Novel case of Parkinson’s disease and schizophrenia: challenges in the management

2021 ◽  
Vol 14 (7) ◽  
pp. e244028
Author(s):  
Amna Ramzan ◽  
Ruchi Aggarwal ◽  
Fariha Jamal
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Course ◽  
Safety Data ◽  
Clinical Findings ◽  
Current Evidence ◽  
Collateral Information ◽  
Positron Emission ◽  
Receptor Profile ◽  
Symptomatic Control

Coexistence of idiopathic Parkinson’s disease (iPD) and schizophrenia can pose great diagnostic and therapeutic challenges because of their pathophysiology. Our case highlights such challenges in management. We present a case of 73-year-old man who had parkinsonism for last several years and was also diagnosed with schizophrenia. Due to lack of collateral information about the onset of symptoms and clinical course, it was difficult to distinguish iPD from neuroleptic-induced parkinsonism. Even though, certain clinical findings may help to differentiate between the two conditions, single positron emission computerized tomography/DatScan was used to confirm the diagnosis of iPD. Treatment of coexisting iPD and schizophrenia can be challenging, and a delicate pharmacologic balance must be maintained to ensure adequate symptomatic control. Current evidence suggests that clozapine is a better choice for managing psychosis in these patients due to its unique receptor profile and better safety data.

scholarly journals A Review of the Current Evidence Connecting Seborrheic Dermatitis and Parkinson’s Disease and the Potential Role of Oral Cannabinoids

Dermatology ◽  
2020 ◽  
pp. 1-6
Author(s):  
Hope R. Rietcheck ◽  
Jalal Maghfour ◽  
Chandler W. Rundle ◽  
Sameeha S. Husayn ◽  
Colby L. Presley ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Neurodegenerative Disorder ◽  
Seborrheic Dermatitis ◽  
Topical Therapy ◽  
Safety Data ◽  
Current Data ◽  
Current Evidence ◽  
Simultaneous Treatment

Parkinson’s disease (PD) is a neurodegenerative disorder associated with multiple comorbidities, including seborrheic dermatitis (SD), which develops in more than half of PD patients. SD in patients with PD can be severe and frequently intractable by traditional topical therapy. Cannabinoids possess anti-inflammatory and neuromodulatory properties working within the intrinsic endocannabinoid system, the activation of which may alleviate the motor symptoms of PD. The effect of cannabinoids on SD is unknown. Here we explore the pathophysiological mechanisms and possible therapeutic role of oral cannabinoids in PD patients with SD, and review speculative mechanisms underlying the association of PD and SD. Current data supporting the use of cannabinoids in both PD and SD, as well as oral cannabinoid safety and tolerability, are presented. Cannabinoids may provide the possibility of simultaneous treatment of both SD and PD. Specific SD studies and additional safety data on oral cannabinoids are needed.

scholarly journals Azathioprine immunosuppression and disease modification in Parkinson’s disease (AZA-PD): a randomised double-blind placebo-controlled phase II trial protocol

BMJ Open ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. e040527
Author(s):  
Julia C Greenland ◽  
Emma Cutting ◽  
Sonakshi Kadyan ◽  
Simon Bond ◽  
Anita Chhabra ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Immune System ◽  
Phase Ii ◽  
Rating Scale ◽  
Positron Emission Tomography Imaging ◽  
Clinical Markers ◽  
Double Blind ◽  
Positron Emission ◽  
Immunosuppressant Medication

IntroductionThe immune system is implicated in the aetiology and progression of Parkinson’s disease (PD). Inflammation and immune activation occur both in the brain and in the periphery, and a proinflammatory cytokine profile is associated with more rapid clinical progression. Furthermore, the risk of developing PD is related to genetic variation in immune-related genes and reduced by the use of immunosuppressant medication. We are therefore conducting a ‘proof of concept’ trial of azathioprine, an immunosuppressant medication, to investigate whether suppressing the peripheral immune system has a disease-modifying effect in PD.Methods and analysisAZA-PD is a phase II randomised placebo-controlled double-blind trial in early PD. Sixty participants, with clinical markers indicating an elevated risk of disease progression and no inflammatory or immune comorbidity, will be treated (azathioprine:placebo, 1:1) for 12 months, with a further 6-month follow-up. The primary outcome is the change in the Movement Disorder Society-Unified Parkinson’s Disease Rating Scale gait/axial score in the OFF state over the 12-month treatment period. Exploratory outcomes include additional measures of motor and cognitive function, non-motor symptoms and quality of life. In addition, peripheral and central immune markers will be investigated through analysis of blood, cerebrospinal fluid and PK-11195 positron emission tomography imaging.Ethics and disseminationThe study was approved by the London-Westminster research ethics committee (reference 19/LO/1705) and has been accepted by the Medicines and Healthcare products Regulatory Agency (MHRA) for a clinical trials authorisation (reference CTA 12854/0248/001–0001). In addition, approval has been granted from the Administration of Radioactive Substances Advisory Committee. The results of this trial will be disseminated through publication in scientific journals and presentation at national and international conferences, and a lay summary will be available on our website.Trial registration numbersISRCTN14616801 and EudraCT- 2018-003089-14.

Repurposing GLP-1 Receptor Agonists for Parkinson’s Disease: Current Evidence and Future Opportunities

2021 ◽  
Author(s):  
Daniella Balduino Victorino ◽  
Mariana Nejm ◽  
Marcia Guimarães-Marques ◽  
Fulvio Alexandre Scorza ◽  
Carla Alessandra Scorza
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Current Evidence ◽  
Receptor Agonists

scholarly journals Observation of magnetic susceptibility changes within the thalamus: a comparative study between healthy and Parkinson’s disease afflicted cynomolgus monkeys using 7 T MRI

2019 ◽  
Vol 10 (1) ◽  
Author(s):  
Sangwoo Kim ◽  
Youngjeon Lee ◽  
Chang-Yeop Jeon ◽  
Yeung Bae Jin ◽  
Sukhoon Oh ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Parkinson’S Disease ◽  
Positron Emission Tomography ◽  
Parkinson's Disease ◽  
Magnetic Resonance ◽  
Disease Model ◽  
Emission Tomography ◽  
Resonance Imaging ◽  
Cynomolgus Monkeys ◽  
Positron Emission

Abstract Background Although the thalamus is known to modulate basal ganglia function related to motor control activity, the abnormal changes within the thalamus during distinct medical complications have been scarcely investigated. In order to explore the feasibility of assessing iron accumulation in the thalamus as an informative biomarker for Parkinson’s disease (PD), this study was designed to employ quantitative susceptibility mapping using a 7 T magnetic resonance imaging system in cynomolgus monkeys. A 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-injected cynomolgus monkey and a healthy control (HC) were examined by 7 T magnetic resonance imaging. Positron emission tomography with 18F-N-(3-fluoro propyl)-2ß-carboxymethoxy-3ß-(4-iodophenyl) nortropane was also employed to identify the relationship between iron deposits and dopamine depletion. All acquired values were averaged within the volume of interest of the nigrostriatal pathway. Findings Compared with the HC, the overall elevation of iron deposition within the thalamus in the Parkinson’s disease model (about 53.81% increase) was similar to that in the substantia nigra (54.81%) region. Substantial susceptibility changes were observed in the intralaminar part of the thalamus (about 70.78% increase). Additionally, we observed that in the Parkinson’s disease model, binding potential values obtained from positron emission tomography were considerably decreased in the thalamus (97.51%) and substantia nigra (92.48%). Conclusions The increased iron deposition in the thalamus showed negative correlation with dopaminergic activity in PD, supporting the idea that iron accumulation affects glutaminergic inputs and dopaminergic neurons. This investigation indicates that the remarkable susceptibility changes in the thalamus could be an initial major diagnostic biomarker for Parkinson’s disease-related motor symptoms.

scholarly journals Cascading from SARS-CoV-2 to Parkinson’s Disease through Protein-Protein Interactions

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 897
Author(s):  
Ernesto Estrada
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Protein Interactions ◽  
Molecular Level ◽  
Direct Consequence ◽  
Viral Proteins ◽  
Clinical Findings ◽  
Post Translational Modification ◽  
Host Proteins ◽  
Bioinformatic Tools

Extensive extrapulmonary damages in a dozen of organs/systems, including the central nervous system (CNS), are reported in patients of the coronavirus disease 2019 (COVID-19). Three cases of Parkinson’s disease (PD) have been reported as a direct consequence of COVID-19. In spite of the scarce data for establishing a definitive link between COVID-19 and PD, some hypotheses have been proposed to explain the cases reported. They, however, do not fit well with the clinical findings reported for COVID-19 patients, in general, and for the PD cases reported, in particular. Given the importance of this potential connection, we present here a molecular-level mechanistic hypothesis that explains well these findings and will serve to explore the potential CNS damage in COVID-19 patients. The model explaining the cascade effects from COVID-19 to CNS is developed by using bioinformatic tools. It includes the post-translational modification of host proteins in the lungs by viral proteins, the transport of modified host proteins via exosomes out the lungs, and the disruption of protein-protein interaction in the CNS by these modified host proteins. Our hypothesis is supported by finding 44 proteins significantly expressed in the CNS which are associated with PD and whose interactions can be perturbed by 24 host proteins significantly expressed in the lungs. These 24 perturbators are found to interact with viral proteins and to form part of the cargoes of exosomes in human tissues. The joint set of perturbators and PD-vulnerable proteins form a tightly connected network with significantly more connections than expected by selecting a random cluster of proteins of similar size from the human proteome. The molecular-level mechanistic hypothesis presented here provides several routes for the cascading of effects from the lungs of COVID-19 patients to PD. In particular, the disruption of autophagy/ubiquitination processes appears as an important mechanism that triggers the generation of large amounts of exosomes containing perturbators in their cargo, which would insult several PD-vulnerable proteins, potentially triggering Parkinsonism in COVID-19 patients.

Cognitive and Physiological Substrates of Impaired Sentence Processing in Parkinson's Disease

1993 ◽  
Vol 5 (4) ◽  
pp. 480-498 ◽  
Author(s):  
Murray Grossman ◽  
Susan Carvell ◽  
Stephen Gollomp ◽  
Matthew B. Stern ◽  
Martin Reivich ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Frontal Cortex ◽  
Sentence Processing ◽  
Sentence Comprehension ◽  
Short Term Memory ◽  
Brain Regions ◽  
Positron Emission ◽  
Left Caudate ◽  
Regional Cerebral Glucose Metabolism

Sentence comprehension is a complex process involving at least a grammatical processor and a procedural component that supports language computations. One type of cerebral architecture that may underlie sentence processing is a network of distributed brain regions. We report two experiments designed to evaluate the cognitive and physiological substrate of sentence processing diaculties in nondemented patients with Parkinson's disease (PD). In the first experiment, patients answered simple questions about sentences that varied in their computational demands. Group and individual patient analyses indicated that PD patients are significantly compromised on this task, and that their difficulties become more prominent as the computational demands of the sentences increase. We manipulated the set of sentences to stress performance aspects of sentence processing. PD patients were compromised in their ability to detect errors in the presence and nature of a sentence's grammatical morphemes, suggesting a deficit in selective attention, but their ability to answer questions about a sentence was not afFected by short-term memory factors. In the second experiment, positron emission tomography was used to correlate this pattern of sentence comprehension impairment with regional cerebral glucose metabolism (rCMRgl) obtained at rest in a representative subset of these PD patients. Grammatical comprehension and attention in sentence processing correlated significantly with mesial frontal rCMRgl. Regression analyses confirmed the central role of left mesial frontal cortex, and identified a subsidiary role for left caudate in overall sentence comprehension, for left dorsolateral frontal cortex in grammatical processing, and for bilateral dorsolateral frontal cortex in attending to the presence of grammatical features. We conclude that compromised mesial frontal functioning underlies in part the sentence processing deficit of these patients, and these data illustrate one method for mapping portions of a sentence processing mechanism onto a distributed cerebral architecture.

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