How Environmental Factors Could Act As Triggers For Visual Snow
The Human Brain Is Vulnerable To Environmental Influences.
A key gathering from a recent review on visual snow of which the significance may have been overlooked is that there appears to be a common onset in adolescence (my personal experience as well). This suggests that visual snow could in some cases be a developmental disorder of the GABAergic system.
The brain goes through several phases of maturation and varying plasticity, during which neural synchrony and functioning is determined. Interneurons responsible for GABAergic inhibition are maturing during these periods and this maturation can be pathologically disrupted through a variety of mechanisms to create a cortical hyperexcitability, and altered neuronal oscillations. The specific nature and location of an interneuron dysfunction can lead to particular neural circuit abnormalities and is hypothesised to be involved in disorders such as schizophrenia, autism, Tourette’s syndrome, and epilepsy.
Parvalbumin expressing interneurons in the brain, responsible for inhibition and network oscillations, and with a direct role in visual perception, mature particularly slowly and this protracted maturation leaves them vulnerable before adulthood. Synaptic reorganization, hormonal changes, and environmental stresses can combine to interfere with this maturation, alter plasticity and eventually create a unique neuronal imbalance. Adolescence is in this sense a period which threatens itself.
If BCM7 is as hypothesised a possible trigger for visual snow then there is a broad range of aforementioned possible changes resulting from BCM7 which may start a cascade of events leading up to a specific interneuron insult in visual snow. For example oxidative stress is being considered as a primary catalyst of this process in schizophrenia.
- Neuromodulation + Hormone effects
- Oxidative stress
- Immune activation
- Epigenetic changes
The progression of these changes may appear asymptomatic because at the neuronal level there is a certain level of resistance during maturation. Regarding other non-visual symptoms opioid peptides mask their own effects.
In this case an accelerated version of this progressive process could be seen in the very young if they are formula fed, whereas later adult onsets are in general probably indicative of extra environmental or age related triggers. This is hypothesised to be the case in late onset schizophrenia, which is generally believed to have less “negative” symptoms (e.g. depression) but more “positive” symptoms (e.g. hallucinations) and this too may be similar with later onsets of visual snow.
The differentiating factor for a susceptibility towards visual snow specifically is probably genetic but epigenetic changes linked with environmental factors may provide clues to this.
In line with this hypothesis, certain people would be at greater risk from BCM7 according to five key factors. Variations in these may affect their visual snow severity and age of onset.
Written and researched by Neil Salata, with help and input from Nina Salata M.D – both have visual snow