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PHAR 562 > Epilepsy > Flashcards

Epilepsy Flashcards

1
Q

What is the basic definition of all types of epilepsy?

A

A sudden, excessive depolarization of some/all cerebral neurons

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2
Q

What differentiates a focal/partial seizure from a generalized seizure?

A

If the cerebral tissue affected is localised: focal/partial

If cortical neurons are also affected: generalized

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3
Q

What are the two types of partial seizures and the three types of generalized seizures?

A

Simple partial
Complex partial

Tonic-clonic
Absence
Myoclonic

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4
Q

What happens if a seizure occurs in the Motor area?

A

Seizures may cause abnormal movements

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5
Q

What happens if a seizure occurs in the Sensory area?

A

Seizures may cause tingling, numbness or burning in an area of the body

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6
Q

What happens if a seizure occurs in the Olfactory area?

A

Seizures may cause intense, unpleasant smells

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7
Q

What happens if a seizure occurs in the Auditory area?

A

Seizures may cause auditory hallucinations such as buzzing or ringing sounds

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8
Q

What happens if a seizure occurs in the Visual area?

A

Seizures may cause visual disturbances

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9
Q

What are the 6 factors that can trigger seizures?

A 
Strobe lights
Stress
(lack of) sleep
Overeating
Alcohol
Drugs
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10
Q

What is status epilepticus?

A

A medical emergency defined by more than 30 minutes of continuous seizure activity
or
Two or more sequential seizures spanning this period without full recovery between seizures

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11
Q

What is the first symptom of having a brain tumor?

A

Seizure

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12
Q

How can genetics lend a predisposition to epilepsy?

A

Cannelopathies can be passed down

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13
Q

What is the largest relative risk of developing epilepsy besides a brain tumor?

A

Stroke and Hemorrage

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14
Q

How can you cure epilepsy?

A

You can’t. It can only be treated with Antiepileptic drugs

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15
Q

What are some considerations when choosing an antiepileptic drug? (6)

A 
Seizure type
Pharmacokinetic profile
Interactions/other medical conditions
Efficacy
Expected adverse effects
Cost
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16
Q

What are the (4) putative mechanisms of action for AEDs?

A 
Sodium channels
Calcium channels
GABAergic synapses
Other targets (eg glutamate receptors)
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17
Q

True/False? AEDs have good absorption/bioavailability

18
Q

Where does metabolism of most AEDs take place? When would this be an issue?

A

In the liver

If a brain tumor metastasizes to the liver can cause complications

19
Q

What is a symptom of many classic AEDs?

A

CNS sedation

20
Q

What are 4 mechanisms of action of AEDs?

A

Enhancing GABA synaptic transmission
Reducing Cell membrane permeability to voltage-dependent sodium channels
Reducing cell membrane permeability to Calcium T-Channels
Inhibiting excitatory neurotransmitter glutamate

21
Q

What needs to be considered when blocking Na channels as a treatment to epilepsy?

A

You want to block Na channels in the brain but not the heart

22
Q

Why is ethosuximide important?

A

Inhibits T-Type Ca channels (important in rhythm generation)

Useful for Absence seizures

23
Q

Define Post Traumatic Epilepsy and it’s recommended treatment course

A

Epilepsy caused by brain injury, can take years to develop

Use AED within 7 days of injury and maintain use for 3-6 months to minimize further brain damage

24
Q

What happens if a patient does not respond to antiepileptic drugs?

A

Surgical intervention might be necessary
Resection/transection of noneloquent brain

Responsive neurostimulation (electrodes are implanted either in/on surface of epileptogenic tissue

25
What is PTE?
Post-Traumatic Epilepsy Epilepsy following a traumatic brain injury Can take years to develop, injury not always recognized
26
Describe the neuronal network of the hippocampus
CA3 pyramidal cells (excitatory) connect to CA1 cells around the hippocampus CA3 cells form connections within themselves, and sends connections to CA1 which then project out to the rest of the brain CA1 cells don't interconnect as much Common site for lesion therapy
27
Why is PTE difficult to measure in Vivo/Vitro?
In Vivo: too complicated, hard to understand what's going on In Vitro: no network, too simple
28
What was found in cultured tissues following cerebral insult?
Excitatory connections were being made in excess, and more interconnections were being formed as well This could tip the scale in the excitatory/inhibitory balance and lead to PTE
29
Is there a loss of inhibitory cells in PTE?
No | There was no apparent decrease in inhibition after cerebral insult
30
What factors are involved with axonal sprouting?
BDNF (neurotropin, involved with many homeostatic functions including axonal growth)
31
How do levels of BDNF expression determine axonal growth?
BDNF gene lead to proBDNF protein, which can be cleaved into mature BDNF Mature BDNF binds TrkB proBDNF binds to p75 Depending on levels of each, different receptors will be favored (on the same synapse)
32
What happens when BDNF was blocked?
The formation of a recurrent network (seen in epilepsy) was inhibited as well
33
What happens to BDNF levels post CA3-lesion?
Increased mRNA 2 hours PL, and increased protein levels 24 hours PL
34
How does TrkB-Fc attenuate epilepsy PL?
Increases hyperexcitability of CA3 excitability neurons and increases network activity 14 days PL
35
How has cannabis been found to help with epilepsy?
CBD helped treat epilepsy but patients developed a tolerance, leading to increased doses until toxicity symptoms presented
36
What two receptors mediate most of THC's actions and where are they found? What kind of receptors are they?
CB1: found mostly on neurons CB2: found in immune system and microglia Both are GPCRs (slow mechanism)
37
What are the two endogenous messengers of the endocannabinoid system?
2 AG | Anandamide
38
How do endogenous messengers of the endocannabinoid system act on CB1 and CB2?
They close presynaptic GPCRs with differing affinity They act by closing CaVs and opening KVs via Gi/o
39
What systems does endocannabinoid feedback reduce?
GABA, glutamate, DA, NE, 5HT, glycine, etc
40
What THC/CB1 drugs are there?
Antagonists for CB1 receptor (CBD) | Inverse agonists for CB1 Receptor (Remonabant)
41
Is CBD a CB1 agonist?
No
42
Do we know the pharmacology of CBD?
No

PHAR 562 (14 decks)

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