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Clinical symposium > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

define seizures

A

the clinical manifestation of an abnormally excessive and hyper synchronous activity of neurones located predominantly in the cerebral cortex

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2
Q

what does the abnormal neurone activity cause in muscles and in the brain

A

muscles=twitch

brain=seizures

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3
Q

what are 3 classifications of tumours

A

generalised- neuronal activity in both hemispheres.
Partial (aka focal seizures)- initial activation of neurones in both hemispheres
secondary generalised- a partial seizure that later spreads to involve the majority of the 2 cerebral hemispheres.

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4
Q

what are some of the main clinical fetters of a partial seizure

A

absence- starting and blinking without thinking.

Myoclonic- jerking movements of the body

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5
Q

what are the some of the main clinical features of a generalised seizure

A

tonic clonic-stiffening, falling and jerking of the body.

tonic/ atonic- falling heavily to the ground.

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6
Q

in which type of seizure complex or simple are you more alert or aware

A

simple.

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7
Q

which lobe of the brain does the Jacksonian seizure effect and what are it’s clinical symptoms

A

frontal

tingling in hand or arm

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8
Q

which lobe of the brain does the adversive seizure effect and what are its clinical symptoms

A

frontal

eyes or head both turn to one side

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9
Q

what are the clinical manifestations of a temporal lobe seizure

A

strange smell or taste altered behaviour- déjà vu feeling, lip smacking or chewing movements.

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10
Q

what are the clinical manifestations of the occipital lobe seizures

A

Flashing lights or spots vomiting

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11
Q

what are the clinical manifestations of the parietal lobe seizures

A

Tingling in or jerking of leg, Arm and Face.

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12
Q

what device is used to diagnose epilepsy and how is it used

A

EEG- electroencephalogram.

scalp electrodes are used to monitor the firing of neurones within the brain.

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13
Q

define status epilepticus

A

Brian is in a persistent seizure
seizure more than 30 mins long
2 sequential seizures without recovery in between.

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14
Q

what effect to a seizure have if it affects the brainstem

A

affects the body’s autonomic functions e.g. breathing.

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15
Q

what is the treatment for status epilepticus.

A

GABA receptor antagonist + diazapem

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16
Q

define epilepsy

A

Conditions were seizures recur, usually spontaneously.

2 or more unprovoked seizures

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17
Q

How do too little inhibition and too much excitation cause seizures.
(think about what ions go in and out and the neurotransmitters involved)

A

excitation- too much
influx sodium and calcium
neurotransmitter- glutamate and aspartate are released.

Inhibition- too little
efflux- chlorine and potassium.
neurotransmitter released GABA

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18
Q

what is the function of inhibitory interneurones

A

allow activity to spread in one direction, but not to spread out sideways

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19
Q

what inhibitory neurotransmitter do inhibitory interneurones release

A

GABA.

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20
Q

what % of the brains neurones are interneurones

A

10–20% of the total number of neurones

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21
Q

Is GABA a inhibitory neurotransmitter

A

Yes

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22
Q

what type of chemical molecule is GABA

A

Y aminobutyric acid

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23
Q

GABA is penatmeric what is it’s composition (alpha, beta, delta and gamma)

A

2 alpa, 2 beta and one gamma or delta subunit.

24
Q

what are some examples of epilepsy causes by mutation in the GABA subunits

A

CAE (Childhood absence epilepsy)
FS (pure febrile seizures)
GEFS- (Generalised epilepsy with febrile seizure plus)
JME (juvenile myoclonic epilepsy
DS (Dravet syndrome- also known as SMEI (severe myoclonic epilepsy in infancy)

25
Q

patients with dravet’s syndrome typically have what form of mutation.

A

GABRG2 (Q390X)- a truncated subunit with the loss of 78 –C terminal amino acids.

26
Q

what type of seizures do people with dravet’s have

A

Can have different types of seizures over years

Febrile, tonic-clonic, myoclonic, absence, complex partial seizures and tonic seizures

27
Q

what is the pathogenesis behind the mutation in the GABA sub unit

A

changing the subunit from a trans membrane protein to a globular cytosolic protein.

28
Q

what type of drug is pilocarpine

A

proconvulsant.

29
Q

which subunits of GABA are increased and which are decreased in status epileptics

A

A4 increased

A1 decreased.

30
Q

How does the change in GABA subunits lead to epilepsy.

A

The change in receptor subtype from α1βγ2 to α4βγ2 may have dramatic effects on brain inhibition.
α4 containing GABARs have been shown to desensitize rapidly, especially when assembled with β3 subunits

31
Q

what effect does the induction of α1 subunit viral vector have

A

increased latency time and decreased rates of seizure development,

32
Q

what are the modes of action of antieplieptics

A 
1. Suppress action potential
•	Sodium channel blocker or modulator
•	Potassium channel opener
2.  Enhance GABA transmission
•	GABA uptake inhibitor
•	GABA mimetics
3.  Suppression of excitatory transmission
•	Glutamate receptor antagonist
33
Q

what are the main anti epileptics for a partial simple or parietal complex seizure or generalised seizure

A

carbamazepine
phenytoin
Valproic acid

34
Q

what are the main anti epileptics for febrile seizures

A

diazepenem rectal

35
Q

what are the main anti epileptics for absence seizures

A

ethosuximide

Valproic acid

36
Q

what are the main anti epileptics for atypical absence or atonic, myoclonic acid

A

valproic acid.

37
Q

what drugs enhance the action of GABA receptors

A

barbiturates e.g. phenobarbital, benzodiazepines e.g. clonazepam.

38
Q

what are the main drugs which inhibit GABA transminase receptors

A

vigabatrin

39
Q

which drug prevents GABA uptake

A

tiagabine

40
Q

which drug is effective against status epileptics

A

diazapam (valium and lorazepam)

41
Q

what are the 3 main benzodiazepines

A

clonazepam
clorazpate
Diazepam

42
Q

mechanism of action of benzodiazepines.

A

Increase affinity of GABA for its receptor.
– Increases Cl- current (opening frequency)
– Suppresses seizure focus by raising action potential threshold
– Strengthens surround inhibition – prevents spread

43
Q

side effects of benzodiazepines

A

sedation

respiratory depression.

44
Q

which anti epileptics work by inhibiting sodium channels

A
  • Phenytoin
  • Carbamazepine and oxcarbamazepine
  • Lamotrigine
45
Q

mechanism of action of phenytoin

A

Phenytoin binds to the inactivated state of an action potential and slows down its recovery.

46
Q

what are the uses of valproic acid

A

Effective against tonic-clonic and absence.

Bipolar illness

47
Q

Mechanism of action of valproate

A

More than 1 mechanism
Inhibits Na+ channels but weaker than phenytoin
Decreased GABA turnover
• Inhibition of succinic semialdehyde dehydrogenase and thereby indirectly inhibiting GABA transaminase
• May lead to increased synaptic GABA levels
Blocks neurotransmitter release by blocking T-type Ca2+ channels

48
Q

What is often given to pregnant women with epilepsy

A

folic acid

49
Q

what drug causes foetal hydantoin syndromes

A

phenytoin.

50
Q

what are the clinical symptoms of foetal hydantoin syndrome

A
  • intrauterine growth restriction with microcephaly
  • minor dysmorphic craniofacial features and limb defects including hypoplastic nails and distal phalanges (birth defects)
  • a smaller population will have growth problems and developmental delay, or mental retardation
  • Heart defects and cleft lip may also be featured
51
Q

what types of seizures does optogenetic stimulation work for

A

partial seizures

52
Q

mechanism of action of optogenetic stimulation

A

halorhodopsin hyperpolarize the neurones in reaction to yellow light
Put halorhodopsin in the brain, which enables entry of Cl-.

53
Q

define epilepsia partialis continua

A

Patient experiences recurrent motor epileptic seizures that are focal (hands and face)

54
Q

what causes epilepsa partialis continua

A

acute brain lesions

55
Q

what drugs are used to treat epilepsy partialis continua

A

no many drugs work.
light activation of the light-activated chloride-pump, halorhodopsin, transfected into pyramidal cells in the focus
Used lentiviral vectors to transfect predominantly pyramidal neurones with halorhodopsin

Clinical symposium (20 decks)

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