2. Introduction
Seizure is the clinical manifestation of
excessive discharge of hyperexcitable
cerebrocortical neurons
Behavioural changes:
• Increased timidity or aggression
• Circling
• Head pressing
• Aimless walking or compulsive wandering
3. Epilepsy
State of recurrent seizures regardless of
aetiology
Primary epilepsy (functional,
asymptomatic): is result of functional cerebral
disturbances for which there is no underlying
cause other than hereditary disposition e.g.
canine idiopathic epilepsy
Secondary epilepsy (structural,
symptomatic): caused by acquired brain
lesions e.g. posttraumatic
4. Pathophysiology
Seizures occur when there is imbalance between
exitatory and inhibitory processes.
1.Inadequate neuronal inhibition
Major inhibitory neurotransmitters include GABA and
glycine
2.Excessive neuronal excitation
Major excitatory neurotransmitters include aspartate and
glutamate
5. Proposed Mechanisms
1. Defective feed-forward inhibition or feed-back
initiation of inhibitory neurons in cortical circuits
Recurrent excitatory collaterals may be formed
2. Changes in membrane properties of neurons
These may include changes at:
Potassium, sodium, chloride and calcium ion channels
GABA receptors
Nicotinic acetyl choline receptors
NMDA receptors activation
3. Changes in the ionic microenvironment
6. Seizures may then spread:
To adjacent areas of the brain.
Through established anatomic pathways to other
distant areas
7. Nomenclature
Status epilepticus is the term used to describe
A seizure lasting longer than 15 minutes, or
A collection of discrete seizures without full recovery of
consciousness
Clusterseizures occur when 2 or more seizures are
experienced in a brief periods, but the patient regains
consciousness between them
Jacksonian seizure is a partial seizure which begins in one
group of muscles and spreads to adjacent muscle groups in the
same limb and then to the ipsilateral limb
9. Generalised Seizures (grand
mal)
1.Idiopathic
2.Symptomatic
Due to intracranial disease e.g. neoplasia, storage
diseases etc.
3.Cryptogenic
There is probably an underlying cause but it cannot be
identified by the diagnostic tests available.
4.Reactive
Due to some extracranial disorder, for example a toxin
or metabolic disorder
10. Generalized seizures
Absence seizures, appear to be staring into space These
seizures are sometimes referred to as petit mal seizures, which
is an older term.
Tonic seizures cause stiffening of muscles of the body
Clonic seizures cause repeated jerking movements of muscles
on both sides of the body
Myoclonic seizures cause jerks or twitches of the upper body,
arms, or legs.
Atonic seizures cause a loss of normal muscle tone - will fall
down or may drop head involuntarily.
Tonic-clonic seizures cause a mixture of symptoms, older term:
grand mal seizures
11. Generalised seizures result in:
Change in consciousness
Motor activity
Tonic-clonic seizures are most common in dogs and
cats.
Autonomic signs
The bo dy's e ne rg y utilisatio n can incre ase to
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g e ne ralise d se iz ure
12. Stages
1. Prodromal Phase
The animal experiences an indication of a forthcoming
seizure.
This occurs hours to days before the event itself.
2. Aural Phase
This is the very start of the seizure.
Behaviour changes may be apparent.
3. Ictal Phase
The seizure "proper".
4. Postictal phase
Consists of transient neurological and behavious changes,
which can last from hours to days.
13. Focal orpartial Seizures
Focal or assymmetrical sensory or motor activity
affecting any part of the body e.g. facial twitching,
chomping of mouth
Can be associated with autonomic signs e.g.
salivation, vomiting
Almost always an acquired disease
can spread to involve whole cortex and become a
generalized seizure
14. Simple focal motor seizure
Remain conscious - sudden focal jerking of a muscle
group
Complex focal seizure
Change in or loss of consciousness. dreamlike
experience.
may display strange, repetitious behaviors
(automatisms) such as blinks, twitches, mouth
movements, walking in a circle.
16. Investigation of Seizures
It must first be determined whether seizure activity
is in fact a seizure, rather than a non-epileptic
paroxysmal event, for example:
Syncope
Exercise-induced weakness
Obsessive-compulsive behaviour
Narcolepsy
17. Differential diagnosis of
seizures
1. Idiopathic
2. Symptomatic
3. Extracranial
4. Intracranial
Recognition of partial seizures can be useful in
localizing lesion to particular part of brain e.g.
twitching of one leg may suggest lesion in motor
cortex on opposite side to abnormal limb
18. History
Seizure type: partial suggest focal, structural,
intracranial lesion
Age:
Tumour
Drugs
Episodic behavioral abnormalities are suggestive
of extracranial metabolic disorders
Toxins: any age group
0-1 yr Hypoglycemia, portosystemic shunt,
encephalitis, hydrocephalus
1-5 yr Idiopathic epilepsy
5 yr + Neoplasia, hypoglycemia(insulinoma)
19. Examination
Persistant interictal neurological abnormalities
e.g. circling, proprioceptive deficits, blindness
are suggestive of structural intracranial lesion
Active occular lesion in infectious diseases e.g.
distemper
Cardiac abnormalities e.g. arrythmia may result
in hypoxic seizures
Neoplasia detected on physical examination
raises possibility of metastatic disease
20.
21.
22. When/Why to Start
Treatment???
More than 1 seizure in a 4-6 weekperiod
Active intracranial disease (neoplasia,
inflammation)
Clusterseizures
Status epilepticus
24. Drug Species and Dosage
Diazepam Dogs, cats 0.5–2.0 mg/kg, IV bolus; can be repeated 2–3 times at
intervals of 5–10 min; CRIa
0.5–2.0 mg/kg/hr
Foals: 0.05–0.4 mg/kg, IV slowly
Adult horses: 25–50 mg/horse, IV
Ruminants: 0.5–1.5 mg/kg, IV or IM
Phenobarbita
l
Dogs, cats: 2–4 mg/kg/ IV bolus; can be repeated at 20- to 30-min
intervals until a total dosage of 20 mg/kg is reached; CRI 3–10 mg/hr
to effect
Foals, adult horses: loading dose of 12–20 mg/kg, IV over 20 min,
then 6.65–9 mg/kg, IV over 20 min every 8–12h
Sodium
pentobarbital
Dogs, cats: 2–15 mg/kg, IV, to effect to stop motor activity
Foals, adult horses: 2–4 mg/kg, IV to effect
Propofol Dogs, cats: 2.5–4.0 mg/kg, IV, to effect to stop motor activity; CRI:
0.1–0.3 mg/kg/min to effect
Phenytoin Dogs 2–5 mg/kg as slow IV infusion
Foals, adult horses: 5–10 mg/kg, IV followed by 1–5 mg/kg, IV, IM,
or PO every 2–4 hr until seizures stop and maintenance dose started
27. Anticonvul
sant Drug
Dosage and Frequency Half-life Time to
Steady
State
Therape
utic
Level
Adverse
Effects/Com
ments
Phenobarbi
tal
Adjust
dosage in all
species by
monitoring
serum levels
and seizure
diary
Dogs: 2–4 mg/kg, PO, bid
(starting dose); up to 10 mg/kg,
bid
40–90 hr
(Beagles
25–38 hr
10–24
day
15–45
μg/mL
Sedation,
polydipsia,
induces P450
system,
increase in
liver
enzymes;
liver failure is
uncommon.
Horses: 3–5 mg/kg, PO, sid as a
starting dose; up to 11 mg/kg,
PO, sid
18 hr 10–40
μg/ml
(43–175
μmol/L)
Ruminants: 11 mg/kg, PO sid
28. Bromide (potassium salt)
Dogs, cats: 20–40mg/kg, PO, sidordivided
bidif GIupset.
Dogs: loadingdose400–600mg/kg, PO
dividedinto 4doses, givenover1–4days
Horses: 90mg/kg/day, PO
Adverseeffects:Sedation, weakness,
polydipsia, vomiting, polyphagia, skin
rash. Reducedosewithrenal insufficiency.
Highchlorideintakeincreases bromide
elimination. Chloridecontent of diet should
29. Diazepam
Dogs: 0.5–2 mg/kg per rectum at onset of
seizure; repeat up to 3 times in 24 hr
Cats: 0.25-0.5 mg/kg, PO, bid-tid
While oral diazepam is not effective in dogs,
rectal administration can be used to stop
cluster seizures or status epilepticus.
Oral diazepam can be used in cats as a
maintenance drug; sedation, liver failure are
potential problems in cats.