Sören Peters
Ruhr University Bochum
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Featured researches published by Sören Peters.
Acta Neurologica Scandinavica | 2003
J. Uekermann; Irene Daum; Sören Peters; B. Wiebel; H. Przuntek; Thorsten Müller
Objectives – Studies on neuropsychological functions in early Parkinsons disease (PD) have reported changes with respect to memory and executive control related to dysfunction of fronto‐striatal circuitry. The question has been raised, however, whether these findings are at least partly influenced by depression, which as such can also lead to cognitive impairments that depend on the functional integrity of the prefrontal cortex.
Current Biology | 2009
Silke Lissek; Claudia Wilimzig; P. Stude; Burkhard Pleger; Tobias Kalisch; Christoph Maier; Sören Peters; Volkmar Nicolas; Martin Tegenthoff; Hubert R. Dinse
Use is a major factor driving plasticity of cortical processing and cortical maps. As demonstrated of blind Braille readers and musicians, long-lasting and exceptional usage of the fingers results in the development of outstanding sensorimotor skills and in expansions of the cortical finger representations. However, how periods of disuse affect cortical representations and perception in humans remains elusive. Here, we report that a few weeks of hand and arm immobilization by cast wearing significantly reduced hand use and impaired tactile acuity, associated with reduced activation of the respective finger representations in the somatosensory cortex (SI), measured by functional magnetic resonance imaging. Hemodynamic responses in the SI correlated positively with hand-use frequency and negatively with discrimination thresholds, indicating that reduced activation was most prominent in subjects with severe perceptual impairment. We found, strikingly, compensatory effects on the contralateral, healthy hand consisting of improved perceptual performance compared to healthy controls. Two to three weeks after cast removal, perceptual and cortical changes recovered, whereas tactile acuity on the healthy side remained superior to that on the formerly immobilized side. These findings suggest that brief periods of reduced use of a limb have overt consequences and thus constitute a significant driving force of brain organization equivalent to enhanced use.
Brain | 2012
Rudolf A. Kley; Piraye Serdaroglu-Oflazer; Yvonne Leber; Zagaa Odgerel; Peter F.M. van der Ven; Montse Olivé; Isidro Ferrer; Adekunle Onipe; Mariya Mihaylov; Juan M. Bilbao; Hee S. Lee; Jörg Höhfeld; Kristina Djinović-Carugo; Kester Kong; Martin Tegenthoff; Sören Peters; Werner Stenzel; Matthias Vorgerd; Lev G. Goldfarb; Dieter O. Fürst
Mutations in FLNC cause two distinct types of myopathy. Disease associated with mutations in filamin C rod domain leading to expression of a toxic protein presents with progressive proximal muscle weakness and shows focal destructive lesions of polymorphous aggregates containing desmin, myotilin and other proteins in the affected myofibres; these features correspond to the profile of myofibrillar myopathy. The second variant associated with mutations in the actin-binding domain of filamin C is characterized by weakness of distal muscles and morphologically by non-specific myopathic features. A frameshift mutation in the filamin C rod domain causing haploinsufficiency was also found responsible for distal myopathy with some myofibrillar changes but no protein aggregation typical of myofibrillar myopathies. Controversial data accumulating in the literature require re-evaluation and comparative analysis of phenotypes associated with the position of the FLNC mutation and investigation of the underlying disease mechanisms. This is relevant and necessary for the refinement of diagnostic criteria and developing therapeutic approaches. We identified a p.W2710X mutation in families originating from ethnically diverse populations and re-evaluated a family with a p.V930_T933del mutation. Analysis of the expanded database allows us to refine clinical and myopathological characteristics of myofibrillar myopathy caused by mutations in the rod domain of filamin C. Biophysical and biochemical studies indicate that certain pathogenic mutations in FLNC cause protein misfolding, which triggers aggregation of the mutant filamin C protein and subsequently involves several other proteins. Immunofluorescence analyses using markers for the ubiquitin-proteasome system and autophagy reveal that the affected muscle fibres react to protein aggregate formation with a highly increased expression of chaperones and proteins involved in proteasomal protein degradation and autophagy. However, there is a noticeably diminished efficiency of both the ubiquitin-proteasome system and autophagy that impairs the muscle capacity to prevent the formation or mediate the degradation of aggregates. Transfection studies of cultured muscle cells imitate events observed in the patients affected muscle and therefore provide a helpful model for testing future therapeutic strategies.
Journal of Neural Transmission-supplement | 2004
J. Uekermann; Irene Daum; M. Bielawski; S. Muhlack; Sören Peters; H. Przuntek; T. Mueller
Investigations concerning cognitive functions in early PD have revealed memory and executive function deficits related to dysfunction of fronto-striatal circuitry. Despite the range of data base, many previous investigations are limited because of methodological questions and inconsistencies. Thus the pattern of executive function impairments in early PD is far from being established. In the present investigation, twenty PD patients in early stages of the disease were compared to control subjects on a comprehensive neuropsychological test battery, aiming to explore their cognitive profile across a range of executive subcomponents. Results revealed impairments with respect to initiation, reasoning and planning. In summary, the present investigation shows that PD is associated with a differential executive impairment pattern which is (partly) related to disease characteristics and affective variables.
NeuroImage | 2007
Silke Lissek; Markus Hausmann; Frauke Knossalla; Sören Peters; Volkmar Nicolas; Onur Güntürkün; Martin Tegenthoff
In this study, we compared brain activation patterns in men and women during performance of a fine motor task, in order to investigate the influence of motor task complexity upon asymmetries of hemispheric recruitment. Thirty-three right-handed participants (17 males, 16 females) performed a self-paced finger-tapping task comprising three conditions of increasing complexity with both the dominant and the non-dominant hand. Imaging results demonstrated significant sex differences in brain activation patterns. While women showed significantly larger activation of ipsi- and contralateral task-related cortical areas than men, men exhibited significantly stronger subcortical activation in striatal regions. The observed activation differences may reflect sex differences in control of voluntary motor skills related to differential emphasis upon cortical and subcortical correlates of motor sequence processing, as well as differences in hemispheric recruitment, by means of which men and women can nevertheless achieve comparable motor performance.
Frontiers in Human Neuroscience | 2012
Jan-Christoph Kattenstroth; Tobias Kalisch; Sören Peters; Martin Tegenthoff; Hubert R. Dinse
Rehabilitation of sensorimotor impairment resulting from cerebral lesion (CL) utilizes task specific training and massed practice to drive reorganization and sensorimotor improvement due to induction of neuroplasticity mechanisms. Loss of sensory abilities often complicates recovery, and thus the individuals ability to use the affected body part for functional tasks. Therefore, the development of additional and alternative approaches that supplement, enhance, or even replace conventional training procedures would be advantageous. Repetitive sensory stimulation protocols (rSS) have been shown to evoke sensorimotor improvements of the affected limb in patients with chronic stroke. However, the possible impact of long-term rSS on sensorimotor performance of patients with CL, where the incident dated back many years remains unclear. The particular advantage of rSS is its passive nature, which does not require active participation of the subjects. Therefore, rSS can be applied in parallel to other occupations, making the intervention easier to implement and more acceptable to the individual. Here we report the effects of applying rSS for 8, 36, and 76 weeks to the paretic hand of three long-term patients with different types of CL. Different behavioral tests were used to assess sensory and/or sensorimotor performance of the upper extremities prior, after, and during the intervention. In one patient, the impact of long-term rSS on restoration of cortical activation was investigated by recording somatosensory evoked potentials (SEP). After long-term rSS all three patients showed considerable improvements of their sensory and motor abilities. In addition, almost normal evoked potentials could be recorded after rSS in one patient. Our data show that long-term rSS applied to patients with chronic CL can improve tactile and sensorimotor functions, which, however, developed in some cases only after many weeks of stimulation, and continued to further improve on a time scale of months.
Acta Neurologica Scandinavica | 2002
Thorsten Müller; Dirk Woitalla; Sören Peters; K. Kohla; H. Przuntek
Studies on progression of Parkinsons disease (PD) mainly focus on the nigrostriatal dopaminergic decline, but not on the visual system. We determined progression of (i) disturbed color vision, assessed with the Farnsworth–Munsell 100 Hue test (FMT) and (ii) intensity of PD in 18 patients. Significant differences occurred between (i) initial FMT error scores and follow‐up results 3 years later (P=0.002) and analogously (ii) scored intensity of PD (P=0.002). A relation between computed differences of FMT error scores and rated activities of daily living appeared. Deterioration of color vision progresses in PD.
Experimental Neurology | 2012
Björn Enzi; Marc-Andreas Edel; Silke Lissek; Sören Peters; Rainer Hoffmann; Volkmar Nicolas; Martin Tegenthoff; Georg Juckel; Carsten Saft
Recent research using various neuroimaging methods revealed the crucial role of the striatum concerning the neuropathology of Huntingtons disease. Degenerative changes located in the basal ganglia are already observable in premanifest stages of Huntingtons disease (pre-HD), i.e., before the onset of manifest motor symptoms. Although the impact of the striatum on reward and punishment processing is well-established in healthy subjects, these processes have not been investigated in manifest and premanifest HD subjects using functional magnetic resonance imaging (fMRI) so far. We used the Monetary Incentive Delay Task to investigate valence discrimination in terms of rewarding and punishing cues in 30 pre-HD and 15 healthy subjects. According to the probability of disease onset within the next 5 years, pre-HD subjects were categorized as either near to motor symptom onset (pre-HD(near); 9.9 [±2.91] years to onset) or far from manifest disease onset (pre-HD(far); 23.49 [±5.99] years to onset). Compared to pre-HD(far) and healthy subjects, pre-HD(near) subjects showed a disturbed neuronal differentiation between reward and control anticipation located in the left ventral striatum. In contrast to pre-HD(far) and healthy subjects, no significant ventral striatal discrimination between punishing and control cues was detected in pre-HD(near) subjects. In the present study, we demonstrated for the first time significant differences in valence discrimination in pre-HD(near) subjects compared to pre-HD(far) subjects and healthy controls. Altered reward and punishment processing could therefore reflect a motivational deficit that may contribute to the pathogenesis of Huntingtons disease.
Journal of Neural Transmission | 2000
Thorsten Müller; Dirk Woitalla; D. Schulz; Sören Peters; W. Kuhn; H. Przuntek
Summary. No significant increase of the maximum concentration (Cmax) of levodopa after addition of catechol-O-methyltransferase inhibitor tolcapone occurred in previous pharmacokinetic studies predominantly on healthy volunteers. We compared pharmacokinetics of levodopa in plasma before and after addition of tolcapone in 13 treated parkinsonian subjects under standardized conditions. We found a significant increase of Cmax of levodopa after the addition of tolcapone. This may represent one cause for the occurrence of dyskinesia previously early in the course of treatment with tolcapone.
Journal of Clinical Neuroscience | 2001
Sören Peters; E.G. Eising; H. Przuntek; Thorsten Müller
Vascular Parkinsonism (VP) is characterised by sudden onset and rapid progression of clinical symptoms, absent or poor response to dopamine substitution therapy, and postural instability with shuffling gait and absence of tremor, making it a clinically distinct entity from idiopathic Parkinsons disease (IPD). Furthermore, it displays certain typical findings in neurological investigations. We report on a patient presenting features of VP associated with an intracerebral lesion not ascribed to VP to date, namely an isolated ischaemic focal lesion located in the left cerebral peduncle between the substantia nigra and nucleus ruber as evidenced by magnetic resonance imaging (MRI). The pathophysiological organic correlate for contralateral extrapyramidal symptoms in this patient may be an interruption of nigro-thalamic projection, interrupting the final subcortical station in the cortic-striato-pallido-nigro-thalamico-cortical loop central to the pathophysiology of parkinsonian syndromes. Non-response t o levodopa therapy could be a consequence of disruption of the cortico-basal ganglia-cortical loop on account of ischaemic destruction of subcortico-cortical axons, the underlying pathology, therefore, not being the result of a loss of nigral dopaminergic neurons or striatal dopamine deficiency pathogonomonic of IPD. To our knowledge, this is the first case of clinically manifest VP to be described with a single lesion in the contralateral cerebral peduncle between the substantia nigra and nucleus ruber, and suggests alternative intracerebral patterns for the distribution of disease-causing lesions in VP, and possibly new pathophysiological explanations for the nature of this disease.