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what are the two different seizure activity
acute
chronic like epilepsy
when do acute symotomatic seizures occur
occurs at the time of a systemic insult or in close temporal assocition with a documented brain insult
unpoked seizure
relation to prexisting brain lesions or progressive nervous system disorder
what is epilepsy
•At least two unprovoked seizures occurring more than 24 hours apart.
•One unprovoked seizure and a probability of further seizures. More so the case with remote structural lesions such as stroke, central nervous system infection, or certain types of traumatic brain injury.
•Diagnosis of an epilepsy syndrome (genetic)
what are things that can provoke a seizure
Alcohol & drug withdrawal
Drug intoxication
Hyponatremia, hypernatremia
Hypomagnesaemia
Hypocalcemia
Hypoglycemia
Nonketotic hyperglycemia /Hyperosmolar Hyperglycemic State
DKA
Uremia
Hypoxia
Hyperthyroidism
Dialysis disequilibrium syndrome
Porphyria - liver disorders with build up of porphyrins

focal partial seizure
abnormal neuronal discharge from one discrete focus of one hemisphere
focal partial seizure 2 different types of awareness
retained awareness (simple) consciouses fully maintained
imapired awareness (complex) conciousness impaired
motor component of focal seizures
jerky rhythmic movements
jackson march is followed by todd paralysis
jackson march
when a focal seizure starts in one area and spreads to other parts of the body
todd parylsis
paralysis of one side 30-60 min sometimes makes in hard to tall from stroke
sensory components of a seizure
•Paresthesia
•Numbness
•Pain
•Heat
•Cold
•Sensation of Movement
•Olfactory
•Flashing Lights
what can autonomic sx of focal seizure
abdominal pain
cardiovascualr sinus tachy
flustions in BP
bronchoconstriction
can aura be present in focal seizure
prior and after event
psychological componenets of focal seizure
fear
agition
deja vu
hallucination
what are the complex types of focal seizure
behvarioal arrest and staring
automatism
post ictal phase
behavioral arrest and starting time frame
less than 3 min
awareness in behavioral arrest
unaware and unresponsive - type of complex focal
automatism
repitive behvarios (lips smacking, facial grimicing, chewing, manual picking, patting, or repeating words)
post itcal phase
somnolence, confusion, agition, HA, generally lasting minutes to hours
inital w/u for seizure
•CBC, CMP (electrolytes, liver and renal function), tox screen, pregnancy test, RPR (rapid plasma reagin, syphillis)
•MRI is preferred; CT if emergent
Video EEG is gold standard.
A normal EEG after an event does not exclude
Epilepsy
what is the gold standard for focal seizure
EEG
Epilepsy Monitoring Unit (EMU
receive continuous video-electroencephalography (video-EEG) monitoring to diagnose, classify, or manage seizure disorders
EEG findings of focal seizure for simple
focal discharge at onset
EEG findings of focal seizure for complex
interictal spikes or slow waves in the temporal or frontotemporal areas
absence seizure
generalized seizure (in both hemispheres) most common in children (4-10) like a child is daydreaming
how often do petit mal seizures occur
aka absence seizure can occur ten of times a day
cinical manifestation of absence seizure
sudden amrked inmpairment of consciousness & loss of awarness w/o loss of body tone
blank spare
promt return to baseline w/o post ical state or aura
how long do abcence seizure last
5-10 sec
what can be a trigger for abcence siezure
hyperventilation/ emtional like fear and anger
main diagnostic tool of EEG findings for abcence seizure
b/l synchronous & symmetrical 3 hertz (3 cyles per sec) spike and waves discharge that start and end abruptly
what is first line for absence seizure
ethosuximide (Blocks T-type voltage-gated calcium channels in thalamocortical neurons, calming overactive nerve signals in the brain that trigger brief lapses of consciousness)
second line for petit mal seizure and gtc
valprocic acid if gtc= manotrigine or tropiramate
medications to aviod
some sodium channel blockers (Carbamazepine, Gabapentin, Phenytoin, Pregabalin) -- can exacerbate
why do sodium channel blocker exacerbate
•Some gene mutations associated with absence seizures cause a loss of function of the sodium channel that leads to increased seizure activity. The result of this mutation leads to a decrease in the amount of inhibitory neurotransmitter that should balance the excitatory neurotransmitters. This makes a seizure more likely to occur. In this situation, the problem with the balance of excitation and inhibition in the brain is not too much excitation, it is too little inhibition.
•This makes sodium channel blocking anti-epileptics a poor choice for treatment. Giving sodium channel blocking drugs to patients with a loss of function mutation will further decrease the amount of inhibitory neurotransmitters in the brain, making the balance scale tip more toward excitement and more seizure activity.
generalized seaizure =
GRAND mal
what defines grand mal seizure
simultanous neural discharge of both hemisphere (diffuse brain invovement)
what are the two clinical manifestions of generalized seizure
mycolonic
atonic
tonic/ clonic
clonic
tonic
myoclonic
sudden, breif, sporadic involuntary twiching of one muscle or a group of muscle usally w/o loss of consciousness
atonic
sudden partial or complete loss of muscle and postural tone= drops attach may can cause injury
tonic
Loss of consciousness followed by rigidity
clonic gran mal
•repetitive, rhythmic, symmetric jerking (usually 1-2min)
•Post-ictal phase
tonic-clonic grand mal
•Sudden loss of consciousness with tonic activity (contraction & rigidity)
•May have respiratory arrest followed by 1-2min of clonic activity (repetitive, rhythmic, symmetric jerking) <3min
•Followed by post ictal phase
•Cyanosis, tongue-biting & urinary incontinence can occur
inital w/u for grand mal
CBC, CMP (electrolytes, liver and renal function), tox screen, pregnancy test, RPR (rapid plasma reagin, syphillis to r/o reversiable causes
what to check after seiazure to r/o psychogenic nonepileptic seiseizure
prolactin or lattic acid immediately after
what to order to r/o brain lesion or mass after seizure
MRI
what does tonic-clonic siezure show on eeg
generilized high amplitude rapid spiking during active events
how to tx generalized seizure
treat the cause
•Alcohol withdrawal: benzodiazepines; AEDs such as phenytoin are not effective. Why??
•Eclampsia: magnesium sulfate. (Works in multiple ways, but specifically for seizures -- raises the seizure threshold by blocking glutamate receptors, which are responsible for excitatory signaling in neurons)
•Hypoglycemia, hyponatremia, hypocalcemia: correct the abnormality.
•Isoniazid (TB treatment): pyridoxine antidote (through depletion of vitamin B6).
Seizure-threshold drugs: bupropion, tramadol, theophylline. (excess will lower seizure threshold
what antiseizure meds are safest in pregancy
Levetiracetam & Lamotrigine
myoclonic tx with
valporic acid
what defines staus epilepticus
five min or more of convulsion or two or more convulsion in 5 min interval w/o returning toward preconvulsive neurological baseline
status epilepticus is
neurological emergancy
what can cause status eptiliptical
structural abrnoamilites, infx, metabolic abnorm, toxins
status epilepticus should get
CT than MRI
tx of status eplepticu first line
Benzodiazepines (lorazepam/midazolam), IM/IV/nasal
tx status eplicpticus 2nd line
Levetiracetam, Fosphenytoin, Phenytoin or Valproate
tx status eplicpticus 3rd line
•Lacosamide or Phenobarbital (refractory)
anasthesia for status epilepticus.. and what is super refractory
•Midazolam or Propofol Infusion. (airway secured)
•Ketamine infusion/IV (super refractory)
complications of status epilepticus
hypoxia, aspiration, respiratory failure, cardiac arrhythmias
•First line benzodiazepines are frequently under-dosed.
•Initiate a complete workup of the underlying etiology for status epilepticus. Seizures will be difficult to control with antiseizure drugs if they are caused by an underlying uncorrected metabolic problem.
•Consider toxins that can cause seizures: tricyclic antidepressants (look for QRS widening on the EKG, treat with sodium bicarbonate); theophylline; cocaine / sympathomimetic; alcohol withdrawal (rarely causes SE, treat with accelerating doses of a benzodiazepine)
•almost any agent in overdose may cause a seizure indirectly if they cause hypoxia, hypotension, or electrolyte (including hypoglycemia) abnormalities
when is the onset of alc withdraw
4-6 hrs after you stop drinking to reduce the amount significantly
what kind os seaizures does alc withdraw cause
tonic clonic can be single or in clusters
what are risk factors for seizure in alc withdraw
concurrent withdraw from benzo, low potassium and low platlets
how to tx seizure from alc withdraw
iv benzo with taper
iv fluids, iv thiamine, mg, multivitamin (b12 and folate), electrolyte replacement
what are the benzo names
diazepam, lorazepam, chlordiazepoxide, and oxazepam
moa of benzo
they potentiate GABA mediated CNS inhibition, alc mimics GABA so in withdraw there is increase CNS activity
why is iv thiamine given in alc withdraw
prior to glucose to prevent wernike encephalopathy
how to tx febrile seaizure
tx fever with antipyretics, use rescue meds for active seiazure and admit if unstable
what are the two type of febrile seaizure
complex and simple
difference between complex and simnple febrile seizures
complex last over 15 min if docal , reccures or has postictal deficits
tx different between compllex and simple febrile seizures
complex: EEG, LP, teach seizure aid to parents as there is an increase risk of epilepsy. neuro f/u within 2 wks
simple no imaging needed is discharge
first line for infants seizures
ACTH(ACTH signals the adrenal glands to produce cortisol and other glucocorticoid) or high dose steriods or vigabtrin if tuberous sclerosis
childhood 4-10 tx of seizure
ethosuximide this is for abcence seizures
ask someone what slide 38 means
carbamazepine moa
blocks sodium channels
when to use carbamazepine
epilepsy
generalized tonic clonic
focal
mood stabilization
carbamazepine AE
SJS
worsen HF
can worsen abscence seiazure
ethosuximide MOA
blocks Ca channels
ethosuximide AE
SJS, GI upset w
what is CI in abscent siezures
carbampizine
what is the drug of choice for petitee mal seizures
ethosuximide
what can ethosuximide worsen
renal and hepatic failure
phenytonin moa
blocks voltage gated Na
when to use phenytoin
GTC, focal seizures, prophylasis
ADE of phenytonin
P - 450 inducer = can induce lupus-like syndrome
H yperplasia of the gums & Hirsutism
E rythema Multiform, Stevens-Johnson
N europathies: vertigo, ataxia & headache
Y ield = Give Slow. Hypotension/Arrythmia
T eratogenicity: Cleft lip/palate, microcephaly
O steopenia
I nhibits Folic Acid absorption (megaloblastic anemia)
N ystagmus
phenobarbital moa
barbituarate that binds GABA receptrs and potentiates GABA mediated CNS inhibition
is phenobarbital safe in pregancy
yes also safe for children
phenobarbital indications
focal of generalizes. second line after phenytonin for status seaizures (lasting over 5 min) also good with alc withdraw seiazures
phenobarbital AE
depression, SJS, osteoproosis
names of the benzos
loprazepam, diazepam, midazolam
moa of benzo
POTENTIATES GABA CNS inhibitions
which benzo is the most effective for seizures
lorazepam have shorter half life means faster peak
when are benzo used
FIRST LINE to all acute seizures
what to give in a benzo
first line for all acute seizures
what to give in benzo overdose
flumazenil
what is flumaxzenil
antagonizes benzo receptors
valproic acid (divalproex sodium) moa
•GABA, inhibits glutamate & NMDA receptors, increases refractory period of voltage-gated sodium channels
when to used valproic acid (divalproex sodium)
myoclonic seizures
ae for valproic acid (divalproex sodium)
pancreatitis, hepatotoxic, inhibition of drug metab
what is the black box warning for valproic acid (divalproex sodium)
highest risk of birth defects (mainly in the neural tube like spina bifida)