Vestibular disease (Proceedings)

     • The vestibular system functions to maintain an animal's balance and orientation with respect to gravity

          o Maintains steady visual image by stabilizing the eyes during head movement

          o Maintains steady body position by stabilizing head positioning in space

     • Clinical anatomy

          o Peripheral components – within inner ear, petrous temporal bone, close to CN VII and sympathetic innervation to the face

               ▪ Membranous labyrinth

                     Utricle, saccule – detect gravity and linear acceleration

                     Semicircular canals – detect head rotation

               ▪ Vestibular portion of CN VIII

          o Central components – at the level of the brain

               ▪ Synapses of CN VIII on vestibular nuclei and neurons at rostral cerebellum

               ▪ Connections of vestibular nuclei to:

                     CN III, IV, VI via medial longitudinal fasciculus

                     Descending pathways to spinal cord

               ▪ Important local anatomy

                     Cerebellar peduncles

                     CN V motor and sensory nuclei

                     CN VII motor nuclei

                     Descending motor and ascending sensory pathways

                     Reticular activating system (RAS)

     • Clinical signs

          o Head tilt – named for the most ventral side

          o Circling, leaning, falling and rolling

          o Ataxia – may be asymmetrical, often in absence of weakness

          o Nystagmus – spontaneous, named for the fast phase

          o Strabismus – generally ventral or ventrolateral

          o "Nausea" – hypersalivation, inappetence, vomiting, seen with acute disease

     • Localization

          o Peripheral vestibular disease classically:

               ▪ Head tilt, circling, leaning, falling, rolling TOWARDS side of lesion

               ▪ Nystagmus conjugate, non positional, horizontal or rotary, fast phase AWAY from lesion

               ▪ Strabismus ipsilateral

               ▪ +/- CN VII deficits

               ▪ +/- Horner's syndrome (NOT expected in central disease)

          o Central vestibular disease classically:

               ▪ Head tilt, circling, falling, rolling TOWARDS side of lesion

               ▪ Nystagmus conjugate or non-conjugate, positional or non-positional, horizontal, rotary or vertical, fast phase AWAY from lesion

               ▪ Strabismus ipsilateral

               ▪ +/- Mentation change

               ▪ +/- Asymmetric conscious proprioceptive deficits, paresis, IPSILATERAL

               ▪ +/- Other CN deficits (CN VII, as well as V, IX, X, XI, XII)

               ▪ +/- Overt cerebellar signs (e.g. hypermetria, intention tremor)

          o Paradoxical vestibular disease – Central disease involving cerebellum specifically Head tilt, circling, falling, rolling AWAY from side of lesion Nystagmus as for classic central disease, but fast phase TOWARDS lesion Strabismus ipsilateral

               ▪ +/- Mentation change

               ▪ +/- Asymmetric conscious proprioceptive deficits, paresis, IPSILATERAL

               ▪ +/- Other CN deficits (CN VII, as well as V, IX, X, XI, XII)

               ▪ +/- Overt cerebellar signs (e.g. hypermetria, intention tremor)

          o Bilateral vestibular disease – almost always peripheral in origin

               ▪ Head tilt not present, but wide excursions of head and neck side to side

               ▪ Absence of spontaneous and physiologic nystagmus

               ▪ Strabismus may not be present

                     Symmetrical ataxia

               ▪ Characteristic wide based stance with crouched posture and gait

               ▪ +/- CN VII deficits or Horner's syndrome

     • Differentials

          o Peripheral vestibular disease

               ▪ Degenerative – uncommon

               ▪ Anomalous – congenital vestibular disease described in cat and dog breeds

               ▪ Metabolic – hypothyroidism?

               ▪ Neoplastic – involving middle and inner ear

               ▪ Infectious – otitis media-interna

               ▪ Inflammatory – nasopharyngeal polyps

               ▪ Idiopathic – most commonly older canine patients

               ▪ Toxic – e.g. aminoglycosides, chlorhexidine topically

               ▪ Traumatic

               ▪ Vascular?

          o Central vestibular disease

               ▪ Degenerative – lysosomal storage diseases

               ▪ Anomalous – Chiari-like malformation, arachnoid cysts

               ▪ Metabolic – hepatic encephalopathy?

               ▪ Neoplastic – primary or metastatic

               ▪ Nutritional – thiamine deficiency

               ▪ Infectious – bacterial, viral, fungal, protozoal, rickettsial, parasitic

               ▪ Inflammatory – granulomatous meningoencephalitis, necrotizing encephalitis

               ▪ Toxic- metronidazole

               ▪ Traumatic

               ▪ Vascular – ischemic, hemorrhagic

     • Diagnostics

          o Thorough history, physical and neurologic exams

          o Extra nervous system evaluation – to rule out concurrent/related pathology

               ▪ CBC, chemistry panel, UA

               ▪ BP measurement

               ▪ Thyroid panel

               ▪ Thoracic radiographs

               ▪ Abdominal US

               ▪ +/- Serology for infectious disease

          o Peripheral vestibular disease

               ▪ Otoscopic exam

               ▪ Imaging of middle/inner ear via radiography, CT or MRI

               ▪ +/- myringotomy for sampling for cytology, culture and sensitivity

               ▪ +/- CSF analysis to rule out central extension of disease process

               ▪ +/- brainstem auditory evoked response (BAER) test

          o Central vestibular disease

               ▪ Otoscopic exam

               ▪ Advanced imaging (MRI preferably, CT)

               ▪ CSF analysis, preferably following imaging

               ▪ +/- brainstem auditory evoked response (BAER) test

               ▪ +/- CSF titers, PCR for infectious disease, CSF culture

               ▪ +/- CT guided or surgical brain biopsy

     • Treatment

          o Compensation is possible with stable or slowly changing disease, via use of visual and somatosensory cues, changes in movements and postural responses and changes to the vestibular system itself via feedback mechanisms

          o Controlled activity encourages recovery – potential role for physical rehabilitation in veterinary medicine

          o Antihistamines (e.g. meclizine), benzodiazepines (e.g. diazepam) and phenothiazines (e.g. acepromazine) can all be used to decrease signs associated with acute vestibular disease, but long term use is not indicated, as they may suppress vestibular input necessary for recovery

          o Maropitant – Potential role, but at what dosage and for how long?

          o Treat underlying disease specifically if possible – e.g. antimicrobials if infectious disease confirmed, surgery (e.g. bulla osteotomy, craniectomy)

          o Potential role of corticosteroids in presence of progressive central disease

Suggested reading:

Vestibular Dysfunction, Thomas, WB, The Veterinary Clinics of North America: Small Animal Practice, Common Neurologic Problems, 30(1), 2000