This document provides information on seizures in animals. It begins by defining a seizure as excessive discharge of excitable neurons in the brain. There are two main types of seizures - generalized seizures which involve the whole brain and cause loss of consciousness, and focal or partial seizures which start in one area of the brain. Epilepsy is defined as recurrent seizures regardless of cause. Seizures occur due to an imbalance between inhibitory and excitatory neurotransmitters in the brain. The document outlines the classification, causes, diagnosis and treatment of seizures including anti-seizure medications.

1. SEIZURE IN ANIMALS
ICTUS
FIT
CONVULSION
SUBMITTEDBY:
Radhika Vaidya
M5444
MVSc

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

8. Classification of seizures

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
aro und 250 % o f the no rm alvalue during a
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.

15. Causes of Acquired Seizures

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

22. When/Why to Start
Treatment???
More than 1 seizure in a 4-6 weekperiod
Active intracranial disease (neoplasia,
inflammation)
Clusterseizures
Status epilepticus

23. Drugs Used forTreatment of
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

25. Anticonvulsants
Stop an ongoing seizure or to decrease the
frequency or severity of anticipated future
seizures

26. First-LineMaintenance
Anticonvulsant Drugs

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.

30. Second-Line(Add-on) Anticonvulsant
Drugs

31.  Zonisamide (Zonegran) 5-10mg/kg BID
 25,50,100mg capsules
 Levetiracetam(Keppra) 20-60mg/kg TID
 250mg, 500mg, 750mg
 Pregabalin (Lyrica) 2-4mg/kg BID
 25, 50, 75, 100, 150, 200, 225, and 300 mg capsules
 Rufinamide (Banzel) 10-20mg/kg BID
 200mg, 400mg tablets
 Topiramate (Topomax) 2-5mg/kg BID
 25, 50mg tablets
 Gabapentin (Neurontin) 10-30mg/kg T-QID
 100, 300, 400, 600, 800mg Capsules/tablets

34. LiverDisease
 Levetiracetam(Keppra) orPotassium
Bromide
 Gabapentin (Neurontin)
 Pregabalin (Lyrica)
 Topiramate (Topimax)

35. Refractory Combos
 Phenobarbital and levetiracetam
 Phenobarbital and KBr(side effects)
 Zonisamide and KBr
 Zonisamide and levetiracetam
 Phenobarbital and zonisamide (double
zonisamide)

36. Thank
you