7) Epilepsy Flashcards

1
Q

Epileptic seizure (definition)

A

= paroxysmal change in behaviour due to synchronised rhythmic firing of populations of CNS

Transient loss of conciousness due to
- epileptic seizures: acute- symptomatic OR unprovoked
- non-epileptic seizures
- unclear

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2
Q

Epilepsy (definition)

A

defined by recurrent unprovoked (=spontaneously occurring) seizures

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3
Q

Epidemiology

A

Prevalence
- approx. 70 Mio worldwide
- in Germany 5.5/1000 (around 450,000 patients, 22,000 in Berlin)
- acutal prevalence unknwon due to lack of diagnosis in rural areas

Life-time risk of one epileptic seizue
- 5 % of the general population

Age-dependent incidence
- epilepsy incidence higher in younger patients (until age of around 20) and in older adults (increase starting around the age of 60)

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4
Q

Epileptic seizure: epileptic - actue symptomatic

A

= provoked
- transient loss of consciousness

Triggers:
- acute brain lesion (eg intracranial bleeding, stroke, head trauma, infection)
- alcohol withdrawal
- metabolic disturbances (eg hypogycemia < 36mg/dl)
- intoxication (all ‘upper drugs’ such as MDMA)
- in children: fever > 35,8 °C

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5
Q

Non-epileptic seizure: non-epileptic

A

Differential diagnoses (epilepsy imitator)
- syncope
- dissociative seizure (PNEA)
- migraine with aura
- hypoglycaemic episode
- transient ischaemic attack (TIA)

Syncope vs tonic-clonic seizure (most prominent differences)
- duration: mostly < 30s – 1-2 min
- reorientation: < 30s – 4-45 min

Psychogenic non-epileptic seizure vs tonic-clonic seizure
- eyes: closed – open, deviation frequently

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6
Q

Epileptic seizure: epileptic - unprovoked: Epilepsy diagnosis

A
  • two unprovoked seizures occurring > 24hrs apart
  • one unprovoked seizure and a probability of further seizures similar to the general recurrence risk after two unprovoked seizures (at least 60%) over the next ten years
  • causative CNS disease
  • pathological EEG alternations
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7
Q

Classification of epileptic seizures - Focal onset

A
  • initial symptoms/signs (clinical and EEG) indicate origin of seizure activity
  • within an area of ONE hemisphere

Seizure types
- aware/impaired awareness
- Motor onset (automatisms, atonic, clonic, epileptic spasms, hyperkinetic, myoclonic, tonic)
- Non-motor onset (automatic, behaviour arrest, congitive, emotional, sensory)

focal to bilateral tonic-clonic

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8
Q

Localisation of focal aware seizures (= ‘aura’)

Distribution across brain areas

A

frontal lobe
- 25 %
- tonic/clonic movements

temporal lobe
- 65%
- lateral (10%)
- >auditory symptoms
mesial (90%)
- psychic or autonomic symptoms

parietal lobe
- 5%
- paraesthesia (abnormal sensation, tickling/pricking)
- vertigo

occipital lobe
- 5%
- visal symptoms

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9
Q

Classification of epileptic seizures - Generalised onset

A
  • initial symptoms/signs (clinical and EEG) indicate origin of seizure activity
  • simultaneously in BOTH hemispheres

Seizure types
- Motor (tonic-clonic, clonic, tonic, myclonic, myoclonic-tonic-clonic, myoclonic-atonic, atonic, epileptic spasms)
- Non-motor - absence (typical, atypical, myoclonic, eyelid myoclonia)

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10
Q

Overview Epilepsy classification

A

Seizure types
- focal
- generalised
- unknown

|

Epilepsy types
- focal
- generalised
- combined generalised & focal
- unknown

|

Leads to epilepsy syndomes

Co-morbidities can occur

Etiology
- structural
- genetic
- infectious
- metabolic
- immune
- unkown

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11
Q

Causes of focal onset epilepsy

A
  • including all etiological causes (structural, genetic, infectious, metabolic, immune, unknown)
  1. Hippocampal sclerosis
    - neuronal loss: CA1and CA4
    - relative resistance: CA2 and CA3
    - gliosis
    - axonal and synaptic reorganisation
  2. Malformation of cortical development (MCD)
    2.1 Neuronal proliferation:
    -> cortical dysplasia with ‘balloon cells’
    -> hemimegalencephalia
    2.2 neuronal migration:
    -> heterotopias
    -> lissencephaly/subcortical band-heterotopia spectrum
    2.3 cortical organisation:
    -> polymicrogyria
    -> cortical dysplasia without ‘balloon cells’
  3. Vascular malformations
  4. (postnatal) acquired CNS lesions
    - neoplasia
    - cerebro-vascular
    - traumatic brain injury
    - neurodegeneration
    - infectious/inflammatory
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12
Q

Causes of generalised epilepsy

A

Genetic (!) causes

Ion channel mutation
- Na+ channel
- K+ channel
- Cl- channel

Receptor mutation
- GABA receptor
- Acth - receptor

Ion transporter mutation
- Na+-K+-ATPase

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13
Q

Clincial features of psychogenic non-epileptic seizures

A
  • undulating head movement
  • eyes closed
  • resistance on passive eye opening
  • asynchonous movement
  • long duration (> 2min)
  • undulating movement of both extremities
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14
Q

Diagnostic

A

Standard Clinical Diagnostic
- MRI with epilepsy-specific protocoll (HARNESS)
- routine EEG with hyperventilation and photostimulation

Additional Clinical Diagnostic
- longterm video EEG (in Germany only as inpatient in few specialsied centres)
- neuropsychology

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15
Q

Treatment: Antiseizure Medication (ASM)

A
  • pharmacotherapy surpresses the symptom
  • the chronic disorder epilepsy cannot be modified or treated
  • no anti-epileptogenic effects have been shown for current available ASM
  • increase of ASM since 1980s
  • target different neurotransmitter receptors
  • few drugs reach 50% probability of seizure freedom with first drug regimen
  • after that cummulative effects
  • and pharmacoresistance with later antiepileptic durg regimen
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16
Q

Treatment goal in chronic epilepsy

A

maintenance of normal life style
- complete seizure freedom

+

  • no or minimal substance adverse effects
17
Q

Treatment success of ASM

A

60%
- good prognosis
- seizure-free with first or second monotherapy
- no relevant adverse effects
- commonly seizure-free with AED termination

30%
- pharmacoresistant with polytherapy

10%
- seizure-free with polytherapy

18
Q

Epilepsy surgery - Eligibility criteria

A
  • pharmacoresistance
  • identification of one epilelptic focus with EEG
    -suitable MRI lesion
  • resection possible without persistent neurological/neuropsychological deficits
19
Q

Epilepsy surgery - Resective epilepsy surgery

A

Temporal lobe (hippocampal sclerosis)
- resection of amygdala, hippocampus, temporo-basal structures
- significant reduction of seizure frequency and 55% seizure-freedom 2 years after TL-resection

20
Q

Epilepsy surgery - laser treatment

A

MRI guided
- in mesial temporal lobe epilepsy 62% (total) efficacy

21
Q

Unreceived epilepsy surgery

A
  • increase in rejection rate
  • decrease in sugery
  • increase in contraindication (no resection)
  • 57% patients not referred
  • 70% of the referred patients refused
  • 5 % of referred patients agreed to evaluation but did not schedule appointment
  • 10% of referred patients scheduled appointment for evaluation
  • reluctance by epileptologists and patients
22
Q

Syncope vs tonic-clonic seizure

A

Syncope vs tonic-clonic seizure (most prominent differences)
- duration: mostly < 30s – 1-2 min
- reorientation: < 30s – 4-45 min

23
Q

Psychogenic non-epileptic seizure vs tonic-clonic seizures

A

Psychogenic non-epileptic seizure vs tonic-clonic seizure
- eyes: closed (in almost all cases) – open (in most cases)