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

2. 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

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
Seizure
Reduced GABA
Rcptr function

6. 20 40 60 80
100
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Yaş 4 5 10 15 25 30 35 45 50 55 65 70 75

9. EEG interpretation !!

11. Seizure Classification

12. 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

13. Seizure Phenotypes think of anatomy!!

14. 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

15. Partial Seizures Homunculus

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 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

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
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