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Author: admin | 23.08.2013 | Category: Treatment For Ear Ringing

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In Belgium the product is sold under the name "Rilatine" and in Brazil and Portugal as "Ritalina". I also sent it to all SIDS Foundation addresses found in the 1986 published book Cot Deaths by Jacquelynn Luben (Thornsons). I was able to prove for the first time that SIDS deaths shared the same mechanism as adult forms of Sudden deaths.
Over a two year period of studying the literature relating to TRICHLOROETHYLENE (TCE), I became quite familiar with the subject of sudden death from TCE poisoning. It is proposed that Sudden Infant Death Syndrome (S1DS) is caused by a delayed toxic effect from latent perinatal medication poisoning.
There are over 100,000 similar synthesised compounds, all with molecular differences; but in reality many are almost identical - one is often substituted for the other. By studying one anaesthetic with abundance of evidence regarding human exposure one can begin to understand all anaesthetics. The delayed toxic effect from perinatal medication is really a latent poisoning that can he reactivated in the same way that aspirin effects REYES Syndrome or alcohol affects Trichloroethylene (TCE) poisoned subjects, (9) If the toxic burden is great enough, death may occur around the time of exposure, infection or vaccination, but more frequently it happens at an unsuspecting time long after the toxic insult. With growth and development the threat of death diminishes but, paradoxically, during the first months of life the toxic burden increases.
Mortality of mice, exposed to either 290 or 170-ppm chlorine for various durations, as a function of time elapsed after exposure. Mortality of mice, exposed to either 750 or 240 ppm bromine for various durations, as a function of lime elapsed after exposure.
The fact that subsequent births are more at risk than first births supports my hypothesis that there is an accumulative poisoning effect; the higher risk associated with smoking also supports the hypothesis of chemical poisoning since Nicotine was one of the first generation of insecticides.
When gas and air was first introduced in childbirth, it was observed that newborn babies were often born in a sleepy state. Schwartz describes a possible pathogenic link with cardiac sympathetic enervation and SIDS. Stolman, referring to the interaction of drugs and chemicals, slates that "interest in the combined effects of drugs in the toxicological field was originally aroused by the observations of the suddenness of death in some known instances or where the available evidence suggested that death may have supervened after several drugs in small quantities were ingested.
Some anaesthetics are used in the manufacture of chemical warfare agents (18) - for example, TCE is used to make phosgene.
Rementaria and Bhatt state an apparent increase in the incidence of SIDS among infants of narcotic-addicted women and describe the sudden death of an infant born to a mother taking diazepam.
Protestos, Carpenter et al, in their paper on the obstetric and perinatal histories of children who died unexpectedly (cot deaths) found a highly significant difference in the length of second stage labour, (26) the very time when gas and air is most used. The toxicology of a human adult is a giant step away from the toxicology of a newborn infant; likewise, anaesthetics are a giant step away from nerve gases.
SIDS occurs more in winter than in summer (40): seasonal distribution can he explained by the similar seasonal distribution of all infectious diseases and all infant mortalities as they are all synergistically connected to SIDS.
Death can he delayed or reactivated from any point in the chain reaction, but death is caused by the original poisoning because vaccines and illness do not possess the innate power to cause sudden death; they only have the power to synergistically reactivate or cause a physical illness with natural death. This hypothesis demonstrates the possibility that SIDS is the product of subtle latent CNS poisoning following exposure to medication at birth.

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Sudden Infant Death Syndrome (SIDS) was first defined in 1969 in the USA as the sudden death of any infant or young child which is unexpected by history and in which a thorough post mortem examination fails to demonstrate an adequate cause of death. I examined many reports of the phenomenon of delayed death which occurred on rare occasions, usually a few hours or even the day following industrial exposure to TCE. The main culprits are the CNS gases used as analgesics; these gases are often inhaled over long periods during labour. The gases, combined with other forms of medication given at birth, have a profound effect on the central nervous system. In animal experiments with inhalation gases designed to determine lethal doses, the results often reveal that a percentage die on exposure and a percentage of the remainder die over the following few weeks. For each group of combined experiments, the range of exposure durations and number of animals are specific in the figure.
For each group of combined experiments, the range of exposure durations and number of animals are specified in the figure.
Similarly, the expanding use of certain drugs appears to he related to the expanding recognition of SIDS: Benzodiazepines, for example in the same year that Valium became the number one prescription drug in America, SIDS was clinically defined as a disease entity.
Workers have observed that in persons, who had taken both alcohol, and barbiturates, death was more rapid and the clinical picture different from that produced by either one acting alone. The mechanism responsible for this is unknown, but it clearly demonstrates how one chemical can reactivate another in an unsuspecting way. CNS drugs, on the other hand, do not only possess the innate power to cause unnatural sudden death but also possess the innate power to delay it. Biological Aspects of Chemical and Biological Weapons in AMBIO; 4 (5-6), 1975 (Recd 1976) pp. Sudden Death from Ventricular Fibrillation After Voluntary Inhalation of Chlorothene in a Mechanics Apprentice in Schweitz Med Wochenschr  1976.
Death From inhalant Abuse: Toxicological and Pathological Evaluation of 34 Cases in Clinical Toxicology. Sudden Deaths in Adolescents resulting From the Inhalation of Typewriter Correction Fluid in JAMA. Obstetric and Perinatal Histories of Children Who Died Unexpectedly (Cot Death) in Archives of Disease in Childhood.
Psychological picture of manifest and Latent Carbon Disulphide Poisoning in British Journal of Industrial Medicine. Upon download of any film Licensed Material, you will be invoiced a non-refundable access service fee of one hundred fifty dollars ($150) USD or such other local currency amount as Getty Images may apply from time to time. Sudden Infant Death Syndrome can, therefore, be logically regarded as the result of exposure to those same toxins. I saw a logical possible connection with SIDS and the analgesic gas TCE used in childbirth. The delayed effect, or latent poisoning, may contribute to all post-natal deaths, especially deaths attributed to respiratory deaths (Graph) as these deaths often present the physician with a dilemma in diagnosis. Tesh of Life Science Research believes that a child"s central nervous system continues to develop after birth for perhaps two years.

If the dose was lowered, instant death would disappear, leaving only delayed deaths, Reduce the exposure yet further and the delayed death ratio that is found in SIDS is reached, without any deaths occurring at the time of exposure. Toxicology is a comparatively new science: recommended ambient levels of exposure in industry are continuously being reduced.
If the infant survives the initial delayed effect the poison remains latent but can be reactivated by illness or vaccination etc. Cardiac Sympathetic Enervation and the Sudden Infant Death Syndrome in The American Journal of Medicine. You will be asked to submit information concerning your intended use of the product, which will determine the scope of usage rights granted.Available for Editorial uses.
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During subsequent investigations, I discovered a known delayed effect from other gases and insecticides that resembled the delayed effect I was searching [or.
All the delayed deaths display the same mode of action - ventricular fibrillation - without evidence of cause of death. Once reactivated, if death is not the immediate outcome, the insult takes on the same course of delayed action as the original poisoning. Could a similar mechanism he responsible for SIDS from exposure to analgesic gases in childbirth, affecting the infant but not the mother? This book is recommended together with this document as evidence of the harmful effects of the Chlorinated Hydrocarbons. No sooner is one chemical spotlighted and removed from use than another of equally unknown hazard often becomes a less-than-completely-tested surrogate.
Death can occur even when the infant is well on the way to recovery from what appeared to he an uneventful normal illness. Are longer and lesser amounts of TCE more harmful than larger acute doses, as is known to be the case with CO poisoning? Adults exposed to anaesthetics can easily survive exposure without sequelae: the only indication of a delayed effect is post-natal or post-operative depression.
Examination of deaths described here reveals that they are not dying from anaesthetic death or asphyxiating death but that another mechanism is in action: that mechanism is identical to the mechanism found in SIDS. Can the same mechanism that is responsible for a delayed effect from CO poisoning he applied to infant exposure to analgesic gas?
In the infant this subtle effect is magnified and is responsible for the hulk of deaths that occur in the second and third months of life. It is interesting to note that both of these reports are less distorted by high seasonal distribution of mortalities.

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Comments to “Medication for sudden hearing loss”

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