Seizure & epilepsy 3) Epilepsoa partialis continua(rare): seizure may Generalised Seizure
continue for hours or days (refractory to therapy)
Defnition Simple sensory seizure: * Arises from subcortical
Seizure: Arise in sensory cortex (area 3,1,2) structures and involve both
A paroxysmal event d/t abnormal,excessive, hypersynchronous Paraesthesia in limbs/face sometimes associated with hemisphere simultaneously
discharges from an aggregate of neurons in CNS feeling of distortion of body * motor manifestations are
Epilepsy: ‘march’ similar to Jacksonian motor seizure may occur bilateral
A condition of recurrent seizures d/t a chronic underlying Autonomic or Psychic(auditory & visual) simple * consciousness may be impaired
process. (defined as occurrence of at least 2 unprovoked partial seizure: very rare
seizures with 24 hours apart)
(b) Complex (if consciousness is impaired) Partial Seizure a) Absence Seizure / Petit Mal
International Classification of Seizures Usually originate within temporal lobe Characterised by:
Classified based on clinical features of seizures and Characterised by: a) Sudden, brief lapses of consciousness without loss of
associated electroencephalographic(EEG) findings: i. Focal seizure activity postural control (lasts only for seconds)
ii. Transient impairment of consciousness (any degree as b) Consciousness return as suddenly as it’s lost
(A) Partial Seizures: long as pt lost ability to maintain normal contact with c) May be accompanied by subtle bilateral motor signs:
a. Simple Partial Seizures with motor/sensory/ environment) rapid blinking of eyelids, chewing, clonic movement of
autonomic or psychic signs iii. Preceded by aura hands
b. Complex Partial Seizures Aura (symtoms immediately before LOC) d) No postictal confusion
c. Partial Seizure with 20 Generalisation ↓ Onset in childhood (4-8 yrs old): main seizure in children
(B) Primarily Generalised Seizures Ictal (seizure) phase: with epilepsy
a. Absence seizure / Petit mal a) Sudden behavioural arrest/motionless stare: onset Might be seen as unexplained “daydreaming”
b. Tonic-clonic seizure / Grand mal of amnesia Distinguish from complex Partial seizure which lasts for
c. Tonic b) Accompanied by automatisms: involuntary more than 30 seconds, followed by headache, confusion
d. Atonic autonomic behaviour such as basic behaviour and lethargy
e. Myoclonic (chewing,swallowing) or more elaborate bahaviour
(C) Unclassified Seizures (running / display of emotion) b) Atypical Absence Seizure:
a. Neonatal seizures ↓ Deviate clinically and electrophysiologically from absence
b. Infantile spasms Postictal phase: Longer duration , less abrupt in onset & cessation
Confused, anterograde amnesia, Headache More obvious motor signs
Partial Seizures
Occur within discrete (c) 20 Generalisation c) Atonic Seizure:
regions in cerebral cortex Sudden loss of postural muscle tone 1-2 s
Brief consciousness impairment & no postictal confusion
(a) Simple (if consciousness Brief seizurequick headdrop or nodding movement
is preserved): Longer seizurecollapserisk of direct head injury
Simple motor seizure:
arise in frontal motor cortex (area 4) d) Myoclonic Seizure(MS):
clonic (repetitive flexion/extension) movements in Myoclonus: sudden/brief muscle contraction that may
contralateral face, trunk or limbs involve 1 part/the entire body
Spread from the point of origin(e.g frontal cortex)
3 additional features to be noted: Distinction from other forms of myoclonus (e.g metabolic
subcortical structures (thalamus,reticular formation)
1) Jacksonian march: spread of seizure over a larger disorder, degenerative disorder of CNS) is imprecise
release discharges that spread back to involve both
region of motor cortex manifested as a abnormal MS is considered as true epileptic event as it is caused
cerebral hemisphere produces generalised seizure
movement in restricted region (e.g:little finger) by cortical/subcortical dysfunction
(usually tonic-clonic variant)
that progress to involve a larger muscle group Dominant feature of juvenile myoclonic epilepsy
Eye witness is very important as the aura before
2) Todd’s paralysis: localised paresis after seizure (i.e May be associated with tonic-clonic seizures
tonic/clonic convulsion give a clue to the site of initial
remain weak for minutes-hours before return of
function)
discharge (simple partial/complex partial) Joen
e) Primary Generalised Tonic-Clonic Seizures / Grand Mal b) Lennox-Gastaut Syndrome (children 3-5 years) b. Paroxysmal Depolarisation Shift:.
Abrupt onset without warning sign (*distincting feature of Defined by a triad of: Consists of a sequence of events occuring in a single
partial seizure2oGeneralisation) a) Multiple seizure types (tonic clonic/absence/atonic) neurons:
b) EEG: slow spike-and-wave discharges
Tonic phase (initial phase 10-20 seconds): c) Impaired cognitive function (learning)
c) Mesial Temporal Lobe Epilepsy Syndrome
Most common syndrome associated with complex partial
seizure i. Burst of action potentials: d/t influx of Ca2+ which
MRI: detect a characteristic hippocampal sclerosis opens the voltage gated Na+ channel Na influx
Tonic contraction of: Important to recognise as it is refractory to plateau like depolarisation
a) Muscles of expiration & larynx loud moan / “ictal cry”, anticonvulsants but responds well to surgical intervention ii. Rapid repolarisation
impaired respiration & cyanosis iii. Hyperpolarising afterpotential:
b) Jaw muscle biting of tongue Etiology & Factor affecting Seizure mediated by GABA-A (Cl-) receptor or K+ efflux
c) Limbs muscle: elbows flexed, arm pronated, legs 1. Genetic: PDS increases possibilty of hypersynchronisation
extended low threshold level for seizures (explains why only a small When multiple neurons fire PDS produces interictal
d) Detrusor muscle urinary incontinence group of children develop febrile seizure) spike (possible of transforming into epileptic seizure)
↑sympathetic tone ↑heart rate, ↑pupil size 2. Epileptogenic factors (changes that ↓threshold): Transformation epileptic seizure is usually inhibited by:
↓ Trauma (especially penetrating head trauma), stroke, a) Hyperpolarisation
Clonic Phase (1-2 minutes) infection, abnormal CNS development b) GABA inhibition thru GABA-A / B receptor
3. Precipitating factors: Factors involved in transformation of interictal spike into
Psychological/physical stress, sleep deprivation, toxic epileptic seizure are:
substances & certain medications Decrease Inhibition Increase excitation
Defective GABA-A & B ↑[A] of NMDA receptor
Epileptogenesis inhibition ↑synchronization
Paroxysmal manifestation of electrical properties of brain Defective activation of between neurons (e.g by
Occur when imbalance occur between excitatory & GABA neuron epathic interaction)
Due to superimposition of periods of muscle relaxation on inhibitory forces
the tonic contraction Pathophysiology of focal-onset seizure differs from TaKE NotE!!!
Tremor violent generalised shaking generalised-onset seizure
The relaxation period progressively increase until the end a) Main Excitatory force in Brain is GLUTAMATE
on ictal phase a) Partial Seizure Produces EPSP (excitatory postsynaptic potential) by binding
↓
2 important events are: to receptors
Post-ictal Phase 1. NMDA: open Ca2+ channel (divalent channel)
a. Hypersynchronisation of neurons
unresponsiveness, muscular flaccidity 2. AMPA: open Na+ & K+ channel (monovalent)
Occur by epathic connection (non-synaptic relation
excessive salivation stridorous breathing & partial 3. Metabotropic (slow channel):not significant
between neurons):
airway obstruction b) Main Inhibitory force in Brain is GABA
1. Gap junction
after regaining consciousness confusion, headache, GABA-A: direct induction of IPSP on postsynaptic neurons
2. Changes in extracellular ion: e.g during repetitive
muscleache as it is coupled with Cl-channel (Cl influx)
firing, K+ efflux from neuron (during repolarisation
phase) will ↑ extracellular [K+] reducing the K+ GABA-B: indirect inhibition by inhibiting release of
epilepsy Syndrome excitatory neurotransmitter(glutamate) from presynaptic
electrical gradient of neighbouring cells blunts
Disorders in which epilepsy is a predominant feature. 3 neurons
the hyperpolarisation no refractory period
important syndromes are:
neighbouring neurons are capable of repetitive
stimulation & firing of A.P b) Generalised seizure
a) Juvenile Myoclonic Epilepsy (early adolescence) Pathophysiology are not well known except for absence
Single/repetitive bilateral myoclonic jerks frequently in seizure which is thought to be related to the :
morning & provoked by lack of sleep 1. normal oscillation in resting potential of thalamic neurons
Consciousness is preserved 2. transient low threshold Ca2+ channel/T-Ca2+ channel
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Investigation I. Valproic acid: GCSE is a medical emergency:
Can be used for any kind of seizure Prolonged seizure
1. Routine blood studies: MOA: block T-calcium channel ↓
Identify the more common metabolic cause of seizures II. Lamotrigine Cardiorespiratory dysfunction, hyperthermia,
E.g: disturbances in electrolyte, glucose, calcium, Can be used for any kind of seizure metabolic disturbances
magnesium, hepatic/renal disease Sodium channel blockers ↓
2. Lumbar Puncture & CSF examination: MOA: act presynaptically on Na+ channel prevent Irreversible neuronal injury
Indicated if suspicion of meningitis or encephalitis release of neurotransmitter (glutamate/aspartate)
Mandatory in all patient’s with HIV infection III. Carbamazepine
3. Electrophysiologic studies MOA: (1) stabilizes the inactivated state of Na+ Treatment:
Presence of electrographic seizure activity during the channel ↓excitability of neurons Anticonvulsant therapy should begin without delay:
event establishes the diagnosis (2) potentiates GABA inhibition Thiamine IV, Lorazepam Iv for 2 mins if no
E.g: abnormal, repetitive rhythmic activity of abrupt onset IV. Phenytoin rapid IV access diazepam is given per-rectal or
& termination MOA: ↑sodium efflux from cell depress Na+ action midazolam intranasally/intramuscular
Absence of it do not exclude seizure as it may arise from potential in PDS stabilise threshold against
a deep region of cerebrum which is not detected by scalp hyperexcitability
electrodes V. Ethosuximide
4. Brain Imaging
Determine presence of abnormal structure responsible for b) Surgical Treatment of Refractory Epilepsy
seizure (applies to all pts with new-onset) Might be useful when the diagnosis suggests that there is
MRI is superior to CT in detecting cerebral lesion possibility that patient has epilepsy syndrome that is
likely to be drug-resistant
Treatment & management E.g:
temporal lobectomy/amygdalohippocampectomy in
1. Treatment of underlying conditions temporal lobe epilepsy
correcting metabolic problem prevent recurrence hemispherectomy for patients with severe seizures
If medication is the cause avoid taking the drugs with hemispheric abnormality (e.g: hemimegalencephaly)
corpus callosum section to prevent spread to opposite
2.Avoidance of precipitating factors hemisphere
E.g: Sleep deprivation, alcohol intake, stress
**reflex epilepsy: seizures induced by highly specific Status Epilepticus
sensory stimuli ( musicogenic/reading/arithmetic epilepsy) refers to continuous seizures / discrete seizure with
impaired consciousness in interictal period
3.Treatment of Epilepsy: in other words, 2 or more seizures without recovery
a) Antiepileptic Drug (AED) Therapy: of consciousness in between (interictal period)
types:
1. Generalised convulsive (GCSE): persistent
generalised tonic-clonic movements
2. Non convulsive: persistent absence
seizure/partial seizure , partial impaired
consciousness
3. simple partial
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