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Video on Demand Associated Lectures
Moderators
Room
Hall 714
Date
07/19/19, Friday
Time
08:00 AM - 08:50 AM
Presentation Type
Level 2: Requires general knowledge of the literature and professional practice within the areas covered
Session Description
Session Sponsored by Canopy Animal Health
Associated Lectures

Rock & roll, turn and dance in circles - Work-up and manage vestibular diseases successfully

Lecture Time
08:00 AM - 08:50 AM
Authors
Room
Hall 714
Date
07/19/19, Friday
Time
08:00 AM - 08:50 AM

Abstract

Abstract Body


Rock & roll, turn and dance in circles - Work-up and manage vestibular diseases successfully

Prof. Holger A. Volk, DVM, PhD, PGCAP, DipECVN

University of Veterinary Medicine Hannover, Germany

The vestibular system main function is to maintain an animal’s equilibrium during movement and orientation against gravity. It is divided into two main sections, the peripheral and the central. The peripheral one is composed of cranial nerve VIII (CNVIII; vestibulocochlear nerve) and sensory receptors contained within the petrosal bone. The central one is that part of the vestibular system held within the cranial vault, i.e., the vestibular nuclei of CNVIII. The peripheral system detects linear acceleration and rotation movement of the head. It is responsible to maintain the position of the eyes, neck, trunk and limbs in reference to the position of the head.

The sensory receptors of the vestibular system are located in the inner ear. The sacculus and the utriculus are located in the vestibule and detect linear acceleration and head positioning against gravity. The semicircular ducts with their ampullae detect rotational acceleration. There are three semicircular ducts, which are orientated in each dimensional direction.

The vestibular nerve fibres travel in CNVIII, terminate mainly in one of the four vestibular nuclei, but also in the cerebellum. A pathway (medial longitudinal fasciculus) connects the medial vestibular nucleus with the nuclei of III (N. occulomotorius), IV (N. trochlearis) and VI (N. abducens) to control eye movements. Other pathways connect the vestibular nuclei with the cerebellum, cerebrum, other brainstem centre (e.g. vomiting centre) and the spinal cord. The vestibular system is mainly unilateral. The lateral vestibular nucleus give rise to a pathway to the spinal cord ventral grey matter and is facilitatory to the extensor muscle (inhibiting the contralateral extensor tone and the ipsilateral flexor muscle).

Keeping this in mind, it is logically that a head tilt and a reduced extensor tone of the limbs are on the side of the lesion. “It looks like the animal is running around a curve”. The jerk nystagmus develops from the dysfunction of the pathways connecting the vestibular nuclei with the cranial nerve nuclei responsible for the eye movement. When the head moves, no / uncoordinated eye movements can be seen. The slow phase of the jerk nystagmus goes into the direction of the lesion; the fast phase is the compensatory one. Vision and proprioception can help to compensate the vestibular dysfunction. This can be often observed in clinics as vestibular disease can progressively improve.

Clinical signs of dysfunction of the vestibular system are: loss of balance, head tilt, leaning, rolling, circling, nystagmus, strabismus, and depending on the type of vestibular disease, other cranial nerve deficits, Horner's Syndrome, cerebellar signs, mental depression and hemiparesis with postural reaction deficits. By defining the clinical signs present the clinician will be able to determine central vs. peripheral vestibular disease. Because the list of differentials depends on the location of the lesion, this determination is most important (see below).

Nystagmus -There is the "normal" physiological nystagmus that we can elicit performing the occulovestibular test or by spinning the animal (together with the clinician) around its on axis. Another type of "normal" nystagmus would be the pendulous nystagmus of particular cat breeds (Siamese, Birman and Himalayan), which is caused by a larger numbre of fibres crossing at the optic chiasm. The pendulous nystagmus is characterised by equal speed of eye movement to both sides. There is also a searching type nystagmus described in animals, which have been born blind.

Abnormal types of nystagmus would be the jerk nystagmus with a slow and a fast phase with varied directions; horizontal, rotatory or vertical. These may be conjugate or disconjugate, they may also be positional. Positional nystagmus will vary with the patient depending on its head position. The direction of the nystagmus is always defined by the fast phase, even if the slow phase is to the side of the lesion.

Strabismus -Certain cat breeds (Siamese) may have congenital divergent strabismus. A divergent strabismus may also be seen in severe cases of hydrocephalus. The strabismus seen with vestibular disease is ventrolateral (unilateral) and is not responsive to the occulovestibular test. It is seen in the eye ipsilateral to the lesion. This does not differentiate central from peripheral vestibular disease.

Leaning, falling, circling - The patient tends to lean or fall toward the affected side because the vestibular system facilitates the extensors of the ipsilateral side (see also above). The patient also tends to circle toward the affected side as with lesions of the forebrain. However, the circles of vestibular disease tend to be closer and tighter rather than the large roaming circles of forebrain disease. The patient with central vestibular disease is more likely to be non-ambulatory.

The head tiltis on the side ipsilateral to the lesion, unless, the lesion is in the flocculonodular lobe of the cerebellum or the cerebellomedullary pontine angle; then the patient may have aparadoxical head tilt. In this case, the head tilts to the contralateral side. Because the lesion involves the cerebellar projections to the vestibular nuclei, and because the cerebellum is predominantly inhibitory in effect, the side of the lesion becomes overactive, giving excessive tone to the extensors of that side and causing the patient to lean and tilt away from the lesion. However, the side of the lesion can be determined by testing the proprioception, especially paw positioning which are reduced to absent on the side of the lesion.

Horner’s syndromeis characterised by the loss of sympathetic innervation to the eye. In dogs and cats fibres of the postganglionic sympathetic fibres travel through the middle ear before following the ophthalmic nerve of the trigeminal nerve. A damage at this site can cause a Horner’s syndrome. The postganglionic sympathetic fibres innervate the smooth muscle of the periorbit and eyelids (also third eyelid in the cat). Furthermore, they innervate the dilator pupillaris and iris muscle. Therefore, the cardinal signs decribed by Dr. Horner were: 1. Enophthalmos; 2. Third eyelid protrusion; 3. Ptosis; 4. Miosis. As the sympathetic system also controls the smooth muscles in blood vessel, a failure of the system results in congested vessels. This can be best appreciated on the sclera and the ear.

Sometimes the patient may present with bilateral vestibular disease. One typically sees wide excursions of the head, symmetrical ataxia, no head tilt and the patient may not demonstrate a "normal" physiological nystagmus. Examples would be aminoglycoside toxicity, bilateral otitis media/interna in cats, and congenital bilateral vestibular disease in young Doberman Pinchers.

Differentials to consider for peripheral vestibular disorders

Category

Acute nonprogressive

Acute progressive

Chronic progressive

Degenerative

Congenital vestibular syndrome

Metabolic

(Diabetes mellitus; indirect)

Hypothyroidism

Neoplastic

Metastatic

Soft tissue tumours

Nerve sheath tumour

Inflammatory / infectious

Otitis media/interna (bacterial)

Protozoal

Otitis media/interna (bacterial)

Protozoal

Idiopathic

Idiopathic (vascular?)

Traumatic

Fracture

Toxic

Streptomycin

Gentamycin

Streptomycin

Gentamycin

Vascular

Infarction

Septic emboli

Hemmorrhage

The diagnostic work-up may vary greatly between central versus peripheral disease but all patients should have a complete blood count, biochemistries, thyroid screening and blood pressure evaluation. Even if it is only a geriatric with idiopathic vestibular syndrome, there may be an underlying renal deficiency and the nausea/vertigo may be enough to keep the patient from drinking adequately, precipitating renal failure.

Given a peripheral vestibular location, radiography of the skull with oblique views and open mouth can be considered, but the main investigation will be an otoscopic examination of the external ear canal and the tympanic membrane. If the potential for otitis media exists then myringotomy is simple and quick. It does necessitate some form of short acting sedation. Cultures and cytology may be obtained from within the bullae. Take note that the bullae of the canine are different from the cat. The feline has two compartments in the bulla. Myringotomy is done in the ventrocaudal aspect of the tympanic membrane. The resultant puncture in the membrane is quick to heal.

Central vestibular disease will almost always require advanced imaging. This is the most important reason to localise as it will change the way how you work up the case. It is generally believed that it has to do with determining the prognosis. But the prognosis is determined by the diagnosed disease process and not by the location of the lesion. We have diagnosed many animals with soft tissue sarcomas invading the middle ear (poor prognosis) and vice versa have diagnosed dogs with cerebellar infarcts (usually good prognosis).

Differentials to consider for central vestibular disorders

Category

Acute nonprogressive

Acute progressive

Chronic progressive

Anomalous

(Hydrocephalus)

Degenerative

Neurodegenerative diseases

Storage diseases

Metabolic

Hypoglycaemia

Neoplastic

Metastatic

Primary: Choroid plexus papilloma,Glioma,

Meningioma or secondary such as lymphoma

Nutritional

Thiamine def. (usually bilateral)

Inflammatory / infectious

FIP

Protozoal

FIP

Protozoal

Toxic

Lead

Hexachlorophene

Metronidazole (usually bilateral)

Lead

Hexachlorophene

Traumatic

Fracture/bleed

Vascular

Infarction

Septic emboli

Haemmorrhage

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