Parkinson's disease, chronic hydrocarbon exposure and striatal neuronal damage: a 1-H MRS study.
Several patients with Parkinson' s disease (PD) reveal an history of chronic exposure to hydrocarbon-solvents. Chronic exposure to hydrocarbon-solvents has been proposed as a risk factor for more severe forms of PD with earlier onset of symptoms and reduced response to dopaminergic therapy. A direct correlation between disease severity and exposure degree has been previously shown. Seven exposed PD patients (two with low degree exposure and five with high degree exposure), 10 unexposed PD patients matched for sex, age and Hoehn and Yahr scale (=3 in the "on" phase), and 10 unexposed PD patients matched for sex, age and l-dopa daily intake instead of disease severity (Hoehn and Yahr scale=3.5 in the "on" phase) were studied. Twenty normal subjects without previous exposure to hydrocarbon-solvents and matched for age and sex with HPD patients were studied for comparison. The purpose of the study was to assess neuronal degeneration in the striatum of exposed vs unexposed PD patients. The authors investigated whether neuronal damage/loss was detectable in the lentiform nucleus measuring N-acetylaspartate (NAA) levels by 1-H MRS. Multiple single voxel MRS water-suppressed spectra were obtained also from the white matter and the occipital lobe. NAA was normal in the lentiform nucleus of patients with low exposure as well as in patients with no exposure whereas it was decreased in PD patients with high degree exposure. White matter and occipital lobe NAA content was normal both in exposed and unexposed PD patients. Clinical expression is more severe in PD patients with previous high degree solvent exposure because of the associated post-synaptic damage of the nigro-striatal pathway.
Rango
M
M
Dipartimento di Scienze Neurologiche-Centro per il Morbo di Parkinson, Ospedale Maggiore Policlinico, IRCCS, Università degli Studi di Milano, Milano, Italy. mariocristia@yahoo.it
Canesi
M
M
Ghione
I
I
Farabola
M
M
Righini
A
A
Bresolin
N
N
Antonini
A
A
Pezzoli
G
G
D000368:Aged; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D002794:Choline / Q000378:metabolism; D003401:Creatine / Q000378:metabolism; D006801:Humans; D006838:Hydrocarbons / Q000633:toxicity*; D008279:Magnetic Resonance Imaging; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D017072:Neostriatum / Q000473:pathology*; D009474:Neurons / Q000473:pathology*; D016273:Occupational Exposure; D010302:Parkinson Disease, Secondary / Q000139:chemically induced* / Q000473:pathology*; D012997:Solvents / Q000633:toxicity*
D006838:Hydrocarbons; D012997:Solvents; D001224:Aspartic Acid; C000179:N-acetylaspartate; D003401:Creatine; D002794:Choline