Lecture 18 -- Seizure Types and Mechanisms Flashcards Preview

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Flashcards in Lecture 18 -- Seizure Types and Mechanisms Deck (14):

seizures vs epilepsy?

Seizure -- hyperactive neuronal activity; may be provoked --eg from infection, etoh withdrawal, sleep deprivation

Epilepsy -- recurrent, unprovoked seizures


focal vs generalized seizures?

Focal -- there is a region of neuronal hyperactivity

Generalized --
No focus or abnormal lesion, but have general propensity for seizures; a lower threshold for seizure activity


Types of focal sz ?

Simple partial - -- a focal area of hyperactivity, but consciousness still intact

aka aura (motor, autonomic, sensory, psychic)

Complex Partial -- focal sz with LOA

either may p


types of generalized sz

Absence (Petit Mal) -- global activity, but not necessarily any convulsions. Very short. Can have 100s in a day.

General Tonic Clonic (Grand mal) - global + lots of convulsive activity




what is status epilepticus?

Classically defined as sz that persist for > 30 minutes (but practically > 5 minutes) or repetitive seizures that recur without recovery of consciousness

May be:

Non Convulisve: Comatose vs Non comatose


Mechanisms in Epilepsy

name two familial forms of Epilepsy

Juvenile Myoclonic Epilepsy -- JME --
Usually in otherwise healthy young individuals
Often comes on in College; no history
Present with generalized tonic clonic
Will require treatment for life

Childhood Absence -- very common; benign prognosis; children grow out of these seizures;


what is kindling? why is it limited?

Kindling -- animal model which LTP is developed in the Amygdala from repeated stimulation, mimics epilepsy
But limited - only Glutaminergic seizures


what is the underlying general pathophysiology of epilepsy?

what are some processes that may lead to acquired focal epilepsy?

Hyper-excitability - arising from decreased inhibition and increasd excitation

May be Acquired: Trauma, anoxia, tumors, infection, metabolic,

Cryptogenic -- idiopathic


mechanisms of Hyperexcitabiliy: Paroxysmal Depolarization Shift

what is it?
what ions are involved?
what NTs?

• Altered receptor protein-conductance channels favor development of PDS and enhanced excitability

Incr Ca conductance and reduced outward K currents

Caused by
Decreased GABA-mediated inhibition

Increased excitation (glutam,aspartate)


mechanisms of Hyperexcitabiliy
excitability from the environment:

what elements comrpise "the environemtn"

Functional Alterations: NTs

Structural Alterations -- Neurons and Glia


what are the functional alterations which can lead to hyperexcitability?

what receptor is involved in absence sz ?

imbalances of excitatory and inhibitory processes

GABA-b involved with absence sz

GABA -- inhibitory
Glutamate -- Excitatory


what is the role of catecholamines (dopamine)?

Decreased dopamine facilitates sz by lowering seizure threshold


structural alterations which may lead to sz?

Glial Abnormalities --responsible for the buffering K concentration; can lead to imbalance

Mossy Fiber Sprouting --- neuronal alteration increasing excitability -
More focal injury (temporal lobe epilepsy) --
Mesial temporal Sclerosis which can be seen on MRI


what immopathologic disease is known to cause epilepsy? what is the mechanism?

Rasmussen's Encephalitis -- antibodies to a GluR3 receptor
Auto-immune inflammatory state