Appendectomy and risk of Parkinson's disease: A nationwide cohort study with more than 10 years of follow-up

Here the authors actually observe the opposite to their starting hypothesis... as always an association does not mean that appendicectomy causes PD as such... it may be that there are other confounding factors that were not measured (residual confounding), something for example that increases both the risk of inflammation of the appendix and also increases the risk of PD...

Mov Disord. 2016 Sep 13. doi: 10.1002/mds.26761. [Epub ahead of print]

Svensson E, Horváth-Puhó E, Stokholm MG, Sørensen HT, Henderson VW, Borghammer P.

http://onlinelibrary.wiley.com/doi/10.1002/mds.26761/abstract

OBJECTIVES:

The appendix may be a key site for the initiation of Parkinson's disease (PD) pathology. We examined the hypothesis that appendectomy is associated with lower PD risk.

METHODS:

We used Danish medical and administrative registries to construct a cohort of all patients in Denmark with an operation code of appendectomy during 1980-2010 (n = 265,758) and a matched general population comparison cohort (n = 1,328,790). Using Cox regression, we computed hazard ratios and corresponding 95% confidence intervals for PD, adjusting for potential confounders and stratifying on age at appendectomy (≤45 years / > 45 years), sex, and follow-up time.

RESULTS:

During follow-up ( > 10 years), PD incidence was 0.19 and 0.15 per 1,000 person-years at risk in the appendectomy cohort and in the general population comparison cohort, respectively, yielding a slightly increased risk of PD (adjusted hazard ratio = 1.14; 95% confidence interval 1.03-1.27). Findings were consistent after more than 20 years of follow-up and when stratified on age of appendectomy and sex.

CONCLUSION:

Appendectomy was associated with a small increase in PD risk 10 or more years after surgery. © 2016 International Parkinson and Movement Disorder Society.

Predicting first fall in newly diagnosed Parkinson's disease: Insights from a fall-naïve cohort

Increased fracture risk in PD has been reported multiple times on this blog... falls are one of the key precipitants of fractures and patients with PD are at high risk... here the authors report multiple predictors of falls... we should be looking out for these things in the clinic to try and prevent adverse outcomes...

Mov Disord. 2016 Sep 13. doi: 10.1002/mds.26742. [Epub ahead of print]

Lord S, Galna B, Yarnall AJ, Coleman S, Burn D, Rochester L.

http://onlinelibrary.wiley.com/doi/10.1002/mds.26742/abstract;jsessionid=34CD352381C016ED6CFECDD9E175D8DE.f03t04

BACKGROUND:

Falls are common and associated with reduced independence and mortality in Parkinson's disease. Previous research has been conducted on falls-prevalent or advanced disease cohorts.

OBJECTIVE:

This study identifies risk factors for first fall for 36 months in a newly diagnosed, falls-naïve cohort.

METHODS:

A total of 121 consecutive Parkinson's disease patients were recruited. Falls data were collected prospectively during 36 months from diagnosis via monthly falls diaries and telephone follow-up for 117 participants. Assessment comprised a comprehensive battery of clinical, gait, and cognitive measures. Significant predictors were identified from decision-tree analysis and survival analysis with time to first fall during 36 months as the dependent variable.

FINDINGS:

At baseline, 26 (22%) participants reported retrospective falls. At 36 months, the remaining cohort (n = 91) comprised 47 fallers (52%) and 30 (33%) nonfallers and 14 (15%) participants with incomplete diaries. Fallers presented with a significantly higher disease severity, poorer ability to stand on one leg, slower gait speed, increased stance time variability, and higher swing time asymmetry. Median time to first fall was 847 days. Gait speed, stance time, and Hoehn & Yahr III stage emerged as significant predictors of first fall, hazard ratio 3.44 (95% confidence interval [CI] 1.58 to 7.48), 3.31(95% CI 1.40 to 5.65), and 1.97 (95% CI 1.40 to 7.80), respectively. The hazard ratio for risk factors combined was 7.8 (CI 2.79 to 21.8).

CONCLUSIONS:

Interventions that target gait deficit and postural control in early Parkinson's disease may limit the potential for first fall. © 2016 International Parkinson and Movement Disorder Society.

Loss of independence in early Parkinson disease: A 5-year population-based incident cohort study

The things that cause patients to be admitted to long term care facilities are not surprising... each of these are considered independent outcomes in their own right. An important observation here is the irreversible nature of dependency... I suspect that relatively small changes can prompt a switch from independence to dependence, such as prolonged hospital admission or long bone fracture...

Neurology. 2016 Sep 2. pii: 10.1212/WNL.0000000000003213. [Epub ahead of print]

Bjornestad A, Tysnes OB, Larsen JP, Alves G.

OBJECTIVE:

To determine the risk, predictors, and prognosis of independence loss and institutionalization in patients with early Parkinson disease (PD).

METHODS:

We conducted a prospective population-based 5-year longitudinal study following 189 patients with incident PD and 174 controls matched for age, sex, and comorbidity. Health care status was assessed repeatedly with standardized interviews.

RESULTS:

More newly diagnosed patients with PD (15.9%) than controls (5.7%) were dependent in activities of daily living at baseline (relative risk [RR] 2.8, p = 0.004). During follow-up, 40.9% of the initially independent patients lost their independence vs 9.1% of controls (RR 4.5, p < 0.001). Higher age, shorter symptom duration, increasing motor severity, and presence of mild cognitive impairment at PD diagnosis independently predicted independence loss during follow-up. Dependency was irreversible in most (>95%) patients. Long-term care facility placement was needed in 8.8% of patients vs 0.6% of controls (RR 15.4, p = 0.001). More patients with PD admitted to long-term care facilities were fallers (RR 4.8, p < 0.001), had hallucinations (RR 4.4, p = 0.001), or had dementia (RR 4.2, p < 0.001) than home-dwelling patients. Once admitted to a long-term care facility, the age-adjusted RR for death during the study period was 5.5 (p = 0.002) vs patients never admitted and 25.1 (p < 0.001) vs controls.

CONCLUSIONS:

Patients with early PD face a substantially greater risk of independence loss and institutionalization than well-matched controls. Independence loss is irreversible in most patients and represents a sinister prognostic factor in early PD. These findings have implications for patient management and health care planning.

Multicenter Assessment of Immunohistochemical Methods for Pathological Alpha-Synuclein in Sigmoid Colon of Autopsied Parkinson's Disease and Control Subjects

This series of papers from these opinion leaders in the field will be very important... if gut biomarkers are to be found, consensus on an approach or series of approaches is absolutely vital.

J Parkinsons Dis. 2016 Aug 31. [Epub ahead of print]

Beach TG, Corbillé AG, Letournel F, Kordower JH, Kremer T, Munoz DG, Intorcia A, Hentz J, Adler CH, Sue LI, Walker J, Serrano G, Derkinderen P.

http://content.iospress.com/articles/journal-of-parkinsons-disease/jpd160888

BACKGROUND:

Conflicting results from studies of Lewy-type α-synucleinopathy (LTS) in colonic biopsies of subjects with Parkinson's disease (PD) prompted a two-part multicenter assessment. The first assessment, now published (Acta Neuropathol Commun 4 : 35, 2016), examined archived colonic biopsies and found that none of the tested methods was adequately sensitive or specific.

OBJECTIVE:

As the amount of nervous tissue in typical colonic biopsies may be insufficient, and the clinical diagnosis of PD not completely accurate, the objective of the current study was to use instead full-thickness sections of sigmoid colon from autopsy-proven PD and normal subjects.

METHODS:

Seven different immunohistochemical (IHC) methods were used, employing five different primary antibodies and four different combinations of epitope exposure and signal development protocols. Specific staining was defined as being restricted to morphological features consistent with neuronal elements. Stained slides from each subject were independently categorized as being positive or negative for LTS, and their density semi-quantitatively graded, by four raters blinded to diagnosis.

RESULTS:

Agreement and mean diagnostic performance varied markedly between raters. With the two most accurate raters, 5 methods achieved diagnostic accuracies of 70% or greater; one method had 100% accuracy and 100% inter-rater agreement. The submucosa had the highest prevalence of pathological LTS staining, followed by the muscularis and mucosa.

CONCLUSIONS:

The major conclusion of this study is that, when sufficient submucosa and LTS is present, and when specific staining is defined as being consistent with neuronal morphology, adequately-trained raters may reliably distinguish PD colon from control using suitable IHC methods.

Impulsive-compulsive behaviors in parkin-associated Parkinson disease

Another slow week updating the blog... but this is important work. Really interesting to see that the ICB predated the diagnosis of PD in a number of the cases. As well has further characterising parkin clinical features, I think this has the potential to tell us more about the pathological substrate of ICBs given that parkin cases tend to have restricted pathology compared with idiopathic PD...

Neurology. 2016 Sep 2. pii: 10.1212/WNL.0000000000003177. [Epub ahead of print]

Morgante F, Fasano A, Ginevrino M, Petrucci S, Ricciardi L, Bove F, Criscuolo C, Moccia M, De Rosa A, Sorbera C, Bentivoglio AR, Barone P, De Michele G, Pellecchia MT, Valente EM.

OBJECTIVE:

The aim of this multicenter, case-control study was to investigate the prevalence and severity of impulsive-compulsive behaviors (ICBs) in a cohort of patients with parkin-associated Parkinson disease (PD) compared to a group of patients without the mutation.

METHODS:

We compared 22 patients with biallelic parkin mutations (parkin-PD) and 26 patients negative for parkin, PINK1, DJ-1, and GBA mutations (PD-NM), matched for age at onset, disease duration, levodopa, and dopamine agonist equivalent daily dose. A semistructured interview was used to diagnose each of the following ICBs: compulsive sexual behavior, compulsive buying, binge eating, punding, hobbyism, and compulsive medication use. The Questionnaire for Impulsive-Compulsive Disorders in Parkinson's Disease-Rating Scale (QUIP-RS) was adopted to rate ICB severity.

RESULTS:

Frequency of patients with at least one ICB was comparable between parkin-PD and PD-NM. Nevertheless, when analyzing the distribution of specific ICBs, a higher frequency of compulsive shopping, binge eating, and punding/hobbyism was found in the parkin-PD group. Compared to PD-NM, parkin-PD patients with ICB had younger onset age and higher frequency of smokers; in 5 patients, ICB had predated PD onset. Total and partial (compulsive buying, compulsive sexual behavior, binge eating, hobbyism/punding) QUIP-RS scores were higher in patients with parkin-PD compared to patients with PD-NM. Logistic regression analysis showed that the presence of parkin mutations was associated with smoking status and higher QUIP-RS total score.

CONCLUSIONS:

Our data expand the parkin-associated phenotypic spectrum demonstrating higher frequency and severity of specific ICBs, and suggesting an association between the parkin genotype, smoking status, and ICB severity.

Comparing the Incidence of Falls/Fractures in Parkinson's Disease Patients in the US Population

This is a topic that I have looked at in the past... it adds further support to the results of our systematic review and meta-analysis on the subject... I cannot understand why the authors present combined results for falls and fractures (they are different) but in the main body of the paper (via the link) they present them separately.

PLoS One. 2016 Sep 1;11(9):e0161689. doi: 10.1371/journal.pone.0161689. eCollection 2016.

Kalilani L, Asgharnejad M, Palokangas T, Durgin T.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161689

Patients with Parkinson's disease (PD) may experience falls and/or fractures as a result of disease symptoms. There are limited data available from long-term studies estimating the incidence of falls/fractures in patients with PD. The objective was to compare the incidence rate of falls/fractures in PD patients with non-PD patients in a US population. This was a retrospective study using a US-based claims database (Truven Health MarketScan®) that compared the incidence rate of falls/fractures in PD subjects with non-PD subjects. The study period included the 12 months prior to index date (defined as earliest PD diagnosis [International Classification of Diseases, Ninth Revision, Clinical Modification code 332.0]) and a postindex period to the end of data availability. Fractures were defined by inpatient/outpatient claims as a principal or secondary diagnosis and accompanying procedure codes during the postindex period. Incidence rates and 95% CIs for falls/fractures were calculated as the number of events per 10,000 person-years of follow-up using negative binomial or Poisson regression models. Twenty-eight thousand two hundred and eighty PD subjects were matched to non-PD subjects for the analysis (mean [SD] age, 71.4 [11.8] years; 53% male). A higher incidence rate (adjusted for comorbidities and medications) of all fall/fracture cases and by fall and fracture types was observed for PD subjects versus non-PD subjects; the overall adjusted incidence rate ratio comparing PD to non-PD subjects was 2.05; 95% CI, 1.88-2.24. The incidence rate of falls/fractures was significantly higher in subjects with PD compared with non-PD subjects in a US population.

Short chain fatty acids and gut microbiota differ between patients with Parkinson's disease and age-matched controls

To my knowledge this is the third paper now looking at the gut microbiome and again it demonstrates differences between patients and controls... however my recollection is that the previous papers found different results to one another... a key thing to determine is whether these changes are cause or effect of PD and indeed constipation PD... i.e. does a slowing of gut transit in PD alter the intestinal microbiome or does a change in microbiome drive disease in PD via the gut??? Testing these hypotheses in pre-diagnostic cohorts may be one way to uncover this....

Parkinsonism Relat Disord. 2016 Aug 26. pii: S1353-8020(16)30323-6. doi: 10.1016/j.parkreldis.2016.08.019. [Epub ahead of print]

Unger MM, Spiegel J, Dillmann KU, Grundmann D, Philippeit H, Bürmann J, Faßbender K, Schwiertz A, Schäfer KH.

http://www.prd-journal.com/article/S1353-8020(16)30323-6/abstract

BACKGROUND:

Patients with Parkinson's disease (PD) frequently have gastrointestinal symptoms (e.g. constipation) and exhibit the PD-typical pathohistology in the enteric nervous system (ENS). Both, clinical symptoms and pathohistological changes in the ENS occur at early stages and can precede the motor manifestations of PD. Two recent studies reported an association between changes in gut microbiota composition and PD. We hypothesized that alterations in gut microbiota might be accompanied by altered concentrations of short chain fatty acids (SCFA), one main metabolic product of gut bacteria.

METHODS:

We quantitatively analyzed SCFA concentrations (using gas chromatography) and microbiota composition (using quantitative PCR) in fecal samples of 34 PD patients and 34 age-matched controls.

RESULTS:

Fecal SCFA concentrations were significantly reduced in PD patients compared to controls. The bacterial phylum Bacteroidetes and the bacterial family Prevotellaceae were reduced, Enterobacteriaceae were more abundant in fecal samples from PD patients compared to matched controls.

CONCLUSIONS:

Our study confirms the recently reported association between PD and the abundance of certain gut microbiota and shows a reduction in fecal SCFA concentrations (one main metabolic product of certain gut bacteria). The reduction in SCFA might, theoretically, induce alterations in the ENS and contribute to gastrointestinal dysmotility in PD. Prospective longitudinal studies in subjects at risk for PD are required to further elucidate the causal role of gut microbiota and microbial products in the development of PD and PD-associated dysmotility.

Association of GBA Mutations and the E326K Polymorphism With Motor and Cognitive Progression in Parkinson Disease

There are now many lines of evidence to suggest that E326K has a role in determining the course of PD. Even though it is not a recognised cause of Gaucher's disease, it has come up frequently in genetic studies looking at PD-related GBA variants and functional work supports the claim... my experience fits with the observations in this study and those of others... the tendency is towards akinetic rigidity, gait problems and cognitive impairment, rather than a tremor predominant form of PD...

JAMA Neurol. 2016 Aug 29. doi: 10.1001/jamaneurol.2016.2245. [Epub ahead of print]

Davis MY, Johnson CO, Leverenz JB, Weintraub D, Trojanowski JQ, Chen-Plotkin A, Van Deerlin VM, Quinn JF, Chung KA, Peterson-Hiller AL, Rosenthal LS, Dawson TM, Albert MS, Goldman JG, Stebbins GT, Bernard B, Wszolek ZK, Ross OA, Dickson DW, Eidelberg D, Mattis PJ, Niethammer M, Yearout D, Hu SC, Cholerton BA, Smith M, Mata IF, Montine TJ, Edwards KL, Zabetian CP.

http://archneur.jamanetwork.com/article.aspx?articleid=2546252

IMPORTANCE:

Parkinson disease (PD) is heterogeneous in symptom manifestation and rate of progression. Identifying factors that influence disease progression could provide mechanistic insight, improve prognostic accuracy, and elucidate novel therapeutic targets.

OBJECTIVE:

To determine whether GBA mutations and the E326K polymorphism modify PD symptom progression.

DESIGN, SETTING, AND PARTICIPANTS:

The entire GBA coding region was screened for mutations and E326K in 740 patients with PD enrolled at 7 sites from the PD Cognitive Genetics Consortium. Detailed longitudinal motor and cognitive assessments were performed with patients in the on state.

MAIN OUTCOMES AND MEASURES:

Linear regression was used to test for an association between GBA genotype and motor progression, with the Movement Disorder Society-sponsored version of the Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) score at the last assessment as the outcome and GBA genotype as the independent variable, with adjustment for levodopa equivalent dose, sex, age, disease duration, MDS-UPDRS III score at the first assessment, duration of follow-up, and site. Similar methods were used to examine the association between genotype and tremor and postural instability and gait difficulty (PIGD) scores. To examine the effect of GBA genotype on cognitive progression, patients were classified into those with conversion to mild cognitive impairment or dementia during the study (progression) and those without progression. The association between GBA genotype and progression status was then tested using logistic regression, adjusting for sex, age, disease duration, duration of follow-up, years of education, and site.

RESULTS:

Of the total sample of 733 patients who underwent successful genotyping, 226 (30.8%) were women and 507 (69.2%) were men (mean [SD] age, 68.1 [8.8] years). The mean (SD) duration of follow-up was 3.0 (1.7) years. GBA mutations (β = 4.65; 95% CI, 1.72-7.58; P = .002), E326K (β = 3.42; 95% CI, 0.66-6.17; P = .02), and GBA variants combined as a single group (β = 4.01; 95% CI, 1.95-6.07; P = 1.5 × 10-4) were associated with a more rapid decline in MDS-UPDRS III score. Combined GBA variants (β = 0.38; 95% CI, 0.23-0.53; P = .01) and E326K (β = 0.64; 95% CI, 0.43-0.86; P = .002) were associated with faster progression in PIGD scores, but not in tremor scores. A significantly higher proportion of E326K carriers (10 of 21 [47.6%]; P = .01) and GBA variant carriers (15 of 39 [38.5%]; P = .04) progressed to mild cognitive impairment or dementia.

CONCLUSIONS AND RELEVANCE:

GBA variants predict a more rapid progression of cognitive dysfunction and motor symptoms in patients with PD, with a greater effect on PIGD than tremor. Thus, GBA variants influence the heterogeneity in symptom progression observed in PD.

Correlation of Quantitative Motor State Assessment Using a Kinetograph and Patient Diaries in Advanced PD: Data from an Observational Study

The PKG is one of the better examples of wearable tech that is available for monitoring PD. Clearly there remains some improvements to be made, but it has already entered the clinical arena and is being used to supplement patient care. Other studies that used it showed improvements in total 'On' time and reductions in 'dyskinesia time'. One problem with the present study is that the home diary method is not without its flaws. Sometimes it is hard to marry up exactly what one sees objectively and what the patient experiences subjectively...

PLoS One. 2016 Aug 24;11(8):e0161559. doi: 10.1371/journal.pone.0161559. eCollection 2016.

Ossig C, Gandor F, Fauser M, Bosredon C, Churilov L, Reichmann H, Horne MK, Ebersbach G, Storch A.

http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161559

INTRODUCTION:

Effective management and development of new treatment strategies for response fluctuations in advanced Parkinson's disease (PD) largely depends on clinical rating instruments such as the PD home diary. The Parkinson's kinetigraph (PKG) measures movement accelerations and analyzes the spectral power of the low frequencies of the accelerometer data. New algorithms convert each hour of continuous PKG data into one of the three motor categories used in the PD home diary, namely motor Off state and On state with and without dyskinesia.

OBJECTIVE:

To compare quantitative motor state assessment in fluctuating PD patients using the PKG with motor state ratings from PD home diaries.

METHODS:

Observational cohort study on 24 in-patients with documented motor fluctuations who completed diaries by rating motor Off, On without dyskinesia, On with dyskinesia, and asleep for every hour for 5 consecutive days. Simultaneously collected PKG data (recorded between 6 am and 10 pm) were analyzed and calibrated to the patient's individual thresholds for Off and dyskinetic state by novel algorithms classifying the continuous accelerometer data into these motor states for every hour between 6 am and 10 pm.

RESULTS:

From a total of 2,040 hours, 1,752 hours (87.4%) were available for analyses from calibrated PKG data (7.5% sleeping time and 5.1% unclassified motor state time were excluded from analyses). Distributions of total motor state hours per day measured by PKG showed moderate-to-strong correlation to those assessed by diaries for the different motor states (Pearson's correlations coefficients: 0.404-0.658), but inter-rating method agreements on the single-hour-level were only low-to-moderate (Cohen's κ: 0.215-0.324).

CONCLUSION:

The PKG has been shown to capture motor fluctuations in patients with advanced PD. The limited correlation of hour-to-hour diary and PKG recordings should be addressed in further studies.

Medium-term prognosis of an incident cohort of parkinsonian patients compared to controls

This is a well conducted study and there are surprisingly few of these high-quality incident PD cohorts in the world... the survival times are worryingly low at first glance and much shorter than we tend to quote. The authors draw attention to this but much of it will be driven by age. The average age in the incident cases is pretty high at 75 years old... the average age of diagnosis of PD is usually quoted as 65 years old. Playing devils advocate, for PD at least, the average survival of 6 years means that patients tend to die around the normal UK life expectancy mark (late 70's, early 80's)... 

The other thing that varies tremendously is access to high quality care around the UK... the Parkinson's UK Excellence Network is trying to achieve equal care for all...

Parkinsonism Relat Disord. 2016 Aug 12. pii: S1353-8020(16)30307-8. doi: 10.1016/j.parkreldis.2016.08.010. [Epub ahead of print]

Fielding S, Macleod AD, Counsell CE.

http://www.sciencedirect.com/science/article/pii/S1353802016303078

BACKGROUND:

The best data on prognosis comes from population-based incident cohorts but few such cohorts exist for Parkinson's disease and atypical parkinsonism.

METHODS:

The PINE study is a prospective follow-up study of an incident cohort of people with degenerative or vascular parkinsonism and age-sex matched controls. Participants have annual follow-up from diagnosis until death with review of primary/secondary care records and linkage to the UK death register. Data are collected on survival, disability (dependency on others for activities of daily living) and institutionalization. Research criteria are used to guide the clinical diagnosis, which is updated annually. We compared all-cause mortality, disability and institutionalization in patients (subdivided by diagnosis) and controls, adjusted for important confounders.

RESULTS:

323 incident parkinsonian patients (199 Parkinson's disease, 124 atypical parkinsonism, mean age at diagnosis 75yrs) and 262 controls (mean age 75yrs) had 1349 and 1334 person-years follow-up respectively (maximum follow-up 10 years). All outcomes were worse in parkinsonian patients than controls, especially in atypical parkinsonism (adjusted mortality hazards ratios Parkinson's disease 2.49, 95%CI 1.72-3.58, atypical parkinsonism, 6.85, 95%CI 4.78-9.81). Median survival times for Parkinson's disease and atypical parkinsonism were 7.8 and 2.7 years respectively but were very age-dependent. At three years the rates of death or dependency were controls 21%, Parkinson's disease 46%, atypical parkinsonism 96% whilst overall institutionalization rates were 5%, 15% and 55% respectively.

CONCLUSION:

The prognosis of Parkinson's disease and atypical parkinsonism in this unselected incident cohort was significantly worse than previously reported. This has important implications for patient management.

Copyright © 2016 The Authors. Published by Elsevier Ltd.. All rights reserved.

Cerebral peduncle angle: Unreliable in differentiating progressive supranuclear palsy from other neurodegenerative diseases

Not to be confused with the cerebellar pontine angle... this CPA (the cerebral peduncle angle) is seen in axial MRI imaging... in PSP the angle is said to widen, which along with midbrain atrophy, gives the appearance of Mickey Mouse's face... see below

Parkinsonism Relat Disord. 2016 Aug 11. pii: S1353-8020(16)30306-6. doi: 10.1016/j.parkreldis.2016.08.009. [Epub ahead of print]

Tipton PW, Konno T, Broderick DF, Dickson DW, Wszolek ZK.

http://www.prd-journal.com/article/S1353-8020(16)30306-6/abstract

INTRODUCTION:

The significant symptom overlap between progressive supranuclear palsy (PSP) and other parkinsonian neurodegenerative diseases frequently results in misdiagnosis. However, neuroimaging can be used to quantify disease-related morphological changes and specific markers. The cerebral peduncle angle (CPA) has been shown to differentiate clinically diagnosed PSP from other parkinsonian diseases but this result has yet to be confirmed in autopsy-proven disease.

METHODS:

Magnetic resonance imaging (MRI) scans were obtained for 168 patients representing 69 medical facilities. Following randomization, the images were divided into two groups (Type 1 and Type 2) based upon midbrain morphological differences. Two readers were blinded and independently measured the CPA of 146 patients with autopsy-proven progressive supranuclear palsy (PSP; n = 54), corticobasal degeneration (n = 16), multiple system atrophy (MSA; n = 11) and Lewy body disease (n = 65).

RESULTS:

Applying two separate measurement techniques revealed no statistically significant differences in CPA measurements among any study groups regardless of classification measurement approach. The interobserver agreement showed significant differences in measurements using the Type 2 approach.

CONCLUSION:

Measuring the CPA on MRI is not a reliable way of differentiating among patients with PSP, corticobasal degeneration, MSA, or Lewy body disease.

The second image is taken from Fatterpekar et al. AJR 2015