease. When the head tilt is opposite to the side of the lesion, it is termed paradoxical.2 This can be seen with lesions of the flocculonodular lobe of the cerebellum or the supramedullary part of the caudal cerebellar peduncle, with sparing of the vestibular nuclei in the rostral medulla; the head tilt often is accompanied by ipsilateral cerebellar signs, paresis, and proprioceptive deficits.3