Vestibular disease Flashcards by Hannah Leech

What are the differentials for central vestibular disease?

FIP/ other infections
GME
Neoplasia
Degenerative disease
Trauma
Cerebrovascular disease
Hypothyroidism
Brain malformation
Thiamine deficiency
Lysosomal storage diseases
MTZ

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What are the differentials for peripheral vestibular disease?

Idiopathic
Middle/ inner ear infections/ trauma/ neoplasia
Hypothyroidism
Congenital vestibular disease
ototoxic preparations

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What are the ddx for acute vestibular disease?

 Idiopathic vestibular disease
 Cerebrovascular disease
 Head trauma
 Trauma to middle/inner ear
 Hypothyroidism
 Metronidazole
 Ototoxic drugs

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What are the ddx for chronic disease?

 Otitis media/interna
 MUEs, FIP
 Brain and middle ear tumours
 Thiamine deficiency
 Lysosomal storage diseases
 Degenerative diseases
 Brain malformation
 Congenital vestibular disease
 Hypothyroidism
 Metronidazole
 Ototoxic drugs

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What is a stroke?

Clinical manifestation of cerebrovascular disease

Mostly ischaemic in animals

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How do you dx a stroke?

 clinical signs vary but acute and nonprogressive; signs of central vestibular disease
MRI:
 well-defined, sharply demarcated lesions with minimal to no mass effect
 limited to the vascular territory of a main cerebral or perforating artery
 hyperintense on T2WI and FLAIR

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What condtitions can cause a stroke?

 chronic kidney disease
 hyperadrenocorticism
 hypertension
 cardiac disease
 neoplasia
 Angiostrongylus vasorum
 diabetes mellitus, hypothyroidism

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How do you treat a stroke and what is the px?

 treatment – supportive or if underlying disease
 prognosis fair to good
 1/2 - 2/3 good outcome
 concurrent medical conditions:
• shorter survival times
• more likely to have recurrence

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What are the types of MUO?

MUOs – meningoencephalomyelitis of unknown origin:
 GME – Granulomatous ME
 NME – Necrotising ME
 NLE – Necrotising leukoencephalytis

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What are the signs of MUO and how do you diagnose it?

 +/- acute and progressive, often multifocal
 rarely extraneural signs (pyrexia, leukocytosis)
Differential diagnosis:
 infectious ME
 neoplasia
 toxic
 metabolic disease
 genetic disease
Dx by:
 advanced imaging
 cerebrospinal fluid analysis (sometimes can't do this as often have high ICP)
 sometimes biopsy

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What are the signs of GME?

 young adults (3-8y), toy and terrier breeds
 multifocal signs
 often caudal fossa (vestibular and cerebellar) but anywhere
 can effect spinal cord (+/- brain)
 may just cause acute blindness
 3 forms:
1. Disseminated – most common; multifocal signs
involving forebrain, brainstem, cerebellum, spinal cord
2. Focal – can be confused with neoplasia
3. Ocular – acute onset visual impairment, dilated and
non-responsive pupils and optic disc oedema

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How do you diagnose GME?

MRI:
 multiple hyperintensities on T2WI and FLAIR
 irregular margins
 predilection for WM but in both GM and WM
 variable degrees of contrast enhancement
CSF analysis:
 pleocytosis (lymphocytic, neutrophilic or mixed)
 increased protein concentration
 occasionally can be normal

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What is necrotising encephalitis?

 Pug, Maltese, Chihuahua, Yorkie, Pekingese,
Shih-Tzu, WHWT, Boston terrier, Japanese Spitz,
Miniature pinscher
 NME and NLE very difficult to differentiate antemortem so often combined and called NE
 acute onset and rapidly progressive signs, worse
prognosis
 non suppurative ME and cerebral necrosis

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What is necrotising myeloencephalitis?

 18m (usually under 4y); Fs
 seizures very frequent (>90%), blindness, altered behaviour, circling, depression
 DNA test available – risk only
 GM and WM; mostly in cerebral hemispheres but can also affect brainstem
 extensive necrosis with mononuclear infiltration of meninges and cerebral cortex

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What is NLE?

 middle aged Yorkies; French Bulldog
 circling, head tilt, blindness, abnormal gait
 mainly periventricular cerebral WM (but affects both cerebrum and brainstem)
 areas of necrosis often coalesce to form large areas of cavitation

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How do you Tx MUO?

Immunosuppressives

MST much better if pred + something else (normally cytarabine)

What is the px of MUO?

GME:
 if controlled quickly – better outcome
 if tricky to control (relapses) – treatment long-term; variable survivals
 if not responding initially – poor outcome

NE
Shorter survival times, often few months only
Often have permanent deficits

Outline neurological signs of FIP

 ~ 30% of cats with clinical FIP have CNS involvement; lesions result from immunecomplex-mediated vasculitis
 Neurological signs:
 insidious signs, progressive, can be focal, diffuse or multifocal
 more commonly localise to the cerebellomedullary region (tetraparesis, ataxia, nystagmus and loss of balance)
 occasionally only progressive spinal cord disease
 sometimes also behavioural changes, seizures
 +/- iritis, anterior uveitis, chorioretinitis

How do you diagnose FIP?

 clinical signs +/- ocular changes
 lymphopenia, neutrophilia, non-regenerative
anaemia
 increased serum α-1-acid glycoprotein (AGP)
 high serum titres of FCoV Ab
 albumin to globulin ratio >0.8g/dL
 CSF (variable): usually high protein and pleocytosis (mononuclear or mixed)
 anti-coronavirus IgG in CSF (not diagnostic as accompanies serum titres)
 MRI or CT: periventricular contrast enhancement, ventricular dilation and hydrocephalus

Outline MTZ as a cause of vestibular disease

 uncommon; signs of CVS, seizures, tremors, rigidity
 usually when doses ≥60mg/kg/day but lower doses
have been reported
 mechanisms of neurotoxicity suggested:
 RNA and DNA binding
 modulation of inhibitory neurotransmitter GABA receptor within cerebellar and vestibular systems
 discontinuation of drug; faster improvement with
diazepam (12h vs. 4d) (competitively inhibits MTZ binding to GABA)

Outline ototoxic drugs as a cause

antibiotics
 aminoglycosides (streptomycin and gentomicin)
 tetracyclines
chemotherapy agents:
 cisplatin
 vinblastine and vincristine
perforated ear drum:
 chorhexidine
 reversible or permanent

Outline thiamine deficiency in cats

 low amount in food; overcooked food
 cats fed with all-fish diet
 essential for complete oxidation of Glucose in Krebs cycle
 tissues dependent on glucose for energy (brain, heart) more affected
 anorexia, lethargy
 vestibular signs
 seizures
 reduced physiol nystagmus, mydriasis with reduced PLR
Dx - very specific bilateral areas of brain affected on MRI, can do bloods (but this is harder)
Tx - thiamine infusion

Outline otitis media/ interna as a cause

 Remember structures passing by middle ear:
 CN VII
 CN VIII
 Sympathetic supply to eye
 Signs may include:
 Facial paralysis
 Peripheral vestibular signs
 Horner’s syndrome
 Pain opening the mouth

How do you tx otitis media/ interna?

• flush middle ear cavity
• prednisolone 1-2mg/kg
• treat infection
Often need sx (TECA/ VBO)

Outline idiopathic vestibular dz in the dog

``` • acute onset of peripheral signs  rolling, falling, vomiting, ataxia  head tilt  nystagmus (horizontal or rotatory) • can be bilateral, can happen simultaneously with facial paralysis • middle to older age dogs • usually some spontaneous improvement within 2-3d, often resolved within ~3-4 wks  nystagmus/ataxia  head tilt ```

How do you tx idiopathic dz?

``` in general, patients may be nauseous  meclozine  maropitant stimulation is important  do not keep quiet all the time  take out slowly but ensure gets up often for short periods of time  teaches the vestibular system all over again what is normal  tempt to eat  cozy beds ```

How is idiopathic disease different in the cat?

 2 forms???  acute onset of PVD, non-progressive, improving over 2-4 weeks  atypical form – acute onset of PVD but clinical signs progressive over a 3 week period  recovery over 3 months; residual deficits (mild head tilt) not uncommon

How quickly should you investigate vestibular disease?

```  peripheral  if suspicious for middle ear disease investigate  otherwise wait and see…  central  advanced imaging of brain ```

Outline the anatomy of the hearing system

``` Outer ear  pinna  ear canal  ear drum Middle ear  3 ossicles  vestibular window Inner ear  cochlea ```

What is the cochlea?

 spiral shaped, fluid filled  part of inner ear along with balance receptors  share the same nerve (vestibulocochlear)  fluid inside moves when the ossicles pull  Organ of Corti  hair cells

What is the process of hearing?

```  sound wave  external ear canal and ear drum  3 ossicles (malleus, incus, stapes)  fluid in cochlea - movement of hair cells  impulse in cochlear neurons  message to brain ```

How can you classify deafness?

 age of onset - congenital or late onset  underlying cause - inherited or acquired  location - peripheral or central  sensorineural (from the cochlea to the auditory cortex of the brain) or conductive (failure to conduct sound from the outer ear to the inner ear)

What are the most common types of deafness?

 congenital sensorineural deafness  acquired sensorineural deafness (chronic otitis interna and/or media, ototoxicity, noise trauma or presbycusis in older animals)  acquired conductive deafness (otitis externa and media)

Outline congenital sensorineural deafness

 dog breeds with white pigmentation and blue eye colour  reported in over 80 dog breeds and several cat breeds  stria vascularis (vascularised epithelium of cochlea) develops normally, but undergoes degeneration shortly after birth and resulting in the death of hair cells of organ of Corti  Dalmatian has highest incidence in the UK (18%)  Brainstem Auditory Evoked Responses (BAER) used to diagnosed, typically at 8 weeks of age

Outline inflammatory polyps

Peripheral signs Normally <2 years old, with signs of middle ear disease Diagnosis may require examination of the external ear canal, tympanic membrane and pharynx under general anaesthesia, and imaging of the middle/inner ear by either radiography or MRI. In some cases exploratory surgery is required. The polyps are usually only attached by a narrow stalk to the Eustachian tube and can readily be removed by traction. In some cases a ventral bulla osteotomy may be necessary.