Research brain damage

The demonstration that injected or force-fed neonatal rodents given extremely high doses of MSG showed evidence of brain lesions, has led to much additional research to determine any possible link between neurotoxicity and human use of MSG (33). However, no evidence from animal tests indicates that MSG in the diet causes brain damage in humans (34). 

Innovative methodologies for in vivo microdialysis in immature subjects have facilitated research in multiple areas. Clinically driven experimentation on neonatal anoxia, hypoxia, or ischemia indicates that perinatal manipulations of oxygen and blood flow result in acute and chronic disruptions of neurotransmission and transmitter turnover (Chen et al., 1997 Nakajima et al, 1999 Ogasawara et al., 1999). Recently, a role for toxic free radicals in brain damage induced by prenatal infection was also delineated by in vivo microdialysis in rat pups (Cambonie et al, 2000, 2004). More subtle neonatal manipulations, such as maternal separation or periodic neonatal isolation, coupled with subsequent in... 

Other people thought the opposite that some of the LSD is sequestered in the brain for extended periods, possibly providing an explanation for flashbacks. Some believed that these small amounts of residual LSD could also cause brain damage. Additional research has fairly well refuted both beliefs. The possibility remains, however, that subtle changes at the sub-microscopic level, perhaps involving specific enzymes within nerve cells, might result from... 

New research on the antioxidative properties of creatine shows that the supplement may have even therapeutic properties beyond the treatment of musculoskeletal disease and injury. A 2000 study in Annals of Neurology reported that creatine had a protective effect against traumatic brain injury (TBI) in animal studies, reducing brain damage in mice and rats by up to 50%. 

The ecstasy epidemic, its potential for causing permanent brain damage, and the deaths associated with ecstasy usage led to the passage of the Ecstasy Prevention Act of 2001. The Ecstasy Prevention Act of 2001 built on the Ecstasy Anti-Proliferation Act of 2000 by allotting funding for the education of law enforcement officials and the public, and for medical research done by the National Institute on Drug Abuse (NIDA). In... 

In that article I covered a number of salient theories—steppingstone to heroin, amotivational syndrome, brain damage, chromosome damage (i.e., birth defects), immune responses, psychosis, incitement to crime, general health hazard and sex impairment. None of this research proved that use of marijuana caused problems. 

Many clinical studies have now confirmed the existence of persistent cognitive deficits and dementia in association with neuroleptic use. However, to some extent, researchers have lost their enthusiasm for demonstrating over and over again that neuroleptics cause cognitive deficits, and textbooks of psychiatry simply do not want to mention it (e.g., Hales et al., 2003). This is reminiscent of the history of research into the brain-damaging effects of shock treatment (chapter 9). When repeated... 

Animal research provides definitive and apparently incontrovertible evidence that neuroleptics often cause irreversible brain damage. This is consistent with more recent studies reviewed earlier in the chapter that demonstrate how both older and newer atypical neuroleptics are highly toxic to living cells in animals. 

Originally, it was thought that, except in extreme cases, lithium-induced neurotoxicity was reversible. However, it eventually became apparent that many patients develop irreversible brain damage and dysfunction, often involving the cerebellum (Grignon et al., 1996). In the last two decades, researchers have defined a syndrome of irreversible lithium-effectuated neurotoxicity (SILENT). Adityanjee et al. (2005) reviewed the literature from 1965 to 2004 for cases of lithium neurotoxicity with the persistence of sequelae for at least 2 months after cessation of treatment. They found 90 cases of SILENT, with persistent cerebellar dysfunction as the most commonly reported persistent aftereffect. These... 

Since the 1997 edition of this book, my task has been lightened by research from the heart of the ECT establishment confirming that ECT causes permanent brain damage and dysfunction with widespread cognitive deficits and that ECT greatly elevates the suicide risk, especially in the first week following treatment. In addition, a recent review of controlled clinical trials for ECT demonstrated once again that the so-called treatment is ineffective. And finally, for the first time in history, an ECT malpractice case has been won in court. 

BREAKING NEWS IN ECT RESEARCH SHOCK TREATMENT CAUSES IRREVERSIBLE BRAIN DAMAGE AND DYSFUNCTION... 

Based on the original large-animal studies that demonstrated ECT-induced brain damage, organized psychiatry should have banned the treatment decades ago. Even without the animal studies, Sackeim et al. s (2007) demonstration of permanent ECT-induced memory loss and other cognitive deficits consistent with dementia should have been sufficient to stop all use of the treatment. This chapter has also reviewed a mountain of additional research confirming that ECT damages both the brain and the mind. 

There is no need to advocate for additional research. Why damage the brains of more animals and more people The facts have been conclusively established. Shock treatment physically damages the brain, irreversibly impairs mental function, and ruins the lives of many if not most... 

Nitric oxide has been found to be an important cell-signalling molecule and research is continuing into its role in causing migraines and brain damage after heart attacks (due to causes described above, linked with SOD).2... 

Wall, H.G., N.K. Jaax and I.J. Hayward. 1990. Motor activity and brain lesions in soman intoxicated rhesus monkeys. Proc. of the Workshop on Convulsions and Related Brain Damage Induced by Organophosphorous Agents, ADA222912, Army Medical Research Institute of Chemical Defense, Aberdeen Proving Ground, pp. 21-29. (cited in Baze, 1993)... 

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