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      Managing Bipolar Disease Complicated with Psychosis in Conjunction with Polypharmacy, Parkinson's Disease, and Multiple Comorbidities

      case-report

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          Abstract

          The lifelong prevalence of bipolar disorder in adults, including subsyndromal forms, has increased over the years in the United States. By contrast, neurodegenerative diseases such as Parkinson's disease have demonstrated an age-related rise in prevalence. As the global population manages to live longer thanks to sociomedical developments, it is expected to observe a rise in the occurrence of comorbid neuropsychiatric disorders. Herein, we present the case and management regimen of a 51-year-old female patient with multiple comorbidities and in the presence of polypharmacy. She was diagnosed with Parkinson's disease and bipolar disorder type I alongside multiple comorbidities; her polypharmacy and medical history presented a significant clinical challenge in managing her condition. This case report focuses on the pharmacologic management of neuropsychiatric disorders titrated to this patient's particular needs, which were complicated by psychosis and comorbidities.

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          Most cited references46

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          Epidemiology of Parkinson's disease

          The causes of Parkinson's disease (PD), the second most common neurodegenerative disorder, are still largely unknown. Current thinking is that major gene mutations cause only a small proportion of all cases and that in most cases, non-genetic factors play a part, probably in interaction with susceptibility genes. Numerous epidemiological studies have been done to identify such non-genetic risk factors, but most were small and methodologically limited. Larger, well-designed prospective cohort studies have only recently reached a stage at which they have enough incident patients and person-years of follow-up to investigate possible risk factors and their interactions. In this article, we review what is known about the prevalence, incidence, risk factors, and prognosis of PD from epidemiological studies.
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            Detection of oligomeric forms of alpha-synuclein protein in human plasma as a potential biomarker for Parkinson's disease.

            To date there is no accepted clinical diagnostic test for Parkinson's disease (PD) based on biochemical analysis of blood or cerebrospinal fluid (CSF). alpha-Synuclein (alpha-syn) protein has been linked to the pathogenesis of PD with the discovery of mutations in the gene encoding alpha-syn in familial cases with early-onset PD. Lewy bodies and Lewy neurites, which constitute the main pathological features in the brains of patients with sporadic PD and dementia with Lewy bodies, are formed by the conversion of soluble monomers of alpha-syn into insoluble aggregates. We recently reported the presence of alpha-syn in normal human blood plasma and in postmortem CSF. Here, we investigated whether alpha-syn can be used as a biomarker for PD. We have developed a novel ELISA method that detects only oligomeric "soluble aggregates" of alpha-syn. Using this ELISA, we report the presence of significantly elevated (P=0.002) levels of oligomeric forms of alpha-syn in plasma samples obtained from 34 PD patients compared with 27 controls; 52% (95% confidence intervals 0.353-0.687) of the PD patients displayed signals >0.5 OD with our ELISA assay in comparison to only 14.8% (95% confidence intervals 0.014-0.281) for the control cases. An analysis of the test's diagnostic value revealed a specificity of 0.852 (95% confidence intervals 0.662-0.958), sensitivity of 0.529 (95% confidence intervals 0.351-0.702) and a positive predictive value of 0.818 (95% confidence intervals 0.597-0.948). These observations offer new opportunities for developing diagnostic tests for PD and related diseases and for testing therapeutic agents aimed at preventing or reversing the aggregation of alpha-syn.
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              Parkinson’s Disease: Biomarkers, Treatment, and Risk Factors

              Parkinson’s disease (PD) is a progressive neurodegenerative disorder caused mainly by lack of dopamine in the brain. Dopamine is a neurotransmitter involved in movement, motivation, memory, and other functions; its level is decreased in PD brain as a result of dopaminergic cell death. Dopamine loss in PD brain is a cause of motor deficiency and, possibly, a reason of the cognitive deficit observed in some PD patients. PD is mostly not recognized in its early stage because of a long latency between the first damage to dopaminergic cells and the onset of clinical symptoms. Therefore, it is very important to find reliable molecular biomarkers that can distinguish PD from other conditions, monitor its progression, or give an indication of a positive response to a therapeutic intervention. PD biomarkers can be subdivided into four main types: clinical, imaging, biochemical, and genetic. For a long time protein biomarkers, dopamine metabolites, amino acids, etc. in blood, serum, cerebrospinal liquid (CSF) were considered the most promising. Among the candidate biomarkers that have been tested, various forms of α-synuclein (α-syn), i.e., soluble, aggregated, post-translationally modified, etc. were considered potentially the most efficient. However, the encouraging recent results suggest that microRNA-based analysis may bring considerable progress, especially if it is combined with α-syn data. Another promising analysis is the advanced metabolite profiling of body fluids, called “metabolomics” which may uncover metabolic fingerprints specific for various stages of PD. Conventional pharmacological treatment of PD is based on the replacement of dopamine using dopamine precursors (levodopa, L-DOPA, L-3,4 dihydroxyphenylalanine), dopamine agonists (amantadine, apomorphine) and MAO-B inhibitors (selegiline, rasagiline), which can be used alone or in combination with each other. Potential risk factors include environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular damage, and genomic defects. This review covers molecules that might act as the biomarkers of PD. Then, PD risk factors (including genetics and non-genetic factors) and PD treatment options are discussed.
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                Author and article information

                Contributors
                Journal
                Case Rep Psychiatry
                Case Rep Psychiatry
                CRIPS
                Case Reports in Psychiatry
                Hindawi
                2090-682X
                2090-6838
                2022
                5 May 2022
                : 2022
                : 3813929
                Affiliations
                1South Texas Health System, USA
                2Saint James School of Medicine, USA
                3University of Medicine and Health Science, USA
                Author notes

                Academic Editor: Lut Tamam

                Author information
                https://orcid.org/0000-0002-4556-5457
                https://orcid.org/0000-0002-5699-6631
                https://orcid.org/0000-0002-1246-8546
                https://orcid.org/0000-0001-5449-6070
                Article
                10.1155/2022/3813929
                9098339
                35571149
                8035b16c-59d0-4dce-bf2d-7b819accf879
                Copyright © 2022 Ricardo Irizarry et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 9 February 2022
                : 8 April 2022
                : 11 April 2022
                Categories
                Case Report

                Clinical Psychology & Psychiatry
                Clinical Psychology & Psychiatry

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