Epileptic seizures and link to memory processes

Abstract

<abstract> <p>Epileptogenesis is a complex and not well understood phenomenon. Here, we explore the hypothesis that epileptogenesis could be “hijacking” normal memory processes, and how this hypothesis may provide new directions for epilepsy treatment. First, we review similarities between the hypersynchronous circuits observed in epilepsy and memory consolidation processes involved in strengthening neuronal connections. Next, we describe the kindling model of seizures and its relation to long-term potentiation model of synaptic plasticity. We also examine how the strengthening of epileptic circuits is facilitated during the physiological slow wave sleep, similarly as episodic memories. Furthermore, we present studies showing that specific memories can directly trigger reflex seizures. The neuronal hypersynchrony in early stages of Alzheimer's disease, and the use of anti-epileptic drugs to improve the cognitive symptoms in this disease also suggests a connection between memory systems and epilepsy. Given the commonalities between memory processes and epilepsy, we propose that therapies for memory disorders might provide new avenues for treatment of epileptic patients.</p> </abstract>

Termination of convulsion seizures by destabilizing and perturbing seizure memory engrams

“…Recognizing the commonalities between memory processes and epilepsy, there has been a recent proposal to apply therapies for memory disorders to the treatment of epileptic patients ( 2 ). However, the effectiveness of applying the reconsolidation theory to epilepsy treatment remains unclear.…”

“…Temporal lobe epilepsy, one of the most common neurological diseases, arises from long-lasting changes in synaptic strength between neurons. These changes resemble both the mechanistic and phenotypic aspects of hippocampus-dependent memory formation (1,2). Decades ago, Goddard and Douglas (3) put forward the opinion that the engram of epilepsy is analogous to the engram of normal long-term memory.…”

“…Recently, modeling studies suggested that epilepsy may arise as an abnormal learned response; thus, it could potentially be treated and reversed through unlearning (4). The high similarity between memory formation and epileptogenesis is increasingly noticed and highlighted to provide promising avenues for epilepsy research (1,2). For example, despite seizures occurring spontaneously in most patients with epilepsy, reflex epileptic seizures occur recurrently in response to specific triggers (5)(6)(7).…”

Neurophotonic methods in approach to in vivo animal epileptic models: Advantages and limitations

“…LTP-induced changes result in a long-lasting postsynaptic increase in the sensitivity of αamino-3hydroxy-5-methylisoxazole-4-propionate receptors, and this increase may play a role in lowering excitability thresholds, leading to increased epileptiform activity. 74 In another recent study, the authors explored optokindling regulation of the excitability of neural circuits. 75 The level of excitability is affected by synaptic efficiency and internal excitability of neurons.…”

“…LTP is a long‐term enhancement of synaptic transmission, which is a cellular correlate of learning and memory. LTP‐induced changes result in a long‐lasting postsynaptic increase in the sensitivity of α‐amino‐3‐hydroxy‐5‐methylisoxazole‐4‐propionate receptors, and this increase may play a role in lowering excitability thresholds, leading to increased epileptiform activity 74 …”