10-22 Epilepsy Flashcards
define EPSP, IPSP
EPSP = excitatory postsynaptic potential
IPSP = inhibitory postsyn “
When EPSPs»_space; IPSPs —> szs
What neurotransmitter mediates excitation? How so? Drugs that act on it?
Glutamate (e.g. via NMDA-Rs) opens Na+ and Ca2+ channels depolarizing cell —> excitation —> sz
—some rxs block glutamate release (lamotrigine)
—others are glutamate receptor antagonists (topiramate)
What neurotrans mediates inhib? Relation to sz/drugs?
GABA —> Cl- channel —> hyperpolarize —> inhibiton —> fewer szs
benzos and barbs are GABA—R agonists
What is the etiology behind most heritable epilepsies?
ion channelopathies
Tonic-Clonic/Convulsive/Grand Mal CATEGORY? PRESENTATION? EEG? NATURAL HX? FYI? BEST RX?
CATEGORY: GENERALIZED Epilepsy w/ Convulsive Szs
PRESENTATION: —loss—of—CONSCIOUSness —muscles become TONIC (rigid) bilaterally —resp inhib (CYANOSIS) —CLONIC (rhythmic jerking) bilaterally —bite tongue/INJURY —INCONTINENCE of bowel and bladder —post-ictal CONFUSION
NATURAL HX: Usually starts in childhood; good prognosis; severe sz does NOT mean severe dz
FYI: tonic part is due to firing, clonic jerks are actually brief periods of relaxation
Rx: usually effective (80%); valproate single best; levetiracetam other good one; lamotrigine for preg women
JME-Junvenile Myoclonic Epilepsy
_BRIEF
convulsive szs w/ diffuse EEG abnormalities prominently in MOTOR CORTEX
—MUTATED GABA receptor
Childhood Petit Mal (Absence/ Staring) CATEGORY? PRESENTATION? EEG? NATURAL HX? FYI? BEST RX?
CATEGORY: GENERALIZED Epilepsy w/ Non-Convulsive Szs; GENETIC
PRESENTATION: —presents in school-aged children —brief LOC/STARING (10-20s) —subtle MYOCLONUS —simple AUTOMATISMS* —NO POSTICTAL period
EEG: diffuse, but not every neuron (e.g. motor cortex thus no convulsions)
NATURAL HX: good prognosis, many grow out, some do develop convulsive szs, though
FYI: *finger rubbing, lip smacking, chewing, or swallowing
RX: Ethosuximide
Atonic Seizures CATEGORY? PRESENTATION? EEG? NATURAL HX? FYI? BEST RX?
CATEGORY: GENERALIZED Epilepsy w/ Non-Convulsive Szs
PRESENTATION:
—Sudden LOSS OF MUSCLE TONE and HEAD DROPS
—go hand in hand WITH TONIC SZS (i.e. some muscle groups stiffen while others lose tone)
—cause FALS/INJURIES
EEG: diffuse FLATTENING (? cortical inhib probs from thal or b.s.)
NATURAL HX: Seen in context of global brain damage; not a good prognosis in terms of response to tx
RX: presuming same as other generaized (valproate best, levetiracetame, too, lamotrigine for preg women)
Complex Partial Seizure (Temporal Lobe Sz/Psychomotor Sz*) *prolly best name CATEGORY? PRESENTATION? EEG? NATURAL HX? BEST RX?
CATEGORY: FOCAL
PRESENTATION:
—IMPAIRED CONSCIOUSness for ~1m
—blank STARE, simple & reactive AUTOMATISMS
—AMENISA of event
EEG: focal abnl; SHARPS over area w/ lesion
NATURAL HX: results from focal brain lesion (e.g. mesial temporal sclerosis)
RX: carbamazepine best (=ly effective to phenytoin w/o SEs); lamotrigine and levetiracetam reasonable options
Trauma and Szs
CATEGORY: ?FOCAL
—trauma causes szs acutely and long-term epilepsy thereafter
—blood break-down prods (e.g. hemosiderrin) are eliptogenic
Mesial Temporal Sclerosis
CATEGORY: ?FOCAL
—MTS common cause of epilepsy
—caused by: trauma, infx, congen malform, prolonged febrile convulsion
—commonly has AURA
Secondarily Generalized Sz
partial seizure that spread to whole body
Auras + location
#Gastric/olfactory/gustatory sensations, déjà vu: Mesial temporal. #Auditory: Lateral temporal. #Lateralized parasthesias: Frontal, Parietal. #Visual changes: Occipital. #Vague feelings in the head: Frontal or Generalized.
Physical Exam findings in epileptic patients?
usu neuro exam is nl; may find neurocutaneous lesions or rarely hemi-paresis or hemi-atrophy
—look for clues of DDx’ers: carotid bruit, orthostatic hypoten, murmur, arrythmia
DDX
- GENERALIZED: Is it a fit or faint?: vasovagal sync, orthostasis, arrythmia and AS can mimic generalized sz
- FOCAL/TODD’S PARALY: transient ischemia 2° to carotid dz
- AURAS: migraine (usually longer, mins-hrs vs. secs-mins)
- pyschogenic szs