Epilepsy and Seizures Definition of seizures and epilepsy Epidemiology Classification of seizures Examples Diferential 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 NMDA Rcptr Activation Seizure Reduced GABA Rcptr function

20 40 60 80 100 120 140 160 Yaş 4 5 10 15 25 30 35 45 50 55 65 70 75

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 Phenotypes think of anatomy!!

Cortex Central Sulcus Sylvian Fissure Frontal Eye Field Visual Assoc. Brocas’s Speech Area Primary Visual Cortex Wernicke’s Speech Primary Auditory Cortex Sylvian Fissure

Partial Seizures Homunculus

Frontal Lobe Frontal 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 Lobe Hippocampal Cortex Wernicke’s Speech area (Brodman’s 22) 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 System Means “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 Lobe Primary Sensory Cortex (Brodman’s 3,1,2) Lesion: contralateral hemihypestheisa and astereognosis Sz: contralateral sensory symptoms ie: tingling, heat Occipital lobe (Brodman’s 17) Lesion: contralateral hemianopsia with macular sparing Sz: flashing or colored lights in contralateral visual field

Psychogenic non-epileptic seizures -PNES 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