Hi Derok and MindOverMatter,
The ultimate message by First Bad Comedown is a positive one, in that the scalp sensations and brain zaps seem to improve over time and in many cases entirely vanish. This is supported anecdotally by several people on this forum. Although I dont know of any data in the medical literature to support this in the setting of MDMA abuse, the fact that we see this trend based on personal reports on this forum is encouraging, and highlights the power of Bluelight to fill in the gaps left open by the published medical literature on this topic. So I think everyone reading these forums who are experiencing scalp pressure and brain zaps can maintain some hope since others are improving, they have a decent chance of improving as well.
The weakness of Bluelight, however, is to correlate the prognosis of these symptoms we suffer with hard data in the literature, as well as our poor ability to correlate our symptoms with neurophysiological theory and studies. One reason is because of the paucity of definitive prospective studies that examine the long term outcome and effective treatment of the various symptoms we experience. However, ScaredFirstTimer may show you some new very long-term studies that have emerged over the last year, albeit retrospective, that look at the very long term outcomes of some of the symptoms we experience, if you dare to read it.
The other reason is that most of us do not have the neurophysiological background to properly explain our symptoms. I think in First Bad Comedown's desperate attempt to understand his situation and to find a solution, he acquired as much neuroanatomical and physiology theory in a short time period as possible, and then extrapolate from that knowledge a speculative theory on exactly what is going on in our brains. However, inevitably, although I find him to be extremely smart, since he does not possess the theoretical foundation required, his theories will be based on misinterpretations and faulty associations of the underlying physiologic mechanisms driving the studies he read. However, FBC's main message, that clinical recovery is often seen in the 12-18 month range, is good, and if he has read the studies that support that claim then more power to us suffering. I think that main message of his, along with the anecodotal improvement we see among users on this site, gives us hope, and that is what Bluelight is all about.
If on the other hand, we look beyond FBC's main message, and try to dissect his arguments more scientifically, I don't think everything he says makes perfect physiologic sense, and I don't think I would put too much faith in his more technical assertions. For example, in his post that has been reposted by MindOverMatter, FBC attempts to assert that the face and scalp sensations are related to altered cerebral blood flow induced by MDMA damage. I think he is trying to draw parallels to the mechanisms underlying migraine headaches. One theory behind migraines is that vasodilation in the arteries/arterioles to the scalp/dura occurs due to a serotonin disturbance. This is why medications such as the triptans, which are 5-HT1 agonists seem to be effective in migraines. This mechanism may similarly explain why some of us experience these sensations in our scalp, as the 5HT-1 activity innervating the blood vessels in our scalp is significantly decreased, but in our case this is very unproven.
Also, unlike FBC's claim, I dont think that the vascular supply or innervation to the scalp or dura, which are the major pain generators in the head causing headaches/weird sensations have anything to do with rCBV, or regional Cerebral Blood volume, since the vascular supply to these structures come from the extracranial circulation, and rCBV pertains to the intracranial circulation. The anterior scalp and face derives much of its blood supply from the facial and superficial temporal arteries, which is a branch off the external carotid artery, with some anastamotic connections from the ophthalmic artery. The dura surrounding the brain is derived largely from the middle meningeal artery, which is also from the extracranial circulation. There is no evidence that the blood flow via this artery to the scalp is compromised or altered after MDMA use, nor is there evidence that blood flow in this distribution resolves over time. However, it IS theoretically possible, however, since the precapillary arterioles from the facial artery in the scalp are enriched in 5HT-1 receptors, which regulate the smooth muscle tone surrounding these vessels. This scalp perfusion however, cannot be measured by rCBV, however, since vascular supply to this area is separate from the cerebral circulation.
If instead, you attempted to explain the sensations in your scalp via cerebral blood flow, then the argument again by FBC has some flaws. You have to first understand what rCBV really is. rCBV is a parameter, along with cerebral blood flow (CBF) and mean transit time (MTT), to measure the perfusion of various areas of the brain. In a stroke, for example, when you have an obstruction in of the main arteries at the skull base, the CBF to the area of the brain which is supplied by the involved area is markedly decreased, and the MTT of blood flowing into that area is thus increased. The brain responds by dilating end arterioles and capillaries in that region of the brain in order to decrease the overall resistance in the circuit and optimize blood flow, and this dilation results in increased rCBV (since the vessels are dilating as a compensatory attempt, the volume in a "pixel" of a brain perfusion scan that is being taken up by blood vessels is increased). So in the setting of an ischemic stroke, increased rCBV correlates with decreased blood flow.
These small arterioles, in some parts of the brain, are highly populated with 5-HT1 receptors, which when activated, facilitate constriction. These vascular receptors seem to have the highest density in some parts of the basal ganglia, thalamus, and striate (visual) cortex. Not suprisingly, several studies that look at CT/MR perfusion or SPECT scans in people with MDMA abuse show altered CBF and CBV in these same areas. It is likely this is the cause of the very rare hemorrhagic strokes post MDMA ingestion reported in a few case reports in the literature.
However, the scalp and dura are innervated by the trigeminal nerve and upper cervical spinal nerves such as the greater occipital nerve. The trigeminal nerve provides sensation, including light touch, vibratory, pain and temperature sensation, to your face and anterior part of your scalp. The trigeminal nerve arises from the mid-pons section of the brainstem, proceeds along the skull base to its next major relay station (Gasserian ganglion), then branches and and leaves the skull via various foramina to go the face. The blood supply to the nuclei of the trigeminal nerve arises largely from the anterior inferior cerebellar artery as well as short and long pontine perforators, and the Gasserian ganglion likely derives its supply from the tentorial artery off the meningohypophyseal trunk. However, neither of these areas have been shown to have altered CBV/CBV after MDMA abuse based on those studies. Therefore, there is nothing to suggest FBC's claim that altered rCBV affects the trigeminal nerve, thus causing these scalp sensations.
It is true that some of these studies have shown restoration of cerebral blood flow over time. However, there has been no evidence to show that the resolution of clinical symptoms correlate with the restoration of normal blood flow in the brain. If the abnormal scalp sensations are a result of a vascular problem to the scalp, then it is independent of CBV/CBF, and there is no good data I found as to how this resolves. If this is simply due to altered serotonin transmission, due to neuronal dysfuction, in the trigeminal nerve or principal trigeminal nucleus or spinal trigeminal tract, then again we don't have good data as to how this resolves. However, as I mentioned in the beginning, the anecdotal information on here that this problem does get better in several people carries far more weight than any unsupported theoretical speculation.
