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Epilepsy Flashcards

1
Q

What percentage of the population suffer from epilepsy?

A

1

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2
Q

What percentage of epilepsy begins in childhood?

A

75%

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3
Q

Define seizure

A

Sudden alteration of neurologic function caused by excessive hypersynchronous discharge of neurons in the brain.

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4
Q

State difference between seizure and epileptic seizure

A

Epileptic seizure is caused by abnormal neuronal firing.

Seizure is broader term and could refer to psychogenic seizure.

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5
Q

Define refractory epilepsy

A

Seizures not controlled by 2+ antiepileptic medication.

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6
Q

What type of seizures are often pre-ceded by an aura?

A

Temporal lobe: patient remains conscious and aware. Can describe motor, sensory, autonomic or psychic symptoms.

Aura = precedes seizures by seconds or minutes.

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7
Q

What are epileptic spasms?

A

Manifests in sudden extension or flexion of extremities, held for seconds and then occurs in clusters.

Can occur at any time (infantile spasms to note).

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8
Q

Are adults or children more susceptible to seizures?

A

Children as developing brain GABA is excitatory and excitatory function develops before inhibitory function.

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9
Q

Describe Nonepileptic seizures

A

Psychogenic: changes in motor activity or behaviour that reflects epileptic seizures but no epileptic activity in the brain.

Reflect major underlying pschopathology, anxiety or psychological stress can manifest into seizures so treatment is based on
teaching patient alternative coping skills.

Presents clinically in different ways and some previously thought to be nonepileptic have been found to be epileptic so very hard.

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10
Q

What is the most frequent psychiatric comorbidity?

A

Depression (30%): associated with hippocampal and limbic dysfunction (structures commonly implicated in epileptic circuits).

Thought to be bi-directional: epilepsy patients with depression more likely to be refractory and people with epilepsy more likely to develop depression.

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11
Q

Link between epilepsy and bone health

A

Antiepileptics: phenytoin, phenobarbiral and carbamazepine thought to lead to decrease in bone mineral density via induction of CYP450 enzyme.

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12
Q

SUDEP?

A

Sudden Unexpected Death in Epilepsy: when you have seizures all neurons firing at once, comparable to brain oscillations. When close eyes you have alpha waves - stops visual processing. When sleep delta - stops all processing. So When all neurons fire in epilepsy stops brain carrying out function. Therefore, when this occurs in brainstem - cardiac and respiratory dysfunction.

Risk factors: onset of epilepsy before 16yrs and poor control of generalised tonic-clonic seizures.

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13
Q

When is surgical epilepsy treatment appropriate?

A

Candidates with drug-resistant focal epilepsy.

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14
Q

Outline chemoconvulsant epilepsy animal model

A

Kainic acid (L-glutamate analog) or pilocarpine (muscarinic acetylcholine agonist). Temporal lobe.

Kainic: damage to hippocampal formation
Both:Elicits damage to neocortical regions
The above refers to damage to pyramidal cells but GABAergic somatostatin cells also showed damage.

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15
Q

Outline repetitive stimulation of the brain epilepsy animal model

A

Repeated electrical stimulation of limbic brain structures that leads to behavioural seizures.

In this protocol spontaneous seizures do not usually occur and overstimulation only elicits spontaneous seizures.

Results in neuronal loss and aberrant plasticity.

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16
Q

Outline potential role of BDNF and epilepsy

A

Human TLE tissue suggests chronic seizure activity is negatively correlated with BDNF expression levels.

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17
Q

Outline focal cortical dysplasia animal model

A

FCD type IIB resembles tuberous sclerosis complex (TSC) = presence of undifferentiated giant cells like balloon cells in FCD.

Somatic mTOR mutations described in both FCD and TSC: hyperactivation of pathway = abnormal cell growth.

So TSC rodent models where TSC genes are inactivated and evidence of lower seizure threshold in rodents but no evidence of spontaneous seizures.

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18
Q

Outline how synaptic scaling works and why it is important in development.

A

Synaptic scaling refers to mechanisms that regulate total strength of a neuron: all of a neurons synaptic inputs increased or decreased in strength as a function of activity.

Chronic blockade: increases mEPSC amplitude and blocking GABA initially increases friring rates but over 48hours mEPSC decreased and returned to control values.

Ensures that firing rates do not become too high during development and preserves relative differences between inputs (like normalisation)

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19
Q

Outline AMPAR encephalitis

A

Patients develop AMPAr antibodies (ab): anti-GluA1/2. These receptors found highly expressed in hippocampus and other limbic regions.

Treatment resistant disorder: short term memory loss and seizures.

Decreased surface level of protein and synaptic localisation of AMPArs without dismantling of excitatory synapses. Loss of AMPAr mediated transmission causes compensatory decrease in GABA transmission and increase in intrinsic excitability thought to cause seizures. As neuron recieves less input but fires more.

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20
Q

Outline the RISE model for epilepsy

A

RISE: Reduced Intensity Status Epilepticus, low mortality and high morbidity model of chronic temporal lobe epilepsy. Long latent (seizure free period) between induction and development of spontaneous recurrent seizures (SRS).

Successfully recapitulates: restriction to temporal lobe structures, variation in seizure freq and intensity between animals.

Loss of AMPAr GluA1 in latent period, increase in PSD95 in SRS. Lower expression of AMPAr in SRS. Loss of hippocampal GABA aBeta3 subunit in SRS. E/I imbalance.

How: pilocarpine to induce seizure and when reached certain activity xylazine to reduce severity.

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21
Q

Role of GABA in epilepsy

A

Previously believed: less GABA causes E/I imbalance as block of GABA in healthy brains produces acute epileptic discharges. Drugs that enhance GABAergic transmission can alleviate seizures eg benzodiazepines.

Real story is more complex: possibly hyperinhibition that masks hyperexcitability and GABAergic interneurons may act as network synchronisers during certain epileptiform activities.

Kainic acid application to hippocampus in rats evokes population spikes at gamma frequency that is synchronised by GABA.

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22
Q

Role of GABA developmentally

A

In early development GABA is excitatory due to elevated intracellular Cl- levels. Higher levels due to Na/Cl cotransporteer KCC2 that causes.

If this persists in adulthood not good. Homeostasis needed or epilepsy (some types associated with altered cl).

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23
Q

How does GABA create neuronal oscillations?

A

Causes neurons to stop firing for a set amount of time (25-30ms) then due to background excitation, neurons will fire again simultaneously when they have recovered from this inhibition.

This often in form of GABAergic neurons connected to 200+ cells (often pyramidal).

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24
Q

Role of synchronisation?

A

Good: need synchronisation to sleep - delta rhythm (2Hz) supresses brain functions. Similarly alpha waves when close eyes suppresses visual function.

Bad: can cause seizures and also loss of consciousness in a seizure (unable to move etc) and therefore pathological.

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25
Q

What percentage of epilepsy cases are refractory?

A

30%

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26
Q

What percentage of epilepsy surgery patients show no improvement after surgery?

A

20%

27
Q

Generalised epilepsy

A

In a lot of parts of the brain, otherwise known as bilateral/whole cortex.

28
Q

Tonic

A

Muscle clenched

29
Q

Clonic

A

Twitching muscles

30
Q

Absence

A

People just stop what they are doing (eg if middle of pouring tea will not stop pouring).

31
Q

Focal

A

Partial/localised: only occurs in small part of brain and effect on body is related to where it is.

32
Q

Secondary generalised

A

When spreads from focal point.

33
Q

Main difference between bilateral and focal?

A

Focal not always accompanied with loss of consciousness and often come with aura if temporal lobe epilepsy.

34
Q

Outline temporal lobe epilepsy

A

Most common.

2/3 of surgeries related to intractable TLE.

Often have aura: deja vu, auditory illusions, orgasmic auras described.

Consciousness lost/altered and amnesia is often seen.

Body movements: hand picking, lip smacking, ictal speech.

35
Q

Outline absence epilepsy

A

Aetiology thought to be genetic, WAG/Rij rats demonstrate spike wave discharges due to genetic disposition

Onset: 3-10 yrs.

Signs: staring, unresponsiveness, loss of postural tone.

Duration is brief ~10s but can occur hundreds of times per day.

EEG: regular rhythm as occurs in thalamus, 3Hz.

36
Q

Outline CAE and evaluate genetic model for absence epilepsy

A

CAE: childhood absence epilepsy.

Aetiology: underlying pathophysiology of CAE involves abnormal thalamocortical firing as a result of aberrant T-type calcium channels.

WAG/Rig: age related onset of spike wave discharges that are accompanied by absent spells. Treated by ethosuximide which is effective drug in CAE but not treated by drugs not effective for CAE.

All above is good but unlike in humans: do not grow out of this and still get SWDs in adulthood.

37
Q

Outline Focal Cortical Dysplasia

A

Part of cortex layered incorrectly, often with stereotypically large abnormal cells.
Most common cause of intractable paedriatic epilepsy and can cause mild to severe mental retardation.

Seizures: focal onset with up to 100 per day.

38
Q

Outline West Syndrome

A

Epileptic spasms with age of onset 4-9 months.

Prognosis: developmental delay with many having seizures later on in life - commonly Lennox Gastaut syndrome.

Treatment: keto diet and surgery as well as drugs.

39
Q

Outline Lennox-Gastaut syndrome

A

Onset: 1-7 yrs.
Seizures: tonic (often nocturnal), myoclonic, atypical absence, generalised tonic clonic (bascially v varied).

EEG: generalised 1-2Hz and sudden fast activity during sleep.

Prognosis: intellectual impairment, depends on aetiology (up to 40% of cases = more severe).
Treatment: drugs, keto diet, corpus callosotomy.

40
Q

Outline Doose syndrome

A

Onset: 2-5yrs.
Seizures: generalised, atonic and absence, bi-parietal theta as well as 3Hz spike.

Aetiology: most unidentified but others have Glut1 deficiency or Na channel mutations.
Prognosis: 50% seizure free with normal development and other half intractable with developmental and behavioural co-morbidities.
Treatment: keto diet, drugs.

41
Q

Outline Dravet syndrome

A

Onset: initially presents as febrile seizures in first year of life.
Seizures: triggered by temp (hot bath) and will rarely have fever without seizure. After 2yrs frequent status epilepticus.

Aetiology: Na channel mutations (SCN1A - 70% have mutation) on interneurons.
MRI: may show cerebral atrophy.

42
Q

Define status epilepticus

A

When come out of seizure only to rapidly enter into another.

This can cause irreversible damage to brain and more seizures due to plasticity. Eg: if going on longer than hour cannot induce coma as receptors can be lost.

Mortality rate can be as high as 1 in 5 with convulsive as majority of cases. over 50% of cases occur in non-epileptic.

43
Q

How can you tell that someone in status epilepticus?

A

Obviously EEG but really can only tell if they show motor symptoms.

If no motor may be completely unable to tell.

44
Q

What is refractory status epilepticus?

A

20-40% of status epilepticus popultation will progress into refractory where continused seizures despite treatement with benzodiazepines and other antiepileptic.

Mortality rates up to 2 in 5.

45
Q

Outline reflex epilepsy

A

Affects 7% of epilepsy sufferers: where seizures are triggered by TV, strobe lighting, music, brushing teeth, playing chess etc.

46
Q

Why can seizures spread to other parts of the brain so easily?

A

Brain is like small world network: v efficient which makes recruitment of more neurons in a seizure very easy to do.

47
Q

How do most Antiepileptic drugs work?

A

Work at the synapse.

48
Q

Outline vagal nerve stimulation for epilepsy

A

Not all patients respond: those who do respond have reduced interictal cortical synchronicity on scalp EEG.

VNS: found to stop experimentally induced seizures in dogs.

VNS - lower risk surgery, placement of electrodes on vagus nerve with intermittent stimulation, studies show periodic (half min on and 5 mins off) 20-30Hz stim provides max seizure protection.

  • Up to 40% of patients observe 5-% seizure reduction freq.
  • Less drugs needed with VNS.

Side effects: coughing/hoarseness of voice.

Only certain branches and fibres are stimulated.

Only A and B fibres need stim: activation threshold lower (less current) than C fibre stim and produces antiepileptic effects.

Only applied to left cervical trunk: if applied to all adverse side effects such as cardiopulmonary.

Krahl 2012

49
Q

Outline deep brain stimulation for epilepsy

A

Thalamus : anterior thalamic nucleus

Most widely used target for treatment of drug resistant epilepsy.

“preferred because of its size, its distance from vascular structures (24), and its extensive connections.”

  • prev trials reported up to 68% seizure freq decrease after 3 years.

Side effects

Invasive (infection) and stimulation related paresthesias.

Zangiabadi at al., 2019

50
Q

How does autoimmune epilepsy usually present?

A

usually new-onset refractory epilepsy along with features of autoimmune encephalitis such as - cognitive decline and autonomic dysfunction.
Husari and Dubey 2019

51
Q

Autoimmune epilepsy treatment?

A

immunosuppressant use and removal of trigger such as tumour when applicable.

largely unresponsive to antiepileptic agents.

Husari and Dubey 2019

52
Q

Possible pathophysiology of autoimmune epilepsies?

A

1) Tumour: cells express onconeural antigen which leads to misdirection of immune response.

2) Infection: diff mechanisms eg amino acid similariity between pathogen and self antigen or may lead to lymphocyte activation and response against self-antigens.

Husari and Dubey 2019

53
Q

Outline LGI1 autoimmune epilepsy

A

disruption of LGI1–ADAM22 interaction which reduces synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor function, subsequently disrupting ca influx

mostly found in over 40yr olds

Husari and Dubey 2019

54
Q

Outline NMDAr autoimmune

A

Binds to GluN1 subunit of NMDAR which disrupts interaction between NMDAR and ephrin B2 receptor causing NMDAR receptor internalisation (this is reversible).

  • Trigger usually overian teratoma 2/3rds and therefore effects young women with mean age of 22yrs

Husari and Dubey 2019

55
Q

What is the ketogenic diet?

A

Strict low carb with 5-10% of total daily calorie intake.

56
Q

How does the ketogenic diet increase ketone concentration in the body?

A

Increased liver ketogenesis - increased production of liver ketone bodies due to lack of glucose.

Ruan et al., 2022

57
Q

Reasons why people discontinue keto diet?

A

regardless of efficacy some patients do not continue due to unpalatability and restrictive nature.
Ruan et al., 2022

58
Q

Side effects of keto?

A

moderate weight loss, GI issues, anorexia and hypercalciura

Ruan et al., 2022

59
Q

Link between keto and mood disorders?

A

ncreased prevalence in epilepsy, seen in young adults at both onset and during course of disorder.

Combined therapy = improvements in Depression levels and overall quality of life.

Attention

Improved altertness and attention: research suggests ketone bodies increase visual attention.

Cognition

Esp beneficial for Dravet syndrome as cognitive improvement observed.

Ruan et al., 2022

60
Q

How is keto diet anticonvulsant?

A

Largely unknown.

1) Ketone bodies have anticonvulsant effects (controversial).

Ketone bodies are byproducts of fatty acid oxidation in mitochondrial hepatocytes.

  • rats exposed to KD showed no difference in synaptic plasticity using PP stim and LTP (unsupportive)
  • In spontaneously epileptic Kcna1 null mice ketone body supplementation associated with attenuation of seizure like events (supports)
  • Ma et al., 2007 found reduction in spontaneous firing rate (supports).

2) Neuronal metabolism

Glucose metab is quick and produces rapidly available energy that can be used for seizure activity.

  • KD patients blood glu conc is low so brain must use keto bodies for energy.
  • Anaerobic metab slows energy availability which in turn reduces seizures.
  • Experimental models showed glucose infusion reverses anti-convulsant effects.

3) increased GABA synthesis

KD diet decreases aspartate levels = aspartate has inhib effect on glutamate decarboxylase so.

  • more GABA made.

4) KD alters gut microbiome

Increases putatively beneficial bacteria, leads to increase of GABA:glu ratio in the brain.

5) increases decanoic acid which inhibits ampar

D’Andrea Meira et al., 2019

61
Q

is CBD safe and effective treatment?

A

CBD:no psychoactive properties, no euphoric or intrusive side effects and largely devoid of abuse liability.

Pharmacological interactions

Drowsiness is most common side effect and higher incidence among patients concomitantly taking clobazam.

CBD can increase the plasma conc of biologically active clobazam metaboliste N-desmethylclobazam.

Therefore strictly observe.

Paper results

Aim to evaluate efficacy and safety in patients with epilepsy uncontrolled by concomitant therapy (Lennox-Gastaut and Dravet).

Reduction in all types of seizure freq by at least 50% observed in 37% patients - greater than placebo.

Lattanzi et al., 2018

62
Q

CBD mechanism

A

Cannabinoid receptors: CBD low affinity and no known effect on epilepsy.

Glycine receptors: CBD causes 9 fold increase in current amp compared to just glycine alone.

VGSC: blocks channels but not thought to confer anticonvulsant effects.

T-type VGCC: low voltage activated channels, antiepileptics sucj as valproate thought to act on this and thought to inhibit synchronised depol. CBD also blocks and produces hyperpolarising shift which thought to induce block when channel is in both open or closed state.

Ibeas Bih et al., 2015

63
Q

Define epilepsy

A

Neurological disorder marked by sudden recurrent episodes of seizures that cause sensory disturbance and are associated with abnormal brain activity.

64
Q

mTOR in epilepsy

A

mTOR: regulates cell metabolism and growth - synapse formation and plasticity. Upregulated…

Rapamycin is inhibitor and successful in rodents - decrease seizure freq and duration and positively effect cell growth and morphology.
Also improves survival in animal models.

Mutations described in FCD

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