Enhanced neural plasticity of the primary visual cortex in visual snow syndrome: evidence from magnetoencephalographic gamma oscillations

TL;DR

This study found that people with visual snow syndrome show heightened brain plasticity in the visual cortex, as seen through increased gamma brain waves during repeated visual stimulation.

Contribution

The study provides the first experimental evidence linking enhanced activity-dependent neuroplasticity to visual snow syndrome.

Findings

Patients with visual snow syndrome showed a steeper increase in gamma power with repeated visual stimuli compared to controls.

Both groups exhibited activity-dependent plasticity, but it was more pronounced in patients.

Heart rate variability correlated with gamma power changes, supporting a link between parasympathetic activation and neuroplasticity.

Abstract

Visual snow syndrome is a neurological disorder characterized by persistent visual disturbances and associated symptoms. Although the neural basis of the visual snow syndrome remains poorly understood, it may involve increased neuronal excitability and/or altered neuroplasticity in the visual cortex, which could, in turn, affect visual gamma oscillations. An altered excitation-inhibition balance is hypothesized to alter the modulation of gamma power and frequency by stimulation intensity, while maladaptive neuroplasticity may impact time-dependent changes in gamma power during repeated stimulation. To investigate potential alterations in the excitation–inhibition balance and neuroplasticity in visual snow syndrome, we used magnetoencephalography to record visual gamma oscillations in 26 patients with this disorder and 27 healthy controls. Participants were exposed to repeatedly presented high-contrast annular gratings, which were either static or drifting at varying speeds to systematically manipulate stimulation intensity. We also assessed heart rate variability during rest and repetitive visual stimulation to explore the relationship between time-dependent gamma changes and parasympathetic activation, which is known to promote activity-dependent plasticity. Our results showed no significant group differences in gamma power or frequency, nor in their modulation by drift rate, suggesting that the excitation–inhibition balance in the V1 area remains largely intact in visual snow syndrome. Both groups exhibited an initial brief decrease in gamma power followed by a sustained linear increase with stimulus repetition, likely reflecting activity-dependent plasticity. Heart rate variability parameters were comparable across groups, with the parasympathetic–sympathetic balance index correlating with repetition-related increase in gamma power, further supporting the link between time-dependent gamma changes and neuroplasticity. Notably, patients with visual snow syndrome exhibited a steeper repetition-related increase in gamma power, indicating atypically heightened activity-dependent plasticity in this group. These findings provide the first experimental evidence suggesting that altered activity-dependent neuroplasticity plays a role in the pathophysiology of the visual snow syndrome. Furthermore, they identify repetition-related increases in gamma power as a potential biomarker of aberrant neuroplasticity, offering novel insights into the pathophysiology of the visual snow syndrome and potential avenues for targeted therapeutic interventions.

Orekhova et al. investigated gamma oscillatory responses to repeated visual stimuli to assess short-term plasticity in the visual cortex of patients with visual snow syndrome. Compared to controls, patients exhibited a more pronounced increase in gamma power with stimulus repetition, suggesting abnormally enhanced activity-dependent plasticity.

Graphical Abstract

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