Are all cranial nerve neuralgia’s a manifestation of a brainstem redox deficit?
I think they are. I think all pain syndromes are linked to a lack of redox caused by an inability to maintain your redox potential in your CNS and PNS at some level.
The cell membranes in the cranial nerve nuclei and brainstem nuclei share a blood supply. They are located in close proximity and recieive input from the retinal pathways and from the skin surfaces.
Trigeminal neuralgia is a disorder of paroxysmal and severely disabling facial pain and continues to be a real therapeutic challenge to the clinicians. As a neurosurgeon I see this condition often. Trigeminal neuralgia affects the 5th cranial nerve but this condition can affect other cranial nerves as well. While the exact cause and pathology of this disorder is uncertain. I was taught to believe in residency that trigeminal neuralgia is most often caused by irritation of the trigeminal nerve by calcified blood vessels.
Today I believe that more proximal defect is due to an endocannabinoid defect in the brainstem of the nuclei of these cranial nerves cause by alien electromagnetic fields and manufactured light that cause a stress response in the paraventricular nucleus that control vagal tone in the autonomic nervous system. The damage to the PVN can extend to the cranial nerve nuclei via the blood vessels in the brain and retina where melanopsin exists.
This irritation results from damage due to the change in the blood vessels, the presence of a tumor or other lesions that cause the compression of the trigeminal root. The pain of trigeminal neuralgia is characterized by unilateral pain attacks that start abruptly and last for varying periods of time from minutes to hours. The quality of pain is usually sharp, stabbing, lancinating, and burning. The attacks are initiated by mild stimuli such as light touch of the skin, eating, chewing, washing the face, brushing the teeth, and exposure to wind.
Although antiepileptic drug therapy may be beneficial in the treatment of trigeminal neuralgia, up to one-half of the patients become refractory or intolerant to these medications. At present there are few other effective drugs. In cases of lacking effect after pharmacotherapy, surgical options may be considered. Currently there is growing amount of evidence to suggest that the psychoactive ingredient in cannabis and individual cannabinoids may be effective in alleviating neuropathic pain and hyperalgesia.
Evidence suggests that cannabinoids may prove useful in pain modulation by inhibiting neuronal transmission in pain pathways. Considering the pronounced anti-nociceptive effects produced by cannabinoids, they may be a promising therapeutic approach for the clinical management of trigeminal neuralgia.
BLOOD SUPPLY brings many things to bear in many mitochondrial diseases because since 2014 we know that melanopsin is present in aterial trees of almost every organ.
Anterior and posterior branches of the circle of Willis provide arterial blood to the hypothalamus. The hypothalamus also receives arterial supply from the hypothalamic branches of the superior hypophyseal artery from the carotid system.
The vertebrobasilar arteries supply the posterior two-fifths of the cerebrum, part of the cerebellum, and most areas in the brain stem where the cranial nerve nuclei are located.
The circulatory system of the anterior carotid system and vertebral basilar system have lipid rafts in them that create a charged state that is SHARED. The shared area is between the hypothalamus where the PVN is located and the cranial nerve nuclei. So when redox charging is ruined in one the clinician should know that it is the arterial tree that connects the two.
Inside of the arterial tree is melanopsin, dopamine, and the machinery for creation of nitric oxide.
All of these proteins are acted upon by excited electrons that fall back to the their ground state and give the charge up to the lipid rafts in the cell membranes of these areas in the brain.
Sunlight provides the redox charge that allows mitophagy and aopotosis to optimize the vessels anatomy using cicradian programming. I have a deep sense this is why melanopsin is present in our vessels.
What happens when this system does not work? People wind up with mitochondrial diseases, a low dopamine state, and lowered melatonin level, lowered DHA, are more likely to clot and sustain an alteration of their endogenous cannabinoid system.
One of the key metabolites from DHA is the key endocannabinoid that maintains the charge of the lipid raft in PVN and brainstem nuclei of the cranial nerves. When this charge transfer does not occur within proper ultradian or circadian cycles, we can see cranial nerve pain syndromes, and migraines manifest. Many times these will be associated with calcified brainstem arteries that cannot liberate nitric oxide (NO). NO is designed to relax microcirculations. It turns out the 7 alpha helices also need electrons to help relax the microcirculation in the brainstem too.
Almost every person I have seen with these pain syndromes have evidence of circadian cycle disruption when I look for it. I believe this happens in humans because melanopsin signaling is destroyed in those arteries as the paper below shows.
It turns out light-induced isomerization of melanopsin is up to several tens of femtoseconds faster than the analogue isomerization of invertebrate and vertebrate visual pigments. It also has been revealed that melanopsin’s thermal isomerization is controlled by an energy barrier higher than the barrier of dim-light visual pigments. These properties support the idea of why evolution has favored the use of extreme light sensitivity of melanopsins in many tissues in our body.
What happens to human circadian biology is damaged, with respect to melanopsin biology in our arteries?
Melanopsin/retinol dysfunction occurs when the covalent bond between melanopsin and retinol is disrupted by blue light absorption. This unleashes retinol to become a toxin in the arterial wall and surrounding neurons and this toxic liberation is what lowers melatonin levels locally in those tissues to cause them to lose control of local mitophagy and apoptosis in neurons and vessels. The collateral signaling cascade leads to lower DHA replacement in the cell membranes of humans. It turns out that neurons and arteries of the brain have the highest levels of DHA within them.
Lowering DHA in the eye and skin directly ruins clock maintenance.
This cascade of events also lowers electrophiles in the blood plasma like CO2 and free electrons made from melanin’s ability to split water using visible light. Remember all hormones are derived from cholesterol when T3 and Vitamin A convert it to pregnenolone. Without T3 (AM light) or Vitamin A (retinol from melanopsin), you cannot make the substrates of ALL the hormones humans use. This is how it all works in symphony inside the brainstem too. Progesterone protects arteries from damage. All the hormone panels that also work via circadian biology too as the slide from my Vermont 2017 slide shows. Tyrosine needs sunlight to activate and program the aromatic ring to make T3 and T4.
As a result of the breaking of the melanopsin/retinol weak covalent bond the arteries calcify and they become like lead pipes and can strike the exiting cranial nerves in the cisterns filled with CSF around the brain. When retinol is freed it becomes a neurotoxin in the body and is linked to poor sleep and regeneration. This was covered in my Vermont 2018 talk from the slide below.
The eye, iris, sclera, RPE, have massive amounts of melanin and I think this is present to provide the opthalmic arteriole bed with a massive factory of free electrons from the action of melanin on water in this arterial tree. I believe those free electrons are critically lost in most pain syndromes of the head and neck in humans. A loss of free electrons sets the stage for arterial calcificiation.
Most of you know I think diabetes is a blue light hazard disease. Few of you know that I believe the disease is linked to melanopsin damage of the arterial tree. This is why diabetics always have poor vessels that are stiff and do not deliver an adequate amount of blood, oxygen, and electrons to distal tissues.
Vascular calcification in humans can occur in either the intimal or medial layers of the arterial wall. Intimal calcification is associated with athero sclerosis, which is characterized by lipid accumulation, inflammation, fibrosis and development of focal plaques.
Medial calcification is associated with arterio sclerosis, i.e. age- and metabolic disease-related structural changes in the arterial wall which are related to increased arterial stiffness. It has been hypothesized that vascular calcification, either intimal or medial, may directly increase arterial stiffness. I think both are linked to the amount of melanopsin damage in the system. This is why the CAC blog was given to you as a warning shot of what to expect in a 5G world. I think nnEMF will demolish the arterial melanopsin system.
Neurosurgeons are taught that the calcified vessel is the main problem in cranial nerve pain syndromes. It turns out this is not true as the video shows. My patient was in scrubs. It turns out he was a nurse who worked in the ICU at night under blue light and nnEMF.
I beleive this environment destroyed his melanopsin mechanism in his arterial tree in his brainstem and caused a myriad of problems in the lipid rafts of the cell membranes. This is why understanding the Bazan effect (below) is very important in these diseases.
If you can restore the melanopsin/retinol function back to the arterial bed, you can restore the return of NO, melanopsin, and natural cannabinoids to the lipid membrane rafts to increase their redox potential in these vessels. If you can increase their charge potential you can reverse the process without opening the skull, in my opinion (below)
You can see in the picture below the cranial nerve nuclei are quite close to the PVN in the hypothalamus (grey nuclei below) but they are not directly connected to one another in most cases via tracts. This raises the question, what connects them?
You can see in the picture above the brainstem is outlined but left blank. If you find the mammillary bodies in red above you’ll see that small tube above it. That is the floor of the third ventricle that connects directly to the brainstem which is outlined. The picture below colors in the brainstem and shows you where all the cranial nerve nuclei are.
Both sets of neurons are directly connected by the circulatory system in the brain. The circle of Willis surrounds this area and it is where the anterior carotid system links to the vertebral basilar system at the posterior floor of the third ventricle. We call this a watershed region in the blood supply. This sits right above the trigeminal ganglion picture below.
Many of you might get lost with this neuroanatomy lesson but the slide below shows you how physiology of the hypothalamus and pituitary and brainstem couple (yellow boxes below). The circadian control in the eye and skin is very important to these systems because it is linked via the arterial supply of this region because melanpsin is located in these arterial trees. Since it is there it is subject to damage.
The picture above shows you how they are linked, but does not show you the wireless connection via the RBC’s in the circulatory system of the region.
Life can begin when you gain control of the processes where the environment first meets your tissues. This happens on the surfaces of our of cells where membranes exist. Human membranes are unique because they are loaded with DHA in their lipid rafts.
This change in evolution was done to take massive advantage of the free energy in sunlight to create a massive electric charge across a small membrane in our RBC’s.
During the day, when the sun is present terrestrial to your eyes and skin the RBC’s in your vessels come closer to the surface to sense the electric and magnetic fields in daytime. It turns out the daytime ionosphere has massive quantities of electric fields and very low magnetic fields. This is due to the presence of sunlight. The RBC cell membranes allow us to harness this free energy from sunlight by using melanin as an intermeidate to create a ton of electrons from splitting water in our arterial tree.
Life begins by creating wireless power transmitters in our surface membranes (surface topology) that work by collecting energy buried in the electric and magnetic resonance of fields in sunlight. They can do this in many ways wirelessly from our environment.
This is how life became supercharged by sunlight and the dynamo in Earth. The technologic problem using this method that evolution had to solve, was that the original surface transmitters in early life forms had a poor range and fidelity to share their information. This kept life simple for 3.8 billion years. The reason for the poor range is due to the inverse square law which states that the intensity of electromagnetic oscillations varies inversely to the distance of the emitting source (S) as the slide below shows.
The further away our skin/blood is from the point source the worse transmission rates are for this energy source. So how did evolution fix this problem?
Nitric oxide and melanopsin both work in unison to bring blood vessels closer to our skin and retinal surfaces in our circulatory system to create the free electrons from water. This effect is very complex. I laid out that complexity in the Vermont 2018 talk. The slide below shows you some of the changes sunlight induces when terrestrial sunlight hits your skin.
Mother Nature built cell membranes in our skin and retina that could absorb light and she placed proteins in their lipid rafts to slow the light down (Vermont 2017) to create a mechanical vibrations after light collide with these things in our cells.
Because of this evolutionary design, human membranes no longer suffer from limited signal creation or amplification. Their specificity and fidelity are improved compared to bacterial systems.
The inner mitochondrial membrane however has to be controlled differently in humans, because it is the only human membrane that retains its bacterial origin. It has no DHA, by design.
The outer mitochondrial membrane is loaded with DHA and it is contiguous with the Golgi body and rough endoplasmic reticulum where proteins are made.
Why did Mother Nature do this?
When you harness mechanical vibrations and couple them to piezoelectric transducers you can amplify weak signals from the environment easily. This is how Mother Nature solved the inverse square law for animal photosynthesis. The signal transduction pathways built by evolution go way back and are still maintained in melanopsin and the G couling systems today. This is why human melanopsin resembles innvertebrate opsins. When evolution uses something for a long time without many changes it would be wise for the Black Swan to discover why this is the case.
Piezoelectric and flexoelectric transducers convert mechanical energy into DC electric current. This ability is amplified in humans because of DHA quantum abilities.
Sunlight, like sound, creates vibration in atoms in the air and in cell membranes and is fully able to transfer energy and information of these oscillations. This makes your skin and cell membranes a universal wireless charging system for sunlight.
That system is fed by the magnetic field and photons of the sun. Sunlight powers up electrons via the photoelectric effect. Excited electrons fall back to the ground state. This is how life really powers itself. It is not really a story of ATP, as modern biology believes.
Photons are released from electrons after they are energized by the sun then fall back to the ground state by giving off a photon to our tissues.
In the blood plasma, the tissue most affected by this action is the lipid rafts in the arteriole walls. I believe this is why nature put melanopsin and dopa carboxylase in arterial walls.
They were put there to make dopamine (time) and tightly control circadian signaling to melanopsin/retinol dysfunction. This is why a Jablonski diagram is so common in life’s blueprint in many tissues. DHA is the lipid that does this most effectively on Earth and this is why DHA has not been replaced one time in evolutionary history in 600 million years.
This is why RBC’s are overloaded with DHA in their cell membranes.
They are loaded with carbonic anhydrase and ascorbate to control protons. Proton control helps the shape of RBC’s too. Diabetes is associated with hyperglycemia and blue light damage. Taken together, hyperglycemia in diabetes produced lower RBC ascorbate with increased RBC rigidity, and are more osmotical fragile making them less likely to navigate small capuillary beds. As melanopsin damage rises RBC ascorbate levels drop and RBC look like echinocytes. This makes melanopsin a key candidate to drive microvascular angiopathy in diabetes.
We also know that RBC’s are loaded with hemoglobin that looks almost identical to a chloroplast atomically. And we know hemoglobin’s absorption spectrum for light is strong in the visible spectrum of sunlight in the 250-600 nm range.
In fact, the cut off is strong at 600 nm. All this evidence tells us that RBC’s likely contain the key electric sensor for the sun’s light. If you ask most biologic researchers they would tell you the identity of the electric field sensor is unknown today. If you asked a bio-physicists or a mitochondriac they would tell you the electric sensor resides in the lipid raft of the RBC. When the RBC looks abnormal it is a sign of melanopsin damage. This won’t allow the RBC to get into the capillaries of the brainstem.
Lipids in cell are well known excellent electrical conductors. This will be an important fact to remember in a 5G world. Fats, like DHA, are loaded with pi electrons and all lipid rafts in cell membranes are associated with massive amounts of DHA and sphingolipids.
The arrangement of the lipid raft also tells us why an RBC is shaped the way it is when sunlight hits them. Charge affects size, shape, and density in anything made of mass. Electron colonies around RBC’s are most dense in the toroid region of the RBC and electrons are less dense in the hollowed-out center portion of the RBC.
This surface arrangement makes it a perfect sine wave antenna for wave transformation into other forms of energy. Proteins change light into other energy waves. The solar plasma is one such waveform that has an electric component. Bio-physical research has now demonstrated that the detergent-resistant membrane nano-domains, known as lipid rafts, act as the primary sensor to electric field-induced directional cell migration in morphogenesis.
This is why Robert O.Becker found that RBC had to be present in his limb regeneration experiments on frogs and salamanders. And he believed the reason humans lost the ability to regenerate was that our skin heals too fast that the RBC’s component could not generate a large enough electric current to drive the stem cells in the injured limb.
Isothiocyanates in foods are weak electrophiles in organic chemistry. Carbon dioxide in the air and our blood is also an electrophile. Voltage-gated channels act as electrophiles too to free more electrons up to do physiologic work when they are excited by sunlight.
Electrophiles in food act like the reactions of carbon dioxide in cells. Things with a lot of carbon are nucleophiles (DHA), and nucleophiles tend to attack carbon in lipids, proteins, and carbohydrates in cells. This means that when electrophile compounds are added to a lipid raft moiety they become excellent at delocalizing electrons (freeing them) and fostering non-linear optical signaling by allowing them to move to lipids and proteins in a cell.
This enhances their redox state as the slide above shows. This is a Jablonski diagram. This is how DHA and water turn sunlight into the DC electric current that Becker found.
To take circadian advantage of this, compounds need large electronic dipole moments, and isothiocyanates have them.
So does the lipids in human cell membranes. The other key way they work in a lipid raft in our cell membranes with DHA is the electron donor and acceptor portions of the raft have to be far away from one another…….and with DHA this occurs because of the 22 carbons and their alternating double bonds.
Those 22 alternating double bonds are critical in making the huge pi-electron clouds that interact with the sun’s light to create massive electric fields that can oscillate with sunlight. Please remember Becker found that the DC electric current vanished at night in all hi animals.
Amines are methylene donors and cyan’s, halogens, and nitro’s are acceptors (DeMartino 1988) in chemistry. This is why nature favored biologic amines in proteins. This is why I kept putting all those pictures up of the aromatic amino acids in the last 2 Vermont Talks to explain to you how animal photosynthesis.
When they bind to DHA they also make the DHA planar (flat) which also helps the electronic effect of the pi electron clouds to interact with sunlight to capture the sun’s power in these electrons to excite them. Melanin in skin augments the DHA effects.
That stored energy can then be transferred to water and to Tensegrity system in the cell membrane and within the cytoarchitecture of the cell to electrify it.
DHA facilitates the transmission because of the pi electron cloud when flattened acts like a giant wire of electrons that has very low resistance. A semiconducting electric current like this has low resistance compared to resistance in a copper wire or the filament of a light bulb which thermalize and let go of the light back to the environment.
This is how melatonin, melanin, and DHA work together to store energy from the sun for use later without the light ever becoming thermalized. Once it is thermalized you lose it by thermodynamic laws. This keeps cells powered and far from equilibrium in the living state.
People need to gear up on 3D atomic chemistry to get why certain foods work in mitochondrial disease states that all are associated with a low DC electric current. A low DC electric current = poor regeneration = poor healing = melanopsin damage = poor sleep.
The sun’s power is changed from photons to a DC electric current photoelectrically by cell membranes.
This is why I showed this as the first slide in my Vermont 2018 talk. Cranial nerve pain syndromes are great diseases I can use to teach/show/educate you just how the complex things you are learning manifest in humans.
This is why I had this as my first slide in Vermont 2018 above.
All diseases = melanopsin defect at some level = low DC electric current = poor electronic flow across the cell membrane. Remember melanopsin is in those lipid rafts too. The collateral signaling cascade of melanopsin dysfunction deerves your extreme focus.
CITES:
https://www.ncbi.nlm.nih.gov/books/NBK279126/