Epilepsy

Question 1

Seizure

Answer 1

episode causing movements or feelings patient cannot control. Electrical activity in the brain –> neurons fire at abnormally high rate

Question 2

epilepsy

Answer 2

multiple seizures; group of disorders

Question 3

What causes seizures

Answer 3

most are idiopathic; may also be caused by withdrawal from CNS depressant drugs (causes brain to rebound)

Question 4

Two types of focal seizures

Answer 4

simple partial and complex partial

Question 5

Two types of generalized seizures

Answer 5

primary and secondary

Question 6

Where do focal seizures start

Answer 6

localized point in cortex –> agitates neighboring regions, but starts and stays in cortex

Question 7

Where do secondary generalized seizures start

Answer 7

starts as focal –> activates thalamus –> causes all other regions to depolarize/fire abnormally

Question 8

Thalamus

Answer 8

main relay station; connections to all other brain regions

Question 9

Where do primary generalized seizures start

Answer 9

original seizure activity STARTS in the thalamus and leads to activation of both hemispheres

Question 10

Describe simple partial seizures

Answer 10

WITHOUT altered mental state; patient stays awake; unexplained feelings of joy, anger, sadness, etc; ONLY time pt does not lose consciousness

Question 11

Describe complex partial seizures

Answer 11

WITH altered mental status; loss of consciousness; repetitive behaviors; automatisms; lasts 30 seconds to 2-3 minutes

Question 12

Absence seizure

Answer 12

Generalized. Very brief, often no symptoms, rapid blinking or nose rubbing, common in children –> often outgrow

Question 13

Tonic seizure

Answer 13

Generalized. Bilateral increase in limb tone, arms curl inward

Question 14

Clonic seizure

Answer 14

Generalized. Bilateral jerking of limbs –> rapid

Question 15

Tonic-Clonic

Answer 15

Generalized. Bilateral increase in tone followed by bilateral jerking

Question 16

Atonic

Answer 16

Generalized. Sudden loss of muscle tone and consciousness –> patient passes out

Question 17

Myoclonic

Answer 17

Generalized. Brief, rhythmic jerks, lasts a few seconds

Question 18

Tonic-Clonic (grand mal) description

Answer 18

Can be primary or secondary –> entire brain activated either way. Sensory aura often precedes seizure, followed by post-ictal state. Patient is unconscious and has no memory of event

Question 19

Role of AMPA in Tonic stage

Answer 19

Sodium channel, open

Question 20

Role of GABA in Tonic stage

Answer 20

Chlorine channel, open briefly at beginning

Question 21

Role of NMDA in Tonic stage

Answer 21

Calcium channel, Opens after AMPA (AMPA must depolarize NMDA)

Question 22

Role of G-coupled Calcium channels in Tonic stage

Answer 22

open

Question 23

Role of AMPA in Clonic stage

Answer 23

Opens and closes

Question 24

Role of GABA in Clonic stage

Answer 24

Opens and closes opposite of AMPA - when one is open the other closes

Question 25

Role of NMDA in Clonic stage

Answer 25

closed - no role

Question 26

Role of G-coupled Calcium channels in Clonic stage

Answer 26

open

Question 27

Role of AMPA in Post-ictal stage

Answer 27

low level --> not much activity

Question 28

Role of GABA in Post-ictal stage

Answer 28

open on full power --> pt unconscious

Question 29

Role of NMDA in Post-ictal stage

Answer 29

no activity

Question 30

Role of G-coupled Calcium channels in post-ictal stage

Answer 30

On full-power --> tons of Cl- leads to CNS depression

Question 31

Status epilepticus

Answer 31

continuous seizure activity lasting more than 30 minutes OR two or more sequential seizures without full recovery of consciousness btwn seizures. Can lead to brain damage or death if not stopped.

Question 32

Causes of status epilepticus

Answer 32

sudden withdrawal of meds (remove CNS depressant get seizure activity), stroke, acute head trauma

Question 33

Sodium channel blockers

Answer 33

``` thought to be more effective in treatment of focal and secondary generalized, but can be used in primary generalized. Phenytoin (Dilantin) Carbamazepine (Tegretol) Lamotrigine (Lamictal) Valproic Acid (Depakene) ```

Question 34

What do Sodium channel blockers do

Answer 34

Keep channels in refractory period for longer. When refractory, no ions flow --> difficult to reopen Blockers increase time in refractory period so no ions flow AP dives below -70, making it harder to generate an AP (hyperpolarized). No AP = harder to get abnormal neuron firing

Question 35

Phenytoin kinetics

Answer 35

Zero order (rare) drug eliminated at constant, set rate regardless of concentration system can become saturated take more drug than body can clear --> build-up --> can lead to CNS depression

Question 36

Valproic Acid (Depakene)

Answer 36

not typical sodium blocker also blocks calcium channels increases GABA synthesis Inhibits enzyme activity that degrades GABA

Question 37

Side effects of Penytoin

Answer 37

Rash, gingival overgrowth, confusion | At high doses: CNS depression, hypotension, hyperglycemia

Question 38

Side effects of Carbamazepine and Lamotrigine

Answer 38

Rash, constipation, N/V, dizzy. Can cause drowsiness or aplastic anemia

Question 39

Side effects of Valproic acid

Answer 39

alopecia, weight gain, back pain. Tremor, pancreatitis, hepatic failure, depression

Question 40

Calcium channel blockers

Answer 40

Ethosuximide (Zarontin) Zonisamide (Zonegran) Block Calcium - block NMDA - block tonic phase

Question 41

Calcium channel modulators

Answer 41

``` Gabapentin (Neurontin) - modulator Pregabalin (Lyrica) - modulator unknown mechanism of action reduces clonic seizures may induce GABA release ```

Question 42

Side effects of Ethosuximide (Zarontin)

Answer 42

sedation, headache, GI issues, rash

Question 43

Side effects of Zonisamide (Zonegran)

Answer 43

Fatigue, dizziness, confusion, kidney stones, weight loss

Question 44

Side effects of Gabapentin (Neurontin)

Answer 44

sedation, dizziness, ataxia, weight gain, blurred vision

Question 45

How do Benzo's work to reduce seizures

Answer 45

Target GABA system typically given IV during status epilepticus inducess GABA release

Question 46

Vigabatrin (Sabril)

Answer 46

inhibits GABA transaminase --> leads to increase in GABA levels. For seizures, NOT status epilepticus Want LOTS of GABA in epilepsy

Question 47

Tiagabine (Gabitril)

Answer 47

GABA transporter blocker. Blocks reuptake from synapse, so increases synaptic levels of GABA

Question 48

Felbamate

Answer 48

Mixed mechanism | NMDA receptor antagonist --> antagonize, less calcium in so less depolarization --> less activity

Question 49

Rufinamide

Answer 49

Sodium channel blocker and metabotrophic glutamate receptor blocker

Question 50

Topiramate (Topamax)

Answer 50

Blocks sodium and calcium channels, enhances GABA and blocks AMPA/Kinate (prevents depolarization)

Question 51

Levetriacetam (Kepra)

Answer 51

disrupts vesicles to prevent release of neurotransmitters; blocks calcium channels, may increase GABA activity