Stone Lion Veterinary Hospital, Goddard Veterinary Group, 41 High Street Wimbledon Common London SW19 5AU
Email: CRusbridge@goddardvetgroup.co.uk
Telephone: 020 8946 4228, Fax: 020 8944 0871
Copyright Clare Rusbridge ©
Central (BRAIN)
|
Peripheral (
|
Vestibular signs
|
Vestibular signs
|
Proprioceptive deficits (ipsilateral)
|
Proprioception normal
|
Paresis (ipsilateral)
|
Normal strength
|
Altered mental status
|
Mental status normal
|
Cranial nerve deficits (esp. CN V,
|
Cranial nerve deficits (CNVII and Horner’s only
|
|
D |
DEGENERATIVE |
As
part of polyneuropathy |
|
A |
Congenital
peripheral vestibular disease (Siamese). Onset at 2-3 weeks old and usually regress/compensate
at 2-4months old (may have recurrences, some permanent). Also in Burmese Cat
where it is typically permanent, non progressive and from birth. Also
reported in Doberman |
|
|
M |
METABOLIC |
As part of polyneuropathy associated metabolic disease e.g.
hypothyroidism |
|
N |
NEOPLASTIC |
Neoplasia
involving temporal bone (fibrosarcoma, osteosarcoma, chondrosarcoma, squamous
cell carcinoma) |
|
|
|
Neoplasia of the vestibulocochlear nerve (e.g. lymphoma or nerve root
tumour) |
|
I |
IDIOPATHIC |
Idiopathic
vestibular disease (sometimes referred to as “Stroke” by veterinary surgeons
however it is not a “brain” vascular event and carries a fair to good
prognosis) |
|
|
INFECTIOUS |
Otitis
media-interna |
|
T |
TOXIC |
Aminoglycoside
antibiotics |
|
|
TRAUMA |
Associated fracture of the petrosal bone |
|
D |
DEGENERATIVE |
Thiamine
(vitamin B1) deficiency |
|
N |
NEOPLASTIC |
Primary or secondary (at the
cerebellopontine angle) |
|
I |
INFECTIOUS - ACQUIRED |
FIP, Toxoplasma, Cryptococcus, Polioencephalomyelitis,
Distemper |
|
|
INLAMMATORY |
Granulomatous meningoencephalomyelitis ( |
|
|
TOXIC |
Metronidazole |
|
T |
TRAUMA |
Injuries
can appear devastating however many pets
can make an excellent recovery so it is worth being patient |
|
V |
VASCULAR |
Infarction
to the territory of the cerebellar /medulla arteries (i.e. stroke – this is rare
and not to be confused with idiopathic vestibular syndrome) |
Vestibular Disease
Damage to the vestibular system results in a vestibular syndrome which comprises one or more of the following signs
• Asymmetric ataxia i.e. drunken gait (worse on the side of the problem)
• Abnormal posture e.g. leaning or head tilt (towards the side of the problem)
• Circling/deviating (towards the side of the problem)
• Nystagmus (rapid eye flick – the slower flick is towards the side with problem)
• Vestibular (positional) strabismus (i.e. a squint, typically down, when the head position is changed)
• Vomiting (motion sickness
A Border Collie with idiopathic vestibular syndrome. There is a dramatic right sided head tilt. This dog was also had abnormal eye position and movement and was unable to stand and walk. The onset of signs was very sudden and severe; however, following supportive care she made a spontaneous recovery. A few weeks later the only signs that she ever had this problem was a subtle head tilt.
Investigation of vestibular disease
The most important “test” is a good neurological examination as this is used to determine if the vestibular syndrome is peripheral or central. The table below illustrates the salient differences between the two
To further elucidate the diagnosis, imaging may be recommended. The most useful is MRI as this allows both the ears and the brain to be appreciated. However ear infections can also be appreciated on CT and sometimes with radiographs.
Additional tests which may be recommended are cerebrospinal fluid (CSF) analysis in which the fluid which bathes the brain and spinal cord is analysed for abnormalities in protein concentration, cell counts and other parameters. This test is most useful to determine if there is an inflammatory and / or infectious disease. Tests for infectious agents such as viruses and protozoa may also be appropriate. Some neurologists use BAER (Brainstem Auditory Evoked Response) to assess the hearing pathways which are close to the vestibular pathways.
Vestibular syndrome is one of the most common neurological presentations in neurology and can be one of the most challenging. For prognostic purposes it is vital to distinguish between peripheral (ear and nerve) and central (brain) disease. The most reliable indication of central disease is depressed mental status (e.g. poorly interactive and disorientated) and postural deficits i.e. loss of strength and proprioception (i.e. the sense of where the joints are in space).
(ABOVE) MRI of a cat with vestibular syndrome as a consequence of a severe ear infection (otitis media / interna). The arrows indicate pus within the tympanic bullae. This case was successfully managed with a several week course of antibiotics however in some cases surgery is required especially if the infection is recurrent and/or associated with an inflammatory polyp.
If diagnostic tests are not possible e.g. for financial reasons then the best course of action is to monitor the neurological examination as knowing if the disease is central (brain) or peripheral (ear or nerve) can be a guide as to both prognosis and management.
Examples of peripheral vestibular disease
– common conditions highlighted in red
This miniature schnauzer was presented with depression, head tilt and stumbling (left picture). Tests including MRI, CSF analysis and blood work resulted in a diagnosis of hypothyroidism. Following thyroid supplementation she made a dramatic improvement (right picture 6 weeks post supplementation)
Examples of central vestibular disease
– common conditions highlighted in red
MRI images from a 10 year old female Golden Retriver with a a 2 week progressive history of vestibular ataxia. This started with a favouring of the right side and progressed to a right sided head tilt and leaning to the right. She was described as subdued and more anxious. These T1W gadolinium enhanced MRI images revealed a mass extending from the skull base (arrows). It covered the entire basioccipital bone and extended out of the foramen magnum to C1. The characteristics are most suggestive of a meningioma however a final diagnosis was not made. This dog was given palliative care (corticosteroids) and made a temporary improvement lasting a few weeks following which she was euthanatized.
Transverse TW2 weighted image from a 3 year old male cavalier King Charles spaniel that presented following acute onset (intention) tremor, depression and weakness with a right sided head tilt, facial nerve paresis and lateral strabismus. MRI reveals a sharply delineated wedge shaped lesion of the left rostral cerebellar hemispheres typical of cerebellar infarction (i.e. stroke). Obstruction of the mesencephalic aqueduct by swelling resulted in secondary hydrocephalus contributing to raised intracranial pressure and cerebellar vermis herniation. The problem was compounded by Chiari-like malformation. Magnetic resonance angiography of the vertebral, carotid, brainstem and cerebral arteries and investigation for cardiac disease and
bleeding disorders was unremarkable. This dog made a temporary improvement to intravenous methylprednisolone, furosemide and mannitol infusions. Ultimately an occipital craniectomy was required to relieve the rising intracranial pressure and brain herniation following which the dog made a good recovery.
Treatment of vestibular disease
Treatment of vestibular disease is twofold 1) dealing (if possible) with the underlying cause and 2) providing supportive care. Supportive care can include intravenous fluids especially if the pet is unable to drink and/or is vomiting. Anti-nausea drugs are recommended if vomiting occurs. Recovery for some causes of vestibular disease, e.g. idiopathic (old dog) vestibular syndrome, is by compensation - i.e. the brain (especially vision) compensates for a permanent deficit. Consequently the dog may be left with a permanent head tilt and a slight balance problem especially when doing more complex tasks. In some cases it can be worth arranging a session with a chartered physiotherapist (e.g. contact ACPAT, email - acpat@calra.net) with the aim of learning techniques to hasten / aid this compensation. There is some experimental evidence (in rats) that suggests that Propentofylline speeds up the brain’s ability to compensate after unilateral vestibular damage. Therefore some vets may advise a (1 month or more) course of this drug. If the pet is aged then it is also recommended to supplement the diet with antioxidants and essential fatty acids (many suitable veterinary formations and diets are available).
Occasionally there can be an acute decompensation (e.g. after suddenly being deprived of vision e.g. by turning of the lights). In this circumstance acute signs such as nystagmus etc can return for a few hours. In this circumstance it is advisable to keep the pet in a quiet environment and monitor. If signs are persistent then re-examination / re-investigation is warranted.