Flashcards in Seizure Active Learning Deck (26)
What is a seizure?
It's abnormal synchronized electrical activity in the brain
manifests as episodes of altered consciousness, involuntary movements or convulsions
What are the causes of secondary seizures? i.e. provoked seizures?
focal neurologic lesions
Epilepsy is the diagnosis for a primary seizures disorder. What would it be characterized by?
at least 2 episodes of UNPROVOKED seizures
note that a single seizures or cluster of seizures within a 24 hours period does NOT imply epilepsy
How are generalized and focal seizures different?
generalized seizures START IN BOTH HEMISPHERES - synchronized
focal seizures have a LOCAL ONSET
How are generalized seizures further characterized?
convulsive = grand mal/tonic clonic
nonconvulsive = petit mal or absence
How are focal seizures further characterized?
simple = no alteration of consciousness (so just motr, autonomic or psychic)
complex = impaired or loss of consciousness
What are some signs of a focal temporal lobe seizures?
- behavioral arrest
- automatisms with licking, blinking, lip smacking, etc
- auditory phenomena
- auras (deja vu, jamais vu, smells, tastes)
What are some signs of a focal frontal lobe seizures?
contralateral arm extension, ipsilateral arm flexion
bizarre complex behaviors
contralateral eye deviation and head turning
What are some signs of a focal occipital lobe seizure?
Describe a Jacksonian Motor Seizure.
it starts as an initial focal tonic seizure with motor involvement in a small area like the fingers, face on one side, or muscles of one foot.
then it spreads from the first muscles affected to those nearby on the motor homunculus - in the "jacksonian march"
What are the 3 physiological bases for seizures?
1. population of pathologically excitable neurons
2. increase in excitatory GLUtaminergic activity
3. decrease in inhibitory GABAnergic projections
How does the ion channel type number and distribution affect neuron excitability?
These are just examples...
the VG Na+ channels form the basis of rapid depolarization and AP, so more = more excitable
the GABA receptor complex mediates influw of Cl-, which hyperpolarizes the cell, so more = neuronal inhibiiton
How does descreasing extracellular volume lead to increased excitability?
Decreased extracellular volume leads to an increased extracellular K+ concentration
this resists the otuward movement of K+ ions
thus, you don't get the hyperpolarization of the cell after the AP, effectively increasing the excitability
Thy synchronized bursts from a sufficient number of neurons will result in what on EEG?
What is the paroxysmal depolarizing shift?
the sequence of electrical activity seen in a seizure:
1. sustained neuronald epolarization resulting in a burst of APs
2. a plateau=like depolarization at completion of the APs
3. rapid repolarization followed by hyperpolarization
What does the bursting activity result from in terms of ion movement?
relatively prolonged influx of Ca2+, which leads to the opening of the VG Na+ channels, influx of Na+ and generation of repetivie action potentials
What receptors and ions then mediate the subsequent hyperpolarizing?
GABA receptors with Cl- influx or K+ efflux depending on the cell type
What is a tetanus?
a high frequency train of stimulations
What is post-tetanic potentiation?
after a tetanus, there is a high level of residual calcium in the presynaptic cell, temporarily increasing the release probability
this increases excitability and synchronous activity wihtin neighboring neurons - so acts on groups of neurons
What is kindling?
After repeated brief, low-intensity stimulation, you get a progressive intensification of seizures, culmination in tonic-clonic seizures
it reflects plasticity of the brain and synaptic connections - essentially it's how a seizures can be "learned"
What glutamate receptor is a particular target of AEDs and why?
the NMDA - because it is an activity dependent channel
if you block it, you can still get activity thoruhg AMPA, but you don't get prolonged electrical activity - blocks seizures
How do AEDs utilize the GABA receptor to decrease seizures?
Benzos and Barbs activate the GABA receptor, allowing Cl- to flow in and out. Because Cl's reversal potential is -61, near the -70 RPM, this acts as a membrane stabilizer - making the cell less excitable
How are use-dependant Na+ channels targeted by AEDs?
they will act on the inactivating plug to put the Na+ into the inactivated phase longer after firing an AP
What types of voltage gated Ca2+ channels are where?
N type and P/Q type are all on the presynaptic terminal
T type is found on the postsynaptic terminal
What does the SV2A receptor do and hwere is it located?
it aids in vesicle docking, so it's located at the presynaptic axon terminal