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Transcript
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
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10 15 20 25 30 35 40 45 50 55 60 65 70 75 80
Yaş
Fokal Epilepsi
Jeneralize Epilepsi
EEG interpretation !!
Seizure Classification
Seizure terms
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
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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