seizures Flashcards
seizure
cortical events characterized by excessive or hypersynchonrnous discharge by cortical neruons
what are idiopathic sz?
usually begin bw 5-10 yrs old and have no specific cause
what are secondary sz?
may result from congenital abnormalities or pernatal injury, metabolic disorders, trauma, tumors, vascular dz, infex dz, or degenerative dz
generalized sz
sudden loss of consciousness; invovles both cerebral hemispheres w/ an alteration of consciousness
convulsive generalized
grand mal or tonic clonic; associated w. a postictal obtundation and confusion lasting for mins to hours
nonconvulsive generalized
absence; associated w/ only minor motor activity, such as blinking
absence is also called…
petit mal!
it begins in childhood, are often familial, and typically subside before adulthood
what are signs and sx of an absence sz?
brief, often unnoticable episodes of imparied consciouness, lasting only seconds and occuring up to hundreds of time sper day
**think staring spells
work up of an absence?
EEG
**3 per second generalized spike and wave tracing
how do you tx an absence sz?
ethosuximide is first line. valproic acid or zonisamide may be used
tonic clonic?
aka GRAND MAL
signs and sx of tonic clonic
begin suddenly w/ loss of consciousness and tonic extension of the back and extremities, continuing w/ 1-2 mins of repetitive, symmetric clonic movements
** classic sz incontinence and tongue biting
**pt may also appear cyanotic druing the ictal owing to poor respiratory fxn during sz
tx of grand-mal
emergent tx w/ benzo to abort thesz
-give antiepiliptics for seconary prevention-phenytoin, phenobarbital, valproate, lamotrigine, etc
partial sz
simple or complex
arise from discrete region of 1 cerebral hemisphere
simple partial sz are NOT accompanied by an impariment of consciousness- may be an isolated tonic or clonic activity of a limb or transient altered 8
pediatric partial sz tx?
treat with phenobarbital
how do you tx intractable temporal lobe sz?
surgical options include anteriro temporal lobectomy or vagal nerve
Postictal?
Todd’s paralysis= wkness or paralysis that is often unilatral and resolves over 24 hrs
status epilepticus
can be convulsive or nonconvulsinve
how is SE dx?
sz fail to cease spontaneously or recur so frequently that full consciousness is not restored between successive episodes
what are complications o SE?
possibility of permanent brain damage secondary to hyperthermia, circulatory collapse, or excitotoxic neuronal damage
how to tx SE?
Immediate management -ensure patent airway, including positioning the patient to prevent aspiration of stomach contents-Management of hyperthermia, related to increased motor activity and high levels of circulating catecholamines, may include a cooling blanket or induction of motor paralysis with a neuromuscular blocking agent-Diazepam or lorazepam is administered IV until the seizure stops; a loading dose of phenytoin or fosphenytoin is also given
EEG findings in partial sz?
focal rhythmic discharge; but sometimes, no ictal activity will be seen
EEG in complex partial?
interictal spikes or spikes associated w/ slow waves in the temporal or frontotemporal are
what will EEG of epileptic sz show>
epileptiform
what happens to the serum prolactin levels?
usually incrased after tru tonic-clonic zx, but are unaffected by psuedosz
sz vs syncope (onset)
sz: sudden onset +/- preceding aura, focal sensory or motor phenomena, sensation of fear, smell, memor
syncope: progressive lightheadedness, diming of vision, faintness
sz vs syncope course
sz: sudden loss of consciousness w/ tonic-clonic activity; tongue laceration, head trauma, bowel/urninary incontinence
syncope: gradual loss of consciousness limp or w/ jerking, rarely lasts > 14 sec
sz vs syncope post spell
sz: postictal confusion and disorentation
syncope: typically immedicate return to lucidity
tx for generalized convulsive, simple partial complex parital sx
carbamazepine, phenytoin, valproic acids, topiramates, lamotrigine, oxcarbazepine, levetiracetam, zonisamide
potientialy side effects of felbamate?
aplastic anemia, hepatic failure
tx for generallized nonconvulsive (absence) sz
valproic acid or ethosuximide
Epilepsy
Disorder of the brain characterized by an enduring predisposition to generate epileptic seizures, and by the neurobiologic, cognitive, psychological, and social consequences of this condition
2 unprovoked sz occuring > 24 hrs apart
what is a simple partial sz?
focal motor, no imparied cognition
what is a complex partial?
dyscognitive focal seizure= impaired response
what are all the types of generalized seizures?
Absence Tonic-clonic Tonic Clonic Myoclonic Atonic (drop attack
aura?
simple partial sz
Symptoms correspond to the area of brain affected by the abnormal electrical activity. Most commonly seen with complex partial seizures
what is ictus?
what is seen/felt during abnormal lecctricl activity
what is postictal?
what is seen/ felt until the brain recovers to baseline
-some pts don’t have one, others can e sleepy, confused, or have impaired awarness
Todd’s paralysis
. Some patients who have seizures involving the motor strip may experience a paralysis of the arm or leg until that part of the brain recovers;
when can you stop AEDs?
Seizure free for 2 – 4 years Depends on seizure type Complete control within one year of onset Onset btw ages 2 and 35 Normal neuro exam Normal EEG Withdraw slowly over at least 6 months Relapse 25% after 1 yr, 29% after 2 years
what is the Pathophys of a sz?
occurs when the message delivery systme becomes unbalanced
-normally, GABA keeps the system by triggering signals in the form of charged particles: causes large conentration of Cl ions to enter recieving neruon = stop message
when there isnt enough GABA, a sz can occur bc receiving neruons can be flooded with signals that say pass on message
-“go” messages are triggered by a diff type of Neurotransmitter that are postitive (sodium particles enter neuron)
what are drugs that can inhivit the high frequency firing?
Carbamazepine, lamotrigine,phenytoin, andvalproic acid
what is the brains major excitator NT?
glutamate
what are the two groups of glutamate receptors?
1) Ionotropic—fast synaptic transmission
Three subtypes – AMPA, kainate, NMDA
Glutamate-gated cation channels
2) Metabotropic—slow synaptic transmission
G-protein coupled, regulation of second messengers (cAMP and phospholipase C)
Modulation of synaptic activity
what is the mjor inhibitory NT?
GABA
what are the 2 types of GABA receptors?
GABAA—post-synaptic, specific recognition sites, linked to CI- channel
GABAB —presynaptic autoreceptors that reduce transmitter release by decreasing calcium influx, postsynaptic coupled to G-proteins to increase K+ current
what are the cellular mechanisms of seizure generation?
Excitation (too much go) Ionic: inward Na+ and Ca++ currents Neurotransmitter: glutamate, aspartate Inhibition (too little stop) Ionic: inward CI-, outward K+ currents Neurotransmitter: GABA
what is an ADR commont to all aeds?
suicidality
what are some examples of blockers of reptitive activation of sodium channels?
phenytoin, carbamazepine, oxcarbazepine, valproate, felbamate, lamotrigine, topiramate, zonisamide, rufinamide , lacosamide
carbamazepine is first line for what type of sz?
focal
*calso used for generalized tonic-clonic, mixed, pain control in trigeminal nerualgai
what is carbamazepine CI in?
h/o bone marrow depression (risk of agranulocytosis, aplastic anemia)
MAOIs
HLA-B 1502
majore ADR of carbamazepine?
-neruogocnitive (Drowsiness, diplopia, HA, ataxia, dizziness)
-GI
-leukopenis
hypona
rash
hepatitis, pancreatitis, aplastic anemai
PCD
