Lecture 18 -- Seizure Types and Mechanisms

Question 1

seizures vs epilepsy?

Answer 1

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

Epilepsy -- recurrent, unprovoked seizures

Question 2

focal vs generalized seizures?

Answer 2

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

Question 3

Types of focal sz ?

Answer 3

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

Question 4

types of generalized sz

Answer 4

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

Myoclonic

Atonic

Question 5

what is status epilepticus?

Answer 5

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

May be:
Convulsive

Non Convulisve: Comatose vs Non comatose

Question 6

Mechanisms in Epilepsy

name two familial forms of Epilepsy

Answer 6

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;

Question 7

what is kindling? why is it limited?

Answer 7

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

Question 8

what is the underlying general pathophysiology of epilepsy?

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

Answer 8

Hyper-excitability - arising from decreased inhibition and increasd excitation

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

Cryptogenic – idiopathic

Question 9

mechanisms of Hyperexcitabiliy: Paroxysmal Depolarization Shift

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

Answer 9

• 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)

Question 10

mechanisms of Hyperexcitabiliy
excitability from the environment:

what elements comrpise “the environemtn”

Answer 10

Functional Alterations: NTs

Structural Alterations – Neurons and Glia

Question 11

what are the functional alterations which can lead to hyperexcitability?

what receptor is involved in absence sz ?

Answer 11

imbalances of excitatory and inhibitory processes

GABA-b involved with absence sz

GABA – inhibitory
Glutamate – Excitatory

Question 12

what is the role of catecholamines (dopamine)?

Answer 12

Decreased dopamine facilitates sz by lowering seizure threshold

Question 13

structural alterations which may lead to sz?

Answer 13

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

Question 14

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

Answer 14

Rasmussen’s Encephalitis – antibodies to a GluR3 receptor

Auto-immune inflammatory state