DMSO et cerveau
extrait de : https://www.midwesterndoctor.com/p/dmso-heals-blood-vessels-and-could?
How DMSO Protects the Brain
In addition to the extensive research showing that DMSO restores blood circulation and prevents reperfusion injuries in those (previously ischemic) tissues, numerous studies have shown DMSO mechanistically protects the brain from strokes:
•In anesthetized cats, DMSO significantly enhanced brain oxygenation (particularly in the caudate nucleus).
•DMSO was shown to preserve the neurological function of hippocampal brain tissue samples once their oxygen or glucose were withdrawn (with similar results seen in this study).
•When infused directly into the rat brain, DMSO alone reduced ischemia-induced (blood loss induced) extracellular glutamate (the excitotoxin that drives much of the neuronal death in a stroke) by 51% and modestly preserved the vulnerable hippocampal CA1 neurons relative to controls.
•DMSO down-regulated aquaporin-4 expression (a key driver of the brain swelling that follows an occlusion) after MCA occlusion in the rat.
•DMSO was found to protect the integrity of the blood-brain barrier integrity after MCA occlusion.
•Diazoxide and DMSO prevented the learning dysfunction and brain damage that follow carotid artery occlusion (with DMSO alone restoring) Morris-water-maze learning and preventing COX-2-positive neuron loss in the dentate gyrus.
Reader Stroke Reports
Corroborating DMSO’s benefits for strokes, numerous readers here shared the following with me:
•A medicinal chemist with a background in neuroscience, recognized his own stroke the moment it began: “Right after waking up I went to the toilet and noticed that I had lost control of my palm. I walked to bed and I froze, unable to lay down.” He had his wife get him diluted DMSO, drank most of it over the next hour, and went to the hospital—by which point he had lost speech (Polish entirely, English partially), leaving him, a Pole, to communicate in English in a Polish hospital. “I credit DMSO for not losing movement ability,” he wrote. His speech recovered well enough that he returned to full-time work as a scientist six weeks later, and he now drinks a small maintenance dose daily.1
•One week after her husband’s stroke, which had left him with severe pain, vertigo, exhaustion, and partial paralysis of the left side of his face, arm, and leg, a reader discovered this series. She then applied undiluted DMSO to his face, neck, and shoulder two to three times a day; the pain, she reported, “went away almost instantly every time.” Within about two weeks he began walking short distances without a cane. “Only 3 months after the stroke he walked with me unassisted to a friend’s house carrying a guitar, and was able to play the guitar and sing flawlessly while standing with one foot on a chair. My jaw was on the floor... ‘You’re all witnessing a freakin’ miracle right now. This man had a stroke three months ago, and now he’s playing his guitar like nothing happened!’”1
Thanks for saving my life. I had a stroke recently, and because of your article on dmso and strokes, was given some by my partner. Three minutes later I was OK again. I continue to read your articles daily.1
I have been in health chats where twice now, folks were in the chat and were having a stroke, they both had DMSO on hand & took 1 oz it both were stopped within 10-15 min and reversed any damage.1
I just recently had a stroke but used DMSO immediately ( I had my wife apply it in the hospital within hours of my stroke) and I’m about 95% back to normal and hoping to be 100% soon.1
•A wife whose husband had atrial fibrillation and two microclot strokes in 2024 treated a recurrence herself the following year: when both his legs went numb with pins and needles, she applied DMSO and “Within two hours he was 70% better,” and after a second identical treatment “everything was cleared up and did not return” (months later she used the same protocol over his chest for a suspected pulmonary embolism, with the same result).
•Another wife, reported DMSO “Made a world of difference” for her husband’s entire-left-side deficit,1 another reported their husband’s two mini-strokes cleared within a few hours,1 another reported that when her husband woke up unable to speak and with numbness in his cheeks, she began DMSO, and there was “a huge improvement from a week ago” as he was speaking in complete sentences most times.1
•A reader who saved her mother from a third stroke shared “It was miraculous!”1; another reported it saving a family member from a stroke.1 Likewise, a reader whose father began showing stroke symptoms wrote: “Thankfully I had some 99.9% DMSO on hand. The improvement was remarkable….“The Lord might have just used you to save my dad’s life.”1
Interestingly, many readers have reported stories matching my own experience of giving someone DMSO and then having the ER be confused because they could not find any signs of stroke:
•After a reader woke at 4:30 a.m. and found his left side would not respond when he tried to walk stated he immediately knew to use his DMSO and over the next 4 hours “My walking returned to normal but my reach and grab with my left arm/hand would not allow me to pick green beans in my garden.” He hence called 911, walked down his own hill to greet the firemen, and talked the EMTs out of taking him; the next morning his clinic’s nurses sent him to the hospital by ambulance, where monitoring, a CT scan, and echocardiograms found “no evidence of stroke,” and his remaining left-hand impairment recovered over two weeks with self-directed therapy. His conclusion: “In every interaction with medical personnel I strongly recommended that DMSO should be the first/immediate action when stroke symptoms are detected. Waiting for an ambulance or an emergency room visit to respond is a tragic waste of time.”1
•A 76-year-old man in excellent health had a nearly identical experience 36 hours after giving a double-red blood donation: he woke at 4 a.m. with trouble walking and gripping on his left side, and applied DMSO based on what he had read here. Hospital testing “has not found/confirmed stroke,” and he reported rehabbing himself until symptoms had “disappeared 97%.”1
•Another reader who was already familiar with DMSO and kept it on hand took it during an apparent stroke: “The ER doc came in to tell me that I had not stroked, despite speech impairment and other signs. I told him I took DMSO.”1
•The reports extend well beyond the acute window into recovery from established strokes. One reader’s husband, who had suffered eight strokes, takes DMSO three times a week; two years after his last stroke, in her words, “recovery great, he has some aphasia but still thinking great speaking to others although he’s an introvert and has lost some confidence in himself he is still living life to its fullest playing with grandkids gardening home renovations and going to the gym and doing a full work out which includes 30 chin ups!”1 A caregiver eight weeks into treating a stroke patient (who noted the changes “began almost immediately, after the very first treatment”) observed a cascade of gains: stronger voice and markedly improved speech, dramatically improved swallowing (he could again eat normal-sized meals, and even swallow while the TV was on, previously a choking hazard), self-feeding with the affected hand; improved energy, strength, and balance; and, “the most recent and undeniable change,” the return of his sense of taste. On one lucid day he zipped up his own jacket—notable, she wrote, “because the fine motor skills in his right hand were quite impaired by the stroke” and “even he commented at the time that it was remarkable.”1 Another reader watching his mother’s recovery described her damaged right side visibly “waking up”, regaining feeling and strength until one day she exclaimed, “Hey look, I’m sanding with my right hand!”1
•Others report gains across the full range of stroke severity. One reader had a large stroke that “affected every joint on my right side” and used DMSO with CBD: “One year later? Only my knee and two fingers (pinky and ring) are still ‘lazy’ but each month I notice an improvement... I couldn’t write but I can now. I’ve learned to type with 8 fingers but the other two are still improving.”1
•Another reader began giving her 72-year-old husband DMSO six weeks after his stroke; over two and a half weeks “he improved and slowly regained more function so that he could swim again,” and a later course brought further gains. She noted the oral route seemed to act faster, though its garlic-like odor kept him homebound—so he switched to applying DMSO nightly to his temples, forehead, and neck, on which he continued to slowly improve.1
•A 65-year-old who’d had a series of small strokes reported that after starting DMSO the improvement in mental acuity was “amazing” alongside whole-body pain relief;1 a physician who ran an IV chelation and ozone clinic recalled an “amazing recovery” in a stroke patient given IV DMSO;1 and caregivers successfully treating loved ones after strokes (e.g. “a very bad stroke1”) or an ischemic stroke and reporting steady, believable progress.1,2,3
•A grandfather who nebulized DMSO for decades survived multiple strokes and “amazed doctors by how quickly he recovered,” living to 94.1 Another reader stated flatly that DMSO saved him from a stroke a decade ago.1
Finally, many readers describe using oral DMSO as ongoing stroke prevention. One was having strokes two or three times a week until he started DMSO (originally bought for sciatic nerve pain): “the strokes stopped happening... once it is in the blood stream it works everywhere.”1 Another also reported DMSO stopped their strokes,1Likewise, a diabetic who’d had two strokes from clotting that monitoring his own blood under a microscope, found daily oral DMSO kept his red cells out of rouleaux formation and “the clots at bay.”1
Note: these readers were almost certainly suffering from what would be diagnosed as “TIAs” and the fact that both DMSO prevented their recurrence and that one reader could link this to DMSO eliminating blood sludging argues for my theory many TIAs are actually microstrokes triggered by things like zeta potential disruption.
In short, I hope all of this (and what is to come) makes it clear why I feel so strongly about DMSO becoming a standard therapy for strokes. Nonetheless, as discussed earlier, it is absolutely critical you do not avoid emergency care just because DMSO is available and rather treat it as complementary therapy as you wait for conventional care.
DMSO Stroke Combination Therapies
Since DMSO is both a non-toxic solvent and able to deliver a variety of agents (e.g., through the skin), that rare combination results in it being used as a “vehicle control” in many studies. In these studies, DMSO is typically assumed to be inert (and hence not independently tested for an effect), but in some cases is tested, where it often yields a therapeutic effect (which I’ve noticed authors often do not disclose). As a wide number of agents combined with DMSO all yield therapeutic effects similar to those seen with DMSO, this suggests that DMSO plays a direct role in the effects observed, particularly since DMSO frequently potentiates the agents it is combined with. This dynamic I believe likely accounts for why many agents that succeed in preclinical studies (where DMSO is also used) fail in clinical studies where DMSO is not also used.
Note: replication failure is one of the largest problems in science.
As such, I include these combinations here (most of which were used for focal brain ischemia) both to highlight the shared effects seen across many agents (that potentially are due to DMSO) and to provide insights to readers looking for additional treatment strategies. To make these section easier to skim, all natural agents are marked with a ⬖.
Natural agents
Polyphenols & flavonoids — curcumin⬖ (reduced infarct size and cell death)1,2,3,4,5,6,7,8,9,10,11,12,13,14; resveratrol⬖ (reduced infarct size and preserved neurons, including in elderly and recurrent-stroke rats)1,2,3,4,5,6,7,8,9,10,11; baicalein⬖ (reduced infarct size and cell death)1,2; chrysophanol⬖ (reduced infarct size and cell death as a pre-treatment)1,2; quercetin⬖ (reduced infarct size)1,2; chrysin⬖ (improved movement and memory and reduced oxidative stress)1,2; nordihydroguaiaretic acid⬖ (reduced neurological deficits and infarct size)1; apigenin⬖ (reduced inflammation)1; mangiferin⬖(reduced neurological deficits when given before ischemia)1; shikonin⬖ (reduced infarct size and oxidative stress)1; trifluoro-icaritin (reduced neurological deficits and infarct size)1.
Alkaloids & related plant compounds — berberine⬖ (reduced infarct size and cell death)1,2,3,4; evodiamine⬖ (reduced infarct size)1,2,3; rutaecarpine⬖ (improved movement and raised neurotrophic factors)1,2,3; cynandione A⬖1; vinpocetine⬖ (reduced infarct size and inflammation)1; sinomenine⬖ (reduced inflammation)1; piperine⬖ (reduced injury)1; carvacrol⬖ (reduced injury)1.
Terpenoids, saponins & quinones — astragaloside IV⬖ (protected neurons and reduced cell death)1,2,3,4,5; celastrol⬖ (reduced neurological deficits and infarct size)1,2; the cembranoid 4R⬖ (reduced infarct size and cell death)1; ginsenoside Rb1⬖ (reduced neuronal death)1; bilobalide⬖ (reduced neurological deficits and infarct size)1; tanshinone IIA⬖ (reduced infarct size when given after stroke)1; sulforaphane⬖ (reduced infarct size and inflammation)1; triptolide⬖ (reduced infarct size, swelling, and neurological deficits)1; picroside⬖ (protected mitochondria and reduced cell death)1; ursolic acid⬖ (reduced infarct size and improved neurological scores)1; Z-guggulsterone⬖ with boswellic acid⬖ (improved neurological function and promoted new blood-vessel growth)1; salvinorin A⬖ (reduced inflammation and swelling and protected the blood-brain barrier)1,2,3,4; herkinorin (reduced brain swelling and improved neurological function)1,2.
Whole-herb & multi-herb extracts — kava extract⬖ (reduced cell injury and inflammation)1; Gastrodia elata extract⬖ (reduced infarction by shifting immune cells toward healing)1; Ptychopetalum olacoides extract⬖ (protected brain tissue from oxygen deprivation)1; Angelica sinensis extract⬖ (improved neuronal survival and regrowth)1; Ginkgo biloba extract⬖ (prolonged survival and reduced injury)1,2; Viola spathulata extract⬖ (reduced infarct size)1; Zhenbao Pill⬖ (reduced inflammation and cell death)1; Qing-Nao-Tong-Luo Recipe⬖ (reduced infarct size and improved neurological function)1; Tongxinluo⬖ (protected the blood-brain barrier and circulation)1; Shenmai injection⬖ (reduced deficits and infarct size)1.
Other natural compounds — stilbazulenyl nitrone⬖ (was highly neuroprotective as an antioxidant)1; docosahexaenoic acid⬖ (protected brain cells from oxygen deprivation)1.
Synthetic & pharmacological agents
Kinase & MAPK-pathway inhibitors — an ERK inhibitor (improved survival and protected mitochondria after cardiac arrest, and reduced infarct size)1,2,3,4,5,6; a PI3K inhibitor (reduced injury in diabetic brain injury)1; a p38 MAPK inhibitor (reduced cell death and swelling and improved neurological function)1,2,3,4,5,6,7,8; a JNK inhibitor (protected neurons and improved survival)1,2,3; rapamycin (reduced infarct size)1,2,3,4; Mdivi-1 (reduced oxidative stress and cell death)1,2; a STAT3 inhibitor (reduced injury)1; anisomycin (improved neuronal survival)1; a PTEN inhibitor (promoted neuronal repair)1; HIF prolyl-hydroxylase inhibitors (induced protective autophagy)1; bosutinib (reduced infarct size and inflammation)1; a TAK1 inhibitor (improved neurological scores and reduced infarct size)1; 5’-deoxy-5-iodotubercidin (reduced infarct size by up to 57%)1; 2-Cl-MGV-1 (promoted new blood-vessel growth)1.
Cell-death & protease inhibitors — caspase inhibitors (reduced infarct size and cell death)1,2,3,4,5; cathepsin inhibitors (reduced infarct size and cell death)1,2,3,4; a Notch/γ-secretase inhibitor (drove stem cells toward neurons and aided post-stroke regrowth)1,2; necrostatin-1 (reduced necroptosis and improved myelination and memory)1,2,3; cyclosporin A (protected neurons)1; a calpain inhibitor (reduced cell death and injury)1,2; a PARP inhibitor (reduced infarct size)1; thalidomide (reduced infarct size and cell death)1.
HDAC & epigenetic inhibitors — an HDAC inhibitor (trichostatin A) (reduced infarct size and inflammation)1,2,3; an HDAC inhibitor (SAHA) (reduced infarct size by up to 57%)1,2; an HDAC inhibitor (MS-275) (reduced infarct size)1; an HDAC inhibitor (TSA) (reduced infarct size and inflammation)1; an EZH2 inhibitor (improved coordination and reduced injury)1.
Nuclear-receptor & metabolic modulators — pioglitazone (reduced neurological deficit, swelling, and inflammation)1,2,3,4; all-trans retinoic acid (reduced infarct size as a post-treatment)1,2,3; a PPARγ inhibitor1,2; LXR agonists (reduced infarct size)1; rosiglitazone (reduced infarct size, and in DMSO cut it by roughly half where DMSO alone was inert)1; a thyronamine analog (induced protective hypothermia)1; a PPARα agonist (bezafibrate)1; an SGLT2 inhibitor (empagliflozin) (reduced microvascular injury)1; an Nrf2 activator1; an ALDH2 activator1.
Receptor ligands & ion-channel modulators — an adenosine A1 agonist (improved outcomes and reduced injury)1,2,3,4; an α7-nicotinic modulator (reduced damage after stroke)1; dexmedetomidine (reduced mitochondrial fission and cell death)1,2,3; octanol, a gap-junction blocker (reduced infarct size after longer ischemia (worsening it after brief ischemia))1,2,3; a TRPC1 blocker (reduced calcium overload and cell death)1,2; nimodipine (improved neuronal survival)1; bumetanide (reduced swelling)1,2; an LPA2 agonist (improved survival)1; a GABAA α5 inverse agonist (promoted motor recovery)1; a nucleoside-transporter inhibitor (reduced infarct size)1.
Cannabinoid-system modulators — a CB1 agonist (acted through mitochondrial CB1 receptors)1,2; a CB2 agonist (reduced injury)1,2.
Hormones, steroids & vitamins — estrogen (reduced infarct size and cell death)1,2,3,4,5,6,7,8,9; progesterone (reduced infarct size and improved recovery, less so in aged animals)1,2,3,4,5,6,7,8,9; tamoxifen (reduced injury)1; vitamin D3⬖ (reduced infarct size and increased blood flow)1; vitamin K2⬖ (reduced swelling, cell death, and inflammation)1; erythropoietin (reduced injury, including intranasal delivery)1,2; leukemia inhibitory factor (protected neurons)1.
Repurposed clinical drugs — 4-methylcyclopentadecanone (reduced infarct size and inflammation)1; a norcantharidin MMP-9 inhibitor (improved scores and protected the blood-brain barrier)1; modafinil (reduced infarct size and swelling)1; cilostazol (protected brain blood vessels)1,2.
Other synthetic / pharmacological agents — an nNOS inhibitor (reduced infarction by 70-92%)1; an azulenyl nitrone (STAZN) (was neuroprotective)1; Z-11 (reduced neurological deficits and infarct size)1; a 12/15-LOX inhibitor (reduced infarct size and inflammation)1; electroacupuncture with microRNA delivery (reduced deficits and promoted stem-cell regrowth).1,2,3,4
Other injury models
The combination data also extend beyond focal ischemic stroke to the following models:
Neonatal & perinatal hypoxic-ischemic models — hesperidin⬖ (reduced oxidative stress and improved survival)1; baicalin⬖ (cut neonatal infarct size roughly in half)1; notoginsenoside R1⬖ (improved survival)1; melatonin⬖ (reduced infarct size and improved brain metabolism)1,2,3; a JNK inhibitor (reduced neonatal cell death)1,2; dantrolene (reduced cell death and injury)1; an adenosine A2A antagonist (reduced brain damage and cell death)1,2,3; 2-methoxyestradiol (reduced swelling and cell death)1; indomethacin (reduced infarct size and protected the blood-brain barrier)1; miconazole (improved myelination in white-matter damage)1; G-CSF (reduced neonatal cell death)1; H2S donors (reduced injury and promoted remyelination)1,2.
Cardiac-arrest & global-ischemia models — ellagic acid⬖ (improved kidney function after global ischemia)1; Gynostemma pentaphyllum⬖ (improved outcomes after cardiac arrest)1; necrosulfonamide (improved recovery by blocking programmed cell death)1; a TLR4 inhibitor (reduced neuron loss after cardiac arrest)1; oxcarbazepine (protected neurons after cardiac arrest)1; WIN 55,212-2 (reduced infarct size and induced protective hypothermia that prolonged survival)1,2,3,4,5; salubrinal (improved outcomes and preserved mitochondria after cardiac arrest)1,2; glibenclamide (raised 7-day survival after cardiac arrest)1; genistein⬖ (increased neuron survival after cardiac arrest)1,2; paclitaxel (protected neurons after cardiac arrest)1,2.
Cerebral Blood Flow & Vascular Reactivity
Beyond protecting brain tissue once a stroke is underway, as highlighted previously in the endothelial data, DMSO also acts directly on the cerebral vessels themselves, changing their tone, their reactivity to constrictors and dilators, and the blood flow they carry.
Like many other properties of DMSO, its effect on cerebral vessel caliber (width) depends heavily on dose. In a cat study examining pial (brain) arterioles both in vitro and in vivo, DMSO concentrations from 0.0001% to 0.5% produced no significant change in arteriolar caliber, while 1% DMSO dilated them by 19%—and on isolated cerebral arteries, high-concentration DMSO reversed constriction induced by PGF₂α (85% reversal), serotonin (60%), and potassium (13%).1 That study also found that intravenous 10% DMSO (1 g/kg) produced rapid, measurable brain shrinkage within 10–15 minutes, consistent with DMSO’s edema reducing properties.1
Conversely, some of DMSO’s effects on cerebral vessels actually work by blocking dilation, and this too traces back to its radical scavenging. This is because hydroxyl radicals themselves dilate cerebral microvessels, so when acetaldehyde and xanthine oxidase were used to dilate mouse pial arterioles, free-radical scavengers including DMSO stopped that dilation.1 Likewise, DMSO inhibited the pial arteriole dilation produced by a radical-generating xanthine oxidase acetaldehyde system while leaving carbon dioxide induced dilation untouched.1 This selectivity (blocking only the radical-driven dilation) hence indicated DMSO was scavenging radicals rather than acting as a general vasomotor agent.1 Likewise, in canine basilar arteries, DMSO reduced the Fe²⁺-mediated inhibition of endothelium-dependent relaxation by scavenging hydroxyl radicals.1 DMSO hence does not push vascular tone in a fixed direction like a typical pharmaceutical, rather normalizes vascular function by removing the radical signal, so it dilates a vessel radicals were constricting and blocks a dilation radicals were driving.
DMSO also independently blocks ATP-sensitive potassium (KATP) channel mediated cerebral vasodilation, and it does so at very low concentrations (within the range routinely used just to dissolve a test compound). In anesthetized rats, DMSO dose-dependently inhibited pinacidil-induced dilation of pial arterioles at 0.01-0.2%, with significant inhibition at the very bottom of that range.1 Notably, DMSO alone did not change the baseline vessel diameter, and the effect reversed within 15 minutes of washing the DMSO out.1 A companion report found the same for very low dilutions of both ethanol and DMSO,1 and in cats, DMSO inhibited the cerebral arteriolar dilation produced by hydrogen peroxide and KATP openers at under 1 mmol/L (which those authors attributed to potassium-channel blockade rather than radical scavenging).1
That said, when perfusion is measured across the whole brain rather than in isolated vessels, DMSO consistently raises cerebral blood flow (e.g, this was a key focus of forgotten Russian research on reversing the effects of chronic stress). In a 1986 rabbit brain-edema study, a 20% DMSO bolus raised cerebral blood flow by roughly 75-77% in both hemispheres almost immediately, with flow still elevated an hour later.1Pretreating with indomethacin did not prevent this rise, which indicated the increase was not prostaglandin-mediated, and the intracranial pressure still fell despite the higher flow (as DMSO rapidly pulls water out of the brain).1 Low-dose intravenous DMSO did much the same in a canine model of myocardial ischemia, raising both cardiac output and cerebral blood flow while lowering vascular resistance, with no adverse change in heart rate or blood pressure.1 Likewise, when given an hour after an experimental brain hemorrhage, DMSO held brain oxygen and glucose consumption near baseline, curbed the excess lactate, stabilized or increased blood flow (partly by raising blood osmolarity), completely prevented the surge in lipid peroxidation, and eliminated the early mortality seen in the untreated animals (0% versus 25%).1
Note: DMSO’s effect on central cardiovascular control has been found to be transient and local rather than systemic. Injected directly into the brainstem cardiovascular center (the NTS),40% DMSO produced only a brief 1-2 minute drop in blood pressure and heart rate before returning to baseline, with no lasting change (consistent with DMSO’s rapid diffusion out of tissue).
Agents dissolved in DMSO have also been shown to dilate the cerebral vessels such as an activator of ATP-sensitive potassium channels,1 various PDE5 inhibitors,1apigenin,⬖1 (which relaxed the basilar artery), tetrahydroxystilbene glucoside,⬖1 (which in rats relaxed the mesenteric artery while protecting carotid flow),1 a gamma-secretase inhibitor (that reduced the vasospasm following a subarachnoid hemorrhage).1
Finally, these cerebral-perfusion effects are often used as a rationale for clinical applications. For example, in a horse that developed seizures and blindness after surgery, intravenous DMSO was given specifically for its radical scavenging and thromboxane inhibition to maintain the brain’s blood supply, after which the seizures stopped by day 3 and the vision partially returned over the following months.1Likewise, the Russian clinical literature describes dimexide (DMSO) as relieving brain-tissue swelling, improving cerebral blood flow, and normalizing cerebral hemodynamics.1 One unusual Russian diagnostic protocol even applied a DMSO, nicotinic acid,⬖ and novocaine compress to the forehead to test whether increasing forehead blood flow improved a patient’s vision, using that result to predict who would benefit from surgery on the branches of the carotid artery.1
Hemorrhagic Strokes
Hemorrhagic strokes are among the most difficult conditions in all of medicine to treat, and despite decades of work, there has been remarkably little progress in neurocritical care—particularly in preventing the long-term paralysis and disabilitythat so often follow a brain bleed. This is because a hemorrhage sets off a cascade of injuries that conventional medicine has no single agent to address, whereas DMSO, remarkably, addresses each of them at once.
When blood escapes into the brain, three things happen more or less simultaneously. First, the swelling and accumulating blood raise the pressure inside the rigid skull (the intracranial pressure, or ICP), and brain tissue is exquisitely sensitive to being compressed—yet there is no good agent for lowering ICP (the most commonly used drug, mannitol, can produce a “rebound” in which pressure climbs higher than where it started). Second, the blood-brain barrier begins to break down, allowing still more fluid into the brain. Third, as the spilled blood cells die, the iron they release generates free radicals that destroy surrounding brain cells,1 while inflammatory processes triggered by the blood injure tissue further and drive additional cell death.
Remarkably, DMSO addresses each of these.1 It rapidly lowers ICP without the risk of rebound,1 and unlike most ICP-lowering agents it does not do so by cutting blood flow to the brain—instead it increases cerebral perfusion without raising blood pressure or heart rate,1 which matters because brain cells die within minutes of losing their blood supply. That improved flow is also what clears the leaked blood, and DMSO is excellent at reducing the accompanying brain edema.1
Note: I suspect rebound ICP is the brain’s attempt to restore its own blood supply; because DMSO already guarantees that supply, there is nothing to rebound from. Consistent with an osmotic rather than a direct vascular mechanism, one study in anesthetized cats found IV DMSO never constricted the cerebral arteries across an enormous concentration range, and only relaxed already-contracted vessels—while still shrinking the brain by pulling out excess fluid.
Beyond pressure and perfusion, DMSO lowers the inflammatory cytokines (IL-1α, IL-1β, IL-6) tied to stroke and tissue injury1,2 and calms overactive immune signaling.1,2 It also directly counters the damage from blood breakdown products: its free-radical scavenging limits platelet aggregation at injured microvessels and prevents blood from flooding the injury site (reducing secondary ischemic injury).1 At just 0.5% DMSO protected basilar-artery smooth muscle from oxyhemoglobin-induced contraction membrane blebbing, and cell death by scavenging hydroxyl radicals1 and it reversed iron-mediated damage to vessel relaxation in canine basilar arteries.1 DMSO likewise prevented bilirubin toxicity in myelinated axons, protecting nerve fibers from another toxic product of degrading blood.1
In short, no comparable agent exists for lowering ICP—one of the greatest unsolved challenges in neurocritical care—and many drugs that succeeded in animals have failed in human trials.1 Beyond removing edema, limited human work also suggests DMSO can somehow reduce the ongoing spilling of blood into the brain, through a mechanism that has not yet been definitively worked out.
Note: DMSO additionally lowers JAK2/STAT signaling,1 suppresses neurotoxic NMDA/AMPA ion currents,1 prevents iron-induced lipid peroxidation and focal edema,1 and partially inhibits PARP-1.1
De la Torre’s Discovery
The potential of DMSO here was recognized decades ago by Jack de la Torre, who when watching a near-dead experimental animal revive with DMSO recounted:
It was, as if the hand of God had somehow touched the animal’s forehead. “I don’t believe it,” I stammered. But it was true. I felt a tingling in my spine because this reawakening of a virtually dead animal had all the markings of a medical breakthrough.
Note: de la Torre’s observations were based partly on his repeated finding that animals with flatlined EEGs—which normally precede brain death—had their EEGs return within about ten minutes of receiving DMSO. As so often in this story, the discovery was never developed and was instead quietly laid to rest in the coffers of forgotten medicine.1
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