The Neurological Horse with Abnormal Mentation

Question 1

What are different mentation statuses?

Answer 1

• Normal: Animal is alert and somewhat apprehensive and curious during examination
• Depressed: Animal is awake but not alert to surroundings; not interested in normal stimuli. Not exclusively neurological in origin. is it appropriate or not?
• Obtunded: Animal is dull and slow to respond, but will respond appropriately.
• Stuporous: Animal is unresponsive to normal stimuli; can be aroused with strong stimuli.
• Comatose: State of unconsciousness in which the animal cannot be aroused, even with noxious stimuli
• Other: Abnormal behaviour, disoriented, delirious, aggression, head-pressing, fly biting, tail chasing, circling

Question 2

What are the general signs of forebrain disease?

Answer 2

➢ OBTUNDATION
➢ HEAD-PRESSING
➢ ODONTOPRISIS (TEETH GRINDING)
➢ HYPERSTESIA/IRRITABILITY
➢ BLINDNESS (LACK OF MENANCE WITH NORMAL PLRs)
➢ SEIZURES
➢ CIRCLING
➢ HEAD TURN
➢ ATAXIA

Question 3

What are possible causes of abnormal mentation?

Answer 3

• viral encephalitides
• head trauma
• hepatic encephalopathy
• idiopathic seizures

Question 4

What causes hepatic encephalopathy?

Answer 4

• Accumulation of ammonia in the blood because of a dysfunctional liver.
• Blood crosses the BBB and the astrocytes metabolise ammonia to generate glutamine.
• Stimulates the production of GABA, a neurotransmitter that depresses neural condution within the central nervous system.
• Also causes accumulation of fluid in neurons - leads to brain oedema

Question 5

What clinical signs are associated with hepatic encephalopathy?

Answer 5

• Depression, obtundation
• Head pressing
• Compulsive walking
• Ataxia
• Seizures

Question 6

How is hepatic encephalopathy diagnosed? How is it treated?

Answer 6

Diagnosis
Liver enzymes elevation: SDH, GDH, GGT, AST, bile acids
if severe disease
✓ hyperammonaemia
✓ Low BUN
✓ Prolonged clotting times (PT, APTT)

Treatment
* Treat liver disease and support neuronal function
* Intravenous fluids with dextrose» liver is not functioning
* Oral Lactulose and/or mineral oil»reduced absorption of ammonia in GI system
* Xylazine/Detomidine to sedate cases with compulsive walking/head pressing
* Avoid Benzodiazepines (increase GABA activity) unless severe seizures
* Plasma transfusion if low clotting factors due to severe liver disease
* Steroids?
* Diet: Low prot + high CH: Sorghum, milo, beet pulp + molasses/Karosyrup

Question 7

Why are horses predisposed to head trauma?

Answer 7

Flighty - will run into walls or get kicked or flip over backwards

Question 8

What clinical signs are associated to head trauma? How is it treated?

Answer 8

• Epistaxis, sometimes haemoptysis
• Ear bleeding: temporal damage
• Retropharyngeal swelling> inspiration dyspnoea
• Blindness
• Cranial nerve deficits
• Irregular breathing pattern
• Anisocoria
• Obtundation/comatose

Treatment
* Establish airway: nasal or frontal fractures
* Obtain vascular access: hypotension, administer medication, control seizures
* Clean and dress wounds: stanch bleeding
* Antibiotics: prevent meningeal infection
* Padded helmet: avoid further trauma
* Control temperature: hyperthermia possible> hypothalamic damage
* Control brain swelling: Hypertonic saline, mannitol
* Oxygen, antioxidants (Vit E, DMSO), Steroids, NSAIDs, magnesium sulphate.

Question 9

What are causes of epilepsy? How is it diagnosed?

Answer 9

More than two unprovoked episodes no more than 30 days apart

Idiopathic: genetical predisposition (Arabs) or unknown causes
Structural
* Skull fractures
* Masses
* Haemorrhages
* Leukoencephalomalacia (mycotoxins)
* Hypoglycaemia, foal maladjustment syndrome
* Intracarotid injections

Diagnosis
Rule out structural aetiology
* Good physical exam: mentation problems, cranial nerves, facial asymmetry, nasal discharge, ocular exam (strabismus, retina, mydriasis, myosis, retinal haemorrhages),postural deficits, signs of skull trauma..
* Full haematology and biochemistry: inflammatory markers, liver profile, glucose and magnesium
* CSF tap: neutrophilia, high protein, xanthochromia, abnormal cells
* Skull x-rays, guttural pouch endoscopy?
* MRI, CT contrast
* Electroencephalography

Question 10

How are seizures treated?

Answer 10

Acute phase
* Midazolam 0.05-0.1mg/kg IV q 15 min (3 doses)
* Diazepan 0.05-0.2mg/kg IV q 5 min (3 doses)
* Phenobarbital 5mg/kg q 12h
* Do not approach an adult horse during the crisis. Normally, seizure activity ceases within 5 min, if persistent activity is noticed administration of medication might be necessary but only if safe for personnel

Maintenance
* Phenobarbital 5mg/kg q 12h if no effect increase 1mg/kg q 15 days
* K-bromide can be added for additional control
* Levetiracetam (32mg/kg q 24h)

Foals: treatment for 3 months then tapering over 2 months (1/2 dose, then q 48h)
Adult : 6 months free of seizures tapering over 4 weeks
If no seizures in following 6 months»> no longer considered epileptic

Question 11

What viral encephalomyelitis causes are notifiable in the UK?

Answer 11

• West nile virus
• Eastern/ western/ venezuelan
• Rabies

Question 12

What clinical signs are associated with west nile virus? How can it be prevented?

Answer 12

• Ataxia (71%) and limb weakness (58%)
• Muscle twitching (45%): muzzle
• Obtundation (43%)
• Dog-sitting posture (10%)
• Thoracic limb knuckling
• Recumbency, circling…
• Facial and tongue paralysis, head tilt…
• Mortality around 31% (USA studies)

Vaccination of horses travelling to Europe in warmer months