Dealing with seizures and sore heads

01 January 2014, at 12:00am

Marion McCullagh presents her third and final report on the sessions at the 2013 congress of the British Equine Veterinary Association with a review of some of the papers on neurological problems

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.


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.