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35 Cards in this Set

  • Front
  • Back
what is epilepsy
chronic, unprovoked, unavoidable seizures
what is a symptomatic seizure
results from a known lesion
what is an idiopathic seizure
cause is not known
ex. genetic cause
what is a cryptogenic seizure
from a suspected lesion whose location is not known
focal onset vs generalized onset
focal - restricted to a specific area or hemisphere

generalized - bilateral, symmetric seizure

focal may spread and become secondarily generalized
___ is req'd to diagnose seizure
generalized seizure vs. partial seizure?
-affects both hemispheres
-all EEG channels affected
-loss of awareness

-affects limited area of brain
-only a few EEG channels are activated
-patient is aware, but may or may not be responsive
what is a generalized tonic-clonic seizure?
generalized tonic-clonic seizure is a grand mal (primary) seizure with a sudden onset, tonic, then clonic, abrupt offset
what is an absence seizure
absence seizure is a petit mal sz where the patient is totally unaware and unresponsive then rapidly returns to normal. cut and splice
what is the difference between a simple partial and a complex partial seizure
in a simple partial the patient is aware and can respond.

in a complex partial, the patient is aware but unresponsive. may have secondary generalization. bottom line- in a complex partial, the patient cannot interact with the environment.
what is ictal semiology
the symptoms of a seizure relate to the location of the seizure in the brain
this kind of seizure has motor symptoms, bizarre behaviors and beliefs, people act like they're crazy
frontal lobe sz
this kind of seizure may produce fear, loss of consciousness, deja vu, amnesia, and automatisms
temporal lobe sz
this kind of seizure may cause somatosensory problems, dizziness
parietal lobe sz
this kind of seizure may cause visual changes
occipital lobe sz
what is an interictial spike?
an EEG spike inb/t seizures. may be the trigger
what kind of imaging is appropriate for someone presenting to the ER with a seizure?
in prescribing anticonvulsants, the physician must balance __ and ___
efficacy in preventing seizures and side effects/ Q of L
how does vagal nerve stimulation treat seizures?
tickling this nerve may disrupt rhythmicity of ongoing seizures
how is icital SPECT useful in treating seizures?
seizures use a lot of glucose at their location, so icital SPECT can be used to determine the location of hyperactivity
how does an implantable electrode treat seizures?
it record brain waves and senses the onset of seizure activity and stimulates the cortex to prevent the rhythmic rise
what is status epilepticus and why is it bad?
an unresolving seizure of more than 30 minutes whose metabolic activity literally cooks the brain
how do you treat status epilepticus?
1. IV benzodiazepines (stimulate GABA release)
2. IV Anti convulsants
3. pharmacologically induce coma (general anesthesia) for 24 hrs
how do female hormones play into seizures?
estrogen may irritiate, progesterone is protective. females may get more seizures at diff times in their menstrual cycle
describe the EEG conventions for pos and negative deflection
pos deflection = negative current = sink (synapse) is close than source

neg deflection = pos current = source is closer than sink
if the EEG measures a negative deflection, are you measuring the sink or the source?
if the EEG measures a positive deflection, are you measuring the sink or the source?
how could modification of intrinsic membrane currents cause hyperexcitability?
gaining Na currents or losing K currents cause them membrane to depolarize, making it more excitable
how is rewiring of the brain relate to seizures?
if the brain is rewired, and synapses are gained/lost, a cell could gain more excitatory synapses or lose its inhibitory synapses. also the cell could synapse on a cell it shouldnt resulting in new circuits w/in the brain that could cause the kind of rhythmic increase in activity needed to trigger a seizure
what is a paroxysmal depolarization shift?
when a cell's RMP depolarizes so it is hyperexcitable. in neurons with NMDA receptors, these receptors become active as the cell depolarizes. the loss of hyperpolarization can lead to a seizure
what is kindling?
electrical stimulation of the brain to produce a seizure. electrodes are implanted in the amygdala or hippocampus
where is synaptogenesis observed in the kindling model?
reorganization (sprouting) of the dentate gyrus of the hippocampus. the mossy fibers sprout and synapseback on the granule cells, where NMDA receptors will be opened by GABA due to paroxsymal depolarization shift. the dentate granule cells are hyperexcitable and are responsible for the seizures
how does a paroxysmal depolarization shift affect glutamate receptors?
NMDA receptors are not active at resting membrane potential. they are blocked by Mg unless the membrane is depolarized. with a paroxysmal depolarization shift, the NMDA receptors can be stimulated to open by GABA.
how does cortical displasia cause seizures?
some neurons are not located where they are supposed to be and also lack K channels they should have. these heterotypic cells are hyperexcitable
the kindling model sheds light on human ___ lobe seizures