TY  - JOUR
A1  - Volkmann, Jens
A1  - Albanese, Alberto
A1  - Antonini, Angelo
A1  - Chaudhuri, K. Ray
A1  - Clarke, Karl E.
A1  - de Bie, Rob M. A.
A1  - Deuschl, Günther
A1  - Eggert, Karla
A1  - Houeto, Jean-Luc
A1  - Kulisevsky, Jaime
A1  - Nyholm, Dag
A1  - Odin, Per
A1  - Ostergaard, Karen
A1  - Poewe, Werner
A1  - Pollak, Pierre
A1  - Rabey, Jose Martin
A1  - Rascol, Olivier
A1  - Ruzicka, Evzen
A1  - Samuel, Michael
A1  - Speelman, Hans
A1  - Sydow, Olof
A1  - Valldeoriola, Francesc
A1  - van der Linden, Chris
A1  - Oertel, Wolfgang
T1  - Selecting deep brain stimulation or infusion therapies in advanced Parkinson’s disease: an evidence-based review
JF  - Journal of Neurology
N2  - Motor complications in Parkinson’s disease (PD) result from the short half-life and irregular plasma fluctuations of oral levodopa. When strategies of providing more continuous dopaminergic stimulation by adjusting oral medication fail, patients may be candidates for one of three device-aided therapies: deep brain stimulation (DBS), continuous subcutaneous apomorphine infusion, or continuous duodenal/jejunal levodopa/carbidopa pump infusion (DLI). These therapies differ in their invasiveness, side-effect profile, and the need for nursing care. So far, very few comparative studies have evaluated the efficacy of the three device-aided therapies for specific motor problems in advanced PD. As a result, neurologists currently lack guidance as to which therapy could be most appropriate for a particular PD patient. A group of experts knowledgeable in all three therapies reviewed the currently available literature for each treatment and identified variables of clinical relevance for choosing one of the three options such as type of motor problems, age, and cognitive and psychiatric status. For each scenario, pragmatic and (if available) evidence-based recommendations are provided as to which patients could be candidates for either DBS, DLI, or subcutaneous apomorphine.
KW  - Parkinson’s disease
KW  - apomorphine
KW  - deep brain stimulation
KW  - duodenal levodopa infusion
Y1  - 2013
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-132373
VL  - 260
ER  - 
TY  - JOUR
A1  - Doppler, Kathrin
A1  - Brockmann, Kathrin
A1  - Sedghi, Annahita
A1  - Wurster, Isabel
A1  - Volkmann, Jens
A1  - Oertel, Wolfgang H.
A1  - Sommer, Claudia
T1  - Dermal phospho-alpha-synuclein deposition in patients with Parkinson's disease and mutation of the glucocerebrosidase gene
JF  - Frontiers in Neurology
N2  - Heterozygous mutations in the glucocerebrosidase gene (GBA1) represent the most common genetic risk factor for Parkinson's disease (PD) and are histopathologically associated with a widespread load of alpha-synuclein in the brain. Therefore, PD patients with GBA1 mutations are a cohort of high interest for clinical trials on disease-modifying therapies targeting alpha-synuclein. There is evidence that detection of phospho-alpha-synuclein (p-syn) in dermal nerve fibers might be a biomarker for the histopathological identification of PD patients even at premotor or very early stages of disease. It is so far unknown whether dermal p-syn deposition can also be found in PD patients with GBA1 mutations and may serve as a biomarker for PD in these patients. Skin biopsies of 10 PD patients with different GBA1 mutations (six N3705, three E326K, one L444P) were analyzed by double-immunofluorescence labeling with anti-p-syn and anti-protein gene product 9.5 (PGP9.5, axonal marker) to detect intraaxonal p-syn deposition. Four biopsy sites (distal, proximal leg, paravertebral Th10, and C7) per patient were studied. P-syn was found in six patients (three N370S, three E326K). P-syn deposition was mainly detected in autonomic nerve fibers, but also in somatosensory fibers and was not restricted to a certain GBA1 mutation. In summary, dermal p-syn in PD patients with GBA1 mutations seems to offer a similar distribution and frequency as observed in patients without a known mutation. Skin biopsy may be suitable to study p-syn deposition in these patients or even to identify premotor patients with GBA1 mutations.
KW  - Parkinson's disease
KW  - glucocerebrosidase mutation
KW  - alpha-synuclein
KW  - skin biopsy
KW  - biomarker
Y1  - 2018
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-222828
VL  - 9
ER  -