Chlorprothixene was the first neuroleptic of the thioxanthene group and was marketed in 1959 under the trade names of Taractan and Truxal. Since then 20 years have passed and the authors were of the opinion that it would be opportune to study the literature published during these 20 years. They perused 801 publications, hereof 542 clinical works. Of these clinical works 109 were suited for statistical analysis. They represented 7109 patients. The other publications comprise 4378 patients which means that all the literature studied consists of a total of 11487 patients. The chlorprothixene proved to be a broad-spectrum neuroleptic with good therapeutic effects. Side effects, especially the extrapyramidal symptoms, appeared only seldom. Among the 11487 patients only 1.02% showed extrapyramidal symptoms and of these only 0.05% had tardive dyskinesias. Sme evidence seems to exist that these are schizophrenic patients showing extrapyramidal symptoms, without having received neuroleptics. It is the authors' opinion that chlorprothixene is still a neuroleptic of topical interest.
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http://dx.doi.org/10.1055/s-2007-1019608 | DOI Listing |
J Mol Neurosci
January 2025
Department of Neurology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Science/Peking Union Medical College, Beijing, 100730, China.
CSF1R-related leukoencephalopathy (CSF1R-L) and AARS2-related leukoencephalopathy (AARS2-L) were two disease entities sharing similar phenotype and even pathological changes. Although clinically, radiologically, and pathologically similar, they were caused by mutation of two different genes. As the rarity of the two diseases, the differential diagnosis of them was difficult.
View Article and Find Full Text PDFMicrographia, characterised by small handwriting, is often linked to Parkinson's disease, but also resulted to injured brain lesions. The left-handed women in her 20s developed 'fast micrographia' after a traumatic brain injury from a traffic accident, showing bilateral subdural haematomas and frontal lobe contusions, but she had no paralysis and extrapyramidal symptoms. Neuropsychological tests showed reduced processing speed and memory deficits, aligning with frontal lobe damage.
View Article and Find Full Text PDFPediatr Emerg Care
January 2025
From the Medical University of South Carolina, Pharmacy Services, Charleston, SC.
Objectives: In the treatment of agitation in a pediatric emergency department (PED), it is common to use once or as needed (PRN) medications when nonpharmacological management options have failed. Currently, there is limited available evidence on the treatment of pediatric agitation. The objective of this analysis was to characterize the prescribing practices of once or PRN medications for the treatment of agitation in a PED at an academic medical center.
View Article and Find Full Text PDFFree Neuropathol
January 2024
Department of Pathology, Nash Family Department of Neuroscience, Department of Artificial Intelligence & Human Health, Neuropathology Brain Bank & Research CoRE, Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
This review highlights a collection of both diverse and highly impactful studies published in the previous year selected by the author from the neurodegenerative neuropathology literature. As with previous reviews in this series, the focus is, to the best of my ability, to highlight human tissue-based experimentation most relevant to experimental and clinical neuropathologists. A concerted effort was made to balance the selected studies across neurodegenerative disease categories, approaches, and methodologies to capture the breadth of the research landscape.
View Article and Find Full Text PDFNeurol Genet
February 2025
Memory Center, Keio University School of Medicine, Tokyo, Japan.
Background And Objectives: A previous postmortem study of men with Christianson syndrome, a disorder caused by loss-of-function mutations in the gene , reported a mechanistic link between pathologic tau accumulation and progressive symptoms such as cerebellar atrophy and cognitive decline. This study aimed to characterize the relationships between neuropathologic manifestations and tau accumulation in heterozygous women with mutation.
Methods: We conducted a multimodal neuroimaging and plasma biomarker study on 3 middle-aged heterozygous women with mutations (proband 1: mid-50s; proband 2: early 50s; proband 3: mid-40s) presenting with progressive extrapyramidal symptoms.
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