1883 Phenothiazines are developed as synthetic dyes.
1934 USDA develop phenothiazines as insecticides
1949 Phenothiazines shown to hinder rope-climbing in rats.
1950 Rhone Poulenc synthesizes chlorpromazine, a phenothiazine, for use as an anaesthetic.
1954 Chlorpromazine marketed in the US as Thorazine, found to induce symptoms of Parkinson’s disease.
1955 Chlorpromazine said to induce symptoms similar to encephalitis lethargica.
1959 First reports of permanent motor dysfunction linked to neuroleptics, later named tardive dyskinesia
1960 French physicians describe a potentially fatal toxic reaction to neurocepltics later named neurocelpetic malignant syndrome.
1962 California Mental Hygiene Department determines that chlorpromazine and other neuroleptics prolong hospitalisation.
1964 Neuroleptics found to impair learning in animals and humans.
1965 A one year follow up of NIMH collaborative study finds drug treated patients more likely than placebo patients to be rehospitalised .
1968 In a drug withrawal study NIMH find a direct relationship between relapse rates and dosage. The higher the dosage patients were on before withdrawal, the higher the relapse rate.
1972 Tardive dyskinesia is said to resemble Huntington’s disease, or ‘postencephalitic brain damage’
1974 Boston researchers report relapse rates are lower in pre- neuroleptic era. And drug treated patients were more likely to be socially dependent.
1977 A NIMH study, that randomised schizophrenic patients into drug and non drug, reports that only 35% of no drug patients, relapsed within a year of discharge, as opposed to 45% drugged patients.
1978 California investigator Maurice Rappaport reports markedly superior three year outcomes in patients treated without neuroleptics.
Only 27% of drug free patients relapsed in the three years following discharge, compared to 62% of drugged patients.
1978 Canadian researchers describe drug induced changes in the brain that make a patient more vulnerable to relapse, and term it ‘neuroleptic induced super sensitive psychosis’
1978 Neuroleptics found to cause 10% cellular loss in the brains of rats.
1979 Prevalence of tardive dyskinesia in drug treated patients is reported to range from 24% to 56%.
1979 Tardive dyskinesia found to be associated with cognitive impairment.
1979 Loren Mosher, chief of schizophrenia studies at NJMH, reports superior one and two year outcomes for Soteria patients treated without neuroleptics.
1980 NIMH researchers find an increase in ‘blunted effect’ and ‘emotional withdrawal’ in drug treated patients, and that neuroleptics do not improve ‘social and role performance’ in non relapsers.
1982 Anticholinergic medications used to treat Parkinsonian symptoms induced by neuroleptics reported ‘to cause cognitive impairment’
1985 Drug induced akathisia is linked to suicide.
1985 Case reports link drug induced akathisia to violent homicides
1987 Tardive dyskinesia is linked to worsening of negative symptoms, gait difficulties, speech impairment, psychological deterioration and memory deficits. They conclude it is both a ‘motor and dementing disorder’.
1992 World Health Organisation reports that schizophrenia outcomes are much superior in poor countries, where 16% of patients are kept continuously on neuroleptics.
The WHO reports that living in a developed nation is a ‘strong predictor’ that a patient will never recover.
1992 Researchers acknowledge that neuroleptics cause a recognisible pathology, which they name neuroleptic induced deficit syndrome .
In addition to Parkinson’s, akathsia, blunted emotions and tardive dyskinesia, patients treated with neuroleptics suffer from an ‘increased incidence of blindness, fatal blood clots, arrhythmia, heat stroke, swollen breasts,, leaking breasts, impotence, obesity, sexual dysfunction, blood disorders, skin rashers, seizures and early death’.
1994 Neuroleptics found to cause an increase in the volume of caudate region in the brain.
1994 Harvard investigators report that schizophrenia patients in the US, appear to have worsened over past 20 years, and are now no better than in first decades of 20th century.
1995 ‘Real World’ relapse rates for schizophrenia patients treated with neuroleptics said to be above 80% in the two years following hospital discharge, which is much higher than in the pre neuroleptic era.
1995 Quality of life’ in drug treated patients reported to be ‘very poor’
1998 MRI scans show that neurocelptics cause hypertrophy of caudate, putamen and thalamus,with the increase ‘associated with greater severity of both negative and positive symptoms’.
1998 Neuroleptics use is found to be associated with atrophy of cerebral cortex
1998 Harvard researchers conclude that ‘oxidative stress’ may be the process by which neuroleptics cause neuronal damage to the brain.
1998 Treatment with two or more neuroleptics is found to increase the risk of early death.
2000 Neuroleptics linked to fatal blood clots.
2003 Atypicals linked to an increased risk of obesity, hyperglycemia, diabetes and pancreatitis.
‘The Case against antipsychotic drugs: a 50 eat record of doing more harm than good.’
Despite this history, a cross party government mental health taskforce only this year recommended an increase in the use of neuroleptics, as they consider they have transformed mental care in the last 50 years.
These drugs, have been fed to the autistic, and learning disabled, off label, without monitoring from 5 in schools, and, in institutions for life, causing untold suffering and death.