Graham Exelby June 2023
“Visual snow is the persistent visual experience of fine acromatic dots or static in the whole visual field likened to ‘static analogue TV noise’. This frequently occurs with other visual symptoms such as persistence of previously viewed stimuli (palinopsia) and disorders of sensory perception such as migraine with or without aura, tinnitus and tremor. “(1) It is hypothesized that this is from a thalamocortical dysrhythmia of the visual pathway. (3)
It “can be associated with stress, depression and previous illicit drug use.” (1) This results in patients often being misdiagnosed and inappropriate treatments being used, or their labeled as psychiatric disorders. All of these visual symptoms “relate to an increase in sensitivity of sensory perception.”(1)
It is felt that that the underlying mechanism in visual snow is increased neuronal excitability, as described by Dean Watson in his work on migraine. This same hypersensitivity is thought to be a possible cause of tinnitus. (1) “It is further thought that in migrainous brains the hypothalamic and brainstem neurons that are responsible for regulation of responses from physiological and emotional homeostasis can lower the threshold for transmission of nociceptive (perception of pain) trigeminal vascular signals from the thalamus to the cortex (1) in the brain, and “may also explain other associated features such as autonomic symptoms (nausea), affective symptoms (irritability and depression) and cognitive symptoms (attention deficit), some of which have been previously associated with visual snow. (1)
The pattern of this disorder is reflected and I believe best described by the cervical nerve root sensitivity in the underlying cause of migraine by Dean Watson.(2) This emerging research supports the role of a sensitised brainstem in migraines, cervicogenic, and tension headaches. The brainstem sits at the bottom of the brain, and functions as the control centre for the flow of messages between the brain and the rest of the body.
Muscles, joint capsules and ligaments of the upper neck share a common nerve pathway with the trigeminal nerve, which passes sensation from facial skin, jaw muscles, and the inner lining of the brain via the brainstem. The shared nerve pathway between the neck, face, and head supports the potential link between the upper neck and headaches or migraines.
“The cervical afferents of C1-3 are the reason we get increased sensitisation of the brainstem. The common pathway with the Trigeminal nerve will present as the head pain or facial pain (Headache) plus associated symptoms of dizziness and nausea etc (C2/3). The head pain is a representation of the input from the cervical afferent nerves C1-3. This constant input will reduce the latency period (ie someone will get symptoms earlier than the normal person). This constant input then causes the brainstem to become sensitised and effectively “ready to go” with small input. This is why small variations (small C2 rotation perhaps from bad posture) or triggers will bring on large changes so quickly. “(2)
Genetic information points to the involvement of transient receptor potential (TRP) channels in pain mechanism. TRPA1, an ion channel on the trigeminal (and most other sensory) nerves is the major oxidative threat sensor. It is activated by various irritants and agents releasing the pro-migraine peptide, calcitonin gene-related peptide through this nerve pathway. TRPA1 agonists release chemicals that cause vascular dilation.
Working out the things that are triggering the body’s threat receptors (Toll-like receptors) is critical to dealing with these problems. The work by Dean Watson and other researchers eg Roger O’Toole has changed the way we look at migraine, and I believe, should also be applied to Visual Snow. But as in migraine, once these processes are activated, and brainstem sensitization has occurred, other potential drivers come into play. But each one you remove can improve the quality of life in someone with this immeasurably.
1. Lauschke,J., Plant, G., Fraser, C.: Visual Snow: A thalamocortical dysrhymia of the visual pathway?. Journal of Clinical Neuroscience 28 (2016) 123-127.
2. Watson,D. https://watsonheadache.com/
3. Lauschke,J, Plant,J, Fraser,C. Visual snow: A thalamocortical dysrhythmia of the visual pathway? 2015. Journal of Clinical Neuroscience. doi: 10.1016/j.jocn.2015.12.001. Epub 2016 Jan 11. PMID: 26791474.