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Brain and Behaviour Year 2 > Epilepsy > Flashcards

Epilepsy Flashcards

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1
Q

What are seizures

A

abnormal paroxysmal changes in the electrical activity of the brain, they reflect large scale synchronous discharges of neuronal networks

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2
Q

What is epileptogensis

A

the process by which normal brain function progresses towards generation of abnormal electrical activity

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3
Q

What is epilepsy

A

a neurological disorder that represents a brain state that supports recurrent, unprovoked seizures

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4
Q

describe the prevelance of epilepsy

A

Prevalence in the UK is 1%
65 million people worldwide
A third of patients are resistant to treatment

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5
Q

What is the difference between generalised seizures and focal seizures

A

Generalised
- both hemispheres are affected and this is always associated with loss of awareness

Focal
- limit to one hemisphere and then further divided into whether or not there is los of awareness

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6
Q

What are the classification of seizures

A
  • Focal onset
  • Generalized onset
  • Unknown onset
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7
Q

What is status epileptics

A

– a form of epilepsy which is a life threatening medical emergency, seizures which last more than 5 minutes ( or more than a seizure in 5 minutes, without regain of consciousness)

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8
Q

describe what happens in a petit mal seizure

A

=begins in childhood.
= Loss of awareness and a vacant expression for <10 seconds before returning abruptly to normal and continuing as though nothing had happened.
= Apart from slight fluttering of the eyelids there are no motor manifestations.
= Patients often do not realize they have had an attack but may have many per day

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9
Q

What happens in a clonic seizure

A

= these are rarer

= there are rapidly alternating contraction and relaxation of a muscle = jerking

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10
Q

what is jerking

A

alternating contration and relaxation of a muscle

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11
Q

what is another term for grand mal seizures

A

tonic clonic seizures

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12
Q

what is another word for absent seizures

A

petit mal

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13
Q

name the phases of a grand mal seizure

A 
= premonition
= pre-tonic clonic phase 
= tonic phase 
= clonic phase 
= postictal period
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14
Q

describe the phases of a grand mal seizure

A
  • Premonition (a vague sense that a seizure is imminent) this is sometimes called aura
  • Pre-tonic-clonic phase (a few myoclonic jerks or brief clonic seizures)
  • Tonic phase (tonic contraction of the axial musculature; upward eye deviation and pupillary dilatation; tonic contraction of the limbs; cyanosis; respiratory muscle contraction - “epileptic cry”; tonic contraction of jaw muscles)
  • Clonic phase - jerks of increasing amplitude followed by relaxation (sphincter opening may occur)
  • Postictal period (generalized lethargy; decreased muscle tone, headaches, muscle soreness)
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15
Q

What is an atonic seizure

A

(decrease in tone) brief lapse in muscle tone causing fall

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16
Q

what is a myoclonic seizure

A

momentary brief contractions of a muscle or muscle groups, e.g. causing a sudden involuntary twitch of a finger or hand.

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17
Q

name some generalised seizures

A
  • petit mal
  • grand mal
  • clonic
  • atonic
  • myoclonic
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18
Q

How do you diagnose epilepsy

A
  • Clinical history = occurrence of 2 or more seizures.
  • The account of witnesses is essential.
    = Investigations = help diagnosis and classification as well as identify aetiology. EEG, MRI, fMRI, PET (positron emission tomography - radioactive tracers), ECG.
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19
Q

describe the causes of epilepsy at different age groups

A

Children and teenagers = genetic, perinatal and congenital disorders

Young adults = trauma, drugs, alcohol

> 60 = cerebrovascular disease, neoplasms

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20
Q

what can cause temporal lobe epilepsy and is also a major cause of epilepsy

A

= Hippocampal sclerosis (damage with scarring and atrophy of the hippocampus and surrounding cortex) is a major cause of epilepsy (temporal lobe epilepsy).
= Usually visible on MRI and may be amenable to surgical resection of the damaged temporal lobe.
= there is loss of cells in the CA2 and CA3 hippocampal areas.
= there may be Sprouting of the mossy fibres of granule cells which may lead to reverberant excitatory circuits.
= Neurogenesis may also occur which can lead to abnormal circuits.

21
Q

What is hippocampus sclerosis

A

= Hippocampal sclerosis (damage with scarring and atrophy of the hippocampus and surrounding cortex) is a major cause of epilepsy (temporal lobe epilepsy).

22
Q

what are two things that can cause primary epilepsy

A

= hippocampal sclerosis

= loss of chandelier cells

23
Q

What are chandelier cells

A

= the are a special population of GABAergic cortical interneurones in the CNS that can control the activity of cortical pyramidal cells

24
Q

what happens when there is loss of chandelier cells

A

this increases the risk of abnormal excitatory activity and epilepsy

25
Q

what can cause a secondary epilepsy

A
  • Traumatic brain injury
  • Stroke
  • Aneurysm
  • Brain tumour
  • CNS infection
  • Craniotomy for any reason
26
Q

what are the 3 cellular mechanisms that are linked to the development of epilepsy

A

Abnormal neuronal excitability (ion channels)

Decreased inhibition (GABA-dependent)

Increased excitation (Glu-dependent)

27
Q

what is a paroxysmal depolarising shift theory

A

= cellular manifestation of epilepsy.
= GABA-activated Cl− influx causes hyper-polarisation.
= Glial abnormalities may also be involved in epilepsy as they have an important role in glutamate transport and clearance through glutamate transporters such as EAAT1 and EAAT2.

28
Q

What is interneuronopathy

A

= theory that epilepsy is a disorder of intracellular signalling.
= Epilepsy may involve activation of distinct major signalling pathways (for example the mTOR pathway or the REST pathways).
= The mTOR pathway is a major regulator of growth and homeostasis.
= The REST pathway leads to negative regulation of the expression of many genes in the CNS.

29
Q

what is the MTOR pathway

A

= The mTOR pathway is a major regulator of growth and homeostasis.

30
Q

What is the REST pathway

A

= The REST pathway leads to negative regulation of the expression of many genes in the CNS.

31
Q

describe how channelopathy and genetic can lead to epilepsy development

A

= Genetic analysis confirms the important role of ion channels in many epilepsy syndromes; however, the genetics of epilepsy is far more complex and also includes genetic hits not linked to ion channels.

32
Q

name three theories of how epilepsy is developed

A
  • paroxysmal depolarising shift
  • interneuronopathy
  • channelopathy and genetic
33
Q

name the drugs used for epilepsy that are targeting sodium channels

A
  • phenytoin
  • carbamazepine
  • sodium valproate
  • lamotrigine
  • topiramate
34
Q

describe the drugs used for epilepsy that are targeting sodium channels

A

• Phenytoin
= - uses Zero order kinetics,
= it also causes liver enzyme induction which are involved in drug metabolism;
= not used in absence seizures because they can be increased by these drugs
= as it has zero order kinetics just a small increase in the dose can lead to toxicitiy as you cannot get rid of it quick enough

• Carbamazepine
= enzyme induction; not used in absence seizures
= has tendcy to induce liver enzymes – this can accelerate the metabolism of other drugs that the patient is taking – increased risk of tetrogentictiy

• Sodium valproate
= can be used in all types of seizures
• Lamotrigine
= also activity at calcium channels; presynaptic inhibition of glutamate release
• Topiramate
= also augmentation of GABAA and inhibition of glutamate AMPA/kainate signalling

35
Q

define zero order kinetics

A

zero order kinetics means that its elimination is independent of the concentration

36
Q

what drugs target GABAa receptors (benzodiazepines)

A

• Clonazepam (sedation)
= binds to a site on the GABAa receptor different to what GABA binds to) positive allosteric modulators- enhance activity in the prescnece of GABA they enhance the effects of GABA

37
Q

What other drug targets GABAa receptors (Barbiturates)

A

Phenobarbitone (microsomal enzyme induction)

= ( can become full agonist if they increase the dose a lot) – GABAA receptor positive allosteric modulators

38
Q

What drugs target calcium channels

A
  • Ethosuximide (used in absence seizures, targets T-type calcium channels)not to be used in grand mal seizures
  • Gabapentin (pregabalin)(alpha2delta subunit of calcium channels)
39
Q

what drug targets neurotransmitter release

A

• Levetiracetam

= (binds to synaptic protein SV2A; modulates neurotransmitter release)

40
Q

what drug targets neurotransmitter uptake

A

• Tiagabine
= unique mechanism of action; mainly as add-on therapy; targets the GAT-1 transporter preventing the reuptake of GABA
= used as an add on therapy in partial seizures with or without generalisation
= possible interaction with the GABAA receptor?)

41
Q

What drug targets neurotransmitter synthesis

A

• Vigabatrin

= inhibition of GABA transaminase prevention the breakdown of GABA – possibly also affects glutamate synthesis?)

42
Q

What drugs target neurotransmitter receptors

A

• Perampanel
= selective non-competitive antagonist of AMPA receptors – first drug targeting AMPA glutamate receptors
• Felbamate
= NMDA receptors; also GABAA receptors? )

43
Q

What are the challenges of epilepsy management

A
  • Choice of initial treatment
  • Choice of best drug for monotherapy
  • Define the best drug combinations
  • Complex shape of drug dose-response curve
  • Variability of response between patients
  • Long-term efficacy issues
44
Q

how many patients are treatment resistant

A

1/3

45
Q

name the prescription guidelines for epilepsy

A
  • Focal seizures with or without secondary generalisation (carbamazepine, lamotrigine, sodium valproate)
  • Tonic-clonic seizures (carbamazepine, lamotrigine, sodium valproate)
  • Absence seizures (ethosuximide, sodium valproate)
  • Myoclonic seizures (sodium valproate, clonazepam, levetiracetam)
46
Q

name some consequences of epilepsy

A
  • Tiredness
  • Memory problems
  • Problems with concentration
  • Depressed
  • Headche
  • Vertigo
47
Q

what are the other treatment options beyond drugs for epilepsy

A

Neuromodulation: vagal nerve stimulation, deep brain stimulation
Ketogenic diet (diet high in fat and low in carbohydrates, e.g. 4:1 ratio)
New anti-epileptic drugs: example of cannabidiol for treatment-resistant epilepsy

48
Q

How do you treat status epilepticus

A

Status epilepticus is a medical emergency – treatment includes lorazepam or diazepam IV

Brain and Behaviour Year 2 (36 decks)

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