Lacosamide Works by Calming Overactive Brain Cells That Cause Seizures

If you've been prescribed Lacosamide (brand name Vimpat) for seizures, you might be curious about how it actually works. Understanding your medication can help you feel more confident about your treatment — and it's not as complicated as it sounds.

Here's the short version: Lacosamide helps stabilize overexcited nerve cells in the brain by slowing down the electrical signals that trigger seizures.

Now let's break that down in plain English.

What Happens in Your Brain During a Seizure

Your brain runs on electricity. Billions of nerve cells (neurons) communicate by sending tiny electrical signals to each other. Normally, this happens in an organized, controlled way.

During a seizure, something goes wrong. A group of neurons starts firing too rapidly and out of control — like a traffic jam of electrical signals. This abnormal burst of activity is what causes the symptoms of a seizure, whether it's a momentary blank stare, jerking movements, or a full-body convulsion.

How Lacosamide Calms Things Down

To send electrical signals, neurons rely on tiny gates called sodium channels. Think of sodium channels like doors that open and close rapidly, allowing electrical current to flow through the neuron. When these doors open too fast or too often, neurons fire too quickly — and that's when seizures happen.

Most seizure medications work by blocking these sodium channel "doors" when they're open. Lacosamide does something slightly different — and this is what makes it unique.

Slow Inactivation vs. Fast Inactivation

Sodium channels have two ways of shutting down:

• Fast inactivation: The channel closes quickly after opening (milliseconds). Most older seizure medications like Carbamazepine, Phenytoin, and Lamotrigine target this.
• Slow inactivation: The channel enters a deeper "rest" state where it can't be activated for a longer period. Lacosamide selectively enhances this slow inactivation.

Think of it like this: imagine a hyperactive child bouncing off the walls. Fast inactivation is like briefly holding them still — they'll start bouncing again the moment you let go. Slow inactivation is more like getting them to take a nap — a deeper, more sustained calm.

By enhancing slow inactivation, Lacosamide preferentially targets neurons that are already firing too rapidly (the ones causing seizures) while having less effect on normal brain activity. This is why many patients find Lacosamide causes fewer cognitive side effects compared to some older medications.

CRMP-2 Binding

Lacosamide also binds to a protein called CRMP-2 (collapsin response mediator protein-2). Scientists believe this may play a role in the drug's antiseizure effects, but the exact contribution is still being studied. CRMP-2 is involved in nerve cell growth and signaling, and its role in Lacosamide's mechanism adds another layer of uniqueness to this medication.

How Long Does Lacosamide Take to Work?

Lacosamide is absorbed quickly after you take it — peak blood levels are reached within 1 to 4 hours. However, your doctor won't start you at the full dose. Instead, you'll begin at 50 mg twice daily and increase by 50 mg twice daily each week until you reach the target dose (usually 150-200 mg twice daily).

This gradual approach (called titration) minimizes side effects like dizziness and nausea. Most patients reach their full maintenance dose within 3-4 weeks, and full seizure control may take a bit longer as the drug reaches steady-state levels in your blood.

How Long Does Lacosamide Last?

Lacosamide has a half-life of approximately 13 hours, which is why it's taken twice daily (every 12 hours). This provides consistent medication levels throughout the day and night — important for round-the-clock seizure protection.

If you miss a dose, take it as soon as you remember unless it's almost time for your next dose. Never double up.

What Makes Lacosamide Different from Other Seizure Medications?

Lacosamide stands apart from other AEDs in several important ways:

• Unique mechanism: It's one of the few AEDs that targets slow inactivation of sodium channels. Most others (Carbamazepine, Phenytoin, Lamotrigine, Oxcarbazepine) primarily target fast inactivation.
• Fewer drug interactions: Lacosamide has relatively few drug interactions compared to older AEDs like Carbamazepine and Phenytoin, which are potent enzyme inducers.
• Simple dosing: Twice daily, with or without food.
• IV option: Unlike many oral AEDs, Lacosamide has an intravenous formulation, making it useful in emergency settings.
• Cardiac monitoring: One notable consideration — Lacosamide can prolong the PR interval on an EKG, so cardiac monitoring may be needed, especially in patients with existing heart conditions.

The closest medication to Lacosamide in terms of mechanism is Eslicarbazepine (Aptiom), which also enhances slow inactivation of sodium channels, though through a slightly different chemical pathway. For more comparisons, see our guide on alternatives to Lacosamide.

Final Thoughts

Lacosamide works in a fundamentally different way than most other seizure medications. By targeting slow inactivation of sodium channels, it calms overactive neurons more selectively, which is why many patients tolerate it well. If you want to learn more about what Lacosamide is and how to take it, read our overview: What Is Lacosamide?

And if you're having trouble finding or affording your medication, Medfinder can help you locate a pharmacy with stock near you.