Epilepsy and Seizures Definition of seizures and epilepsyEpidemiologyClassification of seizuresExamplesDiferential diagnosis

Clinical Definition of Seizure Paroxysmal uncontrolled discharges of neurons

within the central nervous system (grey matter disease).

“These Paroxysmal episodes of brain dysfunction manifested by stereotyped alteration in behavior” Clinical manifestations of a seizure based on anatomy

of the brain that is seizing Symptoms: sensory, motor, autonomic with or without loss of

consciousness

Epilepsy is a disease in which recurrent and unprovoked seizures occur spontaneously

What are seizures?

• Cellular definition: excessive or oversynchronized discharges of cortical neurons

• GABA receptor mediates inhibition responsible for normal termination of a seizure

• NMDA (Glutamate) receptor activation required for propagation of seizure activity

SeizureNMDA RcptrActivation

Reduced GABARcptr function

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Fokal Epilepsi J eneralize Epilepsi

EEG interpretation !!

Seizure Classification

Seizure terms

Ictal= during seizure Post-ictal= confusion following

seizure Aura= abnormal sensation Automatisms= nonsensical

involuntary movements Tonic= tonic contraction producing

extension and arching Clonic= alternating muscle

contraction-relaxation

Partial= focal region involved Generalized= whole brain Convulsions= shaking

Seizure Phenotypesthink of anatomy!!

Cortex

Frontal EyeField

Brocas’s Speech Area

Primary Auditory Cortex

Sylvian Fissure

Wernicke’s Speech

Primary VisualCortex

Visual Assoc.Cortex

Central Sulcus

Partial SeizuresHomunculus

Frontal LobeFrontal Eye Field (Brodman’s 8)

Lesion: deviation of eyes to ipsilateral side Sz: overstimulation->eyes to contralateral side

Prefrontal Cortex (Brodman’s 9-12,46,47) Lesion: deficits in concentration, judgment and behavior Sz: agitation, odd behavior

Broca’s Speech Area (Brodman’s 44,45) Lesion/Sz: expressive nonfluent aphasias

Primary Motor Cortex (Brodman’s 4) Lesion: contralateral spastic paresis Sz: contralateral posturing/convulsions

Temporal LobeHippocampal Cortex

Bilateral lesions: inability to process short term to long term memory Sz: chronic seizures lead to deficits in short term memory

Wernicke’s Speech area (Brodman’s 22) Lesion/Sz: loss of receptive speech, fluent aphasia

Anterior Temporal Lobe Bilateral lesions: “Kluver-Bucy syndrome” of visual agnosia, oral

tendencies, hyperphagia, hypersexuality, docility Sz: pts “freeze” and might have oral automatisms

Primary Auditory (Brodman’s 41, 42) Bilateral lesion: cortical deafness Sz: auditory hallucinations

Olfactory Bulb (Brodman’s 34) Lesion: ipsilateral anosmia Sz: olfactory and gustatory hallucinations

Limbic SystemMeans “border” in Latin

Border between cortex and hypothalamus

Involved with emotional behavior Fear/anger/sexual behavior Short term memory

Includes: Hippocampus Fornix Mammilary bodies Ant. Nucleus thalamus Cingulate cortex

Seizures involving the hippocampus can have clinical symptoms of poor short term memory and abnormal mood

Parietal and Occipital LobePrimary Sensory Cortex (Brodman’s 3,1,2) Lesion: contralateral hemihypestheisa and

astereognosis Sz: contralateral sensory symptoms ie:

tingling, heatOccipital lobe (Brodman’s 17)

Lesion: contralateral hemianopsia with macular sparing

Sz: flashing or colored lights in contralateral visual field

Psychogenic non-epileptic seizures -PNES

Non-epileptic seizures May be manifestation of conversion disorder,

factitious disorder or malingering Features that may distinguish from epileptic

seizures Pre-attack preparation, absence of post-ictal confusion “Disorganized” movements, pelvic thrusting, thrashing Bilateral convulsions without loss of consciousness Violent or goal-directed behavior, obscene language, Forcefull eye closure Tongue biting Time!!!!!

Video EEG may help to diagnose