Seizure Medications in ICU

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

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

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

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

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

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

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

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

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

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

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.

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

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.

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

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.

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

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

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

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

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.

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.

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.

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.

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.

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.

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.

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

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

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.

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.

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.

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.

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.

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.

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.

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.

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.

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

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

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.

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.

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

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

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.

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.

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.

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.

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

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.

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.

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.

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.

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.

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.

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.

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

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

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

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

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

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

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

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

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

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

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.

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

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

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.

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.

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

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

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

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

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