title: Neurovascular coupling in Parkinson's disease patients: effects of dementia and acetylcholinesterase inhibitor treatment.
abstract: Alzheimer's disease (AD) and Parkinson's disease (PD) lead to a cholinergic deficit in the brain which is not only related to dementia, but may also lead to a disturbed neurovascular coupling. We investigated the effect of cholinergic decline on neurovascular coupling in PD patients. Patients with idiopathic PD were divided in groups without (n=59; 65 ± 9 y) or with moderate dementia as specified by Mini-Mental State Examination. The demented patients were assigned to groups with (n=55; 73 ± 6 y) or without (n=61; 72 ± 8 y) acetylcholinesterase inhibitor treatment. Neurovascular coupling was assessed by a simultaneous electroencephalography-Doppler technique applying a contrast-based visual stimulation task. Visually evoked potential amplitudes (N75-P100) and parameters of the hemodynamic response in the posterior cerebral artery were obtained using a control system approach (resting flow velocity, gain, attenuation, rate time, and natural frequency). Data were compared to a healthy control group of a similar age range (n=20; 63 ± 8 yr). Compared to controls, patient groups presented no differences in evoked potential amplitudes or neurovascular coupling parameters. The reported 30% decline in acetylcholinesterase activity in PD patients did not lead to measurable changes in neurovascular coupling. In AD patients additional factors might explain the uncoupling and higher cerebrovascular risk detected in clinical studies.
authors.affiliation: Department of Neurology of the Justus-Liebig University-Giessen, Giessen, Germany. bernhard.rosengarten@neuro.med.unigiessen.de
authors.forename: Bernhard
authors.initials: B
authors.lastname: Rosengarten
authors.forename: Veren
authors.initials: V
authors.lastname: Dannhardt
authors.forename: Ole
authors.initials: O
authors.lastname: Burr
authors.forename: Matthias
authors.initials: M
authors.lastname: Pöhler
authors.forename: Susanne
authors.initials: S
authors.lastname: Rosengarten
authors.forename: Matthias
authors.initials: M
authors.lastname: Oechsner
authors.forename: Iris
authors.initials: I
authors.lastname: Reuter
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D016022:Case-Control Studies; D002536:Cerebral Arteries / Q000473:pathology*; D002800:Cholinesterase Inhibitors / Q000627:therapeutic use*; D003704:Dementia / Q000150:complications / Q000188:drug therapy*; D004569:Electroencephalography / Q000379:methods; D005074:Evoked Potentials, Visual / Q000187:drug effects / Q000502:physiology; D005260:Female; D006801:Humans; D008297:Male; D008609:Mental Status Schedule; D008875:Middle Aged; D009483:Neuropsychological Tests; D010300:Parkinson Disease / Q000150:complications / Q000188:drug therapy*; D048448:Phenylcarbamates / Q000627:therapeutic use*; D010775:Photic Stimulation / Q000379:methods; D000068836:Rivastigmine; D018615:Ultrasonography, Doppler, Color / Q000379:methods
chemical_list: D002800:Cholinesterase Inhibitors; D048448:Phenylcarbamates; D000068836:Rivastigmine