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
Work-Up
IMAGING: CT for sure (maybe MRI to r/o tumor); chest film (cardio)
LABS: CHC, chem, LFTs (hepatic encephalopathy? uremia? hyponatremia?)
EKG
I.D.: spinal tap if infx suspected
Neuro: (consider EEG)
Acute TX (including status)
- 3mg lorazepam IV (works just as fast and lasts longer than diazepam)
- consider adding long-term drug IV (e.g. 1gm of phenytoin or fosphenytoin; OR 1.5mg valproate or levetiracetame
- For status epilepticus (>15mins): phenobarb 500mg; —> intubate midazolam, propofol or pentobarbital
midazolam trade name
Versed
Principles of Chronic Tx
- First seizures are often not treated, because only 50% recur.
- Provoked seizures, e.g. with trauma, high fever, or alcohol withdrawal, are acutely treated for a few days but not long term.
- Recurrent seizures are treated on a long term basis. Medications can be successfully withdrawn after several years in about 50% of patients
lamotrigine vs. carbamazepine
—equal efficacy
—LTg has fewer med interactions b/c not a liver enzyme inducer and fewer SEs in geriatrics
—wayy pricerier though, so stick
Vagus Nerve Stim
L vagus n. b/c less arrythmias than R
—hard to detect early sz with portable EEG inside, so shocks given for 30s q5m
—also approved for refractory depression (and many intractable sz pts depressed)
Cerebral Stim
—cortex or into parenchyma
surgery
—good for mesial temporal sclerosis (remove scarred area) which is usually refractory to RX
SPECT Scanning
—inject w/in seconds of sz onset (can scan later)
—sz foci are HYPO perfused inter- and post-ictally, and hyperperfused ictal period
Callosotomy
palliative
prevents 2° generaization
stop drop-attack szs
qqf decr sz freq
