about 15 minutes into the visual migraine, I can start to see in the center of vision again

Visual Migraine, Ocular Migraine Causes and Cures: Part 1, Exploration

My Experience with Visual Migraines

I had my first visual migraine about ten years ago in 2014. The frequency varies – sometimes I don’t have them for several months, and then I can get several in the same month. I just had one today, Sept 29, 2024 and at first, it was just blind spots and inability to read and to integrate my left and right eye images to build my face in the mirror. (I later determined this was due to blind spots in each eye). This visual migraine started without any flashing this time. About 8 minutes later, I got the flashing curved rip and then a long lasting mild headache I still feel 8 hours later.

On April 6th, 2024, I had one and asked people on a large Listserv about their experiences. Around 16 people shared their insights and what has helped them.Their clues sparked my deeper interest, and after a full day of research, I believe I now understand much more about the cause of visual migraines and some means to avoid them. Despite starting to implement some of the things I discovered, I had my strongest visual migraine yet on the evening of April 9th, 2024.

The Visual Migraine Experience

The flashing C shape with red and other colors of flashing lights started this time on the periphery of vision and moved toward the center over about 30 minutes. I’ve always had the opposite experience until this one. I had taken a large dose of vitamin C and was exercising before it happened. The trigger was the bright light of my computer screen, even though I had the f.lux screen saver blocking blue light at the time.

Understanding the Cause

The punchline is that an injury along the path of our interconnected visual system’s cells, such as by a change in microscopic blood and fluid circulation, can trigger a wave of spreading nerve cell reactions (depolarization and repolarization) which then moves across the visual cortex at a speed determined by the reactions taking place.

Various internal and external triggers, including but not limited to bright lights, dehydration, lack of sleep, hormones, oxidative stress, and bacterial infections, can each contribute to initiating visual migraine by causing or enhancing the root cause: direct damage to brain cells or damage to normal cellular function via small temporary micro blood flow impairment in the visual cortex of the brain.

My Question to the List:

“I sometimes get visual migraines. Anyone else out there have this experience? Having one now. For me it is a blind spot that grows over about 30 minutes as flashing expanding rip in my vision that expands slowly and leaves me functionally blind in an area, both eyes. Bright light sometimes triggers it. Kaiser is worthless on this, just say they don’t know the cause and to let them know if anything more dramatic happens. (They have scripts; Did you pass out? Did you have episodes of ESP? Did you hear the voice of the Pope coming from one of your shoes again? Standard questions.) Well, this time the visual migraine came with super loud tinnitus, nausea, headache and slight choking for a while. After about 40 minutes I can see again, but feel still a bit dizzy. Have any of you had this go on and did you find a solution? Thanks for any clues. “

Summary of Listserv Responses

#1: This person has had about half a dozen visual migraines in their life, which seem to occur randomly and without a clear trigger, and they have found that taking an Excedrin migraine pill, resting in a dark room, and waiting 20-60 minutes for the visual disturbances to subside is the most effective way to manage these episodes.

# 2: This person was told to take an aspirin immediately to avoid an actual migraine headache.

# 3: This person provided links which show a potential remedy for visual migraine appears to be the use of psychedelic substances, particularly psilocybin and LSD. Several studies and anecdotal reports suggest that these 5-HT2A receptor agonists can provide long-lasting therapeutic effects in treating both migraine and cluster headaches, even after a single or infrequent dose[52][53][54]. The research indicates that psilocybin, in particular, has shown promise in reducing the frequency and intensity of migraine attacks in controlled studies[54]. While the exact mechanisms are not fully understood, the search results highlight the growing interest and potential of psychedelic-assisted therapies for managing debilitating headache disorders, including visual migraines[52][53].

#4: This person got them the evening following surgery on the carotid artery and then again a few days later.

#5: This person’s experience with visual migraine suggests that dehydration is a consistent trigger for them and their adult son, and that drinking water seems to work best as a preventative measure, though they have not tried other methods. They note that even if they drink a good amount of water the next day, if they did not get enough water the previous day, they can still experience an ocular migraine. In one case, when they were having migraines daily, even twice a day, the suspected culprit was poor quality water from a refrigerator filtering system that needed a filter change.

#6: This person’s experience with visual migraine involved them thinking they were experiencing it, and upon contacting their eye doctor, the doctor said it was dangerous. Person suggested visiting the Eye Institute in Santa Rosa.

#7: This person’s experience with visual migraine suggests that dehydration, caffeine withdrawal, and exposure to bright/flashing lights are potential triggers for them. They have found that resting and taking aspirin can help provide relief when they experience visual migraine episodes, though they have not had them severe enough to cause vomiting, unlike some other people they know.

#8: This person suffered from totally incapacitating visual migraines for decades, finding little relief from medications and home remedies. However, a chiropractor’s specialized adjustment of the person’s skull plates, which were out of alignment from previous head injuries, ultimately resolved the migraines, though the person is now unable to find a similar practitioner in their area.

#9: This person suggests trying migraine glasses, like those from Axon Optics, as a possible remedy for their visual migraine experiences[66]. They note that two local friends have found these glasses to greatly reduce their migraine episodes, and the person themself uses the glasses when driving in the city to reduce the painful glare of sunlight, though they acknowledge there are now many other companies producing similar migraine glasses as well.

# 10: This person has experienced visual migraines with a zigzag light and rainbow edges, which made it difficult to see while driving. Based on a relative’s success, the person is advised to speak to their doctor about getting a prescription for the medication Imitrex (sumatriptan) to help stop the visual disturbances and headaches associated with their migraines.

#11: This person has experienced episodes of visual disturbances that resemble a visual migraine, where she has had to pull over while driving. She suspects dehydration may be a contributing factor, and staying hydrated could potentially help reduce the frequency or severity of these episodes.

#12: This person has experienced visual migraines their entire life, which always start with an ocular migraine symptom like a neon squiggle or vision loss in one eye. This is then followed by a severe, pounding headache on one side of their head, which is accompanied by a lingering “hangover” feeling for 24 hours. The person has been treated with medications since childhood, but found that triggers like caffeine and stress were contributing factors. They have also found that consuming cold water and bananas at the onset of the ocular migraine symptoms can sometimes stop the migraine from progressing.

#13: Visual migraines can be triggered by exposure to toxins, such as those released during building renovations. After the remodeling of the building this person worked in, they began experiencing frequent migraines, which they believe were caused by off-gassing from the new carpet, paint, and other building materials.

#14: This person experiences occasional visual migraine episodes without headaches, which they can attribute to triggers like bright light, such as sunlight or a computer screen. To manage these episodes, they have found that reducing bright light exposure, like turning down computer screen brightness, can help prevent the visual disturbances. They also find that resting in a quiet, dark room provides relief when an ocular migraine occurs. The person suggests keeping track of potential triggers and finding ways to avoid or mitigate them, as the specific triggers can vary from person to person. Provided was a link to a YouTube Video: Dr. Rupa Wong, board-certified ophthalmologist and eye surgeon, explains the 3 types of migraines that many people call ocular migraines and when you should see your eye doctor.[67]

#15: This person recommend trying Cranial Sacral Therapy (CST) and suggested a local practitioner by name.

#16: This person has experienced both painful migraines with nausea, vomiting, and light sensitivity, as well as non-painful visual migraines that caused a kaleidoscope effect in their vision. They found that smoking a small amount of marijuana (2-3 puffs) could provide relief from their migraine symptoms. The person notes that they are surprised that no one has suggested using marijuana as a potential remedy, given that they found it to be effective for them in the past.

Data Mining YouTube Comments

Based on one user telling me about a YouTube video with many comments, I next extracted all 5,643 comments from a popular video with 912,870 views about Visual Migraine posted April 1, 2022, by Dr. Rupa Wong, board-certified ophthalmologist and eye surgeon. I processed these comments using various techniques and created three lists, one of possible causes as phrases, one of possible cures as phrases, and one of relevant citations as URLs.

The Many Causes and Cures From YouTube Comments Data Mining (text file)

The Experience

I next considered my own experience and that of others. When experiencing a visual migraine you may first notice that parts of words you are looking at are missing or incomprehensible in areas of your vision. This quote is from a 2010 NPR interview with neurologist Oliver Sacks, who describes experiencing visual migraines from a young age and having them explained to him by his doctor mother:

“In a visual migraine, part of the world may disappear, outlines may become distorted. You may see a giant scintillating zigzag. Andwhen this first happened with me, I was terrified. But my mother, who was a doctor, and herself had visual migraine, explained to me, you know, in terms which a five-year-old could understand, that this was a little brain attack, it would only last a few minutes, and it wouldn’t do one any harm.”[25]

Symptoms of a visual migraine (also called migraine with aura) include:

Blind spots or scotomas – A small, flickering, jagged blind spot that can grow bigger and form a “C” shape in the visual field.[1][3] Flashes of light or seeing stars – Bright, shimmering, sparkling areas or patterns that slowly expand outward.[1][3] Other visual distortions – Seeing zig-zag lines, shapes, or other patterns.[1][3]

The visual symptoms typically last 20-30 minutes before resolving[1][3]. The visual symptoms of migraine with aura typically last 5-60 minutes and are usually followed by the headache phase.[3][4] In some cases, visual migraine can occur without a headache, which is called an “acephalgic” or “silent” migraine.[1][2][3][7][12] Ocular migraine is a distinct type that only affects one eye.

Associated Symptoms

Other associated symptoms that can occur with visual migraine include:

Tinnitus (ringing in the ears)
Tingling or numbness
Difficulty speaking
Weakness on one side of the face[1][3]
Dry eyes
Floaters

The visual symptoms of visual migraine are considered “positive” symptoms, meaning there is something the person sees, rather than just vision loss or darkness.[3] In contrast, retinal migraine specifically affects one eye and can cause temporary vision loss or blindness in that eye.[2][4]

Visual Migraine vs Regular Migraine

The key differences between visual migraine and regular migraine are:

In visual migraine, the visual symptoms typically last 20-30 minutes and can include blind spots, flashes of light, zigzag patterns, or other visual distortions. This occurs in both eyes.[6][7][8]

Regular migraine, on the other hand, is characterized by a severe, pounding headache, often accompanied by nausea, vomiting, and sensitivity to light and sound.[6][1][7]

Ocular migraine is a rarer type that only affects one eye and can cause temporary vision loss. This is distinct from visual migraine which affects both eyes.[6][1]

The underlying causes of visual and regular migraine are similar – they involve changes in blood flow in the brain or eye. But the specific mechanisms and symptoms differ between the two types.[1][7][5]

In summary, visual migraine is characterized by temporary visual disturbances, while regular migraine involves a severe headache and other associated symptoms.

Mechanism

Visual migraine, also known as migraine with aura, is a neurological phenomenon that occurs in about 25-30% of people with migraine.

The visual disturbances experienced during a migraine with aura are thought to be caused by a wave of neuronal excitation followed by inhibition, known as cortical spreading depression (CSD). [9][10] This CSD wave originates in the occipital lobe, the visual processing center of the brain, and then propagates across the cerebral cortex. Migraine-related visual symptoms can arise from disturbances at various stages of the visual system.[20][22]

The initial phase of neuronal excitation leads to the positive visual symptoms, such as flickering lights, zig-zag lines, and scintillating scotomas (blind spots) [9][11]. This is followed by a period of neuronal inhibition, which results in the negative visual symptoms like blind spots or tunnel vision. [9]11]

The exact mechanisms triggering this CSD wave is believed to involve a complex interplay of various neurotransmitters and ion imbalances.[9][10] Increased levels of excitatory neurotransmitters like glutamate, as well as changes in calcium, potassium, and sodium ion concentrations, may contribute to the initiation and propagation of the CSD wave.[9][10]

Additionally, the CSD wave is thought to activate the trigeminovascular system, which is involved in the generation of migraine pain.[9][10] This activation leads to the release of inflammatory mediators and vasodilation, which can cause the headache phase of the migraine attack.

In summary, the visual disturbances experienced during a migraine with aura are the result of a complex neurological process involving a wave of neuronal excitation and inhibition, known as cortical spreading depression, originating in the visual cortex of the brain. This CSD wave triggers the activation of the trigeminovascular system, leading to the development of the migraine headache.

What Are Astrocytes?

Astrocytes are star-shaped cells that are a type of glial cell in the brain and spinal cord, making up a significant portion of the central nervous system (CNS). They play several crucial roles, including:

Blood-Brain Barrier: Astrocytes are crucial for maintaining the blood-brain barrier (BBB), which controls what substances enter the brain from the bloodstream. They help form and regulate this protective shield, allowing necessary nutrients to pass while blocking harmful substances. Their star-shaped extensions, called “end-feet,” wrap around blood vessels, creating a physical barrier essential for the BBB’s integrity.
Support: Astrocytes provide structural support to neurons, helping to maintain the overall architecture of the brain.
Nutrient Supply: They help supply nutrients to neurons and maintain the balance of chemicals in the brain, which is essential for proper signaling between nerve cells.
Neurotransmitter Regulation: They are involved in clearing excess neurotransmitters, such as glutamate, from the synaptic space after nerve signals, which helps prevent overstimulation of neurons.
Communication: Astrocytes communicate with each other and with neurons through specialized connections, allowing them to respond to changes in their environment quickly.

Cortical Spreading Depression (CSD) Wave

Cortical spreading depression (CSD) is associated with diseases including migraine, trauma, cerebrovascular disease, and mitochondrial disease. While the exact mechanisms triggering the cortical spreading depression (CSD) wave during visual migraine are not yet fully understood, it involves a complex interplay of various neurotransmitters and ion imbalances:

Astrocytes are now recognized for their active involvement in modulating CSD through mechanisms like endfoot swelling, which affects neuroinflammatory responses and vascular dynamics. In the early stages of CSD, astrocytes provide neurons with energy support and clear K⁺ and glutamate from synaptic gaps, but in late stages, astrocytes release large amounts of lactic acid to exacerbate hypoxia. This occurs when the energy demand exceeds the astrocytes’ compensatory capacity.
Astrocyte endfoot swelling primarily due to K⁺ influx and abnormally active calcium (Ca²⁺) signaling is a characteristic of CSD. Neurons are not similarly altered[131].
Both NMDARs and Ca_V channels are necessary for CSD initiation, which is not determined by the extracellular K⁺ or neuronal depolarization levels per se, but requires the Ca_V-dependent activation of a threshold level of NMDARs. This occurs with a delay of several seconds relative to the rapid depolarization produced by the KCl stimulus[132].
Increased levels of excitatory neurotransmitters like glutamate, as well as changes in calcium, potassium, and sodium ion concentrations, may contribute to the initiation and propagation of the CSD wave.[1][2]
Depletion of serotonin (5-HT) has been shown to increase cortical excitability and sensitivity, as well as the frequency of the CSD wave.[1] This suggests that normal serotonin levels play an important role in regulating the neurocognitive system and preventing migraines.
The CSD wave is thought to activate the trigeminovascular system, which is involved in the generation of migraine pain[1][2]. This activation leads to the release of inflammatory mediators and vasodilation, contributing to the headache phase of the migraine attack.
Other factors like sex and genetic variables associated with migraine can also alter the brain’s vulnerability to CSD and influence migraine susceptibility[4].
Advances in neuroimaging have also allowed researchers to identify abnormal perfusion and metabolism in visual processing regions of the brain during migraine attacks[19].
The high density of neurons in the visual cortex makes it particularly susceptible to the cortical spreading depression that is thought to underlie migraine aura[19].
The initiation and propagation of these SD waves are driven by increased extracellular levels of potassium ions (K+) and excitatory amino acids like glutamate[121]. The increased K+ and glutamate levels disrupt the normal ionic homeostasis and lead to the intense depolarization of neurons and glial cells[121].

In summary, the exact mechanisms triggering the CSD wave during visual migraine involve a complex interplay of neurotransmitter imbalances, ion dysregulation, and activation of the trigeminovascular system, which together contribute to the initiation and propagation of the CSD wave and the subsequent migraine symptoms.

Natural History of Visual Migraine

The history of migraine and its visual symptoms dates back thousands of years. Ancient physicians like Hippocrates and Galen described visual symptoms associated with severe headaches, recognizing migraine as a distinct condition.[21] Over the centuries, physicians continued to document and classify the different types of visual disturbances that can occur with migraine, such as fortification spectra, flashes of color, and visual field defects.[20][21][22]

The first paper to describe scintillating scotomas appears to be the 1870 publication by Sir George Biddell Airy, as described in the JSTOR article “Sir G. B. Airy, F.R.S. (1801-1892) and the Symptomatology of Migraine”.[38] The article states that Airy provided “the classic description of the scintillating scotoma of migraine: I saw a great star, most splendid and beautiful, and with it an exceeding multitude of smaller stars.”[3] This account from Airy is cited as one of the earliest documented descriptions of the visual phenomenon known as a scintillating scotoma, which is a key symptom of migraine with aura.

In the mid-20th century, clinical studies began to systematically document the various types of visual aura symptoms experienced by migraine patients. One key study from this period was by Fisher in the 1940s-1960s, who described a total of 205 cases of “migrainous accompaniments” in subjects over 40 years old.[32] Fisher noted that these visual disturbances often included “scintillating scotoma” – a phenomenon characterized by “flashes of bright light, ‘foggy’ or blurred vision, zigzag or jagged lines, and small bright dots”.[32] Another study by O’Conner and Tredici in the 1960s examined 61 cases of migrainous visual symptoms, again often featuring “flashes of bright light” as a common complaint.[32]

Lashley’s Description of Visual Auras (1941).— Although scientific study of the migraine aura had been undertaken in the 19th century by scientists who suffered from migraine, a study that significantly furthered the understanding of the phenomenon was that carried out by the American psychologist Karl Spencer Lashley (1890-1958), a professor of psychology at Harvard University.[41]

In summary, the history of migraine and its visual symptoms dates back thousands of years, with ancient physicians like Hippocrates and Galen documenting the various visual disturbances associated with severe headaches. Over the centuries, physicians continued to classify and study these visual phenomena, such as the scintillating scotoma described by Sir George Biddell Airy in the 1870s. In the mid-20th century, clinical studies by researchers like Fisher and O’Conner further explored the different types of visual aura symptoms experienced by migraine patients, often featuring descriptions of flashes of light, blurred vision, and zigzag patterns. A significant contribution to the understanding of visual auras was the study conducted by the American psychologist Karl Spencer Lashley in 1941, which provided valuable insights into this aspect of the migraine experience.

The Speed of Spread

The reason the Cortical Spreading Depression (CSD) wave spreads in the visual cortex at a velocity of around 3 mm/min, causing the resulting visual migrane duration is:

The CSD wave is a slowly propagating wave of near-complete depolarization of neurons and glial cells across the cortex.

CSD waves propagate at a velocity of around 2-3 mm/min in the gyrencephalic (folded) human and feline cerebral cortex[42][43].
The propagation of the CSD wave is driven by the rise in extracellular potassium (K+) concentration, which depolarizes adjacent cells and causes them to also enter the CSD state[44][45].
The exchange of ions and molecules during CSD, such as the influx of Na+, Ca2+, and water, and efflux of K+, H+, glutamate, and ATP, is what leads to the near-complete depolarization of neurons and glia[2][44][45][46].
The relatively slow 2-3 mm/min propagation velocity of the CSD wave is a characteristic feature that distinguishes it from other types of neuronal excitation waves[42][43][45].

Lashley suggested that “an inhibitory process, in the case of the blind areas, or an excitatory process, in the case of scintillations, is initiated in one part of the visual cortex and spreads over an additional area.” Thus, distinguishing the excitatory from the inhibitory part of the aura, he realized that during the spreading of the process, “activity at the point where it is initiated is extinguished, and the process of extinction also spreads over the same area at about the same rate as does the active process.”

Lashley was able to determine the rate of spread. “Ten to twelve minutes is required for spread of the outer margin from the region of the macula to the blindspot of the homolateral eye” and the total time for the spread from the macular to the temporal area was what we also hear from our patients: 20 minutes. The anteroposterior length of the striate area being about 67 mm, he concluded that the “wave of intense excitation is propagated at a rate of 3 mm/minute or less across the visual cortex” and that “the wave is followed by complete inhibition of activity, with recovery progressing at the same rate,” adding that sometimes “the inhibition spreads without the preceding excitatory wave.” Later Lashley’s theories had great impact, not least because of the description of Leão’s cortical spreading depression (CSD) in 1944,¹⁰ 3 years after his paper was published in 1941.

In summary, the 3 mm/min propagation velocity of the CSD wave is an inherent property of the underlying ionic and metabolic changes that drive the wave of near-complete depolarization across the cortical tissue. This slow, wave-like propagation is a key aspect of CSD that links it to migraine aura and other neurological phenomena.

Visual Migraine, Ocular Migraine Causes and Cures: Part 2, Causes

In part one of this three part series, we explored the topic of visual or ocular migraine. In this section we will explore in great detail the causes for visual migraines.

Causes

At the level of neurons, the cause of visual migraine is changes in electrical activity in the brain that lead to a rapid positive charge or depolarization of neurons and glial cells.[30]

Changes In Blood Flow

The visual symptoms of ocular migraine are thought to be due to this transient hypoperfusion (temporary blood flow problem) or ischemia in the eye, which then resolves as the blood vessels relax and normal blood flow is restored.[83] The key change in blood flow that causes visual migraine is a temporary constriction or narrowing of the blood vessels in the eye or visual cortex of the brain which reduces blood supply and triggers the visual disturbances.[84]

This was a key discovery for me, a way to tie the various seemingly unrelated triggers together that started to make sense.

Common Visual Migraine Triggers

Knowing the above, let’s look through the filter of blood flow dis-regulation at common triggers for people predisposed to migraine with aura,[30] These include:

Bright lights: Activation by blue light (~480 nm wavelength) occurs in intrinsically photosensitive retinal ganglion cells (ipRGCs). Optogenetic activation of vascular smooth muscle cells can rapidly induce constriction of brain arterioles, including those in the visual cortex.[91] Bright light exposure could directly trigger vasoconstriction in the visual cortex through photostimulation of light-sensitive opsins. Melanopsin cells could trigger a cascade of neural signals that ultimately lead to vasoconstriction in the visual cortex.

Dehydration – Dehydration can disrupt the normal matching of cerebral blood flow to neuronal activity and metabolic demand in the brain.[86] This impairment of neurovascular regulation may be particularly pronounced in the visual cortex, leading to localized vasoconstriction and reduced perfusion in this brain region. Chronic dehydration and the associated “allostatic overload” can lead to endothelial injury, increased inflammation, and impaired vasodilatory mechanisms in the cerebral vasculature.[88]

Too much or too little sleep – Sleep profoundly transforms neurovascular dynamics, with changes in the strength and timing of the coupling between neural activity and vascular responses.[93] Sleep deprivation can lead to blood vessel expansion and decreased vascular compliance in the brain.[92] This prolonged vascular dilation during sleep deprivation may eventually reach physical limits, resulting in blunted hemodynamic responses and reduced blood flow to the visual cortex.[92] Both sleep deprivation and excessive sleep could impair this normal neurovascular coupling in the visual cortex, leading to dysregulation of blood flow and potentially vasoconstriction.[92]

Stress (Chronic) – Mechanisms by which chronic stress can induce cerebrovascular changes include increased inflammation, oxidative stress, and impairment of vasodilatory pathways like nitric oxide signaling.[86] Chronic stress, in particular, may impair the neurovascular balance responsible for matching cerebral blood flow to brain metabolic demand, leading to sustained vasoconstriction and potential brain injury.[86]

Anxiety – Anxiety can have systematic effects on cortical activity, including a linear decrease in cerebral metabolic rate and blood flow in the visual cortex.[87]

Consuming aged cheese and food additives like nitrates – In some cases, nitrates can promote vasodilation and improved blood flow. But in high doses or with certain genetic/health factors, nitrates may also contribute to vasoconstriction and impaired vascular function.[85]

Caffeine consumption – Caffeine is associated with cerebral hypoperfusion and can reduce global cerebral blood flow by 22-30% in humans.[88][89] Caffeine’s effects on the cerebrovascular system are particularly pronounced in the visual cortex. Caffeine has been shown to delay the normal neurovascular coupling response in the retina and macular capillary plexuses during the transition from dark to light adaptation. [90] Long-term, high caffeine intake is associated with increased arterial stiffness, vascular resistance, and blood pressure.[88]

Menstruation – Changes in circulating levels of estrogen (E2) and progesterone (PG) across the menstrual cycle are associated with oscillations in cerebrovascular reactivity (CVR)[94][95] Specifically, lower levels of estrogen during the early follicular phase may be linked to increased vasoconstriction and reduced blood flow in the visual cortex.[94][95]

WiFi and Cell Radiation Explored

Given claims that telecommunications radiation can trigger voltage sensing calcium ion channels, causing neurological effects, I spent time verifying the first mentions of scintillating scotoma to rule out EMF radiation as a primary cause.

Background: Several studies have found that RF exposure can alter calcium ion movements and signaling in cells, including in the central nervous system[61][62][63]. The proposed mechanism is that the electromagnetic fields can interact with and activate voltage-gated calcium channels, leading to increased intracellular calcium levels[63][64]. This calcium dysregulation could then trigger downstream effects like changes in neurotransmitter metabolism, oxidative stress, and apoptosis pathways that may contribute to neurological impacts[63]. The experimental evidence comes mainly from cell and animal studies, and more research is needed to confirm the relevance to human health[62][63]. Nonetheless, the available data suggests a plausible pathway by which RF exposure could influence neurological function, warranting further investigation.

Visual migraines with flashing blind areas have been reported clearly in two cases I reviewed. The first in the 1870s and the next clearly in 1941, both long before the advent of cell phones. For historical reference, the first portable cell phone was the Motorola DynaTAC 8000X, which was developed by Motorola engineer Martin Cooper. On April 3, 1973, Cooper made the first-ever cell phone call on this prototype device.

The phenomena of visual migraine predates cell phone use by over 30 years, seemingly removing it from suspicion as a primary cause.

Nevertheless, recent studies indicate that electromagnetic fields (EMF) can have significant effects on astrocytes, which are crucial for maintaining brain health and the blood-brain barrier (BBB), and which are involved in SCD which is the neurological root of visual migraines. Here are the key findings related to how EMF spikes can lead to catastrophic damage to glial cells like astrocytes:

1. Impact on Astrocytic Function:
– EMF exposure can alter the secretion of critical substances by astrocytes, including ATP, which is essential for cellular communication and energy metabolism. Changes in ATP levels can affect the inflammatory response mediated by microglia, another type of glial cell [133].

2. Reactive States:
– Astrocytes can become reactive in response to inflammatory signals, such as tumor necrosis factor (TNF). This reactive state can lead to dysfunction of the BBB, characterized by increased permeability and loss of barrier integrity. Reactive astrocytes may secrete harmful cytokines that exacerbate neuroinflammation and further compromise BBB function [134][135].

3. Molecular Mechanisms:
– EMF exposure has been shown to increase the expression of heat shock proteins (HSP70) while inhibiting factors like hypoxia-inducible factor 1α (HIF1α). These changes can lead to decreased inflammation and promote neurorestoration processes, but excessive or prolonged exposure may push astrocytes into a more destructive reactive state [133].

4. Consequences of Dysfunction:
– When astrocytes are unable to perform their functions effectively due to EMF spikes or other stressors, it can result in a cascade of negative effects, including brain edema, increased leakage of substances from blood vessels into brain tissue, and potential neuronal damage [135][136][137].

In summary, EMF spikes can disrupt the normal functioning of astrocytes, leading to inflammatory responses that compromise the blood-brain barrier and overall brain health.

Secondary Cause, by Oxidative Stress

Many animal and cell studies have shown that exposure to RF electromagnetic fields (RF-EMF) from sources like mobile phones can increase oxidative stress markers such as reactive oxygen species (ROS), lipid peroxidation, and nitric oxide production[101][103][104]. These effects have been observed in various tissues, including the testes, endometrium, uterus, and ovaries[101].

Specifically, studies on male rats and mice have found that exposure to RF-EMF at specific absorption rates (SAR) ranging from 0.043-0.9 W/kg can lead to increased oxidative stress markers in the testes[101]. Similarly, exposure of female rats to 900 MHz RF-EMF at 0.014-4 W/kg resulted in increased lipid peroxidation and decreased antioxidant levels in the uterus and ovaries[101].

The proposed mechanism is that RF-EMF can target the mitochondria, leading to perturbation of proton flux and promoting electron leakage, which generates superoxide anions and triggers further reactive oxygen species production, causing oxidative stress[104].

However, the search results also note that the effects of long-term RF-EMF exposure on age-induced oxidative stress and neuroinflammation in the brain were not significantly altered in a study on aging mice[103]. This suggests the biological effects may depend on factors like tissue type, exposure duration, and age.

Overall, the preponderance of evidence from animal and cell studies indicates that telecommunications RF radiation can induce oxidative stress in various tissues of the body[101][104]. But more research is still needed, especially on the long-term effects in humans[102].

Oxidative Stress Role in Visual Migraine

Oxidative stress can potentially cause visual cortex blood vessel constriction through the following mechanisms:

1. Impairment of Neurovascular Coupling: The neurovascular unit (NVU), which includes the cerebral blood vessels, is highly sensitive to oxidative stress.[99][100] Oxidative stress can disrupt the normal neurovascular coupling mechanisms that match cerebral blood flow to neuronal activity in the visual cortex.[99][100] This impairment of the vascular response to neuronal activation in the visual cortex could lead to sustained vasoconstriction and reduced perfusion.[99][100]

2. Vascular Endothelial Dysfunction: Oxidative stress can directly damage the vascular endothelium, impairing its ability to regulate vascular tone and promote vasodilation.[98][99] This endothelial dysfunction can shift the balance towards vasoconstriction in the cerebral blood vessels supplying the visual cortex.[98][99]

3. Activation of Vasoconstrictor Pathways: Oxidative stress can activate signaling pathways that promote vasoconstriction, such as those involving angiotensin II and NADPH oxidases.[98][99] The increased production of reactive oxygen species (ROS) can directly trigger constriction of the visual cortex blood vessels.[98][99]

4. Structural Vascular Remodeling: Chronic oxidative stress can lead to structural changes in the cerebral vasculature, including increased arterial stiffness and reduced vessel density.[99][100]
– These vascular remodeling effects can impair the ability of the visual cortex blood vessels to regulate blood flow and maintain proper perfusion.[99][100]

In summary, the search results indicate that oxidative stress can cause visual cortex blood vessel constriction through multiple mechanisms, including disruption of neurovascular coupling, endothelial dysfunction, activation of vasoconstrictor pathways, and structural vascular remodeling.[3][4][5] This impairment of blood flow regulation in the visual cortex may contribute to the visual disturbances associated with various neurological and cerebrovascular disorders.

Impaired Perfusion (Micro Blood Flow)

Impaired perfusion can contribute to the development and propagation of Cortical Spreading Depression (CSD) in the following ways:

1. Reduced oxygen and metabolic supply: During CSD, there is a massive increase in metabolic demand and energy consumption by neurons and glia[47][48][50]. However, the vascular response to this increased demand is often impaired, leading to a mismatch between supply and demand. This can result in tissue hypoxia and metabolic distress, which further propagates the CSD wave[47][48][50].

2. Altered neurovascular coupling: CSD disrupts the normal coupling between neuronal activity, metabolism, and cerebral blood flow (CBF)[50]. This neurovascular uncoupling can prevent the appropriate vasodilatory response to the increased metabolic needs during CSD, exacerbating the mismatch between supply and demand[47][50].

3. Vasoconstriction and reduced perfusion: CSD can trigger vasoconstriction and reduce CBF, which in turn can impair the ability of the tissue to recover from the depolarization and metabolic disturbances[47][48][50]. This can lead to a vicious cycle of spreading depolarization and reduced perfusion.

4. Ionic and metabolic disturbances: The massive ionic shifts and metabolic changes that occur during CSD, such as increases in extracellular K+ and glutamate, can directly impair vascular function and autoregulation, further reducing perfusion[47][48][49][51].

Search results indicate that impaired perfusion and neurovascular coupling play a key role in the propagation and consequences of CSD. The mismatch between metabolic demand and vascular supply during CSD can exacerbate the ionic, metabolic, and electrical disturbances, leading to a self-propagating wave of depolarization across the cortex[47][48][50][51].

Based on the search results provided, the evidence suggests that ischemic changes can be responsible for triggering and propagating the cortical spreading depression (CSD) wave.

Ischemia Induces CSD

CSD is a wave of mass neuronal depolarization associated with a net influx of cations and water, leading to a negative DC shift in the EEG[2].

Imaging studies have shown that CSD can be accompanied by ischemia, as indicated by BOLD signal changes and reductions in tissue oxygen levels[106][107].

The ischemic changes during CSD are thought to be caused by vasoconstriction and reduced vascular reactivity, which can lead to a “spreading ischemia” coupled to the depolarization phase[109][110].

Mechanism of Ischemia-Induced CSD

Potassium released during CSD is believed to act as a vasoconstrictor, inducing the spreading ischemia[110].

Pericytes, contractile cells on capillaries, may also contribute to the capillary constrictions that reduce cerebral blood flow during CSD[110].

This ischemia-induced reduction in blood flow and oxygen levels can further propagate the CSD wave by increasing neuronal excitability through mechanisms like persistent sodium currents and NMDA receptor activation[110].

Ischemic Implications

The ischemic changes associated with CSD are thought to be relevant to human disease states like migraine and stroke, where CSD may play a role in the pathophysiology[108][110].

Understanding the interplay between CSD and ischemia is important, as therapies that can modify the vascular response to CSD, such as nitric oxide donors or calcium channel blockers, may prove useful in treating these conditions[110].

In summary, the search results indicate that ischemic changes, driven by vasoconstriction and reduced blood flow, are a key mechanism by which CSD waves are initiated and propagated across the cerebral cortex[106][107][109][110].

Microbial Ischemia-Induced CSD

Microbes can contribute to the development of ischemia and cerebral spreading depression (CSD) through several mechanisms:

1. Disruption of the gut microbiome: Studies have shown that ischemic stroke can lead to dysbiosis of the gut microbiome, with an increase in bacteria from the Enterobacteriaceae family[111]. This gut microbiome imbalance can enhance systemic inflammation and contribute to cerebral infarction injury.

2. Induction of inflammation: Bacterial infections can trigger an inflammatory response, which can lead to the formation of blood clots and reduced blood flow, causing ischemia[113]. The excessive release of inflammatory cytokines during sepsis can also result in vasodilation, edema, and blood clot formation, further exacerbating ischemia[113].

3. Toxin production: Certain bacteria, such as Clostridium perfringens, can produce toxins like α-toxin and θ-toxin that can damage cell membranes and contribute to the spread of ischemia[3]. These toxins can also disrupt the integrity of blood vessels, leading to thrombosis and ischemia.

4. Disruption of the blood-brain barrier: Bacterial infections can compromise the blood-brain barrier, allowing the entry of pathogens and inflammatory mediators into the brain, which can trigger CSD[114][115]. CSD is a wave of neuronal and glial depolarization that can lead to vasoconstriction, reduced blood flow, and ischemia.

In summary, microbes can contribute to ischemia and CSD through various mechanisms, including disruption of the gut microbiome, induction of inflammation, production of bacterial toxins, and compromising the blood-brain barrier. Understanding these microbial-host interactions is crucial for developing targeted therapies to prevent and manage ischemic stroke and its associated complications.

Gut Bacteria Differences

There is evidence that the gut microbiome may play a role in the development of migraine, including the visual aura symptoms that some migraine sufferers experience:

Studies show that migraine sufferers have a different composition of gut bacteria compared to healthy individuals[73][74]. Specifically, migraine patients tend to have higher levels of bacteria that can break down nitrates[74]. When these nitrates are broken down, it can lead to the production of nitric oxide, which can dilate blood vessels in the brain and trigger migraine symptoms like visual aura[74].

The review article[76] also notes that certain neurotransmitters involved in pain perception, like glutamate and GABA, are produced by gut bacteria and can influence migraine through the gut-brain axis. Imbalances in these neurotransmitters may contribute to migraine symptoms.

Additionally, the study[75] found causal links between specific gut bacterial taxa and the development of migraine, including migraine with aura (MA). This provides more direct evidence that the gut microbiome can influence the underlying mechanisms of visual migraine symptoms.

In summary, the search results indicate that dysbiosis, or an imbalance in gut bacteria, may be a contributing factor to the development of visual migraine symptoms through the modulation of neurotransmitters, inflammatory pathways, and vascular function in the brain. Further research is still needed to fully elucidate the mechanisms involved[73][76].

Low Level Immune Signaling

The immune system plays an important role in the pathophysiology of migraine, including migraine with visual aura (MA):

– Neuroinflammation involving the activation of innate immune cells like microglia and astrocytes has been observed in the central nervous system during cortical spreading depression, which is considered the pathophysiological substrate of migraine with aura.[118]

– Increased levels of pro-inflammatory cytokines like TNF-α, IL-1β, and IL-6 have been found in migraine patients, both during and between attacks.[118] This suggests low-level immune signaling may contribute to migraine pathogenesis.

– Mast cells, which can release inflammatory mediators, are found in high numbers in the dura mater and can interact with trigeminal afferents, potentially contributing to migraine pain.[119]

– Dendritic cells and T lymphocytes have also been reported in the dural vessels and subarachnoid space of migraine patients, indicating the involvement of adaptive immune responses.[120]

– The anti-inflammatory cytokine IL-10 has been found to be decreased in migraine patients compared to controls, further suggesting an imbalance in immune regulation.[120]

In summary, the search results indicate that low-level immune signaling, involving both innate and adaptive immune components, likely plays an important role in the pathophysiology of migraine with visual aura. The activation of inflammatory pathways and imbalance in immune regulation may contribute to the development of cortical spreading depression and other neurological events underlying the visual symptoms of MA.[116][117][118][119][120]

The Perils of Blue Light

Why does blue light trigger CSD through activation of ipRGCs and potentially other photoreceptor pathways in some people and not in others?

Blue light exposure can trigger the death of photoreceptor cells in the retina, leading to age-related macular degeneration, a leading cause of blindness. This occurs through a process where blue light activates retinal molecules in the eye, which then generate toxic chemical reactions that kill the photoreceptor cells.[68]

The key factors are:

1. Blue light from digital devices and the sun can penetrate the eye’s cornea and lens and reach the retina.[68]

2. In the retina, blue light causes retinal molecules to trigger reactions that produce poisonous chemicals, which then kill the photoreceptor cells.[68] These photoreceptor cells do not regenerate, so once they are dead, vision loss is permanent.[68]

3. As people age or their immune system is suppressed, they lose the ability to fight against the toxic effects of retinal and blue light, leading to accelerated damage and vision loss.[68]

4. Certain individuals may be more susceptible to this blue light-induced retinal damage due to genetic or other factors that affect their ability to protect against the toxic reactions.[68][71][72]

In summary, the variability in how individuals respond to blue light exposure likely stems from differences in factors like age, immune function, and underlying genetic predispositions that influence the eye’s vulnerability to blue light-induced photoreceptor cell death.[68][71][72]

What Else May Help or Exacerbate CSD?

This is A.I. search and logic, so check with your doctor before taking any of these recommendations. As an experiment, I took all of the supplements with the thumbs up tonight since I had a visual migraine around noon today. Will see how I sleep and so on.

???? Astaxanthin – Effectively scavenges reactive oxygen species (ROS) and enhances mitochondrial function, potentially offering neuroprotective benefits that could be beneficial in conditions associated with CSD. Additionally, its ability to cross the blood-brain barrier supports its role in protecting brain cells from oxidative damage and inflammation linked to CSD[141][142][143].

???? Carnitine, L-Carnitine L-Tartrate – May help mitigate cortical spreading depression (CSD) by reducing markers of hypoxic stress and enhancing muscle oxygenation during exercise, which could support overall brain health.

???? Chlorella – Chlorella may help mitigate cortical spreading depression (CSD) due to its antioxidant properties, which can reduce oxidative stress and inflammation in the brain, as indicated by studies showing that it improves the velocity of CSD propagation in animal models. Research has demonstrated that Chlorella vulgaris contains beneficial biomolecules that can enhance brain health and protect against oxidative damage, potentially offering a protective role during CSD events.

???? Cistus Tea – Cistus tea may help mitigate cortical spreading depression (CSD) due to its antioxidant properties, which can reduce oxidative stress and inflammation in the brain.

???? Claritin – Claritin, an antihistamine, may help alleviate symptoms associated with migraines and cortical spreading depression (CSD) by reducing inflammation and histamine-related reactions in the brain, although direct effects on CSD initiation are not well established. Research indicates that managing allergic responses and inflammation can potentially reduce the frequency of migraine attacks, often linked to CSD.

???? CO2 Build Up in Room – Accumulation of carbon dioxide (CO2) in a room can lead to cortical spreading depression (CSD) due to its potential to induce hypercapnia,

???? Concrobium Exposure – Exposure to Concrobium, which is used for mold remediation, may lead to cortical spreading depression (CSD) due to potential neurotoxic effects from its chemical components, particularly if they trigger an inflammatory response in the brain.

???? Cranberry Fruit – Research indicates that cranberries contain unique phytonutrients, such as A-type proanthocyanidins, that not only help prevent bacterial adhesion in urinary tract infections but also exhibit neuroprotective effects. These properties suggest that cranberry consumption could be beneficial in managing conditions associated with CSD, potentially improving overall brain health and reducing the risk of neurodegenerative diseases linked to oxidative damage.

???? D-Ribose – may help mitigate cortical spreading depression (CSD) by enhancing ATP production and improving cellular energy metabolism, which is crucial for maintaining neuronal function and integrity.

???? Exercise – Regular exercise may help reduce the frequency and severity of cortical spreading depression (CSD) by improving overall brain health, enhancing blood flow, and promoting neuroplasticity, which can support neuronal function and resilience against stressors.

???? Fluids, Excess – Excessive fluid accumulation can lead to increased intracranial pressure and cerebral edema, which may contribute to cortical spreading depression (CSD) by disrupting normal neuronal function and increasing the risk of neuronal injury.

???? French Maritime Pine Bark Extract – French maritime pine bark extract may help mitigate cortical spreading depression (CSD) due to its rich content of oligomeric proanthocyanidins (OPCs), which possess strong antioxidant and anti-inflammatory properties that can protect neuronal health. Research indicates that OPCs can reduce oxidative stress and improve blood flow, potentially offering neuroprotective benefits that may be advantageous in conditions associated with CSD. Additionally, studies have shown that this extract can enhance cognitive function and support overall brain health, suggesting its utility in managing symptoms related to CSD.

???? Glycine – Glycine may help mitigate cortical spreading depression (CSD) due to its role in modulating NMDA receptor activity, which is crucial for neuronal signaling and can influence the initiation and propagation of CSD. Research indicates that glycine levels are significantly reduced during CSD, suggesting that maintaining adequate glycine concentrations may support neuroprotection and reduce the severity of CSD-related symptoms. Additionally, glycine administration has been associated with improved cognitive function and reduced inflammation, further supporting its potential beneficial effects on CSD.

???? Hyaluronic acid – Hyaluronic acid may help in managing CSD by promoting hydration and tissue repair, potentially supporting the health of astrocytes and the blood-brain barrier.

???? Iron, Chelated – Chelated iron may increase the risk of cortical spreading depression (CSD) due to its potential to influence oxidative stress and excitotoxicity, as excess iron can promote the production of reactive oxygen species (ROS) and disrupt neuronal function.

???? Lysine, L-Lysine HCL – Neuroprotective Effects: L-Lysine may protect against excitotoxicity by inhibiting glutamate-induced neuronal activity, thereby reducing the risk of neuronal damage during stress or ischemic conditions. In the brain, L-lysine and its metabolites interact with various neuronal receptors, including those involved in the GABAergic system. This interaction can enhance the affinity of the GABA-benzodiazepine receptor complex, promoting inhibitory neurotransmission and potentially reducing anxiety.

???? Magnesium Oxide – Magnesium oxide may help mitigate cortical spreading depression (CSD) by supporting magnesium levels in the brain, which are crucial for regulating NMDA receptor activity and preventing excitotoxicity.

???? Magnesium Threonate – Research indicates that magnesium threonate enhances synaptic plasticity and protects against oxidative stress, making it particularly effective in improving cognitive function and reducing neuroinflammation associated with CSD. Its capacity to cross the blood-brain barrier allows it to exert neuroprotective effects, potentially benefiting conditions linked to CSD and enhancing overall brain health.

???? Milk Thistle formula with dandelion, burdock, black radish, ginger and parsley – A formula containing milk thistle, dandelion, burdock, black radish, ginger, and parsley may help mitigate cortical spreading depression (CSD) due to the combined antioxidant and anti-inflammatory properties of these ingredients, which can support liver health and potentially reduce neuroinflammation

???? Moldy Cabbage – Moldy cabbage can potentially contribute to cortical spreading depression (CSD) due to the presence of mycotoxins produced by mold, which may induce neuroinflammation and disrupt normal neuronal function. Mycotoxins can lead to various neurological issues, including inflammation and oxidative stress, both of which are associated with the initiation and propagation of CSD.

???? NAC, N-Acetyl L-Cysteine – May help mitigate cortical spreading depression (CSD) due to its antioxidant properties, which can reduce oxidative stress and inflammation in the brain, as well as its ability to enhance glutathione levels, a key antioxidant that supports neuronal health.

???? Omega3s (EPA 650mg, DHA 450mg) – Research indicates that EPA and DHA can reduce neuroinflammation and promote neuronal membrane fluidity, which is crucial for maintaining proper brain function. Additionally, studies have shown that omega-3 supplementation may improve cognitive function and reduce the risk of neurodegenerative diseases, suggesting potential benefits in managing conditions associated with CSD.

???? Resveratrol (Japanese Knotweed) – has neuroprotective effects, including the ability to modulate inflammatory responses and improve blood flow, suggesting it may be beneficial in managing conditions associated with CSD. Additionally, its role in enhancing mitochondrial function supports its potential protective effects against neurodegenerative processes linked to CSD.

???? Sitting Computer Use, Prolonged – Prolonged sitting while using a computer may increase the risk of cortical spreading depression (CSD) due to its association with decreased cerebral blood flow and increased fatigue, which can exacerbate neurological symptoms.

⇔ Stevia – Stevia is unlikely to have a direct effect on CSD, as there is no substantial evidence linking it to either the initiation or prevention of CSD.

???? Vitamin A (Retinyl palmitate, 15,000 IU) – particularly in its active forms like retinol, can neutralize free radicals and stabilize cellular membranes, potentially offering neuroprotective benefits that are important in conditions associated with CSD. Vitamin A is crucial for maintaining vision and cellular integrity, and it has antioxidant properties that may protect against oxidative stress in the brain[144][145].

???? Vitamin C – May help mitigate cortical spreading depression (CSD) due to its potent antioxidant properties, which can reduce oxidative stress and inflammation in the brain, potentially protecting against neuronal damage associated with CSD.

???? Vitamin D3 – Has neuroprotective effects and can influence calcium homeostasis, which is crucial for maintaining neuronal health and preventing excitotoxicity linked to CSD. Additionally, studies suggest that adequate vitamin D levels are associated with improved cognitive function and reduced risk of neurodegenerative diseases, further supporting its potential benefits in managing conditions related to CSD.

???? Vitamin K2 as MK7 – Research indicates that MK7 plays a crucial role in activating proteins that regulate calcium levels in the body, thereby preventing arterial calcification and promoting cardiovascular health, both of which are important for maintaining overall brain function and reducing the risk of CSD-related symptoms. Additionally, its neuroprotective effects may enhance cognitive function and resilience against oxidative stress, further supporting its potential benefits in managing conditions linked to CSD.

Visual Migraine, Ocular Migraine Causes and Cures: Part 3, Prevention and Cures

In part one of this three part series, we explored the topic of visual or ocular migraine. In part two we explored causes in great detail. In this final section we will explore possible cures for visual migraines. This final segment also includes all citations for the series at the end so you can explore in greater depth.

Relief

Asprin – Taking an aspirin immediately can help avoid an actual migraine headache.[2]
Take Excedrin migraine pill, resting in a dark room, and waiting 20-60 minutes for the visual disturbances to subside is an effective way to manage occasional, randomly occurring visual migraines.[1]
Consuming cold water and bananas at the onset of ocular migraine symptoms can sometimes stop the migraine from progressing.
Smoking a small amount of marijuana (“2-3 puffs”) can provide relief from migraine symptoms for some people.

Prevention

Lifestyle changes to avoid known triggers, such as reducing caffeine intake and practicing stress relief techniques[12]
Prescription medications like beta-blockers, antidepressants, anticonvulsants, and calcium channel blockers to prevent future visual migraine episodes[12][26]
Over-the-counter pain relievers or anti-nausea medication to relieve headache and nausea symptoms[12]
Dehydration is a consistent trigger for some people, and drinking water seems to work best as a preventative measure.
Migraine glasses, like those from Axon Optics, have helped reduce migraine episodes for some people.
The medication Imitrex (sumatriptan) can help stop visual disturbances and headaches associated with migraines.
Inject-able monoclonal antibody
Staying hydrated may help reduce the frequency or severity of visual disturbance episodes.
Triggers can include dehydration, caffeine withdrawal, and exposure to bright/flashing lights. Resting and taking aspirin can provide relief.
Reducing bright light exposure and resting in a dark, quiet room can provide relief during visual migraine episodes.

Potential Cures

Here is a list of possible remedies for visual migraines from everything used to create this article. Each of these should be carefully considered for side effects and for some of them, you should consult your doctor before attempting. Things that might help:

Cranial Sacral Therapy (CST) has been recommended as a potential remedy.
Remedy dry eye syndrome: Treating the dry eyes (finding the source such as allergy) will reduce the migraines
Remove toxins: Exposure to toxins released during building renovations can trigger visual migraines.
Psychedelic substances like psilocybin and LSD may provide long-lasting therapeutic effects in treating both migraine and cluster headaches, even after a single or infrequent dose.
Visual migraines can occur following certain medical procedures, like surgery on the carotid artery.
Visiting an eye doctor is important to rule out other dangerous conditions that can cause similar visual disturbances.
A specialized chiropractic adjustment to correct skull plate misalignment resolved long-term, incapacitating visual migraines for one person.

Probiotics

According to the search results, several studies have found that probiotic supplements can help reduce the frequency and severity of migraine headaches, including visual migraines:

– A large double-blind, randomized placebo-controlled trial found that a probiotic supplement containing 14 strains of “gut-friendly” bacteria significantly reduced both the frequency and severity of migraine attacks in patients with chronic and episodic migraines.[78]

– Another study showed that supplementation with a probiotic mixture of 7 bacterial strains reduced the frequency of migraine attacks by about a quarter and improved migraine-related symptoms.[82]

– An open-label trial found that 12-week supplementation with a probiotic along with minerals, vitamins, and herbs resulted in significant improvement in quality of life and pain relief in around 80% of migraine patients.[82]

The proposed mechanisms by which probiotics may help with migraines include reducing gut inflammation and permeability, modulating the gut-brain axis, and decreasing levels of compounds like tyramine that can trigger migraines.[80][81] The specific probiotic strains that have shown benefits for migraines include multi-strain formulations as well as strains like Lactobacillus and Bifidobacterium.[78][79][82]

So in summary, the available evidence suggests that certain probiotic supplements, particularly those containing multiple strains, may be effective at reducing the frequency and severity of visual migraines and other types of migraine headaches.[78][79][80][81][82]

Strategy: Reduce Glutamate

There is evidence that reducing brain glutamate levels can help prevent ocular (visual) migraine:

1. Glutamate is the main excitatory neurotransmitter in the central nervous system and is implicated in the initiation of migraine as well as central sensitization, which increases the frequency of migraine attacks.[128]

2. Excessive levels of glutamate can lead to excitotoxicity in the nervous system, which can disrupt normal neurotransmission and contribute to migraine pathophysiology.[128]

3. Glutamate-mediated excitotoxicity also leads to neuroinflammation, oxidative stress, blood-brain barrier permeability, and cerebral vasodilation, all of which are associated with migraine.[128]

4. Preclinical evidence supports the role of cortical spreading depression (CSD), which is triggered by local release of glutamate, in stimulating trigeminal neurons and causing migraine aura, including visual aura.[128]

5. Higher levels of glutamate have been observed in the plasma of both chronic and episodic migraine patients compared to healthy controls, supporting the important role of glutamate in migraine pathophysiology.[128][129]

6. Anti-glutamatergic anti-epileptic drugs have shown prophylactic efficacy in preventing migraine with and without aura, further suggesting that reducing brain glutamate levels can help prevent migraine attacks, including ocular migraine.[130]

In summary, the evidence indicates that excessive glutamate levels in the brain contribute to the initiation and progression of migraine, including visual aura, and that reducing brain glutamate through dietary, pharmacological, or other interventions may help prevent ocular migraine attacks.[126][127][128][129][130]

How to Reduce Brain Glutamate

There are several ways to reduce excess glutamate levels in the brain:

1. Dietary interventions: Removing or reducing foods high in free glutamate, such as gluten, dairy, soy, processed foods, bone broth, and certain fermented foods can help lower glutamate levels.[122]

2. Medications: Prescription drugs like Namenda (Memantine) and Amantadine can help reduce free glutamate levels.[122]

3. Supplements: Supplements that can help reduce glutamate include magnesium, selenium, B12, alpha lipoic acid, berberine, and certain herbs like cat’s claw, licorice root, ginseng, and ginkgo biloba.[122]

4. Lifestyle changes: Reducing screen time and avoiding alcohol can also help lower glutamate levels.[122][123]

5. Dietary alternatives: Choosing low-glutamate foods like cheddar cheese, certain fish (cod, mackerel, salmon), and avoiding high-glutamate foods like tomatoes, mushrooms, and peas can help manage glutamate intake.[124]

In summary, a combination of dietary changes, medications, supplements, and lifestyle modifications can be effective in reducing excess glutamate levels in the brain.[121][122][123][124][125]