Neurology: vestibular disease in Horses (Equis) | Vetlexicon
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Neurology: vestibular disease

ISSN 2398-2977


Introduction

  • Cause: damage to the vestibular system which is responsible for maintenance of the normal orientation of the trunk, limbs and eyes with respect to the position and movements of the head.
  • Signs: disturbed equilibrium and ataxia, without paresis.
  • Diagnosis: history and clinical signs (exacerbated by blindfolding).
  • Treatment: appropriate treatment of the primary cause of the vestibular damage.
  • Prognosis: guarded - affected animals often centrally accommodate with time and can return to their previous function, although signs can still be elucidated by blindfolding.

Presenting signs

  • Ataxia (inco-ordination).
  • Head tilt.
  • Nystagmus.
  • Weakness of ipsilateral extensor muscles; may lean against walls.
  • Ear droop, twisted muzzle and corneal ulcer if cranial nerve VII is concurrently affected.

Acute presentation

  • Falling or rolling to side of lesion.
  • Head tilt.
  • Nystagmus.
  • Circling.
  • Panic attacks, disorientation, wild thrashing attempts to stand.
  • Ear droop, paralyzed facial muscles of eye, ear, cheek and muzzle and corneal ulcer if cranial nerve VII is concurrently affected.

Pathogenesis

Etiology

Specific

Pathophysiology

  • The vestibular system maintains balance, and orientation of the trunk, limbs and eyes with respect to the position and movements of the head.
  • The vestibular system comprises a receptor organ within the inner ear (within the petrous temporal bone) and the vestibulocochlear nerve (VIIIth cranial nerve).
  • The facial nerve (VIIth cranial nerve) is closely associated with the vestibulocochelar nerve and the petrous temporal bone, and they enter the internal auditory meatus together.
  • Vestibular disease usually results in disturbed equilibrium and ataxia, without paresis.
  • Disorders are usually unilateral.
  • Extension of the suppurative process in otitis media   Ear: otitis externa / otitis media  into the adjacent facial canal and internal auditory meatus or temporohyoid joint disease    Temporohyoid joint: osteoarthropathy  may   →    sudden fracture of the petrous bone    →   acute signs of vestibular and facial nerve dysfunction.
  • Extension of the infection through the internal acoustic meatus can   →    focal suppurative meningitis, fever and depression; complicating the signs and worsening the prognosis.
  • Idiopathic vestibular syndrome may be the result of transient disease of the vestibular nerve, eg viral or immune-mediated neuritis or labyrinthitis.

Timecourse

  • Central and visual accommodation often occurs with time, and the horse can return to its former use, although signs of vestibular disease can still be stimulated by blindfolding (Rombergs test).
  • Idiopathic vestibular syndrome: can be very acute in onset and full recovery occurs in 2-3 weeks without treatment. 
  • Tremorgenic mycotoxocosis: full recovery occurs a few days to several weeks following early removal of the affected fodder.

Diagnosis

Presenting problems

  • Ataxia.
  • Gait change.
  • Twisted muzzle away from side of lesion, ear droop, corneal ulcer if cranial nerve VII is concurrently affected.

Client history

  • Head tilt.
  • Inco-ordination and loss of balance.
  • Gait changes.
  • Corneal ulcer.

Clinical signs

  • All signs are exacerbated by blindfolding the animal.

Unilateral

  • Peripheral disease:
    • True head tilt towards affected side, ie ventral deviation of the poll to the affected side.
    • Spontaneous rotary or horizontal nystagmus with the fast phase away from the affected side.
    • Ipsilateral ventrolateral strabismus.
    • Head elevation.
    • Staggering dysmetric gait with a tendency to lean or circle towards the affected side.
    • Extensor hypotonia ipsilateral to lesion.
    • Hyperextension of contralateral limbs.
    • Asymmetrical ataxia.
    • Malfunctioning righting reflex    →   exaggerated attempts to stand.
    • Clinical signs of cranial nerve VII dysfunction if concurrently affected. Twisted muzzle, droopy ear, corneal ulcer, inability to shut eye, foul breath due to paralysis of the buccinator muscle.
    • Clinical signs of cranial nerve VIII and IX in cases of skull fracture secondary to temporohyoid osteoarthropathy.
    • Difficulty in eating.
  • Central disease:
    • Variable nystagmus: horizontal, rotatory or vertical.
    • General proprioceptive deficiencies.
    • Head tilt towards or away (rare) from lesion.
    • Depression.
    • Frequently adjacent brainstem structures are involved    →   other signs:

Bilateral

  • Dysmetria.
  • Severe, more symmetric, ataxia.
  • Wide, swinging head movements.
  • Deafness if cochlear branch of cranial nerve VIII is involved bilaterally.

Diagnostic investigation

Neurological examination

Radiography

  • Radiography of the head    Head: radiography  , especially the lateral obliques and ventrodorsal views. Best done under general anesthesia for correct alignment. May indicate cause, eg head trauma, temporohyoid osteoarthropathy.

Scintigraphy

Endoscopy

  • Otoscopy in otitis media/interna.
  • Endoscopy of pharynx and guttural pouch   Respiratory: endoscopy  to identify proliferative osteitis of the stylohyoid bone and possibly hemorrhage subsequent to a skull fracture.

CSF collection

  • Cerebrospinal fluid (CSF) analysis   CSF: collection  to identify secondary bacterial meningitis, primary infectious causes, abscess, verminous encephalomyelitis.

Other

  • Rombergs test: blindfolding the horse forces it to rely on the impaired vestibular system for orientation, causing the clinical signs to be exaggerated.

Perform blindfold test with caution, on a padded surface, with good footing the horse may panic.

Caloric testing

  • Useful in differentiating central from peripheral vestibular disease.
  • Irrigate the external auditory meatus with ice-cold (12°C) water for 3-5 min.
  • The normal horizontal nystagmus with a fast phase away from the tested labyrinth is not induced in the case of a non-functional labyrinth.
  • An asymmetric response indicates a unilateral condition in the depressed side.
  • Animals may resist the procedure and it may be more reliable in the anesthetized or comatose horse.

Brainstem auditory evoked response testing

  • Useful in differentiating central from peripheral disease and monitoring disease progress.
  • The cochlea is damaged by damage to the vestibular receptor organs and may   →   hearing loss.
  • Functional loss of the cochlea or VIIIth cranial nerve results in the loss of the entire waveform on the side of the injury.
  • Abnormalities of a specific waveform can identify a lesion of the corresponding neurologic structure.
  • Reliable under sedation or anesthesia.

Confirmation of diagnosis

Discriminatory diagnostic features

Definitive diagnostic features

  • Rombergs test.
  • Caloric testing.
  • Brainstem auditory evoked response.

Gross autopsy findings

  • Dependent on cause.

Histopathology findings

  • Dependent on cause.

Differential diagnosis

Treatment

Initial symptomatic treatment

  • Sedation of an anxious horse may be necessary in the acute case to prevent self-harm or injury to personnel: diazepam   Diazepam  50 mg/450 kg horse IV.
  • Appropriate supportive care.

Standard treatment

Monitoring

  • Brainstem auditory evoked response testing is useful in monitoring disease progress.
  • Careful observation is necessary to differentiate genuine improvement from adaptation or compensation.

Prevention

Outcomes

Prognosis

  • Guarded: affected animals often centrally and visually accommodate with time and can return to their previous use, although vestibular function deficits can still be elucidated by blindfolding.
  • If blindness is present the prognosis worsens because of the loss of visual compensation for vestibular malfunction.
  • Associated facial and other cranial nerve deficits often remain, with only slight improvement over time. If even mild improvement of facial nerve function is noted in the first 4 months, full function may return.
  • Early removal of toxic fodder can   →   a complete recovery from mycotoxicosis over a period of a few days to several weeks.

Extreme care should always be taken when riding animals with vestibular disease: reduced light situations can instigate a rapid return of clinical signs or cause increased anxiety in the horse, which could be dangerous to the rider.

Expected response to treatment

  • Affected animals often centrally accommodate with time.

Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Hahn C (2008) Common peripheral nerve disorders in the horse. In Pract 30 (6), 322-329 VetMedResource.
  • Sargent S J, Frank L A, Buchanan B R et al (2006) Otoscopic, cytological and microbiological examination of the equine external ear canalVet Dermatol 17 (3), 175-181 PubMed.
  • MacKay R J (2004) Brain injury after head trauma: pathophysiology, diagnosis, and treatmentVet Clin North Am Equine Pract 20 (1), 199-216 PubMed.
  • Pease A P, van Biervliet J, Dykes N L et al (2004) Complication of partial stylohyoidectomy for treatment of temporohyoid osteoarthropathy and an alternative surgical technique in three casesEquine Vet J 36 (6), 546-550 PubMed.
  • Walker A M, Sellon D C, Cornelisse C J et al (2002) Temporohyoid osteoarthropathy in 33 horses (1993-2000)J Vet Intern Med 16 (6), 697-703 PubMed.
  • Bedenice D, Hoffman A M, Parrott B & McDonnel J (2001) Vestibular signs associated with suspected lightning strike in two horsesVet Rec 149 (17), 519-522 PubMed.
  • Tabamo R E & Donahue J E (1999) Eastern equine encephalitis: case report and literature reviewMed Health R I 82 (1), 23-26 PubMed.
  • Paradis M R (1998) Tumors of the central nervous systemVet Clin North Am Equine Pract 14 (3), 543-561 PubMed
  • Blythe L L (1997) Otitis media/interna and temporohyoid osteoarthropathyVet Clin North Am 13 (1), 21-42 PubMed.
  • Tietje S, Becker M & Bockenhoff G (1996) Computed tomographic evaluation of head diseases in the horse: 15 casesEquine Vet J 28 (2), 92 PubMed.
  • Mayhew I G & Washbourne J R (1990) A method of assessing auditory and brainstem function in horsesBr Vet J 146 (6), 509-518 PubMed.

Other sources of information

  • Rush B R (2004) Vestibular Disease. In: Equine Internal Medicine. Eds: Reed S M, Bayly W M & Sellon D C. Elsevier, USA. pp 579-588. ISBN: 0 7216 9777 1.
  • Hahn C H, Mayhew I G & Mackay R J (1999) Diseases of Vestibular and Cerebellar Structures. In: Equine Medicine & Surgery. Eds: Colahan P T, Mayhew I G, Merritt A M & Moore J N. Mosby Inc, USA. pp 941-945. ISBN: 0 8151 1743 4.