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Medical articles on neuroleptic brain damage

These are a few of the many mainstream medical articles indicating that using neuroleptic psychiatric drugs (also known as antipsychotics) can lead to significant structural brain damage.

Brain Damage Associated with Neuroleptic Drug Treatment:


The below was compiled by several sources by the late psychiatrist Loren Mosher, MD. For more on this citations click here.

Ballesteros J, Gonzales-Pinto A, & Bulbena A. Tardive dyskinesia associated with higher mortality in psychiatric patients: results of a meta-analysis of seven independent studies. J Clin Psychopharmacology, 20:2, 188-194, 2000.


E Christensen. "Neuropathological investigations of 28 brains from patients with dyskinesia." Acta Psychiatrica Scandinavica, 46,14-23, 1970. (TD patients have structural abnormalities in the basal ganglia, enlarged ventricles, and sulcal markings.)


OO Famuyiva. Tardive dyskinesia and dementia. British Journal of Psychiatry, 135, 500-504, 1979. (TD associated with cognitive impairment.)


JT Wegner. Cognitive impairment in tardive dyskinesia. Psychiatry Research, 16, 331-337. 1985. (TD associated with cognitive impairment.)


James Wade. Tardive Dyskinesia and Cognitive Impairment. Biological Psychiatry, 22, 393-395, 1987. (Association between TD and cognitive impairment. "The relationship appears to be linear: individuals with severe forms of the disorder are most impaired cognitively.")


JL Waddington. Cognitive dysfunction, negative symptoms, and tardive dyskinesia in schizophrenia. Archives of General Psychiatry, 44, 907-912, 1987. (TD associated with cognitive impairment and worsening of negative symptoms.)


Waddington J et al, Mortality in schizophrenia: Antipsychotic polypharmacy and absence of adjunctive anticholinergics over the course of a 10-year prospective study, Br J Psych, 1998, 173; 325-329. (This study found that a reason that schizophrenics have a shorter life expectancy was neuroleptic drug treatment)


JB Wade. Cognitive changes associated with tardive dyskinesia. Neuropsychiatry, Neuropsychology, and Behavioral Neurology. 1, 217-227. 1989. (TD associated with cognitive impairment. The researchers conclude: "TD may represent both a motor and dementing disorder.")


R. Yassa. Functional impairment in tardive dyskinesia: medical and psychosocial dimensions. Acta Psychiatr Scand 80, 64-67. 1989. (TD associated with gait, speech difficulties, and psychosocial impairment.)


Michael S. Myslobodsky. Central Determinants of Attention and Mood Disorder in Tardive Dyskinesia (Tardive Dysmentia.). Brain and Cognition, 23, 88-101. 1993. (TD patients lose the motor part of their "road map of consciousness." TD may represent "larval dementia.")


Herbert Spohn. The effect of attention/information processing impairment of tardive dyskinesia and neuroleptics in chronic schizoprhenics." Brain and Cognition 23, 28-39, 1993. (TD exacerbates cognitive impairment.)


Jacinthe Baribeau. Tardive dyskinesia and associated cognitive disorders: a convergent neuropsycological and neurophysiological approach. Brain and Cognition 23, 40-55, 1993. (TD associated with cognitive dysfunction.)


John Waddington. Cognitive dysfunction in schizophrenia: organic vulnerability factor or state marker for tardive dyskinesia? Brain and Cognition 23, 56-70, 1993. (He reviews 22 studies from 1979 to 1991 that concluded that patients with TD were cognitively impaired on a variety of measures, which include learning, memory, cognitive function, intellectual function, visual retention, orientation, etc.)


James Wade. Factors related to the severity of tardive dyskinesia. Brain and Cognition 23, 71-80, 1993. (A review of research shows that "biochemical and neuropathological changes associated with TD indicates that similar alterations are associated with Hungtington's disease and or Parkinson's." In their own research, "cortical dysfunction, characterized by impairment in nonverbal function, is associated with TD severity.")


Emmanuelle Pourcher. Organic brain dysfunction and cognitive deficits in young schizophrenic patients with tardive dyskinesia. Brain and Cognition 23, 81-87, 1993. (This is a study of patients under 40. They find that TD is associated with cerebral dysfunction, which in turn is associated with exposure to neuroleptic drugs.)


Thomas Gualtieri. The problem of tardive akathisia. Brain and Cognition 23, 102-109, 1993. (He states that tardive akathisia may be thought of as a disease of the basal ganglia, much like Parkinson's, Huntington's and Wilson's. MRI studies have demonstrated basal ganglia lesions in TD patients, especially in the caudate nucleus. Basal ganglia diseases all cause behavioral instability and intellectual impairment (even psychosis and dementia)).


Miranda Chakos. Increase in Caudate Nuclei Volumes of First-Episode Schizophrenic Patients Taking Antipsychotic Drugs. Am Jour Psych 151, 1430-1435. 1994. (Neuroleptics increase caudate volumes 5.7% during first 18 months of treatment in first-episode schizophrenic patients. Higher dosage is associated with larger increase in caudate volumes.)


J.S. Paulsen. Neuropsychological impairment in tardive dyskinesia. Neurospsychology 8, 227-241. 1994. (Review of 31 studies that compared cognitive function in schizophrenics with and without TD. In 24 studies, TD patients were found to do worse. The more severe the TD, the greater the impairment in cognitive function. They conclude that "TD involves an alteration of brain function that affects both motor and cognitive control.")


P. Sachdev. Negative symptoms, cognitive dysfunction, tardive akathisia and tardive dyskinesia." Acta Psychiatr Scand. 93, 451-459. 1996. (Both tardive akathisia and tardive dyskinesia are associated with more cognitive deficits and negative symptoms. This association is stronger with TA than with TD. The implication is that movement disorders seen in TA and TD are "but one feature of complex syndromes that include motor and cognitive features. A comparison must be made with other movement disorders, such as Parkinson's disease and Huntington's disease, in which neuropsychological deficits, and indeed subcortical dementia are known to occur.")


John Waddington. Cognitive dysfunction in chronic schizophrenia followed prospectively over 10 years and its longitudinal relationship to the emergence of tardive dyskinesia. Psychological Medicine, 26, 681-688. 1996. (Progressive deterioration in cognitive function is seen even late in chronic phase of schizophrenic illness. Deterioration derives primarily from emergence of TD. They find that marked deterioration in cognitive function occurs at same time as emergence of movement disorder.)


Rupert McShane. Do Neuroleptic Drugs Hasten Cognitive Decline in Dementia? Prospective Study with Necropsy Follow Up. British Medical Journal, 314, 266-270. 1997. (The decline in cognitive function in dementia patients who take neuroleptics is twice the decline in patients who did not take he drugs.)


Raquel Gur,et. Al. Subcortical MRI Volumes in Neuroleptic-Naïve and Treated Patients with Schizophrenia. American Journal of Psychiatry, 155, 1711-1717. 1998. (Drugs cause hypertrophy of the caudate, putamen, and thalamus, which is thought to be "structural adaptation to receptor blockade." The drug-induced hypertrophy is also "mildly associated with greater severity of both negative and positive symptoms.")


Raquel Gur, et. Al. A follow-up of magnetic resonance imaging study of schizophrenia. Archives of General Psychiatry, 55, 145-151, 1998. (Use of neuroleptics is associated with volume reduction (or atrophy) of frontal lobes and temporal lobes. As the brain atrophies in this way, here is said to improvement in delusions and thought disorder (the brain-damaging principle at work). A greater rate of reduction in volume is associated with higher dose. At the same time, reduction in volume is associated with decline in some neurobehavioral functions.)


Al Madsen. Neuroleptics in progressive structural brain abnormalities in psychiatric illness. The Lancet, 352, 784-785. Sept. 5, 1998. (Neuroleptic use is associated with atrophy of cerebral cortex. The estimated risk of atrophy increases by 6.4% for each additional 10 grams of neuroleptic drug.)


G. Tsai. Markers of glutamergic neurotransmission and oxidative stress associated with tardive dyskinesia. American Journal of Psychiatry, 155, 1207-1213. 1998. (This study suggests that neuroleptics cause neuronal damage as a result of oxidative stress, and that this is the degenerative process that produces TD.)


Conclusion: the brain abnormalities attributed causal significance in mental illness are most likely the result of neuroleptic drug treatment.


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