DMSO et radicaux libres

 extrait de   : https://www.midwesterndoctor.com/p/dmso-heals-blood-vessels-and-could?

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Human Antioxidant Trials

A separate line of human research, largely published in the Ukrainian and Russian literature, approached DMSO from the angle of its free-radical scavenging rather than its pressure-lowering effect, and provides some of the strongest controlled human TBI data in this section.

The most substantial came from a 2003 dissertation at the Romodanov Neurosurgery Institute in Kyiv, which combined rat experiments with a controlled trial in 135 severe TBI patients. It established that lipid peroxidation, a key driver of secondary brain damage, activates within 3 hours of injury, peaks around days 3 to 7, tracks with injury severity, and persists for at least a year. In a controlled arm of 75 of those severe TBI patients, adding intravenous DMSO (first dose 3 to 5 hours after trauma and a second the following day) to standard therapy reduced lipid peroxidation markers by 22% by day 8 (versus a 15% rise in controls), raised the peroxide resistance of red cells by 71% (versus 13% in controls), and accelerated the regression of major neurological syndromes, with significant improvement in general cerebral (66.6%), meningeal (95.8%), asthenic (46.1%), and vegetative (95.6%) symptoms compared to standard therapy alone.¹ The parallel rat work found that the same intraperitoneal DMSO regimen significantly reduced lipid peroxidation products in brain and blood (TBARS by 8 to 34%, Schiff bases by 27 to 68%) and raised red-cell resistance to peroxide-induced hemolysis by 11 to 51%, with the antioxidant effect sustained out to 21 days.
Note: these results have many intriguing correlations to Plotnikov’s previously mentioned research and the Russian chronic stress discussed in the first part of the series all of which suggests DMSO can counteract primary causes of acute and chronic neurodegeneration.

Likewise, this antioxidant framing recurs throughout the Russian-language reviews, where DMSO is classified as a synthetic radical scavenger noted for trapping the highly damaging hydroxyl radical and for providing a “high and stable” antioxidant effect in severe craniocerebral trauma, raising the body’s antioxidant status and preventing secondary brain damage.¹

Animal Brain Injury Research

The human findings above have been reproduced and mechanistically dissected across a wide range of animal brain injury models.

•Compression and pressure injuries: Because any brain bleed or concussive impact risks putting pressure on part of the brain (for instance from an expanding clot), the models that mimic this are especially relevant. The most dramatic was a study in which an expanding balloon was placed in the brains of 40 rhesus monkeys to simulate a hematoma. All 10 saline-treated monkeys died, versus 10 of 15 surviving with urea (66.7%) and 14 of 15 with DMSO (93.3%), and among survivors neurological deficits occurred in 4 of 10 urea-treated animals versus only 1 of 14 given DMSO.^1,2 This study, in turn, was preceded by an earlier study of 30 monkeys with similar results.¹
Note: urea was previously regularly used as a diuretic,¹ and while it is now mostly (but not completely¹) forgotten. We have found one oral urea formulation to be very helpful for certain types of edema and swelling.

Pressure injuries in dogs told the same story. In dogs with reduced blood pressure, pressure was applied directly to the brain for an hour, cutting off cerebral blood flow and producing necrosis, cavitation, edema, and deficits on the opposite side of the body. Against a panel of agents (barbiturates, mannitol, dextran, methylprednisolone), DMSO was the most effective: compared to no treatment, it improved neurobehavioral scores by 220%, reduced lesion volume by 93%, and prevented death in 5 of 6 dogs. Since blood alcohol worsens the damage from a traumatic brain injury (as occurs in drunk driving), the experiment was repeated with high blood alcohol, where DMSO still reduced brain tissue damage by 60%.^1,2,3 In a related model, pressure-induced ischemia applied to the somatosensory cortex killed every untreated dog within days, whereas with IV DMSO five of six survived with no neurological or behavioral changes and preserved evoked potentials. A further comparison of seven therapies likewise found DMSO the most effective against pressure-induced focal ischemia. Likewise in rats with diffuse axonal brain injury, DMSO significantly reduced c-fos and c-jun gene expression in neurons across the cortex, white matter, brain stem, thalamus, and cerebellum, with the most pronounced reduction 2 hours post-injury compared to controls¹—which is noteworthy as these genes drive inflammation and neuronal cell death in the window immediately after traumatic brain injury.

Note: one of the more intriguing findings across these compression studies was that neurological function was frequently preserved even when injury was still present in the brain tissue itself, suggesting DMSO protects function above and beyond what its effect on visible damage would predict.

•Edema models: A large body of rabbit work established DMSO’s anti-edema effect. A rabbit study that created lethal brain edema by freezing part of the brain found DMSO significantly reduced ICP and edema within 5 minutes while raising cerebral perfusion and leaving central venous pressure unchanged.¹ This was reproduced repeatedly, including a follow-up with similar results,¹ one using slow infusion rather than a bolus,¹ another one that also found a 20% solution reduced ICP more reliably than 30% or 40% (at 1.0 to 2.0 g/kg),¹ two others showing a synergistic effect with a barbiturate (where DMSO enhanced the ICP reduction while counteracting the barbiturate’s reduction of brain blood flow),^1,2 one indicating the effect was mediated through sodium mobilization,¹ and a final set showing indomethacin partly blocked DMSO’s ICP reduction, implicating prostaglandins.^1,2,3

Note: highlighting DMSO’s normalizing properties, while DMSO lowers pathologically elevated ICP, in anesthetized rabbits with normal pressures, intravenous DMSO produced a prompt, significant rise in cerebrospinal fluid pressure (up to 66 mm H₂O, lasting under a minute)—and, unlike norepinephrine or epinephrine, it did so with no change in systemic blood pressure, respiration, or anything else, pointing to a local cerebral vascular or blood-CSF barrier effect.¹

A Chinese study likewise used DMSO for acute cerebral edema.¹ The effect held in other edema models too: in rabbits with brain edema induced by injecting pertussis vaccine into the carotid artery, IV DMSO effectively reduced ICP and edema,¹ and in rats with edema induced by injecting iron (FeCl₂) into the brain, intraperitoneal DMSO reduced edema by 23% initially and left treated rats with far less edema at 24 hours.¹ Similarly in cats exposed to standardized cortical freeze injury, DMSO reduced Evans blue extravasation—a marker of blood-brain-barrier disruption and vasogenic edema—acting as a hydroxyl-radical scavenger and grouped with deferoxamine as effective.¹ Finally in a rat frozen-brain-injury model, DMSO (0.4 g/kg*) significantly reduced brain water content and neuronal apoptosis, outperforming tetramethylpyrazine at relieving the edema.¹

Note: the older pertussis vaccine (which was notorious for causing severe brain injuries) contained a toxin that disrupted the blood-brain barrier and created brain inflammation. In that study, injecting it into the artery feeding the brain was used as a reliable way to induce brain damage.

•Missile and penetrating injuries: To simulate DMSO’s protective effects against gunshot wounds, missile injuries (frequently with BB pellets) were created in monkeys. Compared to mannitol, DMSO produced significantly better cerebral perfusion and oxidative metabolism along with an 86% survival rate (versus 75% for mannitol and 55% untreated).¹ These results were replicated in a more detailed follow-up¹ and by two other groups.^1,2 A direct comparison to mannitol in rhesus monkeys with a standardized occipitofrontal missile injury confirmed DMSO better preserved cerebral blood flow, perfusion pressure, and oxidative metabolism than mannitol,¹ and a further monkey study comparing 50% DMSO to mannitol for experimental brain gunshot wounds tested repeat dosing whenever ICP exceeded 20 mmHg.¹

•Impact and weight-drop models: Numerous studies simulate closed head trauma by dropping weights on the heads of animals, and DMSO consistently protected against the resulting damage. In injured rats it reduced neuronal apoptosis, increased anti-apoptotic Bcl-2 expression across 6 to 168 hours post-injury,¹ and raised Survivin and NF-κB expression in injured tissue, all reducing cell death.¹ Functionally, DMSO improved cognitive and locomotor performance (such as solving mazes) while reducing anxiety, oxidative stress, inflammation, necrosis, and axonal damage,¹ and separately reduced memory deficits by 62% a week after injury.¹ A particularly rigorous study found that DMSO significantly reduced secondary neuronal degeneration in the hippocampus, with a magnitude of neuroprotection statistically indistinguishable from curcumin^⬖ or alpha-tocopherol^⬖ tested alongside it, leading the authors to conclude DMSO itself acted as a neuroprotective agent.¹ In mice, DMSO combined synergistically with fructose 1,6-diphosphate (FDP) to protect motor function, survival, and cortical and hippocampal neurons from these injuries.¹

Note: in animal experiments simulating severe brain injury, DMSO has also been shown to strengthen respiration (which otherwise becomes shallow and may stop), and in both humans and animals it often significantly increases urination through its diuretic action.

•Free-radical scavenging: DMSO also attenuated free-radical-mediated neurotoxicity in traumatized rat hippocampal neuron cultures, reducing apoptosis in uninjured neighboring cells by scavenging reactive oxygen species,¹ providing a cellular-level mechanism to for its protective effects here.

Jacob and de la Torre’s capstone review of this literature,¹ summarized the whole picture: low-dose intravenous DMSO restores cardiac output and cerebral blood flow, inhibits tissue-factor expression, scavenges free radicals, suppresses platelet aggregation, and in CNS models and patients rapidly lowers intracranial pressure without rebound, reduces edema, raises cerebral perfusion pressure, limits infarct volume, and preserves vulnerable hippocampal neurons. 

To put all of this into context:

A January 11, 1981, news report in the Ocala Star Banner [page 6] carried the headline “DOCTOR CLAIMS DMSO SAVED 11.” The story read:

SAN DIEGO (AP) - A doctor at the University of San Diego [UCSD] credits the controversial drug DMSO with saving the lives of 11 people who suffered severe head injuries.

Dr. Perry E. Camp, a UCSD Medical School neurosurgeon, said Friday that dimethyl sulfoxide was effective for 11 of 30 people judged near death and for which other lifesaving methods have proved useless.

“To take patients like that and have even one out of 10 survive is phenomenal,” Camp said. “The fact that we have any survivorship at all . . . doesn’t sound like much, but it is extremely encouraging,” Camp said.

Note: many of the same principles discussed above hold true for concussions, and the pioneers of DMSO felt DMSO was an essential treatment for athletes after they experienced one, particularly since concussions can predispose the athlete to long-term cognitive issues (e.g., both boxers and professional football players have a threefold risk of dementia).

Traumatic Brain Injury DMSO Combinations

Like many other neurological conditions, a variety of agents dissolved in DMSO have shown promise in treating traumatic brain injuries, and convergent effects seen suggest some of the effects arise from DMSO rather than the active agent.

For example, in a controlled cortical impact study using DMSO as the vehicle for glibenclamide, the authors reported “unexpected independent beneficial effects” of DMSO itself, particularly in female mice, in which DMSO alone significantly downregulated the neurodegeneration markers TDP43 and TAU and helped restore cerebral blood flow by 21 days post-injury, comparable to the drug it was merely supposed to be dissolving. The authors flagged these as novel, previously unrecognized protective effects.
Note: this response illustrates why the protective effects of DMSO are rarely recognized in combination studies as the authors frequently can’t even conceive they could be present to begin with (despite a vast body of evidence already showing it).

Traumatic Brain Injury Combinations

The TBI combinations were as follows:

Natural agents — curcumin^⬖ (reduced inflammation, oxidative stress, and seizure susceptibility)^1,2,3; tetrahydrocurcumin^⬖ (curcumin’s more absorbable form; enhanced autophagy and restored antioxidant enzymes)¹; resveratrol^⬖ (reduced cell death and modulated autophagy)^1,2,3,4; quercetin^⬖ (reduced swelling and cell death)¹; sulforaphane^⬖ (reduced swelling, contusion size, and oxidative stress)¹; alpha-lipoic acid^⬖ (improved neurological scores and reduced cell death)¹; honokiol^⬖ (from magnolia bark; protected the blood-brain barrier and reduced oxidative stress)¹; vitamin K₂^⬖ (reduced inflammation)¹; docosahexaenoic acid (DHA)^⬖ (the omega-3 fatty acid; improved autophagy and reduced inflammation)^1,2,3,4; erianin and the mangrove-fungus derivative C53N (from Dendrobium; reduced inflammation, oxidative stress, and cell death (isolated research compounds rather than accessible remedies))^1,2; Morin^⬖ with MK-801 (lowered dementia and inflammatory markers after repetitive TBI)¹; Auraptene^⬖ (reduced oxidative stress and inflammation)¹.

Note: the hormones progesterone and 17β-estradiol were also repeatedly delivered in DMSO and found protective after TBI, reducing swelling, oxidative stress, and inflammation while improving neurological outcomes. ^1,2,3 Notably, in one progesterone study the DMSO-only arm itself showed the same pattern of benefit¹ (reduced swelling and cell death and improved neurological scores over time), an ambiguity in the source data that again points to how independent DMSO effects get folded into the “vehicle” group.

A far larger set of studies used DMSO to deliver targeted pathway inhibitors and other synthetic compounds. Across these, the agents below repeatedly reduced brain swelling, cell death, oxidative stress, and neurological deficits, with the DMSO-only arm often following the same protective direction.

Oxidative-stress & Nrf2 agents — Nrf2 activators apocynin^1,2; and tert-butylhydroquinone¹.

HDAC & epigenetic inhibitors — HDAC inhibitors^1,2,3.

Cell-death & protease inhibitors — necroptosis inhibitors^1,2; a cathepsin, a calpain inhibitor¹ and a selective PAR-1 inhibitor (improved depression-associated behaviors, social interaction and hippocampal-associated cognitive impairment).¹

Autophagy & mTOR modulators — autophagy modulators^1,2,3; an Epac2 inhibitor¹; an mTOR inhibitor (rapamycin)¹.

Receptor ligands & agonists — an S1P1 agonist and a bile-acid-receptor agonist^1,2; a translocator-protein ligand¹; a histamine-receptor ligand¹.

Other pathway & enzyme modulators — a matrix metalloproteinase inhibitor^1,2; a PTEN inhibitor¹; an adenosine kinase inhibitor¹; mitochondrial uncouplers¹; a spinogenic agent¹; a CRMP2-derived peptide¹; cypin activators¹; an anti-inflammatory (ATB-346)¹; salubrinal (improved motor and cognitive function and reduced lesion size)¹; an ADAM inhibitor (reduced lesion size and axonal injury)¹.

Edema model combinations — curcumin^⬖ (reduced brain swelling and inflammation)¹; quercetin^⬖ (reduced oxidative stress, brain swelling, cell death, and vasospasm)¹; kadsura pepper stem extract^⬖ (reduced hematoma size)¹; a JAK2 inhibitor with dexmedetomidine (reduced brain swelling and cell death)¹; a KMO inhibitor¹.

TBI and Concussion Reader Reports

Within the DMSO literature, there are periodic cases of dramatic concussion recoveries following DMSO. For example, one author shared the case of a woman who had received a severe concussion from falling off a horse, after which she had trouble walking, would suddenly neurologically decompensate (e.g., dropping things), and had memory issues alongside foggy headaches. Thirteen years later, she received an injection of DMSO, immediately had a large improvement, and further improved with subsequent injections.

Readers recovering from traumatic brain injuries, concussions, and related head trauma have reported similar benefits from DMSO.

The most mechanistically intriguing report came from a reader who is post-traumatic brain injury since 2017 and lives with cervical instability and a CSF leak that leaves her with recurring concussion-like symptoms. Even at a low dose she could tolerate, she found DMSO noticeably lowered her intracranial pressure, along with reducing daytime fluid retention, improving her distance vision and bowel function, and lessening food reactivity. She noted this could be particularly helpful for others with raised intracranial pressure, since, as in her case, elevated ICP can itself produce CSF leaks.¹

Other readers reported briefer successes: one for sciatica and brain trauma¹ (”It works!”), and another for finger joints and a head injury.¹

Concussion Reports

Several readers have described using DMSO specifically for concussion. One with a concussion said it was “saving me and helping me to continue working,”¹ another used it for post-concussion and whiplash injury,¹ and another, recovering from fifteen concussions and a broken back after a 1992 Grand Canyon fall found success with castor oil^⬖ and DMSO.¹

Another reader described slipping on a wet floor and landing on her cheekbone with nothing but her glasses to break the fall—”I could feel my brain slam inside my head.” Within 30 minutes her cheek and eye had puffed up severely; she ingested DMSO and lathered it on her face, continuing for three days. By day five the bruising was already in its final yellowing stage. “I think had I not had DMSO in my house, I would be suffering from symptoms of concussion now,” she wrote, adding that she now keeps a bottle in her handbag at all times.¹

The most detailed concussion account came from a reader who said DMSO “gave me my life back” after a shoulder injury with a concussion of the upper back left everything from his neck to his left hand inflamed and painful, and left him feeling systemically ill for months. Standard anti-inflammatories were useless. Starting a topical DMSO once nightly, he felt “not sick for the first time in months” within about three weeks. He described the pain first being suppressed, then localizing to its true source (his neck rather than the shoulder), then resolving, alongside a range of incidental benefits (a chronic wrist problem, thumb inflammation, eye floaters, a fading scar, and body odor all improved). He also found an on-off strategy worked best, applying for several days then pausing, observing that each time he stopped, the pain would briefly spike and then settle to a new low, as though removing DMSO let the body “better see where the problems really are.”¹

One reader even tried it for a rare eye condition tied to an old concussion. He has superior oblique myokymia, a “twitch behind the eye” that makes his vision jump and occasionally double (alarmingly, sometimes while driving at speed), which had been attributed to a concussive injury from a serious car accident in which an airbag knocked him out. After a neuro-ophthalmologist offered only anti-convulsant drugs with “awful” side effects, he tried a 10% DMSO solution in distilled water as an eye drop, which temporarily “hit the off switch.” It didn’t cure the condition, but gave him, in his words, an actual tool in the toolbox.¹

Note: concussions are notoriously difficult to manage (e.g., I have only found one approach that seems to work consistently for them), so the possibility a simple and widely accessible option exists is immensely encouraging as it would benefit many. However, while the evidence strongly argues for DMSO’s use in severe traumatic brain injuries, there is much less data for typical concussions, and it is quite likely the results for DMSO on those injuries were will be highly variable with not everyone experiencing a noticeable benefit from DMSO.