Epilepsy pathogenesis
The brain, an enigmatic masterpiece of nature, continues to shroud itself in mystery. Esteemed neuroscientists around the globe tread cautiously around these mysteries, acknowledging the profound intricacies that still elude our understanding. In our pursuit, we endeavor to unravel these enigmas.
Before delving into the hypothesis, let us contemplate the conventional perception of the brain’s functionality, both from our standpoint and that of others. Regarded as an organ operating on electricity, the brain relies on the conduction of electric currents by neurons. Intriguingly, the brain does not generate electricity autonomously; rather, it draws upon the electricity potentially produced within the skeletal muscles. During the restorative embrace of sleep, this electricity traverses from muscles to the brain, finding its reservoir in the reticular nucleus. In essence, the reticular nucleus acts as a biological battery, storing electrical energy during slumber, later utilized by neurons upon awakening.
Our exploration into intracranial pressure dynamics, facilitated by video monitoring and eye bottom observations, has illuminated variations between the right and left hemispheres in afflicted individuals. The irregularities in intracranial pressure, stemming from the intricate multistage cavity within the skull, may induce deformation in the soft, pliable substance of the brain, particularly in the interhemispheric and reticular nucleus regions.
Enter the realm of inhibitory neurons, overfilled with electricity, or hyperpolarized neurons. Activation, in the form of depolarization, triggers their functional state. Subsequently, discharged neurons must undergo inhibition once more, transitioning back to an activated state through repolarization, a process fueled by the energy of reticular cells.
The hypothesis on the pathogenesis of epileptic seizures, colloquially referred to as ‘the hypothesis of a short circuit in the subcortical batteries of electricity,’ posits that asymmetric increases in intracranial pressure deform and potentially damage axons of certain reticular neuron batteries, particularly near synapses. This deformation culminates in the rupture of one of their isolated layers, unleashing a torrent of electrical energy into the extracellular space—a short circuit. The cortex, stripped of its electrical equilibrium, witnesses the discharge of Betz cells, culminating in their depolarization or activation, signifying tonic seizures. The released electricity permeates the intercellular space, influencing the depolarized Betz cells, resulting in their periodic polarization—clonic seizures.
Post-seizure, the depleted brain yearns for rejuvenation, compelling the patient to succumb to the embrace of sleep, initiating the vital process of recharging.
In the world, over 100 million people suffer from epilepsy. The leading organization dedicated to these patients globally is the International League Against Epilepsy, established in 1909. It includes epilepsy centers from more than 100 countries, with a membership exceeding 10,000. Despite this, the number of people with epilepsy continues to rise, indicating a gap in understanding and treating the disease. The physiology of an epileptic seizure and its pathogenesis remain unknown.
The kindling theory proposed by Goddard in 1960 lacks logic but is established in the pathogenesis of epilepsy. In other words, in our view, there is no pathogenetic treatment for epilepsy. Modern explanations of epileptogenesis include disruptions in molecular and genetic mechanisms, neurotransmission pathways, glutamate-calcium complex disturbances, structural, neurochemical, and cellular changes, immunological, inflammatory, apoptotic disorders, gene and protein regulation disturbances, and other perspectives.
To understand our hypothesis, it’s crucial to know that some authors, including us, believe that the brain’s reticular nuclei act as capacitors of electricity, not as something abstract or nonspecific. Like tissues, these capacitors are susceptible to damage. While modern neurology makes no mention of reticulopathy, our hypothesis on the pathogenesis of epilepsy has been around for 20 years. Presenting it again, we don’t expect a decisive breakthrough. We lack the means to research the hypothesis and reach a definitive scientific conclusion simply because Armenia lacks a neurosurgery and neurology institute, let alone epileptology.
This presentation is made in the hope that future doctors intending to work with epilepsy will approach scientific materials more seriously and seek logic in what is said. They must know that there is an alternative opinion, and this opinion, for some reason, is not in favor of current epileptologists.
We believe that epilepsy is a disease of the reticular nuclei, and the explanations proposed to date for epileptogenesis only show what can affect the reticular nuclei. Our hypothesis needs research as it is highly logical. If proven, modern epileptology will need a complete reevaluation. Primarily, the name of this disease should be changed to “Reticular Encephalopathy.”