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Marcus Heldmann

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4 papers
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4

YNIMG Journal 2020 Journal Article

Effects of hunger, satiety and oral glucose on effective connectivity between hypothalamus and insular cortex

  • Arkan Al-Zubaidi
  • Sandra Iglesias
  • Klaas E. Stephan
  • Macià Buades-Rotger
  • Marcus Heldmann
  • Janis Marc Nolde
  • Henriette Kirchner
  • Alfred Mertins

The hypothalamus and insular cortex play an essential role in the integration of endocrine and homeostatic signals and their impact on food intake. Resting-state functional connectivity alterations of the hypothalamus, posterior insula (PINS) and anterior insula (AINS) are modulated by metabolic states and caloric intake. Nevertheless, a deeper understanding of how these factors affect the strength of connectivity between hypothalamus, PINS and AINS is missing. This study investigated whether effective (directed) connectivity within this network varies as a function of prandial states (hunger vs. satiety) and energy availability (glucose levels and/or hormonal modulation). To address this question, we measured twenty healthy male participants of normal weight twice: once after 36 ​h of fasting (except water consumption) and once under satiated conditions. During each session, resting-state functional MRI (rs-fMRI) and hormone concentrations were recorded before and after glucose administration. Spectral dynamic causal modeling (spDCM) was used to assess the effective connectivity between the hypothalamus and anterior and posterior insula. Using Bayesian model selection, we observed that the same model was identified as the most likely model for each rs-fMRI recording. Compared to satiety, the hunger condition enhanced the strength of the forward connections from PINS to AINS and reduced the strength of backward connections from AINS to PINS. Furthermore, the strength of connectivity from PINS to AINS was positively related to plasma cortisol levels in the hunger condition, mainly before glucose administration. However, there was no direct relationship between glucose treatment and effective connectivity. Our findings suggest that prandial states modulate connectivity between PINS and AINS and relate to theories of interoception and homeostatic regulation that invoke hierarchical relations between posterior and anterior insula.

YNICL Journal 2020 Journal Article

Patients with mutations of the Thyroid hormone beta-receptor show an ADHD-like phenotype for performance monitoring: an electrophysiological study

  • Jan Uter
  • Marcus Heldmann
  • Berenike Rogge
  • Martina Obst
  • Julia Steinhardt
  • Georg Brabant
  • Carla Moran
  • Krishna Chatterjee

Resistance to thyroid hormone beta (RTHβ) is a syndrome of reduced responsiveness of peripheral tissue to thyroid hormone, caused by mutations in the thyroid hormone receptor beta (THRB). Its cognitive phenotype has been reported to be similar to attention deficit hyperactivity disorder (ADHD). This study used electrophysiological biomarkers of performance monitoring in RTHβ to contribute further evidence on its phenotypical similarity to ADHD. Twenty-one participants with RTHβ aged 18-67 years and 21 matched healthy controls performed a modified flanker task during EEG recording. The RTHβ and control groups were compared on behavioural measures and components of event related potentials (ERPs), i.e. the error related negativity (ERN), the error positivity (Pe) and P3 component. There were no significant group differences with regard to behaviour. RTHβ subjects displayed significantly reduced ERN and Pe amplitudes compared to the controls in the response-locked ERPs. In addition, we observed reduced P3 amplitudes in both congruent and incongruent trials, as well as prolonged P3 latencies in RTHβ subjects in the stimulus-locked ERPs. Our findings reveal alterations in error detection and performance monitoring of RTHβ patients, likely indicating reduced error awareness. The electrophysiological phenotype of RTHß subjects with regard to action monitoring is indistinguishable from ADHD.

YNICL Journal 2018 Journal Article

Increased insula-putamen connectivity in X-linked dystonia-parkinsonism

  • Anne J. Blood
  • Jeff L. Waugh
  • Thomas F. Münte
  • Marcus Heldmann
  • Aloysius Domingo
  • Christine Klein
  • Hans C. Breiter
  • Lillian V. Lee

Preliminary evidence from postmortem studies of X-linked dystonia-parkinsonism (XDP) suggests tissue loss may occur first and/or most severely in the striatal striosome compartment, followed later by cell loss in the matrix compartment. However, little is known about how this relates to pathogenesis and pathophysiology. While MRI cannot visualize these striatal compartments directly in humans, differences in relative gradients of afferent cortical connectivity across compartments (weighted toward paralimbic versus sensorimotor cortex, respectively) can be used to infer potential selective loss in vivo. In the current study we evaluated relative connectivity of paralimbic versus sensorimotor cortex with the caudate and putamen in 17 individuals with XDP and 17 matched controls. Although caudate and putamen volumes were reduced in XDP, there were no significant reductions in either "matrix-weighted", or "striosome-weighted" connectivity. In fact, paralimbic connectivity with the putamen was elevated, rather than reduced, in XDP. This was driven most strongly by elevated putamen connectivity with the anterior insula. There was no relationship of these findings to disease duration or striatal volume, suggesting insula and/or paralimbic connectivity in XDP may develop abnormally and/or increase in the years before symptom onset.

YNIMG Journal 2017 Journal Article

Valsalva-induced elevation of intracranial pressure selectively decouples deoxygenated hemoglobin concentration from neuronal activation and functional brain imaging capability

  • Martin Knauth
  • Marcus Heldmann
  • Thomas F. Münte
  • Georg Royl

During neuronal activation, neurovascular coupling leads to a local decrease of deoxygenated hemoglobin concentration (deoxy-Hb) and thus forms the basis of many functional brain mapping methods. In animals, an elevated intracranial pressure (ICP) can attenuate or even reverse this deoxy-Hb signaling. To study the effect of an elevated ICP on functional brain imaging in humans, we used different breathing tasks to modify ICP and analyzed the resulting effect on neurovascular coupling in the motor cortex. Functional near-infrared spectroscopy (fNIRS) was performed on 45 subjects during alternating conditions of finger tapping and resting state combined with four different breathing maneuvers (normal breathing (NB), breath holding without Valsalva maneuver (BH), Valsalva maneuver with 15 mm Hg forced expiratory pressure against resistance (V15) and Valsalva maneuver with 35 mm Hg forced expiratory pressure against resistance (V35)) in randomized order. With escalation of breathing tasks the median amplitude of the functional deoxy-Hb decrease during finger tapping became smaller. In contrast, functional oxygenated hemoglobin concentration (oxy-Hb) and total hemoglobin concentration (total-Hb) responses did not show a significant alteration. The functional oxy-Hb map evoked by finger tapping withstood Valsalva challenges while the functional deoxy-Hb map identified the correct motor cortex in normal breathing conditions only and did not reveal a functional contrast during Valsalva maneuvers. In summary, we conclude that during ICP elevation, deoxy-Hb is not a reliable basis for functional brain imaging. This suggests that the validity of BOLD fMRI during increased ICP might be impaired.