Epilepsy (include pharmacology) Flashcards

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1
Q

What is epilepsy?

A

Epilepsy is the most common neurological disorder, characterised by recurrent seizures

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2
Q

How many different types of seizures are there?

A

Over 40

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3
Q

How can you diagnose epilepsy?

A

EEG/MRI/CAT(CT) (hard to see anything in an MRI or CAT scan

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4
Q

According to the international league against epilepsy (ILAE), what are the main categories of epilepsy?

A

Focal and generalised

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5
Q

What are the characteristics/auras of a temporal onset of seizure?

A

Auras: smell/taste, ‘déjà vu’, ‘jamais vu’, emotional changes
Oral automatisms: gestures eg dystonic or fidgetting

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6
Q

What are the characteristics/auras of a frontal onset of seizure?

A

Motor seizures: Brief, frequent, cluster,
Often bilateral eg kicking, cycling, violent, bizarre. Head version
Commonly on waking from sleep

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7
Q

What are the characteristics/auras of a parietal onset of seizure?

A

Sensory seizures: somatosensory (tingling/warmth)

Auras: Nausea, choking, sinking sensations, Illusions of body distortion

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8
Q

Look at these symptoms: Visual hallucinations – simple or complex (shapes to scenes)
Vision may black out
Visuo-spatial distortions
Head turning, headache, nausea
An epilepsy induced from which location would get these symptoms?

A

Occipital

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9
Q

What is the main characteristic of focal aware seizures?

A

No loss of consciousness or post-ictal confusion

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10
Q

Which lobe of the brain are focal aware seizure mostly found?

A

Temporal lobe

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11
Q

What are the main characteristic of focal with impaired awareness seizures?

A

Altered consciousness, but may seem fully aware. There may be some post-ictal confusion
May experience auras

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12
Q

If the patient presented with automatisms (chewing, swallowing, repeated displacement behaviour), what type of focal seizure is this?

A

Focial with impaired awareness

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13
Q

Which lobe of the brain are focal with impaired awareness seizures mostly found?

A

Temporal lobe

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14
Q

What are the two types of jacksonian seizures?

A

Focal aware motor and focal aware sensory

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15
Q

What are the characteristics of a focal aware motor (jacksonian) seizure?

A

Short-lasting, ripple of muscle activity, may be localised to one group of muscles or progress, usually distal to proximal, through the limbs and trunk (following HAL)

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16
Q

What are the characteristics of a focal aware sensory (jacksonian) seizure?

A

Short lasting sensory changes, may be localised to one area or progress, usually distal to proximal, through the limbs and trunk (following HAL)

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17
Q

What are the characteristics of a focal to bilateral tonic clonic seizure?

A

Focal seizure progressing to generalised (tonic-clonic)

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18
Q

If a patient presented with unilateral motor effects during the seizure and experienced an aura prior to the onset, what type of seizure do they have?

A

Focal to bilateral tonic clonic

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19
Q

What are the symptoms of a generalised tonic clonic seizure?

A

Tonic phase - whole body stiffness, breathing may stop (cyanosis), loss of bladder control
Clonic phase – muscle jerks

Followed by unconsciousness, muscle relaxation, slow regain of consciousness, confusion, sleepy, headaches and aching limbs, no recall of episode

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20
Q

What is a generalised obsence seizure?

A

Rare in adults, generally starts between 6-12 yrs

Girls > Boys

Symptoms: seem to ‘switch-off’ but cannot be alerted or woken up

Whole brain involved, low level activity

Responds well to anti-epileptics

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21
Q

Why is a status epilepticus generalised tonic clonic seizure treated as a medical emergency?

A

Whole brain involved
Ictal period of > 5 mins
Repeated seizures with no recovery between (>30 mins)

Other forms: long-lasting, absence or focal-type seizures

22
Q

What is the type of seizure which Sav, Risheka and Arpita have?

A

Generalised myoclonic - sudden jerks (like when falling asleep), possibly familial

23
Q

What are the symptoms of each form of seizure?
Generalised clonic

Generalised tonic

Generalised Atonic

A

Generalised clonic – repeated twitches and jerks no stiffness

Generalised tonic – all muscle contract, whole body stiffness

Generalised Atonic – ‘drop attacks,’ muscle tone lost

24
Q

How can you diagnose an NEAD?

A
Diagnosis can be made through a video EEG.
There may be differences in:
Duration
Eye opening
Location of tongue biting - tips
Recollection
25
Q

What are the advantages of using an Electroencephalogram (EEG)?

A

Useful for investigating gross cortical activity
Non-invasive and painless
Can be used over long periods
Cost effective

26
Q

How many plate electrodes does the EEG have?

A

24-158

27
Q

Where is the ground electrode for the EEG?

A

ear

28
Q

What do EEG’s record?

A

Activity patterns of populations of neurons by recording changes in gross current flow

Levels of synchrony between neurons causes changes in patterns, if fire together give larger amplitude oscillations

Patterns of synchrony cause rhythms

29
Q

What are the different types of rhythms seen in EEG?

A

Alpha – 8-13Hz
Mainly occipital, quiet, eyes shut, meditation
Beta >14Hz
Parietal and frontal, activity and tension, sleep spindles
Gamma – 40Hz
‘binding,’ learning and memory
Theta – 4-7Hz
Parietal and temporal, alertness, L&M
Delta <3.5 Hz
Cortical, deep sleep, coma

30
Q

During a seizure, what happens to GABA, Ach transmission, Na+ channel activity and K+ channel activity?

A

Reduction in GABA
Increase in ACh transmission
Increase in Na+ channel activity
Decrease in K+ channel activity

31
Q

What are the three types of treatment for epilepsy?

A
Pharmacological 
First line approach for seizures
Anticonvulsants/Antiepileptic drugs (AEDs)*	
Surgical
removal of aberrant areas (found by MRI/CAT/electrical stim)
Implants 
VNS – vagal nerve stimulation
DBS – deep brain stimulation
32
Q

What is the treatment for Focal and Focal to generalised seizures?

A

First Line:
Carbamazepine
Lamotrigine
Sodium valproate

Second Line (adjuncts):
Clobazam, gabapentin, topiramate
33
Q

What is the treatment for generalised tonic clonic?

A
First Line:
Sodium valproate
Lamotrigine
Also:
Carbamazepine
Oxcarbazepine
Second Line (adjuncts):
Clobazam, levetiracetam, topiramate
34
Q

What is the treatment for generalised absence atypical?

A

First Line:
Ethosuximide
Sodium Valproate*†

Second line:
Lamotrigine*

35
Q

What is the treatment for status epilepticus?

A

Status epilepticus generalised tonic clonic :
Commence i.v. Lorazepam (repeated after 10 mins) (can use buccal Midazolam/i.v. diazepam)
Buccal Midazolam/Rectal diazepam (if resusc facilities not available)
After 25 mins: phenytoin sodium or phenobarbital sodium*
After 45 mins: Anaesthetize with thiopental, midazolam or non-barbiturate anaesthetic (propofol)

36
Q

What is the treatment for a generalised myoclonic seizure?

A

First Line: Sodium valproate.

37
Q

Name some Na+ channel blocker epilepsy drugs.

A
Phenytoin
Carbamazepine
Lamotrigine
Sodium Valproate
Zonisamide
38
Q

How do Na+ channels blockers block?

A

Only block channels in inactivated state

39
Q

What are some side effects of Na+ channel blockers?

A

Teratogenicity! - especially Sodium Valporate
CNS effects, cognitive impairment, visual impairment
Peripheral neuropathy
Skin problems
Gum hyperplasia
Anaemia and other blood disorders
Osteomalacia

40
Q

Name some Ca2+ channel blockers.

A

Ethosuximide (T-type Ca2+ blocker)
Gabapentin
Lamotrigine

41
Q

What is Antiepileptic Hypersensitivity Syndrome?

A

Major side-effect
Starts 1-8 weeks from treatment initiation
Initial signs: Fever, rash, swollen lymph nodes
Severe signs: Blood, liver kidney and respiratory abnormailites, vasculitis and organ failure

42
Q

What would you do if your patient had Antiepileptic Hypersensitivity Syndrome?

A

Withdraw drug immediately
Topical steroids and antihistamines for rash
Systemic corticosteroids?
Beware of rebound seizure activity

43
Q

What drug inhibits GABA transporters?

A

Tiagabine

44
Q

What drug inhibits GABA transaminase?

A

Vigabatrin

45
Q

What is the mechanism of action of Gabapentin?

A

Enhance activation of GABAA mediated channels, indirectly alter the activity at the GABA channel. Increases GABA synthesis and also acts as a muscle relaxant

46
Q

What is the difference between Benzodiazepines and Barbiturates?

A

Benzodiazepines act as a co-agonist to the GABAA receptors (of the gamma unit), whereas Barbiturates act on the beta unit. Thus both increase GABA activity.

47
Q

How do Benzodiazepines and Barbiturates work?

A

Reduce neuronal transmission by enhancing inhibition

48
Q

Which drug acts as a GABA antagonist and therefore can cause seizures?

A

Flumazenil

49
Q

What type of modulators for Barbiturates?

A

Positive allosteric modulators (co-agonists) of GABAA receptors.

50
Q

Name some examples of Benzodiazepines?

A

Diazepam and Lorazepam

51
Q

What are the Side Effects of BDZs and Barbs?

A
Short-term use only (< 12 weeks)
Tolerance and dependency can develop
Withdrawal on termination
Impaired motor coordination (↓muscle tone)
Impaired cognitive performance
Sedation
Disturbed sleep patterns (↓SWS)
Retrograde amnesia
52
Q

What are some future targets of epilepsy drugs?

A
Glutamate Antagonists
AMPA
Metabotropic
Gap Junction inhibitors
Enzymes
Cannabinoids
Steroids
CO2