This document presents the Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's disease (PD). The Movement Disorder Society PD Criteria are intended for use in clinical research but also may be used to guide clinical diagnosis. The benchmark for these criteria is expert clinical diagnosis; the criteria aim to systematize the diagnostic process, to make it reproducible across centers and applicable by clinicians with less expertise in PD diagnosis. Although motor abnormalities remain central, increasing recognition has been given to nonmotor manifestations; these are incorporated into both the current criteria and particularly into separate criteria for prodromal PD. Similar to previous criteria, the Movement Disorder Society PD Criteria retain motor parkinsonism as the core feature of the disease, defined as bradykinesia plus rest tremor or rigidity. Explicit instructions for defining these cardinal features are included. After documentation of parkinsonism, determination of PD as the cause of parkinsonism relies on three categories of diagnostic features: absolute exclusion criteria (which rule out PD), red flags (which must be counterbalanced by additional supportive criteria to allow diagnosis of PD), and supportive criteria (positive features that increase confidence of the PD diagnosis). Two levels of certainty are delineated: clinically established PD (maximizing specificity at the expense of reduced sensitivity) and probable PD (which balances sensitivity and specificity). The Movement Disorder Society criteria retain elements proven valuable in previous criteria and omit aspects that are no longer justified, thereby encapsulating diagnosis according to current knowledge. As understanding of PD expands, the Movement Disorder Society criteria will need continuous revision to accommodate these advances.

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MDS clinical diagnostic criteria for Parkinson's disease

Interpretation of clinical trials comparing different drug regimens for Parkinson's disease (PD) is complicated by the different dose intensities used: higher doses of levodopa and, possibly, other drugs produce better symptomatic control but more late complications. To address this problem, conversion factors have been calculated for antiparkinsonian drugs that yield a total daily levodopa equivalent dose (LED). LED estimates vary, so we undertook a systematic review of studies reporting LEDs to provide standardized formulae. Electronic database and hand searching of references identified 56 primary reports of LED estimates. Data were extracted and the mean and modal LEDs calculated. This yielded a standardized LED for each drug, providing a useful tool to express dose intensity of different antiparkinsonian drug regimens on a single scale. Using these conversion formulae to report LEDs would improve the consistency of reporting and assist the interpretation of clinical trials comparing different PD medications.

Systematic review of levodopa dose equivalency reporting in Parkinson's disease

Background: A consensus conference on multiple system atrophy (MSA) in 1998 established criteria for diagnosis that have been accepted widely. Since then, clinical, laboratory, neuropathologic, and imaging studies have advanced the field, requiring a fresh evaluation of diagnostic criteria. We held a second consensus conference in 2007 and present the results here.Methods: Experts in the clinical, neuropathologic, and imaging aspects of MSA were invited to participate in a 2-day consensus conference. Participants were divided into five groups, consisting of specialists in the parkinsonian, cerebellar, autonomic, neuropathologic, and imaging aspects of the disorder. Each group independently wrote diagnostic criteria for its area of expertise in advance of the meeting. These criteria were discussed and reconciled during the meeting using consensus methodology.Results: The new criteria retain the diagnostic categories of MSA with predominant parkinsonism and MSA with predominant cerebellar ataxia to designate the predominant motor features and also retain the designations of definite, probable, and possible MSA. Definite MSA requires neuropathologic demonstration of CNS alpha-synuclein-positive glial cytoplasmic inclusions with neurodegenerative changes in striatonigral or olivopontocerebellar structures. Probable MSA requires a sporadic, progressive adult-onset disorder including rigorously defined autonomic failure and poorly levodopa-responsive parkinsonism or cerebellar ataxia. Possible MSA requires a sporadic, progressive adult-onset disease including parkinsonism or cerebellar ataxia and at least one feature suggesting autonomic dysfunction plus one other feature that may be a clinical or a neuroimaging abnormality.Conclusions: These new criteria have simplified the previous criteria, have incorporated current knowledge, and are expected to enhance future assessments of the disease.

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Second consensus statement on the diagnosis of multiple system atrophy

Mini Mental State

ContextPostmenopausal women have a greater risk than men of developing Alzheimer
disease, but studies of the effects of estrogen therapy on Alzheimer disease
have been inconsistent. On July 8, 2002, the study drugs, estrogen plus progestin,
in the Women's Health Initiative (WHI) trial were discontinued because of
certain increased health risks in women receiving combined hormone therapy.ObjectiveTo evaluate the effect of estrogen plus progestin on the incidence of
dementia and mild cognitive impairment compared with placebo.Design, Setting, and ParticipantsThe Women's Health Initiative Memory Study (WHIMS), a randomized, double-blind,
placebo-controlled clinical trial, began enrolling participants from the Women's
Health Initiative (WHI) estrogen plus progestin trial in May 1996. Of the
4894 eligible participants of the WHI study, 4532 (92.6%) postmenopausal women
free of probable dementia, aged 65 years or older, and recruited from 39 of
40 WHI clinical centers were enrolled in the WHIMS.InterventionParticipants received either 1 daily tablet of 0.625 mg of conjugated
equine estrogen plus 2.5 mg of medroxyprogesterone acetate (n = 2229), or
a matching placebo (n = 2303).Main Outcome MeasuresIncidence of probable dementia (primary outcome) and mild cognitive
impairment (secondary outcome) were identified through a structured clinical
assessment.ResultsThe mean (SD) time between the date of randomization into WHI and the
last Modified Mini-Mental State Examination (3MSE) for all WHIMS participants
was 4.05 (1.19) years. Overall, 61 women were diagnosed with probable dementia,
40 (66%) in the estrogen plus progestin group compared with 21 (34%) in the
placebo group. The hazard ratio (HR) for probable dementia was 2.05 (95% confidence
interval [CI], 1.21-3.48; 45 vs 22 per 10 000 person-years; P = .01). This increased risk would result in an additional 23 cases
of dementia per 10 000 women per year. Alzheimer disease was the most
common classification of dementia in both study groups. Treatment effects
on mild cognitive impairment did not differ between groups (HR, 1.07; 95%
CI, 0.74-1.55; 63 vs 59 cases per 10 000 person-years; P = .72).ConclusionsEstrogen plus progestin therapy increased the risk for probable dementia
in postmenopausal women aged 65 years or older. In addition, estrogen plus
progestin therapy did not prevent mild cognitive impairment in these women.
These findings, coupled with previously reported WHI data, support the conclusion
that the risks of estrogen plus progestin outweigh the benefits.

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Estrogen plus progestin and the incidence of dementia and mild cognitive impairment in postmenopausal women: the Women's Health Initiative Memory Study: a randomized controlled trial.

Impact of coexistent Alzheimer pathology on the natural history of dementia with Lewy bodies

The Frontal Assessment Battery in RLS patients with and without augmentation

Introduction Sarcopenia and Parkinson's disease are closely related diseases of the elderly population leading to progressive disability and nursing-dependent care. Objective The aim of this study was to estimate the prevalence of sarcopenia in PD patients with three different approaches: (1) the screening tool SARC-F, (2) EWGSOP-1 criteria, and (3) EWGSOP-2 criteria. Moreover, we aimed to evaluate the diagnostic accuracy of the screening tool SARC-F to detect sarcopenia according to the updated EWGSOP-2 criteria. Methods Eighty-one patients with Parkinson's disease aged 65 years and above were interviewed in a cross-sectional study at a tertiary referral center. All patients were screened with the SARC-F questionnaire and were evaluated for motor and non-motor symptoms, exercise, quality of life, and frailty. Muscle mass was assessed with bioelectrical impedance analysis, handgrip strength with a dynamometer, and gait speed was assessed with the 8-m walk test. EWGSOP-2 criteria were considered the gold standard to diagnose sarcopenia in our study. Results Eighty-one patients were evaluated (mean age: 73.82; SD 5.30). The prevalence of sarcopenia was 28.4% according to the EWGSOP-2 criteria. The concordance between EWGSOP-2 and EWGSOP-1 was poor (weighted kappa of 0.361[95% 0.164–0.557]). The sensitivity of the SARC-F screening test for detecting sarcopenia was 60.9%. The corresponding AUC in the ROC curve analysis showed 0.598 (0.462, 0.734 CI). The item assessing strength was found to have the highest sensitivity (69.6%). Conclusion Sarcopenia prevalence in patients with PD in Tirol, Austria is higher with EWGSOP-1 criteria compared to EWGSOP-2 criteria. The sensitivity and specificity of the SARC-F scale to detect sarcopenia in this population are poor.

Different assessment tools to detect sarcopenia in patients with Parkinson's disease

Parkinsonian disorders are characterized by both motor and nonmotor symptoms with varying degrees of treatment response and disability. While current conventional magnetic resonance imaging (MRI) methods are unable to confirm a diagnosis of idiopathic Parkinson disease, they may provide a means for identifying other atypical parkinsonian syndromes. This chapter will review the state of current structural MRI modalities, the structural imaging findings in various parkinsonian disorders and disease mimics, and the use of structural MRI as a biomarker of neurodegeneration. The discussion will also provide insights into the integration of high-field MRI and multimodal imaging to future clinical practice.

Structural MRI in Idiopathic Parkinson Disease and Parkinsonism

We read with interest the article by Buchman et al.,1 which reported that depressive symptoms, neuroticism, urinary incontinence, sleep complaints, and chronic health conditions were associated with incident parkinsonism (48.2% over 5 years) in the elderly. We previously reported on incidence and risk factors of mild parkinsonian signs, a similar concept to possible parkinsonism,1 in the cohort of the prospective population-based Bruneck Study of 2005.2 We now present an analysis of risk factors for parkinsonism according to the definition used by Buchman et al. in this population. Of 393 participants without parkinsonism at baseline undergoing 5-year follow-up, a markedly lower proportion of 16.0% (95% confidence interval [CI] 12.7%–20.0%) developed incident parkinsonism (excluding participants developing secondary parkinsonism). A logistic regression analysis adjusted for age and sex revealed that, out of single markers for prodromal Parkinson disease as defined per movement disorder society research criteria,3 assessed in the Bruneck study,4 substantia nigra hyperechogenicity on transcranial sonography (odds ratio 1.99; 95% CI 1.10–3.62, p = 0.024), probable REM sleep behavior disorder (6.88; 95% CI 1.10–43.10, p = 0.039), olfactory loss (1.96; 95% CI 1.01–3.81, p = 0.047), urinary dysfunction (5.15; 95% CI 1.65–16.14, p = 0.005), and depression/anxiety (2.85; 95% CI 1.28–6.36, p = 0.011) were significantly associated with incident parkinsonism, thus confirming and expanding the findings of Buchman et al.

Klaus Seppi

Papers

Impact of coexistent Alzheimer pathology on the natural history of dementia with Lewy bodies

The Frontal Assessment Battery in RLS patients with and without augmentation

Different assessment tools to detect sarcopenia in patients with Parkinson's disease

Structural MRI in Idiopathic Parkinson Disease and Parkinsonism

Letter re: Incident parkinsonism in older adults without Parkinson disease.