The uncontrollable jerking of limbs, loss of consciousness, and lifeless stares that accompany seizures have been well known for millennia, but it was only until recent scientific past, that humans have been able to describe the biochemical background behind them. From a neuroscientific perspective, seizures can be described as involuntary neuronal firing, occurring either in a localized area, or throughout the entire brain. These irregular electrical impulses in the brain stimulate the abnormal physical and emotional behavior experienced by seizure patients, meaning the symptoms have a dependence on the locality at which this unwanted firing of neurons is taking place. Any scientist working in this field would ask the obvious question of “why does this happen”, and there are many reasonable answers, which include brain tumors, strokes, and chemical imbalances. Unfortunately, there are many cases in which there may be no cause, and when these types of seizures occur multiple times in a short period of time, they are characterized as an epileptic disorder. This unresolved causation for epilepsy has led epileptic researchers to focus on lessening the symptoms for the patients, which is done primarily through the use of drugs.
Antiepileptic drugs (AED’s) have been used effectively for over a century, but there will always be ways to improve them and lessen the symptoms for the patients. With the thousands of drugs that have been developed, they can be classified based on their mechanism of action.
The most common AEDs are grouped as sodium channel blockers, and they do exactly as their name suggests. They are part of the anticonvulsant class of medication, which suppresses neuronal activity. To understand what this involves, the basics of neuron activation, or more commonly known as action potentials, must be acknowledged. Action potentials, the firing of a neuron in the brain, are mediated by sodium channels, found on the cell membrane. These channels open and close allowing the diffusion of sodium cations (positively charged ions), which transmit the signal across the neuron. As the positive sodium ions enter the cell, they create a rapid change in voltage, which induces an electrical charge within the cell. This electrical current can then be passed on to other neurons and transmit a signal from one part of the body to another. In AED’s, sodium channel blockers inhibit the activation of sodium channels, which prevents the sodium ions from entering the cell, which maintains the resting state voltage of the cell, and disallows for a signal to be emitted. This can be very beneficial during seizures, when there is involuntary neuron activity. Some of the main sodium channel blockers include:
Carbamazepine
Phenytoin
Fosphenytoin
Oxcarbazepine
Eslicarbazepine
Zonisamide
For more information of the science behind sodium channel blockers and how they help suppress epileptic symptoms, feel free to read Voltage gated sodium channel inhibitors as anticonvulsant drugs.
Another common group of AED’s used in epileptic treatment are GABA reuptake inhibitors, and once again, they do exactly as the name suggests. The basics of neuron communication must be understood to fully grasp the concept of GABA reuptake inhibitors. When a neuron is activated, it will transmit its signal to other neurons by sending neurotransmitters to the target cell, which is known as the postsynaptic neuron, through a synaptic cleft. These neurotransmitters will bind to receptors on the postsynaptic cleft and transmit the signal to the next cells. Once neurotransmitters have fulfilled their role, they will be brought back into the original cell through a process known as reuptake. GABA, short for gamma-aminobutyric acid, is an inhibitory neurotransmitter that suppresses the activity of neurons. These neurotransmitters will bind to chloride channels, sending in negatively charged chloride ions into the cell. This process known as inhibitory postsynaptic potential (IPSP’s), lowers the probability of the neuron becoming active, since it lowers the voltage of the cell even further. Normally, GABA will be brought back by the pre-synaptic cell, so it can be recycled. With GABA reuptake inhibitors, this process is terminated, and the GABA neurotransmitters are left in the synaptic cleft to bind to more receptors and further hyperpolarize the cell. In epilepsy, this lowers the chance neurons are activated at random, reducing epileptic symptoms. One of the main GABA reuptake inhibitors is Tiagabine and it is an anti-convulsant that can also be used as anxiety medication.
For more information on the chemical basis of GABA reuptake inhibitors feel free to read GABA Reuptake Inhibitor.
These are only two types of the many drugs used deal with epilepsy, while many other types of AED’s deal with the same underlying principles associated with sodium channel blockers, and GABA reuptake inhibitors. The variety in AED’s allows physicians to accommodate for each individual and their needs to find the right prognosis, since there is no one drug that will completely cure epilepsy. Other treatments for epilepsy deal with the surgical removal of the area of the brain that seizes, which is known as resective brain surgery, or deep brain stimulation which involves putting a device in the body, that sends signals disrupting the electrical impulses emitted by the seizure. There will always be better ways to deal with this disorder, thanks to the advancements in technology, so we should keep our hopes up and not give up on finding a cure for epilepsy.
If you have any questions, concerns, comments, or ideas on epilepsy, seizure and medications, or just Neuroscience in general, feel free to write back to us. We would love to hear your ideas and opinions to help educate and inform the community about the beauty of neuroscience.
-Jaiden