shaolinbomber Posted March 19, 2012 Report Posted March 19, 2012 http://brain.oxfordj...awr157.full.pdf Here's another good article I found about the newer types of diagnostic tools they are using in neurology to identify the problems with disorders involving persisting visual disturbances. Also notice that on all of the readings from the mEEG done on all of the test groups who complained of visual disturbances, the Persistent Visual Aura crowd (I believe HPPDers can be summed in with this group) had the highest readings of cortical excitability. " The present finding of persistent hyperexcitability across ictal-interictal phases suggests that sustained cortical spreading depression reverberations might be the culprit in persistent visual aura. We hereby provide two possible reasons why a vicious cycle of sustained cortical spreading depression is formed in persistent visual aura. First, persistent potentiation in persistent visual aura may lead to enduring and excessive neuronal stress, and the accumulation of metabolites such as lactate and protons that may induce repetitive cortical spreading depression (Scheller et al., 1992). Given the protective nature of habituation, persistent potentiation leads to brain sensory overload, depletes the cortical energy reserve and finally leads to neuronal stress and a biochemical shift that triggers cortical spreading depression (Coppola et al., 2009; Rankin et al., 2009). On the other hand, the excitatory waves piloting each cortical spreading depression propagation and the detrimental effects of repetitive cortical spreading depression upon intracortical inhibition (Kruger et al., 1996) may upregulate cerebral excitability and eventually increase vulnerability to cortical spreading depression (Holland et al., 2010). The association between cortical spreading depression and hyperexcitability here is further supported by a clinical observation that 45% of patients with persistent visual aura had worsening headache during aura persistence (Wang et al., 2008). Despite PET evidence of sustained metabolic activation in the medial occipital cortex with persistent visual aura, there was no corresponding metabolic change during a typical migraine aura (Andersson et al., 1997). Therefore, single cortical spreading depression propagation per se (hence migraine aura) cannot explain the persistent potentiation in persistent visual aura. The culprit should be, again, the complex interaction between cortical spreading depression reverberations and central excitability. The entanglement between central excitability and cortical spreading depression reverberations may further explain the lack of correlation between magnetoencephalography and most clinical measures." CONCLUSION "Persistent visual aura is characterized by persistent hyperexcitability of the visual cortex without interictal-ictal variation, compatible with the excitatory effect of sustained reverberations of cortical spreading depression. Our magnetoencephalography data on the excitability changes in the visual cortex differentiates persistent visual aura from other migraine disorders (migraine with aura, migraine without aura and chronic migraine). Therefore, while belonging to the migraine spectrum, persistent visual aura may be considered a distinct disorder."
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