Seizures Flashcards
1
Q
Seizure v. Epilepsy
A
Seizure- discrete clinical event of temporary brain dysfunction characterized by abnormal electrical discharge
Epilepsy - paroxysmal disease of recurring, unprovoked seizures
- Continuous tendency to generate unpredictable seizures w/o provoking factors
2
Q
Epilepsy Criteria
A
- Specific criteria = 2 unprovoked seizures in > 24 hr OR dx after 1 seizure if risk of recurrent seizure is 60% or more
- Cannot be cured but “resolved” if no seizures for 10yrs and have not taken seizure meds in 5 yrs
3
Q
PDS
A
Paroxysmal Depolarization Shift
- Large, prolonged depolarization of neuronal membrane —> bursts of spike activity on EEG (interictal epileptiform discharges on scalp)
- Inc excitation (EPSPs) and dec inhibition (IPSPs) —> depolarization —> progresses to train of action potentials (ictal phase) —> ACTIVATE inhibitory currents —> recovery
4
Q
3 types of epilepsy due to ion channel mutations
A
- Benign Familial Neonatal Convulsions (BFNC) - K+ channel problem
- Genetic Epilepsy w/ Febrile Seizures Plus (GEFS+) - Na+ channel problem
- Idiopathic Generalized Epilepsy (IGE) - Cl- channel problem
5
Q
Temporal Lobe Epilepsy + Circuit Associated
A
FOCAL
Hippocampus Circuit
- Excitation from enterohinal cortex —> granule cell layer of hippocampus —> AP propagates down mossy fibers —> project to hilar interneurons AND CA3 region pyramidal neurons (excitatory)
- Hilar mossy cells then excite basket cells that inhibit the original granule cell layer (FEEDBACK)
- C3 pyramidal —> CA1 pyramidal via Schaffer collaterals
6
Q
Kindling Model (+ what does this look like in hippocampus?)
A
- repeated admin of sub convulsive electric stim or other agents —> after discharges —> progression to more intense seizures
- Tissue develops enhanced sensitivity (“kindled”)
- repeated admin of sub convulsive electric stim or other agents —> after discharges —> progression to more intense seizures
- In hippocampus this leads to …
- 1- Enhanced excitement of dentate granule cells (via NMDA receptors)
- 2- Loss of hilar neurons that normally activate inhibitory basket cells (loss of feedback inhibition)
- 3- Synaptic reorganization of granule cell output and feedback to dentate -> hyper-excitability
7
Q
Absence Seizures + Circuit Associated
A
GENERALIZED
- Sudden episodes of staring w/o awareness
- Involves thalamocortical circuitry (central and deep)
- Cortex pyramidal cells excite reticular neurons in thalamus + relay cells excite reticular neurons—> reticular neurons are GABAergic so they inhibit fellow reticular cells and relay neurons —> relay neurons excite cortex pyramid cells
- Thalamic reticular and relay neurons both use low-threshold transient Ca++ channels (T channels) which allow influx of Ca++ after only mild depolarization —> burst firing followed by inactive mode (takes awhile for de-inactivation)
8
Q
8 Postulated Causes of Epilepsy
A
- Abnormal ion channels
- Abnormal neurotransmitter metabolism
- Abnormal receptors
- Defects in neuronal migration
- Disorders of cell growth and differentiation
- Abnormal organelle function
- Abnormal storage products
- Abnormal chromosomes
9
Q
Status Epilepticus
A
- Research Definition - seizure lasting > 5 min in adults or > 10 min in children OR series of seizures in which conscious or function does not recover in-between
- Classic Definition - seizure of 30 min duration
- Non-convulsive SE - prolonged but no tonic or clonic movements
- Convulsive SE - medical emergency; must treat w/ benzo and long-term AED (fosphenytoin)
- Mortality and morbidity is high but more due to underlying disease than seizure itself
10
Q
4 Common Causes of SE
A
- Withdrawal of AEDs, sedative hypnotic drugs or alcohol
- High fever (esp b/f age 5)
- Metabolic disorders
- Cerebral lesions (meningitis, encephalitis, stroke, tumor)
11
Q
Epidemiology of Epilepsy
A
- 5-1% US population
- U curve - highest incidence in young and old
- 150,000-200,000 new cases in US / yr
- Inc risk if… parent w/ epilepsy, severe alcoholism, civilian or military head trauma, heroine use, past stroke or viral encephalitis, etc
12
Q
5 Broad Etiology Categories of Seizures
A
- Toxic
- Systemic Illness, drugs, wihdrawal, pyridoxine deficiency
- AcquiredStructural Lesions
- Infections, vascular, trauma, neoplastic, mesial temporal sclerosis
- Familial
- Primary Generalized Epilepsy
- Benign Focal Epilepsy in Childhood
- Febrile convulsions
- > 200 other genetic syndromes related to seizures
- Idiopathic Genetic
13
Q
3 Categories of Etiology of Epilepsy
A
- Structural-Metabolic (“symptomatic”) - known pathology
- Genetic (“idiopathic”) - no detectable structural abnormality but susceptibility genes
- Unknown (“cryptogenic”)
14
Q
Seizure Etiology by Age
A
- Developmental if < 14
- Injury if 15-24
- Brain tumor if 25-44
- Vascular if 45+
15
Q
Types of Focal Seizures
A
FOCAL = CONSCIOUS
- W/o impairment of conscious or awareness
- Involving subjective sensory phenomena only (touch, smell, taste, vision, hearing, hallucinations
- Involving subjective psychic phenomena only (aura w/ staring and automatisms)
- Observable autonomic component (change in HR or resp, goose bumps, perception of viscera)
- Observable motor component (muscle groups including vocal; may have post-ictal Todd’s paralysis) - W/ impairment of consciousness or awareness (still conscious but unable to respond to stimuli b/c altered awareness or responsiveness)
- *Important distinction b/c these patients cannot drive or operate machinery
- Evolving to bilateral/convulsive seizure
