Seizure Medications in ICU

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Questions and Answers

What is the preferred benzodiazepine for acute seizure cessation due to its longer duration of action?

  • Lorazepam (correct)
  • Phenobarbital
  • Diazepam
  • Midazolam

Which medication acts as a prodrug of phenytoin and has fewer infusion-related side effects?

  • Lacosamide
  • Valproic Acid
  • Levetiracetam
  • Fosphenytoin (correct)

What risk is particularly associated with midazolam when used for continuous infusion?

  • Respiratory depression (correct)
  • Sedation
  • Cardiovascular instability
  • Neurotoxicity

Which mechanism is associated with levetiracetam in its role as an antiepileptic drug?

<p>Inhibits neurotransmitter release by modulating SV2A (A)</p> Signup and view all the answers

In which situation is propofol typically indicated?

<p>Refractory status epilepticus unresponsive to benzodiazepines (B)</p> Signup and view all the answers

Which medication should be avoided in patients with liver dysfunction or metabolic disorders?

<p>Valproic Acid (B)</p> Signup and view all the answers

What is the primary risk associated with the use of thiopental or pentobarbital?

<p>Ventilation requirement and hemodynamic instability (A)</p> Signup and view all the answers

Which antiepileptic drug is known for its favorable side effect profile and minimal drug interactions?

<p>Levetiracetam (C)</p> Signup and view all the answers

What mechanism does phenobarbital primarily utilize in treating refractory status epilepticus?

<p>Enhances GABA-A receptor activity (D)</p> Signup and view all the answers

Which of the following describes a critical monitoring consideration for patients receiving propofol?

<p>Monitoring triglycerides and metabolic status (C)</p> Signup and view all the answers

What is the primary mechanism of action for ketamine in treating super-refractory status epilepticus?

<p>Antagonizes NMDA receptors (D)</p> Signup and view all the answers

Which of the following agents is used specifically for seizures caused by isoniazid toxicity?

<p>Pyridoxine (Vitamin B6) (D)</p> Signup and view all the answers

What is a key consideration when using corticosteroids and immunomodulators to treat seizures?

<p>They require confirmation of autoimmune etiology (C)</p> Signup and view all the answers

Which potential side effect should be monitored when administering ketamine?

<p>Tachycardia (B)</p> Signup and view all the answers

What role does continuous EEG monitoring have in the management of seizures?

<p>It helps detect non-convulsive seizures (B)</p> Signup and view all the answers

Which of the following mechanisms do magnesium sulfate employ to aid in seizure management?

<p>Blocks NMDA receptors (D)</p> Signup and view all the answers

What is the primary use of pharmacological treatment with magnesium sulfate in seizure disorders?

<p>To manage hypomagnesemia seizures (A)</p> Signup and view all the answers

What does laboratory monitoring in the context of seizure treatment typically involve?

<p>Regularly assessing drug levels and organ function (A)</p> Signup and view all the answers

What is the risk associated with many anticonvulsants and anesthetics noted in monitoring considerations?

<p>Hypotension and respiratory depression (B)</p> Signup and view all the answers

Which clinical scenario would require the use of intravenous immunoglobulin (IVIG)?

<p>Autoimmune encephalitis with confirmed diagnosis (D)</p> Signup and view all the answers

Which medication is indicated for absence seizures and is considered the drug of choice?

<p>Ethosuximide (A)</p> Signup and view all the answers

Which medication is commonly used as an adjunctive therapy for focal seizures and also for neuropathic pain?

<p>Gabapentin (D)</p> Signup and view all the answers

What is the preferred first-line benzodiazepine for managing status epilepticus in an emergency setting?

<p>Lorazepam (B)</p> Signup and view all the answers

Which of the following medications is primarily used off-label for status epilepticus treatment?

<p>Lacosamide (B)</p> Signup and view all the answers

Which antiepileptic medication is also used to treat bipolar disorder in addition to its seizure control properties?

<p>Valproic Acid (D)</p> Signup and view all the answers

Which medication is specifically indicated for treating Lennox-Gastaut syndrome?

<p>Clobazam (C)</p> Signup and view all the answers

Among the following, which medication is indicated for Dravet syndrome?

<p>Cannabidiol (A)</p> Signup and view all the answers

Which anti-seizure medication is known for utilizing AMPA receptor antagonism?

<p>Perampanel (B)</p> Signup and view all the answers

Which of the following medications is typically used for adjunctive therapy in generalized tonic-clonic seizures?

<p>Topiramate (D)</p> Signup and view all the answers

Which medication requires careful monitoring due to its risk of causing significant sedation when used intravenously?

<p>Midazolam (A)</p> Signup and view all the answers

What is the primary reason for using fosphenytoin over phenytoin in IV treatments?

<p>Fosphenytoin has fewer infusion-related side effects. (C)</p> Signup and view all the answers

Which medication is considered the first-line treatment for neonatal seizures?

<p>Phenobarbital (B)</p> Signup and view all the answers

In the context of SE treatment, what is the primary goal of using pentobarbital?

<p>To achieve burst suppression in super-refractory cases. (C)</p> Signup and view all the answers

Which of the following treatments is specifically indicated for patients with anti-NMDA receptor encephalitis?

<p>IVIG/Plasmapheresis (C)</p> Signup and view all the answers

What is a significant concern when using propofol for rapid seizure control?

<p>It is linked to propofol infusion syndrome (PRIS). (C)</p> Signup and view all the answers

Which medication is contraindicated due to its high teratogenic risk in pregnant patients?

<p>Valproic Acid (D)</p> Signup and view all the answers

What type of seizures is cannabidiol (Epidiolex) primarily used for?

<p>Lennox-Gastaut and Dravet syndrome (C)</p> Signup and view all the answers

Which of the following medications is an NMDA receptor antagonist used in super-refractory status epilepticus?

<p>Ketamine (D)</p> Signup and view all the answers

During which phase of status epilepticus should benzodiazepines be administered?

<p>Initial Phase (0–5 minutes) (C)</p> Signup and view all the answers

Which anxiolytic is preferred for its route of administration in acute seizure situations?

<p>Midazolam IM (A)</p> Signup and view all the answers

What is a key indicator of toxic levels of Dilantin (Phenytoin)?

<p>Marked diffuse delta activity (D)</p> Signup and view all the answers

Which of the following is NOT a recognized effect of chronic use of AEDs?

<p>Increased muscle strength (D)</p> Signup and view all the answers

Which side effect is specifically associated with Depakote (Valproic Acid)?

<p>Fatal liver failure (C)</p> Signup and view all the answers

What common effect does Carbamazepine (Tegretol) have on EEG readings?

<p>Diffuse slowing (C)</p> Signup and view all the answers

Which statement best describes the impact of acute intoxication with Dilantin (Phenytoin)?

<p>Increased vestibular dysfunction (A)</p> Signup and view all the answers

What is a characteristic feature of Tegretol toxicity?

<p>Drowsiness and ataxia (A)</p> Signup and view all the answers

What unusual withdrawal symptom is primarily associated with Lamictal (Lamotrigine)?

<p>Rash (B)</p> Signup and view all the answers

Which effect is associated with therapeutic doses of Depakote?

<p>Reduction or disappearance of generalized spikes (A)</p> Signup and view all the answers

What is a long-term consequence of chronic use of Phenytoin?

<p>Chronic Phenytoin Encephalopathy (A)</p> Signup and view all the answers

During withdrawal from which of the following AEDs is a rash commonly observed?

<p>Lamotrigine (D)</p> Signup and view all the answers

What is the primary reason for the limited administration of RASH?

<p>Potentially life-threatening effects (B)</p> Signup and view all the answers

What EEG findings are typically seen in non-epileptic patients treated with RASH?

<p>Widespread attenuation without slowing (D)</p> Signup and view all the answers

Which effect is NOT indicated for Topamax (topiramate)?

<p>Designed for adult epilepsy only (B)</p> Signup and view all the answers

What kind of EEG changes can lithium cause?

<p>Marked generalized slowing and spikes (A)</p> Signup and view all the answers

What side effect is commonly associated with Zarontin (ethosuximide)?

<p>Lethargy and emotional instability (D)</p> Signup and view all the answers

Which of the following statements regarding lithium and EEG is true?

<p>Triphasic patterns can be seen without indicating lesions (A)</p> Signup and view all the answers

In which scenario would EEG abnormalities be marked with lithium use?

<p>During acute intoxication (D)</p> Signup and view all the answers

Which of the following is NOT considered a primary use of Zarontin?

<p>Treatment of generalized tonic-clonic seizures (C)</p> Signup and view all the answers

Which of the following EEG findings is NOT associated with lithium intoxication?

<p>Increased alpha activity (B)</p> Signup and view all the answers

What role does Zarontin specifically play in the treatment of epilepsy?

<p>It is the main AED for absence epilepsy (D)</p> Signup and view all the answers

What is the primary action of SV2A modulators in the context of antiepileptic drugs?

<p>Moderate neurotransmitter release to stabilize neuronal activity (D)</p> Signup and view all the answers

Which mechanism is NOT primarily associated with sodium and calcium channel blocking antiepileptic drugs?

<p>Increasing the frequency of dopamine release (D)</p> Signup and view all the answers

How do AMPA receptor antagonists help in seizure management?

<p>By blocking excitatory signals from glutamate (C)</p> Signup and view all the answers

What is a key function of carbonic anhydrase inhibitors in antiepileptic therapy?

<p>They alter the pH balance in neurons (C)</p> Signup and view all the answers

Which antiepileptic drug primarily functions as a potassium channel opener?

<p>Retigabine (C)</p> Signup and view all the answers

Which of the following accurately describes the function of ethosuximide in epilepsy treatment?

<p>It specifically targets T-type calcium channels (C)</p> Signup and view all the answers

What effect does retigabine primarily have on neuronal activity?

<p>Opens potassium channels to stabilize membrane potential (A)</p> Signup and view all the answers

What is the primary result of using GABA modulators in the brain?

<p>Increased inhibitory signals within the central nervous system (A)</p> Signup and view all the answers

Which antiepileptic drug primarily functions as an NMDA receptor antagonist?

<p>Perampanel (A)</p> Signup and view all the answers

How do sodium channel blockers primarily affect excessive neuronal firing?

<p>By stabilizing the inactive state of sodium channels (D)</p> Signup and view all the answers

What is the primary effect of enhancing GABA's action in the context of antiepileptic drugs?

<p>Hyperpolarization of neurons leading to decreased excitability (C)</p> Signup and view all the answers

In what way do NMDA receptor antagonists contribute to seizure control?

<p>By reducing excitatory neurotransmission (C)</p> Signup and view all the answers

Which mechanism is involved in the activity of calcium channel blockers as AEDs?

<p>Limiting calcium influx to dampen neurotransmitter release (B)</p> Signup and view all the answers

What role do benzodiazepines play in the context of GABA receptors as AEDs?

<p>They enhance the effects of GABA by increasing chloride influx (A)</p> Signup and view all the answers

Which analogy best describes the action of sodium channel blockers in the control of seizures?

<p>A brake that slows down moving vehicles (C)</p> Signup and view all the answers

Which drug is commonly associated with enhancing GABA availability as a mechanism to control seizures?

<p>Valproic Acid (D)</p> Signup and view all the answers

How do NMDA receptor antagonists function in the context of excitatory neurotransmission?

<p>They block excitatory signals (C)</p> Signup and view all the answers

What is the role of calcium channels specifically referenced in absence epilepsy?

<p>To regulate neurotransmitter release (D)</p> Signup and view all the answers

Which of the following EEG changes is NOT typically associated with therapeutic levels of Dilantin (Phenytoin)?

<p>Marked diffused delta activity (D)</p> Signup and view all the answers

What EEG finding is most indicative of Dilantin (Phenytoin) toxicity?

<p>Marked diffused delta activity (B)</p> Signup and view all the answers

Which of the following is a potential long-term effect of chronic Dilantin (Phenytoin) use?

<p>Gum hypertrophy (A)</p> Signup and view all the answers

What neurological sign would be least expected during acute intoxication with Dilantin (Phenytoin)?

<p>Improved cognitive function (A)</p> Signup and view all the answers

Which of the following is a common effect of Tegretol on EEG?

<p>Diffuse slowing (A)</p> Signup and view all the answers

Which of the following is a sign of Tegretol toxicity?

<p>Nystagmus (A)</p> Signup and view all the answers

What change on an EEG can be expected when Depakote is working to reduce seizures??

<p>Reduction of generalized spikes (C)</p> Signup and view all the answers

What is a side effect of Depakote (Valproic Acid Valproate)?

<p>Tiredness (B)</p> Signup and view all the answers

What is the most common factor that would cause a patient to withdraw from Lamictal (lamotrigine)?

<p>RASH (A)</p> Signup and view all the answers

Which option is true about the effects of Lamictal(lamotrigine) on EEGs for those without epilepsy?

<p>Shows widespread attenuation but no slowing (B)</p> Signup and view all the answers

Which statement is true about Lamictal(lamotrigine) and EEGs for those who have epilepsy?

<p>NO slowing in epileptic patients! (A)</p> Signup and view all the answers

Which statement is true about Topamax (topiramate)?

<p>Multiple modes of action (C)</p> Signup and view all the answers

What is true about reports of Topamax(topiramate) on EEG readings?

<p>No reports of EEG correlate (D)</p> Signup and view all the answers

Which of the following is true regarding lithium's effects on EEG?

<p>Can lead to diverse &amp; prominent EEG changes (C)</p> Signup and view all the answers

Which of the following is a potential effect of lithium on EEG?

<p>PDR slowing (B)</p> Signup and view all the answers

What EEG abnormalities are typical during lithium intoxication?

<p>Diffuse slow waves (C)</p> Signup and view all the answers

Which of the following are NOT evidence of structural lesion?

<p>Occasional spikes &amp; frontal slowing (D)</p> Signup and view all the answers

What type of epilepsy does Zarontin (ethosuximide) primarily treat?

<p>Absence Epilepsy (A)</p> Signup and view all the answers

Which is the following is NOT a side effect of Zarontin (ethosuximide)?

<p>Hyperactivity (C)</p> Signup and view all the answers

What part of the brain do Intermittent rhythmic deltas tend to be most prominent in, when seen on EEGs?

<p>Frontal or occipital regions (C)</p> Signup and view all the answers

What is a potential alternative to Zarontin today?

<p>Lamictal (B)</p> Signup and view all the answers

Flashcards

Ketamine

A drug used for super refractory status epilepticus (SRSE), acting as an NMDA receptor antagonist with neuroprotective effects.

Pyridoxine (Vitamin B6)

The drug used for seizures caused by pyridoxine-dependent epilepsy or isoniazid toxicity.

Magnesium Sulfate

Used for seizures caused by eclampsia or hypomagnesemia. Blocks NMDA receptors and stabilizes neuronal membranes.

Continuous EEG

A continuous record of brain activity used for detecting non-convulsive seizures or assessing treatment efficacy.

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Hemodynamic Support

Monitoring of blood pressure and heart rate crucial for managing potential adverse effects of anticonvulsants and anesthetics.

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Laboratory Monitoring

Regular monitoring of drug levels (e.g., phenytoin, valproic acid) and organ function (liver, kidney) to ensure medication efficacy and patient safety.

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Corticosteroids and Immunomodulators

Steroids and agents that modulate immune responses, used for autoimmune encephalitis or seizures with immune-mediated causes.

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Methylprednisolone

Steroid used for autoimmune encephalitis or seizures with immune-mediated causes.

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Intravenous Immunoglobulin (IVIG)

A protein-based therapy used for autoimmune encephalitis or seizures with immune-mediated causes.

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Plasmapheresis

A procedure that removes harmful antibodies from the blood, used for autoimmune encephalitis or seizures with immune-mediated causes.

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Benzodiazepines

A class of drugs that enhance the activity of GABA-A receptors, leading to increased inhibitory neurotransmission in the brain, reducing neuronal excitability. This action helps to suppress seizures.

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Lorazepam (Ativan)

A common benzodiazepine used for acute seizure cessation, known for its longer duration of action in the central nervous system.

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Phenytoin/Fosphenytoin

A second-line medication used for status epilepticus when benzodiazepines fail. It blocks voltage-gated sodium channels, stabilizing neuronal membranes and decreasing the chance of firing.

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Levetiracetam (Keppra)

A newer anti-epileptic drug increasingly replacing traditional second-line agents. It modulates a specific protein involved in neurotransmitter release, reducing excessive firing.

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Propofol (Diprivan)

A general anesthetic commonly used for refractory status epilepticus unresponsive to typical medications. It potentiates the activity of GABA-A receptors, leading to deep sedation.

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Thiopental/Pentobarbital

A powerful anesthetic used for status epilepticus requiring barbiturate coma induction, providing deep sedation and halting seizure activity.

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Anti-Epileptic Drugs (AEDs)

A class of drugs commonly used for seizures that function by blocking voltage-gated sodium channels, stabilizing neuronal membranes by preventing excessive firing.

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Valproic Acid (Depakote)

A specific AED used for seizures, especially focal seizures. It increases GABA availability and modulates sodium and calcium channels, reducing neuronal hyperexcitability.

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Lacosamide (Vimpat)

An AED adjunct therapy for seizures, particularly in focal seizures. It enhances the slow inactivation of sodium channels, reducing the frequency of action potentials.

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Propofol (Diprivan)

An anesthetic used in extreme cases of status epilepticus when traditional medications fail. It enhances GABA-A receptor activity and inhibits NMDA receptors, suppressing excessive neuronal activity.

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Fosphenytoin

A medication used as a second-line treatment for status epilepticus, when benzodiazepines are ineffective. It works by blocking sodium channels, stabilizing neuronal membranes and reducing the likelihood of excessive neuronal firing. It's often preferred over phenytoin due to improved IV tolerability.

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Valproic Acid

A commonly used anti-epileptic medication for status epilepticus, especially when benzodiazepines fail. It's often the first-line choice for neonatal seizures. It exerts its effects by increasing GABA levels and modulating sodium and calcium channels.

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Levetiracetam

A newer anti-epileptic drug with a favorable safety profile and fewer drug interactions. It's commonly employed for status epilepticus when traditional medications fail.

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Propofol

A powerful general anesthetic used for refractory status epilepticus when traditional medications fail. It potentiates the activity of GABA-A receptors, leading to deep sedation and suppression of seizures.

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Pentobarbital

A potent anesthetic agent reserved for super-refractory status epilepticus when other medications fail. It induces a burst suppression pattern on the EEG, effectively halting seizures by drastically reducing brain activity.

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Super-Refractory Status Epilepticus

A phase in status epilepticus lasting more than 24 hours, characterized by persistent seizure activity despite maximal medical therapy. It requires intensive management and potentially specialized interventions.

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Status Epilepticus Treatment Protocol

A treatment protocol designed to manage status epilepticus, consisting of sequential phases with escalating treatment options based on the duration and severity of seizures.

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Refractory Status Epilepticus

A specific type of status epilepticus where seizures continue despite aggressive treatment with conventional medications. It requires more specialized and aggressive therapeutic approaches.

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What are ASMs used for?

Anti-seizure medications (ASMs) aim to control seizures in outpatient settings. They work by blocking or modulating the activity of specific channels or receptors in the brain, affecting neuronal excitability and reducing the likelihood of seizures.

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How does Phenytoin (Dilantin) work?

Phenytoin blocks sodium channels, reducing the electrical activity that triggers seizures. It's effective for focal seizures, including those that can progress to generalized tonic-clonic seizures.

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What is Carbamazepine (Tegretol) used for?

Carbamazepine, another sodium channel blocker, is used for focal and generalized tonic-clonic seizures. It also helps with trigeminal neuralgia, a painful facial nerve condition.

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How does Ethosuximide (Zarontin) work?

Ethosuximide specifically targets calcium channels, particularly in the thalamus, a brain region essential for controlling absence seizures. It's the go-to drug for these seizures.

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What is Gabapentin (Neurontin) used for?

Gabapentin, a calcium channel modulator, is often used as an add-on therapy for focal seizures and also helps manage neuropathic pain caused by nerve damage.

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How does Phenobarbital work?

Phenobarbital increases the effects of GABA, an inhibitory neurotransmitter, leading to reduced neuronal excitability. It's valuable for treating generalized tonic-clonic seizures, focal seizures, and as an alternative for status epilepticus.

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How does Levetiracetam (Keppra) work?

Levetiracetam targets SV2A, a protein involved in neurotransmitter release, effectively modulating neuronal communication and reducing the chances of seizures. It's effective for a range of seizure types, including generalized and focal seizures.

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What makes Valproic Acid (Depakote) so versatile?

Valproic Acid has a broad spectrum of action, affecting multiple mechanisms like increasing GABA levels, modulating sodium and calcium channels, and influencing neuronal excitability. It's highly versatile for treating various types of seizures.

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How does Topiramate (Topamax) work?

Topiramate, like Valproic Acid, has a wide-ranging action on brain activity. It inhibits glutamate release, enhancing GABA effects, and modulating sodium and calcium channels. It's effective for focal, generalized, and Lennox-Gastaut seizures.

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How does Lorazepam (Ativan) work?

Lorazepam, a benzodiazepine, enhances the effects of GABA, a calming neurotransmitter. This leads to reduced neuronal activity, effectively controlling seizures.

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Topamax (topiramate)

A powerful antiepileptic drug used in the treatment of partial and childhood epilepsies. It acts through several mechanisms but has no reported EEG correlates.

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Zarontin (ethosuximide)

This medication is primarily used for absence seizures but is being replaced by Depakote and Lamictal. It can cause side effects like somnolence, lethargy, emotional instability, and altered vigilance on EEG.

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Lithium (not an AED)

This medication is not an antiepileptic drug (AED) but can induce various EEG changes. It can cause slowing, rhythmic delta activity, triphasics, and occasional spikes.

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Zarontin (ethosuximide)

This medication is not an AED, but it's the primary treatment for absence seizures. It is being replaced by Depakote and Lamictal.

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RASH (rapid acting sodium channel blocker)

A medication that has a significant impact on spontaneous and photosensitive generalized spikes and waves.

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Topamax (topiramate)

A powerful antiepileptic drug with multiple modes of action that is effective in the treatment of partial and childhood epilepsies. Its effects can be difficult to detect on an EEG.

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RASH (rapid acting sodium channel blocker)

This antiepileptic drug is known for its marked decreasing effect on the occurrence and frequency of spontaneous and photosensitive generalized spikes and waves, spike-and-wave discharges.

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RASH (rapid acting sodium channel blocker)

A medication that is potentially life-threatening when used in children. It can cause widespread attenuation in the EEG but no slowing in non-epileptic patients.

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RASH (rapid acting sodium channel blocker)

A medication that is effective at reducing the frequency of seizures, specifically spontaneous and photosensitive generalized spikes and waves. It does not cause any significant slowing on the EEG.

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Zarontin (ethosuximide)

A medication used for absence seizures; however, it's less commonly prescribed now, replaced by drugs such as Depakote and Lamictal.

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What is the effect of Dilantin on the EEG at therapeutic levels?

Dilantin (Phenytoin) and Cerebyx (Phosphenytoin) can increase theta-range slow waves in the EEG, which is a sign of therapeutic levels. This is unlike other anti-epileptic drugs like benzodiazepines and barbiturates, which increase fast activity.

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How does Dilantin toxicity show up on the EEG?

High levels of Dilantin, or Cerebyx, can cause a distinctive EEG pattern with marked diffused delta activity, paroxysmal slow wave abnormalities, and possibly cerebellar atrophy.

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What long-term side effects can occur with chronic Dilantin use?

Chronic use of Dilantin is associated with cerebellar atrophy and chronic phenytoin encephalopathy. This encephalopathy can alter seizure patterns, leading to increased tonic and opisthotonic components, lower seizure frequency, and characteristic facial features.

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What are the symptoms of acute Dilantin intoxication?

Acute Dilantin intoxication presents with cerebellar dysfunction – potentially mimicking a cerebellar tumor – alongside cognitive impairment, pyramidal signs, and movement disorders. In some cases, it may even trigger seizures.

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What effect does Tegretol have on the EEG?

Carbamazepine (Tegretol) often doesn't significantly change the background frequency on the EEG. However, it can cause generalized paroxysmal activity, like spikes, which may indicate potential for seizures.

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What are the signs of Tegretol toxicity?

High doses of Tegretol can lead to a range of symptoms, including ataxia, nystagmus, diplopia, drowsiness, and diffuse EEG slowing. Notably, it can also worsen seizures.

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How does Depakote affect the EEG in therapeutic doses?

Depakote (Valproic Acid/Valproate) is known for its potential to reduce or even eliminate generalized spikes on the EEG, often leading to a corresponding decrease in seizures. In therapeutic doses, it may have a minimal effect on background activity.

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How does Depakote toxicity manifest on the EEG?

High doses of Valproic Acid can cause marked diffuse slowing on the EEG, with high variability in prognosis for patients who attempt suicide.

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Why is a rash the most common reason for discontinuing Lamotrigine?

The most common reason for withdrawal from Lamotrigine is an allergic reaction (rash). This is why close monitoring for any skin changes is important.

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What is a serious side effect of Depakote?

Depakote (Valproic Acid) can cause fatal liver failure. With this risk in mind, it's crucial to monitor liver function regularly during Depakote therapy.

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Sodium and Calcium Channel Blockers

AEDs that target sodium and calcium channels in neurons, reducing the likelihood of excessive firing.

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GABA Modulators

AEDs that enhance the activity of GABA, an inhibitory neurotransmitter, leading to reduced neuronal excitability.

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NMDA and AMPA Receptor Antagonists

AEDs that reduce excitatory signals by blocking NMDA and AMPA receptors, which are involved in fast neurotransmission.

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SV2A Modulators

AEDs that bind to SV2A, a protein involved in neurotransmitter release, controlling the release of neurotransmitters and stabilizing neuronal activity.

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AMPA Receptor Antagonists

AEDs that block AMPA receptors, ultimately leading to a reduction in excitatory signals and a decreased likelihood of seizures.

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Topiramate (Topamax)

AEDs that enhance GABA effects, inhibit glutamate release, and modulate sodium and calcium channels, leading to a broad spectrum of action.

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Sodium Channel Blockers

A class of AEDs that work by blocking voltage-gated sodium channels, stabilizing neuronal membranes and preventing excessive firing.

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Anti-Seizure Medications (ASMs)

A class of drugs that work specifically by blocking or modulating the activity of certain channels or receptors in the brain, directly affecting neuronal excitability.

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How do sodium channels work?

Voltage-gated sodium channels open to allow sodium ions (Na⁺) to flow into the neuron, causing depolarization and triggering electrical signals.

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How do sodium channel blockers work?

Sodium channel blockers bind to these channels, primarily in their open or inactivated state, reducing neuronal firing and the spread of seizure activity.

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How does GABA work to inhibit neuronal activity?

GABA, the brain's main inhibitory neurotransmitter, binds to its receptor (GABA receptor), allowing chloride ions (Cl⁻) to flow into the neuron and make it less likely to fire.

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How do GABA receptor modulators work?

GABA receptor modulators enhance GABA's effects by increasing chloride influx, resulting in hyperpolarization (harder for neurons to fire). Some drugs also increase GABA levels by inhibiting its breakdown or reuptake.

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How do NMDA receptors work?

NMDA receptors are a type of glutamate receptor that mediate excitatory neurotransmission. They allow calcium (Ca²⁺) and sodium (Na⁺) to flow into neurons when activated, promoting synaptic plasticity and excitability.

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How do NMDA receptor antagonists work?

NMDA receptor antagonists block these receptors, reducing excitatory signals and preventing seizure propagation.

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How do calcium channels contribute to seizures?

Calcium channels, particularly T-type, regulate neurotransmitter release and neuronal excitability. Overactive calcium channels can contribute to seizures, especially in absence epilepsy.

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How do calcium channel blockers work?

Calcium channel blockers reduce calcium influx, dampening neuronal activity and reducing seizure activity.

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Name some examples of sodium channel blockers.

Phenytoin, Carbamazepine, Oxcarbazepine, Lamotrigine, and Lacosamide are examples of sodium channel blockers.

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Name some examples of GABA receptor modulators.

Benzodiazepines (Lorazepam, Diazepam), Barbiturates (Phenobarbital), and Valproic Acid are examples of GABA receptor modulators.

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AEDs

A class of drugs used to treat seizures.

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Tegretol Toxicity

Medication toxicity that can be demonstrated by color vision tests.

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Lamictal (Lamotrigine)

An anti-epileptic drug that is associated with a rash.

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Fatal Liver Failure

A potentially fatal side effect caused by Depakote.

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Marked diffuse slowing

Diffuse slowing on EEG

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No change in background frequency

When a medication has minimal effect on the background frequency.

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Diplopia

Visual disturbance in the eye, seeing double.

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Ataxia

Lack of coordination.

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Nystagmus

Involuntary eye movement.

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Somnolence

Feeling of sleepiness.

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Lethargy

Being abnormally sleepy or tired.

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Emotional Instability

Unstable or rapidly changing feelings.

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Altered Vigilance

Decreased alertness or attention span.

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PDR Slowing

Slowing of the posterior dominant rhythm.

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Non-epileptic patients

EEG may show widespread attenuation but no slowing

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Study Notes

  • This is an update to existing study notes with new information
  • The final output contains all existing information from the previous notes, with the new information integrated appropriately

Medications for Seizures and Status Epilepticus (SE) in ICU

  • Benzodiazepines (First-Line):

    • Lorazepam (Ativan): Preferred for IV administration for status epilepticus. Rapid onset and longer CNS action, potential for respiratory depression and hypotension.
    • Midazolam (Versed): Used for continuous infusions in refractory cases, or for prehospital/early ICU management via intranasal, buccal, or IM routes. Effective for continuous infusions in refractory cases.
    • Diazepam (Valium, Diastat): IV or rectal gel for acute seizures.
    • Mechanism: Enhance GABA-A receptor activity for increased inhibition.
  • Anti-Epileptic Drugs (AEDs) (Second-Line):

    • Phenytoin/Fosphenytoin (Cerebyx): Fosphenytoin preferred due to better IV tolerance, second-line for SE if benzodiazepines fail. Blocks voltage-gated sodium channels. Monitor for arrhythmias and hypotension.
      • At therapeutic levels, it does not increase fast activities, unlike benzodiazepines and barbiturates.
      • Influence on Interictal Epileptiform Discharges (IEDs) is mixed.
      • Withdrawal is used to provoke seizures in Epilepsy Monitoring Units (EMUs).
      • May increase theta-range slow waves.
      • At toxic levels, it can trigger marked diffused delta activity, paroxysmal slow wave abnormalities, and cerebellar atrophy.
      • Chronic use can lead to cerebellar atrophy, chronic phenytoin encephalopathy (changes in seizure pattern, increased tonic and opisthotonic components), lowered Posterior Dominant Rhythm (PDR) frequency, gum hypertrophy, and coarsening of facial features.
      • Acute intoxication can cause cerebellovestibular dysfunction (may be mistaken for cerebellar tumor), altered cognitive function, pyramidal signs, extra-pyramidal movement disorders and may exacerbate epileptic seizures.
    • Levetiracetam (Keppra): Increasingly used as second- or adjunct therapy, well-tolerated with fewer drug interactions; IV form available. Modulates synaptic vesicle protein SV2A to inhibit neurotransmitter release.
    • Valproic Acid (Depakote): Alternative second-line, especially for focal seizures; IV form available. Increases GABA availability; modulates sodium and calcium channels. Avoid in liver dysfunction or metabolic disorders.
      • At therapeutic doses, there may be no significant change in background activity or diffuse slowing, depending on the source.
      • It can reduce or even eliminate generalized spikes, with photosensitive spikes disappearing.
      • Toxic levels may cause marked diffuse slowing and are associated with high variability in the prognosis of suicide attempts, including tiredness.
      • Side effects include the potential for fatal liver failure.
    • Lacosamide (Vimpat): Adjunct therapy for SE, particularly in focal seizures; IV form available. Enhances slow inactivation of sodium channels. Well-tolerated with minimal sedation.
    • Phenobarbital: Alternative for refractory cases, neonates, or when other agents fail, has a long half-life. Enhances GABA-A receptor activity and decreases glutamate release. Risks respiratory depression and sedation.
    • Carbamazepine (Tegretol): May cause diffuse slowing, has minimal effect on background frequency, but can increase generalized paroxysmal activity, including spikes.
      • Toxicity can be detected through color vision tests.
      • Clinical signs of toxicity include ataxia, nystagmus, diplopia, drowsiness and diffuse slowing on EEG; it may also exacerbate seizures.
  • Anesthetics for Refractory Status Epilepticus:

    • Propofol (Diprivan): For RSE unresponsive to benzodiazepines and AEDs. Potentiates GABA-A receptor activity & inhibits NMDA receptors. Risk of Propofol Infusion Syndrome (PRIS) with prolonged use. Monitor triglycerides and metabolic status.
    • Thiopental/Pentobarbital: For RSE requiring barbiturate coma induction. Potentiation of GABA-A receptor activity, producing deep sedation/coma. Requires mechanical ventilation and close hemodynamic monitoring. Reserved for super-refractory status epilepticus (SRE).
    • Ketamine: Adjunct in super-refractory status epilepticus (SRSE) with potent NMDA receptor antagonism. Provides neuroprotective effects and additional analgesia. Increased risk of tachycardia and increased intracranial pressure.
    • Inhalational Agents (Isoflurane, desflurane): For refractory seizures in extreme cases.
  • Corticosteroids & Immunomodulators:

    • Methylprednisolone, IVIG, Plasmapheresis: Used for autoimmune encephalitis or immune-mediated seizures. Confirmation of autoimmune etiology is crucial.
  • Other Agents:

    • Pyridoxine (Vitamin B6): For seizures due to pyridoxine-dependent epilepsy or isoniazid toxicity. Corrects deficiency in the GABA synthesis cofactor.
    • Magnesium Sulfate: Used for seizures from eclampsia or hypomagnesemia. Blocks NMDA receptors & stabilizes neuronal membranes.
    • Lamotrigine (Lamictal): Rash is a common cause of withdrawal, limiting its use in children due to potential life-threatening reactions.
      • In non-epileptic patients, EEG shows widespread attenuation without slowing, but there is no slowing observed in epileptic patients.
      • It markedly decreases the occurrence and frequency of spontaneous and photosensitive generalized spikes and waves, and spike-and-wave discharges.
      • Toxicity is low with only reports of QRS prolongation.
    • Topiramate (Topamax): It is a powerful AED used in partial & childhood epilepsies, with multiple modes of action, but with no reported EEG correlates.
    • Lithium (not an AED): It can lead to diverse & prominent EEG changes:
      • EEG changes include PDR slowing and increased diffuse slowing, intermittent rhythmic delta most prominent in frontal or occipital regions, and triphasics.
      • Occasional spikes and frontal slowing should not be considered evidence of a structural lesion.
      • Intoxication is marked by EEG abnormalities like diffuse slow waves, triphasics, and multifocal epileptiform discharges.
    • Ethosuximide (Zarontin): It is mainly used for absence epilepsy but is being that is replaced by Depakote and Lamictal.
      • Side effects include somnolence, lethargy, emotional instability, and altered vigilance on EEG.

ICU Monitoring and Considerations

  • Continuous EEG: Essential for detecting non-convulsive seizures and measuring treatment effectiveness.
  • Hemodynamic Support: Anticonvulsants & anesthetics can cause hypotension and respiratory depression. Close monitoring of blood pressure and oxygen saturation is critical.
  • Laboratory Monitoring: Regularly assess drug levels (e.g., phenytoin, valproic acid) and organ function (liver, kidneys). Monitor relevant lab values for renal and hepatic function.

Status Epilepticus Treatment Protocol (Updated)

  • Initial Phase (0–5 minutes):

    • Benzodiazepines (Lorazepam IV, Midazolam IM/IV/intranasal/buccal, or Diazepam IV/rectal).
  • Second Phase (5–20 minutes):

    • Fosphenytoin, Valproic Acid IV, or Levetiracetam IV.
    • Lacosamide IV (alternative).
  • Third Phase (>20 minutes):

    • Continuous infusions: Midazolam, Propofol, or Pentobarbital. Consider continuous infusion therapy after 20 minutes to quickly and efficiently manage seizures.
    • Adjuncts: Ketamine, corticosteroids, or immune-modulating agents. Adjust treatment strategies to individual needs and seizure patterns.
  • Super-Refractory Phase (>24 hours):

    • Burst suppression strategy with continuous infusions of suitable agents.
    • Alternative therapies: Ketamine, inhalational anesthetics, or surgical options (e.g., VNS, responsive neurostimulation). Consider surgical options in severe cases, such as VNS or responsive neurostimulation.

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