Vestibular disease Flashcards
Anatomy of the vestibular system
Peripheral part:
- sensory receptors (in the vestibular apparatus)
- vestibulocochlear nerve CNVIII
Central part:
- Brainstem - vestibular nuclei
- (cerebellum, thalamus, cranial cervical spine)
Function of the vestibular system
Maintain an animals balance and orientation wrt gravity
Including maintaing position of eyes, trunk, and limbs
It also controls eye movements in relation to movements of the head
Clinical signs of unilateral vestibular dysfunction
Imbalance
Abnormal head, limb/body, and eye position
Abnormal eye movements
Head tilt towards the lesion (unless paradoxical)
Ataxia with a wide based stance, circling, leaning, falling, or rolling towards a lesion
Strabismus (often positional), nystagmus
Clinical signs of bilateral vestibular dysfunction
Wide excursions of the head from side to side and a lack of physiological nystagmus
Neurological exam findings in central vestibular disease (brainstem and cerebellum)
Mentation: may be affected
Head tilt: ipsilateral or contralateral
Gait: vestibular ataxia, can present paresis, proprioceptive ataxia, dysmetria
Postural reaction deficits: may be ppresent on the side of the lesion
Nystagmus: pure vertical, horizontal, rotatory. Can change direction with change of head position
Intention tremor: with cerebellar lesion
Neurological exam findings in peripheral vestibular disease (inner ear and CN VIII)
Mentation: normal
Head tilt: ipsilateral
Gait: vestibular ataxia, no paresis
Postural reaction deficits: normal
Nystagmus: VII, sympathetic innervation of the eye (Horner’s)
Intention tremor: no
Types of nystagmus
Horizontal, rotatory, or vertical
Spontaneous or positional
Jerk or pendular
Spontaneous nystagmus
observed when head in normal position
Due to different stimulation of the vestibular system
Postional nystagmus
Elicited by moving the head in an unusual position i.e. either by lifting the head or by lying the animal on its back
Jerk nystagmus
Has a slow and rapid phase
Typically observed in vestibular disorders
Pendular nystagmus
Sinusoidal
Typically observed in cerebellar disorders
Circling
Seen in vestibular and fore brain diseases.
CIrcles are usually narrow in vestibular diseases, compared with wide compulsive circles in forebrain diseases.
Paradoxical vestibular disease
The head tilt is paradoxical
Cerebellar lesion (caudal cerebellar peduncle and flocculonodular lobe)
Sometimes other cerebellar signs
Vascular central vestibular diseases
Infarction, haemorrhage
Infectious/inflammatory central vestibular diseases
Meningoencephalitis (MUO)
Empyaema, Toxoplasma/neospora, FIP
Idiopathic central vestibular diseases
Arachnoid cysts
Traumatic central vestibular diseases
Head trauma
Toxic central vestibular diseases
Metronidazole
Anomalous central vestibular diseases
Congenital malformation
Neoplastic central vestibular diseases
Brain tumours - primary or metastatic
Nutritional central vestibular diseases
Thiamine deficiency
Degenerative central vestibular diseases
Lysosomal storage disorders
Neurodegenerative diseases
Infectious/inflammatory peripheral vestibular diseases
Otitis media/interna
Nasopharyngeal polyps
Idiopathic peripheral vestibular diseases
Idiopathic vestibular disease
Traumatic peripheral vestibular diseases
Trauma to middle or inner ear
Toxic peripheral vestibular diseases
Aminoglycosides
Chlorhexidine
Anomalous peripheral vestibular diseases
Congenital vestibular disease (most common cause in dogs)
Metabolic peripheral vestibular diseases
Hypothyroidism
Neoplastic peripheral vestibular diseases
Tumours of the middle and inner ear
Pathogenesis of otitis media/interna
Infeciton of the middle/inner ear, most commonly as an extension of otitis externa
Staphylococcus intermedius and Pseudomonas are the most common organisms
Can also occur by ascent from the oral cavity through auditory tube or by haematogenous spread
Clinical signs of otitis media/interna
Vestibular signs (peripheral)
Facial nerve paralysis and/or Horner’s syndrome can be seen due to close association of CN VII nd the sympathetic nerve with the petrous temporal bone
Diagnosis of otitis media/interna
Otoscopic exam: tympanic membrane often ruptured
X-ray/MRI/CT: to visualise the tympanic bullae
Myringotomy: to obtain some fluid for cytology or culture - needle through tympanic membrane to aspirate
Treatment of otitis media/interna
Systemic antibiotics ideally on results of culture, for 4-6 weeks (amoxycillin/clavulanate, cephalosporin, or fluoroquinolone)
Bulla osteotomy can be needed if unresponsive to medical treatment
Prognosis of otitis media/interna
Good for resolution of infection, although neurological damafe may persist due to irreversible damage of neural structures
Pathogenesis of idiopathic vestibular disease
Cause not determined, potentially various
Epidemiology of idiopathic vestibular disease
Common in dogs and cats
Most common cause in dogs
Typically older dogs so sometimes called canine geriatric vestibular disease
Clinical signs of idiopathic vestibular disease
Peripheral vestibular dysfunction
Signs usually unilateral and severe
Peracute onset
Vomiting is common at the initial stage of the disease
Horner’s syndrome can be seen in dogs but not in cats
In cats can get facial paralysis
Diagnosis of idiopathic vestibular disease
Exclusion of other causes
MRI contrast enhancement of CN VIII
Treatment of idiopathic vestibular disease
No treatment is recommended other than supportive care
Prognosis of idiopathic vestibular disease
Usually good
Spontaneous improvement typically seen within 2-3 days
Complete resolutions takes 2-4 weeks and in some cases may be prolonged for months
Mild head tilt may persist
Can re-occur
Middle ear polyps
Cats of all ages (often young, and male)
Middle ear localisation, Horner’s common
May show respiratory signs
Sub-acute onset, progressive signs of vestibular disease
Diagnosis of polyps
Visualisation (with or without otoscope)
Imaging (CT, MRI)
Treatment of polyps
Traction-avulsion vs central bulla osteotomy vs TECA
+/- antibiotics and corticosteroids
Recurrence depends on technique (14-50% traction avulsion, 2% VBO)
Ototoxic medication causing disease
Causes: animoglycosides, tetracyclines, cisplatin, chlorhexidine, loopdiuretics, propylene glycol
Signs of peripheral vestibular disease
Peracute/acute onsest
Progressive
Diagnose on clinical signs and history
Treatment: stop medications
Prognosis good for recovery of vestibular signs but poor for hearing
Neurodiagnostic investigation (especially when central vestibular syndrome suspected)
Routine haem and biochem (metabolic, inflammatory, infectious disease)
ACTH stimulation: Cushing’s disease and chronic renal failure - hypertension
T4/TSH testing: hypothyroidism
Toxoplasma/neospora serology
Coagulation testing
Angiostrogylus vasorum testing: haemorrhagic stroke
Urinalysis: protein losing enteropathy can predispose ischaemic stroke (loss of anticoagulant factors)
Systemic blood pressure: persistent hypertension
CT/MRI: structural abnormalities
Pathogenesis of cerebrovascular accident (CVA)
Ischaemic (>70%):
- endocrine
- renal
- cardiac
- neoplasia
- sepsis
- parasitic
- hypertension
Haemorrhagic (<30%):
- neoplasia
- coagulopathy
- parasitic
- malformations
- trauma
- hypertension
- vasculitis
Signs of cerebrovascular accident (CVA)
SIgns of central vestibular disease
Peracute/acute onset
Minimal progression/gradual movement
Diagnosis of cerebrovascular accident (CVA)
Confirm clinical suspicion
- MRI (ischaemic: T2W hyperintense, sharly marginated, mainly GM, lesions confined to vascular territory of affected vessel.; Haemorrhagic: mass lesion, intensities vary with time)
- CSF (exclusion of other causes
Look for concurrent disease process:
- CBC, biochemistry, UA
- BP
- imaging (chest/abdomen)
- endocrine testing if clinically appropriate
Treatment of cerebrovascular accident (CVA)
If concurrent disease identified then treat that
Symptomatic (nursing, anti-emetics, physiotherapy)
Prognosis of cerebrovascular accident (CVA)
Good if no concurrent disease found
Ischaemic disease has better prognosis than haemorrhagic
Metronidazole toxicity - central vestibular disease
Dogs and cats treated with high doses of metronidazole for at least a month can develop signs of neurotoxicity, usually presenting as central vestibular syndrome
Can happen at lower doses in shorter time
Resolution of signs after discontinuation of therapy takes 3-5 days, may be quicker is diazepam given orally
Cerebellovestibular ataxia, head tilt, nystagmus, seizures
Thiamine deficiency - central vestibular disease
In cats, females overrepresented
Encelopathy, including the medial vestibnular nuclei
Impaired energy metabolism
Bilateral, central vestibular signs. Subacute/acute onset. Wax- and-waning
Diagnose with brain MRI - symmetrical hyperintense leions in specific nuclei. Serum testing can reveal low thiamine levels but ranges poorly defined.
Treat by injecting vitamin B1 (thiamine), and correcting diet
Prognosis is good - reversible in most cases
FIP - central vestibular disease
Signs sometimes multifocal/diffuse. Subacute/acute onset. Progressive
CNS form often associated with ocular form and non-effusive form
Immune-complex mediated development of vasculitis
Diagnosis of FIP - central vestibular disease
PCR on CSF, free fluid, or tissue
Immunohistochemistry
MRI
CSF: increase in microprotein and leocytosis
Treatment of FIP - central vestibular disease
Remdesivir IV
Adenosine nucleoside analogue
80-90% response - good prognosis
Hypothyroidism - central vestibular disease
Central and peripheral signs
Subacute/acute onset. Progressive
Central disease can be related to CVA
Abnormal axonal function and transport/polyneuropathy; abnormal lipid metabolism and arteriosclerosis; myxoedematous compression
Diagnosis: T4/TSH
Treatment: Levothyroxine
Prognosis: good, reversible
