DMSO - More Evidence from the "Midwestern Doctor"

To read the original article (and support the doctor's work), go here.

https://www.midwesterndoctor.com/p/therapeutic-dmso-combinations-revolutionize?utm_source=post-email-title&publication_id=748806&post_id=148476894&utm_campaign=email-post-title&isFreemail=true&r=1bz278&triedRedirect=true&utm_medium=email

I'm culling out a few key points with a focus on stroke.

Here is the specific article by the Midwestern doctor on stroke.

https://www.midwesterndoctor.com/p/dmso-could-save-millions-from-brain?utm_source=substack&utm_medium=email

Firstly, the standard of care again proves that it does NOT want to help people. Minocycline is an effective stroke treatment, especially when taken as soon as possible after the event. However, it's never too late, given the multiple modes of action of minocycline. More on this later.

Minocycline - an effective agent for stroke. And maybe even enhanced in the presence of DMSO, based on another MWD article discussing how DMSO improves cellular permeability, which often reduces antibiotic resistance.

Lewis' comment: Based on information aggregated by the MWD, A DMSO / Minocycline combination may provide more efficacy.

Here is a review study on minocycline and stroke:

Abstract

Background: Various randomized-controlled clinical trials (RCTs) have investigated the neuroprotective role of minocycline in acute ischemic stroke (AIS) or acute intracerebral hemorrhage (ICH) patients. We sought to consolidate and investigate the efficacy and safety of minocycline in patients with acute stroke.

Methods: Literature search spanned through November 30, 2017 across major databases to identify all RCTs that reported following efficacy outcomes among acute stroke patients treated with minocycline vs. placebo: National Institute of Health Stroke Scale (NIHSS), Barthel Index (BI), and modified Rankin Scale (mRS) scores. Additional safety, neuroimaging and biochemical endpoints were extracted. We pooled mean differences (MD) and risk ratios (RR) from RCTs using random-effects models.

Results: We identified 7 RCTs comprising a total of 426 patients. Of these, additional unpublished data was obtained on contacting corresponding authors of 5 RCTs. In pooled analysis, minocycline demonstrated a favorable trend towards 3-month functional independence (mRS-scores of 0-2) (RR = 1.31; 95% CI 0.98-1.74, p = 0.06) and 3-month BI (MD = 6.92; 95% CI - 0.92, 14.75; p = 0.08). In AIS subgroup, minocycline was associated with higher rates of 3-month mRS-scores of 0-2 (RR = 1.59; 95% CI 1.19-2.12, p = 0.002; I2 = 58%) and 3-month BI (MD = 12.37; 95% CI 5.60, 19.14, p = 0.0003; I2 = 47%), whereas reduced the 3-month NIHSS (MD - 2.84; 95% CI - 5.55, - 0.13; p = 0.04; I2 = 86%). Minocycline administration was not associated with an increased risk of mortality, recurrent stroke, myocardial infarction and hemorrhagic conversion.

Conclusions: Although data is limited, minocycline demonstrated efficacy and seems a promising neuroprotective agent in acute stroke patients, especially in AIS subgroup.

Here is an AI overview of minocycline for the treatment of stroke.

Yes, minocycline has shown promising potential as a neuroprotective agent for stroke victims, particularly those who have experienced an ischemic stroke. 

Here's why:

• Neuroprotective Effects: Minocycline possesses multiple neuroprotective properties, including anti-inflammatory, anti-apoptotic, and antioxidant effects. It has been shown to reduce brain damage after ischemic stroke in animal studies by protecting the blood-brain barrier and influencing various molecular pathways.

• Potential for Improved Outcomes: Clinical studies have indicated that minocycline may significantly improve neurological and functional outcomes in patients with ischemic stroke, as measured by scales like the National Institute of Health Stroke Scale (NIHSS) and the modified Rankin Scale (mRS).

• Delayed Therapeutic Window: Unlike some conventional stroke treatments, minocycline may offer a relatively delayed therapeutic window, potentially providing a treatment option for a larger number of patients.

• Safety Profile: Minocycline is a known antibiotic with a generally good safety profile. It has been safely administered intravenously and orally in clinical trials for stroke.

The literature on minocycline to treat stroke is actually quite robust, yet it has hardly been used.

---

Minocycline is just an antibiotic, right? (And functional medicine largely does NOT believe in antibiotic use).

WRONG and shame on too many functional medicine doctors for being very close-minded on this treatment for the key AGING PATHWAY - Immunosenescence.

Here are some of the many properties of minocycline and its cousin, doxycycline.

Minocycline's 12 Anticancer and Longevity mechanisms

1) Matrix Metalloproteinase (MMP) Inhibition: Minocycline inhibits MMPs, which play a role in tissue remodeling and can facilitate tumor invasion and metastasis.

2) Inhibition of Cell Proliferation: Minocycline has been shown to inhibit the proliferation of various cancer cell lines.

3) Induction of Apoptosis: Minocycline can induce apoptosis or programmed cell death in cancer cells.

4) Mitochondrial Disruption: Minocycline affects the mitochondrial function in cancer cells leading to reduced cancer cell viability.

5) Inhibition of Angiogenesis: Angiogenesis is the process by which new blood vessels form. Tumors require these vessels to grow. Minocycline has anti-angiogenic properties, thus preventing tumor growth.

6) Stem Cell Modulation: Minocycline can target cancer stem cells, preventing tumor initiation, metastasis, and resistance to therapy.

7) Reduction in Tumor Growth: In animal models, Minocycline has been shown to reduce tumor size.

8) Enhancement of Chemotherapeutic Effects: In some studies, Minocycline has been shown to enhance the effects of traditional chemotherapeutic agents.

9) Inhibition of Epithelial-to-Mesenchymal Transition (EMT): EMT is a process by which cancer cells gain migratory and invasive properties. Minocycline has been shown to inhibit this process.

10) Autophagy Modulation: Autophagy is a cellular mechanism that can sometimes aid cancer cell survival through the process of reusing damaged and old cell parts. Minocycline has been found to modulate this process in cancer cells, downregulating the cancer cells’ ability to repair.

11 Immune Modulation: Some research suggests that Minocycline can modulate the tumor microenvironment, potentially positively impacting the immune response to tumors.

12) Targeting Microbial Influence: There's an evolving understanding of the role of microbes in cancer progression. Given its antibiotic properties, Minocycline might influence the tumor-associated microbiome and thereby enhance anticancer response.

---

The MWD and DMSO for ischemic strokes

Lewis' Comment: You will note that most of the information on DMSO and stroke treatment is either anecdotal or based on animal studies. I'm not discouraging its use - just pointing this out. If I had a stroke, it would be minocycline orally and DMSO orally - at appropriate doses - for months, not just a one-and-done treatment.

Note the substantial difference in the number of publications for minocycline vs DMSO and stroke. Also, note that these are "title only" searches - thus the "tip of the iceberg" of published studies.

Ischemic Strokes

After I learned how unconscionable the FDA’s prohibition against DMSO was, I made a point to begin telling people (e.g., friends, relatives, patients) I felt were at risk of a stroke to stock DMSO at home, and since then, I’ve had instances where someone (or their caretaker) called me up, described a stroke, I gave them instructions on what to do (since they already had DMSO at home), and by the time they got to the ER, the stroke was “resolved” and in some cases, the ER was confused by the CT scan because it both looked like a stroke had happened and simultaneously that one had not.

Note: in my opinion, IV DMSO would have been ideal (and more effective) in those situations, but in each case, it was not feasible to implement.

Likewise, many compelling cases have been recorded of individuals who treated their strokes with DMSO:

A Los Angeles school teacher had a major stroke shortly after the start of the Christmas break. She was unconscious on her living room floor. DMSO treatment was started immediately after the stroke. The DMSO was first applied topically to her head within minutes of the stroke. Less than one hour after the stroke she was given DMSO by intramuscular injection. This patient was never taken to the hospital for this stroke. A prominent surgeon who was a family friend told the husband of this patient that it was important to keep her out of the hospital. The surgeon said that even though the treatment was completely legal, it would be difficult to get approval to give the DMSO especially by injection at his hospital. This patient made a dramatic recovery. She regained consciousness later in the day in which she had her stroke. Treatment continued for the next week. Each day she received two topical applications of DMSO, one intramuscular injection of DMSO, and two doses of one teaspoonful of DMSO in juice. Her condition improved each day. When school resumed after the first of January, this teacher was back in the school teaching the students as if nothing had happened during the Christmas vacation. She never even mentioned it to the other people at the school. She continued teaching until she retired. She retired healthy with no disability. 

Note: if you drive someone to the ER (and call in ahead to let the ER know you are coming), you have numerous opportunities to administer DMSO prior to placing the patient in the ER without delaying their care there (e.g., emergency brain surgery for a hemorrhagic stroke).

A lady was in a coma in a convalescent hospital and had been in the coma since her stroke three months ago. She was given little chance of recovery and was expected to remain in a vegetative state until her death. When I first observed this lady, there was no response to any type of stimulus. She was alive, but appeared lifeless. It was decided that her treatment should be topical DMSO applied to her head daily either by her husband or by one of the nurses at the facility. One month after the start of treatment, there were positive signs in the lady. Her brain was starting to respond to the DMSO. The treatment continued, and four months after treatment started this lady was able to return to her home. After her return to her home, this patient started drinking one teaspoonful of DMSO in a small glass of water each day in addition to the daily topical treatment. This treatment continued for a period of years. Three years after the start of DMSO treatment this writer returned to visit this patient. At this time the lady was living a normal life, not the life of a stroke victim. She was able to look after the house and walked normally. The only lingering effect of the stroke was a slight speech defect. At this time she said that her memory was better than that of her husband who had not had a stroke and who was considered to be completely normal. 

Note: there are also many reported cases of individuals who took DMSO for musculoskeletal or pain disorders (by far the most common use of DMSO) who then experienced a permanent improvement of stroke symptoms.

As shown earlier in this article, DMSO has numerous properties that make it uniquely suited to protect from the damage of ischemic strokes. These benefits have in turn been shown to occur for brain tissue. For example:

DMSO was shown to preserve the neurological function of brain tissue samples once their oxygen or glucose were withdrawn (with similar results seen in this study).

Giving DMSO to rats 30 minutes prior to cutting off the blood flow in their MCA (a key artery in the brain) significantly reduced the amount of permanently damaged brain tissue. Additionally, this study and this study had similar results.A more recent rat study found giving DMSO 20 hours before blocking the MCA reduced the damaged brain tissue by 65%, by 44% when given an hour after, and by 17% when given two hours afterwards.

Note: these results argue that giving IV DMSO beforehand could reduce the complications of many challenging surgeries (e.g., a coronary bypass). Unfortunately, much in the same way ultraviolet blood irradiation dramatically reduces bad surgical outcomes, neither has been adopted for this purpose.A gerbil study (this species is more susceptible to strokes) found blocking carotid blood flow to the brain and then restoring blood flow to the brain caused significantly less neuronal loss if DMSO was given 30 minutes before the carotid blood supply was cut off. Another gerbil study had similar results.

A dog study cut off cerebral blood flow, then restored it and used a variety of biochemical measurements to monitor cellular metabolism (along with EEGs). Dogs who received DMSO (and an anti-platelet agent) had significantly higher mitochondrial function (which was almost identical to controls who had not suffered the occlusion).

Another dog study induced a stroke by introducing an embolus (clot) into the MCA and then giving DMSO. Compared to controls, those given DMSO were observed to have normal behavior and no neurological deficits afterward, whereas 3 of the 9 controls died (with significant tissue death in the brain), while the survivors had contralateral paralysis (a typical stroke consequence) and impaired consciousness.

A cat study found DMSO protected brain tissue from MCA occlusion and increased cerebral blood flow (CBF) by 27%. When DMSO was given in conjunction with PGI2, a greater improvement was seen (e.g., a 68% increase in CBF).

A rhesus monkey study blocked the MCA for 4 hours, gave DMSO, dexamethasone, or nothing, and then opened the MCA after it had been blocked for 17 hours. DMSO gave significant protection from the severe neurological deficits and loss of arterial blood flow the other two groups developed.

A squirrel monkey study blocked the left MCA for 4 hours, and then given a variety of different treatments (e.g., saline, hemodilution, or hyperbaric oxygen at 2 atmospheres). Seven days after treatment, 8 of 10 DMSO treated monkeys were alive (with 2 having mild contralateral muscle weakness), while 75% of those receiving hyperbaric survived, and just 34% of those receiving hemodilution survived (with the last two groups also having more significant neurological deficits). Finally, combining either of these treatments with DMSO produced slightly worse results than just DMSO alone.

Lastly, a rat study found that when hemorrhagic shock was induced, DMSO downregulated the inflammatory response (NF-kappaB) and upregulated a key protein cells use for survival (HSP70).

Note: small strokes can still cause significant long-term issues (which DMSO often completely prevents), so as a general rule, I advise using DMSO anytime someone has a suspected stroke.

Lastly, DMSO has been shown to treat Bell’s palsy (facial paralysis caused by either microstrokes, inflammation, or ischemic strokes). In one study of 65 patients, DMSO mixed with 1% nicotinic acid applied to the affected part of the face as a compress 10-12 times and was shown to provide a statistically significant improvement in the number cured and the duration of therapy they required.Note: DMSO has also been used to treat diseases of the peripheral nervous system.

---

Hemorrhagic Strokes and Traumatic Brain Injuries

While ischemic strokes are difficult to treat, hemorrhagic ones (and other traumatic brain injuries) are even more challenging, and after decades, there has been surprisingly little progress in neurologic intensive care, particularly in preventing long-term paralysis and disability.

Note: conflicting evidence exists supporting the use of progesterone, hypothermia, and hyperbaric oxygen therapy for traumatic brain injuries, but none of these approaches are in widespread use. Strong evidence also supports the use of methylene blue but it also is rarely used. Finally, certain trials (e.g., with progesterone or with an adenosine kinase inhibitor) find those therapies work even better if combined with DMSO.

 It was, as if the hand of God had somehow touched the [experimental] 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 [Jack de la Torre MD].Instead, the discovery, the potential for saving lives and the continued research that should have uncovered other uses for dimethyl sulfoxide and similar agents was quietly laid to rest in the coffers of forgotten medicine.

Note: Torre’s observations were partly based on the fact he saw numerous animals with flatlined EEGs (which typically precede brain death and then actual death) have the EEGs come back within 10 minutes of receiving DMSO.

When treating severe brain bleeds, a few major challenges exist.

First, swelling and the leaking of blood into the brain can dramatically increase the pressure on the brain (known as intracranial pressure or ICP). The brain’s tissue in turn is very sensitive to increased ICP or masses (e.g., a large blood clot) compressing it. Unfortunately, there is no good agent for reducing ICP (e.g., the most commonly used agents like mannitol can create a “rebound ICP” which is higher than it was at the start).Note: there can also often be a breakdown of the blood brain barrier which causes even more fluid to enter the brain.

Additionally, inflammatory processes begin once the blood enters the brain which injures brain tissue (and triggers cell death), while simultaneously, the iron released by dying blood cells generates free radicals which then destroy brain cells.

Remarkably DMSO addresses each of these issues. For example, it rapidly lowers ICP (without the risk of a rebound) and unlike many other ICP lowering agents, does not cut the blood supply to the brain (rather it increases cerebral perfusion without increasing blood pressure or heart rate—which is important because brain cells rapidly die without a sufficient blood supply to maintain their metabolism). Likewise, improved cerebral blood flow is necessary to remove the blood that leaked into the brain (with DMSO in turn being excellent for reducing brain edema). Finally, DMSO lowers many of the inflammatory cytokines (e.g., IL-1α, IL-1β, and IL-6) associated with strokes and tissue injury (along with macrophage chemoattractant protein-1) and inhibits capping of surface receptors including those in lymphocytes (which calms an overactive inflammatory response).Note: I suspect rebound ICP is the brain’s attempt to get enough blood, and since DMSO ensures this, that’s why it doesn’t cause rebound ICP.

In short, as far as I know, no comparable agent exists for lowering ICP (one of the greatest challenges in neurocritical care), and in turn, many (unsuccessful) agents have been tried (in part because what works in animals often does translate to human brains).

Note: one monkey study that compared mannitol to DMSO in experimentally induced missile (bullet) injuries found DMSO created significantly better cerebral perfusion, and had a 86% survival rate (vs. 75% for mannitol and 55% for the untreated group). Those results were then confirmed in a followup study.

Furthermore, beyond directly removing edema (water) from the brain and bringing it back to the bloodstream (which is how it lowers ICP), limited experiments done in humans show DMSO is somehow able to reduce the spilling of blood into the brain (the mechanisms of which has not been worked out).

Additionally, DMSO also addresses many other critical aspects of traumatic brain injuries and brain bleeds (which under conventional care requires many different drugs):

Note: DMSO also lowers the JAK2/Stat pathway, suppresses neurotoxic NMDA-AMPA-induced ion currents, prevents iron induced lipid peroxidation and focal edema, and as mentioned above, protects cell membranes.

A variety of studies have been conducted that demonstrate DMSO’s remarkable therapeutic potential in these situations:

•Ten patients with closed head trauma and elevated ICP (40-127 mmHg compared to the normal 5-13 mm Hg) received IV DMSO, with an ICP drop in most cases happening within 30 minutes, and averaging 28mmHg after 24 hours, and 58mmHg after six days. Most patients then took 2-10 days to have the fluctuations in their ICP diminish (this study can be read here).

The reduction in brain swelling following DMSO treatment was confirmed by CT scans. All patients had a neurological assessment six days after the DMSO treatment. Six patients had mild or no problems, two had moderate impairment, and two had severe impairment (two patients eventually died of their injuries). Three months later, seven patients had minimal to no impairment, while one patient showed no improvement. No adverse effects from DMSO were observed.

•A follow-up study (at the same hospital) of 10 patients with severe closed head injuries (causing brain edema and increased ICP) found DMSO rapidly reduced ICP, increased cerebral perfusion without affecting the systemic blood pressure and patient responsiveness (except only in one patient), and most importantly improved the neurological course and outcome of the illness.

•A study examined 11 adult patients with high ICP and a GCS score of 4–6 following brain trauma or subarachnoid hemorrhage (standard therapy did not work) who were on the verge of dying. DMSO was then given, which immediately reduced the ICP (and induced diuresis), with 3 (who had been expected to die) then surviving.Note: it was also concluded this study demonstrated the value in keeping the cerebral perfusion pressure above 60mmHg (something DMSO helps with) even in the presence of high ICP.

•At a 1980 Congressional hearing on DMSO, Dr. Stanley Jacob discussed data presented at his medical school on 11 patients with severe head injuries and markedly elevated ICP, 6 of whom did not respond to other ICP treatments, but within 3-5 minutes all had their ICP come down to normal, along with similar 5 patients who were started on DMSO and ultimately had a much better outcome than those where DMSO was started later.

•One paper reported on nine patients who suffered a partial or total hemiplegia (paralysis) after surgical repair of an aneurysm:

• In a 61 year old male (R. MCA and R. carotid), DMSO was initiated after surgery due to blood pressure climbing and left-sided paralysis developing, and in 30 minutes, blood flow increased in the right brain region by 20% (and 11% on the left), the patient’s condition greatly improved. DMSO was then stopped day 5, and paralysis (and confusion) rapidly came back, after which DMSO was resumed and the patient fully recovered.

• A 67-year-old woman (L. MCA) lost the ability to speak and developed right-sided paralysis after surgery. After 8 hours DMSO was started (as mannitol didn’t work), and within 45 minutes she became fully alert and regained her strength, within 2 hours her cerebral blood flow improved, and within 12 hours her motor strength permanently normalized.

• A 25-year-old woman was hospitalized with severe headache and high blood pressure from a L. MCA aneurysm (and spasm in the internal carotid). 12 days after surgery, she suddenly developed right-sided weakness, right-leg paralysis, and difficulty speaking. After 8 hours of mannitol didn’t help, DMSO was started, and within 90 minutes she could lift her leg, and by the following day she had fully recovered.

• A 28-year-old woman developed excruciating headache and right sided weakness from an MCA aneurysm who then developed a severe internal carotid spasm that did not respond to standard care but did from DMSO (allowing her to have a completely recovery).

• The remaining five cases of a hemorrhaging aneurysm had a similar course to the above cases after rapidly responding to DMSO, with all but one patient (who had a variety of severe exacerbating factors) making a full recovery. Additionally, no adverse events were observed in any cases.

•Finally a report discussed by Dr. de la Torre (which I could not locate), detailed five patients with closed head injuries and a high ICP which rapidly lowered from IV DMSO. A 1.5 year old with a GCS of 7 and ICP of 30mmHg fully recovered over 3 weeks, while a 7-year old child admitted with a GCS of 5 and an ICP of 25 mmHg fully recovered after 8 weeks at the hospital. The three other patients (aged 17-52 with GCS scores of 3-5 and two having ICPs above 50 mmHg) initially responded to DMSO but did not survive.

Animal research in turn supports the above results:

•A rabbit study created lethal brain edema (and increased ICP) by freezing part of the brain. DMSO was observed to significantly reduce ICP after 5 minutes while increasing cerebral perfusion and not changing central venous pressure. This was then followed up with a study that had similar result, with a study that achieved similar results with a different DMSO dose and a final study that showed indomethacin blocked DMSO’s reduction of ICP.

•A monkey study, had an expanding balloon (designed to stimulate a hematoma) was placed in the brains of 40 monkeys, 15 of whom received DMSO. Of the DMSO treated monkeys, 1 (7%) died, and 1 developed mild right side paralysis. In contrast, 90% of those who received saline died (with the survivor having severe neurological deficits and dying the next day).

Note: in animal experiments simulating severe brain injury, DMSO has also been shown to strengthen their respiration (whereas in many cases it instead becomes shallow and may eventually stop). Additionally, in both humans and animals, DMSO (due it functioning as a diuretic) will often significantly increase urination.

To put all of this into context:

A January 11, 1981, a 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 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.

Sadly, however, despite the immense amount of research conducted and these results being dramatically better than what the standard of care can offer, this remains an almost completely forgotten side of medicine. That said, one treatment for brain bleeds (Onyx) is composed of a polymer dissolved in DMSO which solidifies into a solid coating which “patches” the leaking vessel.

---

Current Stroke Management:

Roughly 3.1% of adult Americans have experienced a stroke (a figure I expect to rise from the COVID-19 vaccines). Each year, this translates to about 800,000 people in the United States having a stroke, and in 2022, 165,393 died (making it the fifth most frequent cause of death in the United States), with between 20-40% of survivors experiencing long-term disability from the stroke.

Because of the harm strokes pose to society, and the rate at which brain tissue deteriorates once its blood supply is lost, the medical system emphasizes doing everything that can be done to identify and treat strokes as soon as possible.

Unfortunately, there are different types of strokes. In most cases, the blood supply is cut off due to something (e.g., a clot) blocking the artery (an ischemic stroke).

However, in 13% of cases, it’s instead due to a blood vessel rupturing and leaking out. This is problematic because the primary treatment for strokes is to inject a powerful clot-busting medication (tPA), but in cases where the stroke is coming from a bleed, this can be disastrous. As a result, nothing can be done until the patient is accurately diagnosed (which requires a brain CT scan at the hospital), which in turn results in an even longer delay before tPA can be used to save a patient’s brain tissue. Note: there are a few diagnostic signs that are more suggestive of a hemorrhagic stroke (e.g., a severe headache or unusual neurologic symptoms), but to our knowledge, no reliable method besides a CT scan exists to differentiate the two.

When that window is met (which only happens about 25% of the time and ultimately results in roughly 1.8%-8.5% of ischemic stroke patients receiving tPA), the existing data shows that only 13% percent of patients who receive tPA significantly benefit from it (39% return to normal, compared to 26% who would return to normal without treatment), with an additional 19% of tPA users experiencing some degree of improvement (but not a full recovery) from it. Worse still, tPA can cause significant bleeding, which is sometimes minor (e.g., gum bleeding), but also carries a 6.4% risk of a symptomatic brain bleed, and a 1.6% risk of a severe systemic hemorrhage (along with other issues such as a 1.3% to 5.1% risk of angioedema and tPA frequently causing reperfusion injuries).

In turn, many risk factors exist for the increased bleeding (e.g., a few common risk factors can lead to a 33% chance of tPA causing a fatal bleed), and there have been many lawsuits for either giving or not giving tPA to a stroke patient. Additionally, tPA is a poor choice for larger obstructions (e.g., those within the internal carotid artery), which must be physically removed instead. In short—many ICU doctors I know are quite hesitant to use tPA as they have seen cases where it dramatically improved patients, many where it did not do anything, and quite a few disasters (especially in the early days of the therapy where it was used for heart attacks and then often caused the patient to have a fatal or debilitating brain bleed).

Note: the best data exists for tPa being injected directly into the obstructed artery with interventional radiology. Unfortunately, while many premier institutions offer this, it is a specialized procedure that is not available at most hospitals.

Finally, there is essentially no therapy for recovery from stroke—which in short explains why stroke is the second leading cause of death and the third leading cause of disability worldwide.

---

Weekly Webinar Links: Join us for detailed health information at no charge. All are welcome.

Monday at noon EST -

https://zoom.us/j/94642492535?pwd=c2IyOTRoQTdNQ3JhTFdlVXpPMGErUT09

Wednesday at 8 pm EST -

https://zoom.us/j/96863715606?pwd=VTRCNTQ1dEVoWnlRQjRkeGJYRXlSdz09

---

Be Bold - Be Brave - Stay Well

---