THE session on neurology at the
2013 BEVA congress was chaired
by David Rendle of the Liphook
Equine Hospital, with Richard
Piercy of the RVC describing
“How to investigate and treat the
horse with seizures”.
Seizure disorders make up a large
proportion of neurological cases seen
in practice. Generalised seizures are
obvious,
characteristic
and
dangerous to
the patient,
rider and
surrounding
people. Focal
seizures are
more subtle and so are harder to
diagnose.
Generalised seizures are the result
of depolarisation in the cerebral
cortex, often starting in the motor
cortical area that controls the head and
the lips. Twitching starts around the
eyes or the lips and then spreads over
the body.
Involuntary urination and
defaecation may occur and the horse
may fall and loose consciousness. If
the twitching progresses to rhythmic
involuntary muscle spasms, this is
known as status epilepticus, which is
usually brief, lasting only a few
minutes, but the potential for injury to
horse and bystanders is significant, so
it is wise to stand back until the fit
subsides.
Post-ictal period
After the seizure there is a post-ictal
period where the horse may be blind,
depressed and disorientated. This
blindness, amaurosis, comes from the
brain. The post-ictal period can last
from a few hours to a day but there
will be full recovery.
Focal seizures come from
depolarisation of a small area of the
forebrain, but the area involved may
spread, leading to a generalised seizure.
The clinical signs start locally, a facial
twitch for example, or isolated muscle
fasciculation, or isolated limb
movements. The brain disturbance will
be contralateral to the signs as the
motor pathways cross over below the
cerebrum.
Dummy foals suffering from toxic
ischaemic encephalopathy may have
fits of chewing, nystagmus and
paddling. This seizuring can look like
colic. It will resolve once the primary
problems are treated.
Arabian foals may seizure for a
year or a year and a half. If these
seizures can be controlled with
phenobarbitone the foals will grow out of the problem. In adult horses,
metabolic derangements or hepatic
encephalopathy can give rise to
secondary seizures but this is rare.
Tumours, such as cholesterol
granuloma, and space-occupying brain
lesions are likely to cause neurological
signs other than seizures. If the horse
has neurological or clinical signs in the
period between fits, it is more likely to have structural brain disease.
Most seizures happen without a veterinary surgeon being present but a
video taken by the owner can provide
good information.
In generalised
seizures, advanced imaging, (MRI or
CT) usually does not provide any new
information, unless there is a structural
lesion. Cerebro-spinal fluid (CSF) may
show low grade inflammatory
degenerative cytological or biochemical
changes for a few days after a seizure
but if these persist on further
monitoring it may indicate underlying
cerebral disease.
If seizures occur more than once a
week, treatment or euthanasia is
warranted. Infrequent seizures (more
than six months apart) do not require
treatment. The veterinary surgeon
needs to give the owners a good idea
of the commitment required to
maintain treatment for a seizuring
patient: it is expensive and it may need
to be life-long.
Phenobarbitone (5mg/kg
bodyweight by mouth once daily,
increasing by 25% every second week
until seizures are controlled) is the
most frequently used drug. If this
causes too much sedation, potassium
bromide (given orally at 30mg/kg
bodyweight ) can be added.
Treatment is not reduced until the
animal has been free from seizures for
six months. Return to being ridden is
usually avoided for at least six months
but owners need to be aware of the
risk of repeated seizures at any time.
In the light of this information, many
owners decide on euthanasia.
Osteoarthropathy
Kristopher Hughes of Charles Sturt
University in Wagga Wagga, Australia,
discussed “How to manage
temperohyoid osteoarthropathy”. This
is a rare condition, affecting mostly
middle-aged horses.
The stylohyoid and petrous temporal bones and the temperohyoid
(TH) joint are involved and often the
associated nerves are affected. There is
bony proliferation and the joint suffers
degenerative disease which can lead to
ankylosis. The condition can progress
without clinical signs until the altered
biomechanical forces due to the bone
distortion lead to fracture of the
petrous temporal bone or the
stylohyoid bone.
Surgical treatment such as partial
stylohyoidectomy or
ceratohyoidectomy can be used to
prevent fracture or treat it by reducing
the abnormal biomechanical forces.
Surgery can give a rapid improvement
in clinical signs. The prognosis is
guarded to fair.
Cause unknown
The cause of temperohyoid
osteoarthropathy (THO) is unknown.
It may be an extension of infection
from otitis media or externa or from
the guttural pouch, or a crib-biter may
present aseptic degenerative joint
disease which may lead to fracture.
THO may be clinically silent or
start as head shaking, pain over the
TH joint, resenting having the bridle
put on, or dysphagia. There may be
neurological signs associated with
damage to the vestibular, facial or
glossopharyngeal nerves with a head
tilt towards the affected side.
There may be exposure keratitis and keratitis sicca (KCS) due to lack of the
aqueous component of the tears caused
by damage to the parasympathetic
fibres which run through the petrous
temporal bone along with the facial
nerve. If the KCS becomes bilateral,
the horse should be euthanased.
Assessment of THO relies on
history and clinical examination backed
up by radiography, bilateral endoscopy,
scintigraphy and computed
tomography. CT is both sensitive and
specific. Tympanocentesis and cerebro-
spinal fluid analysis can also be useful.
The choice of antimicrobial should
be determined by culture and
sensitivity testing. If there is central
nervous system involvement, drugs
which cross the blood:CSF and
blood:brain barriers should be
selected.
Where there is otitis media or
interna or CNS involvement, the
treatment will need to extend over at
least 30 days and deciding when to
stop may need repeated testing.
Trimethoprim-sulfonamide
combinations or third generation
cephalosporins are suitable.
Treatment consists of attacking the
presenting signs – pain, inflammation
and infection – and surgical
intervention. Many horses improve
with treatment and return to athletic
function though there may be residual
cranial nerve dysfunction; improvement can continue for up to a year.
