Shortly after I began to get migraine auras in my early 20’s my auras became prolonged and diverse. My most common persistent migraine aura is a mass of scintillation, or multi-colored sparkles that arch over both sides of my vision in the upper field and sometimes pulsing down in a open and closing fist sort of motion. I say most common because this is daily. However I get a varied amount of visual auras that are persistent. My other auras, tactile and such are prior to the migraine itself. I will get flashing lights, scintillation scotomas, vortex like effects, warping illusions of lines and patterns, that heat wave wave effect. Other things like halos, starbursts, ghosting and trailers I also have but I attribute to the fact I have a rare neurological condition called visual snow… that not so long ago was once considered a migraine persistent aura in itself but recent research has discovered it is a disease in itself as well as the location in the brain that is malfunctioning. But that is an aside, for those that may also have that (causing vision to be ‘staticy’). Now, I don’t believe that research is well spread because some neuros still refer to this as a persistent migraine aura. And in fact 50% of people with visual snow have migraines, so there may be some sort of link between the two. There simply isn’t that much know about PAWOI to know what is actually going on. If in fact they were looking at two distinct entities all along, that might explain some of the complications with research. Both being rare as is and subjects with VS being in the PAWOI study. But one can have both. I do wonder if VS makes one more sensitive to the aura phenomena or vice versa. However, I do know I developed VS around the age of 12 and PPAWOI around 25.
Generally speaking, typically, with PAWOI the research suggests it is the same aura on repeat. Like my multi-colored light show. Yet in my case and other people I have met we have variety in our mix up. Other auras are in there. Like the fellow who originally name PAWOI stated one ‘type’ was those who had oscillation, scotoma, and fortification in one hemifield persisting and the second ‘type’ was those that had intermittent scotoma or oscillating lights as as well as visual snow. Well I would be oscillating lights visual snow type with other auras tossed in the mix, so really there is no ‘type’ for this phenomena. I do know it is all visual. Any non-visual aura comes prior to a migraine and is my only migraine pending doom alert system. But it can be hard to say, since I have had numbness and tingling last for 4 to 5 hours. I believe I read one study that said that is in the realm of normal though.
But with PAWOI I can’t even say what the realm of normal is, I just get a mass of fluctuating auras that are not dependent on my actual migraines. They just occur all day long, not an hour prior to the migraine. Into the migraine, after the migraine. Well before it. Directly before it. Definitely stronger in the evening. And triggered a lot by light, they can be spurned on to get more intense. For a whole six months every time I stepped outside I would get this magnificent blue and rose… some other colors in there… vortex in the middle of my vision. I had not been working at the time, so not driving fortunately. But it was spectacular to look at. It was like a pulsing flower and the petals would pulse open and closed. If it wasn’t smack in the middle of my visual field obscuring every damn thing it would be beautiful to look at. If I was getting a ride to the doctor I would just stare at it. That distracting. Point is, damned thing, seemed to be trigger by sunlight. Stopped happening abruptly. As some of them do. Some get worse and others crop up and others fade away.
I remember distinctly my visual aura was like without Persitent migraine auras. It was your classic oscillation, scotoma, and fortification in one hemifield. Well… the scintillating scotma. I had that every migraine, every time, same aura.
Then one day… it got weird. I had the edge part with all the lights and I had a lot of colored dots there and it last for a week. Then stopped. Then I got halos. And trailers. And warpy vision. Then the warping field of colored dots came back and lasted longer. It just got weird. I went to the neuro once it was lasting for a year nonstop of this jumble of visual stuff. And my regular aura before the migraine was gone, never happened like that again. It was just all this new weird mishmash of auras.
Here is the Criteria from The International Classification of Headache Disorders, 3rd edition:
1.4.2 Persistent aura without infarction Description: Aura symptoms persisting for 1 week or more without evidence of infarction on neuroimaging.
A. Aura fulfilling criterion B
B. Occurring in a patient with 1.2 Migraine with aura and typical of previous auras except that one or more aura symptoms persists for 1 week C. Neuroimaging shows no evidence of infarction D. Not better accounted for by another ICHD-3 diagnosis.
Comments: Persistent aura symptoms are rare but well documented. They are often bilateral and may last for months or years. The 1-week minimum in criterion B is based on the opinion of experts and should be formally studied. Diagnostic work-up must distinguish 1.4.2 Persistent aura without infarction from 1.4.3 Migrainous infarction, and exclude symptomatic aura as a result of cerebral infarction of other causes. Attacks lasting more than 1 hour and less than 1 week and not fulfilling criteria for 1.2.1 Migraine with typical aura are coded 1.5.2 Probable migraine with aura.
Here in general is what you are looking at for PAWOI. Now keep in mind research has been minimal at best.
The primary explanation for PAWOI is cortical spreading depression [3, 4, 7]. Cortical spreading depression involves a wave depolarization spreading across a region of the cortex, principally in the visual cortex of the occipital lobe, followed by an inhibitory wave. These waves are implicated in regular migraines with aura but it is believed that in people with PAWOI, these waves are sustained and repeated . The brains of people with PAWOI may also be more susceptible to cortical spreading depression . Furthermore, alterations in energy metabolism has been implicated, based on Positron Emission Tomography (PET) scans finding that blood flow changes often occur in the occipital lobe during migraine attacks that involve aura . Generally, this involves a decrease in blood flow in the affected areas, like the occipital lobe of the brain . Changes in magnesium levels, increased sensitivity of NMDA receptors to the excitatory neurotransmitter glutamate, and decreased activity of the inhibitory neurotransmitter GABA have also been suggested to be involved with the pathogenesis of PAWOI .TripleHelix
Here is some recent research I have found. But the thing is, PMA is rare and variable… from short duration to long. I have had it for 14 years or so myself but people can have it for anywhere from one week to decades. Lifetime even. It can stop as quickly as it started. So this is a review of that research… and not much to say about it.
Objectives.—This case-based review article describes four new cases of PMA as well as reviews all cases reported, trying to identify relevant associations, in particular with respect to functional investigations.
Methods.—We performed a systematic literature search, extending from the period when it was first described (1991) to March 2014. We included all case descriptions of which criteria for PMA formulated in the International Classification of Headache Disorders, second edition, were met. In addition, we described four new cases.
Results.—We identified 47 cases of PMA, 27 PMA-PPVD and 19 PMA-TA. In one case, there was not enough information to define the type of PMA. The mean age of onset was 30 years, varying from 7 to 74 years. The duration of symptoms varied from 9 days to 28 years. Besides a longer duration in symptoms in the PMA-PPVD group, we could not identify any differences between these groups. Some authors report occipital hypoactivity on Tc99m-hexamethylpropylene amine oxime -single-photon emission computed tomography (Tc99m-HMPAO-SPECT) or fluorodeoxyglucose-positron emission tomography (FDG-PET) in PMA cases, but data are inconsistent. Multiple drugs have been used for the treatment of PMA, usually with little effect. Lamotrigine seems to be the most effective drug.
Conclusion.—Despite the fact that 47 cases of PMA have been reviewed in this paper, many questions remain. The cases that have been described so far show inconsistent data with respect to the results of functional studies as well as treatment effects. The pathophysiology of PMA is still largely a matter of conjecture.MedScape
As far as treatment goes it is in general treated like migraines are with the same preventatives. But some specific are used. For example a lot of research mentions Lamotrigine