Journal ArticleDOI
Striatal binding of 11C-NMSP studied with positron emission tomography in patients with persistent tardive dyskinesia: no evidence for altered dopamine D2 receptor binding.
TLDR
The lack in difference in k3 values between TD patients, neuroleptic treated patients without TD and control subjects throws doubt on the hypothesis that changes in striatal D2 dopamin receptor number or binding affinity is an etiological mechanism for persistent TD.Abstract:
Dopamine D2 receptor binding characteristics were studied by positron emission tomography (PET) using N-11C-methyl spiperone as receptor ligand in patients on longterm treatment with neuroleptic drugs and in control subjects. Eight of the patients had symptoms of tardive dyskinesia whereas three patients did not have any symptoms. Control subjects comprised 5 healthy volunteers and 7 patients with pituitary tumors. All patients had been free of neuroleptic drugs for at least 4 weeks. The time dependent regional radioactivity in the striatum was measured and the receptor binding rate, k3, proportional to receptor number, Bmax and association rate for the receptor was calculated in relation to the cerebellum. The lack in difference in k3 values between TD patients, neuroleptic treated patients without TD and control subjects throws doubt on the hypothesis that changes in striatal D2 dopamin receptor number or binding affinity is an etiological mechanism for persistent TD.read more
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Blind, controlled, long-term study of the comparative incidence of treatment-emergent tardive dyskinesia with olanzapine or haloperidol.
TL;DR: The findings support an atypical extrapyramidal symptom profile and the potential of a significantly lower risk of tardive dyskinesia with olanzapine than with haloperidol among patients requiring maintenance antipsychotic treatment.
Journal ArticleDOI
Loss of striatal cholinergic neurons as a basis for tardive and L-dopa-induced dyskinesias, neuroleptic-induced supersensitivity psychosis and refractory schizophrenia
TL;DR: It is proposed that this syndrome is not the consequence of dopamine receptor proliferation, but results from damage or degeneration of striatal cholinergic interneurons, which occurs when they are released from dopaminergic inhibition following neuroleptic administration.
Journal ArticleDOI
Tardive dyskinesia is caused by maladaptive synaptic plasticity: a hypothesis.
TL;DR: Newer atypical antipsychotics with less nonspecific activity at dopamine receptors have not heralded the end of tardive dyskinesia and merely highlight the incomplete understanding of the disorder.
Journal ArticleDOI
The vacuous chewing movement (VCM) model of tardive dyskinesia revisited: is there a relationship to dopamine D2 receptor occupancy?
TL;DR: The results demonstrate that the incidence of VCMs is significantly related to HAL dose, and significant levels ofVCMs only emerge when haloperidol is continually present, consistent with the possibility that total D(2) occupancy, as well as 'transience' of receptor occupation, may be important in the development of late-onset antipsychotic-induced dyskinetic syndromes.
Journal ArticleDOI
Acute administration of haloperidol induces apoptosis of neurones in the striatum and substantia nigra in the rat.
TL;DR: It is reported here that the in vivo, acute administration of a large dose of haloperidol resulted in a microglial response indicative of neuronal damage, accompanied by an increase in the number of apoptotic cells in the striatum and in the substantia nigra pars reticulata.
References
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Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data:
TL;DR: A theoretical model of blood–brain exchange is developed and a procedure is derived that can be used for graphing multiple-time tissue uptake data and determining whether a unidirectional transfer process was dominant during part or all of the experimental period.
Journal ArticleDOI
Graphical Evaluation of Blood-to-Brain Transfer Constants from Multiple-Time Uptake Data. Generalizations:
TL;DR: General equations are derived that can be used to analyze tissue uptake data when the blood–plasma concentration of the test substance cannot be easily measured and for situations when trapping of theTest substance is incomplete and for a combination of these two conditions.
Journal ArticleDOI
Antischizophrenic drugs: chronic treatment elevates dopamine receptor binding in brain
TL;DR: Chronic treatment of rats with the neuroleptic drugs haloperidol, fluphenazine, and reserpine elicits a 20 to 25% increase in striatal dopamine receptor binding assayed with [3H]haloperidols, which may account for behavioral supersensitivity to dopamine receptor stimulants in such animals and for tardive dyskinesia in patients treated with these drugs.
Journal ArticleDOI
Positron emission tomography reveals elevated D2 dopamine receptors in drug-naive schizophrenics
Dean F. Wong,Henry N. Wagner,Larry E. Tune,Robert F. Dannals,Godfrey D. Pearlson,Jonathan M. Links,Carol A. Tamminga,Emmanuel P. Broussolle,Emmanuel P. Broussolle,Hayden T. Ravert,Alan A. Wilson,J. K. Thomas Toung,Jan Malat,Jeffery A. Williams,Lorcan A. O'Tuama,Solomon H. Snyder,Michael J. Kuhar,Michael J. Kuhar,Albert Gjedde,Albert Gjedde +19 more
TL;DR: Schizophrenia itself is associated with an increase in brain D2 dopamine receptor density, and the densities in the caudate nucleus were higher in both groups of patients than in the normal volunteers.