anti seizure drugs Flashcards
What primarily differentiates epilepsy from a single seizure event?
A) Epilepsy is caused by provoked seizures, while a single seizure is unprovoked.
B) Epilepsy is characterized by spontaneous, recurrent seizures, while a single seizure may not recur.
C) Epilepsy is caused by genetic mutations, while a single seizure is always due to trauma.
D) Epilepsy occurs only in adults, while seizures can occur in people of any age.
b
seizures= lots of firing in the brain (abnormally excessive and synchronous firing in the brain)
epilepsy= disorder with periodic seizures and unpredictable seizures
what does it mean when epilepsy can be symptomatic or asymptomatic
symptomatic= occur due to an event (head injury)
asymptomatic= epilepsy due to genetics
Which of the following best explains why high-frequency bursts of action potentials contribute to seizure initiation?
A) High-frequency bursts result in excessive sodium influx, leading to prolonged neuronal depolarization.
B) High-frequency bursts cause potassium channels to remain permanently open, increasing hyperpolarization.
C) High-frequency bursts reduce calcium entry into neurons, thereby increasing inhibition.
D) High-frequency bursts activate the GABAergic system, reinforcing inhibitory pathways.
High-frequency bursts result in excessive sodium influx, leading to prolonged neuronal depolarization.
seizures happen due to asynchronous nueral firing and man y action potentials
Surround inhibition is critical in preventing seizure propagation because it:
A) Strengthens the refractory period, limiting excessive neuronal firing.
B) Increases the rate of neurotransmitter release at excitatory synapses.
C) Prevents excessive inhibition by blocking GABAergic activity.
D) Enhances the sensitivity of sodium channels to depolarization.
Strengthens the refractory period, limiting excessive neuronal firing.
*the refractory period is a period in which an action potential CANNOT be generated
which of the following characterizes seizure initiation?
a. scynchronous firing Gaba receptors
b. high frequency bursts of action potentials
c. asynchronous firing of nuerons
d. hyper synchronization nuerons
high frequency bursts of action potentials
hyper synchronization of a nueronal population
What is hypothesized on why do seizures often stop on their own?
A) The brain runs out of neurotransmitters like glutamate.
B) Surround inhibition is suddenly restored, shutting down activity.
C) The refractory period of neurons is extended indefinitely.
D) The seizure exhausts all available ATP, preventing further activity.
The brain runs out of neurotransmitters like glutamate.
The seizure exhausts all available ATP, preventing further activity.
glutamate is an excitatory nuerotransmitter, and seizures occur due to so much nueral excitement
Atp is needed for nuerons to fire, and drive the sodium/potassium atp ase pump
what causes the burst of synchronous action potentials?
calcium influx through NMDA receptors
Which of the following correctly describes the three phases of seizure mechanisms and their underlying processes?
A) Initiation: Loss of ion gradients → Propagation: Increase in GABAergic inhibition → Termination: Enhanced neurotransmitter release
B) Initiation: High-frequency neuronal bursts → Propagation: Breakdown of hyperpolarization and surround inhibition → Termination: Loss of ionic gradients and ATP depletion
C) Initiation: Neuronal synchronization and calcium influx → Propagation: Strengthening of refractory periods → Termination: Sustained glutamate release
D) Initiation: Increased GABAergic activity → Propagation: Excitatory neurons firing asynchronously → Termination: Accumulation of sodium in presynaptic terminals
Initiation begins with high-frequency bursts of action potentials and neuronal hypersynchronization, often driven by calcium influx through NMDA receptors.
Propagation occurs when the brain loses normal inhibitory controls, such as hyperpolarization and surround inhibition, leading to uncontrolled spread of seizure activity.
Termination is not well understood but likely involves loss of ionic gradients, depletion of ATP, neurotransmitter exhaustion (especially glutamate), and activation of inhibitory circuits (GABA).
b
alternative answer
Initiation:
High-frequency neuronal bursts → Excessive sodium (Na+) and calcium (Ca2+) influx.
NMDA receptor activation → Increased excitatory activity.
Hyper-synchronization → Neurons fire abnormally together.
Propagation:
Loss of hyperpolarization → Increased extracellular potassium (K+).
Accumulation of presynaptic calcium → Increased neurotransmitter (glutamate) release.
Failure of surround inhibition → Seizure activity spreads uncontrollably.
Termination:
Loss of ionic gradients (ATP depletion, neurotransmitter exhaustion).
Activation of inhibitory circuits (GABAergic activity increases).
Postictal period (temporary cognitive impairment, confusion, fatigue).
What key factors contribute to seizure propagation, allowing abnormal neuronal activity to spread?
A) Increased extracellular potassium, which reduces hyperpolarization, accumulation of calcium in presynaptic terminals, and activation of NMDA receptors, leading to sustained excitation.
B) Increased extracellular sodium, which enhances depolarization, accumulation of GABA, and inhibition of NMDA receptors, preventing further neuronal activation.
C) Increased extracellular chloride, causing hyperpolarization, reduced calcium accumulation, and blockade of glutamate receptors, stopping seizure activity.
D) Increased intracellular magnesium, leading to reduced neurotransmitter release, decreased NMDA activation, and prolonged refractory periods.
Explanation: During seizure propagation:
Increased extracellular potassium weakens hyperpolarization, making neurons more excitable.
Accumulated presynaptic calcium leads to excessive neurotransmitter release, amplifying excitation.
NMDA receptor activation results in further calcium influx, sustaining depolarization and preventing inhibition.
a
Why is surround inhibition lost during seizure propagation, allowing the seizure to spread uncontrollably?
A) Increased extracellular potassium blunts hyperpolarization, excessive glutamate release overwhelms inhibitory circuits, and NMDA receptor activation leads to sustained depolarization.
B) Surround inhibition is lost because GABAergic neurons are hyperactivated, leading to excessive inhibition of excitatory neurons and seizure termination.
C) Surround inhibition is lost because sodium channels become permanently inactivated, preventing excitatory neurons from continuing to fire.
D) Surround inhibition is lost because potassium influx increases, reinforcing the resting membrane potential and limiting excitatory spread.
Extracellular potassium increase reduces the brain’s ability to maintain hyperpolarization, making neurons more likely to fire.
Excessive glutamate release excites surrounding neurons, overwhelming inhibitory circuits.
NMDA receptor activation causes prolonged calcium influx, reinforcing excitatory signaling and preventing GABAergic neurons from restoring balance.
a
a disease?disorder? of a seizure lastng longer than 5 minutes or having more than one seizure in a 5 minute period, life threatening
a. status eliepticus
b. postacial period
status
condition where seizure last 5-30 minutes after seizure, characterized by drowsiness, confusion, depression, anxiety, and psychosis
a. status eliepticus
b. postacial period
postacial
the brain rebounds after lots of nueral excitement and has lots of inhibition effects
Which of the following mechanisms would be LEAST effective in stopping a seizure?
A) Blocking NMDA receptors to prevent calcium influx.
B) Enhancing GABAergic activity to increase neuronal inhibition.
C) Increasing extracellular potassium to reduce hyperpolarization.
D) Extending the refractory period of sodium channels.
Increasing extracellular potassium to reduce hyperpolarization.
identify the condition of a seizure type that starts in a specific area of the brain area. and what kind of seizures are expected:
focal seizures
kinds of focal seizures:
- simple (no loss of conciousness)
- complex (loss of conciousness)
- Jacksonian March (seizure gradually spreads through body, unusual activities that are not created conciously)
what are the differences between tonic clonic and myoclonic Generalized seizures? and what are the similarities?
all involve losing conciousness, happens without warning
tonic-clonic: seizures involve contractions of muscles with periods of muscle relaxation
myoclonic seizures have a sudden shock or contraction of muscles (localized or generalized)
what are the differences and similarities between absence and atonic non-convulsive seizures?
absence seizures: impaired conciousness, loss of awareness, subtle movements (slight turn of head), may be a period of postictal disorientation (confusion)
atonic seizures: characterized by sudden loss of muscle strength. conciousness is maintained, falls without warning
Why do anti-seizure drugs that block sodium channels often have a “use-dependent” effect?
A) They only target neurons that are firing excessively, reducing side effects on normal neurons.
B) They remain inactive unless the neuron is at resting potential.
C) They selectively bind to inhibitory neurons, amplifying their effects.
D) They are only effective if used continuously without interruptions.
They only target neurons that are firing excessively, reducing side effects on normal neurons.
What distinguishes a focal seizure from a generalized seizure?
A) Focal seizures originate in one area and may remain localized or spread, while generalized seizures involve the entire brain from onset.
B) Focal seizures always cause loss of consciousness, whereas generalized seizures never do.
C) Focal seizures are associated with muscle jerks, while generalized seizures are only characterized by absence episodes.
D) Focal seizures do not involve neurotransmitter release, while generalized seizures are triggered by excessive glutamate.
Focal seizures originate in one area and may remain localized or spread, while generalized seizures involve the entire brain from onset.
Why might a drug that enhances GABA activity cause sedation and cognitive impairment?
A) GABAergic drugs decrease the firing rate of neurons, leading to reduced overall brain activity.
B) GABAergic drugs cause a rapid influx of calcium into neurons, increasing neurotransmitter release.
C) GABAergic drugs inhibit only excitatory neurons, causing unopposed inhibition.
D) GABAergic drugs increase glutamate release, overloading the brain with excitatory signals.
GABAergic drugs decrease the firing rate of neurons, leading to reduced overall brain activity.
What is a key reason benzodiazepines are considered safer than barbiturates?
A) Benzodiazepines require the presence of GABA to exert their effects, while barbiturates can activate GABA receptors independently.
B) Benzodiazepines increase the duration of GABA receptor opening, while barbiturates only increase frequency.
C) Benzodiazepines have a lower risk of dependence compared to barbiturates.
D) Benzodiazepines can block sodium channels, whereas barbiturates cannot.
Benzodiazepines require the presence of GABA to exert their effects, while barbiturates can activate GABA receptors independently (direct gating at GABA receptor)
How do anti-Seizure drugs act?
Anti-seizure medications work by either increasing inhibition (calming the brain) or reducing excitation (preventing excessive activity). They do this by:
Blocking ion channels (sodium, calcium, potassium) to slow down brain signals.
Blocking neurotransmitter release to prevent overactive brain communication.
Affecting receptors on neurons to change how they respond to signals.
what kind of of drugs are benzodiazepines and barbiturates at the GABA a receptor and what is their overall effect?
benzodiazepines and barbiturates are positive allosteric modulaters at the Gaba A receptor,.
since they have positive allostery, they enhance the activity of GABA
How are benzodiazepines and barbiturates different and the same?
Both drugs enhance inibitory nuerons and are positive allosteric modulators at the GABA a receptor
Benzo’s
- need GABA to do its effects
- increase the frequency of GABA a receptors opening
- increases the potency of GABA
Barbiturates:
- can act as gaba agonists at high concentrations
- increase the duration og the GABA a receptors being opened (which increases the efficacy)
How are viganatrin and tiagabine similar and different?
- both enhance inhibitory nuerotransmitters
- anti seizure drugs
0 inhibit nuerotransmission in synapse of presynaptic cell
Tiagabine inhibits GABA transporter (GAT-1, in nuerons and glia), increases GABA signalling
Vigabatrin
- inhibits gaba aminotransaminase GAVA-T (an enzyme that that breaks down GABA)
*gaba-t is an enzyme that degrades GABA
