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SaraSara

Glutamate and some theory about visual snow

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Someone on the visual snow fb group posted this . U guys might wanna read it , The person who wrote this believes that we need a combination of gene and stem cell therapy: 

 

'' I spend a lot of time researching how our nervous system works and what may contribute to the development of Visual Snow and other symptoms. Remember that there is a lot of vital information that I do not know, and may greatly benefit our understanding of this condition. 

Visual snow is described as an "epileptic" firing in the visual system in the brain. NMDA glutamate receptors, which are overexpressed after excitotoxic injury may well be the trigger of an increased spontaneous firing in the nerves. In turn, the brain would decode this increased firing as "visual snow"  The idea is that remaining nerve endings have been damaged enough to overexpress NMDA Glutamate receptors, thus increasing their spontaneous firing.

There are various factors that contribute to the development of this condition. Everybody first had an initial trigger, and this varies from person to person. Common causes include stress, trauma, recreational and prescription drugs, Lyme, mold, heavy metals, and other toxic exposures. But what they all result in is brain injury and neuronal damage. The consequences of such injury doesn't just cause break in communication between healthy neurons, but a cascade of events that can lead to further neuronal degeneration and cell death. That is where visual snow comes in. Think of a broken radio or a TV where it isn't able to receive and process incoming signals so the outcome is a lot of visual/auditory noise. Our brains behave in a similar manner when there is an interference with proper neuron function and communication.

I strongly believe there are some genetic components that play a huge role in the development of Visual Snow and makes some individuals more susceptible to developing it. They are unknown as more research will be needed in this aspect.

Medical researchers searching for new medications for visual snow often look to the connection between the nerve cells in the brain and the various agents that act as neurotransmitters, such as the central nervous system's primary excitatory neurotransmitter glutamate. Visual snow can be caused when damaged brain cells emit an excess of glutamate. Many treatments use ingredients that work as glutamate antagonists, or inhibitors. 

Communication between nerve cells in the brain is accomplished through the use of neurotransmitters. There are many compounds that act as neurotransmitters including acetylcholine, serotonin, GABA, glutamate, aspartate, epinephrine, norpinephrine and dopamine. These chemicals attach to nerve cells at specific receptors that allow for only one type of neurotransmitter to attach.

Some of the neurotransmitters are excitatory; leading to increased electrical transmission between nerve cells. Others are inhibitory and reduce electrical activity. The most common excitatory neurotransmitters are glutamate and aspartate while the primary inhibitory neurotransmitter is GABA. It is necessary for excitatory and inhibitory neurotransmitters to be in balance for proper brain function to occur.

Communication over synapses between neurons are controlled by glutamate. When brain cells are damaged, excessive glutamate is released. Glutamate is well known to have neurotoxic properties when excessively released or incompletely recycled. This is known as excitotoxicity and leads to neuronal death.

Excess glutamate opens the sodium channel in the neuron and causes it to fire. Sodium continues to flow into the neuron causing it to continue firing. This continuous firing of the neuron results in a rapid buildup of free radicals and inflammatory compounds. These compounds attack the mitochondria, the energy producing elements in the core of the neuron cell. The mitochondria become depleted and the neuron withers and dies.

Excitotoxicity has been involved in a number of acute and/or degenerative forms of neuropathology such as epilepsy, autism, ALS, Parkinson’s, schizophrenia, migraines, restless leg syndrome, tourettes, pandas, fibromyalgia, multiple sclerosis, Huntington's, seizures, insomnia, hyperactivity, OCD, bipolar disorder and anxiety disorders.

(Doctors use two basic ways to correct this imbalance. The first is to activate GABA receptors that will inhibit the continuous firing caused by glutamate. The second way to correct the imbalance is use antogonists to glutamate and its receptor N-methyl-d-aspartate (NMDA). These are termed glutamate or NMDA antagonists. By binding with these receptors, the antagonist medication reduces glutamate-induced continuous firing of the neuron. This explains why some drugs like clonazepam and lamictal are able to help relieve symptoms in some patients. They help reduce excitatory action in the brain temporarily)

Anxiety, depression, brain fog, depersonalizations, visual disturbances (including visual snow, palinopsia, blue field entoptic phenomenon, photophobia, photopsia) headaches, tinnitus, are all common symptoms associated with increased excitatory activity in the brain. Excessive glutamate is the primary villain in visual snow.

Included below is a list of things that can lead to excitotoxicity. The list includes trauma, drugs, environmental, chemicals and miscellaneous causes of brain cell damage. (Keep in mind everybody's bodies behave and react differently to various substances)

-Severe Stress (Most people that are stressed out don’t realize that once the fight-or-flight response gets activated it can release things like cortisol and epinephrine into the body. Although these boost alertness, in major concentrations, the elevated levels of cortisol over an extended period of time can damage brain functioning and kill brain cells)
-Free Radicals – Free radicals are highly-reactive forms of oxygen that can kill brain cells and cause brain damage. If the free radicals in your brain run rampant, your neurons will be damaged at a quicker rate than they can be repaired. This leads to brain cell death as well as cognitive decline if not corrected. (Common causes are unhealthy diet, lifestyle and toxic exposure)
-Head Trauma (like concussion or contusion) MRI can detect damaged brain tissue BUT not damaged neurons. 
-Dehydration (severe)
-Cerebal Hypoxia
-Lyme disease
-Narcolepsy
-Sleep Apnea
-Stroke
-Drugs (recreational or prescription) 
-Amphetamine abuse
-Methamphetamines
-Antipsychotics
-Benzodiazepine abuse
-Cocaine
-Esctasy  
-Tobacco
-Inhalants
-Nitrous Oxide
-PCP
-Steroids
-Air Pollution
-Carbon Monoxide
-Heavy Metal Exposure (such as lead, copper and mercury)
-Mold Exposure
-Welding fumes
-Formaldehyde
-Solvents
-Pesticides
-Anesthesia
-Aspartame
-MSG (Monosodium Glutamate is found in most processed foods and is hidden under many various names)
-Solvents
-Chemotherapy
-Radiation
-Other toxic exposures

Inside the Glutamate Storm 

By Vivian Teichberg, Ph.D, professor of neurobiology 

"The amino acid glutamate is the major signaling chemical in nature. All invertebrates (worms, insects, and the like) use glutamate for conveying messages from nerve to muscle. In mammals, glutamate is mainly present in the central nervous system, brain, and spinal cord, where it plays the role of a neuronal messenger, or neurotransmitter. In fact, almost all brain cells use glutamate to exchange messages. Moreover, glutamate can serve as a source of energy for the brain cells when their regular energy supplier, glucose, is lacking. However, when its levels rise too high in the spaces between cells—known as extracellular spaces—glutamate turns its coat to become a toxin that kills neurons.*

As befits a potentially hazardous substance, glutamate is kept safely sealed within the brain cells. A healthy neuron releases glutamate only when it needs to convey a message, then immediately sucks the messenger back inside. Glutamate concentration inside the cells is 10,000 times greater than outside them. If we follow the dam analogy, that would be equivalent to holding 10,000 cubic feet of glutamate behind the dam and letting only a trickle of one cubic foot flow freely outside. A clever pumping mechanism makes sure this trickle never gets out of hand: When a neuron senses the presence of too much glutamate in the vicinity—the extracellular space—it switches on special pumps on its membrane and siphons the maverick glutamate back in.

This protective pumping process works beautifully as long as glutamate levels stay within the normal range. But the levels can rise sharply if a damaged cell spills out its glutamate. In such a case, the pumps on the cellular membranes can no longer cope with the situation, and glutamate reveals its destructive powers. It doesn’t kill the neuron directly. Rather, it overly excites the cell, causing it to open its pores excessively and let in large quantities of substances that are normally allowed to enter only in limited amounts.

One of these substances is sodium, which leads to cell swelling because its entry is accompanied by an inrush of water, needed to dilute the surplus sodium. The swelling squeezes the neighboring blood vessels, preventing normal blood flow and interrupting the supply of oxygen and glucose, which ultimately leads to cell death. Cell swelling, however, is reversible; the cells will shrink back once glutamate is removed from brain fluids. More dangerous than sodium is calcium, which is harmless under normal conditions but not when it rushes inside through excessively opened pores. An overload of calcium destroys the neuron’s vital structures and eventually kills it.

Regardless of what killed it, the dead cell spills out its glutamate, all the vast quantities of it that were supposed to be held back by the dam. The spill overly excites more cells, and these die in turn, spilling yet more glutamate. The destructive process repeats itself over and over, engulfing brain areas until the protective pumping mechanism finally manages to stop the spread of glutamate."

Recent research has confirmed that hypermetabolism has been primarily found in the right lingual gyrus and left cerebellar anterior lobe of the brain in individuals suffering from visual snow. The definition of hypermetabolism is described as "the physiological state of increased rate of metabolic activity and is characterized by an abnormal increase in metabolic rate." Hypermetabolism typically occurs after significant injury to the body. This means that the brain is trying to compensate for the injured areas in the brain by increasing metabolism to meet it's high energy demands. It is trying to function to the best of it's ability under the circumstances.

Normally the body can heal itself and regenerate under the right circumstances. But it is extremely difficult for the central nervous system - which includes the spinal cord and brain to be able to do so, due to it's inhibitory environment which prevents new neurons from forming. That is where stem cells come in. Stem cells are an exciting new discovery, because they can become literally any cell in the body including neurons. This is an amazing scientific breakthrough and has the potential to treat a whole host of conditions. Scientists are currently doing research and conducting trials.

Excitotoxicity can trigger your "fight or flight" response. If the brain and the body remain in the sympathetic fight or flight state for too long and too often, it is degenerative; it breaks us down. If this cycle continues, then eventually the system burns out. It is this cycle that results in autonomic nervous system dysfunction. The results are disastrous, digestion is shut down, metabolism, immune function and the detoxification system is impaired, blood pressure and heart rate are increased, circulation is impaired, sleep is disrupted, memory and cognitive function may be impaired, neurotransmitters are drained, our sense of smell, taste and sound are amplified, high levels of norepinephrine are released in the brain and the adrenal glands release a variety of hormones like adrenalin and cortisol.

I believe in order to find a treatment or cure for VS and it's accompanying symptoms, we need to address the underlying cause, reduce the excess excitatory activity in the brain, repair the damaged neurons, regain proper communication between neurons, rebalance the autonomic nervous system and prevent further cellular damage. We also need to figure out what genes, if any come into play. There is still a lot we don't know about the brain because it is such an remarkably complex organ. ''

Edited by SaraSara

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I have studied several models.

 

It has become obvious HPPD is NOT purely a glutamate or NMDA-receptor issue.  

 

Dr. A seemed to be leaning more toward Sodium Channel blocking via anti-convulsive drugs.   I looked towards NRIs and DRIs once you are over the main hump of the malady.  

HPPD is somewhat self-limiting.   In other words,  time seems to be the best cure. 

 

I was impressed with Quetiapine in terms of 'resetting' the brain to a default.  

 

Probably, it has to do with genetic predisposition to having more of the big 3 receptors in the prefrontal cortex (S, D, G).  Glucocorticoids, Choline perhaps.  Long-term alteration of plasticity, damage to the hippocampus [as well as potentially thalamus, hypothalamus, amygdala, sensory cortices,  CSF turnover, etc].   Also looking at the 5ht2A receptor inverse agonists, and kappa-opioid antagonists. 

Generally speaking, depending on what stage you are in, if you want to treat this psychopharmacologically, you may need a few drugs addressing a few models.

 

To be honest, nothing seems to work in the early stages, except perhaps Benzos and Antipsychotics to a certain degree: only to the point that you are being tranquillized.   [Also Dr. A's SCB anti-convulsive studies]

Edited by mgrade

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NMDA receptor is an aspartame receptor that accepts Glutamate as well.  

 

Certainly, this has been used as a model for Schizophrenia via PCP (which is a NMDA antagonist). 

-------------------------------------

This is why this is all very complicated.  Look at my last 2 posts (this one and the one before). 

If you have ADD to begin with and have a significant Amphetamine OD and survive, how exactly do you treat your ADD?

If you have a PCP OD, how do you deal with an underlying anxiety issue when prior to this you had been treating by aiding GABA agonism against Glutamate via Benzodiazepines?

____________________________

 

You take things like 1. aspartame and/or Glutamate and 2. Phenylalanine, which especially the latter is a major building block to dopamine (and the former (G) is the most abundant more important NTs in the body), and you bungle those lines up, respectively, you get the G line and D line going absolutely haywire. 

 

So the inhibitory and the adrenaline lines are totally out of whack, and because of the circumstances, some people are predisposed to a longer recovery through plasticity. 

Edited by mgrade

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This is so interesting, especially considering I've been basically pushing this theory -- right or wrong -- the last few months. The way Dr. Teichberg explains it is exactly what I've been envisioning could happen -- again, right or wrong. The fact is, no matter if you have HPPD, DP or VS there are a few common bonds that absolutely cannot be ignored:

1) Anxiety. It's far too common to dismiss. It's not like a few people with HPPD and VS have anxiety -- it's the vast majority, far more than is common in the general population. 

2) Trigger. Though there are reports of people who's VS symptoms come on slowly, these seem to be in the minority. In general people with HPPD, VS and DP have some form of incident (panic attacks) or agent (often times drugs) that acts as the damaging factor in giving them their condition. There is a clear before and after. 

3) Healing. While some people do not "recover" it appears a vast number of people make their way back to a state of normalcy by a process of healthy living. Sometimes it takes many years, but what can't be denied is that a clear recovery is taking place. 

When you consider all of these factors I just can't get past the idea that we aren't experiencing some form of cerebral injury. I really firmly believe accepting this fact will go a long way in bringing about change to this community of sufferers. We are not people who are imagining these symptoms. We are not crazy. We were not always mildly schizophrenic and then became full-blown mad as the result of a few drugs. I really believe we have suffered some form of an injury and that what we're dealing with is far more neurological than a commonly cited DSM condition. 

If I leave one mark on this site and on this condition I really hope that this is it. 

  • Upvote 2

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I agree , some kind of damage has happened. I did think of this possibility but I didn't want to admit it to myself. But as the author of this theory hypothesizes there are also some faulty genes involved that we need to discover and correct . Basically a cure for hppd and visual snow is most likely gene and stem cell therapy.

I also fully agree with u that hppd is pure neurological just like visual snow . 

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