Epilepsy and Memory Loss - What’s the Link

Why does epilepsy cause memory loss? Repeated electrical activity can cause the part of the brain that's responsible for learning and memory to shrink.

The retention of the exact combination of features that helps to restore memory may be impaired in people with chronic epilepsy. At least the findings of a new study published in the journal Brain point in this direction.

Memory deficits are a debilitating symptom of epilepsy, but little is known about the mechanisms underlying cognitive deficits. Here, researchers describe the sodium channel-dependent mechanism underlying altered hippocampal dendritic integration, degraded coding, and deficits in spatial memory.

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Seizure or a convulsion is a result of abnormal electrical activity in the brain. If there are two or more unprovoked seizures at an interval of at least 24 hours, it is referred to as epilepsy.

‘The impairment in the process of dendritic integration may cause memory loss in epileptic patients.’

The hippocampus is a region in the brain that plays a central role in memory processes. This is especially true for spatial memory. There are about one million different place cells in the mouse hippocampus. And each response to a combination of specific environmental characteristics.

These cells have long extensions called dendrites. These are dotted with numerous contact points where the information that the senses convey to us about a place is received (de facto, there are often hundreds or thousands of them). These contacts are called synapses.

When signals arrive at many neighboring synapses at the same time, a strong voltage pulse may form in the dendrite - a so-called dendritic spike.

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In this way, the dendrite integrates different types of location information. Only when they all come together it may generate a spike. And so, it helps to recognize the acquaintance the next time we visit it.

In mice with epilepsy, however, this process is impaired. In them, the spikes already occur when only a few synapses are stimulated. Nor does the stimulation have to occur at the same time.

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Researchers were able to show in our experiments that epilepsy-affected animals had significantly greater problems distinguishing familiar places from unfamiliar ones.

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But what is the reason for this? For a spike to form, large amounts of electrically charged particles (the ions) must flow into the cell. For this purpose, pores open in the membrane that surrounds the dendrite - the ion channels.

In the lab animals, a special channel for sodium ions was significantly more prevalent than normal in the dendrite membrane. This means that just a few poorly synchronized stimuli at the synapses are enough to open many channels and elicit a spike.

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There are inhibitors that very specifically block the affected channel, preventing the influx of sodium ions. This normalized the firing behavior of their dendrites. They were also better able to remember places they had visited.

The study thus provides insight into the processes involved in memory retrieval. In addition, in the medium term, it gives rise to hopes of producing new drugs that can be used to improve the memory of epilepsy patients. These promising results are also the result of fruitful cooperation.

Source-Eurekalert