Seizure Patho Flashcards
Seizure rate in epilepsy
->80% of pt will have first seizure by age 20
-rate dips down from age 25-50 then increases steeply w age
chance of seizure recurrence in epilepsy
-20% after 1st
-60% after 2nd
-75% after 3rd
Types of seizures
-myoclonic: muscles twitching, jerk head, trunk, body
-tonic: children, rigidity
-clonic: babies, rapid motor activity
-atonic: loss of muscle tone, pt falls if standing
-tonic-clonic (most severe, life-threatening)
Seizure definition
-paroxysmal disorder of CNS characterized by abnormal cerebral neuronal discharges w or wo loss of consciousness
paroxysm
-sudden attack
convulsion
-specific seizure type where attack is amnifested by involuntary muscle contractions
epilepsy definition
-repeated seizured due to damage, irritation, chemical imbalance in brain
-leads to sudden excessive, synchronous electrical discharge
seizure patho
-anomalous firing of population of neurons in brain
-comes from gray matter of any (sub)cortical area of brain
-disordered, synchronous, rhythmic firing (synchronized hyperexcitability)
-neurons recruit other neurons to join
-manifestation depends on site, degree of irritability, and intensity of impulse
-brain uses more energy and O2 that can lead to ischemia
Seizure classifications
-focal onset
-generalized onset
-unknown onset
Focal onset seizures
-aware/impaired awareness
-60% of seizures
-only part of brain affected
-begin in cortical region (like temporal lobe)
-usually caused by lesion
-progress to generalized seizure (focal to bilateral)
-motor or nonmotor onset?
example of lesions that cause focal seizures
-head trauma
-tumor
-stroke
-hypoxia at birth
-metabolic disorder
-infection
-malformations
Generalized onset seizure
-40%
-loss of conciousness
-both brain hemispheres
-primary or idopathic (not caused by lesion)
-likely genetic
-motor: tonic-clonic or other
-nonmotor (absent)
Unknown onset seizure
-epileptic spasm
-other
-unclassified
Propogation Pathways of focal seizures*
-activity speads from focus in one part of brain
-progresses to generalized via projections to thalamus (then thalamus propogates to rest of brain) (focus to bilateral seizure)
progression pathway of generalized seizures
-propogate via diffuse interconnections between thalamus and cortex (no discrete focus)
-thalamus propogates to rest of brain
-both brain hemispheres
Electroencehpalogram patterns (EEG patterns)
-focal: abnormal sequence only in 2 (a few) electrodes instead of all of them
-generalized: abnormal sequence shown on all electrodes
Focal seizure awareness
-aware or impaired awareness
Aware type focal seizure
-25%
-limited convulsions (one body part)
-limited sensory disturbance
-NO LOSS OF CONSIOUSNESS
-auras also occur bc electrical activity: ab hurt, sense of fear, unpleasant smell
Impaired awareness focal seizure
-most common
-cloudy consiousness
-staring
-repetitive motor behaviors (swallowing, chewing, lip smacking) pt does know
-disturbances of visceral, emotional, autonomic systems (diarrhea, vomitting)
-followed by confusion, fatigue, headache
-aura common
-postictal state due to impaired awareness
Postical state
-confusion, disorientation, amnesia after seizure
-last seconds to hours depending on severity, meds, age
Absence type generalized seizures
-typical or atypical
-typical:
-brief loss of consiousness (less than minute)
-straining/eye flickering
-abrupt onset
-often repetitive
-may not realize
-no convulsions, aura, postictal period!!!
-atypical:
-slower onset
-harder to control w Rx
Generalized tonic-clonic seizure (grand-mal)
-most dramatic
-first phase: tonic
-abrupt onset
-diaphragm contraction
-NO AURA
-tonic rigidity everywhere (15-30sec)
-interuptted by tremor that = releaxation
-second phase: clonic
-relaxation periods more prolonged
-violent body jerking 1-2 min
-pt in stuporous state after
-tongue/cheek bitten
-might pee
-there may be a brief aura in focal to bilateral tonic-clonic seizure
Stratus epilepticus
-generalized convulsive status epileptic (GCSE)
-repetitive seizure activity in which pt does not regain conciousness between seizures OR episode lasting > 30min
-life threatening
->5min continuous seizure OR recurrent activity without return to baseline
GCSE tx goal
-bring seizure under control within 60 minutes
-minimize complications:
-excess glucose use
-CNS blood flow (oxygen)
-lactic acid
-CV collapse (arrhythmia)
-long-term cognitive effects
-worsening of epilepsy
Epilepsy stats
-1-2% of population
-1 in 5 will experience seizure
-50-75% of pt are successfully tx
-drug therapy can be withdrawn if seizure free for 2-5 years
-sudden unexpected death possible
Which of the following types of convulsions can be preceded by
an aura phase?
(A) typical absence (petit-mal)
(B) primary generalized tonic-clonic (grand-mal)
(C) focal to bilateral (secondary generalized) tonic-clonic
(D) all of the above
C: focal to bilateral tonic-clonic
Paroxysmal depolarizing shift (PDS)
-large depolarization that triggers action potentials
-depolarization requires activation of AMPA and NMDA channels = influx of cation (Ca)
-followed by hyperpolarization involving GABA (Cl influx) and voltage and calcium dependednt K channels = efflux of K
-depolarization dampened by feedback inhibition involving GABA and excitatory pyramidal neurons
-disrupted excitation/inhibitory (E/I) balance
Inhibitory surround
-zone that contains the spread of electrical discharge in seizure focus
-excitatory pyramidal neuron activates another pyr neuron whereas another neuron in surround inhibited region is hyperpolarized bc GABAergic inhibition???
slide 27??
slide 27??
potential triggers of seizure
-prenatal injury
-CV disease
-brain tumor/trauma
-infection
-hemmorhage
-anoxia
-drugs
-metabolic disturbances (hyperventialtion, blood gas, pH, hypoglycemia), sleep deprivation, stress, alcohol withdrawal
-sudden dc of seizure meds
-strobe light
drugs that can inc risk of seizure
-alcohol
-theophylline
-CNS stimulants
-bupropion
-oral contraceptives
-withdrawal from antidepressants
-clozapine
Which of the following occurs during the hyperpolarization
phase of a PDS?
(A) influx of Cl- ions resulting from GABAA receptor activation
(B) influx of K+ through voltage- and calcium-dependent K+
channels
(C) activation of NMDA receptors
(D) all of the above
A. influx of Cl ions resulting from GABA activation
