Phenoconversion in PPMI

Slides:



Advertisements
Similar presentations
Medium-term prognosis of an incident cohort of people with Parkinson’s and their carers vs a community-based control group Carl Counsell.
Advertisements

Parkinson’s Disease (PD)
Frontotemporal Dementia
Parkinson’s Disease Dr Rachel Cary, Warwick Hospital.
PRoBaND Parkinson’s Repository of Biosamples and Networked Datasets History Hypotheses Overview Linkage to other studies Funded by Parkinson’s UK Dr Donald.
Tracking the East Midlands contribution to PD-PROBAND Nin Bajaj Clinical Director NPF International Centre of Excellence in PD, East Midlands Trent CLRN.
Clinical trials with DeNDRoN in the North East Dr Margaret Piggott Data and Communications Manager Dementias and Neurodegenerative.
Knowledge and Attitudes Toward Genetic Testing in Parkinson’s Disease Dana Lundberg 2006.
Dementia with Lewy Bodies
Alexander I. Tröster, Ph.D. Department of Neurology
Is it a neurodegenerative brain disorder that progresses slowly in most people.
Alzheimer’s Disease Neuroimaging Initiative Neuropathology Core John C. Morris, MD Nigel J. Cairns, PhD, FRCPath Erin Franklin, MS Presented by: Beau Ances,
Parkinson ’ s disease. Function Anatomy of Parkinson ’ s Disease.
LATE NEUROLOGICAL SEQUELS AFTER ACUTE POISONING WITH DIMETHOATE Niko Bekarovski, B. Pavlovski, N.Popovski, I.Jurukov Clinic of Toxicology and Urgent Internal.
Dementia Update October 1, 2013 Dylan Wint, M.D. Cleveland Clinic Lou Ruvo Center for Brain Health Las Vegas, Nevada.
Catherine Kober Margaret Johnson Martin Fisher Caroline Sabin On behalf of UK-CHIC BHIVA/BASHH Manchester 2010 Non-uptake of HAART among patients with.
Antipsychotic drugs. Anti-psychotic drugs The CNS functionally is the most complex part of the body, and understanding drug effects is difficult Understanding.
Parkinson’s Plus By: Glen Estrosos.
Joohi Jimenez-Shahed, MD Assistant Professor of Neurology Baylor College of Medicine 8 th Annual IMHO Convention April 30, 2011 – Houston, TX Parkinson’s.
Treatment of Parkinson Disease David Tran, 2013 Mercer University PharmD Candidate.
Is It Essential Tremor or a Parkinsonian Syndrome? Diagnostic Considerations in Primary Care Faculty Tanya Simuni, MD Director, Parkinson's Disease and.
Impact of Highly Active Antiretroviral Therapy on the Incidence of HIV- encephalopathy among perinatally- infected children and adolescents. Kunjal Patel,
CU-1 Summary of Neuropathological and Clinical Features of PDD Clive Ballard, MD Professor of Age Related Diseases Institute of Psychiatry King’s College.
Group 5.  100+  Precise roles not known  3 categories.
HOW TO EXAMINE PATIENTS WITH DEMENTIA Serge Gauthier, MD, FRCPC McGill Centre for Studies in Aging Douglas Mental Health Research Institute.
 Parkinson’s Disease (PD) -progressive neurodegenerative disease affecting motor ability -third most common neurologic disorder of older adults.
CC-1 Benefit-Risk Assessment Murat Emre, MD Professor of Neurology Istanbul Faculty of Medicine Department of Neurology Behavioral Neurology and Movement.
Improvement of life quality and non motor symptoms relief in patients with advanced Parkinson's disease. Natalia Prican Andra Oltean Doctor Jozsef Attila.
PARKINSON’S DISEASE BY: NICOLE MABARDI & SHAINA JOSEPH.
Assessment and Diagnosis of Dementia Dr Alison Haddow.
Α-synuclein transgenic mouse models of Parkinson’s disease Michelle Maurer December 2015.
Conversion Disorder (The Modern Hysteria)*
Parkinson’s Disease in Africa Jacques Doumbé MD Department of Neurology Douala Laquintinie Hospital Cameroon.
Date of download: 6/2/2016 Copyright © 2016 American Medical Association. All rights reserved. From: Pharmacological Treatment of Parkinson Disease: A.
© 2006 American Academy of Neurology Practice Parameter: Diagnosis and Prognosis of New Onset Parkinson Disease (An Evidence-Based Review) American Academy.
Reflections on animal models of neurological disorders Marie-Francoise Chesselet UCLA
My Symptom/s: (What You’re Feeling or Seeing) Your Name Here Class Hour Here Enter the name of your symptoms here (Insert a picture of your symptoms here)
59 year old man w visual hallucinations
Dementia with Lewy Bodies
2. IRCSS, Institute of Neurological Sciences, Bologna, Italy
Basics of New PHASE Reporting
NISCHR Academic Health Science Collaboration Launch
ULTRASONOGRAPHY AND MR IMAGING IN PROGRESSIVE SUPRANUCLEAR PALSY
Table 1. Summary of Study Measures
Dementia: from molecules to minds
Table 2. Data Sharing for (Reporting Period)
The evolving differential diagnosis of Parkinson’s disease
“The effects of chronic changes to the functioning of the nervous system due to interference to neurotransmitter function, illustrated by the role of Dopamine.
III. Parkinson Disease.
Parkinson's disease Parkinson's disease (PD) is the second-most common
FINAL Recommendations
PPMI in the Medical Literature
Parkinson’s progression markers initiative
Elham Rastegari University of Nebraska at Omaha
PPMI Beyond 2018.
Figure 4 Cerebrospinal fluid levels of neurofilament light chain
Atypical Parkinsonian Syndromes
Can we find dementia in the skin?
CSF αlpha-synuclein is not a good diagnostic and progression marker (alone)
Repositories Lunch Meeting, Day 1
PPMI – GOALS 2019 Ken Marek PPMI Annual Meeting May 3, 2018
Figure 2 Diagnostic scheme for MSA
DAT Imaging in a cohort of p.A53T SNCA PD patients versus typical PD
Decision Trees Showcase
Gait Sub study Anat Mirelman PhD.
The Evolution of Genetics: Alzheimer’s and Parkinson’s Diseases
supported study by Dr. Heiko Gaßner and Dr. Cecilia Raccagni
Women and Parkinson’s Disease
HOW DOES EXPERIENCE AFFECT BEHAVIOUR AND MENTAL PROCESSES?
Presentation transcript:

Phenoconversion in PPMI

outline Definitions of phenoconversion Characteristics of phenoconverters

Defining phenoconversion in pppmi Karl

Definition of phenoconversion Data-driven Diagnostic codes …biomarkers… Karl

Data-driven Karl

Data-driven Diagnostic Features Questionnaire responses: Bradykinesia present and typical for PD (Question 7.1=1) and at least one of the following: Resting tremor present and typical for PD (Question 5.1=1) Rigidity present and typical for PD (Question 6.1=1) Postural/gait disturbances present and typical for PD (Question 8.1=1) Karl

Diagnostic codes RBD=23 Hyposmia=23 Karl

Diagnostic codes Asymptomatic genetic=17 Karl

Diagnostic codes Karl

Diagnostic codes Karl

Diagnostic codes Considerations regarding code 97 (see next slide) Karl

Diagnostic codes Notes to site PIs: “Other” (code 97) should not be used to indicate non-specific exam findings (like “tremor NOS”) Code LRRK2-associated PD as idiopathic PD Comorbid conditions should be listed in medical conditions log even if they are neurologic: Multiple Sclerosis Tremor NOS Peripheral Neuropathy Karl

Diagnostic codes Notes to site PIs: Be mindful of code “fluctuations”, especially once a neurodegenerative parkinsonism code is assigned Karl do we want to have a slide like this? Feel free to delete

Biomarker-defined conversion Future work will aim to define biomarker-based algorithms to identify phenoconversion including but not limited to: Imaging CSF Questionnaire responses Smell test Exam findings Wearable data Karl

Characteristics of phenoconverters in ppmi

Converters vs. nonconverters When conversion is defined as code=24: “Prodromal Motor PD” or change to a neurodegenerative parkinsonism 60 cases have “converted” 32 (53.3%) Genetic cohort 12 (20.0%) Hyposmia cohort 16 (26.7%) RBD cohort NOTE: mean follow-up time 34.2 months in converters vs. 19.8 months in non-converters (p<0.0001)

Converters vs. nonconverters

Converters vs. nonconverters

Converters vs. nonconverters

Converters vs. nonconverters When conversion is defined as change to a neurodegenerative parkinsonism code only: PD, PSP, MSA, DLB, CBS, FTD 23 cases (of the 60) have “converted” to diagnosed neurodegenerative parkinsonism 5 (21.7%) Genetic cohort 7(30.4%) Hyposmia cohort 11(47.8%) RBD cohort 19 PD, 3 DLB, 1 PSP (1 PD later changed to MSA) mean follow-up time 35 months in converters vs. 19.8 months in non-converters (p<0.0001)

Converters vs. nonconverters

Converters vs. nonconverters

Summary Clinical features different between converters and non-converters include age, olfactory function, neuropsychiatric and autonomic symptoms, RBD and motor abnormalities Striatal SSBR at baseline is associated with conversion Total CSF α-syn is not associated with conversion, though perhaps change in CSF α-syn is of predictive value

Characteristics of phenoconverters in the Rbd cohort

RBD Converters vs. nonconverters RBD cohort: n=38 RBD symptom duration: mean 9.94 years (range 0.38-30.36 years) RBD duration since diagnosis: mean 2.92 years (range 0.04-11.77) Recruitment heavily stratified toward DaTscan SPECT deficit (~90%:~10%)

RBD Converters vs. nonconverters RBD cohort: 11 converters vs. 27 non-converters Mean follow-up time 40.91 mo in converters vs. 37.33 mo in non-converters (p=0.047) 7 converted to PD 3 to DLB 1 to MSA (first coded as PD then after 4 visits to MSA)

RBD Converters vs. nonconverters

RBD Converters vs. nonconverters

RBD Converters vs. nonconverters

Summary Motor abnormalities are greater among converters; neuropsychiatric symptoms and autonomic symptoms worse Even among a group selected based on DaT binding, DaT measures are strongly associated with conversion

Questions/ comments