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Pathophys, Exam 3: Seizure Disorders
Terms in this set (62)
What is a seizure?
a discrete clinical event that results in the abnormal discharge of a set of neurons in the brain
What is epilepsy?
recurrent seizure activity (>2), often unprovoked without an identifiable cause (w/ or w/o convulsions)
What is status epilepticus?
1 prolonged seizure > 30 minutes or 2 or more seizures back to back in which the pt does not regain consciousness/no resolution inb/t
True or false: having a seizure means you have epilepsy
True or false: seizures always mean you have movements
false - absence seizures in particular do NOT have a motor component, involve staring off into space (esp in children)
When would someone be diagnosed as epileptic?
either have recurrent seizure activity (>2), often unprovoked without an identifiable cause (w/ or w/o convulsions); or if status epilepticus presents
What general region of the brain is affected by epilepsy?
cerebral cortex (four lobes)
What are the four lobes of the cerebral cortex and what is each lobe responsible for?
frontal - focused on in managing depression; responsible for planning, organization, actions, abstract thought, reward
parietal - sense of touch (including pain); spatial recognition
temporal - visual memory; organizing sensory inputs in a coherent manner; associated with emotional reactions
occipital - vision
What is an aura?
simple partial seizure; pt can predict they are getting ready to have a seizure; smell burnt rubber a lot of the time, look psychotic/psychic
What is the association cortex responsible for?
understanding or having meaningful, perceptual sensory processing; abnormality here = perceptual disturbance
What is the motor cortex responsible for?
voluntary motor movements
What is the somatosensory cortex responsible for?
sense of touch; tingling sensations; paresthesias; numbness; pain; where aura originates
Where does the aura originate?
What is Broca's area responsible for?
specific area tied to language and expression
What do seizure symptoms depend on? What can help discover this?
depend on area of the brain affected; EEG helps measure where abnormalities are coming from, pinpointing the seizure type
When does epilepsy most often present itself?
infancy and childhood
What do we mean when we say epilepsy has a bimodal distribution of occurrence, what do we mean?
greater risk in newborn/young children AND >65 years of age
What kind of injury increases your risk of epilepsy?
traumatic brain insults/injuries
True or false: seizures are present as epilepsy only
false - can be present as a result of other disease states
Head injury increases seizure activity rates but what are some other causes?
structural changes; trauma; tumor; stroke; diabetes; renal disease; hepatic disease
What is the general pathophysiology of seizures?
abnormal excessive electrical activity/excessive APs results in seizure development
What is the detailed pathophys of seizures?
excessive excitation or cortical neurons presents in:
-alterations in the properties of ion channels in the neuronal membrane
-defects in ion transport (tied to ATPases) across neuronal membranes (sodium/calcium, potassium)
-biochemical modification of receptors - some sort of alteration/abnormality tied to post-synaptic receptor
-modulation of 2nd messaging systems and gene expression (usually G proteins that form focal lesions in the cerebral cortex)
-changes in EC ion concentrations (Na, K mostly)
-alterations in NT uptake and metabolism is glial cells (glial cells are normally protective and provide neuronal support)
-modifications in the ratio and function of inhibitory circuits (main inhibitory NT is GABA)
also could be disorder inhibition of cortical neurons or transitory imbalance in NTs -- enhanced excitatory neurotransmission (glutamate/aspartate, NMDA/AMPA receptors)
What kind of NT is glutamate? Permeability?
excitotoxic; permeable to Na, K, Ca; stimulation of glutamate means it is permeable to those positive ions
What is NMDA permeable to when stimulated?
What is AMPA permeable to when stimulated?
AMPA glutamatergic receptors permeable to Na, K
What is the main inhibitory NT? What happens when we stimulate it?
main inhibitory NT is GABAa; GABAa is coupled to Cl- channels; when we stimulate GABA we are actually promoting inhibition/calming (Cl- has stabilizing effect on membrane)
What is normal behavior of the Na,K pump?
constant exchange of 3Na from EC to IC and 2K from IC to EC; pump keeps going back and forth to maintain resting membrane potential
What is normal behavior of ligand-activated channels -- GABA? What do we want to do here for seizure tx?
GABAa binding to its receptor opens channel to Cl- ions; goal is to increase the seizure threshold -- resting membrane potential is -70 mV so if we have an abnormality we want to stabilize the membrane by raising the seizure potential, potentiating GABA to allow Cl- ions to raise seizure threshold, hyperpolarizing the membrane with Cl-
What is normal behavior of voltage sensitive channels?
tied to positive/negative charge going back and forth; constant exchange across gradient between EC and IC
In general, when do APs occur?
when there is a depolarization of the neuronal membrane with membrane depolarization propagating down the axon to stimulate NT release
What is Phase 0 of an AP?
-essentially happens right after Phase 4
-start of depol of membrane
-heavy shift from Na EC to IC
-depol starts around +20 mV
What is Phase 1 of an AP?
-gates for Na start to close, door has been shut
-we peak on the graph
-now we have Na and K present in IC
What is Phase 2 of an AP?
-does NOT occur in CNS AP, occurs in cardiac AP
-slow Ca channels open during plateau phase - door to let K out opens; start to have influx of Ca and efflux of K = balance each other out = plateau phase
What AP phase occurs in cardiac APs but NOT CNS APs?
Phase 2 - plateau phase
What is Phase 3 of an AP?
-Ca channels close, IC more negative
-slow K channels fully open = repolarization phase
-exodus of K
What is Phase 4 of an AP?
-back to resting mem potential
-Na starts to enter cell
-K slows its efflux
-IC becomes more postive
-membrane stabilization, start process over
In general, what does seizure activity result from?
abnormality of electrical activity that results in AP formation
What happens neuronally with an AP?
-start with stimulus/AP that propagates down the axon and gets to the synaptic knob/axon terminal -- different second messenger systems and ionic channels here
-NTs stored in and around vesicles - AP gets to vesicles and opens door; NTs released into synaptic cleft to cause an effect on post-synaptic receptors which then trigger their own AP effects (b/c cause and effect)
In terms of seizures, what do we see neuronally?
excessive discharge of NorE, Epi, dopamine; not enough GABA discharge; abnormalities in propagation down the axon to release of NTs
Besides increasing GABAa, what else might we want to do in terms of NTs to tx seizures?
reduce glutamate stimulus because it is permeable to Na, K, Ca; diminish firing of NorE, serotonin
AP Stages/Phases by graph.
What are the additional seizure etiological considerations?
-medications and seizure meds (clozapine, bupropion, carbamazepine)
-drug intoxication (cocaine, ephedrine)
-metabolic disturbance (high or low glucose)
-electrolyte disturbance (calcium, sodium, magnesium)
-prenatal or birth injury
How can carbamazepine cause seizures?
an anticonvulsant but causes phenomenon known as syndrome of ADH -- causes fluid retention, resulting hypervolemic hyponatremia = development of seizure activity
How can clozapine cause seizures?
antipsychotic; causes seizures in dose related phenomenon; worry about levels - 600 mg dose/blood level tied to seizures
How does bupropion cause seizures?
causes seizures in dose-related fashion; higher doses used for eating disorders = increased seizure activity but seating disorders already increase risk so we don't know causation for sure
How does estrogen cause seizures?
What does progesterone do in terms of GABA?
What is delirium tremens?
severe alcohol withdrawal from frequent drinking; treat with benzodiazepines; can cause seizures
What are the main differences between partial (focal) seizures and generalized seizures?
partial seizures begin in one hemisphere in the brain (can grow and become generalized) while generalized begin in both hemispheres; generalized ALWAYS involves loss of consciousness
What are partial (focal) seizures?
-begin in one hemisphere of the brain, can grow and become generalized
-without impairment of consciousness or awareness = simple partial -- patients who are fully aware, have aura (aura is classified as simple partial seizure)
-with impairment of consciousness or awareness = complex partial -- more difficult to treat; start in temporal lobe; can see automatisms - patients grimacing, pulling at clothes, repetitive motor symptoms
Where do complex partial seizures typically start?
What are generalized seizures?
-begin in both hemispheres
-always involve loss of consciousness
-absence: 5-20 seconds; staring off into space; unresponsiveness; don't lose postural control
-myoclonic: muscle jerk
-clonic: continuous shaking/movements
-tonic: stiff and rigid; arching of the back; gasp for ait
-tonic-clonic: stiffness to shaking; what we see on TV; lasts 2-3 minutes; include postictal phase where pt is difficult to wake back up, snoring, incontinent of urine and feces, seizure activity present, pt won't remember event
-atonic: drop attacks; these kids where a helmet (head trauma = seizure exacerbation)
What is one of the most common type of seizures in children? What is best tx?
febrile seizures -- best thing to do is break the fever
True or false: many children with childhood epilepsy become seizure free
What are childhood epilepsy seizures like? What should we rule out before dx?
most seizures are brief; rarely do seizures cause long-term brain damage without neurologic insult (hypoxia in first 24-48 hours increases risk)
rule out fever, infection, trauma
Medications in childhood epilepsy may cause what?
long-term side effects
Childhood epilepsy -- what children have most favorable prognosis?
children with idiopathic first seizure and normal EEG
What is an EEG?
electroencephalogram; graphical representation of cortical electrical activity; provides high temporal resolution, poor spatial resolution of cortical disorder; most important neuropsychological assessment tool for dx and subsequent treatment; place on the scalp and electrical abnormalities sensed = EEG lights up; need to get within first 4 hours of event; best reading in unmedicated patients - benzos and other meds decrease accuracy
What is involved in taking a seizure disorder history?
-identifiable source (infection/trauma/medication) - phenothiazines, TCAs, clozapine, bupropion; unmasking - CBZ, phenytoin, phenobarbital (absence)
-precipitating event (stress) - labs: hypoglycemia, hyponatremia, infection
-age of onset/frequency
-severity (describe type of movements, sounds, visual observations)
-get the before, during, AND after
What would a postictal confusion stage indicate?
generalized tonic clonic seizure
What would an aura indicate?
simple partial (focal) seizure
When is seizure tx appropriate?
-after two or more seizures
-treat after first seizure if: idiopathic and abnormal EEG; symptomatic and abnormal EEG; prior neurologic abnormality; positive family history
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