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Brain Power: Adam and Victor's Neurology > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is the usual EEG finding of primary generalized epilepsies?

A

2.5-4 Hz bifrontally predominant spikes or polyspike-and-slow-wave dischargesthat arise without underlying sturcutral abnormalities

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2
Q

Identify the localization:
1. Masticatory, salivation, speech arrest
2. Head and eye turning associated with arm movement or athetoid-dystonic postures
3. Vertiginous aura
4 Olfactory aura
5 Gustatory aura (salivation or thirst sensation)
6 Visceral or autonomic aura
7 Formed hallucinations
8 Vertiginous
9 Auditory

A
  1. Amygdaloid nuclei, opercular
  2. Supplementary motor cortex
  3. Superoposterior temporal region
  4. Mesial temporal, parahippocampal convolution/ uncus
  5. Insula
    6 Insular orbital frontal cortex (temporal usually)
    7 Temporal neocortex or amygdaloid hippocampal complex
    8 Superoposterior temporal region
    9 Superior temporal convultion, Heschl gyrus
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3
Q

T or F Primarily generalized epilepsies usually are underlied by a genetic component while secondary generalized tonic clonic seizures generally do not have such genetic component

A

T

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4
Q

What part of the tongue is bitten in an epileptic fit? how about in a pseudoseizure?

A

Lateral margin of the tongue

Tip of the tongue

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5
Q

T or F Seizures occurring on awakening are usually focal in nature while those occurring during sleep are usually generalized

A

F

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6
Q

What is the typical EEG of absence?

A

3 per second spike and wave pattern

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7
Q

What percentage of absence seizures are completely motionless?

A

10%

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8
Q

T or F 1/3 of children with absence attacks will, in addition, display symmetrical or asymmetrical myoclonic jerks without LOC while 1/2 will at some time have GTCs

A

T

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9
Q

Lennox Gestaut syndrom is often preceded by?

A

infantile spasms (hypsarrhythmia)

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10
Q

What composes west syndrome?

A
  1. Infantile spasms
  2. Hypsarrhythmia
  3. Arrest in mental development
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11
Q

What is the most common form of idiopathic generalized epilepsy?

A

JME

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12
Q

What is the EEG pattern of JME?

A

4-6 Hz polyspike activity on EEG

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13
Q

If a young female has JME what drug should be given?

A

VA is the most effective but owing to its terarogenicity, levetiraceteam or lamotrigine may be more appropriate

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14
Q

What gene and protein responsible for

  1. Dravet syndrome (severe myoclonic epilepsy of infancy)
  2. Juvenile myoclonic epilepsy
  3. Tuberous sclerosis, generalized epilepsy
  4. Angelman syndrome, myoclonic, tonic clonic, atonic
  5. Lafora body disease with PME (progressive myoclonic epilepsy
  6. Unverricht-Lundborg disease with PME
  7. Familial generalized seizures with febrile seizures
A
  1. Dravet SCN1A, sodium channel alpha subunit
  2. GABRA1 (CACNB4), GABA A receptor subunit
  3. TSC1, 2– hamartin tuberin
  4. Angelman: UBE3A, Ubiquitin-protein ligase
  5. Lafora– EPM2A: Laforin, protein tyrosine phosphatase
  6. ULD: EPM1– Cystatin B
  7. SCN1 A,B– sodium channel subunits/ GABA receptor
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15
Q

Describe a Jacksonian seizure?

Where does contraversive turning of head and eyes originate?

Where does the fencing posture with associated choreoathetotic and dystonic postures?

A

Turning movement of the head and eyes to the side opposite the irritative focus often associated with a tonic extension of limbs on the side contralateral to the affected hemisphere

Superolateral frontal region Area 8 just anterior to Area 6

High medial frontal lesions (Area 8 and supplementary motor cortex)

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16
Q

What is the most common color associated with Visual Seizures?

A

Red

followed by blue green yellow

UP Ateneo DLSU UST

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17
Q

T or F. Nondirected oppositional resistance to restraint may manifest in those with temporal lobe epilepsy.

A

T.

2.4 % may have outbursts of intense rage

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18
Q

T or F. Post ictal nose wiping is seen in half of temporal lobe epilepsy patients is carried out by the hand contralateral to the lesion

A

F. IPSILATERAL TO THE SEIZURE FOCUS

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19
Q

What is the triad of behavioral abnormalities in temporal lobe epilepsy?

A
  1. Hyposexuality
  2. Hypergraphia
  3. Hyperreligiosity
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20
Q

What are risk factors for SUDEP?

A
  1. Postictal period immediately after a tonic clonic seizure
  2. Increasing seizure frequency
  3. Lack of successful treatment
  4. Subtherapeutic AED levels
  5. Early adulthood
  6. Long standing epilepsy
  7. Mental retardation
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21
Q

AKA Epilepsy with occipital spikes manifesting as visual hallucinations

A

Panayiotopoulos syndrome

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22
Q

Salaam or Jacknife seizures are also known as?

A

Infantile spasms on account of the single or brief episodes of gross flexion movements of the trunk and limbs

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23
Q

What drugs may be given to infantile spasms

  1. Not associated with tuberous sclerosis
  2. Associated with TS
A
  1. ACTH, Steroids, Clonazepam

2. Vigabatrin

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24
Q

What is the risk of developing unprovoked seizures later in life for patients with
1. Simple febrile seizures
2. Complex febrile seizures with 1 feature
3. Complex febrile seizures with 2 features
3. Complex febrile seizures with 3 features
Features are: Focal, Prolonged, Repeated episodes

A
  1. 2.4%
  2. 8%
  3. 17%
  4. 49%
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25
Q

What is the most common type of reflex epilepsy?

A

Visual

Seizures are usually myoclonic

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26
Q

In those with intractable focal epilepsy in association with progressive hemiparesis, what should be a consideration?

A

Rasmussen syndrome

May be responsive to corticosteroids, plasma exchange and IVIG

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27
Q

What antibodies are found in Rasmussen encephalitis?

A

Ab to GluR3

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28
Q

T or F Incontinence assists greatly in the differentiation between seizures and pseudoseizures

A

F

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29
Q

What are the 3 conditions for development of a discharging lesion in epilepsy?

A
  1. Pathologically excitable neurons, deafferented neurons that become hyperexcitable on account of increased ionic permeability
  2. Increased glutaminergic activity
  3. Reduction GABAergic activity
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30
Q

What 2 phenomena form the basis of Todd’s paralysis?

A
  1. Excess of inhibitory mechanisms

2. Metabolic exhaustion from bursts of neurons

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31
Q

The interictal EEG is abnormal in how many percent of epileptic patients?

A

30-50%

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32
Q

What epileptic focus usually shows EEG abnormalities during sleep?

A

Temporal lobes

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33
Q

In about 15% of patients what can be seen in the CSF after a seizures?

A

10-50 WBCs

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34
Q

T or F. Serum prolactin like those of other hypothalamic hormones rise 10 to 20 minutes after all types of generalized seizures including complex partial types.

A

T

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35
Q

What is the associated histologic finding in medial temporal sclerosis (neuronal loss with gliosis)?

A

CA1 segment (Sommer sector) of the pyramidal cell layer

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36
Q

In primary generalized epilepsies, how many percent have a familial incidence?

A

5-10%

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37
Q

What forms of progressive myoclonic epilepsy results from mutations of

  1. Cystatin B
  2. Tyrosine phosphatase
A
  1. Unverricht-Lundborg

2. Lafora disease

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38
Q

T or F. Limb shaking TIA and convulsive phenomena at the outset of basilar artery occlusion may be nearly impossible to distinguish from epilepsy.

A

T

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39
Q

Fifth day seizures occur when?

A

Days 2 and 3 up to day 7

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40
Q

What are the most common metallic poisons that cause convulsions?

A

Lead in children

Mercury in children and adults

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41
Q

What antibiotics can cause seizures?

A

Imipinem

Cefempime

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42
Q

T or F. Propofol can cause myoclonus.

A

T

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43
Q

What percentage of embolic cortical infarcts trigger seizures after several months?

A

fewer than 10%

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44
Q

How does pregnancy impact the frequency of seizures in an epileptic?

A

2/3 no change
1/6 worsen
1/6 improve

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45
Q

T or F. CBZ, Phenytoin and VA are all found in mother’s milk

A

VA is highly protein bound. Virtually absent in breast milk

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46
Q

What is the most common the cause of epilepsy in the adult life?

A

Infarct

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47
Q

What drugs can be taken only once daily on account of their long half lives?

A

Phenytoin
Phenobarbital
Ethusuximide

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48
Q

What percentage of epileptics will be controlled AEDs?

A

70% completely controlled

20-25% will have significantly reduced seizure frequency

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49
Q

Indicate the first line drugs

  1. GTC
  2. Myoclonic
  3. Focal
  4. Absence
A
  1. VA, Phenytoin
  2. VA
  3. Carbamazepine, Phenytoin
  4. VA
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50
Q

What are the effective blood levels of the ff

  1. Phenytoin
  2. Valproic Acid
  3. Phenobarbital
A
  1. 10-20
  2. 50-100
  3. 15-40
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51
Q

What drug can lead to the buildup of Carbamazepine epoxide when added?

A

Valproic acid inhibits epoxide hydrolase

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52
Q

At what level does non linear kinetics start for phenytoin?

A

10mg/ml

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53
Q

How do salicylates and valproic acid increase the levels of phenytoin and phenobarbital?

A

Displacing them from their protein binding

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54
Q

How do antacids and histamine blockers affect phenytoin levels?

A

Antacids reduce

Histamine blockers increase

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55
Q

T or F Dialysis removes Pb and ethosuximide

A

T

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56
Q

What are the most common teratogenic effects of AEDs?

A

Cleft lip and palate

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57
Q

Pregnant women in general have what percentage risk of developing a congenital malformation?

A

2-3%.

Lamotrigine 3%

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58
Q

What AEDs may be started in patients off AEDs but with recurrence of seizures while pregnant?

A

Phenytoin + Levetiracetam

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59
Q

Skin eruptions from AEDs are most common with what AEDs?

A

The aromatics:

  1. Phenytoin
  2. Carbamazepine
  3. Phenobarbital
  4. Primidone
  5. Lamotrigine
60
Q

What HLA polymorhphism is associated with skin eruptions with AEDs?

A

HLA-B*1502 in asians

HLA-A*3101 in caucasians

61
Q

After withdrawal of AEDs what is the % of recurrence at 5 years?

62
Q

How is bone density decreased by AEDs?

A

induction of cytochrome p450 which enzymatically degrades vitamin D

63
Q

What supplementation needs to to be given to patients on phenytoin?

A

Vitamin K and Folate

64
Q

What synaptic vesicle protein is acted upon by Levetiracetam?

65
Q

What is the MOA of Topiramate and Tiagabine?

A

Inhibition of GABA reuptake

66
Q

The ff are adverse effects of which AED?

Renal stones + Angle closure glaucoma + Hyperchloremic metabolic acidosis

A

Topiramate

67
Q

What is the MOA of Lacosamide?

A

Lacosamide binds to collapsin response mediator protein-2 (CRMP-2), a phosphoprotein which is expressed primarily in the nervous system and is involved in neuronal differentiation and control of axonal outgrowth.

68
Q

What are the three ways that epilepsy is diagnosed?

A
  1. recurrent unprovoked seizures (ie, two or more unprovoked seizures occurring at least 24 hours apart)
  2. a heightened tendency toward recurrent unprovoked seizures (ie, a single seizure, accompanied by evidence from clinical, electroencephalographic, or neuroimaging tests that a heightened risk [at least 60%] exists for future seizures over the next 10 years)
  3. an epilepsy syndrome is diagnosed
69
Q

Identify the region of onset of these seizures:

  1. Dysmnesic
  2. Gustatory
  3. Olfactory
  4. Complex visual
  5. Complex visua
  6. Simple visual
A
  1. Dysmnesic Mesial Temporal
  2. Gustatory Mesial Temporal
  3. Olfactory Mesial Temporal, parahippocampal convultion or the uncus
  4. Complex visual Lateral/ posterior temporal
  5. Complex visual Lateral/ posterior temporal
  6. Simple visual Occipital
70
Q

T or F Absence seizures unlike focal seizures lack any premonitory aura symptoms or postictal state.

71
Q

Which seizures mimic:

  1. Positive symptoms of photopsia and paresthesia; starts with prolonged sensory march
  2. Negative symptoms of numbness and weakness; with rapid sensory march
  3. Emotional provocation; muscle atonia with preserved consciousness
A
  1. Migraine
  2. TIA
  3. Cataplexy
72
Q

What does EEG show in

  1. Migraine
  2. NREM Parasomnia
A
  1. Focal or generalized
  2. Slowing
    shows generalized or frontal dominant rhythmic delta or theta pat- terns lasting a few seconds following the arousal.
73
Q

What are the ictal characteristics of Paroxysmal nonepileptic seizures?

A

1 Eye closure during the spell (which may rarely be seen in true epileptic seizures as well) 2 Bizarre voluntary movements, including “yes-yes” type head nodding or “no-no” type side-to-side head shaking
3. Prominent pelvic thrusting, 4. Atypical nonanatomic spread of movements (eg, clonic-type move- ments that may begin in a leg, spread to the head, then to an arm, features that also may occur in true epilepsy)

74
Q

Differentiate sharp and spike on the basis of duration

A

Spike discharges are predominantly negative transients with steep ascending and descending limbs and a duration of 20 ms to 70 ms.
Sharp wave is a broader potential with a duration of 70 ms to 200 ms.

75
Q

What is the sensitivity of EEG for epilepsy?

A

The sensitivity of a single EEG study to record an epileptiform abnormality may be 50% or less in people with epilepsy. The diagnostic yield increases to 80% to 90% if three or more serial EEGs are performed.2

76
Q

T or F

Interictal epileptiform discharges are seen rare- ly in adults or children without epilepsy (0.2% to 0.3%).

A

F

0.2% to 3%

77
Q

What drugs predispose to interictal epileptiform discharges?

A
  1. bupropion
  2. cefepime
  3. clozapine
  4. lithium
  5. tramadol
78
Q

T or F

Extracranial (scalp) EEG records activity in only approximately one-half of the cerebral cortex.

79
Q

What regions of the brain may have epilpetiform activity not recorded by EEG?

A
  1. Basal regions
  2. Sulci
  3. Medial temporal lobe
  4. Interhemispheric regions
80
Q

What are of the cortex must be involved in order to produce an epileptiform discharge?

A

6 cm2 of cerebral cortex must be involved to generate a scalp-recorded epileptiform discharge

81
Q

What is the most epileptogenic region of the brain?

A

The most epileptogenic region or zone (the area likely to be associated with seizures) is the medial temporal lobe, including the amygdala and hip- pocampus.

82
Q

What is the most common interictal EEG finding in adult patietns with focal seizures?

A

The most common interictal EEG finding in adult patients with focal seizures is the ante- rior temporal lobe spike discharge. The anterior temporal lobe epileptiform discharge is highly epileptogenic, and 80% to 90% of these patients have a seizure disorder

83
Q

What percentage of patients with extratemporal seizures will have interictal epileptiform discharges local- ized to the correct lobe of seizure origin.

A

Only about 50%. Compared to:
In patients with temporal lobe epilepsy, 80% to 90% will have predominantly tem- poral lobe epileptiform discharges. Bitemporal spike discharges may be identified in 25% to 33%

84
Q

What is usually triggered by

  1. Hyperventilation
  2. Photic stimulation– photoparoxysmal response
A
  1. Absence
  2. Genetic generalized epilepsy such as childhood absence epi- lepsy with or without eyelid myoclonia, juvenile absence epilepsy, and juvenile myoclonic epilepsy
85
Q

What percentage of patients with psychogenic events have coexistent seizure disorders?

86
Q

What sequence has shown an accuracy of 97% for detecting abnor- malities associated with mesial temporal

A

FLAIR imaging sequences have shown an accuracy of 97% for detecting abnor- malities associated with mesial temporal sclerosis

87
Q

The imaging finding of a transmantle sign is a specific alteration that has been shown to be consistent with ____________

A

focal cortical dysplasia

88
Q

T or F
those presenting with multiple seizures in a 24-hour period were no more likely to have seizure recurrence than those presenting with a single seizure, irre- spective of etiology or treatment

89
Q

What is the recurrence risk of an unprovoked seizure after the first seizure? After the second unprovoked seizure?

A

after a first unprovoked seizure, the overall risk for a second seizure was only 33%. After a second seizure, how- ever, the risk of a third unprovoked seizure rose to 76%.

90
Q

What is the only indication for AED prophylaxis?

A

The only evidence supporting AED prophylaxis is in patients with high-risk head injury in the early posttraumatic period1

91
Q

What medications can cause seizures>

A
  1. tramadol
  2. imipenem
  3. theophylline
  4. bupropion
92
Q

What are the indications for medications in benign rolandic epilepsy?

A
  1. Evolution of focal seizures to GTCs

2. Focal seizures causing psychosocial distress

93
Q

What is the definition of acute in ASS?

A

. They defined acute symptomatic as within 7 days of stroke or TBI and during the active infection for central nervous sys- tem (CNS) infections.

94
Q

What is more likely to have a second unprovoked seizure?
Acute SS OR
Remote SS

A

Remote ASS

95
Q

T or F Provoked seizures are usually focal?

A

F. Generalized except for hypoglycemia sometimes causing focal seizures

96
Q

The presence of which of the following increase risk for seizure recurrence after unprovoked first seizure:

  1. Sibling with seizures
  2. Presence of spike wave discharges on EEG
  3. Focal onset of seizures
  4. Generalized onset of seizures
  5. Previous neurologic insult
  6. Generalized spike and wave discharges
A
  1. Yes 29% at 4 months
  2. Yes 50% at 18 months
  3. No
  4. No
  5. Yes. 2.5 increased risk compared to idiopathic
  6. Yes. 60%

History of acute symptomatic seizures also increase risk by 50%

97
Q

In children what are risk factors for seizure recurrence after an unprovoked seizure?

A 
1 remote symptomatology
2 abnormal EEG
3 seizures occurring during sleep
4 history of prior febrile seizures 
5 Todd paralysis
98
Q

In the prognostic scoring based on the MESS trial what 3 factors are looked at?

A
  1. Number of seizures at presentation
    1 =0
    2-3=1pt
    4 or more= 2pts
  2. Neurological disorder or defi cit, learning disability, or developmental delay = 1pt
  3. Abnormal EEG = 1pt

Low risk 0pt
Medium risk 1 pt
High risk 2 pts

99
Q

What drugs are proven to have efficacy for GTCs in class 1 trials?

A

Lamotrigine
Topiramate
Levetiracetam
Perampanel

100
Q

What 2 drugs have class 1 trials to back them up for both Focal AND generalized TC seizures?

A

Perampanel and Levetiracetam

101
Q

What drugs have class 1 trials to back them up for absence seizures?

A

Valproic acid and ethosuximide

102
Q

Which among these drugs are deemed NOT EFFECTIVE for myocloniz seizures?

Phenytoin
Carbamazepine
Oxcarbazepine
Ethosuximide
Gabapentin
Pregabalin
Lacosamide
Phenobarbital
Levetiracetam
A

ALL EXCEPT
Levetiracetam and Phenobarbital are not effective.

Lev has class trials
Pb has class 4 trials
103
Q

What is the MOA of:

  1. Pb
  2. Phenytoin
  3. CBZ
  4. VA
  5. Benzodiazepenes
  6. Felbamate
A
  1. Pb: PROLONG the opening of GABA A channel receptors
  2. Prolongs the inactivated state of the Na channel
  3. Same as Phenytoin
  4. Blocking T type Calcium channels and Na
  5. Diazepam: INCREASE THE FREQUENCY OF OPENING of GABA A channel receptors
  6. NMDA antagonism, Na block and GABA enhancement
104
Q

Hepatic inducer or blocker?

  1. Pb
  2. Phenytoin
  3. CBZ
  4. VA
A
  1. Pb: Inducer
  2. Phenytoin: Inducer
  3. CBZ: Inducer
  4. VA: Blocker!
105
Q

What is the recommended dose for Pb?

A

Pb 1mg/kg to 2.5mg/kg

106
Q

Primidone gets converted in the liver into?

A
  1. pb

2. Phenylethylmalonamide

107
Q

What should be taken into account in an epileptic on phenytoin who has been diagnosed with PTB?

A

INH can reduce metabolism of phenytoin therefore the drug levels increase

108
Q

What is the maximum rate at which phenytoin can be administered?

109
Q

What is the metabolite of CBZ that is responsible for most of its adverse effects?

A

carbamazepine-10,11-epoxide.

110
Q

What are the adverse effects of CBZ?

A
  1. Cerebellar symptoms
  2. Leukopenia
  3. Hyponatremia
  4. Weight gain
  5. Decreased bone density
111
Q

Why does Oxcarbazepine reduce the efficacy of oral contraceptives?

What kind of OCP is affected by perampanel– accelerating metabolism and reducing blood level?

A

Induction of CYPA4

Progesteron containing at doses 12mg per day or moreT

112
Q

How to convert CBZ to OXCBZ?

A

300mg OXCBZ for every 200mg CBZ if CBZ dose is 800 or less

113
Q

T or F Oxcarb is more likely to cause hyponatremia than CBZ

A

T. ESPECIALLY IN ELDERLY and those taking diuretics.

114
Q

What is the critical level of phenytoin for it to cause paradoxical increase in seizures?

A

More than 30mg per ml. happens with renal failure because of decrease in protein and increase in the free phenytoin level

115
Q

What are the MOA of valproic acid?

A
  1. Na blocking

2. Blocking of T type calcium channels

116
Q

How does VA prevent absence seizures?

A

BLOCKING OF T TYPE CALCIUM CHANNELS

117
Q

What is the long acting formulation of VA? How is it started?

A

500mg at bedtime

Divalproex sodium

118
Q

What are the 2 most serious adverse effects of Felbamate?

What is the most common?

A
  1. Lethal aplastic anemia
  2. Hepatic failure

Most common: GI irritation

119
Q

What is the MOA of:

  1. Gabapentin
  2. Lamotrigine
  3. Topiramate
  4. Tiagabine
A
  1. Gabapentin: Binding to alpha 2 delta subunit of the voltage gated calcium channel
  2. Lamotrigine: Blocks sodium channels
  3. Topiramate: AMPA antagonist, Augments GABA, Blocks Na
  4. Tiagabine: Inhibits GABA uptakee
120
Q

Which 3 drugs are proven NOT effective for GTC, Absence and Myoclonic seiuzres?

A

Gabapentin, Pregabalin and Tiagabine ARE FOR FOCAL SEIZURES ONLY

121
Q

What AEDs may be used for bipolar disorder?

A
  1. VA
  2. LTG
  3. CBZ
122
Q

What AED has efficacy against migraine and obesity?

A

Topiramate

123
Q

What is the main problem with Topiramate?

A

The main tolerability issue being cognitive adverse effects includ- ing cognitive slowing, decreased atten- tion and memory, impaired executive function, word-finding difficulty, and reduced verbal fluency

124
Q

Carbonic anhydrase inhibition is brought about by which AED? Causing secondary angle closure glaucoma and kidney stones

A

Topiramate

Zonisamide

125
Q

MOA:

  1. Levetiracetam
  2. Zonisamide
  3. Lacosamide
  4. Vigabatrin
  5. Exogabine
  6. Perampanel
A
  1. Lev: SV2A blockade resulting in decrease in neurotransmitter blockade
  2. Zonisamide: Inhinits T type calcium channels like ethosuximide and valproic acid, blocks Na channels
  3. Lacosamide:Blocks sodium channels enhancing slow inactivation AS OPPOSED TO blocking fast sodium channel infaction
  4. Vigabatrin: IRREVERSIBLE INHIBITOR of GABA transaminase thereby resulting in GABA accumulation
  5. Potassium channel opener
  6. Perampanel: AMPA glutamate receptor antagonist
126
Q

Vigabatrin is especially effective in?

A

Infantile spasms in the presence of tuberous sclerosis

127
Q

What is the most serious adverse effect of vigabatrin?

A

Visual field constriction

128
Q

What is the only evidence based combination therapy in humans?

129
Q

What are automatisms and where are they localized?

A

Lip smacking, chewing, swallowing, fumbling, shuffling of feet. Temporal lobe or limbic structures

130
Q

Where do high voltage spikes occur in the eeg of Rolandic Epilepsy/ Sylvian Epilepsy?

A

Centrotemporal area or lower rolandic area

131
Q

What CNSI manifests with seizures without fever or nuchal rigidity?

A

Syphilitic meningitis

132
Q

T or F: GTCs can occur with gram negative sepsis with shock, hepatic stupor and intractable congetive heart failure

133
Q

Enumerate as many drugs that can cause seizures

A
  1. Imipinem
  2. Cefepime
  3. Lidocaine
  4. Tramadol
  5. Propofol
  6. Aminophylline
134
Q

How is warfarin affected by the addition of Pb or CBZ?

A

Concentrations are decreased

use with phenytoin produces UNSTABLE

135
Q

What drugs are affected by end stage CKD?

A

Pregabalin, Levetiracetam and Gabapentin becuase they are excreted through the kidney
Low protein means measurement of phenytoin levels will be low so check for free levels
Dialysis removes Pb and ethosuximide so dosage of the drugs need to be modified

136
Q

What is the usual risk for congenital defects in the normal population?

A

2-3%

Increased to 4-5% in those taking AEDs

137
Q

What adverese effects of valproic acid are important to remember in women?

A
  1. Menstrual irregularities
  2. PCOS
  3. Weight gain
  4. Congenital anomalies in offspring
138
Q

Women taking phenytoin should be given what supplements prior to delivery?

A

Folate

Vitamin K

139
Q

What are adverse effects of Lacosamide?

A

Prolong PR interval

Worsen heart failure

140
Q

What are the components of the propofol syndrome?

A

Hypotension
Acidosis
Shock

May present with Hypertryglyceridemia pancreatitis as well

141
Q

How to introduce or start ketogenic diet?

A

Starve for a day or two then diet is 80-90% fats

142
Q

What is the main treatment for GLUT1 deficiency syndrome?

A

Ketogenic diet

143
Q

What gene or protein is responsible for:

  1. Myoclonic epilepsy with ragged red fibers
  2. Gaucher disease
  3. Pyridoxine deficiency
A
  1. tRNAlys: Mitochondiral lysine trNA
  2. PSAP: beta glucocerebrosidase
  3. ALDH7A1: Antiquitin
144
Q

What are the manifestations of:

  1. Volvular epilepsy
  2. Epilepsia procursiva
  3. Poriomania
A
  1. Walking repetitively in small circles
  2. Running
  3. Wandering aimlessly
145
Q

Gelastic seizure with precocious puberty =

A

Hypothalamic hamartoma

146
Q

What is also known as early infantile epileptic encephalopathy with burst-suppression?

A

Ohtahara syndrome may evolve into West syndrome and eventually, Lennox Gestaut syndrome

147
Q

What combination of AEDs can result in absence status?

A

VA and clonazepam

Brain Power: Adam and Victor's Neurology (19 decks)

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