Epilepsy and Seizures

1. Epilepsy and Seizures • Definition of seizures and epilepsy • Epidemiology • Classification of seizures • Examples • Diferential diagnosis

2. Clinical Definition of Seizure • Paroxysmaluncontrolleddischargesofneuronswithinthecentralnervoussystem (greymatterdisease). • “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

3. 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 Reduced GABA Rcptr function • Seizure

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9. EEG interpretation!!

11. Seizure Classification

12. Seizure terms Ictal= duringseizure 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

13. Seizure Phenotypesthink of anatomy!!

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

15. Partial SeizuresHomunculus

16. 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

19. 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

20. 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

21. 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

23. 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