Diagnostic considerations in juvenile parkinsonism

Paviour, Dominic; Surtees, Robert; Lees, Andrew J.

doi:10.1002/mds.10644

Cited by 60 publications

(48 citation statements)

References 126 publications

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“…Age was determined using the date of birth. We excluded patients aged < 30 years with a diagnosis of PD to exclude juvenile onset parkinsonism, which is not likely due to PD [17], and patients aged 55 years or older, as these cases could be considered the lower limit of older onset PD. We included cases aged 50 to 54 because of the length of time typically required to apply for and be declared legally disabled, then start receiving Medicare benefits.…”

Section: Methodsmentioning

confidence: 99%

Epidemiology and neuropsychiatric manifestations of Young Onset Parkinson's Disease in the United States

Willis

Schootman

Kung

et al. 2013

Parkinsonism & Related Disorders

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Background To determine the demographic distribution of Young Onset Parkinson’s Disease (YOPD) in the United States and to quantify the burden of neuropsychiatric disease manifestations. Methods Cross sectional study of 3,459,986 disabled Americans, aged 30 to 54, who were receiving Medicare benefits in the year 2005. We calculated race and sex distributions of YOPD and used logistic regression to compare the likelihood of common and uncommon psychiatric disorders between beneficiaries with YOPD and the general disability beneficiary population, adjusting for race, age, and sex. Results We identified 14,354 Medicare beneficiaries with YOPD (prevalence = 414.9 per 100,000 disabled Americans). White men comprised the majority of cases (48.9%), followed by White women (34.7%), Black men (6.8%), Black women (5.0%), Hispanic men (2.4%), and Hispanic women (1.2%). Asian men (0.6%) and Asian women (0.4%) were the least common race sex pairs with a YOPD diagnosis in this population (chi square, p<0.001). Compared to the general population of medically disabled Americans, those with YOPD were more likely to receive medical care for depression (OR: 1.89, 1.83-1.95), dementia (OR: 7.73, 7.38-8.09), substance abuse/dependence (OR: 3.00, 2.99-3.01), and were more likely to be hospitalized for psychosis (OR: 3.36, 3.19-3.53), personality/impulse control disorders (OR: 4.56, 3.28-6.34), and psychosocial dysfunction (OR: 3.85, 2.89-5.14). Conclusions Young Onset Parkinson’s Disease is most common among white males in our study population. Psychiatric illness, addiction, and cognitive impairment are more common in YOPD than in the general population of disabled Medicare beneficiaries. These may be key disabling factors in YOPD.

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Section: Methodsmentioning

confidence: 99%

Epidemiology and neuropsychiatric manifestations of Young Onset Parkinson's Disease in the United States

Willis

Schootman

Kung

et al. 2013

Parkinsonism & Related Disorders

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“…Some of these are Mendelian genetic disorders, including the autosomal-dominant spinocerebellar ataxias (especially SCA-2 and SCA-3), Wilson's disease and neuroferritinopathy. This review focuses on PD only; however, for more detailed discussion of the genetic parkinsonisms we refer readers to recent reviews [19,20].…”

Section: Introductionmentioning

confidence: 99%

Molecular genetic pathways in Parkinson's disease: a review

2005

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Major progress has been made in the last decade in understanding the genetic basis of PD (Parkinson's disease) with five genes unequivocally associated with disease. As a result, multiple pathways have been implicated in the pathogenesis of PD, including proteasome impairment and mitochondrial dysfunction. Although Mendelian genetics has been successful in establishing a genetic predisposition for familial PD, this has not been reiterated in the sporadic form. In fact no genetic factors have been unequivocally associated with increased risk for sporadic PD. The difficulty in identifying susceptibility factors in PD has not only been because of numerous underpowered studies, but we have been unable to dissect out the genetic component in a multifactorial disease. This review aims to summarize the genetic findings within PD.

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“…Importantly, the absence of marked levodopa-induced dyskinesias after sustained treatment will help differentiate DRD from dystonia due to parkin mutations. 44 This difference was explained by the absence of dopaminergic cell loss in the substantia nigra in DRD, where the mutations are thought to cause only dysfunction of the neurons, as opposed to parkin mutations, which result in marked dopaminergic cell loss in the substantia nigra. In addition to the dramatic response to levodopa, low CSF levels of homovanillic acid (HVA), neopterin, and BH 4 are typical findings in DRD, but the biochemical analysis of these compounds is not widely available, limiting its usefulness in routine clinical practice.…”

Section: Dystonia-plusmentioning

confidence: 98%

Dystonia

Bhidayasiri

2006

The Neurologist

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Recent advances in molecular biology have led to the discovery of novel dystonia genes and loci, updating classification schemes, and better understanding of underlying pathophysiology. Treatment strategies for dystonia have significantly been updated with the introduction of different forms of botulinum toxin therapy, new pharmacologic agents, and most recently pallidal deep brain stimulation. A systematic approach to the diagnosis and treatment evaluation of dystonic patients provides optimal care for long-term management.

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Diagnostic considerations in juvenile parkinsonism

Cited by 60 publications

References 126 publications

Epidemiology and neuropsychiatric manifestations of Young Onset Parkinson's Disease in the United States

Epidemiology and neuropsychiatric manifestations of Young Onset Parkinson's Disease in the United States

Molecular genetic pathways in Parkinson's disease: a review

Dystonia

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