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Year 4 Small Animal Studies > Neurology: Seizures > Flashcards

Neurology: Seizures Flashcards

1
Q

What is a seizure?

A

A transient occurrence of convulsions or focal motor, autonomic or behavioural signs due to abnormal excessive or synchronus epileptic neuronal activity in the brain

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2
Q

Where in the brain causes a seizure?

A

Forebrain activity change

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3
Q

What are other possible changes with forebrain localisation?

Other then seizures

A
  • Behaviour change
  • Compulsive circling or pacing
  • Head turn on same side as the lesion
  • Loss of vision on opposite side as the lesion
  • Postural reaction defecits on opposite side
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4
Q

What is the pathogenesis of seizures?

A

Multifactorial

Imbalance in exitation and inhibition
* Either excessive exitation or decreased inhibition
Glutamate- exitatory
GABA- inhibitory

Neurons become hypersynchronised- seizure

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5
Q

What are the stages of a seizure?

A
  1. Prodrome- any preditive or preceding events
  2. Aura- initial manifestation of a seizure
  3. Ictal- seizure event- involuntary muscle tone or movement ± abnormal sensations or behaviour
  4. Post-ictal- minutes to days- can have unusual behaviour or neurological deficits
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6
Q
  1. How long does ictal event last
  2. When does it most commonly occur?
  3. What are the two major phenotypic categories?
A
  1. 60-90 seconds
  2. Sleep or rest
  3. Generalised, focal

Autonomic signs are common- hypersalivate, urinate, defecate

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7
Q

What parts of the brain are involved in generalised seizures?

A
  • Involvment of both cerebral hemispheres simultaneously
  • Consciousness impaired
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8
Q

What different phases may be involved in a generalised seizure?

A
  1. Tonic- clonic- extent all 4 limbs
  2. Tonic
  3. Clonic- repetitive muscle movement
  4. Myoclonic- shock like contractions
  5. Atonic- complete lack of muscle tone

Tonic- clonic most common

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9
Q

What part of the brain is involved in focal seizures?

What are the forms of focal seizures?

A
  • Initial activation of one part of region in the forebrain
  • Clinical signs remain unilateral

Forms
* Motor- twitching ear, facial automations
* Autonomic- pupils dilated, hypersalivation
* Behavioural

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10
Q

What is audiogenic reflex seizure?

How is it treated?

A
  • Reflex seizure that is objectively and consistently precipitated by environmental or internal stimuli
  • Myoclonic seizures progressing to generalised tonic-clonic seizures

Cats- late onset

Levetiracetam typically effective

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11
Q

What are the differentials for a seizure?

A
  • Narcolepsy/cataplexy
  • Neuromuscular collapse
  • Syncope
  • Paroxysmal dyskinesia
  • Painful episodes
  • Metabolic disease
  • Vestibular disease
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12
Q

How is idiopathic head tremor syndrome treated?

A

Stress causes

Distraction stops- stoke, treat

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13
Q

What breed is affected by episodic hypertonicity?

A

CKCS

  • Increased muscle tone in all 4 limbs

Tx
* benzodiazipine- clonazepam

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14
Q

What is paroxsysmal dyskinesia?

A

Spikes disease, paraosysmal gluten-sensitive dyskinesia (border terriers)

  • Disconected movements
  • Dysponesia
  • Not painful- mins to hours

Clonazepam

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15
Q

What- broadly- are the three causes of seizures?

A

Reactive
* Natural response from the normal brain to a transient disturbance in function
* Concurrent neurological signs usually present
* Metabolic or intoxication

Idiopathic
* Genetic or presumed genetic in origin
* No inter-ictal neurological signs

Structural epilepsy
* Epileptic seizures which are provoked by intracranial or cerebral pathology
* Concurrent neurological signs usually
* Inflammatory, neoplastic, traumatic

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16
Q

What are the different causes of seizures?

A
  • V- ischaemic encephalopathy, cerebrovascular accident
  • I- MUO
  • T- traumatic brain injury, toxicity
  • A- congenital malformation
  • M- hepatic enceph, renal enceph, hypoglycaemia
  • I- idiopathic
  • N- entra or intraparenchymal neoplasia
  • D- lafora disease, NCL
17
Q

How is idiopathic epilepsy diagnosed?

A
  • Diagnosis of exclusion
  • Dogs between 6 months and 6 years
  • Normal neurologicl examination between seizures

A- idipathic- genetic epilepsy
* Lagotto romagnlolo
* Belgian shepherd
* Boerboels

B- idiopathic- suspected breed epilepsy
* genetic influence with high breed prevalence

C- idiopathic- unknown cause
* epilepsy in which the nature of the underlying cause is as yet unkown
* no indication of structural epilepsyq

18
Q

When is an MRI appropriate?

A
  • Age of onset <6 m or <6 years
  • Inter-ictal neurological abnormalities consistent with intracranial neurolocalisatoin
  • Stratus epilepticus or cluster seizure
  • Previous presumptive diagnosis of IE and drug resistance
19
Q

When is starting treatment indicated?

A
  • Structural or metabolic epilepsy
  • Status epilepticus or cluster seizures
  • An inter-ictal period of 6 m or less
  • Post- ictal signs are severe or last over 24h
  • Frequency is increasing
  • Severity worsening
  • 1st seizure within 1 months of traumatic event
20
Q

What are the three anti epileptic treatments?

A
  • Phenobarbital
  • Bromide
  • Imepitoin

not licensed- levetiracetam, zonisamide,

21
Q
  1. What is the mechanism of phenobarbital?
  2. How does it need to be monitored?
  3. What are the side effects?
  4. How is it metabolised?
A
  1. Augments the inhibitory effect of GABA- prolongs chloride channel opening at GABA
  2. 2 weeks, 3 months, 6 months (haem/biochem)
  3. Sedation, ataxia, polyuria, hepatotoxicity, haem abnormalities, pseudolymphoma
  4. Hepatic microsomal enzymes- induces cytochrome P450 activity

Care with hepatic dysfunction

22
Q
  1. What is the mechanism of action of bromide?
  2. When should it be monitored?
  3. What are the side effects?
  4. How is it metabolised?

KBr or NaBR

A
  1. Competes with Cl- transport across nerve cell membranes- inhibits Na+ transport
  2. 12 weeks
  3. Sedation, ataxia, paresis, bromism (toxicity)
  4. Excreted unchanged in urine- undergoes tubular reabsorption in competition with chlorine
23
Q
  1. What is the MAO of imepitoin?
  2. How is it monitored?
  3. What are the side effects?
  4. How is it metabolised?
A
  1. Low affinity partial agonist site of GABA receptor
  2. None
  3. Phenobarb but fewer
  4. Liver excreted by faecal
24
Q
  1. What is the action of levetiracetam?
  2. What is the action of zonisamide?
A
  1. Reduced intracellular Ca2+ accumulation
  2. Blocks propogation of epileptic dishcharges- spenny

Levetiracetam fast working- good for liver disease

25
Q

How are seizures treated in cats?

A
  • No licenced medication
  • Diazepam- fulminant hepatic necrosis rare but associated with oral administration
  • Phenobarbitone
  • Potassium bromide- avoid
  • Propofol- heinz body anaemia

Year 4 Small Animal Studies (97 decks)

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