Update on the neurology of Parkinson's disease

Fowler, Clare J.

doi:10.1002/nau.20371

Cited by 41 publications

(29 citation statements)

References 46 publications

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“…In PD, urinary symptoms (nocturia, urgency) usually evolve after motor onset of disease are mostly unresponsive to L ‐dopa and due to loss of inhibitory input to the pontine micturition centre 14. In our study, these symptoms were less common in Parkin disease when compared with PD.…”

Section: Discussioncontrasting

confidence: 39%

Nonmotor symptoms in Parkin gene‐related parkinsonism

Kägi

Klein

Wood³

et al. 2010

Movement Disorders

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The aim of the study was to explore the prevalence and differences of nonmotor symptoms (NMSs) in patients with young-onset Parkinson's disease (YOPD) with and without mutations in the Parkin gene and late-onset Parkinson's disease (LOPD). Twenty-seven patients with YOPD and 27 with LOPD, as well as 16 patients with homozygous or compound heterozygote Parkin mutations filled in the nonmotor symptoms questionnaire, a 30-item self-completed questionnaire that addresses various NMSs. Overall, NMSs were more prevalent in YOPD (12.07 +/- 3.9; P = 0.009) and LOPD (13.26 +/- 5.8; P = 0.001) compared with Parkin mutation carriers (7.38 +/- 4.2). Dribbling of saliva, vivid dreams, loss of smell, and urinary urgency were more prevalent in YOPD compared with Parkin mutation carriers. Only anxiety was more prevalent in the latter. Apart from anxiety, NMSs appear to be less prevalent in Parkin gene-related parkinsonism. Although these results need further study, the presented data might be helpful in the clinical recognition of specific phenotypes and genotypes in YOPD. The data are in keeping with a different pathological disease process in Parkin gene-related parkinsonism.

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Section: Discussioncontrasting

confidence: 39%

Nonmotor symptoms in Parkin gene‐related parkinsonism

Kägi

Klein

Wood³

et al. 2010

Movement Disorders

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“…We also failed to measure history of smoking (i.e., smoker's cough), which is associated with development of both hernia and LUTS and is prevalent in both active duty and retired military personnel (Fiegelman, 1994;Teachman, 2011). The predictive power of PD duration corresponds to the conventional view that LUTS are related to the extent of dopamine depletion and become more troublesome as PD progresses (Fowler, 2007), although findings from an earlier study by Defreitas and colleagues (2003) challenge this assumption.…”

Section: Discussionmentioning

confidence: 98%

Lower Urinary Tract Symptoms in Men With Parkinson Disease

Robinson¹,

Bradway²,

Bunting-Perry³

et al. 2013

Journal of Neuroscience Nursing

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Assessment for LUTS should be a component of every evaluation of a patient with PD. Our findings offer a preliminary profile of the male PD patient with LUTS, which is an important step toward effective screening, detection, and access to care and treatment. Next steps in research include further work to identify predictors of LUTS in both male and female PD populations, explore patient perspectives, begin trials of interventions for LUTS in the PD population, and analyze the economic impact.

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“…GU disorders include bladder and sexual dysfunction and collectively may occur in up to 40–80 % of patients with PD (Winge et al 2006; Fowler 2007; Sakakibara et al 2008). Patients commonly experience symptoms of a hyperactive or ‘irritable’ bladder such as urinary frequency, nocturia and urgency with occasional urgency incontinence.…”

Section: 4 Parkinson Disease: An Evolving Clinical Phenotypementioning

confidence: 99%

Parkinson’s Disease

Mhyre¹,

Boyd²,

Hamill³

et al. 2012

Subcellular Biochemistry

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Parkinson’s disease (PD) is the most common age-related motoric neurodegenerative disease initially described in the 1800’s by James Parkinson as the ‘Shaking Palsy’. Loss of the neurotransmitter dopamine was recognized as underlying the pathophysiology of the motor dysfunction; subsequently discovery of dopamine replacement therapies brought substantial symptomatic benefit to PD patients. However, these therapies do not fully treat the clinical syndrome nor do they alter the natural history of this disorder motivating clinicians and researchers to further investigate the clinical phenotype, pathophysiology/pathobiology and etiology of this devastating disease. Although the exact cause of sporadic PD remains enigmatic studies of familial and rare toxicant forms of this disorder have laid the foundation for genome wide explorations and environmental studies. The combination of methodical clinical evaluation, systematic pathological studies and detailed genetic analyses have revealed that PD is a multifaceted disorder with a wide-range of clinical symptoms and pathology that include regions outside the dopamine system. One common thread in PD is the presence of intracytoplasmic inclusions that contain the protein, α-synuclein. The presence of toxic aggregated forms of α-synuclein (e.g., amyloid structures) are purported to be a harbinger of subsequent pathology. In fact, PD is both a cerebral amyloid disease and the most common synucleinopathy, that is, diseases that display accumulations of α-synuclein. Here we present our current understanding of PD etiology, pathology, clinical symptoms and therapeutic approaches with an emphasis on misfolded α-synuclein.

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Update on the neurology of Parkinson's disease

Cited by 41 publications

References 46 publications

Nonmotor symptoms in Parkin gene‐related parkinsonism

Nonmotor symptoms in Parkin gene‐related parkinsonism

Lower Urinary Tract Symptoms in Men With Parkinson Disease

Parkinson’s Disease

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