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Michaelmas 5th year > Neuro epilepsy > Flashcards

Neuro epilepsy Flashcards

1
Q

Definition of a neurogenic seizure

A

Paroxysmal, transient disturbance of brain function which is characterised by excessive asynchronous neuronal activity and causes motor distrubances

Originates in the forebrain

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2
Q

Excitatory neurotransmitters

A

Main one = glutamate
Also aspartate, acetylcholine

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3
Q

Inhibitory neurotransmitters

A

Main = GABA
Also glycine, taurine, norepinephrine

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4
Q

Pathophysiology of a seizure starting

A

Get out of control activity in neurons where excitation exceeds inhibition
Get sudden depolarisatin oof neurons in a focal area of cerebral cortex causing Ca2+ influx, Na+ channel opening and AP discharge which leads to seizures

Gaba mediated repolarisation and hyperpolarisation puts animal back into refractory peroid

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5
Q

What are inter-ictal spikes

A

Characteristics EEG pattern picked up during (and sometimes between) seizures in epileptic dogs

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6
Q

What is the paroxysmal depolarisation shift in seizure generation

A

= sudden depolarisation of neurons in a focal area of the cerebral cortex which will eventually lead to action potential discharge and seizure

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7
Q

What physiology leads to status epilepticus rather than recovery from seizure

A

Failure of repolarisation and refractor period after seizure

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8
Q

What are the two key types of seizures

A

Generalised = loss of consciousness and tonic/clonic muscular activity affecting all limbs + autonomic changes e.g urination

Focal = non-generalised; could be just one eye, may be non-clinical

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9
Q

What would lateralised signs in a simple focal seizure suggest about lesion location

A

Contralateral forebrain lesion

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10
Q

What are complex focal seizures

A

Also caused automotor
- Some involvement of sensory +/- limbic system
E.g fly-catching, tail chasing, aggression, manic activity
- Can develop into generalised seizure
[vs simple focal where small region of body just twitching/flexing etc]

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11
Q

Characteristics of a generalised seizure

A
  • Loss of consciousness
  • Tonic skeletal muscle contraction
  • Recumbency
  • Periods of clonic muscular activity
  • Jaw clenching, mydriasis, urination/defaecation, sialosis
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12
Q

How long is the actual seizure phase of. aseizure usually

A

<2 mins

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13
Q

What is syncope

A

collapse assocaited with cardio-respiratory distress
Is more floppy than seizure collapse

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14
Q

What accute toxicity could mimis status epilepticus with a persistent whole body tremor

A

Mycotoxin poisoning

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15
Q

What activity might narcolepsy be assocaited with

A

Excitement related to eating

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16
Q

What breed is Spike’s disease seen in and what is it

A

Paroxysmal dyskinesia in Border Terriers related to gluten intolerance

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17
Q

What do REM sleep disorders look like compared to genuine seizure

A

Animal stays asleep during episode

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18
Q

What individuals do we tend to see idiopathic head bobbing in

A

Young boxers
English bulldogs

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19
Q

What does prodrome mean

A

early signs/triggers indicating a seizure is coming on

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20
Q

What is the post-ictal period

A

neurological/behavioural abnormalities AFTER a seizure which lasts from minutes to days

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21
Q

What inflammatory condition is a common cause of seizures

A

Meningoencephalitis of unknown origin

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22
Q

What anomalous condition could cause epileptic seizures

A

Hydrocephalus via causing raised ICP

23
Q

What metabolic conditions may be associated with epileptic seizures

A
  • Hypocalcaemia
  • Hypoglycaemia
  • Hypo/hypernatraemia
  • Hepatic encephalopathy with porto-systemic shunt
24
Q

What is the most common cause of seizures in dogs

A

Idiopathic epilepsy

25
Q

What does term ‘reactive epilepsy’ mean about location of the cause

A

= extra-cranial cause e.g metabolic and toxic
Use haematology and biochemistry to rule out

26
Q

What does the term ‘structural epilepsy’ mean about location and cause

A

= intracranial cause
e.g vascular, inflammatory, neoplastic, anomalous
Use a brain scan to rule out

27
Q

If epilepsy is intracranial non-structural - what is the diagnosis

A

Idiopathic epilepsy
= diagnosis of exclusion

28
Q

What counts as a seizure cluster

A

> 1 seizure in 24hrs with recovery inbetween

29
Q

What is defined as status epilepticus

A

Continuous seizure for more than 5 mins OR two seizures without recovery of consciousness between then

30
Q

What age do we see idiopathic epilepsy

A

Between 6 months and 6 years

31
Q

When might we do a bile acid stimulation test during an epilepsy investigation

A

if you have high suspicion of hepatic encephalopathy e.g due to a portosystemic shunt
- Suspect this if seeing low urea, low albumin, unthirft animal, high serum ammonia

32
Q

When might we measure fructosamine and insulin during epilepsy work up

A

If suspicious of an insulinoma
e.g presented with middle aged dog with hypoglycaemia

33
Q

What infectious agents can lead to seizures

A

FIP in cats
Rarely: toxoplasma/neospora

34
Q

What is tier 1 confidence of idiopathic epilepsy (in exam)

A

2 or more unprovoked seizures with normal inter-ictal neuro exam
Seizures started within 6 months and 6 years age
Normal bloods (biochem and haem) and urinalysis

35
Q

What is tier 2 confidence of idiopathic epilepsy

A

Tier 1 requirements
+ normal brain MRI, normal CSF analysis, normal bile acid stimulation

36
Q

What is tier 3 confidence of idiopathic epilepsy

A

Tier 1 and 2
+ compatible EEG i.e inter-ictal spikes

37
Q

What signalment might point towards MUO rather than idiopathic epilepsy

A

Small breed dog e.g terrier
Seizures over short period which are increasing over time

Vs intermittent seizures in large dogs with no progression

38
Q

What things justify starting epilepsy medical management

A
  • Cluster or status epilepticus
  • Structural epilepsy e.g due to tumour, inflammatory focus
  • Increasing freq/seizure severity
  • Severe post-ictal signs
  • > 2 seizures in 6 months but unclear
39
Q

How does phenobarbitone work to control seizures and what are some potential side effects

A

Enhances GABA and inhibited glutamate
- This raises the seizure threshold

Side effects: sedation, ataxia, polyphagia and weight geain, polydipsia
- rarely can get haematological changes and liver damage

40
Q

How to monitor phenobarbitone treatment

A

Test phenobarbitone serum level 2 weeks after starting/changing treatment and then every 6-12 months or if seizure activity increases

Complete blood count and liver enzymes at start, 3 weeks later, 3 months later, every 6-12 month [expect to see elevation in ALT and AlkP but NOT GGT AND AST]

41
Q

Why might we have to increase the dose over time on an animal on long term phenobarbitone mediation

A

Due to autoinduction of enzymes that metabolise the drug; get fall in serum level

42
Q

What to remember about treating cats with epilepsy

A

Do NOT use potassium bromide to treat

43
Q

What diet changes can cause animals on potassium bromide to start showing signs of bromide toxicity

A

Diets with very different NaCL content

44
Q

Why can potassium bromide be beneficial c/f phenobarbitone

A

It is excreted through the kdineys so takes some pressure off the liver

45
Q

How does imepitoin act to stop seizures and what is an advantage

A

potentiation of GABA receptors
No requirement for monitoring
Lower efficacny than phenobarbitone but can be an add on

46
Q

What is the physiolgy behind failure of cessation of seizure activity in status epileptic (receptors involved etc)

A
  • Failure of inhibition mediated by GABA
  • Excessive excitation mediated by glutamate on NMDA receptors

SO can treat with GABA agonists and NMDA antagonists

47
Q

What is the first line drug to control seizures

A

Benzodiazepine; diazepam or midazolam

48
Q

When might we skip phenobarbitone and go straight to using levetiracetam to treat current seizure that is happening

A

In known idiopathic epileptics which are already being treated with phenobarbitone
- Less leeway for boluses and less effective

49
Q

What advantage can using a CRI of benzodiazepine rather than boluses give in seizure control

A

Avoids accumulation in the CNS and resistance to them

50
Q

What issues can sequential treatment of seizures with different drugs give

A

Pharmacoresistance
- Via internalisation of GABA receptors (inhibitory), upregulation of NMDA receptors (excitation)
+ over-expression of drug transporter systems

So new approach it to do early polytherapy with benzodiazepines, ketamine, phenobarbitone, levetiracetam
+ may add in sedation via dexmedetomidine to buy time

51
Q

Levetiracetam use

A

Short half life so can give animals without side effects or monitoring
- Can be useful in cat epileptics
- Useful in status epilepticus control

52
Q

What is teh most common cause of status epilepticus in young dogs

A

Intoxication = a reactive seizure

53
Q

What metabolic disturbances do we commonly get in status epilepticus and how do we correct

A
  • Hypoglycaemia; use 50% desxtrove IV
  • Hypocalcaemia: 10% calcium gluconate IV
54
Q

Why might we induce hypothermia in prolonged SE cases

A

Neuroprotective

Michaelmas 5th year (41 decks)

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