Hospitals & Asylums

Don’t Forget to Try Atropine and Pralidoxime Chloride Injection for Emergency Stroke Treatment HA-30-1-17

By Anthony J. Sanders

Three quarters of a million Americans suffer a cerebral vascular accident (CVA), also known as a stroke, each year. One-fifth of them die of the stroke, and at least one-third remain permanently disabled (Bradley ’09: 62, 63). Stroke ranks as the number four most common cause of death (behind heart disease, cancer and chronic lower respiratory disease) but number one as the cause of disability and a contributor to dementia. Cerebral vascular disease costs the U.S. health care system an estimated $60 billion each year. Stroke symptoms include a sudden numbness or weakness of the face, arm or leg (especially on one side of the body), sudden confusion or difficulty understanding speech, sudden loss of the ability to speak, sudden trouble seeing in one or both eyes, sudden trouble walking, dizziness, or loss of balance or coordination or a sudden severe headache with no known cause. A stroke is a sudden loss of function of part of the brain. Usually the cause is either (1) ischemic stroke; sudden loss of blood flow to part of the brain because an artery that supplies blood to that part of the brain has become blocked (ischemia) due to atherosclerosis, in 87 percent of strokes or (2) hemorrhagic stroke; bleeding (hemorrhage) into the brain because an artery has burst, due to high blood pressure in 7-10 percent of cases. In about 15 percent of individuals who come to an emergency room with the sudden onset of a brain disorder, the cause of stroke turns out to be an epileptic seizure followed by weakness on one side, or something else such as a brain tumor, low blood sugar (hypoglycemia), an abscess in the brain, a blood clot over the surface of the brain caused by head trauma, or some other condition (Spence ’06: 3). The risk increases with age: nearly three-quarters of strokes occur after age 65, with the risk more than doubling each decade after age of 55. In the United States, strokes increase in a given year from 35 per 100,000 people at age thirty-five to 1,100 to 100,000 at ages seventy-five to eighty. Getting treatment for an ischemic stroke within three hours of the onset of symptoms with tissue plasminogen activator (tPA) can dissolve clots and lessen disability by 40 percent if it is administered within three hours of an ischemic stroke. A hemorrhagic stroke caused when a blood vessel breaks and bleeds into the brain is much harder to treat: more than half are fatal. rtPA, a clot-busting drug, is not for home use because it would increase hemorrhaging and a physician must distinguish between ischemic and hemorrhagic stroke. Extensive physical therapy for many months helps many regain function (Horstman ’12: 70, 72). rtPA (recombinant tissue plasminogen activator) is for mild strokes only <25 on the NIH stroke scale, in patients age <80, without hemorrhage, anticoagulant use or elevated blood pressure (Hazinsky '10: 18-19). It is proposed to introduce atropine or other effective anticholinergic drug for administration by emergency medical technicians and emergency room doctors to neutralize the effect of the lucid dreaming pill galamantine, that cause the side-effect of sleep paralysis that cannot be ignored as a stroke risk, in both ischemic and hemorrhagic strokes with Atropine IV or by endotracheal tube IO (LaBerge '03).

Atropine and pralidoxime (DuoDote®) is indicated for the treatment of poisoning by organophosphorous nerve agents as well as organophosphorous insecticides. Atropine and pralidoxime (DuoDote) is injected into a muscle in the upper thigh - Atropine 2.1 mg/0.7 mL Pralidoxime Chloride 600 mg/2 mL. One injection should be enough for the emergency treatment of a stroke patient of undetermined cause. A healthcare provider will administer this injection. The combination of atropine and pralidoxime is used as an antidote to treat poisoning by a pesticide (insect spray) or a chemical that interferes with the central nervous system, such as nerve gas or galamantine. Atropine competitively blocks the effects of acetylcholine, including excess acetylcholine due to organophosphorous poisoning, at muscarinic cholinergic receptors on smooth muscle, cardiac muscle, and secretory gland cells and in peripheral autonomic ganglia and the central nervous system. Pralidoxime reactivates acetylcholinesterase which has been inactivated by phosphorylation due to an organophosphorous nerve agent or insecticide. Reactivated acetylcholinesterase hydrolyzes excess acetylcholine resulting from organophosphorous poisoning to help restore impaired cholinergic neural function. When atropine and pralidoxime are used together, pralidoxime may potentiate the effect of atropine. When used in combination, signs of atropinization (flushing, mydriasis, tachycardia, dryness of the mouth and nose) may occur earlier than might be expected when atropine is used alone.

Breathing, blood pressure, oxygen levels, kidney function, and other vital signs will be watched closely. After treatment with atropine and pralidoxime, you may be watched for up to 72 hours. Some of the side effects of atropine and pralidoxime may be similar to the symptoms of poisoning. Avoid becoming overheated or dehydrated during exercise and in hot weather. Atropine can decrease sweating and you may be more prone to heat stroke for a short time after receiving this medication. Overdose may occur if the patient receive satropine and pralidoxime but has not actually been exposed to the specific poisons this medication is designed to treat. Symptoms may include vision problems, feeling unsteady, loss of balance or coordination, trouble concentrating, fast heart rate, confusion, hallucinations (seeing or hearing things), decreased sweating, hot and dry skin, fainting, weak or shallow breathing, or breathing that stops after receiving atropine and pralidoxime injection (DuoDote). In a study of organophosphate poisonings one patient is reported recovered from their cerebral hemmorrhage (Quinby '64: 28). Atropine should be included in the emergency medical response to all strokes, both hemorrhagic and ischemic strokes. Further review of galamantine is needed because the lucid dreaming patent application of 2003 found there was also associated with a significantly elevated frequency of sleep paralysis. Sleep paralysis is a parasoma that can be very nightmarish. Essentially, one remains aware during the transition into sleep onset and/or REM sleep while the body undergoes muscle paralysis (LaBerge '03). Drugs with anticholinergic properties and which cross the blood/brain barrier, such as atropine, benztropine (Cogentin) and trihexyphenidyl (Artane) counteract the effects of galantamine (Toro '07).

Dreams are a controversial subject among sleep researchers. Virtually everyone dreams every night, three, four, or five times a night in 5 to 45 minute discrete episodes. Drug use, prior sleep patterns,medical illness and other factors may alter the length, frequency and time of occurrence of dreams, but a truly dreamless sleep is unusual. Most people will have four or five dream, or REM periods each night during which one or more dreams will occur. REM stands for the rapid eye movement that occurs in dreaming sleep. We only remember dreams, however if we awaken during the dream or shortly thereafter. Thus, people who sleep soundly through their REM periods will have little or no dream recall. Most people find even casual analysis of their dreams helpful in understanding themselves and solving problems of everyday life. Stories of dreamers solving important problems in dreams are widely reported. August Kekule, an eighteenth century chemist, discovered the structure of benzene during a dream. Mikhail Tal, a former world chess champion, describes in his autobiography solving a difficult chess problem this same way. Lucid dreams are those in which the dreamer can control the action as if awake. Recurrent dreams usually reveal psychological issues that are interesting for the individual to ponder. When entering the state of

sleep in which we dream, our muscles become paralyzed. The paralysis is very real, it protects us from acting out dreams when we sleep. Even though we are asleep, we may have some awareness of this paralysis, which may cause our minds to create dreams in which we are trapped and unable to escape, one of the most common themes in recurrent dreams (Kavey '95: 33-35).

“Oneirogens” (from the Greek oneiros meaning “dream” and gen meaning “creating”), which produce and also enhance dream-like states of consciousness. These herbs and roots have been used for thousands of years for prophetic divination through dreams, out-of-body experiences, and to consciously awaken during dream states. Oneirogens represent only one specific class of entheogens that can be exclusively used for lucid dreaming. The following legal psychedelics can be safely consumed having minimal effect on waking consciousness, and will only exhibit their effects when you fall into a natural state of sleep. Calea zacatechichi (Mexican Dream Herb), Artemisa vulgaris (Mugwort) contraindicated for use during pregnancy, Heimia salicifolia (Sun Opener), Celastrus paniculatus (Intellect Tree), Silene capensis (Zhosa Dream Root), Nymphaea caerulea (Blue Lotus), Asparagus racemosus (Tian Men Dong) adaptogenic, and Entada reheedii (African Dream Bean) (Sol '17). Galantamine has emerged as the lucid dreaming pill after being patented by LaBerge, S. Substances that enhance recall and lucidity during dreaming, United States Patent Application 604138 (LaBerge '03) in 2004. Galantamine is found in the natural world in many plant sources, including the common daffodil (Narcissus pseudonarcissus). Today, it is used commercially as an extract derived from red spider lily (Lycoris radiata), the Golden spider lily (Lycoris aurea) or from the Snowdrop plant (Galanthus nivalis). The resulting compound is

galanthamine hydrobromide. Galantamine and its derivatives was approved by the FDA in 2001, and is largely used as a memory-improvement supplement for sufferers of Alzheimers disease and mild dementia. Only recently has the substance been used as an oneirogen, or a dream enhancing supplement. Galantamine keeps acetylcholinesterase from breaking down acetylcholine, temporarily leading to increased memory function, dream recall and lucidity. As early as 1975, dream researchers found out that acetylcholine and its inhibitors are somehow involved with dream sleep (Amatruda et al '75). High acetylcholine levels in the brain was associated with the prevention of memory loss, which is why it appears to be effective in treating Alzheimers. The compound acts immediately to increase the duration of REM sleep, and the dream state is made more structurally sound (Riemann et al '94).

There “was also associated with a significantly elevated frequency of sleep paralysis and a 40% increase in estimated time awake during the night”. Sleep paralysis is a parasoma that can be very nightmarish. Essentially, one remains aware during the transition into sleep onset and/or REM sleep while the body undergoes muscle paralysis (LaBerge '03). Drugs with anticholinergic properties and which cross the blood/brain barrier, such as atropine, benztropine (Cogentin), trihexyphenidyl (Artane), and perhaps

amantadine (Symmetrel) counteract the effects of galantamine. Also, the following medical issues have been documented to be irritated or worsened by the use of galantamine: asthma, lung diseases, epilepsy or history of seizures, heart problems, including slow heartbeat or heart murmur, kidney and/or liver problems, stomach ulcer, and urinary tract problems. Taken orally, the galantamine supplement is active and at full strength within an hour of ingestion. The half-life is about 7 hours. Recommended dosage for dream enhancement is on the low side: 4 – 8 mg. (Alzheimer’s patients, on the other hand, often take 12mg or more a day) (Toro '07). Sleep paralysis however poses at least a moderate stroke risk that consumer must be informed of. There seems to be a correlation between the patenting of galantamine and an epidemic of involuntary exposure to what is presumed to be galantamine associated lucid dreaming in geographically diverse family members of a higher education applicant resulting in strokes in the frailest and most elderly of that applicants' family members and perplexing lucid dreaming in others. Lucid dreams are traditionally considered a bad omen. There is reason for the patent holder to believe that galantamine and, to a lesser or greater extent, other oneirogenic herbs and entheogens pose a stroke risk that requires review (LaBerge '03).

The most common identified environmental cause of dementia is E. coli toxin from cow manure contamination of the groundwater. People with memory loss should consume only bottled or professionally filtered water. No beef. The Center for Disease Control reports Escherichia coli (E. coli) bacteria normally live in the intestines of people and animals. Most E. coli are harmless and actually are an important part of a healthy human intestinal tract. However, some E. coli are pathogenic, meaning they can cause illness, either diarrhea or illness outside of the intestinal tract. The types of E. coli that can cause diarrhea can be transmitted through contaminated water or food, or through contact with animals or persons. E. coli consists of a diverse group of bacteria. Pathogenic E. coli strains are categorized into pathotypes. Six pathotypes are associated with diarrhea and collectively are referred to as diarrheagenic E. coli. Shiga toxin-producing E. coli (STEC)—STEC may also be referred to as Verocytotoxin producing E. coli (VTEC) or enterohemorrhagic E. coli (EHEC). This pathotype is the one most commonly heard about in the news in association with foodborne outbreaks. The other types are Enterotoxigenic E. coli (ETEC), Enteropathogenic E. coli (EPEC), Enteroaggregative E. coli (EAEC), Enteroinvasive E. coli (EIEC), and Diffusely adherent E. coli (DAEC). The infectivity or the virulence of an EHEC strain depends on several factors, including the presence of fucose in the medium, the sensing of this sugar and the activation of EHEC pathogenicity island. Wikepedia elaborates a little more on the Verocytotoxin E. coli (VTEC) listing enterohemorrhagic E. coli (EHEC), hemolytic uremic syndrome (HUSEC), shiga toxin producing E. coli (STEC), shigatoxinogenic E. coli (STEC), shiga-like toxin producing E. coli (SLTEC), verotoxin-producing E. coli (VTEC), veroxigenic E. coli (VTEC) verocytotoxin-producing E. coli (VTEC), verocytotoxigenic E. coli (VTEC).

E. coli is a zoonotic infection most commonly transmitted by the manure of cows (Bos taurus) that can cause food and water-born epidemics in humans. Shiga toxin producing E. coli (STEC) seem to be more associated with diarrhea so the water of forgetfulness is assumed to be contaminated by verocytotoxin producing E. coli (VTEC). VTs produced by these bacteria are thought to damage host endothelial cells in small vessels of the intestine, kidney and brain resulting in thrombotic microangiopathy. All VTs have the same subunit structure, glycolipid cell receptor and inhibit protein synthesis. During VTEC infection, it is thought one or more bacterial adhesins initiates colonization and establishes intimate attachment and is responsible for the translocation of a variety of effectors which alter the

structure and function of host cells. VTEC are widespread in animals but ruminants are thought to be their natural reservoir. E. coli O157:H7 colonizes the terminal colon of cattle and can be shed in very large numbers by specific herd-mates known as "super-shedders". Feces containing these organisms act as a source of contamination for a

variety of foods and the environment (Kamali et al '09) in particular groundwater contaminated by watershed injection of un-potable manure contaminated water. Beta-amyloid plaque and/or tau in the brain of the Alzheimer's patient could be caused by Diffusely adherent E. coli (DAEC). Metronidazole is more helpful in the treatment of infectious diarrhea caused by E. coli than Bactrim, but it is contraindicated for use in central nervous system disease and when it comes to verocytotoxin contamination of the groundwater and memory there is not really anything to do but stop drinking and cooking with cow manure contaminated water.

Vasculitis and organophosphate poisoning each occasionally cause a motor neuron disease. Jakob-Creutzfeldt virus (JCV), most commonly presents as progressive dementia with seizures, myoclonus, fasciculations and asymmetrical weakness known as Mad Cow disease. (Wiederholt ’88: 191, 193). Mad Cow disease is a member of a family of diseases called transmissible spongiform encephalopathies, TSEs, seen in various animal species including humans, sheep, cows, mink, deer and cats – for example, Creutzfeld-Jacob Disease (CJD) in humans, scrapie in sheep, chronic wasting syndrome in deer and elk, and bovine spongiform encephalopathy of BSE in cows. They attack the central nervous system, causing disintegration of the brain; they have a long incubation period (measured in years if not decades) between the time

when infection first occurs and the appearance of symptoms; they are always fatal; and they are transmitted by the eating of animals or animal parts; especially brains and spinal cords. More than 167,000 British dairy cattle died between 1985 and 1995. In 2000 to 2001 between 4,700 and 9,800 French cattle had become infected with Mad Cow disease and up to 100 of those had entered the human food chain. When it became clear the disease had spread to Spain and Germany, the European Union called for the destruction of up to another 2 million cattle. European beef consumption plummeted. The infectious agent of Mad Cow disease remains infectious even after exposure for an hour to a temperature of 680 degrees – enough to melt lead – and can withstand antibiotics, boiling water, bleach, formaldehyde and a variety of solvents, detergents, and enzymes known to destroy most bacteria and viruses. The expected rate of occurrence of CJD (the human variation of Mad Cow disease) has been 1 in 1 million people. Yet one study found that people diagnosed with Alzheimer’s disease, whose symptoms were difficult to distinguish from CJD) were examined after death, 5.5

percent of the presumed Alzheimer’s victims were found actually to have CJD. Another study counted 13 percent (Robbins ’01: 144, 145, 146, 149, 150). Organic food only, lots of green leafy vegetables and no red meat. Find concentrated animal feeding operations (CAFO) polluting the watershed.