EPILEPSY

Question 1

Q1: What is epilepsy?

Answer 1

A1: A chronic neurological disorder characterized by recurrent unprovoked seizures due to abnormal excessive or synchronous neuronal activity in the brain.

Question 2

Q2: What causes epilepsy at the neuronal level?

Answer 2

A2: Imbalance between excitatory (glutamate) and inhibitory (GABA) neurotransmission, leading to hyperexcitability

Question 3

Q3: What is the role of ion channels in epilepsy?

Answer 3

A3: Dysfunction of sodium, calcium, and potassium channels can lead to increased neuronal excitability and seizures.

Question 4

Q5: How is epilepsy diagnosed?

Answer 4

A5: Clinical history + EEG findings + neuroimaging (MRI). At least two unprovoked seizures >24 hours apart OR one seizure with high recurrence risk.

Question 5

Q6: What is the role of EEG in epilepsy diagnosis?
Q7: What imaging is preferred in epilepsy workup?

Answer 5

A6: Identifies epileptiform discharges, localizes seizure origin, and classifies seizure type.
A7: MRI is preferred over CT, especially in focal epilepsy, to detect structural causes.

Question 6

Q8: What are the two main types of seizures?

Q9: What distinguishes focal vs generalized seizures?

Answer 6

A8: Focal (partial) and generalized.
A9: Focal: originate in one hemisphere; Generalized: involve both hemispheres from onset.

Question 7

Q10: Name types of focal seizures.

Answer 7

Focal aware (simple partial)
Focal impaired awareness (complex partial)
Focal to bilateral tonic-clonic

Question 8

Q11: Name types of generalized seizures.

Answer 8

Tonic-clonic
Absence
Myoclonic
Tonic
Atonic

Question 9

Q12: What is the mechanism of sodium channel blockers?

Answer 9

A12: They stabilize the inactivated state of voltage-gated sodium channels, reducing high-frequency firing.
Examples: Phenytoin, carbamazepine, lamotrigine.

Question 10

Q13: What AEDs enhance GABA activity?

Answer 10

A13: Benzodiazepines, phenobarbital, vigabatrin, tiagabine

Question 11

Q14: What is the mechanism of levetiracetam?

Answer 11

A14: Binds to SV2A (synaptic vesicle protein), modulating neurotransmitter release.

Question 11

Q15: What AED blocks calcium channels?

Answer 11

A15: Ethosuximide (T-type channels, used in absence seizures).

Question 12

Q16: Which AEDs are broad-spectrum?

Q17: Which AEDs are narrow-spectrum (focal only)?

Answer 12

A16: Valproate, lamotrigine, topiramate, levetiracetam.

A17: Carbamazepine, phenytoin, gabapentin, oxcarbazepine

Question 13

Q18: Common side effects of phenytoin?

Answer 13

A18: Gingival hyperplasia, hirsutism, nystagmus, ataxia, teratogenicity, osteoporosis.

Question 14

Q22: Levetiracetam side effects?

Answer 14

A22: Behavioral changes like irritability, mood swings, aggression.

Question 14

Q21: Topiramate side effects?

Answer 14

A21: Cognitive impairment, weight loss, kidney stones, paresthesias.

Question 14

Q19: Valproate main adverse effects?

Answer 14

A19: Weight gain, tremor, hepatotoxicity, teratogenicity (neural tube defects), thrombocytopenia.

Question 15

Q20: Lamotrigine risk to monitor?

Answer 15

A20: Stevens-Johnson Syndrome—requires slow titration.

Question 16

Q23: Which AEDs require therapeutic drug monitoring?

Answer 16

A23: Phenytoin, valproate, carbamazepine, phenobarbital.

Question 17

Q24: What are the therapeutic ranges?

Answer 17

A24:

Phenytoin: 10–20 mcg/mL

Valproate: 50–100 mcg/mL

Carbamazepine: 4–12 mcg/mL

Phenobarbital: 15–40 mcg/mL

Question 18

Q25: What labs are monitored with valproate?

Answer 18

A25: LFTs, platelet count, serum levels.

Question 19

Q27: When should AEDs be withdrawn?

Answer 19

A27: After 2–5 years seizure-free, with normal neuro exam and EEG, slow taper required.

Question 20

Q26: What labs are monitored with carbamazepine?

Answer 20

A26: CBC (for aplastic anemia/agranulocytosis), LFTs, serum sodium (risk of SIADH).