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Pharma/CDC on Brain damage from vaccines, Fauci, Phages, Bioweapons manufacture HHS.gov is Incompetent; BMJ calls fraud "crime.")
Official: CFIDS and MS-Lyme are the
same disease; Epstein-Barr
ELISA = arbitrary cutoff. 1998, CIA Oilmen & Israelis plan to overthrow Saddam for the oil.
Bush/Gore Oil/War-(Oct,2000)
Iraq was an oil-theft war.
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Psychotropics induced agitation and violence, Forensic Aspects (BLAME THE VICTIM):
Neuroleptic-induced akathisia and violence: a review. Leong GB, Silva JA. Center for Forensic Services, Western State Hospital, Tacoma, WA 98498-7213, USA. leonggb@dshs.wa.gov Surprisingly, the association of neuroleptic-induced akathisia and aggressive behavior was not formally recognized until nearly two and one-half decades of antipsychotic prescribing had passed. Using a search of the anglophonic literature, this phenomenon is reviewed. Advances in psychopharmacology have reduced neuroleptic-induced akathisia and hold promise to eliminate it altogether. Nonetheless, important clinical and forensic aspects of neuroleptic-induced akathisia and aggression remain and are explored. Publication Types:
PSYCHOTROPIC DRUGS ==== Lyme brain needs to be treated with ceftriaxone ==== http://www.psych.org/clin_res/pg_delirium.cfm American Psychiatric Association on Delirium: "Delirium is often misdiagnosed as depression or dementia. These disorders can be diagnosed during a delirium only when the patient's history reveals symptoms that clearly existed before the delirium onset. When delirium is comorbid with other psychiatric disorders, the delirium should be treated first and the treatments for these other disorders, such as antidepressant or anxiolytic medications, should be minimized or not begun until the delirium is resolved. Medications for psychiatric disorders can both be the cause of delirium and exacerbate or contribute to delirium from other causes." Lyme Neuroborreliosis: Brian A. Fallon,MD, Neuropsychiaty, Columbia-lyme.org "The profile of neuropsychiatric Lyme disease typically includes disturbances of cognition and mood. On formal neuropsychological testing, more than 50 percent of patients with chronic neurologic Lyme disease will show impairment in short-term memory, processing speed, or attention. This cognitive impairment, although worsened by marked pain or mood disorders, exists independently of the physical symptoms or the severity of concurrent depression. Typical cognitive symptoms include word-finding problems, word-substitutions, new-onset dyslexia, transient episodes of geographic disorientation, marked inattention and distractibility, difficulty with organization, and the sensation that one’s brain is in a fog. Less commonly, the severity of the cognitive disturbance causes a global impairment, suggestive of a new-onset dementia." --- Shadock’s 2002 Comprehensive Textbook of Psychiatry CHAPTER 2. NEUROPSYCHIATRY AND BEHAVIORAL NEUROLOGY, 2.9 NEUROPSYCHIATRIC ASPECTS OF OTHER INFECTIOUS DISEASES GABA (gamma amino butyric acid) is the vulnerable neurotransmitter in both Lyme and Autism GABA and dementia (MEDLINE) GABA and Autism and Chromosome 15 (NF and anti-apoptotic BCL class repeats) A history in the Inanity of psychotropic drug development: http://www.cpa-apc.org/Publications/Archives/PDF/1997/Mar/lehmann.pdf Originally, the phenothiazines we dyes used in microbial staining (Paul Ehrlich). They "paralyzed" (neuro-leptic >> "nerve siezing") the organism. These were discovered to be sedating to animals and then were used as anesthetics, but eventually, "Psychopharmacotherapy" for humans. It's been "accidental receptorology" ever since (Top-Down). And all psychotropic drugs cause some sort of brain damage. The newer approaches, are, rationally, the Neurotrophins and psychotherapy. Lithium is a promoter of BCL-2; which seems to be neuroprotective See also, but with reservations, since this article is by Psychiatrists, and not real scientists (Neurologists): Molecular Psychiatry, Millenium Article.
Society for the Study of Psychiatry and Psychology (there REALLY needs to be one) http://www.icspp.org/positionpapers.htm Peter Breggin, author of "Toxic Psychiatry" and other books http://www.breggin.com Psychotropic Drugs... and Violence http://www.cchr.org/event/31anni/violence/ ========== Brain damage- -therefore clearly dangerous to children Dyskinesias (movement disorders: akathisia, tardive dyskinesia, tardive akathisia, chorea, Parkinson's "tics" myoclonus, "restless leg") Tardive Dyskinesia (1960 to 1982, back in the days when Psychiatrists were honest) Receptor compensating results (more confusion) "Extrapyamidal Effects" (EPS) MYOCLONUS, Physiology, MEDLINE
BREGGIN: http://www.breggin.com/neuroleptics.html Other closely related, untreatable neurological disorders have now been recognized as variants of tardive dyskinesia. Tardive akathisia involves painful feelings of inner tension and anxiety and a compulsive drive to move the body. In the extreme, the individual undergoes internal torture and can no longer sit still. Tardive akathisia often develops in children who have been treated for "hyperactivity", ironically and tragically subjecting them to permanent inner torture. Tardive dystonia involves muscle spasms, frequently of the face, neck and shoulders, and it too can be disfiguring, disabling and agonizing. Akathisia, Subjective (Akathisia = Psychomotor agitation, pacing, rocking, shifting from foot to foot, fidgeting, restless leg... What already looks like Autism.) Tremor/Parkinsons Psychotropic drug induced
The Science of drug-induced brain damage Mechanisms 1) Dopamine blockers seem to upregulate more dopamine receptors to compensate. It also is a matter of redistribution of normal or inherent receptology (which, quite technically means,. you are not the person you used to be...). The drug therapy itself, and the withdrawal of the drug, creates more confusion. It's interesting science, but it shouldn't be done.
Differential effects of clozapine and haloperidol on dopamine receptor mRNA expression in rat striatum and cortex. Damask SP, Bovenkerk KA, de la Pena G, Hoversten KM, Peters DB, Valentine AM, Meador-Woodruff JH. Mental Health Research Institute, University of Michigan, Ann Arbor 48109-0720, USA. The regulation of the dopamine (DA) receptors is of considerable interest, in part because treatment with antipsychotic drugs is known to upregulate striatal D2-like receptors. While previous studies have focused on the regulation of striatal DA receptors, less is known about the pharmacological regulation of cortical DA receptors. The purpose of this study was to examine the regulation of DA mRNA receptor expression in the cortex compared to the striatum following treatment with antipsychotic agents. Adult male Sprague-Dawley rats were injected daily with haloperidol (2 mg/kg/day), clozapine (20 mg/kg/day) or a control vehicle for a period of 14 days. Following treatment, brains were subjected to in situ hybridization for the mRNAs encoding the five dopamine receptors; only D1, D2, and D3 receptor mRNAs were detected in these regions. Haloperidol tended to either modestly upregulate or have no effect on dopamine receptor mRNAs detected in striatal structures, while clozapine generally downregulated these mRNAs. On the other hand, in the cortex, both drugs had striking effects on D1 and D2 mRNA levels. Cortical D1 mRNA was upregulated by haloperidol, but this effect was primarily restricted to cingulate cortex; clozapine also upregulated D1 mRNA, but primarily in parietal regions. Haloperidol downregulated D2 mRNA in the majority of cortical regions, but most dramatically in frontal and cingulate regions; clozapine typically upregulated this mRNA, but primarily in regions other than frontal and cingulate cortex. These results indicate that clozapine and haloperidol each have regionally-specific effects, and differentially regulate dopamine receptor mRNA expression in striatal and cortical regions of the rat brain. PMID: 8883957 [PubMed - indexed for MEDLINE]
The pathophysiology of agitation. Lindenmayer JP. Manhattan Psychiatric Center-Nathan Kline Institute for Psychiatric Research, New York, NY 10035, USA. Agitation is a nonspecific constellation of relatively unrelated behaviors that can be seen in a number of different clinical conditions, usually presenting a fluctuating course. Multiple underlying pathophysiologic abnormalities are mediated by dysregulations of dopaminergic, serotonergic, noradrenergic, and GABAergic systems. Pathophysiologic mechanisms of agitation that operate in the different clinical disorders where agitation occurs are discussed. These pathophysiologic abnormalities are not associated with distinct clinical features. Although there may be a final common pathway, there is no unifying etiologic pathophysiology. The author suggests that the clinician address the underlying pathophysiology through a treatment intervention that addresses the overarching psychiatric disorder. Generally, agents that reduce dopaminergic or noradrenergic tone or increase serotonergic or GABAergic tone will attenuate agitation, often irrespective of etiology. Publication Types: Review PMID: 11154018 [PubMed - indexed for MEDLINE]
Drug-induced movement disorders. Jimenez-Jimenez FJ, Garcia-Ruiz PJ, Molina JA. Department of Neurology, Hospital Universitario Principe de Asturias, Alcala de Henares, Madrid, Spain. Parkinsonism, tremor, chorea-ballismus, dystonia, tardive dyskinesia, myoclonus, tics and akathisia can be induced by many drugs. The drugs that are most frequently implicated in movement disorders are antipsychotics, calcium antagonists, orthopramides and substituted benzamides (e.g. metoclopramide, sulpiride, clebopride, domperidone), CNS stimulants, antidepressants, anticonvulsants, antiparkinsonian drugs and lithium. It is possible for a single drug to induce 2 or more types of movement disorders in the same patient. Movement disorders are not always reversible after drug withdrawal.
Lithium: occurrence, dietary intakes, nutritional essentiality. Schrauzer GN. Department of Chemistry and Biochemistry, University of California, San Diego, USA. Lithium is found in variable amounts in foods; primary food sources are grains and vegetables; in some areas, the drinking water also provides significant amounts of the element. Human dietary lithium intakes depend on location and the type of foods consumed and vary over a wide range. Traces of lithium were detected in human organs and fetal tissues already in the late 19th century, leading to early suggestions as to possible specific functions in the organism. However, it took another century until evidence for the essentiality of lithium became available. In studies conducted from the 1970s to the 1990s, rats and goats maintained on low-lithium rations were shown to exhibit higher mortalities as well as reproductive and behavioral abnormalities. In humans defined lithium deficiency diseases have not been characterized, but low lithium intakes from water supplies were associated with increased rates of suicides, homicides and the arrest rates for drug use and other crimes. Lithium appears to play an especially important role during the early fetal development as evidenced by the high lithium contents of the embryo during the early gestational period. The biochemical mechanisms of action of lithium appear to be multifactorial and are intercorrelated with the functions of several enzymes, hormones and vitamins, as well as with growth and transforming factors. The available experimental evidence now appears to be sufficient to accept lithium as essential; a provisional RDA for a 70 kg adult of 1,000 microg/day is suggested. PMID: 11838882 [PubMed - indexed for MEDLINE]
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