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SEIZURES
PRESENTER : DR. SHREYA
MODERATOR : DR. RAKESH JADAV
INTRODUCTION
CLASSIFICATION
Focal seizures
(Can be further described as having motor, sensory,
autonomic, cognitive, or other features)
Generalized seizures
Absence
Typical
Atypical
Tonic clonic
Clonic
Tonic
Atonic
Myoclonic
EPILEPSY SYNDROMES
FOCAL :
Localized to one hemisphere
Types:
1. Focal seizures without dyscognitive
features:
Aura
Ictal phase with Automatisms
Post ictal confusion , Anterograde amnesia
Post ictal aphasia
10% of seizures
Tonic contraction of muscles throughout the
body
"ictal cry."
Respirations are impaired, secretions pool in the
oropharynx, and cyanosis develops.
Contraction of the jaw muscles
A marked enhancement of sympathetic tone
After 1020 seconds, the tonic phase of the
seizure.
postictal phase :unresponsiveness, muscular
flaccidity, excessive salivation, bowel and
bladder incontinence
ABSENSE SEIZURES:
TYPICAL : sudden, brief lapses of consciousness
without loss of postural control.
4-8 years and adolesence
major seizure type
15-20% children with epilepsy
EEG : generalized, symmetric, 3-Hz spike-and-wave
discharge
ATONIC SEIZURES :
Characterized by sudden loss of postural
muscle tone lasting 12 seconds.
Consiousness impaired
No post ictal confusion
MYOCLONIC SEIZURES:
Myoclonus is a sudden and brief muscle
contraction that may involve one part of the
body or the entire body
ETIOLOGY
NEONATES(<1 MONTH)
Perinatal hypoxia and ischemia
Intracranial hemorrhage and trauma
Acute CNS infection
Metabolic disturbances
Drug withdrawal
Developmental disorders
Genetic disorders
Trauma
Alcohol withdrawal
Illicit drug use
Brain tumor
Idiopathic
Cerebrovascular disease
Brain tumor
Alcohol withdrawal
Metabolic disorders
Alzheimer's disease and other degenerative CNS diseases
Idiopathic
PATHOPHYSIOLOGY
Causes of Hyperexcitability:
MECHANISM OF SEIZURE
PRODUCTION
1. INITIATION PHASE
2. PROPAGATION PHASE
INITIATION PHASE
(1) high-frequency bursts of action
potentials
(2) hypersynchronization.
PROPAGATION PHASE
Recruitment of surrounding neurons via a number
of synaptic and nonsynaptic mechanisms,
including:
(1) an increase in extracellular K+
(2) accumulation of Ca2+ in presynaptic terminals
(3) depolarization-induced activation of the
N-methyl-D-aspartate
(4) changes in tissue osmolarity and cell swelling.
The recruitment of a sufficient number of neurons
leads to the propagation of seizure activity.
MECHANISM OF EPILEPTOGENESIS
Epileptogenesis refers to the transformation
of a normal neuronal network into one that
is chronically hyperexcitable
Initial injury : trauma, infection, hypoxia, stroke
Lowering of seizure threshold
Structural changes in neuronal network
reorganization or "sprouting" of surviving
neurons affecting its excitability of the
network
APPROACH TO
SEIZURES
CLINICALS
Identify whether it is a true seizure
h/o associated risk factors and predisposing
factors(sleep disturbances, systemic
diseases, electrolyte abnormalities
Past h/o head trauma, tumor, stroke ,infection
On examination look for neurocutaneous
markers, signs of liver cell failure
,organomegaly
Developmental milestones assessment in
children
Complete neurological examination
TREATMENT
GENERALIZED-ONSET TONIC-CLONIC
Valproic acid
Lamotrigine
Topiramate
FOCAL
Lamotrigine
Carbamazepine
Oxcarbazepine
Phenytoin
Levetiracetam
TYPICAL ABSCENSE
Valproic acid
Ethosuximide
ATYPICAL ABSENSE
Valproic acid
Lamotrigine
Topiramate
STATUS EPILEPTICUS
THANK YOU