My Visual Snow Syndrome Genetic Profile

A Personal Analysis of Genes Relevant to Visual Snow, Migraine Aura, and Cortical Hyperexcitability

Derived from 23andMe Raw Genomic Data  |  March 2026

About This Document

My name is not included here for privacy, but I am sharing this document because I believe my genetic data may be of interest to Visual Snow Syndrome researchers and to others in the VSS community who are trying to understand the biological basis of what we experience.

I have Visual Snow Syndrome and I recently got a 23andMe test and have been exploring the genomic data, looking specifically at genes that research has implicated in cortical excitability, thalamocortical function, ion channel regulation, and visual processing.

Across more than a dozen genes, I carry common variants in genes that are involved in neuronal excitability, inhibitory signaling, thalamocortical function, and visual cortex modulation. I want to be upfront about what that does and does not mean — and I will address this directly below. I am not a geneticist or neurologist, but I have tried to research carefully and I am sharing this in the hope that it might contribute — even in a small way — to understanding VSS. I also encourage those with VSS that have done genetic testing to see if their results are similar to mine.

Important caveat: All variants described in this document are common SNPs identified through consumer-grade SNP array testing (23andMe). This platform captures only a fraction of the genome and cannot detect rare structural variants. Nothing here is diagnostic. I am sharing this as a personal data point, not as a medical claim.

What These Variants Actually Mean

Before going any further, I want to address something important — because I think it is easy to misread genetic data like this, and I want to be honest about the limits of what I can claim.

When I say I carry "8 heterozygous variants in HCN1" or "17 heterozygous variants in KCNQ3," here is what that does and does not mean:

• What it means: At those positions in the gene, I carry a version that differs from the most common version in the population.
• What it does NOT mean: That those specific variants have been individually proven to alter how that gene functions, or that they cause any particular effect in my brain.
• What is NOT known: Whether my specific combination of variants meaningfully changes how these genes work, and whether that has anything to do with my VSS.

The honest framing for everything in this document is this: I carry variants in genes that play important roles in visual processing, thalamocortical signaling, and neuronal excitability. Whether those specific variants meaningfully alter those functions (and whether that contributes to VSS) is unknown. What I find interesting is not any single variant, but the pattern: variants in many independent gene systems that all relate to the same biological processes implicated in VSS.

Think of it this way: I cannot say my HCN1 variants disrupt thalamocortical pacing. What I can say is that I carry variants in a gene whose normal function is thalamocortical pacing — and that this gene has never been studied in VSS populations. Whether that connection is meaningful is a question for researchers with proper tools, not something I can answer from a DNA test.

With that important caveat clearly stated, here is what I found.

My Symptoms

For context, here is what I experience:

• Persistent visual snow (static across my entire visual field, present at all times)
• Palinopsia (positive afterimages)
• Photophobia (light sensitivity)
• Depersonalization / Derealization
• Excessive blue field entoptic phenomenon (BFEP): visible on white backgrounds as well as in the sky
• Pattern Glare
• Halos
• Migraine-like aura — a spot in either my right or left eye that lasts about a minute and is not followed by a headache. It looks like an afterimage from a camera flash and is typically worse when blinking.
• Brain Fog

I recently started taking Lamotrigine, which was prescribed specifically for the visual snow. I also take Sertraline (Zoloft) for OCD and anxiety, which are common comorbidities in the VSS community. I have tried Neuro-Optometric Rehabilitation Therapy (NORT) with little improvement. Upon examination I was found to have Binocular Vision Dysfunction (BVD), astigmatism, and issues with depth perception.

The Most Interesting Findings

Before going through every gene, I want to highlight the three findings I think are most worth discussing in the context of VSS. These are the ones that surprised me most, and that I think may be of particular interest to researchers — not because they prove anything, but because of how directly they connect to the biological mechanisms currently being discussed in VSS research.

1. HCN1 — A Gene Involved in Thalamocortical Pacing

Heterozygous variants: rs9292918, rs1501357, rs12517615, rs12513449, rs12519133, rs369451404, rs12522771, rs16902191

The leading theory for what causes VSS is called thalamocortical dysrhythmia. The idea is that the communication between the visual thalamus (the brain's visual relay station) and the visual cortex becomes abnormally desynchronized — generating the persistent visual static we see. Think of it like a TV signal that has lost its proper timing: instead of a clean picture, you get noise.

HCN1 channels play a key role in generating the rhythmic activity that keeps thalamocortical communication synchronized. They are expressed in both the visual thalamus and the visual cortex, and research has shown that disrupting HCN1 function alters thalamocortical oscillations.

I carry 8 heterozygous common variants across this gene. To be clear: I cannot claim these specific variants alter HCN1 function — that is not established. What I can say is that I carry variants in a gene that is central to the very mechanism that VSS researchers have proposed as the basis for our condition, and that this gene does not appear to have been studied in VSS populations.

HCN1 has not, to my knowledge, been investigated in VSS. Given its direct role in thalamocortical pacing — the mechanism most implicated in VSS — it seems like a high-priority candidate gene worth studying in VSS patient cohorts.

2. GABRA1 — A Gene Involved in Visual Cortex Inhibition

Heterozygous variants: rs78679936, rs6878494, rs2279020, rs2290732

GABA is the brain's main inhibitory neurotransmitter — the signal that tells overactive neurons to quieten down. GABRA1 encodes a key receptor for this signal. These receptors are especially concentrated in the visual cortex, where they play a critical role in filtering out background neural noise from the visual signal.

Some VSS researchers have proposed that our condition may involve a failure of this filtering — the visual cortex cannot adequately suppress its own background activity, and what we perceive as visual snow is that unfiltered neural noise reaching conscious awareness.

I carry 4 heterozygous common variants in GABRA1. Again, I cannot claim these variants reduce GABA receptor function — that is not known. What I can say is that I carry variants in a gene whose function is precisely the kind of visual cortex inhibition that researchers have proposed is deficient in VSS.

The convergence of variants in both HCN1 (thalamocortical pacing) and GABRA1 (visual cortex inhibition) is what I find most striking. The thalamocortical dysrhythmia hypothesis for VSS requires both of these things to go wrong simultaneously. I carry variants in the genes responsible for both.

3. HTR2A — The Serotonin Receptor in the Visual Cortex

HTR2A encodes the serotonin 2A receptor. This receptor is densely concentrated in exactly the layer of the visual cortex that receives incoming signals from the thalamus. Its job is to modulate how sensitive the visual cortex is to those incoming signals.

Here is what I find most striking about this gene: psychedelic substances like LSD and psilocybin produce their visual effects — visual snow, trailing images, afterimages, geometric patterns — almost entirely by activating the HTR2A receptor. This tells us something important: HTR2A is a key gatekeeper of visual cortex excitability. When it is overstimulated by a drug, the visual cortex becomes hyperexcitable and generates the kind of visual noise that closely resembles what VSS sufferers experience every day.

This connection also helps explain Hallucinogen Persisting Perception Disorder (HPPD) — a condition where people continue to experience visual disturbances long after a psychedelic substance has left their system. The leading theory for HPPD is that repeated HTR2A overstimulation permanently alters the excitability of the visual cortex, leaving it in a persistently hyperactive state. The overlap between HPPD and VSS symptoms has led some researchers to suggest they may share the same underlying mechanism of a visual cortex that has lost its ability to properly regulate its own activity. Whether that happened through drug exposure or, as may be the case in VSS, through a biological predisposition present from birth.

I carry 8 heterozygous variants across HTR2A, including rs6311. Whether these specific variants meaningfully alter receptor expression or function is not established. But the role of this receptor in visual cortex excitability — and its pharmacological connection to VSS-like symptoms — makes it a gene I think deserves attention in VSS research.

The Full Genetic Picture

Beyond the three highlighted above, I found variants across many additional genes that relate to neuronal excitability and visual processing. The table below summarizes all of them. The "Potential relevance" column describes what these genes do and why they might matter in VSS.

The reason I find this pattern interesting is not any individual row in this table. Individually, common variants in any one of these genes would not be remarkable — everyone carries variants across their genome. What struck me is that the genes where I happen to carry variants are not random: they are disproportionately concentrated in the biological systems like thalamocortical signaling, cortical inhibition, and ion channel excitability. All of which have been implicated in VSS research.

Whether that concentration is meaningful, or whether it is a coincidence produced by the fact that I was specifically looking for these genes, is something I cannot determine. That is a question for properly controlled research.

My Working Hypothesis

I want to be clear that I am not a scientist, and I am not claiming to have discovered the cause of my VSS. What I am saying is that when I look at all of these genetic variants together, they suggest a hypothesis that feels worth investigating.

The hypothesis is this: I may carry a collection of common genetic variants that, individually, each have small or uncertain effects, but that collectively shift multiple biological systems in the direction of visual cortex hyperexcitability. This would be a polygenic predisposition rather than a single causative mutation.

Every gene in this analysis relates to a biological system that VSS researchers have proposed as relevant to our condition. Whether my specific variants are functionally meaningful is unknown. But the pattern — variants in so many independent systems, all pointing the same direction — is what I find potentially significant.

On the excitation side: I carry variants in sodium channels (SCN2A), calcium channels (CACNA1A, CACNA1C, CACNB4), a sensory excitability channel (TRPM8), and glutamate receptors (GRIN2B) — all of which could theoretically lower neuronal firing thresholds if the variants are functional.

On the inhibition side: I carry variants in potassium brake channels (KCNQ2 and KCNQ3) and GABA receptors (GABRA1) — both of which normally prevent neurons from getting stuck in an overexcited state.

And specifically in the visual pathway: variants in HCN1 and HTR2A that relate to thalamocortical timing and visual cortex sensitivity.

I am particularly struck by the HCN1 and GABRA1 findings together. The thalamocortical dysrhythmia hypothesis for VSS requires two things: disrupted thalamic pacing, and insufficient cortical inhibition. I carry variants in the gene most responsible for thalamic pacing (HCN1) and the gene most responsible for cortical inhibition (GABRA1).

The Remaining Genes — More Detail

For those who want to go deeper, here is more information on each gene. In each case, I will describe what the gene does and why it might be relevant.

TRPM8 — Migraine Susceptibility

TRPM8 is one of the most consistently replicated migraine susceptibility genes in large genome-wide association studies. rs10166942 T/T is not a rare or unusual finding — it is a common variant — but T/T does represent the higher-risk genotype at one of the strongest known migraine loci. TRPM8 is involved in sensory excitability, temperature sensation, and pain processing. Migraine and VSS are so commonly comorbid that strong migraine genetic signals feel relevant to this analysis, even if the direct VSS connection is not established.

SCN2A — Sodium Channels and Neuronal Firing

Heterozygous variants: rs6736704, rs17183016, rs10174400, rs9287856, rs1816918, rs3769955

SCN2A encodes a voltage-gated sodium channel — one of the molecules responsible for triggering the electrical signal neurons use to communicate.

CACNA1A — The Primary Migraine Calcium Channel

Heterozygous variants: rs60185051, rs78274743, rs11085841, rs10403191, rs7252316, rs10422305, rs72993592, rs16022, rs16016, rs11085844, rs12977265, rs17777712, rs62111186, rs8105564, rs28696267, rs8109003, rs4632265, rs12610465, rs12974636, rs11085852, rs4244619

CACNA1A is perhaps the most important migraine gene known. Rare loss-of-function mutations cause Familial Hemiplegic Migraine Type 1. The common variants I carry are not pathogenic. What caught my attention was the number of heterozygous variants spread across this gene (21), and the fact that CACNA1A plays a central role in cortical spreading depression — the mechanism underlying migraine aura. I experience migraine-like auras regularly, and CACNA1A is the gene most directly implicated in this biology.

CACNA1C — L-Type Calcium Channels and Thalamocortical Function

Heterozygous variants: rs6489348, rs7304870, rs74062239, rs55884343, rs2238051, rs2239025, rs2239027, rs10848635, rs7312354, rs2239030, rs7975467, rs74806527, rs78006379

CACNA1C encodes an L-type calcium channel that is important for thalamocortical signaling and calcium-dependent gene expression in neurons. The visual thalamus-to-cortex pathway relies on this channel type. I carry 13 heterozygous common variants here.

CACNB4 — The Calcium Channel Regulatory Subunit

Heterozygous variants: rs7419564, rs16830446, rs11895837, rs6748530, rs4146377, rs79872355, rs1879140, rs4664073, rs7604835, rs9784082, rs12327907, rs4664076, rs6725537, rs12693199

CACNB4 encodes a regulatory subunit that influences how CACNA1A calcium channels are expressed and function. Having common variants in both CACNA1A and CACNB4 means I carry variants at two different levels of the same calcium channel system — the channel itself and its regulator.

KCNQ2 and KCNQ3 — The M-Current Braking System

KCNQ2 heterozygous variants: rs7271899, rs11699830

KCNQ3 heterozygous variants: rs1437824, rs2436133, rs2436134, rs13249479, rs4736571, rs7837201, rs16904655, rs4736573, rs16904657, rs2896656, rs10956658, rs59292953, rs6984395, rs73345940, rs16904676, rs2673606, rs7012444

KCNQ2 and KCNQ3 proteins combine to form the M-current — a potassium current that activates when neurons have been firing for a sustained period, acting as a brake on repetitive firing. These are two genes that function as a unit, so variants in both are worth noting together. I have 2 heterozygous variants in KCNQ2 and 17 in KCNQ3.

To use an analogy: if some of my other gene variants were like having a more sensitive accelerator pedal, KCNQ2/3 variants could theoretically be like having less responsive brakes . But only if they meaningfully alter the M-current, which is not known.

There is a drug called Retigabine (ezogabine) that specifically opens KCNQ2/3 channels. It was FDA-approved for epilepsy and has been studied in migraine. Whether this pathway might be therapeutically relevant in VSS is an open question.

HTR1A — The Serotonin Feedback Regulator

Heterozygous variant: rs878567 (A/G)

HTR1A encodes the 5-HT1A receptor, which acts as a feedback sensor on serotonin-producing neurons — detecting when serotonin levels are high and reducing further production. My single heterozygous variant here may or may not affect this feedback system. If it does, it could influence serotonergic tone throughout the brain including in visual processing areas. Together with my HTR2A variants, this suggests that serotonergic modulation of the visual cortex may potentially be altered at two levels.

GRIN2B — Glutamate Receptors and Cortical Excitability

Heterozygous variants: rs765688, rs4764026, rs2192976, rs7297761, rs17833849, rs1861452, rs78495744, rs73053669, rs7301500, rs2058878, rs11055628, rs2160733, rs12298994, rs9988991, rs74067112, rs2193513, rs79037547, rs10845853, rs77384356 (19 variants — more than any other gene in this analysis)

GRIN2B encodes a subunit of the NMDA glutamate receptor. Glutamate is the brain's main excitatory neurotransmitter, and NMDA receptors are central to synaptic plasticity and cortical excitability. I carry 19 heterozygous common variants here. Cortical spreading depression — the mechanism underlying migraine aura — involves massive glutamate release and NMDA receptor activation, which is why this gene feels potentially relevant to both my aura symptoms and VSS.

A Note for Researchers

If you are a researcher working on Visual Snow Syndrome and have found this document, I would be very grateful for any feedback, and I would be happy to participate in any research study that might find this genetic profile useful.

I want to be transparent about the limitations of this data. These are common SNPs from a consumer chip, not clinical sequencing. The specific variants I carry have not been individually validated as functionally significant. What I am offering is information and an idea that VSS may be associated with a polygenic pattern of common variants across excitability-related genes .

With that said, a few specific observations I think may be worth investigating in properly controlled VSS patient populations:

• HCN1 as a candidate gene: To my knowledge, HCN1 has not been specifically studied in VSS. Given its direct role in thalamocortical pacing and the growing evidence for thalamocortical dysrhythmia in VSS, it seems like a high-priority gene to include in future genetic studies.

• GABRA1 and cortical disinhibition: The cortical disinhibition hypothesis for VSS has theoretical support, but I am not aware of specific GABRA1 genetic studies in VSS populations. This gene seems worth investigating.

• HTR2A and visual cortex modulation: The pharmacological relationship between 5-HT2A agonism and VSS-like visual phenomena, and the overlap with HPPD, suggests this receptor may be mechanistically important. HTR2A variants including rs6311 may be worth studying in VSS cohorts.

• Polygenic excitability burden: Individual common variants have small and often uncertain effect sizes. A more interesting question may be whether VSS patients as a group show enrichment for common variants across multiple excitability-related genes simultaneously.

A Note for Fellow VSS Patients

I know how isolating and confusing this condition can be, especially when you are trying to understand why your brain works the way it does.

If you have 23andMe data and want to explore your own results, the genes I found most interesting for VSS specifically were: HCN1, GABRA1, HTR2A, CACNA1A, KCNQ3, and TRPM8. But please go in understanding that carrying variants in these genes does not mean those variants are causing you any problem — it just means you share genetic variation in genes that seem biologically relevant to VSS. Hang in there my friends!

Thank you for reading.

All genetic data derived from 23andMe raw SNP array. March 2026.