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3. Hereditäre Transthyretinamyloidose (ATTRv-Amyloidose)

Author

F. Escolano-Lozano, Ernst Hund, C. Sommer, Wilhelm Schulte-Mattler, Jens Schmidt, C. Geber, M. Auer-Grumbach, Ralf Baron, M. Schilling, J. Sachau, Markus Weiler, H. C. Lehmann, Maike F. Dohrn, N. Grether, F. Birklein, Katrin Hahn, and T. Hagenacker

Subjects
medicine.medical_specialty, business.industry, medicine, business, Dermatology
Published
2020
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6. Das komplexe regionale Schmerzsyndrom (CRPS)

Author

F. Birklein and V. Dimova

Subjects
medicine.medical_specialty, Neurology, Pain medicine, 03 medical and health sciences, 0302 clinical medicine, Pharmacotherapy, 030202 anesthesiology, Internal medicine, Medicine, 030212 general & internal medicine, Gynecology, business.industry, Chronic pain, 030208 emergency & critical care medicine, General Medicine, medicine.disease, Rheumatology, Anesthesiology and Pain Medicine, Complex regional pain syndrome, Anesthesia, Hyperalgesia, Anxiety, Neurology (clinical), medicine.symptom, business, 030217 neurology & neurosurgery
Abstract

The acute phase of complex regional pain syndrome (CRPS) is pathophysiologically characterized by an activation of the immune system and its associated inflammatory response. During the course of CRPS, central nervous symptoms like mechanical hyperalgesia, loss of sensation, and body perception disorders develop. Psychological factors such as pain-related anxiety and traumatic events might have a negative effect on the treatment outcome. While the visible inflammatory symptoms improve, the pain often persists. A stage adapted, targeted treatment could improve the prognosis. Effective multidisciplinary treatment includes the following: pharmacotherapy with steroids, bisphosphonates, or dimethylsulfoxide cream (acute phase), and antineuropathic analgesics (all phases); physiotherapy and behavioral therapy for pain-related anxiety and avoidance of movement; and interventional treatment like spinal cord or dorsal root ganglion stimulation if noninvasive options failed.

Published
2018
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7. [Complex regional pain syndrome (CRPS) : An update]

Author

V, Dimova and F, Birklein

Subjects
Analgesics, Treatment Outcome, Diphosphonates, Hyperalgesia, Pain, Humans, Complex Regional Pain Syndromes
Abstract

The acute phase of complex regional pain syndrome (CRPS) is pathophysiologically characterized by an activation of the immune system and its associated inflammatory response. During the course of CRPS, central nervous symptoms like mechanical hyperalgesia, loss of sensation, and body perception disorders develop. Psychological factors such as pain-related anxiety and traumatic events might have a negative effect on the treatment outcome. While the visible inflammatory symptoms improve, the pain often persists. A stage adapted, targeted treatment could improve the prognosis. Effective multidisciplinary treatment includes the following: pharmacotherapy with steroids, bisphosphonates, or dimethylsulfoxide cream (acute phase), and antineuropathic analgesics (all phases); physiotherapy and behavioral therapy for pain-related anxiety and avoidance of movement; and interventional treatment like spinal cord or dorsal root ganglion stimulation if noninvasive options failed.

Published
2018

8. Komplexes regionales Schmerzsyndrom (CRPS)

Author

F. Birklein

Abstract

Das komplex-regionale Schmerzsyndrom (CRPS) ist durch Schmerz, sensorische, vegetative, motorische und trophische Storungen charakterisiert. Die Symptomatik andert sich jedoch im Verlauf. Zu Beginn ist die Pathophysiologie durch die Aktivierung des Immunsystems dominiert. Danach entwickeln sich zentrale Reorganisations- und Lernvorgange. Dadurch werden Bewegungsstorungen, vegetative und sensible Symptome und Korperschemastorungen generiert. Psychische Faktoren beeinflussen den Verlauf. Die Therapie muss der jeweiligen pathophysiologischen Veranderung angepasst sein: eine antientzundliche medikamentose Therapie (Steroide, Bisphosphonate, DMSO-Creme) in akuten Stadien, gegen die Schmerzen die ublichen antineuropathischen Medikamente; i.v. Ketamin ist nebenwirkungsreich. Wichtige Therapiebestandteile sind weiter Physio- und Ergotherapie, z. T. mit verhaltenstherapeutischen Ansatzen, evtl. Psychotherapie, invasive Verfahren nur in Ausnahmefallen. Die Prognose bezuglich Funktion und Schmerz ist nicht generell schlecht.

Published
2018
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9. Lindernde Wirkung des CGRP-Antagonismus auf Entzündungsschmerz

Author

S. Hirsch and F. Birklein

Subjects
Gynecology, medicine.medical_specialty, Anesthesiology and Pain Medicine, business.industry, Medicine, Neurology (clinical), Calcitonin gene-related peptide, business, Antagonism, Inflammatory pain
Abstract

Das Neuropeptid „calcitonin gene-related peptide“ (CGRP) ist an der Pathogenese verschiedener Schmerzkrankheiten beteiligt. Uber seine Bedeutung bei Entzundungsschmerz ist aber noch nicht viel bekannt. Vor einigen Jahren wurde gezeigt, dass der CGRP-Rezeptor-Antagonist BIBN4096BS Schmerzen bei Migrane und die dazugehorige spinale neuronale Aktivitat afferenter Neurone reduziert. Wird Ratten das komplettierte Freund-Adjuvans (CFA) in eine Hinterpfote injiziert, um eine Entzundung zu erzeugen, finden wir ebenfalls eine analgetische Wirkung von BIBN4096BS. Sowohl das Schmerzverhalten der Tiere als auch die spinale Aktivitat nozizeptiver Projektionsneurone wird durch BIBN4096BS verringert. Im Verhaltensversuch (Randall-Selitto-Test) kann die CFA-induzierte mechanische Hyperalgesie durch systemische Applikation der Substanz vollstandig revidiert werden. Im elektrophysiologischen Experiment, bei dem spinale Neurone extrazellular in vivo abgeleitet werden, verringert sich die Entladungsfrequenz der Nervenzellen („wide dynamic range neurons“) nach systemischer Substanzgabe und uberraschenderweise auch nach deren topischer Applikation auf die Entzundungsstelle. Bemerkenswert ist dabei, dass nach topischer Gabe die Plasmaspiegel im lediglich niederen nanomolaren Bereich liegen. Die spinale Applikation von BIBN4096BS verandert die Nervenzellaktivitat nicht. Zu vermuten ist daher, dass eine Blockade peripherer CGRP-Rezeptoren fur eine Schmerzreduktion durch BIBN4096BS verantwortlich ist und dass diese durch lokale Gabe erzielt werden kann.

Published
2014
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10. [Pain - a neglected neurological issue]

Author

F, Birklein, R, Baron, C, Gaul, C, Maihöfner, O, Rommel, A, Straube, T, Tölle, and G, Wasner

Subjects
Patient Care Team, Health Services Needs and Demand, Neuronal Plasticity, Neglected Diseases, Nervous System, Neurology, Germany, Pain Management, Interdisciplinary Communication, Chronic Pain, Nervous System Diseases, Delivery of Health Care, Intersectoral Collaboration, Diagnosis-Related Groups, Forecasting, Specialization
Abstract

Chronic pain represents a great challenge; according to epidemiological data increasing numbers of patients should be expected. Based on recent advances, a better understanding of the pathophysiology of chronic pain has been achieved and neurologists have made a major contribution to this understanding. Chronic pain is accompanied by substantial maladaptive plastic alterations in both the peripheral and central nervous systems; therefore, neurological knowledge is of paramount importance for pain therapists but this contrasts with the current treatment situation of pain patients in Germany. There are basically too few departments and practices undertaking treatment, and neurologists are an exception in most pain centers. Furthermore, due to economic reasons neurological hospitals are currently experiencing a dearth of inpatients suffering from chronic pain. Diagnostic and/or treatment procedures for neurological pain entities (e.g. headaches or neuropathic pain) are insufficiently represented in the German diagnosis-related groups (DRG) reimbursement system and the obstacles for an efficient pain therapy in neurological practices are too high. Finally, there are too few academic positions for pain medicine in neurological hospitals; therefore, career opportunities for motivated young neurologists with an interest in pain are lacking. In order to address the unmet therapeutic needs of patients with chronic pain there is a high demand for (i) establishment of departments for neurological pain medicine, (ii) modification of the German DRG system and (iii) education of young neurologists with expertise in pain. Pain medicine in particular should be especially appealing to neurologists .

Published
2016

11. Aktuelles zur Pathophysiologie und Therapie des komplex-regionalen Schmerzsyndroms (CRPS)

Author

F. Birklein and M. Fechir

Subjects
Gynecology, medicine.medical_specialty, business.industry, Physiology (medical), Medicine, Complex regional pain syndrome type I, Neurology (clinical), business
Abstract

Bei etwa 2% der Patienten kommt es, meist nach einem Trauma einer Extremitat, einer Lasion eines periphereren Nervs oder des zentralen Nervensystems, zum Auftreten charakteristischer Symptomkonstellationen mit schmerzhafter Funktionseinschrankung, die als „komplex-regionales Schmerzsyndrom“ (CRPS) bezeichnet werden. Die Symptome bestehen aus Storungen der Sensibilitat (z. B. Taubheitsgefuhle, Schmerzen, Hyperalgesie), der Motorik (z. B. Kraftminderung, Tremor, Dystonie), des autonomen Nervensystems (z. B. Anderungen der Hauttemperatur, des Schwitzens sowie Verfarbung der Haut) und der Trophik (z. B. verandertes Wachstum von Haaren, Finger-/Fusnageln). Komplex-regionale Schmerzsyndrome werden in Anhangigkeit des Nachweises einer Nervenlasion unterteilt in Typ I ohne Lasion und Typ II mit Nervenlasion. Jedoch erscheint zudem eine Einteilung nach der Hauttemperatur zu Beginn der Erkrankung sinnvoll, da dies auch pathophysiologische Aspekte berucksichtigt („primar warmes“ bzw. „primar kaltes CRPS“). Dank intensiver Forschungen der letzten Jahre konnten die Mechanismen des CRPS zunehmend besser erklart werden. Die unterschiedlichen beteiligten pathophysiologischen Prozesse sind in der vorliegenden Ubersichtsarbeit dargestellt. Um eine Chronifizierung und bleibende Funktionseinschrankung zu vermeiden bzw. eine gute Extremtitatenfunktion wiederherzustellen, ist moglichst fruhzeitig eine individuell angepasste, multi-disziplinare Therapie unter Einbeziehung medikamentoser und nicht-medikamentoser Verfahren anzustreben. Die zur Verfugung stehenden Optionen werden in dieser Arbeit ebenfalls vorgestellt.

Published
2012
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12. Vom M. Sudeck zum komplexregionalen Schmerzsyndrom

Author

F. Birklein and M. Fechir

Subjects
Neurology (clinical), Family Practice
Abstract

ZusammenfassungNach Extremitätentraumata, Läsionen peripherer Nerven oder des zentralen Nervensystems und selten spontan kann es zum Auftreten von charakteristischen Symptomkonstellationen eines komplex-regionalen Schmerzsyndroms (CRPS) kommen. Diese bestehen aus motorischen, sensiblen sowie autonomen Störungen. Nachdem dieser Symptomkomplex in der Vergangenheit mit wechselnden Bezeichnungen (z. B. M. Sudeck, Kausalgie, sympathische Reflexdystrophie) belegt wurde, lautet die von der International Association for the Study of Pain vorgeschlagene und aktuell verwendete Bezeichnung „komplexregionales Schmerzsyndrom“ (complex regional pain syndrome, CRPS). Aufgrund pathophysiologischer Gesichtspunkte erscheint eine Einteilung in Abhängigkeit der Hauttemperatur prinzipiell sinnvoller (primär warmes oder primär kaltes CRPS) als eine Einteilung in Typ I und II, der die Abwesenheit oder das Vorliegen einer einzelnen und eindeutigen peripheren Nervenläsion zugrunde liegt. Eine frühzeitige Diagnosestellung und Beginn einer auf die Symptomatik individuell abgestimmten Therapie unter Einbeziehung nicht medikamentöser und medikamentöser Therapieverfahren sind wichtig, um eine Chronifizierung zu vermeiden und die Funktion der betroffenen Extremität zu erhalten oder wieder herzustellen.

Published
2012
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13. Therapie chronischer Schmerzen in der neurologischen Praxis

Author

F. Birklein, A. May, and S. Sternberg

Subjects
medicine.medical_specialty, Neurology, business.industry, Chronic pain, Psychosomatic medicine, General Medicine, medicine.disease, Psychiatry and Mental health, Neuropathic pain, Physical therapy, medicine, Outpatient clinic, Neurology (clinical), Neurosurgery, business, Acute pain
Abstract

Although chronic pain is common, especially in elderly patients, its treatment often remains inadequate. One of many reasons for this is that insufficient therapy of acute pain carries the risk of making the pain chronic. Sooner or later most patients suffering from chronic pain will consult a neurologist. However, in most neurological departments, pain treatment is neither one of the common medical activities nor a subject in medical education. In Germany, only specialised centres have associated pain outpatient clinics, so it is almost impossible for neurologist trainees to improve their knowledge in pain treatment. This review provides a synopsis of procedures regarding chronic pain treatments, with particular focus on the most frequent pain disorders. The treatment recommendations follow the current guidelines of the German Society of Neurology.

Published
2008
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14. Das komplexe regionale Schmerzsyndrom

Author

P. M. Rommens, P. Ingelfinger, F. Birklein, Alexander Hofmann, A. Lingawi, and M. H. Hessmann

Subjects
medicine.medical_specialty, Sports medicine, business.industry, Radiography, Acetabular fracture, Hand surgery, medicine.disease, Acetabulum, Surgery, Plastic surgery, Complex regional pain syndrome, Emergency Medicine, medicine, Orthopedics and Sports Medicine, Sciatic nerve, business
Abstract

Complex regional pain syndrome (CRPS) is seldom observed in the lower extremities. A case of a 19-year-old patient with typical symptoms in the lower leg and foot after surgical treatment of an acetabular fracture is described. Differential diagnostic evaluation should include CRPS in patients with persistent or progressive pain in the distal extremity after acetabular fracture. Early diagnosis and therapy contribute significantly to a successful outcome.

Published
2007
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15. Komplex regionale Schmerzsyndrome: Neues zu Pathophysiologie und Therapie

Author

F. Birklein and C. Maihöfner

Subjects
Dystonia, Nervous system, business.industry, medicine.disease, Spinal cord stimulator, law.invention, Psychiatry and Mental health, Pharmacotherapy, Complex regional pain syndrome, medicine.anatomical_structure, Neurology, law, Anesthesia, Hyperalgesia, Neuropathic pain, medicine, Neurology (clinical), medicine.symptom, business, Paresis
Abstract

Complex-regional pain syndromes (CRPS), formerly known as Sudeck's dystrophy and causalgia, belong to the neuropathic pain syndromes. CRPS may develop following fractures, limb trauma or lesions of the peripheral or central (CNS) nervous system. Occasionally, CRPS may also develop spontaneously. The clinical picture comprises a characteristic clinical triade of symptoms including autonomic (disturbances of skin temperature, colour, presence of sweating abnormalities), sensory (pain and hyperalgesia) and motor (paresis, tremor, dystonia) disturbances. Diagnosis is mainly based on clinical signs. However, additional laboratory, neurophysiological and radiological examinations may help to corroborate correct diagnosis. Several pathophysiological concepts have been proposed to explain the complex symptoms of CRPS: 1, facilitated neurogenic inflammation; 2, pathological sympatho-afferent coupling; 3, neuroplastic changes within the CNS. Furthermore, there is accumulating evidence that genetic factors may predispose for CRPS. Therapy is based on a multidisciplinary approach. Non-pharmacological approaches include physiotherapy and occupational therapy. Pharmacotherapy is based on individual symptoms and includes steroids, free radical scavengers, treatment of neuropathic pain, and finally agents interfering with bone metabolism (calcitonin, biphosphonates). Sympathetic blocks are useful for the treatment of sympathetically maintained pain. Invasive therapeutic concepts include implantation of spinal cord stimulators. This review covers new aspects of pathophysiology and therapy of CRPS.

Published
2007
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16. Mechanisms of neuropathic pain and their importance in Fabry disease

Author

F Birklein

Subjects
business.industry, Mechanism (biology), Pain, General Medicine, Bioinformatics, medicine.disease, Fabry disease, Nociception, medicine.anatomical_structure, Disinhibition, Anesthesia, Pediatrics, Perinatology and Child Health, Neuropathic pain, medicine, Etiology, Fabry Disease, Humans, Nervous System Diseases, medicine.symptom, business, Pathological, Sensitization
Abstract

UNLABELLED One of the most prominent features of Fabry disease is neuropathic pain. Neuropathic pain occurs after neuronal damage. In contrast to inflammatory or trauma-related pain, which normally helps to maintain or restore body functions, neuropathic pain tends to become chronic, and must therefore be considered a 'pathological' pain. Neuropathic pain has usually been classified according to the aetiology of nerve damage: traumatic, inflammatory, cancer-related or metabolic (e.g. Fabry disease). However, use of this classification often results in inadequate therapy for neuropathic pain. Recent research has revealed distinct mechanisms that are responsible for neuropathic pain. These mechanisms are independent of the aetiology of nerve damage. The most important mechanisms are accumulation and maldistribution of sodium channels on injured axons, pathological sympatho-afferent coupling, disinhibition of nociception and central or peripheral nociceptive sensitization. CONCLUSIONS Future research should focus on diagnostic tools to identify the predominant mechanisms in individual patients. These mechanism could be targeted specifically by drugs, or non-drug therapy, enabling more effective treatment of neuropathic pain.

Published
2007
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17. Das Horner-Syndrom - Ein Update zur Neuroanatomie, topographischen Differenzialdiagnostik und Ätiologie

Author

J. J. Marx, F. Birklein, and F. Thömke

Subjects
S syndrome, business.industry, Signs and symptoms, Lesion, Sudomotor, Psychiatry and Mental health, medicine.anatomical_structure, Neurology, Neuroimaging, Functional anatomy, Etiology, medicine, Neurology (clinical), medicine.symptom, business, Neuroscience, Neuroanatomy
Abstract

Due to the complex neuroanatomy of the sympatho-excitatory pathway, Horner's syndrome represents a clinical sign that may result from a variety of lesions in the central and peripheral nervous system. The purpose of the present communication is to help the reader to localize the site of the lesion and to demonstrate the most common etiologic mechanisms resulting in Horner's syndrome. The functional anatomy of the sympathetic supply to the iris, eyelids, facial sweat glands and blood vessels is reviewed and in particular the structure of the central pathway updated. Moreover, pharmacological testing and tests of sudomotor function are described that may help to guide the decision regarding useful additional diagnostic, especially neuroimaging procedures. Finally, a schematic overview is given on the most common pathology, considering additional clinical signs and symptoms.

Published
2005
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18. Schmerz ist nicht gleich Schmerz – ein Fallbericht als Plädoyer für eine differenzierte Schmerzdiagnostik und Therapie

Author

F. Birklein and S. Seddigh

Subjects
Physiology (medical), Neurology (clinical)
Abstract

Wir berichten von einer Patientin mit Armschmerzen nach mehrfachen Handgelenkoperationen. Sie wurde jahrelang unter der Diagnose Komplexes Regionales Schmerzsyndrom behandelt. Die sorgfaltige Aufarbeitung der Krankengeschichte und die klinische Untersuchung legte ein myofasziales Schmerzsyndrom nahe. Nach einer Infiltration muskularer Triggerpunkte in der Schulterblattmuskulatur bildeten sich Schmerzen, Sensibilitatsstorungen und vegetative Symptome sofort zuruck. Eine sorgfaltige klinische Untersuchung sollte Grundlage der Behandlung chronischer Schmerzpatienten sein.

Published
2012
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19. Morbus Sudeck - Pathophysiologie und Therapie eines komplexen Schmerzsyndroms

Author

F Birklein, Bernhard Neundörfer, and Margarete Weber

Subjects
medicine.medical_specialty, Pain syndrome, business.industry, General Medicine, Disease, medicine.disease, Dermatology, Pathophysiology, Spontaneous pain, Atrophy, Complex regional pain syndrome, Hyperalgesia, medicine, Autonomic symptoms, medicine.symptom, business
Abstract

UNLABELLED Sudeck's atrophy: pathophysiology and treatment of a complex pain syndrome. SUMMARY The "Morbus Sudeck" or Complex Regional Pain Syndrome (CRPS) forms a typical triad of motor, sensory and autonomic symptoms. It is clinically characterized by spontaneous pain and hyperalgesia not limited to a single nerve territory and disproportionate to the inciting event. An underlying pathophysiology which could explain the whole symptomatology of CRPS is still unknown. Therefore, nowadays therapy is still symptomatic. However, recent research led to a better understanding of the disease and to the beginning of a pathophysiologically orientated therapy.

Published
2002
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20. Neuropathische Schmerzen - Mechanismen und Therapie

Author

F. Birklein

Subjects
business.industry, Mechanism (biology), Peripheral, Psychiatry and Mental health, Nociception, Neurology, Disinhibition, Neuropathic pain, Etiology, Medicine, Neurology (clinical), medicine.symptom, business, Pathological, Neuroscience, Pain therapy
Abstract

Traditionally, neuropathic pain has been classified due to aetiology of nerve damage-traumatic, inflammatory or metabolic, for instance. Based on this classification, pain therapy often is insufficient. Recent research revealed different mechanisms, which are responsible for the generation of pain after nerve lesion. These mechanisms seem to be independent of aetiology of the nerve damage. The most important mechanisms are accumulation of sodium channels on injured nerves, pathological sympatho-afferent coupling, disinhibition of nociception and central or peripheral nociceptive sensitisation. Each individual mechanism could be treated specifically by current available drugs, or by non-drug therapy. However, future research has to focus on exploring tools to recognise individual pain mechanisms in single patients. Thereby treatment will become more effective.

Published
2002
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21. [Pain-relieving effect of CGRP antagonism on inflammatory pain]

Author

S, Hirsch and F, Birklein

Subjects
Inflammation, Neurons, Pain Threshold, Disease Models, Animal, Spinal Cord, Calcitonin Gene-Related Peptide Receptor Antagonists, Quinazolines, Animals, Chronic Pain, Piperazines, Rats, Receptors, Calcitonin Gene-Related Peptide
Abstract

The neuropeptide calcitonin gene-related peptide (CGRP) is known to play a major role in the pathogenesis of pain syndromes, in particular migraine pain; however, its implication in inflammatory processes is not well known. The CGRP receptor antagonist BIBN4096BS was shown to reduce migraine pain and trigeminal neuronal activity. An analgesic action of this compound can also be found in rats with induced acute inflammation by injection of complete Freund's adjuvant (CFA) in one hindpaw. In this model the compound reduced inflammatory pain and spinal neuronal activity. Behavioral experiments (Randall-Selitto test) revealed a reversal of the CFA-induced mechanical hyperalgesia in rats after systemic drug administration. In vivo electrophysiological studies performed in rats injected with CFA using recordings of wide dynamic range neurons in deep dorsal horn layers of the lumbar spinal cord, confirmed a reduction of neuronal activity after systemic drug administration. The same considerable amount of reduction occurred after topical administration onto the paw with resulting systemic plasma concentrations in the low nanomolar range. Spinal administration of BIBN4096BS did not modify the neuronal activity in the CFA model which suggests that peripheral blockade of CGRP receptors by BIBN4096BS significantly alleviates inflammatory pain.

Published
2014

22. Association between pain, central sensitization and anxiety in postherpetic neuralgia

Author

T, Schlereth, A, Heiland, M, Breimhorst, M, Féchir, U, Kern, W, Magerl, and F, Birklein

Subjects
Adult, Male, Pain Threshold, Central Nervous System Sensitization, Neuralgia, Postherpetic, Pain, Anxiety, Middle Aged, Anxiety Disorders, Quality of Life, Humans, Female, Evoked Potentials, Aged
Abstract

In postherpetic neuralgia (PHN), dorsal root ganglia neurons are damaged. According to the proposed models, PHN pain might be associated with nociceptive deafferentation, and peripheral (heat hyperalgesia) or central sensitization (allodynia).In 36 PHN patients, afferent nerve fibre function was characterized using quantitative sensory testing and histamine-induced flare analysis. Psychological factors were evaluated with the Hospital Anxiety and Depression Scale (HADS), disease-related quality of life (QoL) with SF-36 and pain with the McGill questionnaire [pain rating index (PRI)]. The patients were also divided into subgroups according to the presence or absence of brush-evoked allodynia as a sign of central sensitization.For all patients, warm, cold and mechanical detection was impaired (p0.001 each) and the size of the histamine flare was diminished on the affected side (p0.05); pain thresholds with the exception of brush-evoked allodynia (p0.05) were unaltered. Correlation analysis revealed allodynia, anxiety, depression, QoL and age as relevant factors associated with pain severity (PRI). Allodynia was present in 23 patients (64%). In these patients, heat pain perception was preserved; the histamine flare was larger; the pinprick pain was increased as were McGill PRI sensory subscore, actual pain rating and almost significantly pain (McGill PRI) over the last 4 weeks.PHN is associated with damage of afferent fibres. Central sensitization (i.e., allodynia) might contribute to PHN pain. There was a striking association between anxiety, depression and age, and the magnitude of PHN pain.

Published
2014

23. Dose thresholds and duration of the local anhidrotic effect of botulinum toxin injections: measured by sudometry

Author

F. Erbguth, C. Braune, and F. Birklein

Subjects
medicine.medical_specialty, Iontophoresis, business.industry, Dermatology, medicine.disease, Botulinum toxin, Sudomotor, SWEAT, Dose–response relationship, medicine.anatomical_structure, Endocrinology, Sweat gland, Internal medicine, medicine, Axon reflex, business, medicine.drug, Focal hyperhidrosis
Abstract

Background Local injections of botulinum toxin type A (BTX-A) have been used successfully to treat focal hyperhidrosis, but because experimental data were lacking, doses have been chosen arbitrarily or empirically. Objectives To analyse dose dependency and duration of BTX-A-derived suppression of sweat gland activity. Methods Employing a standardized scheme (four injections, square 2 × 2 cm), different doses of BTX-A [Dysport®; 2·5–120 mouse units (MU)] were injected subcutaneously at the lateral aspects of both of the lower legs in 15 healthy volunteers. Sweat tests were performed before, and 3 weeks and 6 months after, BTX-A injections. Sweating was visualized by staining with iodine starch, and quantified by capacitance hygrometry after carbachol iontophoresis, the quantitative sudomotor axon reflex test (QSART). Results Iodine starch staining indicated a threshold dose of 10 MU (2·5 MU cm−2) leading to visible anhidrotic skin spots after 3 weeks in all subjects. This was maintained for 6 months with doses of 50 MU (12·5 MU cm−2) or higher, but the size of the anhidrotic skin area decreased over time (P

Published
2001
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24. Insula and sensory insular cortex and somatosensory control in patients with insular stroke

Author

B, Baier, P, zu Eulenburg, C, Geber, F, Rohde, R, Rolke, C, Maihöfner, F, Birklein, and M, Dieterich

Subjects
Cerebral Cortex, Male, Brain Mapping, Pain Perception, Somatosensory Cortex, Middle Aged, Magnetic Resonance Imaging, Cohort Studies, Hypesthesia, Stroke, Touch Perception, Humans, Female, Perception, Thermosensing, Aged
Abstract

In functional imaging studies, the insular cortex (IC) has been identified as an essential part of the processing of a whole spectrum of multimodal sensory input. However, there are no lesion studies including a sufficient number of patients, which would reinforce the functional imaging data obtained from healthy subjects. Such lesion studies should examine how damage to the IC affects sensory perception. We chose acute stroke patients with lesions affecting the IC in order to fill this gap.A comprehensive sensory profiling by applying a quantitative sensory testing protocol was performed and a voxel-lesion behaviour mapping analysis in 24 patients with acute unilateral cortical damage was applied.Our data demonstrate that patients with lesions of the posterior IC have deficits in temperature perception, but did not show other sensory deficits such as hot or cold pain perception associated with specific lesion locations.Our data allow the conclusion that the posterior IC may represent the major region responsible for encoding warm and cold perception in the brain. To what extent focal IC lesions may also impair pain processing or induce post-stroke pain has to be addressed in future studies including more patients.

Published
2014

25. [The complex regional pain syndrome]

Author

C, Sommer and F, Birklein

Subjects
Neuronal Plasticity, Sympathetic Nervous System, Risk Factors, Terminology as Topic, Humans, Complex Regional Pain Syndromes
Published
2014

26. [Current aspects of the therapy of complex regional pain syndrome]

Author

F, Birklein and T, Schlereth

Subjects
Neuronal Plasticity, Humans, Extremities, Interdisciplinary Communication, Cooperative Behavior, Autonomic Nervous System, Prognosis, Combined Modality Therapy, Complex Regional Pain Syndromes
Abstract

Complex regional pain syndrome (CRPS) constitutes an enigmatic post-traumatic pain disorder.The paper provides state of the art knowledge about CRPS.The typical constellation of symptoms of CRPS includes pain, sensory disturbances, motor symptoms, disturbances of the autonomic control of the limbs and trophic changes. These symptoms generalize distally and go beyond single nerve innervation territories. Diagnosis is made based on clinical findings. Three-phase bone scintigraphy may be the best supporting technical investigation. Symptoms typically change during the course of CRPS. In the acute stage inflammatory symptoms prevail and during chronic stages the most expressed findings are related to central neuroplasticity. These findings include hyperalgesia, sensory loss, CRPS movement disorder, body perception disturbances and autonomic symptoms. Medical treatment with anti-inflammatory agents (steroids) or bisphosphonates is most effective in the early stages and DMSO cream might also be beneficial. Administration of i.v. ketamine has been proven effective against CRPS pain and physical therapy with behavioral components, such as pain exposure helps to overcome central reorganization and functional impairment. Psychotherapy should be offered if there are significant comorbidities. All other forms of treatment are more or less empirical. Invasive treatment should be restricted to selected cases and should only be offered in specialized centers.If these recommendations are followed the prognosis for CRPS is not as poor as commonly assumed. Whether this means a return to the previous quality of life is unclear and often depends on very personal factors.

Published
2013

27. [Non-drug therapies for CRPS]

Author

H H, Krämer, C, Tanislav, and F, Birklein

Subjects
Psychotherapy, Reflex Sympathetic Dystrophy, Spinal Cord Stimulation, Treatment Outcome, Occupational Therapy, Behavior Therapy, Imagination, Transcutaneous Electric Nerve Stimulation, Humans, Combined Modality Therapy, Physical Therapy Modalities, Randomized Controlled Trials as Topic
Abstract

State of the art CRPS therapy comprises medication, interventional therapies and non-pharmaceutical treatments like physiotherapy (PT), occupational therapy, PT with cognitive behavioural elements (mirror therapy, 'motor imagery', and 'graded exposure'), psychotherapeutic methods, local therapies and neurostimulation. These treatments are mostly as successful as medical or interventional treatment. These effects have been demonstrated in small but randomised controlled studies. Adjuvant therapies were shown to reduce pain and the severity of dysfunction in CRPS. Therefore, these non-drug therapies should be an essential part of any multimodal CRPS treatment.

Published
2012

29. Skin innervation at different depths correlates with small fibre function but not with pain in neuropathic pain patients

Author

M, Schley, A, Bayram, R, Rukwied, M, Dusch, C, Konrad, J, Benrath, C, Geber, F, Birklein, B, Hägglöf, N, Sjögren, L, Gee, P J, Albrecht, F L, Rice, and M, Schmelz

Subjects
Adult, Male, Pain Threshold, Hot Temperature, Dermis, Middle Aged, Cold Temperature, Nerve Fibers, Hyperalgesia, Touch, Case-Control Studies, Sensory Thresholds, Humans, Neuralgia, Female, Epidermis, Skin
Abstract

Neuropathy can lead not only to impaired function but also to sensory sensitization. We aimed to link reduced skin nerve fibre density in different levels to layer-specific functional impairment in neuropathic pain patients and tried to identify pain-specific functional and structural markers.In 12 healthy controls and 36 patients with neuropathic pain, we assessed clinical characteristics, thermal thresholds (quantitative sensory testing) and electrically induced pain and axon reflex erythema. At the most painful sites and at intra-individual control sites, skin biopsies were taken and innervation densities in the different skin layers were assessed. Moreover, neuronal calcitonin gene-related peptide staining was quantified.Perception of warm, cold and heat pain and nerve fibre density were reduced in the painful areas compared with the control sites and with healthy controls. Warm and cold detection thresholds correlated best with epidermal innervation density, whereas heat and cold pain thresholds and axon reflex flare correlated best with dermal innervation density. Clinical pain ratings correlated only with epidermal nerve fibre density (r = 0.38, p0.05) and better preserved cold detection thresholds (r = 0.39, p0.05), but not with other assessed functional and structural parameters.Thermal thresholds, axon reflex measurements and assessment of skin innervation density are valuable tools to characterize and quantify peripheral neuropathy and link neuronal function to different layers of the skin. The severity of small fibre neuropathy, however, did not correspond to clinical pain intensity and a specific parameter or pattern that would predict pain intensity in peripheral neuropathy could not be identified.

Published
2012

30. Leitlinien für Diagnostik und Therapie in der Neurologie

Author

Gereon Nelles, Wolfgang Jost, Arne May, Génther Deuschl, Heinz Reichmann, Thomas Klockgether, Christian Bien, Franz Xaver Glocker, Gunnar Wasner, Thorsten Steiner, Konrad Scheglmann, Michael Weller, Christiane Schneider-Gold, Sandra Verena Méller, Wieland Hermann, Reinhard Kaiser, Armin Curt, Gabriele Arendt, Jörg R. Weber, Marianne Dieterich, Marcus Deschauer, Hans-Walter Pfister, Cornelia Kornblum, Rolf R. Diehl, Frank Lehmann-Horn, U. Meier, Eric Jéttler, Josef Georg Heckmann, W. H. Oertel, M. Weller, Kirsten Méller-Vahl, Christian E. Elger, Inga Zerr, Andreas Straubev, Helmuth Steinmetz, Gerhard F. Hamann, Hans-Michael Meinck, Oliver Kastrup, Albert C. Ludolph, Werner Hacke, F. Birklein, Felix Rosenow, Peter-Dirk Berlit, Marcus Pohl, Stefan Hesse, Hermann Ackermann, Uta Meyding-Lamadü, A. Hufschmidt, Claudia Sommer, Claudia Trenkwalder, Uwe Schlegel, Günther Deuschl, Angelika Thöne-Otto, R. Gold, Jens Volkmann, Roland Veltkamp, E. Bernd Ringelstein, Ullrich Wéllner, P. Berlit, Karla Eggert, Erich Schmutzhard, Hans-Otto Karnath, Roland Nau, Walter Sturm, Ralf Gold, Walter Paulus, Dominik Straumann, Stefanie Förderreuther, Heinz Wiendl, Matthias Maschke, Eckhard Thiel, Dieter Heuß, Hans-Christoph Diener, Carsten Saft, Matthias Endres, Wolfram Ziegler, Frank Leypoldt, Claus-W. Wallesch, C. Weimar, Christian Gerloff, H. C. Diener, Joachim Liepert, Ludger Schöls, Heinrich Mattle, Christian Weimar, Michael G. Hennerici, Michael Strupp, Sebastian Rauer, Mario Prosiegel, Geert Mayer, Jörg B. Schulz, Martin Tegenthoff, Rainer Lindemuth, Josef Zihl, H. Reichmann, Paul W. Schönle, Ralf Baron, Dirk Woitalla, E. Schmutzhard, and Dirk Sander

Subjects
business.industry, Medicine, business
Published
2012
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31. Fourth meeting of the European Neurological Society 25–29 June 1994 Barcelona, Spain

Author

H. Hattig, C. Delli Pizzi, M. C. Addonizio, Michelle Davis, A. R. Giovagnoli, L. Florensa, M. Roth, J. de Kruijk, Francisco Lacruz, Ph. Dewailly, A. Toygar, C. Avendano, P.P. De Deyn, J. F. Hurtevent, F. Lomeila, T. W. Wong, Gordon T. Plant, M. Bud, H. J. Willison, DH Miller, D. W. Langdon, R. Cioni, J. Servan, A. Kaygisiz, E. Racadot, D. B. Schens, E. Picciola, L. Falip, C. Bouchard, J. Jotova, A. Jorge-Santamaria, P. Misra, A. Dufour, C. P. Panagopoulos, A. Venneri, B. Sredni, B. Angelard, M. Janelidze, M. Carreno, J. Obenberger, J. Pouget, H. W. Moser, R. Kaufmann, J. A. Molina, D. Linden, A. Martin Urda, E. Uvestad, A. Krone, J. P. Cochin, J. Mallecourt, A. Cambon-Thomsen, K. Violleau, P. Osschmann, A. M. Durocher, E. Bussaglia, D. M. Danielle, H. Efendi, C. Van Broeckhoven, K. G. Jordan, W. Rautenberg, C. Iniguez, J. M. Delgado, Graham Watson, M. Lawden, Gareth J. Barker, K. Stiasny, James T. Becker, G. Campanella, E. Peghi, A. Poli, A. Haddad, T. Yamawaki, Giacomo P. Comi, S. Sotgiu, B. Ersmark, A. Pomes, M. Ziegler, P. Ferrante, P. Ruppi, H. KuÇukoglu, R. Bouton, U. K. Rinne, P. Vieregge, M. Dary, P. Giunti, Peter J. Goadsby, S. Jung, E. Secor, A. Steinberg, N. Vila, M. A. Hernandez, M. Cursi, A. Enqelhardt, A. Engelhardt, J. Veitch, F. Di Silverio, F. Arnaud, B. Neundörfer, R. Brucher, Dominique Caparros-Lefebvre, B. Meyer, Marianne Dieterich, M. H. Snidaro, R. Gomez, R. Cerbo, M. Ragno, J. M. Vance, S. Nemni, A. Caliskan, F. Barros, I. Velcheva, D. Ceballos-Baumann, V. Barak, A. Avila, N. Antonova, F. Resche, S. Pappata, L. Varela, S. R. Silveira Santos, A. Cammarota, L. Naccache, Y. Nara, E. Tournier-Lasserves, R. Mobner, T. Chase, A. Ensenyat, J. Ulrich, G. Giegerich, M. Rother, M. Revilla, N. Nitschke, K. Honczarenko, E. Basart Tarrats, J. Blin, B. Jacob, J. Santamaria, S. Knezevic, J. L. Castillo, M. Antem, J. Colomer, O. Busse, Didier Hannequin, S. Carrier, J. B. Ruidavets, C. Rozman, J. Bogoussslavsky, J. Pascual Calvet, E. Monros, J. M. Polo, M. Zucconl, Javier Muruzabal, R. R. Allen, R. Rivolta, K. Haugaard, A. Nespolo, K. Hoang-Xuang, G. Bussone, T. Avramidis, E. Corsini, Christiana Franke, T. Vinogradova, H. Boot, K. Vestergaard, G. H. Jansen, N. Argentino, M. Raltzig, W. Linssen, Mark B. Pepys, P. Roblot, L. Lauritzen, E. Fainardi, D. Morin, T. X. Arbizu Urdiain, J. Wollenhaupt, S. Bostantjopoulou, G. Pavesi, A. D. Forman, Giovanni Fabbrini, D. Jean, J. J. Archelos, M. I. Blanchs, M. Del Gobbo, Anna Carla Turconi, Ch. Derouesné, Elio Scarpini, A. Visbeck, P. Castejon, J. P. Renou, F. Mounier-Vehier, G. Potagas, Ch. Duyckaerts, A. Filla, R. Schneider, G. Ronen, K. Nagata, J. P. Vedel, A. Henneberg, G. van Melle, C. Baratti, H. Knott, M. C. Prevett, A. Bes, B. Metin, Jos V. Reempts, L. Martorell, Mefkure Eraksoy, H. O. Handwerker, D. S. Younger, O. Oktem, D. Frongillo, C. Soriano-Soriano, L. Niehaus, F. Zipp, A. Tartaro, S Newman, R. H. Browne, P. Davous, R. Sanchez, M. Muros, M. E. Kornhuber, A. Lavarone, M. Mohr, M. R. Garcia, S. Russell, H. Kellar-Wood, M. R. Tola, B. Ostermeyer, Ch. Tzekov, K. Sartor, E. B. Ringelstein, P. P. Gazzaniga, Paul Krack, H. Fidaner, H. Rico, T. Dbaiss, F. Alameda, E. Torchiana, L. Rumbach, I. Charques, J. M. Bogaard, C. D. Frith, L. J. Rappelle, R. Brenner, A. Joutel, K. Fuxe, G. HÄcker, M. J. Blaser, J. Valls-SolÇ, G. Ulm, M. Alberdi, A. Bock, F. W. Bertelsmann, U. Wieshmann, J. Visa, J. R. Lupski, D. D'Amico, L. M. P. Ramos, A. A. Vanderbark, R. Horn, M. Warmuth, Dietmar Kühne, Mark S. Palmer, C. Ehrenheim, E. Canga, S. Viola, O. Scarpino, P. Naldi, R. Almeida, A. A. Raymond, J. Gamez, Stephan Arnold, A. DiGiovanni, J. Dalmau, C. C. Chari, H. F. Beer, J. C. Koetsier, J. Iriarte, E. Yunis, J. Casadevall, E. Le Guern, E. Stenager, S. R. Benbadis, J. M. Warter, F. Burklin, I. Theodorou, L. Johannesen, G. A. Graveland, X. Leclerc, I. Vecchio, L. Ozelius, G. Nicoletti, R. K. Gherardi, E. Esperet, M. L. Delodovici, F. Cattin, F. Paiau, Giorgio Sacilotto, C. A. J. Broere, D. Chavdarov, J. P. Willmer, C. H. Hawkes, Th. Naegele, E. Ellie, E. Dartigues, M. J. Guardiola, S. Hesse, Z. Levic, Marco Rovaris, P. Saugeir-Veber, B. A. Yaqub, H. F. Durwen, R. Larumbe, J. Ballabrina, M. Sendtner, J. Röther, M. Horstink, C. Kluglein, M.P. Montesi, H. Apaydin, J. Montoya, E. Waubant, Ch. Verellen-Dunoulin, A. Nicolai, J. Lopez-Delval, R. Lemon, G. Cantinho, E. Granieri, A. Zeviani, Wolfgang H. Oertel, U. Ficola, V. Di Piero, V. Fragola, K. Sabev, M. V. Guitera, I. Turki, F. Bolgert, P. Ingrand, J. M. Gobernado, L. M. E. Grimaldi, S. Baybas, B. Eymard, Y. Rolland, Y. Robitaille, Ta. Pampols, P. J. Koehler, A. Carroacedo, J. Vilchez, S. Di Vittorio, I. R. Rise, T. Nagy, M. Kuffner, E. Palazzini, A. Ott, J. Pruim, T. X. Arbizu, E. Manetti, C. Cervera, S. Felber, G. Gursoy, J. Scholz, G. A. Buscaino, M. S. Chen, A. Pascual, J. Hazan, J. U. Gajda, J. G. Cea, G. Bottini, G. Damalik, F. Le Doze, G. Bonaldi, J. M. Hew, C. Messina, A. M. Kennedy, J. M. Carney, N. M. F. Murray, M. Parent, M. Koepp, V. Dimova, D. De Leo, K. Jellinger, G. Salemi, S. Mientus, M. L. Hansen, F. Mazzucchelli, J. Vieth, M. Mauri, E. Bartels, L. Johannsen, C. Humphreys, J. Emile, D. N. Landon, E. Kansu, R. Sanchez-Pernaute, Rsj Frackowiak, M. Gonzalez Torres, L. Oller, C. Machedo, J. Kother, M. Billiard, H. Durak, T. Schindler, A. Frank, A. Uncini, A. Sbriccoli, C. Farinas, D. W. Paty, N. Fast, A. T. Zangaladze, A. Kerkhofs, J. M. Pino Garcia, I. De la Fuente, B. Marini, L. Gomez, I. Rubio, Alessandra Bardoni, C. Brodie, P. Acin, U. Sliwka, S. A. Hawkins, S. Tardieu, F. Vitullo, J. M. Pereira Monteino, R. Gagliardi, T. Jezewski, A. Cano, T. Lempert, F. Abad Alegria, G. Rotondo, D. Ince, C. Martinez Parra, Y. Huang, H. Luders, Y. Steinvil, F. G. A. Van Der Meche, R. Bianchi, A. Sanchez, T. Sevilla, J. M. Ketelslegers, A. Domzal-Stryga, M. Pandolfo, M. O. Josse, K. W. Neff, I. Blanco, G. W. Bruyn, O. W. Witte, J. L. Thibault, G. Andersen, J. Pariset, A. Marcone, R. J. M. Lane, A. Hofman, M. Verin, T. Matilla, P. Bedoucha, J. Roche, M. Lai, M. Collard, A. Ugarte, F. Gallecho, D. Silbersweig, C. Kennard, J. P. Azulay, T. W. Ho, P. L. I. Dellemijn, R. Girardello, F. Baas, B. Voss, F. Rozenberg, E. M. Brocker, V. Stanev, A. A. J. Soeterboek, A. Marra, A. Rey, E. Ertem, M. Sawradewicz-Rybak, J. De Keyser, P. Cavallari, F. Proust, Y. Chevalier, H. C. Hansen, D. Leys, C. A. Davie, K. Hoang-Xuan, C. Bairati, H. van Crevel, Thomas T. Warner, B. Bompais, A. Dobbeleir, T Campbell, C. Macko, C. J. M. Klijn, M. Dussallant, T. P. Berlit, W. Rozenbaum, M. J. van den Bent, W. A. Rocca, M. Muller, H. Hundemer, U. Zifko, M. Campera, F. Drislane, D. Ranoux, T. M. Kloss, Anil Kumar, I. Ruolt, C. Bargnani, B. Marescau, N. A. Losseff, S. Notermans, B. Kint, E. T. Burke, C. Aykut, J. Matias Guiu, P. Maquet, T. Drogendijk, M. Leone, K. von Ammon, M. Pepeliarska, C. Prados, L. DiGiamberardino, T. Logtenberg, G. Lenoir, I. Castaldo, Damhaut, M. Radionova, G. Sirabian, R. Navon, Giovanni Antonini, K. Al Moutaery, E. Chamas, R. Schönhuber, M. Giannini, B. Debilly, I. Labatut, H. Henon, J. A. Egido, M. Baudrimont, J. N. Lorenzo, J. E. C. Bromberg, R. Antonacci, J. J. Vilchez, T. Moulin, B. Rautenstrauss, Giovanni Meola, J. Noth, S Mammi, P. Laforet, F. Lopez, C. Gehring, S. Bort, G. Rancurel, D. Decamps, S. Kostadinova, Y. Shapira, B. Neundoerfer, D. Chavrot, M. Solimena, J. P. Salier, W. Deberdt, R. Hoff-Jörgensen, A. Messina, S. Meairs, G. Rosoklija, E. Nelis, I. Bertran, C. Ertekin, J. Lohmeyer, Mitermayer Galvao dos Reis, L. Calo, E. Maccagnano, A. P. Hays, J. Verlooy, M. G. Forno, T. Blanco, L. Bail, Gabriella Silvestri, J. Montero, F. Bertrand, R. T. Ghnassia, C. Besses, T. Sereghy, F. Shalit, G. Bogliun, S. Braghi, St. Baykouchev, C. Franke, A. Lasa, L. C. Archard, J. Kriebel, S. Shaunak, M. Nocito, Alexander Tsiskaridze, E. Manfredini, T. Seigal, David G. Gadian, M. Barlas, J. D. Degos, C. Seeber, J. Caemert, J. L. Mas, R. B. Pepinsky, M. G. D'Angelo, N. Baumann, S. Yorifuji, H. P. Endtz, M. A. Cassatella, R. A. C. Hughes, V. Golzi, A. Bittencourt, A. Ferreira, M. Sanson, C. Alper, M. Vermeulen, M. A. A. van Walderveen, E. Alexiou, C. H. Lucas, M. Fiorelli, Y. N. Debbink, R. Gil, S. Congia, T. Banerjee, J. M. Bouchard, A. N. Pinto, A. Ceballos-Baumann, G. Grollier, P. I. M. Schmitz, M. D. Catata, N. Lahat, N. S. Rao, P. Papathanasopoulos, J. Valls-Solé, D. Claus, G. Schroter, A. Castro, C. Videbaek, R. Martinez Dreke, A. D. Platts, M. Hermesl, A. C. PeÇanha-Martins, M. Cardoso Silva, P. Masnou, M. J. A. Tanner, Ch. Confavreux, B. Mishu, H. Rasmussen, L. Valenciano, Carlo Pozzilli, S. W. Li, V. Salzman, Y. Vashtang, Massimo Franceschi, M. Severo, G. Deuschl, S. Setien, G. Mariani, A. Protti, J. Castillo, M. J. B. Taphoorn, M. Frontali, I. Milonas, D. Decoq, J. A. Navarro, S. Castellvi-Pel, C. Ertikin, M. Urtasun, Y. Lajat, B. E. Kendall, E. Verdu, B. Gueguen, E. Boisen, R. Couderc, A Danek, JM Stevens, F. Nicoli, L. Feltri, M. L. Vazquez-Andre, J. A. Morgan-Hughes, L. D'Angelo, F. Y. Liew, L. F. Pascual, J. Patrignani Ochoa, Vittorio Martinelli, J. Cophignon, L. Zhang, S. Martin, J. F. Meder, H. C. Buschmann, L. Bertin, J. van Gijn, A. Barreiro, A. Cools, C. Leon, A. Berod, E. A. Anllo, E. Zanette, L. Petrov, R. Barona, B. Gallicchio, P. J. Cozzone, N. Diederich, G. Cancel, L. Schelosky, P. Orizaola, K. Yulug, S. Ozer, Valeria A. Sansone, B. Guiraud-Chaumeil, K. Voigt, P. Labauge, M. Eoli, J. Zhu, J. Aguirre, M. Ferrarini, B. Zyluk, E. Planas, A. Cadilha, C. Tortorella, H. Bismuth, C. E. Counsell, A. Laun, A. Ferlini, Rio J. Montalban, N. Biary, L. Becker, M. Fardeau, M. Poloni, V. M. S. de Bruin, C. Fornada, J. Barros, E. Ganzmann, E. Touze, D. Wallach, J. Peila, H. Fujimura, M. T. Iba-Zizen, G. Macchi, C. Villoslada, R. Gouider, Ph. Rondepierre, P. Grummich, P. Chiodi, C. Conte, M. Michels, P. Annunziata, G. Semana, C. Sommer, J. Vajsar, D. Zekin, J. Kulisevsky, David G. Munoz, B. Jacotot, M. Magoni, A. Luxen, T. Garcia-Silva, S. Di Cesare, Christophe Tzourio, M. Gomori, I. Picomell, L. Santoro, F. Villa, Giovanni Pennisi, T. Ribalta, J. M. Molto, L. Marzorati, P. Loiseau, F. Gemignani, A. Gironell, J. Wissel, A. Prusinski, F. Cailloux, P. Villanueva-Hemandez, P. Cozzone, T. Del Ser, J. Sans-Sabrafen, M. Zappia, P. W. A. Willems, G. Tchernia, D. Gardeur, R. Bauer, F. Palomo, H. Metz, S. Lamoureux, C. Chastang, I. Reinhard, A. Goldfarb, S. Harder, Jordi Río, C. Ozkara, E. Tekinsoy, P. Vontobell, J. De Recondo, M. Rabasa, L. Lacomblez, F. Boon, Dgt Thomas, V. Palma, Renato Mantegazza, A. Dervis, M. Nueckel, B. YalÇinerner, I. Duran, G. Dalla Volta, A. Zubimendi, J. Pinheiro, A. Marbini, Xavier Montalban, H. Wekerle, X. Pereira Monteino, F. Crespo, F. Koskas, N. Battistini, C. Ruiz, H. Offner, J. de Pommery, P. Kanovsky, J. Y. Barnett, J. Pardo, G. Tomei, R. Rene, H. M. Lokhorst, P. Thajeb, H. Bilgin, D. McGehee, R. Fahsold, L. Morgante, Katie Sidle, C. Delwaide, M. N. Diaye, P. H. Rice, A. Creange, C. Sabev, K. Stephan, K. WeilBenborn, G. Magnani, L. Grymonprez, F. Cardellach, M. Kaps, N. G. Meco, F. Vega, V. Bonifati, A. Desomer, M. Baldy-Moulinier, G. Kvale, F. J. Authier, B. Yegen, T. Ho, J. M. Rozet, E. A. Cabanis, L. Bruce, L. Ambrosoli, M. A. Petrella, M. Hernandez, P. Timmings, H. B. van der Worp, F. Mahieux, A. Urbano-Marquez, D. A. Krendel, A. A. Garcia, R. Divari, R. Michalowicz, M. R. Piedmonte, M. Bondavalli, M. Zanca, P. F. Ippel, Onofre Combarros, B. Tavitian, E. Hirsch, I. Anastasopoulos, A. Roses, A. Köhler, P. Vienna, V. Timmerman, P. Sergi, F. Cornelio, A. Di Pasquale, R. Verleger, S. Castellvirel, J. Proano, B. van Moll, F. Rubio, W. Hacke, I. Lavenu, L. Zetta, M. W. Tas, N. Bittmann, M. Bonamini, O. R. Hommes, V. Dousset, N. Afsar, S. Belal, R. R. Myers, J. Goes, Giuseppe Vita, E. Clementi, V. G. Karepov, M. Jueptner, A Vincent, P. Emmrich, Th. Heb, A. Caballo, J. Gallego, T. Mokrusch, C. Perla, L. Gebuhrer, O. Titlbach, Alessandro Prelle, A. Czlonkowska, M. Russo, D. Hadjiev, T. S. Chkhikvishvili, M. Oehlschlager, G. Becker, I. Günther, E. N. Stenager, J. Garcia Agundez, J. Casademont, J. Batlle, S. Podobnik-Sarkanji, C. Alonso-Villaverde, B. Delaguillaume, B. Genc, B. Mazoyer, A. Rodriguez-Al-barino, Ch. Hilger, B. Ferrero, R. Price, W. Grisold, L. Fuhry, D. Oulbani, D. Ewing, A. Petkov, W. Walther, A. Gokyigit, John Newsom-Davis, J. Tayot, D. Seliak, G. Pelliccioni, D. Campagne, K. Kessler, F. Boureau, D. Perani, J. P. N'Guyen, N. Tchalucova, B. A. Antin-Ozerkis, C. Lacroix, B. D. Aronovich, I. H. Jenkins, E. A. dos Reis, M. Hortells, H. M. Meinck, H. Ch. Buschmann, S. C. J. M. Jacobs, T. Wetter, P. Creissard, N. Martinez, J. Weidenfeldl, H. J. Sturenburg, G. Damlacik, V. Gracia, J. C. Turpin, A. Pou-Serradell, J. P. Vincent, T. Gagoshidze, U. Ozkutlu, M. McLeod, K. Siegfried, I. Tchaoussoglou, J. Hildebrand, S. Kowalska, M. C. Picot, G. Galardin, L. Crevits, F. Andreetta, S. Larumbe-Lobalde, G. de la Sierra, J. C. Alvarez-Cermeno, R. J. Seitz, P. L. Oey, L. Ptacek, A. M. J. Paans, A. Wirrwar, A. Schmied, J. Uilchez, H. Tounsi, D. Hipola, V. Avoledo, Y. Hirata, P. Vermersch, T. M. Aisonobe, J. Valls-SoIè, H. Staunton, J. Dichgans, R. Karabudak, I. Dones, G. Porta, E. Janssens, Maria Martinez, J. M. Fernandez-Real, R. Villagra, Y. Yoshino, C. Kabus, K. Schimrigk, I. Girard-Buttaz, F. Piccoli, F. Aichner, P. Zuchegna, S. M. Al Deeb, F. Bono, N. Busquets, A. Jobert, Patrizia Ciscato, M. Martin, L. Polman, S. Darbra, V. Le Cam-Duchez, F. Baldissera, B. Baykan-Kurt, D. Guez, M. Bratoeva, H. Matsui, M. Mila, H. Perron, L. Bjorge, G. Husby, Steven T. DeKosky, D. R. Cornblath, J. M. Gabriel, J. J. Poza, Y. Wu, A. Toscano, R. P. Kleyweg, J. Kuhnen, S. O. Confort-Gouny, A. Barcelo, A. M. Conti, C. Fiol, C. Steichen-Wiehn, J. Rodes, M. Cavenaile, C. Vedeler, M. Drlicek, C. Argentino, M. L. Peris, A. Cervello, A. Z. GinaÏ, S. Yancheva, D. Passingham, S. Aoba, D. L. 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Brasic, W. Heide, I. Santilli, W. M. Korn, D. Selcuki, M. J. Barrett, D. Krieger, T. Leon, T. Houallah, M. Tournilhac, C. Nos, D. Chavot, F. Barbieri, F. J. Jimenez-Jimenez, J. Muruzabal, K. Poeck, A. Sennlaub, L. M. Iriarte, L. G. Lazzarino, C. Sanz, P. A. Fischer, S. D. Shorvon, R. Hoermann, F. Delecluse, M. Krams, O. Corabianu, F. H. Hochberg, Christopher J. Mathias, B. Debachy, C. M. Poser, L. Delodovici, A. Jimenez-Escrig, F. Baruzzi, F. Godenberg, D. Cucinotta, P. J. Garcia Ruiz, K. Maier-Hauff, P. R. Bar, R. Mezt, R. Jochens, S. Karakaneva, C. Roberti, E. Caballero, Joseph E. Parisi, M. Zamboni, T. Lacasa, B. Baklan, J. C. Gautier, J. A. Martinez-Matos, W. Pollmann, G. Thomas, L. Verze, E. Chleide, R. Alvarez Sala, I. Noel, E. Albuisson, O. Kastrup, S. I. Rapoport, H. J. Braune, H. Lörler, M. Le Merrer, A. Biraben, S. Soler, S. J. Taagholt, U. Meyding-Lamadé, K. Bleasdale-Barr, Isabella Moroni, Y. Campos, J. Matias-Guiu, G. Edan, M. G. Bousser, John B. Clark, J. Garcia de Yebenes, N. K. Olsen, P. Hitzenberger, S. Einius, Aj Thompson, Ch. J. Vecht, T. Crepin-Leblond, Klaus L. Leenders, A. Di Muzio, L. Georgieva, René Spiegel, K. Sabey, D. Ménégalli, J. Meulstee, U. Liszka, P. Giral, C. Sunol, J. M. Espadaler, A. D. Crockar, K. Varli, G. Giraud, P. J. Hülser, A. Benazzouz, A. Reggio, M. Salvatore, K. Genc, M. Kushnir, S. Barbieri, J. Ph. Azulay, M. Gianelli, N. Bathien, A. AlMemar, F. Hentati, I. Ragueneau, F. Chiarotti, R. C. F. Smits, A. K. Asbury, F. Lacruz, B. Muller, Alan J. Thompson, Gordon Smith, K. Schmidt, C. Daems Monpeun, Juergen Weber, A. Arboix, G. R. Fink, A. M. Cobo, M. Ait Kaci Ahmed, E. Gencheva, Israel-Biet, G. Schlaug, P. De Jonghe, Philip Scheltens, K. Toyka, P. Gonzalez-Porque, A. Cila, J. M. Fernandez, P. Augustin, J. Siclia, S. Medaglini, D. E. Ziogas, A. Feve, L. Kater, G. J. E. Rinkel, D. Leppert, Rüdiger J. Seitz, S. Ried, C. Turc-Carel, G. Smeyers, F. Godinho, M. Czygan, M. Rijntjes, E. Aversa, M. Frigo, Leif Østergaard, J. L. Munoz Blanco, A. Cruz-Matinez, J. De Reuck, C. Theillet, T. Barroso, V. Oikonen, Florence Lebert, M. Kilinc, C. Cordon-Cardon, G. Stoll, E. Thiery, F. Pulcinelli, J. Solski, M. Schmiegelow, L. J. Polman, P. Fernandez-Calle, C. Wikkelso, M. Ben Hamida, M. Laska, E. Kott, W. Sulkowski, C. Lucas, N. M. Bornstein, D. Schmitz, M. W. Lammers, A. de Louw, R. J. S. Wise, P. A. van Darn, C. Antozzi, P. Villanueva, P. H. E. Hilkens, C. Constantin, W. Ricart, A. Wolf, M. Gamba, P. Maguire, Alessandro Padovani, B. M. Patten, Marie Sarazin, H. Ackermann, L. Durelli, S. Timsit, Sebastian Jander, B. W. Scheithauer, G. Demir, J. P. Neau, P. Barbanti, A. Brand, N. AraÇ, V. Fischer-Gagnepain, R. Marchioli, G. Serratrice, C. Maugard-Louboutin, G. T. Spencer, D. Lücke, G. Mainardi, K. Harmant Van Rijckevorsel, G. B. Creel, R. Manzanares, Francesco Fortunato, A. May, J. Workman, K. Johkura, E. Fernandez, Carlo Colosimo, L. Calliauw, L. Bet, Félix F. Cruz-Sánchez, M. Dhib, H. 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Brizioli, J. Calleja, L. Publio, M. Desi, R. Soffietti, P. Cortinovis-Tourniaire, E. F. Gonano, G. Cavaletti, S. Uselli, K. Westerlind, H. Betuel, C. O. Dhiver, H. Guggenheim, M. Hamon, R. Fazio, P. Lehikoinen, A. Esser, B. Sadzot, G. Fink, Angelo Antonini, D. Bendahan, V. Di Carlo, G. Galardi, A. F. Boller, M. Aksenova, Del Fiore, V. de la Sayette, H. Chabriat, A. Nicoletti, A. Dilouya, M. L. Harpin, E. Rouillet, J. Stam, A. Wolters, M. R. Delgado, Eduardo Tolosa, G. Said, A. J. Lees, L. Rinaldi, A. Schulze-Bonhage, MA Ron, C. Lefebvre, E. W. Radü, R. Alvarez, M. L. Bots, P. Reganati, S. Palazzi, A. Poggi, N. J. Scolding, V. Sazdovitch, T. Moreau, E. Maes, M. A. Estelies, P. Petkova, Jose-Felix Marti-Masso, G De La Meilleure, N. Mullatti, M. Rodegher, N. C. Notermans, T. A. T. Warner, S. Aktan, J. P. Louboutin, L. Volpe, C. Scheidt, W. Aust, C. M. Wiles, U. Schneider, S. K. Braekken, W. R. Willems, K. Usuku, Peter M. Rothwell, C. Talamon, M. L. Sacchetti, A. Codina, M. H. Marion, A. Santoro, J. Roda, A. Bordoni, D. J. Taylor, S. Ertas, H. H. Emmen, J. Vichez, V. BesanÇon, R. E. Passingham, M. L. Malosio, A. Vérier, M. Bamberg, A. W. Hansen, E. Mostacero, G. Gaudriault, Marie Vidailhet, B. Birebent, K. Strijckmans, F. Giannini, T. Kammer, I. Araujo, J. Nowicki, E. Nikolov, A. Hutzelmann, R. Gherardi, J. Verroust, L. Austoni, A. Scheller, A. Vazquez, S. Matheron, H. Holthausen, J. M. Gerard, M. Bataillard, S. Dethy, V. H. Patterson, V. Ivanez, N. P. Hirsch, F. Ozer, M. Sutter, C. Jacomet, M. Mora, Bruno Colombo, A. Sarropoulos, T. H. Papapetropoulos, M. Schwarz, D. S. Dinner, N. Acarin, B. Iandolo, J. O. Riis, P. R. J. Barnes, F. Taroni, J. Kazenwadel, L. Torre, A. Lugaresi, I. L. Henriques, S. Pauli, S. Alfonso, Pedro Quesada, A. S. T. Planting, J. M. Castilla, Thomas Gasser, M. Van der Linden, A. Alfaro, E. Nobile-Orazio, G. Popova, W. Vaalburg, F. G. A. van der Mech, L. Williams, F. Medina, J. P. Vernant, J. Yaouanq, B. Storch-Hagenlocher, A. Potemkowski, R. Riva, M. H. Mahagne, M. Ozturk, Ve. Drory, N. Konic, C. Jungreis, A. Pou Serradell, J. L. Gauvrit, G. J. Chelune, S. Hermandez, T. Dingus, L. Hewer, Ch. Koch, M. N. Metz-Lutz, G. Parlato, M. Sinaki, Charles Pierrot-Deseilligny, H. C. Diener, J. Broeckx, J. Weill-Fulazza, M. L. Villar, M. Rizzo, O. Ganslandt, C. Duran, N. A. Fletcher, G. Di Giovacchino, Susan T. Iannaccone, C. Kolig, N. Fabre, H. A. Crockard, Rita Bella, M. Tazir, E. Papagiannuli, K. Overgaard, Emma Ciafaloni, I. Lorenzetti, F. Viader, P. A. H. Millac, I. Montiel, L. H. Visser, M. Palomar, P. L. Murgia, H. Pedersen, Rafael Blesa, S. Seddigh, W. O. Renier, I. Lemahieu, H. M. L. Jansen, L. Rosin, J. Galofre, K. Mattos, M. Pondal, G. M. Hadjigeorgiou, D. Francis, L. Cantin, D. Stegeman, M. Rango, A. B. M. F. Karim, S. Schraff, B. Castellotti, I. Iriarte, E. Laborde, T. J. Tjan, R. Mutani, D. Toni, B. Bergaasco, J. G. Young, C. Klotzsch, A. Zincone, X. Ducrocq, M. Uchuya, O. J. Kolar, A. Quattrone, T. Bauermann, Nereo Bresolin, J. Vallée, B. C. Jacobs, A. Campos, Werner Poewe, J. A. Villanueva, A. W. Kornhuber, A. Malafosse, E. Diez-Tejedor, G. Jungreia, M. J. A. Puchner, A. Komiyama, O. Saribas, V. Volpini, L. Geremia, S. Bressi, A. Nibbio, Timothy E. Bates, T. z. Tzonev, E. Ideman, G. A. Damlacik, G. Martino, G. Crepaldi, T. Martino, Kjell Någren, E. Idiman, D. Samuel, J. M. Perez Trullen, Y. van der Graaf, J. O. Thorell, M. J. M. Dupuis, E. Sieber, R. D'Alessandro, C. Cazzaniga, J. Faiss, A. Tanguy, A. Schick, I. Hoksergen, A. Cardozo, R. Shakarishvili, G. K. Wennlng, J. L. Marti-Vilalta, J. Weissenbach, I. L. Simone, Amalia C. Bruni, Darius J. Adams, C. Weiller, A. Pietrangeli, F. Croria, C. Vigo-Pelfrey, Patricia Limousin, A. Ducros, G. Conti, O. Lindvall, E. Richter, M. Zuffi, A. Nappo, T. Riise, J. Wijdenes, M. J. Fernandez, J. Rosell, P. Vermersh, S. Servidei, M. S. C. Verdugo, F. Gouttiere, W. Solbach, M. Malbezin, I. S. Watanabe, A. Tumac, W. I. McDonald, D. A. 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C. Patrosso, N. L. Gershfeld, P. A. J. M. Boon, O. Sabouraud, M. Lara, J. Svennevig, G. L. Lenzi, A. Barrio, H. Villaroya, JosÇ M. Manubens, O. Boespflug-Tanguy, M. Carreras, D. A. Costiga, J. P. Breux, S. Lynn, C. Oliveras Ley, A. G. Herbaut, J. Nos, C. Tornali, Y. A. Hekster, J. L. Chopard, J. M. Manubens, P. Chemouilli, A. Jovicic, F. Dworzak, S. Smirne, S. E. Soudain, B. Gallano, D. Lubach, G. Masullo, G. Izquierdo, A. Pascual Leone Pascual, A. Sessa, V. Freitas, O. Crambes, L. Ouss, G. W. Van Dijk, P. Marchettini, P. Confalonieri, M. Donaghy, A. Munnich, M. Corbo, and M. E. L. van der Burg

Subjects
Neurology, business.industry, Media studies, Library science, Medicine, Neurology (clinical), business
Published
1994
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32. Within-session sensitization and between-session habituation: a robust physiological response to repetitive painful heat stimulation

Author

A, May, R, Rodriguez-Raecke, A, Schulte, K, Ihle, M, Breimhorst, F, Birklein, and T P, Jürgens

Subjects
Adult, Male, Pain Threshold, Depressive Disorder, Hot Temperature, Adolescent, Pain, Pain Perception, Middle Aged, Physical Stimulation, Humans, Female, Chronic Pain, Habituation, Psychophysiologic, Low Back Pain, Pain Measurement
Abstract

Habituation and sensitization are important behavioural responses to repeated exposure of painful stimuli. Whereas within-session response dynamics to nociceptive stimuli is well characterized, little is known about long-term behaviour due to repetitive nociceptive stimulation. We used a standardized longitudinal heat pain paradigm in 66 healthy participants, 21 patients with chronic low back pain and 22 patients with depression who received daily sessions of 60 suprathreshold heat stimuli (48 °C each) for eight consecutive days. All three groups showed the same response: Repeated painful stimulation over several days resulted in substantially decreased pain ratings to identical painful stimuli. The decreased perception of pain over time was associated with a very robust increase in pain ratings in each single pain session, i.e., all participants sensitized within sessions and habituated between sessions. This uniform pattern was equally present in all examined groups. Chronic pain and depression do not seem to interfere with short-term sensitization and long-term habituation in this model of repetitive phasic heat pain.

Published
2011

33. Naloxone inhibits not only stress-induced analgesia but also sympathetic activation and baroreceptor-reflex sensitivity

Author

M, Fechir, M, Breimhorst, S, Kritzmann, C, Geber, T, Schlereth, B, Baier, and F, Birklein

Subjects
Adult, Male, Behavior, Sympathetic Nervous System, Naloxone, Narcotic Antagonists, Pain, Blood Pressure, Baroreflex, Neuropsychological Tests, Electric Stimulation, Young Adult, Double-Blind Method, Heart Rate, Regional Blood Flow, Stroop Test, Reaction Time, Humans, Female, Analgesia, Stress, Psychological, Pain Measurement
Abstract

Interactions between the sympathetic nervous system and pain are manifold and still have not been sufficiently characterized. Accordingly, several possible neuronal pathways have been described as being involved in mental stress-induced analgesia. We studied the role of the endogenous opioidergic system in stress-induced analgesia in 14 healthy participants in a double-blind cross-over trial. Naloxone or placebo was applied while electrical pain stimulation was started and electrical current increased. After reaching a constant stimulation at 30 mA, a color word interference test (Stroop task) was performed in a stressful and a non-stressful version. Blood pressure, heart rate and baroreflex sensitivity were continuously recorded to assess autonomic activation. Each participant was tested with naloxone and placebo with a randomized and balanced order of trials. The major results are that the opioid-receptor antagonist naloxone prevented (1) stress-induced reduction of tonic current-induced pain, (2) attenuated the simultaneous activation of the sympathetic nervous system, and (3) reduced the counteraction of sympathetic activation by vagal baroreceptor mechanisms. Thus, the opioidergic system not only modulates nociceptive input but also the interplay with vegetative responses. We conclude that acute stress, sympathetic activation and analgesia might be linked via vagal reflexes, which are disturbed when opioid receptors are blocked. This mechanism might underlie increased perception of noxious stimuli in patients with chronic pain or mood disorders.

Published
2011

34. Cortical control of thermoregulatory sympathetic activation

Author

M, Fechir, A, Klega, H G, Buchholz, N, Pfeifer, S, Balon, T, Schlereth, C, Geber, M, Breimhorst, C, Maihöfner, F, Birklein, and M, Schreckenberger

Subjects
Adult, Cerebral Cortex, Male, Glucose, Fluorodeoxyglucose F18, Temperature, Humans, Radiopharmaceuticals, Adrenergic Fibers, Body Temperature Regulation, Brain Stem, Tomography, Emission-Computed
Abstract

Thermoregulation enables adaptation to different ambient temperatures. A complex network of central autonomic centres may be involved. In contrast to the brainstem, the role of the cortex has not been clearly evaluated. This study was therefore designed to address cerebral function during a whole thermoregulatory cycle (cold, neutral and warm stimulation) using 18-fluordeoxyglucose-PET (FDG-PET). Sympathetic activation parameters were co-registered. Ten healthy male volunteers were examined three times on three different days in a water-perfused whole-body suit. After a baseline period (32 degrees C), temperature was either decreased to 7 degrees C (cold), increased to 50 degrees C (warm) or kept constant (32 degrees C, neutral), thereafter the PET examination was performed. Cerebral glucose metabolism was increased in infrapontine brainstem and cerebellar hemispheres during cooling and warming, each compared with neutral temperature. Simultaneously, FDG uptake decreased in the bilateral anterior/mid-cingulate cortex during warming, and in the right insula during cooling and warming. Conjunction analyses revealed that right insular deactivation and brainstem activation appeared both during cold and warm stimulation. Metabolic connectivity analyses revealed positive correlations between the cortical activations, and negative correlations between these cortical areas and brainstem/cerebellar regions. Heart rate changes negatively correlated with glucose metabolism in the anterior cingulate cortex and in the middle frontal gyrus/dorsolateral prefrontal cortex, and changes of sweating with glucose metabolism in the posterior cingulate cortex. In summary, these results suggest that the cerebral cortex exerts an inhibitory control on autonomic centres located in the brainstem or cerebellum. These findings may represent reasonable explanations for sympathetic hyperactivity, which occurs, for example, after hemispheric stroke.

Published
2010

36. Sensitized peripheral nociception in experimental diabetes of the rat

Author

D Fuchs, F Birklein, P.W. Reeh, and Susanne K. Sauer

Subjects
Male, Pain Threshold, medicine.medical_specialty, Diabetic neuropathy, Calcitonin Gene-Related Peptide, Action Potentials, Stimulation, Calcitonin gene-related peptide, In Vitro Techniques, Substance P, Bradykinin, Dinoprostone, Streptozocin, Diabetes Mellitus, Experimental, Nerve Fibers, Diabetes mellitus, Internal medicine, medicine, Reaction Time, Animals, Pain Measurement, Skin, Behavior, Animal, Dose-Response Relationship, Drug, business.industry, Nociceptors, medicine.disease, Sciatic Nerve, Rats, Disease Models, Animal, Anesthesiology and Pain Medicine, Nociception, Endocrinology, nervous system, Neurology, Hyperalgesia, Nociceptor, Neurology (clinical), Sciatic nerve, medicine.symptom, Capsaicin, business
Abstract

Painful neuropathy is a common complication of diabetes. Particularly in the early stage of diabetic neuropathy, patients are characterized by burning feet, hyperalgesia to heat, and mechanical stimuli, as if residual nociceptors were sensitized. Such symptoms are barely explained by common pathophysiological concepts of diabetic neuropathy. Diabetes was induced in Wistar rats by streptozotocin (STZ). After 4 weeks behavioral testing (Plantar test, Randall-Selitto) was conducted. Basal and stimulated release of calcitonin gene-related peptide (CGRP), Substance P (SP) and prostaglandin E(2) (PGE(2)) from isolated skin and sciatic nerve were assessed by enzyme immunoassays. Electrophysiological properties of identified nociceptors under hyperglycemic, hypoxic, and acidotic conditions were investigated using the skin-nerve preparation. The diabetic rats showed hyperalgesia to heat and pressure stimulation. The basal CGRP/SP release was reduced, but chemical stimulation with bradykinin induced greater release of SP, CGRP and PGE(2) than in control animals. In contrast, capsaicin-stimulated CGRP release was reduced in sciatic nerves. Hypoxia per se lowered von Frey thresholds of most C-nociceptors to half. Hyperglycemic hypoxia induced ongoing discharge in all diabetic but not control C-fibers which was further enhanced under acidosis. Sensory and neurosecretory nociceptor functions are sensitized in diabetes. Diabetic C-fibers show exaggerated sensitivity to hyperglycemic hypoxia with and without additional acidosis, conditions that are thought to mimic ischemic episodes in diabetic nerves. Ongoing C-fiber discharge is known to induce spinal sensitization. Together with altered receptor and ion channel expressions this may contribute to painful episodes in diabetic neuropathy.

Published
2010

37. Spinal cord stimulation, from diagnosis-oriented to mechanism-based treatment

Author

V. Tronnier and F. Birklein

Subjects
business.industry, Mechanism based, Pain, Electric Stimulation Therapy, Spinal cord stimulation, Electric Stimulation, Reflex Sympathetic Dystrophy, Anesthesiology and Pain Medicine, Spinal Cord, Physical Stimulation, Sensation Disorders, Medicine, Humans, Pain Management, business, Neuroscience
Published
2009

38. [Prevalence and risk factors of phantom limb pain and phantom limb sensations in Germany. A nationwide field survey]

Author

U, Kern, V, Busch, M, Rockland, M, Kohl, and F, Birklein

Subjects
Adult, Male, Artificial Limbs, Middle Aged, Health Surveys, Cross-Sectional Studies, Amputees, Phantom Limb, Risk Factors, Germany, Sleep Initiation and Maintenance Disorders, Surveys and Questionnaires, Humans, Female, Aged, Pain Measurement
Abstract

Data on the incidence and intensity of phantom limb pain (PLP) and phantom limb sensations (PLS) were collected in a nationwide survey.Supported by a manufacturer of artificial limbs and press notices a total of 537 amputees were contacted and interviewed by questionnaire.The questionnaire containing 62 questions was filled in by 537 out of 1,088 amputees. Of the amputees 14.8% were pain free, 74.5% had PLP, 45.2% stump pain (SP) and 35.5% a combination of both. In addition 62.4% of the amputees reported disturbed sleep, of those with PLP it was even higher at 77.3% and 66.8% of patients with PLP woke up several times during the night. The prevailing features of PLP included burning sensation (13.6%), cramp (15.3%), prickling (23.4%), electrification (21%) and tingling (20.4%). Phantom sensations were felt by 73.4% and were described as being mobile (66.8%), of normal temperature (64%), warm (19.5%), cold (16.5%), bare (35.9%), clothed (13.6%), not unpleasant (31.7%), pressed (29.6%), contorted (7.5%) and blown up (5.8%). Of the patients with PLP, 35.7% described the location as mostly ventral, 26.7% as mostly dorsal. Significantly more PLP was found in the presence of PLS than in its absence (p0.0001), but unrelated to the type of PLS, to demographic factors, or to the level or side of amputation. Perception of the artificial limb being "a foreign body" was highly significantly more often associated with PLP than with a sensation of "fusing with the body" (p0.0001).To our knowledge the present study constitutes the largest field survey on phantom limb pain carried out in Europe and corroborates the high prevalence and intensity of PLP, unusual PLS and amputation-related sleep disturbances. The significance and manageability of phantom feelings and its risk factors need further research.

Published
2009

40. Autonomic Effects on the Skin

Author

F. Birklein and T. Schlereth

Subjects
Sympathetic nervous system, Complex regional pain syndrome, medicine.anatomical_structure, business.industry, Skin blood flow, Anesthesia, Sweat gland, Cold pressor test, Medicine, business, medicine.disease
Published
2009
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41. Neuropathischer vs. nozizeptiver Schmerz bei Tumorerkrankungen: Neurologischer Status, quantitative sensorische Testung und PAINdetect-Fragebogen

Author

J. Legutke, U. Siepmann, F. Birklein, R. Schwab, M Weber, R. Rolke, R. Laufenberg-Feldmann, and J. Spielberger

Abstract

Fragestellung: Tumorschmerzen zeigen eine neuropathische Komponente, wenn im Verlauf von Tumorwachstum oder Therapie eine Schadigung des somatosensorischen Systems auftritt. Ziel der Untersuchung war die Frage, ob mit verschiedenen Testverfahren wie einer klinisch-neurologischen Untersuchung, einem Screening-Fragebogen (PAINdetect) und einer detaillierten quantitativen sensorischen Testung (QST) das Vorhandensein eines neuropathischen Schmerzes mit gleicher Sensitivitat festgestellt werden kann. Methoden: Wir erfassten konsekutiv Patienten der Interdisziplinaren Einrichtung fur Palliativmedizin in Mainz. Eingeschlossen wurden alle Patienten mit Schmerzen, die in der Lage waren, den Schmerzfragebogen und die Instruktionen der QST zu verstehen und bereit zur Studienteilnahme waren. Diese Patienten wurden einer klinisch-neurologischen Untersuchung unterzogen. Mittels PAINdetect-Schmerzfragebogen wurden eine Schmerzzeichnung sowie die Auspragung von 7 Schmerzdeskriptoren erhoben. Im schmerzhaften Areal und einem Kontrollareal folgte eine quantitative sensorische Testung. Entsprechend dem QST Protokoll des Deutschen Forschungsverbunds Neuropathischer Schmerz (DFNS) wurden 13 thermische und mechanische Wahrnehmungs- und Schmerzschwellen bestimmt und bezogen auf Referenzdaten gesunder Kontrollpersonen beurteilt. Mithilfe der genannten Verfahren wurden die Schmerzen als nozizeptiv, neuropathisch oder ohne eindeutige Zuordnung (unklar) klassifiziert. Ergebnisse: 34 von 56 konsekutiv aufgenommenen Patienten berichteten Schmerzen als aktuelles Hauptsymptom (60,7%). Davon erfullten 12 Patienten die Einschlusskriterien. Das durchschnittliche Alter der 12 Studienpatienten betrug 60,3±10,3 Jahre (75% Frauen) mit einem mittleren ECOG-Score von 2,5±0,9 (MW±SD). Nach dem Neurostatus war bei 7 von 12 Patienten (58,3%) eine zusatzliche neuropathische Schmerzkomponente wahrscheinlich. Nach der QST zeigten 6 von 12 Patienten (50%), nach dem PAINdetect-Fragebogen 3 von 12 Patienten (25%) einen neuropathischen Schmerz. Neurostatus und QST korrelierten signifikant (r=0,66; p=0,02). PAINdetect korrelierte weder mit dem Neurostatus noch der QST. Schlussfolgerung: Die vorlaufigen Ergebnisse der laufenden Studie zeigen eine Assoziation von Neurostatus und QST, die belegt, dass QST als standardisierte und formalisierte quantitative klinische Sensibilitatsprufung gut mit der klassischen qualitativen neurologischen Untersuchung ubereinstimmt. Die fehlende Korrelation von Neurostatus/QST und PAINdetect weist darauf hin, dass eine sorgfaltige korperliche Untersuchung nicht durch einen Screening–Fragebogen bei diesem Patientenkollektiv mit Tumorschmerz ersetzt werden kann.

Published
2008
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42. [Ins and outs of neurologic therapy for chronic pain]

Author

S, Sternberg, F, Birklein, and A, May

Subjects
Analgesics, Pain, Antidepressive Agents, Tricyclic, Combined Modality Therapy, Analgesics, Opioid, GABA Antagonists, Chronic Disease, Practice Guidelines as Topic, Humans, Neuralgia, Pain Clinics, Anticonvulsants, Anesthetics, Local, Referral and Consultation, Selective Serotonin Reuptake Inhibitors
Abstract

Although chronic pain is common, especially in elderly patients, its treatment often remains inadequate. One of many reasons for this is that insufficient therapy of acute pain carries the risk of making the pain chronic. Sooner or later most patients suffering from chronic pain will consult a neurologist. However, in most neurological departments, pain treatment is neither one of the common medical activities nor a subject in medical education. In Germany, only specialised centres have associated pain outpatient clinics, so it is almost impossible for neurologist trainees to improve their knowledge in pain treatment. This review provides a synopsis of procedures regarding chronic pain treatments, with particular focus on the most frequent pain disorders. The treatment recommendations follow the current guidelines of the German Society of Neurology.

Published
2008

43. Neurogenic Inflammation in Complex Regional Pain Syndrome (CRPS)

Author

M. Schmelz and F. Birklein

Subjects
Neurogenic inflammation, business.industry, Substance P, Calcitonin gene-related peptide, medicine.disease, Extravasation, chemistry.chemical_compound, Complex regional pain syndrome, chemistry, Anesthesia, Immunology, Nociceptor, Medicine, Body region, Axon reflex, business
Abstract

This chapter explains symptoms and nature of neurogenic inflammation and its importance in posttraumatic complex regional pain syndrome (CRPS). Neurogenic inflammation regularly accompanies excitation of primary afferent nociceptors. It has two major components – plasma extravasation and vasodilatation. The most important mediators are the neuropeptides calcitonin gene-related peptide (CGRP) and substance P (SP). After peripheral trauma, immune reaction (e.g., cytokines) and the attempts of the tissue to regenerate (e.g., growth factors) sensitize nociceptors and thereby amplify neurogenic inflammation. This cascade of events has recently been demonstrated in rat models of CRPS employing distal tibial fractures and nerve transections. Clinical findings in these animals resemble clinical findings in CRPS, and these can be prevented by antineuropeptide treatment. Meanwhile, in CRPS patients, there is plenty of evidence that neurogenic inflammation contributes to clinical presentation. Increased cytokine production was demonstrated and facilitated neurogenic inflammation on the affected side. Surprisingly, there was moderately increased neurogenic inflammation in unaffected body regions also. This favors the possibility that CRPS patients have some genetic similarities. The importance of neurogenic inflammation in acute CRPS also has implications for pathophysiologically oriented treatment.

Published
2008
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44. [Complex regional pain syndrome. A rare complication after acetabular fracture]

Author

A, Lingawi, M H, Hessmann, F, Birklein, A, Hofmann, P, Ingelfinger, and P M, Rommens

Subjects
Adult, Male, Neurologic Examination, Leg, Foot, Multiple Trauma, Acetabulum, Combined Modality Therapy, Sciatic Nerve, Radiography, Fracture Fixation, Internal, Postoperative Complications, Humans, Complex Regional Pain Syndromes, Follow-Up Studies
Abstract

Complex regional pain syndrome (CRPS) is seldom observed in the lower extremities. A case of a 19-year-old patient with typical symptoms in the lower leg and foot after surgical treatment of an acetabular fracture is described. Differential diagnostic evaluation should include CRPS in patients with persistent or progressive pain in the distal extremity after acetabular fracture. Early diagnosis and therapy contribute significantly to a successful outcome.

Published
2007

45. Multiplex neuritis in a patient with autoimmune hepatitis: A case report

Author

W Müller-Forell, Stefan Lüth, Christoph Schramm, F Birklein, E. M. Hennes, Peter R. Galle, Johannes Herkel, and Ansgar W. Lohse

Subjects
Adult, medicine.medical_specialty, medicine.medical_treatment, Neuritis, Azathioprine, Case Report, Autoimmune hepatitis, Gastroenterology, Internal medicine, medicine, Humans, Hepatitis, business.industry, Immunosuppression, General Medicine, medicine.disease, Magnetic Resonance Imaging, Surgery, Hepatitis, Autoimmune, Carotid Arteries, Prednisolone, Female, Vasculitis, business, Cerebral vasculitis, medicine.drug
Abstract

A 37-year old woman presented with a 9-year history of hepatitis of unknown origin and aminotransferases within a 3-fold upper limit of normal. Autoimmune hepatitis (AIH) was diagnosed on the basis of elevated aminotransferases, soluble liver antigen/liver pancreas (SLA/LP) autoantibodies and characteristic histology. Immunosuppressive therapy led to rapid normalization of aminotransferases. Two years later, the patient developed left sided hemisensory deficits under maintenance therapy of prednisolone and azathioprine (AZT). Later she developed right foot drop and paraesthesia in the ulnar innervation territory on both sides. Magnetic resonance imaging (MRI) and cerebral panangiography suggested cerebral vasculitis. Neurological investigation and electromyography disclosed multiplex neuritis (MN) probably due to vasculitis. Consistent with this diagnosis, autoantibodies to extractable nuclear antigens were detectable in serum. Immunosuppression was changed to oral 150 mg cyclophosphamide (CPM0) per day. Prednisolone was increased to 40 mg/d and then gradually tapered to 5 mg. Oral CPM was administered up to a total dose of 40 g and then substituted by 6 times of an intervall infusion therapy of CPM (600 mg/m(2)). Almost complete motoric remission was achieved after 3 mo of CPM. Sensibility remained reduced in the right peroneal innervation territory. Follow-up of cranial MRI provided stable findings without any new or progressive lesions. This is the first report of multiplex neuritis in a patient with autoimmune hepatitis.

Published
2006

48. [Horner's syndrome -- update on neuroanatomy, topographic diagnosis and etiology]

Author

J J, Marx, F, Thömke, and F, Birklein

Subjects
Diagnosis, Differential, Neurons, Horner Syndrome, Humans, Nervous System
Abstract

Due to the complex neuroanatomy of the sympatho-excitatory pathway, Horner's syndrome represents a clinical sign that may result from a variety of lesions in the central and peripheral nervous system. The purpose of the present communication is to help the reader to localize the site of the lesion and to demonstrate the most common etiologic mechanisms resulting in Horner's syndrome. The functional anatomy of the sympathetic supply to the iris, eyelids, facial sweat glands and blood vessels is reviewed and in particular the structure of the central pathway updated. Moreover, pharmacological testing and tests of sudomotor function are described that may help to guide the decision regarding useful additional diagnostic, especially neuroimaging procedures. Finally, a schematic overview is given on the most common pathology, considering additional clinical signs and symptoms.

Published
2005

49. Use of gabapentin to reduce chronic neuropathic pain in Fabry disease

Author

Markus Ries, Eugen Mengel, K. S. Kim, Mathias Beck, F. Krummenauer, G. Kutschke, and F. Birklein

Subjects
Adult, Male, medicine.medical_specialty, Diabetic neuropathy, Gabapentin, Adolescent, Cyclohexanecarboxylic Acids, medicine.medical_treatment, Acetates, Genetics, medicine, Humans, Brief Pain Inventory, Amines, Genetics (clinical), gamma-Aminobutyric Acid, Pain Measurement, business.industry, Vascular disease, Enzyme replacement therapy, medicine.disease, Fabry disease, Surgery, Anticonvulsant, Treatment Outcome, Anesthesia, Neuropathic pain, Fabry Disease, Neuralgia, Anticonvulsants, business, medicine.drug
Abstract

The effect of the anticonvulsant gabapentin on neuropathic pain was studied in six male patients with Fabry disease, aged 15-45 years. After 4 weeks of treatment, pain, as measured using the Brief Pain Inventory, was decreased compared with baseline. Treatment was generally well tolerated. This study indicates that gabapentin should be considered as a treatment option for the neuropathic pain of Fabry disease.

Published
2003

50. 176 LIVER TRANSPLANTATION IN PATIENTS WITH FAMILIAL AMYLOID POLYNEUROPATHY: COMPARISON OF DIFFERENT TRANSTHYRETIN MUTATIONS

Author

Maria Hoppe-Lotichius, F. Birklein, Gerd Otto, C. Theis, AP Barreiros, F. Post, C. Geber, and Peter R. Galle

Subjects
Transthyretin, Pathology, medicine.medical_specialty, Hepatology, biology, business.industry, medicine.medical_treatment, biology.protein, Amyloid polyneuropathy, medicine, In patient, Liver transplantation, business
Published
2012
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