-
Something wrong with this record ?
Striosomal dysfunction affects behavioral adaptation but not impulsivity-Evidence from X-linked dystonia-parkinsonism
C. Beste, M. Mückschel, R. Rosales, A. Domingo, L. Lee, A. Ng, C. Klein, A. Münchau,
Language English Country United States
Document type Journal Article
PubMed
28059473
DOI
10.1002/mds.26895
Knihovny.cz E-resources
- MeSH
- Adult MeSH
- Dystonic Disorders complications diagnostic imaging MeSH
- Electroencephalography MeSH
- Adaptation, Physiological physiology MeSH
- Genetic Diseases, X-Linked complications diagnostic imaging MeSH
- Impulsive Behavior physiology MeSH
- Inhibition, Psychological MeSH
- Cognition Disorders etiology MeSH
- Middle Aged MeSH
- Humans MeSH
- Magnetic Resonance Imaging MeSH
- Brain diagnostic imaging MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Publication type
- Journal Article MeSH
BACKGROUND: Executive functions including behavioral adaptation and impulse control are commonly impaired in movement disorders caused by striatal pathology. However, as yet it is unclear what aspects of behavioral abnormalities are related to pathology in which striatal subcomponent, that is, the matrix and the striosomes. We therefore studied cognitive control in X-linked dystonia-parkinsonism, a model disease of striosomal degeneration, using behavioral paradigms and EEG. METHODS: We studied genetically confirmed X-linked dystonia-parkinsonism patients (N = 21) in their early disease stages and healthy matched controls. Error-related behavioral adaptation was tested in a flanker task and response inhibition in a Go/Nogo paradigm during EEG. We focused on error-related negativity during error processing and the Nogo-N2 and Nogo-P3 in the response inhibition task. Source localization analyses were calculated. In addition, total wavelet power and phase-locking factor reflecting neural synchronization processes in time and frequency across trials were calculated. RESULTS: Error processing and behavioral adaptation predominantly engaging the anterior cingulate cortex was markedly impaired in X-linked dystonia-parkinsonism. This was reflected in abnormal reaction times correlating with error-related negativity amplitudes, error related theta band activity, and the phase-locking factor. Also, abnormal error processing correlated with dystonia severity but not with parkinsonism. Response inhibition and corresponding EEG activity were normal. CONCLUSIONS: This dissociable pattern of cognitive deficits most likely reflects predominant dysfunction of the striosomal compartment and its connections to the anterior cingulate cortex in X-linked dystonia-parkinsonism. The results underscore the importance of striosomes for cognitive function in humans and suggest that striosomes are relays of error-related behavioral adaptation but not inhibitory control. © 2017 International Parkinson and Movement Disorder Society.
Faculty of Neurology and Psychiatry University of Santo Tomas Manila Philippines
Institute of Neurogenetics University of Lübeck Lübeck Germany
XDP Study Group Philippine Children's Medical Center Quezon City Philippines
References provided by Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc17031160
- 003
- CZ-PrNML
- 005
- 20171031110849.0
- 007
- ta
- 008
- 171025s2017 xxu f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.1002/mds.26895 $2 doi
- 035 __
- $a (PubMed)28059473
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xxu
- 100 1_
- $a Beste, Christian $u Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine of the Technische Universität (TU) Dresden, Dresden, Germany. Experimental Neurobiology, National Institute of Mental Health, Klecany, Czech Republic.
- 245 10
- $a Striosomal dysfunction affects behavioral adaptation but not impulsivity-Evidence from X-linked dystonia-parkinsonism / $c C. Beste, M. Mückschel, R. Rosales, A. Domingo, L. Lee, A. Ng, C. Klein, A. Münchau,
- 520 9_
- $a BACKGROUND: Executive functions including behavioral adaptation and impulse control are commonly impaired in movement disorders caused by striatal pathology. However, as yet it is unclear what aspects of behavioral abnormalities are related to pathology in which striatal subcomponent, that is, the matrix and the striosomes. We therefore studied cognitive control in X-linked dystonia-parkinsonism, a model disease of striosomal degeneration, using behavioral paradigms and EEG. METHODS: We studied genetically confirmed X-linked dystonia-parkinsonism patients (N = 21) in their early disease stages and healthy matched controls. Error-related behavioral adaptation was tested in a flanker task and response inhibition in a Go/Nogo paradigm during EEG. We focused on error-related negativity during error processing and the Nogo-N2 and Nogo-P3 in the response inhibition task. Source localization analyses were calculated. In addition, total wavelet power and phase-locking factor reflecting neural synchronization processes in time and frequency across trials were calculated. RESULTS: Error processing and behavioral adaptation predominantly engaging the anterior cingulate cortex was markedly impaired in X-linked dystonia-parkinsonism. This was reflected in abnormal reaction times correlating with error-related negativity amplitudes, error related theta band activity, and the phase-locking factor. Also, abnormal error processing correlated with dystonia severity but not with parkinsonism. Response inhibition and corresponding EEG activity were normal. CONCLUSIONS: This dissociable pattern of cognitive deficits most likely reflects predominant dysfunction of the striosomal compartment and its connections to the anterior cingulate cortex in X-linked dystonia-parkinsonism. The results underscore the importance of striosomes for cognitive function in humans and suggest that striosomes are relays of error-related behavioral adaptation but not inhibitory control. © 2017 International Parkinson and Movement Disorder Society.
- 650 _2
- $a fyziologická adaptace $x fyziologie $7 D000222
- 650 _2
- $a dospělí $7 D000328
- 650 _2
- $a mozek $x diagnostické zobrazování $7 D001921
- 650 _2
- $a kognitivní poruchy $x etiologie $7 D003072
- 650 _2
- $a dystonické poruchy $x komplikace $x diagnostické zobrazování $7 D020821
- 650 _2
- $a elektroencefalografie $7 D004569
- 650 _2
- $a genetické nemoci vázané na chromozom X $x komplikace $x diagnostické zobrazování $7 D040181
- 650 _2
- $a lidé $7 D006801
- 650 _2
- $a impulzivní chování $x fyziologie $7 D007175
- 650 _2
- $a inhibice (psychologie) $7 D007266
- 650 _2
- $a magnetická rezonanční tomografie $7 D008279
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a lidé středního věku $7 D008875
- 655 _2
- $a časopisecké články $7 D016428
- 700 1_
- $a Mückschel, Moritz $u Cognitive Neurophysiology, Department of Child and Adolescent Psychiatry, Faculty of Medicine of the Technische Universität (TU) Dresden, Dresden, Germany.
- 700 1_
- $a Rosales, Raymond $u XDP Study Group, Philippine Children's Medical Center, Quezon City, Philippines.
- 700 1_
- $a Domingo, Aloysius $u Institute of Neurogenetics, University of Lübeck, Lübeck, Germany.
- 700 1_
- $a Lee, Lillian $u Faculty of Neurology and Psychiatry, University of Santo Tomas, Manila, Philippines.
- 700 1_
- $a Ng, Arlene $u XDP Study Group, Philippine Children's Medical Center, Quezon City, Philippines.
- 700 1_
- $a Klein, Christine $u Institute of Neurogenetics, University of Lübeck, Lübeck, Germany.
- 700 1_
- $a Münchau, Alexander $u Institute of Neurogenetics, University of Lübeck, Lübeck, Germany.
- 773 0_
- $w MED00003420 $t Movement disorders official journal of the Movement Disorder Society $x 1531-8257 $g Roč. 32, č. 4 (2017), s. 576-584
- 856 41
- $u https://pubmed.ncbi.nlm.nih.gov/28059473 $y Pubmed
- 910 __
- $a ABA008 $b sig $c sign $y a $z 0
- 990 __
- $a 20171025 $b ABA008
- 991 __
- $a 20171031110939 $b ABA008
- 999 __
- $a ok $b bmc $g 1254753 $s 992187
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2017 $b 32 $c 4 $d 576-584 $e 20170106 $i 1531-8257 $m Movement disorders $n Mov Disord $x MED00003420
- LZP __
- $a Pubmed-20171025