Have you ever took a walk by the ocean and observed the waves in a stormy day. If so, you actually observed what is happening inside your brain during trouble times.
What had been taught
in medical schools
is that the CSF is produced by Choroid Plexuses mainly in lateral ventricles then moves to the third and then to the fourth ventricle. Later on it leaves the ventricular system to subarachnoid spaces and then it is absorbed into the blood via the Arachnoid Villi & Granulations.
It is partially correct, but we must consider that the CSF movement is not a simple one directional like the movement of the tap water inside the pipes of our homes, but rather it moves like the waves of the ocean.
I came up with this hypothesis in early 1980?fs, when I tried to explain what happens in the brains of post-traumatic epileptic patients in order to treat them properly. I didn?ft know how to name this movement of the CSF until I was introduced to the term ?gFluctuation of CSF?h during my studies of Osteopathic
Now, I can use this new terminology ?gFluctuation of CSF?h in explaining my theory of HOW and WHY the post-traumatic epileptic seizures are developed in order to treat them successfully.
Here, I would like to explain my hypothesis of HOW and WHY the post-traumatic epileptic seizures are developed; and to share with you my previous unorthodox method of treating patients who suffer from those post-traumatic epileptic seizures. But, before I do so, lets explore what is conventional:
The conventional theory explains that epileptic seizures are developed as paroxysmal hyper-synchronous transient electrical discharges in the brain due to over excitation or not enough inhibition in the areas in which the abnormal discharges start. Hence, the conventional treatment of epilepsy is based on this theory. The treatment is based primarily on the reduction of this excitation.
As you see, this theory succeeded in explaining the HOW, but failed to explain the WHY. It explains HOW these seizures are produced, but failed to explain WHY this is happening. Eventually, the available antiepileptic drugs (AEDs) that are based on this theory succeeded only in masking the symptoms but failed in treating the epilepsy. Furthermore, these drugs keep the nervous system of these patients depressed throughout their lives.
The available AEDs such as sodium channel blockers, calcium current inhibitors, gamma-aminobutyric acid (GABA) enhancers, glutamate blockers are aimed to inhibit repetitive neuronal discharges and reduce synaptic propagation of the nervous excitatory impulses. Unfortunately, it is a well-known fact that most epilepsy patients only achieve satisfactory seizure control, meaning they still have seizures and experience the severe side effects from these medications. When successful seizure control with monotherapy cannot be achieved, additional AEDs are added to the treatment regimen (polypharmacy). Finally, when a patient fails to respond to an AED protocol, surgery is considered. HERE I DREW THE LINE!!!
I was a neurosurgeon for many years, and avoiding a brain surgery to me was like avoiding the water by a thirsty person. Performing surgeries on the brain was one of my passions. Having said that, I also had another passion, which was NOT to do unnecessary surgeries that wouldn't help the patients, but rather hurt them. This was my way of following one of Hippocrates principal ?gNON NOCERE?h that means ?gDO NO HARM?h.
These surgeries are aimed to remove the post-traumatic scar tissues (adhesions) that cause the epileptic seizures. I was and still advocating against these surgeries because these adhesions will develop again soon after surgeries. Also, in addition to the previous adhesions many new ones will develop in other places; hence more focal regions that will cause more seizures. So, we ended where we started eventually or even worse.
So, lets go back to HOW and WHY these seizures develop in post-traumatic patients from my point of view (i.e. according to my new hypothesis). To understand what is happening we need to understand the process of CSF ?gFluctuation?h. This is the wave movement of the CSF inside the cranium. From our studies of physics and from the English dictionary, we can find that it is a wave if: (1) energy moves from one place to another, and (2) mater doesn?ft move from one place to another, for most part. For example, ocean waves sporadically arrive at the shore without pulling up vast amounts of water. The wave arrives, but most of the water doesn't.
The same thing happens with the waves that are developed by the CSF ?gFluctuation?h. Normally, the amplitudes of this fluctuation allow the CSF to provide nutrition to the nervous tissues and to remove the waste products of cellular metabolism from the nervous system same as the ocean waves clean up and remove the debris from the shores.
The amplitudes of these waves can be increased if the CSF amount or viscosity is increased and/or if there is an obstacle (such as post-traumatic Leptomeningial adhesion) standing in the way that hinders or prevents the progress of these waves. This will result in the increase of energy threshold inside the cranium and eventually cause the development of epileptic seizures.
Thick Leptomeningeal adhesion and/or increasing the amount or viscosity of CSF would cause more energy and eventually more seizures to be developed. Small or thin Leptomeningeal adhesion and/or decreasing the amount or viscosity of CSF would not cause the burst of energy that could cause the seizures development.
My unconventional method of treating
patients who suffered from
post-traumatic epileptic seizures (without going into details) was based on this CSF fluctuation and adhesion hypothesis and was aimed toward the following: