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Brain and Behaviour Year 2 > Epilepsy > Flashcards

Epilepsy Flashcards

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
what can cause a secondary epilepsy
- Traumatic brain injury - Stroke - Aneurysm - Brain tumour - CNS infection - Craniotomy for any reason
26
what are the 3 cellular mechanisms that are linked to the development of epilepsy
Abnormal neuronal excitability (ion channels) Decreased inhibition (GABA-dependent) Increased excitation (Glu-dependent)
27
what is a paroxysmal depolarising shift theory
= 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
What is interneuronopathy
= 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
what is the MTOR pathway
= The mTOR pathway is a major regulator of growth and homeostasis.
30
What is the REST pathway
= The REST pathway leads to negative regulation of the expression of many genes in the CNS.
31
describe how channelopathy and genetic can lead to epilepsy development
= 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
name three theories of how epilepsy is developed
- paroxysmal depolarising shift - interneuronopathy - channelopathy and genetic
33
name the drugs used for epilepsy that are targeting sodium channels
- phenytoin - carbamazepine - sodium valproate - lamotrigine - topiramate
34
describe the drugs used for epilepsy that are targeting sodium channels
• 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
define zero order kinetics
zero order kinetics means that its elimination is independent of the concentration
36
what drugs target GABAa receptors (benzodiazepines)
• 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
What other drug targets GABAa receptors (Barbiturates)
Phenobarbitone (microsomal enzyme induction) | = ( can become full agonist if they increase the dose a lot) – GABAA receptor positive allosteric modulators
38
What drugs target calcium channels
* 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
what drug targets neurotransmitter release
• Levetiracetam | = (binds to synaptic protein SV2A; modulates neurotransmitter release)
40
what drug targets neurotransmitter uptake
• 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
What drug targets neurotransmitter synthesis
• Vigabatrin | = inhibition of GABA transaminase prevention the breakdown of GABA – possibly also affects glutamate synthesis?)
42
What drugs target neurotransmitter receptors
• Perampanel = selective non-competitive antagonist of AMPA receptors – first drug targeting AMPA glutamate receptors • Felbamate = NMDA receptors; also GABAA receptors? )
43
What are the challenges of epilepsy management
* 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
how many patients are treatment resistant
1/3
45
name the prescription guidelines for epilepsy
* 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
name some consequences of epilepsy
- Tiredness - Memory problems - Problems with concentration - Depressed - Headche - Vertigo
47
what are the other treatment options beyond drugs for epilepsy
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
How do you treat status epilepticus
Status epilepticus is a medical emergency – treatment includes lorazepam or diazepam IV

Brain and Behaviour Year 2 (36 decks)

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