Vestibular disease

Question 1

What are the differentials for central vestibular disease?

Answer 1

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

Question 2

What are the differentials for peripheral vestibular disease?

Answer 2

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

Question 3

What are the ddx for acute vestibular disease?

Answer 3

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

Question 4

What are the ddx for chronic disease?

Answer 4

 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

Question 5

What is a stroke?

Answer 5

Clinical manifestation of cerebrovascular disease

Mostly ischaemic in animals

Question 6

How do you dx a stroke?

Answer 6

 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

Question 7

What condtitions can cause a stroke?

Answer 7

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

Question 8

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

Answer 8

 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

Question 9

What are the types of MUO?

Answer 9

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

Question 10

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

Answer 10

 +/- 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

Question 11

What are the signs of GME?

Answer 11

 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

Question 12

How do you diagnose GME?

Answer 12

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

Question 13

What is necrotising encephalitis?

Answer 13

 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

Question 14

What is necrotising myeloencephalitis?

Answer 14

 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

Question 15

What is NLE?

Answer 15

 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

Question 16

How do you Tx MUO?

Answer 16

Immunosuppressives

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

Question 17

What is the px of MUO?

Answer 17

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

Question 18

Outline neurological signs of FIP

Answer 18

 ~ 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

Question 19

How do you diagnose FIP?

Answer 19

 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

Question 20

Outline MTZ as a cause of vestibular disease

Answer 20

 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)

Question 21

Outline ototoxic drugs as a cause

Answer 21

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

Question 22

Outline thiamine deficiency in cats

Answer 22

 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

Question 23

Outline otitis media/ interna as a cause

Answer 23

 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

Question 24

How do you tx otitis media/ interna?

Answer 24

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

Question 25

Outline idiopathic vestibular dz in the dog

Answer 25

• 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

Question 26

How do you tx idiopathic dz?

Answer 26

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

Question 27

How is idiopathic disease different in the cat?

Answer 27

 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

Question 28

How quickly should you investigate vestibular disease?

Answer 28

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

Question 29

Outline the anatomy of the hearing system

Answer 29

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

Question 30

What is the cochlea?

Answer 30

 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

Question 31

What is the process of hearing?

Answer 31

 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

Question 32

How can you classify deafness?

Answer 32

 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)

Question 33

What are the most common types of deafness?

Answer 33

 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)

Question 34

Outline congenital sensorineural deafness

Answer 34

 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

Question 35

Outline inflammatory polyps

Answer 35

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.