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      Possible multiple system atrophy with predominant parkinsonism in a patient with chronic schizophrenia: a case report


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          Multiple system atrophy (MSA) is an adult-onset, rare, and progressive neurodegenerative disorder characterized by a varying combination of autonomic failure, cerebellar ataxia, and parkinsonism. MSA is categorized as MSA-P with predominant parkinsonism, and as MSA-C with predominant cerebellar features. The prevalence of MSA has been reported to be between 1.86 and 4.9 cases per 100,000 individuals. In contrast, approximately 1% of the population is affected by schizophrenia during their lifetime; therefore, MSA-P comorbidity is very rare in schizophrenic patients. However, when the exacerbation or progression of parkinsonism occurs in patients with schizophrenia treated with antipsychotics, it is necessary to consider rare neurodegenerative disorders, including MSA-P, in the differential diagnosis of parkinsonism.

          Case presentation

          A 60-year-old female patient with chronic schizophrenia developed possible MSA-P. She had been treated mainly with typical antipsychotics, and presented with urinary incontinence, nocturnal polyuria, and dysarthria around 2011. In 2014, she developed worsening parkinsonian symptoms and autonomic dysfunction. Although her antipsychotic medication was switched to an atypical antipsychotic and the dose reduced, her parkinsonism was not improved. In 2015, modified electroconvulsive therapy produced slight improvements in the symptoms; however, she shortly returned to her symptomatic state. A combination of cardiac 123I-meta-iodobenzylguanidine scintigraphy and 123I-FP-CIT single-photon emission computed tomography imaging, in addition to brain magnetic resonance imaging findings, helped to discriminate MSA-P from other sources of parkinsonism. L-dopa had been prescribed, but she responded poorly and died in the spring of 2016.


          This case report highlights the importance of considering MSA-P in the differential diagnosis for parkinsonism in a patient being treated with antipsychotics for chronic schizophrenia. MSA-P should be considered in patients presenting with worsening and progressing parkinsonism, especially when accompanied by autonomic dysfunction or cerebellar ataxia. Although a definite diagnosis of MSA-P requires autopsy confirmation, a combination of brain magnetic resonance imaging and nuclear medicine scans may help to differentiate suspected MSA-P from the other parkinsonian syndromes. This case also demonstrates that MSA with parkinsonism that is poorly responsive to L-dopa may improve shortly after modified electroconvulsive therapy without worsening psychiatric symptoms.

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          Most cited references61

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          Olfactory dysfunction in Parkinson disease.

          Olfactory dysfunction is among the earliest nonmotor features of Parkinson disease (PD). Such dysfunction is present in approximately 90% of early-stage PD cases and can precede the onset of motor symptoms by years. The mechanisms responsible for olfactory dysfunction are currently unknown. As equivalent deficits are observed in Alzheimer disease, Down syndrome, and the Parkinson-dementia complex of Guam, a common pathological substrate may be involved. Given that olfactory loss occurs to a lesser extent or is absent in disorders such as multiple system atrophy, corticobasal degeneration, and progressive supranuclear palsy, olfactory testing can be useful in differential diagnosis. The olfactory dysfunction in PD and a number of related diseases with smell loss correlates with decreased numbers of neurons in structures such as the locus coeruleus, the raphe nuclei, and the nucleus basalis of Meynart. These neuroanatomical findings, together with evidence for involvement of the autonomic nervous system in numerous PD-related symptoms, suggest that deficits in cholinergic, noradrenergic and serotonergic function may contribute to the olfactory loss. This Review discusses the current understanding of olfactory dysfunction in PD, including factors that may be related to its cause.
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            Glial cytoplasmic inclusions in the CNS of patients with multiple system atrophy (striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome).

            Glial cytoplasmic inclusions (GCIs) were demonstrated by silver staining, immunocytochemistry and by electron microscopy in the central nervous system (CNS) of 11 patients with various combinations of striatonigral degeneration, olivopontocerebellar atrophy and Shy-Drager syndrome. Although their configuration in light microscope can sometimes resemble neurofibrillary tangles, their cellular localisation, measurements, ultrastructure, immunocytochemical characteristics and regional distribution all differ from these Alzheimer type changes. The majority of GCIs were localized in the white matter and appeared to be accompanied by an increase in the number of interfascicular oligodendroglial cells and pallor or loss of myelin staining. Our histological, ultrastructural and immunocytochemical findings all indicate that the cells which contain GCIs are oligodendrocytes and the inclusions themselves are composed of tubular structures. The presence of the until now unknown GCIs in all the 11 CNS, but not in age- and sex-matched control brains, indicates that GCI is a cellular change characteristic of multiple system atrophy and the three syndromes are various manifestations of the same disease.
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              Oligodendrocyte dysfunction in schizophrenia and bipolar disorder.

              Results of array studies have suggested abnormalities in expression of lipid and myelin-related genes in schizophrenia. Here, we investigated oligodendrocyte-specific and myelination-associated gene expression in schizophrenia and bipolar affective disorder. We used samples from the Stanley brain collection, consisting of 15 schizophrenia, 15 bipolar affective disorder, and 15 control brains. Indexing-based differential display PCR was done to screen for differences in gene expression in schizophrenia patients versus controls. Results were cross-validated with quantitative PCR, which was also used to investigate expression profiles of 16 other oligodendrocyte and myelin genes in schizophrenia and bipolar disorder. These genes were further investigated with an ongoing microarray analysis. Results of differential display and quantitative PCR analysis showed a reduction of key oligodendrocyte-related and myelin-related genes in schizophrenia and bipolar patients; expression changes for both disorders showed a high degree of overlap. Microarray results of the same genes investigated by quantitative PCR correlated well overall. Schizophrenia and bipolar brains showed downregulation of key oligodendrocyte and myelination genes, including transcription factors that regulate these genes, compared with control brains. These results lend support to and extend observations from other microarray investigations. Our study also showed similar expression changes to the schizophrenia group in bipolar brains, which thus lends support to the notion that the disorders share common causative and pathophysiological pathways.

                Author and article information

                +81-22-384-2236 , +81-22-384-9626 , hkomatsu1019@gmail.com
                BMC Psychiatry
                BMC Psychiatry
                BMC Psychiatry
                BioMed Central (London )
                21 May 2018
                21 May 2018
                : 18
                [1 ]Department of Psychiatry, Miyagi Psychiatric Center, Mubanchi, Tekurada, Natori, 981-1231 Japan
                [2 ]Department of Neurology, Minami Tohoku Hospital, Iwanuma, 989-2483 Japan
                [3 ]ISNI 0000 0004 1764 884X, GRID grid.415430.7, Department of Neurology, , Kohnan Hospital, ; Sendai, 982-8523 Japan
                © The Author(s). 2018

                Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

                Case Report
                Custom metadata
                © The Author(s) 2018

                Clinical Psychology & Psychiatry
                multiple system atrophy,schizophrenia,antipsychotics,parkinsonism,autonomic dysfunction,cardiac 123i-meta-iodobenzylguanidine scintigraphy,123i-fp-cit single-photon emission computed tomography image,magnetic resonance imaging,modified electroconvulsive therapy


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