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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

A

True

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
Q

What is PTE?

A

Post-Traumatic Epilepsy
Epilepsy following a traumatic brain injury
Can take years to develop, injury not always recognized

26
Q

Describe the neuronal network of the hippocampus

A

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
Q

Why is PTE difficult to measure in Vivo/Vitro?

A

In Vivo: too complicated, hard to understand what’s going on
In Vitro: no network, too simple

28
Q

What was found in cultured tissues following cerebral insult?

A

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
Q

Is there a loss of inhibitory cells in PTE?

A

No

There was no apparent decrease in inhibition after cerebral insult

30
Q

What factors are involved with axonal sprouting?

A

BDNF (neurotropin, involved with many homeostatic functions including axonal growth)

31
Q

How do levels of BDNF expression determine axonal growth?

A

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
Q

What happens when BDNF was blocked?

A

The formation of a recurrent network (seen in epilepsy) was inhibited as well

33
Q

What happens to BDNF levels post CA3-lesion?

A

Increased mRNA 2 hours PL, and increased protein levels 24 hours PL

34
Q

How does TrkB-Fc attenuate epilepsy PL?

A

Increases hyperexcitability of CA3 excitability neurons and increases network activity 14 days PL

35
Q

How has cannabis been found to help with epilepsy?

A

CBD helped treat epilepsy but patients developed a tolerance, leading to increased doses until toxicity symptoms presented

36
Q

What two receptors mediate most of THC’s actions and where are they found? What kind of receptors are they?

A

CB1: found mostly on neurons
CB2: found in immune system and microglia

Both are GPCRs (slow mechanism)

37
Q

What are the two endogenous messengers of the endocannabinoid system?

A

2 AG

Anandamide

38
Q

How do endogenous messengers of the endocannabinoid system act on CB1 and CB2?

A

They close presynaptic GPCRs with differing affinity

They act by closing CaVs and opening KVs via Gi/o

39
Q

What systems does endocannabinoid feedback reduce?

A

GABA, glutamate, DA, NE, 5HT, glycine, etc

40
Q

What THC/CB1 drugs are there?

A

Antagonists for CB1 receptor (CBD)

Inverse agonists for CB1 Receptor (Remonabant)

41
Q

Is CBD a CB1 agonist?

A

No

42
Q

Do we know the pharmacology of CBD?

A

No

PHAR 562 (14 decks)

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