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2. Human REM sleep recalibrates neural activity in support of memory formation.

Author

Lendner, Janna, Niethard, Niels, van Schalkwijk, Frank, Schuh-Hofer, Sigrid, Schmidt, Hannah, Knight, Robert, Born, Jan, Walker, Matthew, Lin, Jack, Helfrich, Randolph, and Mander, Bryce

Subjects
Humans, Sleep, REM, Sleep, Mental Recall, Calcium, Cardiac Electrophysiology
Abstract

The proposed mechanisms of sleep-dependent memory consolidation involve the overnight regulation of neural activity at both synaptic and whole-network levels. Now, there is a lack of in vivo data in humans elucidating if, and how, sleep and its varied stages balance neural activity, and if such recalibration benefits memory. We combined electrophysiology with in vivo two-photon calcium imaging in rodents as well as intracranial and scalp electroencephalography (EEG) in humans to reveal a key role for non-oscillatory brain activity during rapid eye movement (REM) sleep to mediate sleep-dependent recalibration of neural population dynamics. The extent of this REM sleep recalibration predicted the success of overnight memory consolidation, expressly the modulation of hippocampal-neocortical activity, favoring remembering rather than forgetting. The findings describe a non-oscillatory mechanism how human REM sleep modulates neural population activity to enhance long-term memory.

Published
2023

4. Stress-induced hyperalgesia instead of analgesia in patients with chronic musculoskeletal pain

Author

Löffler, Martin, Schneider, Pia, Schuh-Hofer, Sigrid, Kamping, Sandra, Usai, Katrin, Treede, Rolf-Detlef, Nees, Frauke, and Flor, Herta

Subjects
Quantitative Biology - Neurons and Cognition
Abstract

Many individuals with chronic musculoskeletal pain (CMP) show impairments in their pain-modulatory capacity. Although stress plays an important role in chronic pain, it is not known if stress-induced analgesia (SIA) is affected in patients with CMP. We investigated SIA in 22 patients with CMP and 18 pain-free participants. Pain thresholds, pain tolerance and suprathreshold pain ratings were examined before and after a cognitive stressor that typically induces pain reduction (SIA). Whereas the controls displayed a significant increase in pain threshold in response to the stressor, the patients with CMP showed no analgesia. In addition, increased pain intensity ratings after the stressor indicated hyperalgesia (SIH) in the patients with CMP compared to controls. An exploratory analysis showed no significant association of SIA or SIH with spatial pain extent. We did not observe significant changes in pain tolerance or pain unpleasantness ratings after the stressor in patients with CMP or controls. Our data suggest that altered stress-induced pain modulation is an important mechanism involved in CMP. Future studies need to clarify the psychobiological mechanisms of these stress-induced alterations in pain processing and determine the role of contributing factors such as early childhood trauma, catastrophizing, comorbidity with mental disorders and genetic predisposition.

Published
2019

17. Diabetic neuropathy is a generalized phenomenon with impact on hand functional performance and quality of life

Author

Kender, Zoltan, primary, Groener, Jan B., additional, Jende, Johann M. E., additional, Kurz, Felix T., additional, Fleming, Thomas, additional, Sulaj, Alba, additional, Schuh‐Hofer, Sigrid, additional, Treede, Rolf‐Detlef, additional, Bendszus, Martin, additional, Szendroedi, Julia, additional, Nawroth, Peter P., additional, and Kopf, Stefan, additional

Published
2022
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18. Stress-induced hyperalgesia instead of analgesia in patients with chronic musculoskeletal pain

Author

Löffler, Martin, Schneider, Pia, Schuh-Hofer, Sigrid, Kamping, Sandra, Usai, Katrin, Treede, Rolf-Detlef, Nees, Frauke, Flor, Herta, Löffler, Martin, Schneider, Pia, Schuh-Hofer, Sigrid, Kamping, Sandra, Usai, Katrin, Treede, Rolf-Detlef, Nees, Frauke, and Flor, Herta

Abstract

Many individuals with chronic musculoskeletal pain (CMP) show impairments in their pain-modulatory capacity. Although stress plays an important role in chronic pain, it is not known if stress-induced analgesia (SIA) is affected in patients with CMP. We investigated SIA in 22 patients with CMP and 18 pain-free participants. Pain thresholds, pain tolerance and suprathreshold pain ratings were examined before and after a cognitive stressor that typically induces pain reduction (SIA). Whereas the controls displayed a significant increase in pain threshold in response to the stressor, the patients with CMP showed no analgesia. In addition, increased pain intensity ratings after the stressor indicated hyperalgesia (SIH) in the patients with CMP compared to controls. An exploratory analysis showed no significant association of SIA or SIH with spatial pain extent. We did not observe significant changes in pain tolerance or pain unpleasantness ratings after the stressor in patients with CMP or controls. Our data suggest that altered stress-induced pain modulation is an important mechanism involved in CMP. Future studies need to clarify the psychobiological mechanisms of these stress-induced alterations in pain processing and determine the role of contributing factors such as early childhood trauma, catastrophizing, comorbidity with mental disorders and genetic predisposition.

Published
2022

24. Pain thresholds and intensities of CRPS type I and neuropathic pain in respect to sex

Author

Meyer‐Frießem, Christine H., primary, Attal, Nadine, additional, Baron, Ralf, additional, Bouhassira, Didier, additional, Finnerup, Nanna B., additional, Freynhagen, Rainer, additional, Gierthmühlen, Janne, additional, Haanpää, Maija, additional, Hansson, Per, additional, Jensen, Troels S., additional, Kemp, Harriet, additional, Kennedy, Donna, additional, Leffler, Anne‐Sofie, additional, Rice, Andrew S. C., additional, Segerdahl, Märta, additional, Serra, Jordi, additional, Sindrup, Soeren, additional, Solà, Roma, additional, Tölle, Thomas, additional, Schuh‐Hofer, Sigrid, additional, Treede, Rolf‐Detlef, additional, Pogatzki‐Zahn, Esther, additional, Maier, Christoph, additional, and Vollert, Jan, additional

Published
2020
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25. Understanding Diabetic Neuropathy—From Subclinical Nerve Lesions to Severe Nerve Fiber Deficits: A Cross-Sectional Study in Patients With Type 2 Diabetes and Healthy Control Subjects

Author

Groener, Jan B., primary, Jende, Johann M.E., additional, Kurz, Felix T., additional, Kender, Zoltan, additional, Treede, Rolf-Detlef, additional, Schuh-Hofer, Sigrid, additional, Nawroth, Peter P., additional, Bendszus, Martin, additional, and Kopf, Stefan, additional

Published
2020
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29. Early gamma-oscillations as correlate of localized nociceptive processing in primary sensorimotor cortex.

Author

UCL - SSS/IONS - Institute of NeuroScience, UCL - SSS/IONS/COSY - Systems & cognitive Neuroscience, Heid, C, Mouraux, André, Treede, Rolf Detlef, Schuh-Hofer, Sigrid, Rupp, André, Baumgärtner, Ulf, UCL - SSS/IONS - Institute of NeuroScience, UCL - SSS/IONS/COSY - Systems & cognitive Neuroscience, Heid, C, Mouraux, André, Treede, Rolf Detlef, Schuh-Hofer, Sigrid, Rupp, André, and Baumgärtner, Ulf

Abstract

Recent studies put forward the idea that stimulus-evoked gamma-band oscillations (GBOs; 30-100 Hz) play a specific role in nociception. So far, evidence for the specificity of GBOs for nociception, their possible involvement in nociceptive sensory discriminatory abilities, and knowledge regarding their cortical sources is just starting to grow. To address these questions, we used electroencephalography (EEG) to record brain activity evoked by phasic nociceptive laser stimuli and tactile stimuli applied at different intensities to the right hand and foot of 12 healthy volunteers. The EEG was analyzed in the time domain to extract phase-locked event-related brain potentials (ERPs) and in three regions of interest in the time-frequency domain (delta/theta, 40-Hz gamma, 70-Hz gamma) to extract stimulus-evoked changes in the magnitude of non-phase-locked brain oscillations. Both nociceptive and tactile stimuli, matched with respect to subjective intensity, elicited phase locked ERPs of increasing amplitude with increasing stimulus intensity. In contrast, only nociceptive stimuli elicited a significant enhancement of GBOs (65-85 Hz, 150-230 ms after stimulus onset), whose magnitude encoded stimulus intensity, whereas tactile stimuli led to a GBO decrease. Following nociceptive hand stimulation, the topographical distribution of GBOs was maximal at contralateral electrode C3, whereas maximum activity following foot stimulation was recorded at the midline electrode Cz, compatible with generation of GBOs in the representations of the hand and foot of the primary sensorimotor cortex, respectively. The differential behavior of high-frequency GBOs and low-frequency 40-Hz GBOs is indicating different functional roles and regions in sensory processing. Gamma-band oscillations show hand-foot somatotopy compatible with generation in primary sensorimotor cortex and are present following nociceptive but not tactile stimulation of the hand and foot in humans.

Published
2020

32. Technical and clinical performance of the thermo‐test device “Q‐Sense” to assess small fibre function: A head‐to‐head comparison with the “Thermal Sensory Analyzer” TSA in diabetic patients and healthy volunteers

Author

Pfau, Doreen B., primary, Greffrath, Wolfgang, additional, Schilder, Andreas, additional, Magerl, Walter, additional, Ohler, Carolin, additional, Westermann, Andrea, additional, Maier, Christoph, additional, Doppler, Kathrin, additional, Sommer, Claudia, additional, Orth, Michael, additional, Hammes, Hans‐Peter, additional, Kurz, Jochen, additional, Götz, Marcus, additional, Treede, Rolf‐Detlef, additional, and Schuh‐Hofer, Sigrid, additional

Published
2019
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35. Stratifying patients with peripheral neuropathic pain based on sensory profiles: algorithm and sample size recommendations

Author

Vollert, Jan, Maier, Christoph, Attal, Nadine, Bennett, David L H, Bouhassira, Didier, Enax-Krumova, Elena K, Finnerup, Nanna B, Freynhagen, Rainer, Gierthmühlen, Janne, Haanpää, Maija, Hansson, Per, Hüllemann, Philipp, Jensen, Troels S, Magerl, Walter, Ramirez, Juan D, Rice, Andrew S C, Schuh-Hofer, Sigrid, Segerdahl, Märta, Serra, Jordi, Shillo, Pallai R, Sindrup, Soeren, Tesfaye, Solomon, Themistocleous, Andreas C, Tölle, Thomas R, Treede, Rolf-Detlef, Baron, Ralf, Universitatsklinikum Schleswig - Holstein, Commission of the European Communities, Clinicum, University of Helsinki, Neurokirurgian yksikkö, Department of Neurosciences, and HUS Neurocenter

Subjects
Pain Threshold, Diabetic polyneuropathy, Clinical Neurology, Quantitative sensory testing, PLACEBO-CONTROLLED TRIAL, PHENOTYPE, 3124 Neurology and psychiatry, LIDOCAINE, MECHANISMS, 17 Psychology And Cognitive Sciences, DOUBLE-BLIND, Anesthesiology, Physical Stimulation, Surveys and Questionnaires, Journal Article, Humans, German Research Network on Neuropathic Pain, Pain Measurement, Science & Technology, fungi, 3112 Neurosciences, Neurosciences, food and beverages, POSTHERPETIC NEURALGIA, 11 Medical And Health Sciences, 3126 Surgery, anesthesiology, intensive care, radiology, Hyperalgesia, EVALUATION TOOL, Sample Size, Peripheral nerve injury, GERMAN RESEARCH NETWORK, Neuralgia, GRADING SYSTEM, Neurosciences & Neurology, Life Sciences & Biomedicine, Algorithms, CLINICAL-TRIALS, Research Paper
Abstract

Supplemental Digital Content is Available in the Text. Phenotype stratification of patients with peripheral neuropathic pain can be conducted with a novel algorithm based on sensory profiles., In a recent cluster analysis, it has been shown that patients with peripheral neuropathic pain can be grouped into 3 sensory phenotypes based on quantitative sensory testing profiles, which are mainly characterized by either sensory loss, intact sensory function and mild thermal hyperalgesia and/or allodynia, or loss of thermal detection and mild mechanical hyperalgesia and/or allodynia. Here, we present an algorithm for allocation of individual patients to these subgroups. The algorithm is nondeterministic—ie, a patient can be sorted to more than one phenotype—and can separate patients with neuropathic pain from healthy subjects (sensitivity: 78%, specificity: 94%). We evaluated the frequency of each phenotype in a population of patients with painful diabetic polyneuropathy (n = 151), painful peripheral nerve injury (n = 335), and postherpetic neuralgia (n = 97) and propose sample sizes of study populations that need to be screened to reach a subpopulation large enough to conduct a phenotype-stratified study. The most common phenotype in diabetic polyneuropathy was sensory loss (83%), followed by mechanical hyperalgesia (75%) and thermal hyperalgesia (34%, note that percentages are overlapping and not additive). In peripheral nerve injury, frequencies were 37%, 59%, and 50%, and in postherpetic neuralgia, frequencies were 31%, 63%, and 46%. For parallel study design, either the estimated effect size of the treatment needs to be high (>0.7) or only phenotypes that are frequent in the clinical entity under study can realistically be performed. For crossover design, populations under 200 patients screened are sufficient for all phenotypes and clinical entities with a minimum estimated treatment effect size of 0.5.

Published
2017
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38. Nitric oxide from perivascular nerves modulates cerebral arterial pH reactivity

Author

LINDAUER, UTE, KUNZ, ALEXANDER, SCHUH-HOFER, SIGRID, VOGT, JOHANNES, DREIER, JENS P., and DIRNAGL, ULRICH

Subjects
Acidosis -- Physiological aspects, Endothelium -- Physiological aspects, Nitric oxide -- Physiological aspects, Biological sciences
Abstract

In the isolated rat middle cerebral artery (MCA) we investigated the role of nitric oxide (NO)/ cGMP in the vasodilatory response to extraluminal acidosis. Acidosis increased vessel diameter from 140 [+ or -] 27 [micro]m (pH 7.4) to 187 [+ or -] 30 [micro]m (pH 7.0, P [is less than] 0.01). NO synthase (NOS) inhibition by [N.sup.[Omega]]-nitro-L-arginine (L-NNA, 10 [micro]M) reduced baseline diameter (103 [+ or -] 20 [micro]m, P [is less than] 0.01) and attenuated response to acidosis (9 [+ or -] 8 [micro]m). Application of the NO-donors 3-morpholinosydnonimine (1 [micro]M) or S-nitroso-N-acetylpenicillamine (1 [micro]M), or of 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP, 100 [micro]M) reestablished pre-L-NNA diameter at pH 7.4 and reversed L-NNA-induced attenuation of the vessel response to acidosis. Restoration of pre-L-NNA diameter (pH 7.4) by papaverine (20 [micro]M) or nimodipine (30 nM) had no effect on the attenuated response to acidosis. Guanylyl cyclase inhibition with 1H-[1,2,4] oxadiazolo [4,3-a]-quinoxalin-1-one (5 [micro]M) or NOS-inhibition with 7-nitroindazole (7-NI, 100 [micro]M) reduced baseline vessel diameter (109 [+ or -] 8 or 127 [+ or -] 11 [micro]m, respectively) and vasodilation to acidosis, and restoration of baseline diameter with 8-BrcGMP (30 [micro]M) completely restored dilation to pH 7.0. Chronic denervation of NOS-containing perivascular nerves in vivo 14 days before artery isolation significantly reduced pH-dependent reactivity in vitro (diameter increase sham: 48 [+ or -] 14 [micro]m, denervated: 14 [+ or -] 8 [micro]m), and 8-BrcGMP (30 [micro]M) restored dilation to pH 7.0 (denervated: 49 [+ or -] 31 [micro]m). Removal of the endothelium did not change vasodilation to acidosis. We conclude that NO, produced by neuronal NOS of perivascular nerves, is a modulator in the pH-dependent vasoreactivity. acidosis; endothelium; isolated cerebral artery; nitric oxide synthase; rat; soluble guanylyl cyclase

Published
2001

41. Decrease in parietal cerebral hemoglobin oxygenation during performance of a verbal fluency task in patients with Alzheimer's disease monitored by means of near-infrared spectroscopy (NIRS) — correlation with simultaneous rCBF-PET measurements

Author

Hock, Christoph, primary, Villringer, Kersten, additional, Müller-Spahn, Franz, additional, Wenzel, Rüdiger, additional, Heekeren, Hauke, additional, Schuh-Hofer, Sigrid, additional, Hofmann, Marc, additional, Minoshima, Satoshi, additional, Schwaiger, Markus, additional, Dirnagl, Ulrich, additional, and Villringer, Arno, additional

Published
1997
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