Epilepsy and Seizures Definition of seizures and epilepsy

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

160 140 120 100 80 60 40 20 0 4 5 10 15 20 25 30 35 40 45 50 55 60 65 70 75 80 Yaş

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

Seizure Phenotypes think of anatomy!!

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

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 • • § 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 § 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