epilepsy seizures n.
Download
Skip this Video
Loading SlideShow in 5 Seconds..
Epilepsy & Seizures PowerPoint Presentation
Download Presentation
Epilepsy & Seizures

Loading in 2 Seconds...

play fullscreen
1 / 22

Epilepsy & Seizures - PowerPoint PPT Presentation


  • 99 Views
  • Uploaded on

Epilepsy & Seizures. def. Seizure – clinical event caused by an abnormal synchronised electrical discharge in the brain. Epilepsy – neurological disorder characterised recurrent and unprovoked seizures. p athophysiology.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about 'Epilepsy & Seizures' - hue


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
slide2
def
  • Seizure – clinical event caused by an abnormal synchronised electrical discharge in the brain.
  • Epilepsy – neurological disorder characterised recurrent and unprovoked seizures.
p athophysiology
pathophysiology
  • Normal cortex – recurrent and collateral inhibitory circuits that limit synchronised discharge
  • GABA – inhibitory neurotransmitter, GABA receptor drugs cause seizures
  • Acetylcholine, glutamate & aspartate – excitatory neurotransmitters
  • Epileptic cortex – reduced inhibitory signals or increased excitatory signals
classification
classification

Physiological classification:

  • Partial/focal
  • Generalised (primary)

Clinical seizure description:

  • Pre-ictal
  • Ictal
  • Post-ictal
partial focal seizures
partial/focal seizures
  • Limited to one part of cortex
  • Sx depend on part of the cortex involved:
    • Simple partial seizures – consciousness preserved
    • Complex partial seizures – consciousness impaired (involving centres of awareness – frontal/temporal)
    • Partial seizures with secondary generalisation – focal origin spreading to rest of the brain
partial focal seizures1
partial/focal seizures
  • Focal motor (Jacksonian)
    • Motor cortex origin - Speech arrest, involuntary turning of eyes or head etc
    • Rare – jacksonian march, focal clonus spread from distal to proximal in limbs
  • Temporal lobe
    • Affective and/or cognitive fx. Feelings of unreality, deja vu, vertigo, visual hallucinations etc
  • Parietal lobe
    • Sensory fx – visual, auditory, somatosensory, vertiginous, olfactory etc
  • Frontal lobe
    • Autonomic fx. Pallor, sweating, pupillary dilation, epigastric sensation, piloerection, flushing
p rimary generalised seizures
primary generalised seizures
  • Electrical disturbance originates and spreads from the diencephalon activating pathway (controls cortical activation).
  • Simultaneous bilateral cerebral discharge with LOC.
  • Types:
    • Absence
    • Myoclonic
    • Tonic – clonic
    • Atonic
    • Tonic
a bsence seizure
absence seizure
  • Almost always begins in children; tends to develop into tonic-clonic
  • Generalised absence seizure in children known as petit-mal
  • Characterised by unconscious sudden behaviour arrest and unresponsiveness
  • Discharge doesn't spread out of the hemispheres hence doesn't affect posture
  • Possible eyelid and/or facial clonus, muscle spasms but rarely lasting >10s
  • Normal activity is resumed after attack
  • Atypical presentations – with tonic, clonic and atonic features with above signs.
t onic clonic seizures
tonic-clonic seizures
  • Often preceded by an aura/prodome.
  • Tonic phase
    • patient goes rigid (flexes), unconscious and falls heavily.
    • respiration is arrested and central cyanosis may be seen.
    • Tongue biting, incontinence occurs. A period of generalised extension follows.
  • Clonic phase
    • Generalised convulsions with frothing at mouth
    • Tonic contractions alternate with atonia with increasing duration of atonia between spasms till event ceases
    • May last a few minutes
  • Post ictal– drowsiness, confusion or coma for several hrs after seizure.
slide10

Myoclonic

    • Consciousness maintained
    • Single or repetitive rapid muscle contractions (bilaterally synchronous and symmetric) – shock like jerks.
  • Tonic
    • Intense hypertonia not followed by clonic jerks
    • Usually <10s, maybe up to 1 minute
    • Usually occurs during non REM sleep, and periods of drowsiness
    • Less consciousness impairment than tonic-clonic
  • Atonic – ‘drop attacks’
    • Sudden loss of postural tone for 1-2s
    • Brief LOC but quick recovery
aetiology
aetiology
  • Any cerebral pathology causing sustained synchronised discharge of a group of neurons.
slide12
DDx
  • Syncope
  • TIA
  • Narcolepsy (sleep disorder)
  • Pseudo-seizures (resemble epileptic seizures but not caused by electrical discharge in the brain).
  • Metabolic
  • Epilepsy is essentially a clinical Dx – Hx from witness important.
investigations
investigations
  • EEG +/- video monitoring
    • Performed soon after event or during one
    • Help to characterise the type of seizure
    • Seizure activity is generally shown as either focal cortical spikes or by generalised spikes and wave activity
    • EEG not a sensitive test for epilepsy – an abnormal EEG doesn't prove epilepsy
investigations1
investigations
  • Brain imaging – CT/MRI indications:
    • Epilepsy starts after age of 20
    • Seizures with focal clinical features
    • EEG showing focal source
    • Control of seizures is difficult or deteriorates
  • General tests:
    • Glucose, Na, Ca, Mg
    • Serum prolactin (increased, DDx pseudo-seizures)
    • ECG (DDx syncope)
    • Urine drug screen (amphetamines)
management
management
  • Non pharmacological:
    • Diet + nutrition esp. in young people
    • Stress and anxiety
    • Counselling/psychotherapy – higher risk of depression
    • Passion flower fusion – natural anticonvulsant
    • Massage Rx
    • Support groups
  • Epilepsy implications
    • Driving
    • Avoid solitary/dangerous sports (or hymns!)
    • Jobs – machines
    • In women – decreased fertility, 1/3 of women with epilepsy have ovarian abnormalities
management1
management
  • Pharmacological
    • Control fits in 70-80% with tonic-clonic seizures, 30-40% of absence seizures
    • Patient monitoring essential after commencing drug
    • Anti-epileptics induce liver enzymes:
      • Pregnancy – reduced OCP efficacy
      • Patients on warfarin – increased risk of bleeding
    • Anti-epileptics also highly protein bound – decreased Alb.
    • SEs: hepatotoxicity, ataxia, diploplia, nystagmus + cognitive fx decline.
p harmacological rx
pharmacological Rx
  • Rule of thumb:
    • Valproate
    • Lamotrigine
    • Absence – ethosuximide /vaproate
    • Partial – carbamazepine
  • Partial seizures +/- secondary generalisation:
    • 1st line – carbamazepine
    • 2nd line – lamotrigine, gabapentin, vaproate, levetiracetam, oxcarbazepine.
  • Primary generalised:
    • 1st line – vaproate
    • 2nd line – lamotrigine, topiramate, carbamazepine
    • Ethosuximide – more effective in absence seizures.
slide18

Mode of action of drugs

    • Increase inhibitory transmission
    • Alter sodium channels to prevent transmission
  • Na channel blockers – carbamazepine, valproate, phenytoin.
    • Valproate also seems to increase GABAergin inhibition.
    • Valproate and carbamazepine considered 1st line because of least SEs.
    • Phenytoin – pure Na channel blocker, primarily affects the motor cortex (prevents seizure spreading), can cause cerebellar signs (nystagmus, chorea, ataxia), cognitive fx & other SEs. A lot of SEs.
slide19

Ca channel blockers

    • Ethosuximide
    • SE – abnormal LFTs, liver and renal imparment
  • Inhibits release of glutamate
    • Lamotrigine – also blocks Na channels
    • Fewer SE: CNS Sx, skin rxn esp. in children
  • Potentiate effects of GABA – gabapentin, benzodiazepines, phenobarbital
    • Gabapentin – used as a ‘add-on drug’ when epilepsy is not being controlled, also used in neuropathic pain. Well tolerated.
    • Benzodiazepine - ^ GABA effects, used in ER situations – status epilepticus, prolonged seizures. SE- withdrawal syndrome, cognitive fx.
  • Levetiracetam & topiramate – unknown mech of action, powerful new AEDs for secondary generalisation.
surgical
surgical
  • Temporal lobectomy
    • Amputation of non dominant anterior temporal lobe
    • must have hippocampal sclerosis (imaging and EEG confirmation)
    • These cases represent < 1% of all cases bt cure rates are > 50 %
s tatus epilepticus
status epilepticus
  • Def – two or more continuous seizures where the patient has incomplete recovery of consciousness btw seizures.
  • Medical ER – up to 30% mortality from cardio respiratory arrest
  • >50% have no PHx of epilepsy
  • Rx:
    • Benzodiazepines
    • Phenytoin