Central Clinical School
Faculty of Medicine, Nursing and Health Sciences
Visual Snow is a complex syndrome which is frequently ignored, or misdiagnosed, to the disadvantage of patients.
It can be recognized at any stage of life and may be of varying severity from merely annoying to disabling. Once recognized, it usually stabilises over the first 6-12 months and remains unchanged thereafter. It is differentiated from hallucinogen persistent perceptual deficit (HPPD) only on the basis of history. It may be related to other disorders of sensory processing, such as persistent perceptual postural deficit (PPPD) and some forms of tinnitus. It is closely related to, and often coexists with, migraine.
Suffice to say, vision is so important to us that 53% of all cerebral circuits are related to vision and control of eye movement.
At least at this stage, there is no reliably effective form of therapy although some treatments such as filtered, coloured lenses, and lamotrigine, work in a small percentage of patients.
The purpose of this monograph is to provide some background into the proposed nature of this disorder.
- All sensation and its interpretation are learned through early life experience. Ergo, it can perform differently in different people, in the same way that some people can run fast, and some can’t.
- Vision is not real time. There are 130,000,000 receptors in each eye and 140,000,000 cells receiving that information in each visual cortex before projecting to the various association cortices for interpretation. However, there are only 1,100,000 cells in each optic nerve, so we cannot transfer all that information in real time.
- Moreover, we see our whole visual field in colour, yet we only have colour receptors in the central 5-100. Any colour seen peripherally is a construct of the brain.
In fact, all vision is a percept that is maintained by the brain and is updated constantly depending on visual input. It is however, dependent on the integrity of the neural circuits that maintain the percept and then brain is inherently electrically noisy and leaky at the same time.
- We have a concept of “unimodal” cortex. This implies that visual cortex only has visual information. That is not quite exact. Unimodal cortex (visual, auditory, vestibular, taste, smell, sensory) actually receive polymodal input but only respond with a single perception, in the case of vision, with a visual response. Filtering (noise analysis) is required to permit transmission of only the correct signals. Thus, our visual percept is the result of noise analysis.
- Finally, the eye in visual snow patients is normal but, normally, the individual cells in the retinal are inherently unstable and, although there is inbuilt, ”centre-surround” inhibition, cells will fire inappropriately, and that activity is transmitted centrally, potentially producing what are called entoptic phenomena, although probably not the visual snow.
Thus, the fundamental abnormality appears to be one or all of several phenomena:
- Impaired filtering/inhibition of spontaneous electrical activity arising in the eye.
- Failed filtering of thee spontaneous, extraneous signals to visual cortex.
- Impaired maintenance of the visual percept.
One of the theories currently being evaluated is that there is impaired interaction within the thalamus deep within the brain. The thalamus acts as a relay station for almost all sensory interaction. The same areas that receive sensory information from the periphery, also receive information from various areas of cortex, including sensory.
Whether or not the cells transmitting signals actually fire or not depends on the balance of all inputs to those cells, from above and below, and the balance between excitatory and inhibitory inputs.
It is easy to see how abnormality of function at many levels may result in an imbalance between inhibitory/excitatory inputs at thalamic levels, impacting on eventual perception.
Other theories have not been excluded and active research will help elucidate the process and provide new insights into management.
Prof Owen B White
Director Ocular Motor Laboratory
Central Clinical School
Monash University & Alfred Hospital
Melbourne, VIC 3008
Tel: +61 3 9576 0022
Fax: +61 3 9576 0019
Mob: +61 418 822 996