Clinical aspects and progression of Parkinson's disease in women with detrusor hyperreflexia

2013 ◽  
Author(s):  
Raimundo Nonato Campos Sousa
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Aspects ◽  
Detrusor Hyperreflexia

scholarly journals Urinary dysfunction with detrusor hyperactivity in women with Parkinson's disease cannot be blamed as a factor of worsening motor performance

2013 ◽  
Vol 71 (9A) ◽  
pp. 591-595 ◽  
Author(s):  
Raimundo Nonato Campos-Sousa ◽  
Elizabeth Maria Aparecida Barasnevicius Quagliato ◽  
Kelson James Almeida ◽  
Inacio Augusto Dias de Castro ◽  
Viriato Campelo
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Motor Performance ◽  
Rating Scale ◽  
Clinical Symptoms ◽  
Urinary Dysfunction ◽  
Clinical Aspects ◽  
Yahr Scale ◽  
Disease Rating ◽  
Detrusor Hyperactivity

Introduction Detrusor hyperactivity is the leading cause of urinary dysfunction in Parkinson's disease (PD). There are few studies correlating PD clinical aspects with this autonomic feature. Methods A cohort of 63 women with PD were prospectively examined for assessment of clinical aspects and disease severity using unified Parkinson's disease rating scale and Hoehn-Yahr scale, respectively. The urologic function was evaluated by the urodynamic study. Two groups were categorized at this time - groups with and without detrusor hyperactivity. After seven years, the same parameters were re-evaluated. Results Progression of the disease on mental scores was found in the group with detrusor hyperactivity. On follow-up, clinical symptoms and severity did not show significant worsening between the groups. Conclusion Detrusor hyperactivity is a frequent urodynamic finding in PD, and even though it is associated with dopaminergic dysfunction, it cannot be blamed as a factor of worsening motor performance, but is probably associated with poor cognitive and mental prognosis.

scholarly journals Cognitive and Behavior Deficits in Parkinson’s Disease with Alteration of FDG-PET Irrespective of Age

Geriatrics ◽  
2021 ◽  
Vol 6 (4) ◽  
pp. 110
Author(s):  
Fulvio Lauretani ◽  
Livia Ruffini ◽  
Crescenzo Testa ◽  
Marco Salvi ◽  
Mara Scarlattei ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Disease Progression ◽  
Metabolic Activity ◽  
Fdg Pet ◽  
Surrogate Marker ◽  
Metabolic Imaging ◽  
Clinical Aspects ◽  
Histopathological Diagnosis ◽  
Motor Symptoms

Significant progress has been made in our understanding of the neurobiology of Parkinson’s disease (PD). Post-mortem studies are an important step and could help to comprehend not only the progression of motor symptoms, but also the involvement of other clinical domains, including cognition, behavior and impulse control disorders (ICDs). The correlation of neuropathological extension of the disease with the clinical stages remains challenging. Molecular imaging, including positron emission tomography (PET) and single photon computed tomography (SPECT), could allow for bridging the gap by providing in vivo evidence of disease extension. In the last decade, we have observed a plethora of reports describing improvements in the sensitivity of neuroimaging techniques. These data contribute to increasing the accuracy of PD diagnosis, differentiating PD from other causes of parkinsonism and also obtaining a surrogate marker of disease progression. FDG-PET has been used to measure cerebral metabolic rates of glucose, a proxy for neuronal activity, in PD. Many studies have shown that this technique could be used in early PD, where reduced metabolic activity correlates with disease progression and could predict histopathological diagnosis. The aim of this work is to report two particular cases of PD in which the assessment of brain metabolic activity (from FDG-PET) has been combined with clinical aspects of non-motor symptoms. Integration of information on neuropsychological and metabolic imaging allows us to improve the treatment of PD patients irrespective of age.

scholarly journals Clinical Aspects and Management of Levodopa-Induced Dyskinesia

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Nicola Tambasco ◽  
Simone Simoni ◽  
Erica Marsili ◽  
Elisa Sacchini ◽  
Donatella Murasecco ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dopamine Agonists ◽  
Chronic Treatment ◽  
Clinical Impact ◽  
Clinical Aspects ◽  
Pharmacological Profile ◽  
Early Use

In Parkinson's disease, one of the most troublesome dilemmas is the treatment of levodopa-induced dyskinesia. After a few years, chronic treatment with levodopa is associated with the development of dyskinesias. Strategies to delay or to reduce dyskinesias are based on the change of levodopa dosing or the early use of dopamine agonists. Dopamine agonists with different pharmacological profile are available. Our paper was aimed to analyse the clinical impact and the management of dyskinesias with dopamine agonists.

Does catatonia have a specific brain biology?

2002 ◽  
Vol 25 (5) ◽  
pp. 580-581
Author(s):  
Bernhard Bogerts
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Basis ◽  
Subjective Experience ◽  
Clinical Symptoms ◽  
Clinical Aspects ◽  
Multimodal Approach ◽  
Top Down ◽  
Comprehensive Comparison ◽  
New Strategies

Dr. Northoff's comprehensive comparison of clinical symptoms and neurobiological findings in catatonia with that of Parkinson's disease through integration of various levels of investigation, from neurochemistry up to the subjective experience, is a good example of the new strategies we need to improve our understanding of psychiatric disorders. His multimodal approach, leading to the hypothesis that different pathophysiologies of transcortical “horizontal modulation” and “bottom-up/top-down” – orbitofrontal/basal ganglia – “vertical modulations,” may explain many clinical aspects of catatonia and Parkinson's disease, and thereby fills an important gap in current theories of psychomotor syndromes. However, to analyze more specifically the pathophysiology of catatonia, comparison not only with Parkinson's disease, but also with schizophrenia and anxiety disorders would be helpful. As long as the pathohistological and molecular basis of catatonic syndromes is unknown, theories based mainly on functional considerations remain preliminary.

scholarly journals Impulse Control Disorders Following Deep Brain Stimulation of the Subthalamic Nucleus in Parkinson's Disease: Clinical Aspects

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Polyvios Demetriades ◽  
Hugh Rickards ◽  
Andrea Eugenio Cavanna
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Deep Brain Stimulation ◽  
Brain Stimulation ◽  
Impulse Control ◽  
Case Reports ◽  
Impulse Control Disorders ◽  
Clinical Aspects ◽  
Dopaminergic Medication ◽  
Deep Brain

Parkinson's disease (PD) has been associated with the development of impulse control disorders (ICDs), possibly due to overstimulation of the mesolimbic system by dopaminergic medication. Preliminary reports have suggested that deep brain stimulation (DBS), a neurosurgical procedure offered to patients with treatment-resistant PD, affects ICD in a twofold way. Firstly, DBS allows a decrease in dopaminergic medication and hence causes an improvement in ICDs. Secondly, some studies have proposed that specific ICDs may develop after DBS. This paper addresses the effects of DBS on ICDs in patients with PD. A literature search identified four original studies examining a total of 182 patients for ICDs and nine case reports of 39 patients that underwent DBS and developed ICDs at some point. Data analysis from the original studies did not identify a significant difference in ICDs between patients receiving dopaminergic medication and patients on DBS, whilst the case reports showed that 56% of patients undergoing DBS had poor outcome with regards to ICDs. We discuss these ambivalent findings in the light of proposed pathogenetic mechanisms. Longitudinal, prospective studies with larger number of patients are required in order to fully understand the role of DBS on ICDs in patients with PD.

scholarly journals Parkinson's Disease and Sleep/Wake Disturbances

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Todd J. Swick
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Sleep Disorders ◽  
Sleep Disturbances ◽  
Treatment Options ◽  
Rem Sleep Behavior Disorder ◽  
Behavior Disorder ◽  
Clinical Aspects ◽  
Nonmotor Symptoms ◽  
Sleep Behavior

Parkinson's disease (PD) has traditionally been characterized by its cardinal motor symptoms of bradykinesia, rigidity, resting tremor, and postural instability. However, PD is increasingly being recognized as a multidimensional disease associated with myriad nonmotor symptoms including autonomic dysfunction, mood disorders, cognitive impairment, pain, gastrointestinal disturbance, impaired olfaction, psychosis, and sleep disorders. Sleep disturbances, which include sleep fragmentation, daytime somnolence, sleep-disordered breathing, restless legs syndrome (RLS), nightmares, and rapid eye movement (REM) sleep behavior disorder (RBD), are estimated to occur in 60% to 98% of patients with PD. For years nonmotor symptoms received little attention from clinicians and researchers, but now these symptoms are known to be significant predictors of morbidity in determining quality of life, costs of disease, and rates of institutionalization. A discussion of the clinical aspects, pathophysiology, evaluation techniques, and treatment options for the sleep disorders that are encountered with PD is presented.

Brain Grafting as a Treatment for Parkinson's Disease

Neurosurgery ◽  
1987 ◽  
Vol 20 (2) ◽  
pp. 335-342 ◽  
Author(s):  
Mark J. Perlow
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Clinical Manifestations ◽  
Dopamine Neurons ◽  
Clinical Aspects ◽  
Pathological Changes ◽  
Pharmacological Treatments ◽  
The Central Nervous System ◽  
The Brain

Abstract Parkinson's disease is an illness with neuropathological and neuroanatomical abnormalities in many areas of the central nervous system. Some clinical manifestations of this illness are correlated with pathological changes in the substantia nigra and with a loss of dopamine in the nigra and striatum. The most effective pharmacological treatments have used agents that either replace the lost dopamine or act as agonists on dopamine receptors. Recent studies in animal models of Parkinson's disease demonstrate that the loss of dopamine and many clinical manifestations of dopamine reduction can be reversed by transplantation of fetal dopamine-containing cells to specific dopamine-depleted areas of the brain. Long term viability of these transplants has also been demonstrated. The author suggests that the transplantation of dopamine neurons, even across species barriers, is a reasonable consideration for the treatment of human Parkinson's disease. This article reviews in detail the results of recent experiments and how the experience in these models might be utilized in determining a transplantation strategy for the treatment of specific clinical aspects of this illness.

scholarly journals Genetic Variants in SNCA and the Risk of Sporadic Parkinson’s Disease and Clinical Outcomes: A Review

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Clarissa Loureiro das Chagas Campêlo ◽  
Regina Helena Silva
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Environmental Factors ◽  
Clinical Outcomes ◽  
Association Studies ◽  
Clinical Aspects ◽  
Genome Wide Association Studies ◽  
Snca Gene ◽  
Increased Risk

There is increasing evidence of the contribution of genetic susceptibility to the etiology of Parkinson’s disease (PD). Genetic variations in the SNCA gene are well established by linkage and genome-wide association studies. Positive associations of single nucleotide polymorphisms (SNPs) in SNCA and increased risk for PD were found. However, the role of SNCA variants in individual traits or phenotypes of PD is unknown. Here, we reviewed the current literature and identified 57 studies, performed in fourteen different countries, that investigated SNCA variants and susceptibility to PD. We discussed the findings based on environmental factors, history of PD, clinical outcomes, and ethnicity. In conclusion, SNPs within the SNCA gene can modify the susceptibility to PD, leading to increased or decreased risk. The risk associations of some SNPs varied among samples. Of notice, no studies in South American or African populations were found. There is little information about the effects of these variants on particular clinical aspects of PD, such as motor and nonmotor symptoms. Similarly, evidence of possible interactions between SNCA SNPs and environmental factors or disease progression is scarce. There is a need to expand the clinical applicability of these data as well as to investigate the role of SNCA SNPs in populations with different ethnic backgrounds.

Sign in / Sign up

Export Citation Format

Share Document