The neurological horse with abnormal mentation Flashcards
(40 cards)
What is a normal mentation?
- animal is alert and somewhat apprehensive and curious during exam
What is a depressed mentation?
- animal is awake but not alert to surroundings
- not interested in normal stimuli
- not exclusively neurological in origin, is it appropriate or not?
What is an obtunded mentation?
- animal is dull and slow to respond, but will respond appropriately
What is a stuporous mentation?
- animal is unresponsive to normal stimuli
- can be aroused with strong stimuli
What is a comatose mentation?
- state of unconsciousness in which the animal can’t be aroused, even with noxious stimuli
General signs of forebrain disease
- obtundation
- head-pressing
- odontoprisis (teeth grinding)
- hyperesthesia/irritability
- blindness (lack of menace with normal PLRs)
- seizures
- circling
- head turn
- ataxia
Causes of abnormal mentation
Viral encephalitides
- EEE/WEE/VE
- WNV
- borna
- rabies
Head trauma
Hepatic encephalopathy
Idiopathic seizures
Hepatic encephalopathy - cause
Normally most ammonia is absorbed in the GIT and gets converted to urea in the liver, and released in the urine.
In horses with liver disease, this process is impaired and higher levels than normal reach the brain.
Astrocytes within the brain transform the ammonia to the amino acid glutamine. Glutamine stimulates the production of gaba (a neurotransmitter) that depressed neural conduction in the CNS. It is also able to shift the cellular osmotic gradients, triggers the accumulation of fluid in the neurones. The accumulation of fluid will eventually lead to brain oedema
Hepatic encephalopathy - CS
- depression, obtundation
- head pressing
- compulsive walking
- ataxia
- seizures
Hepatic encephalopathy - diagnosis
Liver enzymes elevation: SDH, GDH, GGT, AST, bile acids
If severe disease
- hyperammonaemia
- low BUN
- prolonged clotting time (PT, aPTT)
Hepatic encephalopathy - tx
Tx liver disease and support neuronal function.
IV fluids with dextrose»_space; liver is not functioning.
Oral lactulose and/or mineral oil»_space; reduced absorption of ammonia in GIT
Xylazine/detomidine to sedate cases with compiles 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 protein + high carbs (Sorghum, milo, beet pulp + molasses/karosyrup)
Head trauma - causes (generally and for each area)
Horses predisposed due to flighty temperament, thin calvaria and activity (fast gaits)
Blows to frontal and parietal area: run into stationary objects, kicks.
Occipital/temporal areas: flipping over backwards, ‘counter-coup’
Temporal/stylohyoid: GP pathology, result of temporal hyoid OA
Base skull: avulsion fractures: flipping backwards
Head trauma: CE & diagnostic points
CE:
- temp
- breathing pattern
- mm
- palpation of skull
- CN assessment
- mentation
Radiographs, CT, GP scope, blood gas (oxygenation, acid-base status)
Head trauma - CS
- epistaxis, sometimes haemoptysis
- ear bleeding: temporal damage
- retropharyngeal swelling > inspiration dyspnoea
- blindness
- CN deficits
- irregular breathing pattern
- anisocoria
- obtundation/comatose
Head trauma - tx
General principles of critical care medicine
- establish airway: nasal or frontal fracture
- obtain vascular access: hypotension, administer meds, control seizures
- clean & 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 (vitE, DMSO), steroids, NSAIDs, magnesium sulphate
- give time (for CNS to recover and the fracture to heal)
Seizure - cause/what is it?
- abnormal synchronous electrical discharges in the neuron’s of the forebrain that lead to spontaneous, paroxysmal, involuntary movements that might begin
- cerebral dysfunction caused by an imbalance between excitation and inhibition in the brain
Epilepsy - what is it?
- more than 2 unprovoked episodes no more than 30d apart
Epilepsy - causes
Idiopathic
- genetical predisposition (Arabs) or unknown causes
Structural
- skull fractures
- masses
- haemorrhages
- leukoencephalomalacia (mycotoxins)
- hypoglycaemia, foal maladjustment syndrome
- intracarotid injections
Seizures - diagnostic plan
Rule out structural aetiology
Good physical exam
- mentation
- CN
- facial asymmetry
- nasal discharge
- ocular exam (strabismus, retina, mydriasis, myosis, retinal haemorrhages)
- postural deficits
- signs of skull trauma
Full haematology & biochemistry
- inflammatory markers
- liver profile
- glucose and magnesium
CSF tap
- neutrophilia
- high protein
- xanthochromia
- abnormal cells
Skull x-rays, GP endoscopy?
- GP endoscopy always indicated as we can assess some portions of the skull
MRI, CT contrast
Electroencephalography
- when haven’t found anything yet
- gives more information on the neurones themselves and their function
Seizures - tx in the acute phase
- midazolam 0.05-0.1mg/kg IV q15mins (3 doses)
- diazepam 0.05-0.2mg/kg IV q5mins (3 doses)
- phenobarbital 5mg/kg q12h
Don’t approach an adult horse during the crisis. Normally seizure activity ceases within 5 mins, if persistent activity is noted administration of meds might be necessary but only if safe to do so
Seizures - maintenance tx
- phenobarbital 5mg/kg q12h
— if no effect increase 1mg/kg q15d
— K-bromide can be added for additional control - levetiracetam 32mg/kg q24h
Seizures - tx length
Foals
- tx for 3 months
- then tapering over 2 months (1/2 dose, then q48h)
Adult
- 6 months free of seizures
- tapering over 4 weeks
- if no seizures in following 6m»_space;> no longer considered epileptic
Seizures - safety considerations
Horse can collapse anytime
- always handled by an experienced person on a long rope
- provide large stable with thick bedding to minimise trauma
- don’t ride the horse for the initial 6months of tx, tapering period (3months) and up to 6months after withdrawal of meds
Ideally horse should only be ridden by an experienced rider over the age of 18 that understands the risk (particularly if the horse had several seizing episodes).
Macrocytic lactones (GABA blocker) should NOT be given to horses on anticonvulsant therapy
Viral encephalomyelitis - causes?
- West Nile Virus
- Easter/Western/Venezuelan
- Borna
- Rabies
