ABSTRACT
OBJECTIVE: Schizophrenic patients who are only partially responsive to clozapine pose a therapeutic challenge. In these circumstances some clinicians would consider adding in a second antipsychotic. We present a case report and review evidence for the efficacy of such augmentation strategies. METHOD: Single case report and literature review. RESULTS: The total number of patients in studies and case reports of combining clozapine with other antipsychotics is small. There has been only one randomized controlled trial. This found the addition of sulpiride to clozapine resulted in clinical improvement in some patients. CONCLUSION: Further randomized controlled studies of augmentation of clozapine therapy are needed to provide scientific justification for this clinical practice.
Subject(s)
Antipsychotic Agents/therapeutic use , Clozapine/therapeutic use , Schizophrenia, Paranoid/drug therapy , Sulpiride/therapeutic use , Antipsychotic Agents/administration & dosage , Clozapine/administration & dosage , Drug Therapy, Combination , Humans , Male , Middle Aged , Randomized Controlled Trials as Topic , Sulpiride/administration & dosage , Treatment OutcomeABSTRACT
It is now a recognized principle that various neuropeptides are neuronally co-localized with biogenic amine or aminoacid neurotransmitters. In the rat CNS it has previously been shown that TRH is co-localized with 5-HT (and also with substance P) in cell bodies of the posterior raphe that project to the spinal cord. Although TRH cell bodies are known to be widely distributed throughout the forebrain there is no other known co-localization with 5-HT. In this study we further specify the forebrain there is no other known co-localization with 5-HT. In this study we further specify the anatomical relationship of TRH with 5-HT by use of surgical and neurotoxic lesioning with reference to limbic forebrain regions wherein TRH is greatly increased following seizures. In groups of rats, the fimbria-fornix was lesioned alone, or combined with a lesion of the dorsal perforant path or the ventral perforant path. There was a sham lesioned control group. Additional groups were lesioned with 5,7 dihydroxytryptamine, 100 micrograms i.v.t., 45 min. after i.p. desipramine, 25 mg/kg. All rats were sacrificed three weeks after lesions. Indoleamines were determined by HPLC in left anterior cortex, left pyriform/olfactory cortex, left dorsal hippocampus and left ventral hippocampus. TRH was determined by specific RIA in the corresponding right brain regions. The modal n was 7 rats.(ABSTRACT TRUNCATED AT 250 WORDS)
Subject(s)
Prosencephalon/metabolism , Serotonin/metabolism , Thyrotropin-Releasing Hormone/metabolism , 5,7-Dihydroxytryptamine/pharmacology , Animals , Frontal Lobe/metabolism , Hippocampus/metabolism , Hydroxyindoleacetic Acid/metabolism , Male , Olfactory Bulb/metabolism , Prosencephalon/drug effects , Prosencephalon/surgery , Rats , Rats, Inbred StrainsABSTRACT
Light and electron microscopic studies of a chemodectoma of the vagus nerve are presented. Forty-four cases of vagal chemodectoma have been reported to date, but no electronmicroscopic studies have been published. The ultramicroscopic studies showed the presence of clear and dark cells and membrane-bound neurosecretory granules, and the absence of sustentacular cells and nerve endings. Similar findings have been reported in cases of carotid body and glomus jugulare tumors.
