Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease

Research output: Contribution to journalJournal articlepeer-review

Standard

Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease. / Reetz, Kathrin; Gaser, Christian; Klein, Christine; Hagenah, Johannes; Büchel, Christian; Gottschalk, Stefan; Pramstaller, Peter P; Siebner, Hartwig R; Binkofski, Ferdinand.

In: Movement Disorders, Vol. 24, No. 1, 2009, p. 99-103.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Reetz, K, Gaser, C, Klein, C, Hagenah, J, Büchel, C, Gottschalk, S, Pramstaller, PP, Siebner, HR & Binkofski, F 2009, 'Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease', Movement Disorders, vol. 24, no. 1, pp. 99-103. https://doi.org/10.1002/mds.22333

APA

Reetz, K., Gaser, C., Klein, C., Hagenah, J., Büchel, C., Gottschalk, S., Pramstaller, P. P., Siebner, H. R., & Binkofski, F. (2009). Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease. Movement Disorders, 24(1), 99-103. https://doi.org/10.1002/mds.22333

Vancouver

Reetz K, Gaser C, Klein C, Hagenah J, Büchel C, Gottschalk S et al. Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease. Movement Disorders. 2009;24(1):99-103. https://doi.org/10.1002/mds.22333

Author

Reetz, Kathrin ; Gaser, Christian ; Klein, Christine ; Hagenah, Johannes ; Büchel, Christian ; Gottschalk, Stefan ; Pramstaller, Peter P ; Siebner, Hartwig R ; Binkofski, Ferdinand. / Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease. In: Movement Disorders. 2009 ; Vol. 24, No. 1. pp. 99-103.

Bibtex

@article{2a440980aac711df928f000ea68e967b,
title = "Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease",
abstract = "A bilateral compensatory increase of basal ganglia (BG) gray matter value (GMV) was recently demonstrated in asymptomatic Parkin mutation carriers, who likely have an increased risk to develop Parkinson's disease (PD). We hypothesized BG morphological changes in symptomatic Parkin mutation carriers (sPARKIN-MC) and idiopathic PD patients (iPD) after the occurrence of PD symptoms, reflecting the breakdown of compensatory mechanisms. Nine sPARKIN-MC, 14 iPD, and 24 controls were studied clinically and with voxel-based morphometry. Analysis of variance revealed mainly BG decrease of GMV in sPARKIN-MC and to a lesser extent in iPD. However, a slight increase in GMV was also found in the right globus pallidus externus in sPARKIN-MC and in the right putamen in iPD. This may reflect a structural correlate of functional compensation that can only partially be maintained when nigrostriatal neurodegeneration becomes manifest. Simple regression analyses with the UPDRS-III and disease duration score revealed a distinct more bilateral linear decrease of BG GMV in sPARKIN-MC than in iPD that may correspond to previous findings showing a symmetric reduction in putaminal (18)F-DOPA-uptake and bilateral manifestation of symptoms in sPARKIN-MC. In symptomatic PD, BG are subject to a progressive atrophy, which gradually increases with disease severity and duration.",
author = "Kathrin Reetz and Christian Gaser and Christine Klein and Johannes Hagenah and Christian B{\"u}chel and Stefan Gottschalk and Pramstaller, {Peter P} and Siebner, {Hartwig R} and Ferdinand Binkofski",
note = "Keywords: Adult; Aged; Basal Ganglia; Caudate Nucleus; DNA Mutational Analysis; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Organ Size; Parkinson Disease; Parkinsonian Disorders; Putamen; Sequence Deletion; Ubiquitin-Protein Ligases",
year = "2009",
doi = "10.1002/mds.22333",
language = "English",
volume = "24",
pages = "99--103",
journal = "Movement Disorders",
issn = "0885-3185",
publisher = "JohnWiley & Sons, Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Structural findings in the basal ganglia in genetically determined and idiopathic Parkinson's disease

AU - Reetz, Kathrin

AU - Gaser, Christian

AU - Klein, Christine

AU - Hagenah, Johannes

AU - Büchel, Christian

AU - Gottschalk, Stefan

AU - Pramstaller, Peter P

AU - Siebner, Hartwig R

AU - Binkofski, Ferdinand

N1 - Keywords: Adult; Aged; Basal Ganglia; Caudate Nucleus; DNA Mutational Analysis; Female; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Organ Size; Parkinson Disease; Parkinsonian Disorders; Putamen; Sequence Deletion; Ubiquitin-Protein Ligases

PY - 2009

Y1 - 2009

N2 - A bilateral compensatory increase of basal ganglia (BG) gray matter value (GMV) was recently demonstrated in asymptomatic Parkin mutation carriers, who likely have an increased risk to develop Parkinson's disease (PD). We hypothesized BG morphological changes in symptomatic Parkin mutation carriers (sPARKIN-MC) and idiopathic PD patients (iPD) after the occurrence of PD symptoms, reflecting the breakdown of compensatory mechanisms. Nine sPARKIN-MC, 14 iPD, and 24 controls were studied clinically and with voxel-based morphometry. Analysis of variance revealed mainly BG decrease of GMV in sPARKIN-MC and to a lesser extent in iPD. However, a slight increase in GMV was also found in the right globus pallidus externus in sPARKIN-MC and in the right putamen in iPD. This may reflect a structural correlate of functional compensation that can only partially be maintained when nigrostriatal neurodegeneration becomes manifest. Simple regression analyses with the UPDRS-III and disease duration score revealed a distinct more bilateral linear decrease of BG GMV in sPARKIN-MC than in iPD that may correspond to previous findings showing a symmetric reduction in putaminal (18)F-DOPA-uptake and bilateral manifestation of symptoms in sPARKIN-MC. In symptomatic PD, BG are subject to a progressive atrophy, which gradually increases with disease severity and duration.

AB - A bilateral compensatory increase of basal ganglia (BG) gray matter value (GMV) was recently demonstrated in asymptomatic Parkin mutation carriers, who likely have an increased risk to develop Parkinson's disease (PD). We hypothesized BG morphological changes in symptomatic Parkin mutation carriers (sPARKIN-MC) and idiopathic PD patients (iPD) after the occurrence of PD symptoms, reflecting the breakdown of compensatory mechanisms. Nine sPARKIN-MC, 14 iPD, and 24 controls were studied clinically and with voxel-based morphometry. Analysis of variance revealed mainly BG decrease of GMV in sPARKIN-MC and to a lesser extent in iPD. However, a slight increase in GMV was also found in the right globus pallidus externus in sPARKIN-MC and in the right putamen in iPD. This may reflect a structural correlate of functional compensation that can only partially be maintained when nigrostriatal neurodegeneration becomes manifest. Simple regression analyses with the UPDRS-III and disease duration score revealed a distinct more bilateral linear decrease of BG GMV in sPARKIN-MC than in iPD that may correspond to previous findings showing a symmetric reduction in putaminal (18)F-DOPA-uptake and bilateral manifestation of symptoms in sPARKIN-MC. In symptomatic PD, BG are subject to a progressive atrophy, which gradually increases with disease severity and duration.

U2 - 10.1002/mds.22333

DO - 10.1002/mds.22333

M3 - Journal article

C2 - 18823048

VL - 24

SP - 99

EP - 103

JO - Movement Disorders

JF - Movement Disorders

SN - 0885-3185

IS - 1

ER -

ID: 21458481