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
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
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?
• Altered receptor protein-conductance channels favor development of PDS and enhanced excitability
Incr Ca conductance and reduced outward K currents
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