Targeting Monoaminergic Neuronal Networks in the Parkinsonian Patients After Carbon Monoxide Intoxication
|ClinicalTrials.gov Identifier: NCT02138864|
Recruitment Status : Unknown
Verified May 2016 by chiungchihchang, Chang Gung Memorial Hospital.
Recruitment status was: Enrolling by invitation
First Posted : May 15, 2014
Last Update Posted : June 1, 2016
|Condition or disease||Intervention/treatment||Phase|
|Carbon Monoxide-induced Parkinsonism||Radiation: 18F-FP-(+)-DTBZ||Phase 3|
With the urbanization of Taiwanese society, there are increasing numbers of people committing suicide by charcoal burning, making carbon monoxide (CO) encephalopathy a new pandemic phenomenon. In CO related parkinsonism, the clinical features included gait disturbances, mask face, rigidities and small steps. From literature searches, the CO related parkinsonism is related to white matter damages or decline in dopamine innervations. From our previous research results, the CO related neuronal damages would started from reversible or progressive white matter demyelination. For some patients, axonopathy or gray matter atrophy developed and became irreversible. The neuronal networks in determining development of Parkinsonism required to be established.
In terms of neurotransmitter, most of the clinical data for Parkinsonism came from studies of idiopathic Parkinson's disease while the data of CO related Parkinsonism were limited to case reports. From neuropathology studies in idiopathic Parkinson's disease, dopamine deficits and decreased in monoamine transporters were observed well before the development of clinical features. Although there is linkage between CO related Parkinsonism and dopamine deficits, patients with CO intoxication had poor response to levodopa. The observation suggested the critical networks and neurotransmitters were still not well understood.
18F-FP-(+)-DTBZ is a newly developed nuclear medicine tracer for monoamine transporter. The study purpose is to determine the clinical values of 18F-FP-(+)-DTBZ in the diagnosis of Parkinsonism in patients with carbon monoxide intoxication, regional distribution and its correlation with clinical parameters. This is a three-year prospective research. For each patient, the PET will be arranged twice, with an interval of 18 months. The regional distribuation of 18F-FP-(+)-DTBZ in relation to Parkinsonism severity and regional reduction patterns longitudially will be assessed in order to understand the regional neurotoxicity and the functional progression.
|Study Type :||Interventional (Clinical Trial)|
|Estimated Enrollment :||25 participants|
|Intervention Model:||Single Group Assignment|
|Masking:||None (Open Label)|
|Official Title:||Targeting Monoaminergic Neuronal Networks in the Parkinsonian Patients After Carbon Monoxide Intoxication|
|Study Start Date :||August 2013|
|Estimated Primary Completion Date :||May 2016|
|Estimated Study Completion Date :||May 2016|
Experimental: 18F-FP-(+)-DTBZ only
PET tracer: 18F-FP-(+)-DTBZ
- Assess the regional decline in 18F-DTBZ uptake of Parkinsonism after carbon monoxide intoxication [ Time Frame: up to 3 years ]This study will assess the brain uptake and distribution of 18F-DTBZ in 25 carbon monoxide intoxication patients with Parkinsonism. For each patient, the PET will be arranged twice, with an interval of 1.5 years.
Please refer to this study by its ClinicalTrials.gov identifier (NCT number): NCT02138864
|Chang Gung Memorial Hospital|
|Kaohsiung, Taiwan, 886|
|Principal Investigator:||Chiung-Chih Chang, M.D.; Ph.D||Chang Gung Memorial Hospital|