Epilepsy and Sleep Flashcards
How should the dose of Lamictal be adjusted in pregnancy?
increased since pregnancy increases lamictal clearance.
what are symptoms of temporal lobe seizures?
altered consciousness, atomotisms, deja vu, complex partial seizures, olfactory hallucinations.
When a patient has the fencer’s posture during a seizure, where does their seizure usually come from.
frontal lobe- supplementary motor cortex.
What is proposed mechanism of action of gabapentin and pregabalin?
binding to L-type Ca channels, modulate presynaptic neurotransmitter release.
How is Gabapentin excreted?
renal
What are advantages and disadvantages of Gabapentin?
Advantage: does not interact with other drugs. Disadvantages: can worsen generalized epilepsy, absorption is non-linear.
Which medications can exacerbate myoclonic epilepsy?
Lamictal, Carbamazepine, Gabapentin, Pregabalin, Vigabatrin.
Which anti-convulsants are hepatic enzyme inducers?
Phenytoin, Carbamazepine, Phenobarbital, Primidone, Oxcarbamazepine and Topirimate >200mg/day.
Which anti-convulsants are hepatic enzyme inhibitors
VPA,
at what age does the posterior dominant alpha rhythm develop to the adult frequency?
8-10 years
which medications can aggravate absence seizures?
phenytoin, carbamazepine, gabapentin, lamictal.
what is the mechanism of action of Benzodiazepines?
GABAa agonists.
what is the interaction between oral contraceptives and Lamotrigine?
OCP’s containing ethinylestradiol increase Lamotrigine clearance.
How is Topirimate metabolized?
Excreted in urine.
What is the mechanism of action of Lacosamide?
inactivation of slow voltage Na channels- leads to decreased membrane hyperexcitability. Also interacts with CRMP2- involved in neuronal differentiation and axon guidance.
What is the mechanism of action of Rufinimide?
prolongation of inactive state of Na channels.
How is Rufininide metabolized?
enzymatic hydrolysis of carboxylamide group (NOT via cyp system), elimination in urine.
What is inheritance of Aicardi syndrome?
X-linked Dominant
what is the pathomenumonic eye findings in Aicardi syndrome?
chorioretinal lacunae
What are the characteristics of Unverricht Lundborg Syndrome?
stimulus induced progressive myoclonic epilepsy that is action related, various seizure types, neurologic decline, ataxia and tremor.
What gene is involved in Unverricht Lundborg Syndrome and what chromosome is it on?
EPM1 on Chr 21q22. Encodes Cytasin B which regulates apoptosis.
What are the clinical features of Sialadosis Type I?
progresive action myoclonus, pregoressive ataxia, vision loss, cherry red spot. Onset in adolescence or adulthood.
What is the enzyme deficiency in Sialadosis Type I?
alpha-neuroaminidase.
What are the clinical features of Sialadosis Type II?
myoclonus, coarse facial features, corneal clouding, hepatomegaly, skeletal dysplasia, learning disability. Onset between birth and 20s.
what is the enzyme defect in Sialadosis Type II?
N-acetyl neuroaminidase and beta-galactosialidase
what is the inheritence of the sialadoses?
autosomal recessive.
what gene is implicated in sialadoses and what chromosome is it on?
Neu1 on Chr6p
what are the clinical features of Lafora body disease?
onset in adolescence, progressive myoclonic seizures and other seizure types. Ataxia, dysarthria and progressive dementia.
what gene is involved in Lafora Body disease and what chromosome is it on?
EPM2A on Chr6q.
what is the pathologic finding in Lafora body disease?
PAS positive Lafora body inclusions in skin biopsy.
what is the frequency of alpha waves?
8-13 Hz
what is the frequency of beta waves?
>13 Hz
What is the frequency of theta waves?
4-7 Hz
what is the frequency of Delta waves?
1-4 Hz
what are the main features of N1 sleep
loss of posterior alpha rhythm, increased theta, loss of muscle artifact, vertex waves, POSTS
What are the features of N2 sleep?
sleep spindles, K-complexes, vertex waves, POSTS
What are the features of N3 sleep?
high amplitude delta, rare spindles, k-comoplexs.
What are the features of REM Sleep?
can have some alpha, spontaneous REM, tonic motor activity suppression on EMG, central sawtooth waves.
what is the AHI in mild OSA?
5-15
What is the AHI in moderate OSA?
15-30
what is the AHI in severe OSA?
>30.
what are the non-REM parasomnias?
confusional arousals, sleepwalking, night terrors.
what stage of sleep do non-REM parasomnias arise from?
Stage III (slow wave)
what is Klein-Levin Syndrome?
recurrent episodes of hypersomnia during which sleep is not refreshing. Can be associated with irritability, aggressiveness, confusion and hypersexuality.
what is idiopathic hypersomnia?
long term inability to obtain adequate sleep.
what is the physiologic basis of narcolepsy?
loss of hypocretin neurons in the lateral hypothalamus.
what degenerative disease have been associated with REM sleep disorders?
alpha-syneuclopathies.
what are some treatments of narcolepsy?
gamma-hydroxybuterate, triciclyc anti-depressants, SSRIs
what are two features of narcolepsy on polysomnography?
MSLT
what structure is responsible for REM sleep?
locus correlius
what aspect of narcolepsy are stimulants helpful for?
sleep attacks
at what age to well formed, synchronous sleep spindles appear?
2 years
at what gestational age does the EEG consist of primarily trace discontinue?
24-28 weeks
starting at what gestational age is trace discontinue confined to quiet sleep?
32 weeks
at what age does trace alternans arise?
36 weeks
what is activite moyenne? at what gestational age does it arise?
continuous low voltage mixed frequency during wakefulenss. 36-40 weeks.
at what gestational age does continuous slow wave sleep arise?
44 weeks
at what gestational age are delta brushes peaking?
32-34 weeks
at what gestational age do asynchronous sleep spindles arise?
44-46 weeks
what percentage of the time does the term neonate spend in the waking state?
30%
what term neonatal sleep state is characterized by decreased muscle tone, irregular respirations and occasional face and body movements. What percentage of time is spent in this state?
active sleep, 50-60%
what term neonatal sleep state is characterized by muscle tone similar to waking, regular respirations, and little movement. what percentage of the time is spent in this sleep state?
quiet sleep, 30-40%
What is Bancaud’s phenomenon?
failure of one side to abolish alpha rhythm with eye opening. Indicates abnormality on that side.
sail waves over the posterior region
posterior slowing of youth
Episodic theta occurring over the sylvian area
temporal transients- seen in normal aging.
what EEG pattern is seen in dialysis dementia? Due to the accumulation of what substance?
bilateral spike and wave discharges. Aluminum
what are the 5 grades of EEG after anoxic injury?
- reactive alpha with some theta 2. Dominant Theta 3. continuous polymorphic slow delta 4. invariant low amplitude delta without change with stim 5. nearly iso-electric
in what type of injury is there reactive alpha most predominant over the posterior head?
vascular lesion to ventral pons
when do benign epileptiform transients of sleep occur?
during drowsiness in adults
what EEG finding is circled?
Wicket spikes- arc like spikes that occur in trains. Normal variant.
what are the blue arrows pointing to?
Lambda waves- evoked waves due to shifting saccades when a visual stimulus is presented
rolandic alpha that slows with aging and abolishes when you move contralateral arm
mu rhythm
at what serum concentration does phenytoin reach zero order kinetics?
15
what class of drugs alters free phenytoin level without changing total level?
siacylates
addition of what drug can cause immediate phenytoin toxicity?
Valproate because it displaces protein bound phenytoin resulting in immediately higher level
which wave of auditory evoked brainstem potential corresponds to activation of the distal CN VIII?
I
what brainstem auditory evoked potential corresponds to activation of the proxiam CN VIII?
II
what brainstem auditory evoked potential corresponds to activation of the superior olive and trapezoid body?
III
what brainstem auditory evoked potential corresponds to activation of the upper pons?
IV
what brainstem auditory evoked potential corresponds to activation of the midbrain?
V
what wave corresponds to pattern reversal visual evoked potential?
p100
what corresponds to the N9 wave?
Erb’s point after stimulation of median nerve
What is the wave at the cerico-medullary junction after stimulation of the median nerve? WHat does it represent?
N14. Medial lamniscus
what is the wave in contralateral somatosensory cortex after median nerve stimulation?
N20
what is the wave over the lumbar spinal cord after stimulation of the tibal nerve?
N22
what is the wave over contralateral somatosensory cortex after stimulation of the tibial nerve?
P38
what are the two potentially serious side effects of felbamate?
hepatic toxicity and aplastic anemia
what is the risk of having a baby with major malformations if you are on one anti-convulsant?
5-7%
in which type of seizure are there well formed visual hallucinations?
lateral temporal
is motor arest more commen in medial or lateral temporal seizures?
mesial
which anti-convulsant increases seizures in patients with porphyria?
carbamazepine
in what disorder is generalized paroxysmal fast activity seen?
porencephaly
what is the mechanism of action of tetrototoxin?
blocks opening of V-gated Na channels
which sensory receptors in the skin respond to sustained touch? What sensory fibers do they stimulate?
Merckle cells. Type II afferents.
which skin sensory receptors resond to descret onset and offset fo touch, but not to sustained touch?
Meissner’s corpuscles.
what is the resting membrane potential of rods?
-40
what is the rod cell response to light?
hyperpolarization and decrease in tonic release of glutamate.
what is the effect of nerve cooling on motor action potentials?
slowed conduction velocity and increased distal latency
what is the effect of nerve cooling on SNAPs?
INCREASED amplitude
what is the mechanism of action of the nerve cooling effects?
increased time of opening of Na channels, increasing refractory period.
