Gunnar Wasner
University of Kiel
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Featured researches published by Gunnar Wasner.
Lancet Neurology | 2010
Ralf Baron; Andreas Binder; Gunnar Wasner
Neuropathic pain develops as a result of lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Examples of neuropathic pain include painful polyneuropathy, postherpetic neuralgia, trigeminal neuralgia, and post-stroke pain. Clinically, neuropathic pain is characterised by spontaneous ongoing or shooting pain and evoked amplified pain responses after noxious or non-noxious stimuli. Methods such as questionnaires for screening and assessment focus on the presence and quality of neuropathic pain. Basic research is enabling the identification of different pathophysiological mechanisms, and clinical assessment of symptoms and signs can help to determine which mechanisms are involved in specific neuropathic pain disorders. Management of neuropathic pain requires an interdisciplinary approach, centred around pharmacological treatment. A better understanding of neuropathic pain and, in particular, of the translation of pathophysiological mechanisms into sensory signs will lead to a more effective and specific mechanism-based treatment approach.
Pain | 2010
Christoph Maier; Ralf Baron; Thomas R. Tölle; Andreas Binder; Niels Birbaumer; Frank Birklein; Janne Gierthmühlen; Herta Flor; Christian Geber; Volker Huge; Elena K. Krumova; G.B. Landwehrmeyer; Walter Magerl; Christian Maihöfner; Helmut Richter; Roman Rolke; A. Scherens; A. Schwarz; Claudia Sommer; V. Tronnier; Nurcan Üçeyler; Michael Valet; Gunnar Wasner; Rolf-Detlef Treede
&NA; Neuropathic pain is accompanied by both positive and negative sensory signs. To explore the spectrum of sensory abnormalities, 1236 patients with a clinical diagnosis of neuropathic pain were assessed by quantitative sensory testing (QST) following the protocol of DFNS (German Research Network on Neuropathic Pain), using both thermal and mechanical nociceptive as well as non‐nociceptive stimuli. Data distributions showed a systematic shift to hyperalgesia for nociceptive, and to hypoesthesia for non‐nociceptive parameters. Across all parameters, 92% of the patients presented at least one abnormality. Thermosensory or mechanical hypoesthesia (up to 41%) was more frequent than hypoalgesia (up to 18% for mechanical stimuli). Mechanical hyperalgesias occurred more often (blunt pressure: 36%, pinprick: 29%) than thermal hyperalgesias (cold: 19%, heat: 24%), dynamic mechanical allodynia (20%), paradoxical heat sensations (18%) or enhanced wind‐up (13%). Hyperesthesia was less than 5%. Every single sensory abnormality occurred in each neurological syndrome, but with different frequencies: thermal and mechanical hyperalgesias were most frequent in complex regional pain syndrome and peripheral nerve injury, allodynia in postherpetic neuralgia. In postherpetic neuralgia and in central pain, subgroups showed either mechanical hyperalgesia or mechanical hypoalgesia. The most frequent combinations of gain and loss were mixed thermal/mechanical loss without hyperalgesia (central pain and polyneuropathy), mixed loss with mechanical hyperalgesia in peripheral neuropathies, mechanical hyperalgesia without any loss in trigeminal neuralgia. Thus, somatosensory profiles with different combinations of loss and gain are shared across the major neuropathic pain syndromes. The characterization of underlying mechanisms will be needed to make a mechanism‐based classification feasible.
Pain | 2003
Torsten Meier; Gunnar Wasner; Markus Faust; Thierry Kuntzer; François Ochsner; Michael Hueppe; Julien Bogousslavsky; Ralf Baron
&NA; Peripheral neuropathic pain syndromes (PNPS) are difficult to treat because commonly used analgesics are often ineffective when, for example, touch‐evoked allodynia, hyperalgesia, and pain paroxysms are present. To investigate whether lidocaine patch 5% treatment is also effective in postherpetic neuropathy (PHN) and in other PNPS, 40 patients with various forms and localizations of PNPS completed a prospective, randomized, placebo‐controlled, two‐way, cross‐over study in three medical hospitals. Patients suffering from pain in a localized skin area with intensity above 40 mm visual analog scale (VAS) and a stable consumption of pain medication were included in this study. The study was divided into four phases: 3‐day run‐in phase, treatment phase 1, wash‐out period, and treatment phase 2, each lasting 1 week. At the discretion of the patients, up to four patches (covering a maximum of 560 cm2) were applied onto the maximally painful area for 12 consecutive hours daily, always either by day or at night. Throughout the four phases, ongoing pain, allodynia, quality of neuropathic symptoms, quality of sleep, and adverse events were assessed. When, after the wash‐out period, the pain intensity scores did not return to the pre‐treatment values (±20%), these patients were excluded from the study. The present study revealed that, as an add‐on therapy, the lidocaine patch 5% was clearly effective in reducing ongoing pain (P=0.017) and allodynia (P=0.023) during the first 8 h after application and that the patches also worked well over a period of 7 days (P=0.018) in diverse focal PNPS. Calculation of the numbers needed to treat (NNT) to obtain one patient with more than 50% relief of ongoing pain revealed that the NNT of 4.4 in the present study compared reasonably well with other studies of PHN, such as topically applied capsaicin (NNT: 5.3–∞) or systemic treatment with gabapentin (NNT: 3.2–5.0).
The Lancet | 2002
Ralf Baron; Jörn Schattschneider; Andreas Binder; Dieter Siebrecht; Gunnar Wasner
BACKGROUND Complex regional pain syndromes can be relieved by sympathetic blockage. The mechanisms of sympathetically maintained pain (SMP) are unclear. We aimed to establish the effect of physiological sympathetic cutaneous vasoconstrictor activity on pain and hyperalgesia in patients with complex regional pain syndromes. METHODS High and low cutaneous vasoconstrictor activity was produced by whole-body cooling and warming (thermal suit) in 13 patients with type I disease and in ten controls. The degree of cutaneous vasoconstrictor discharge was monitored by measurement of skin blood flow and temperature at the arm and leg. Local skin temperature at the affected region was fixed at 35 degrees C. Pain was quantified during high and low cutaneous vasoconstrictor activity (intensity of spontaneous pain, area of mechanical hyperalgesias, heat-pain thresholds). Furthermore, pain was measured before and after diagnostic sympathetic blockage to identify patients with SMP and sympathetically independent pain. FINDINGS In patients with SMP, intensity of spontaneous pain significantly increased, by 22%, and spatial distribution of mechanical dynamic and punctate hyperalgesia increased by 42% and 27%, respectively, during high sympathetic activity compared with low activity. Heat-pain thresholds did not differ during high and low cutaneous vasoconstrictor activity (cold and warm state, 43.6 degrees C vs 44.6 degrees C). Pain relief after sympathetic blockage correlated with augmentation of spontaneous pain after experimental stimulation of cutaneous vasoconstrictor activity (r=0.6, p=0.0244). INTERPRETATION We have shown that in complex regional pain syndromes with SMP, physiological activation of cutaneous vasoconstrictor neurons projecting to the painful arm or leg enhances spontaneous pain and hyperalgesia. We postulate that there is a pathological interaction between sympathetic and afferent neurons within the skin.
Journal of Neurology | 2005
Gunnar Wasner; Anne Kleinert; Andreas Binder; Jörn Schattschneider; Ralf Baron
AbstractObjectivesTopical lidocaine is effective in postherpetic neuralgia (PHN). The aim of the present investigation was to classify patients according to their predominant peripheral nociceptor function and to compare these data with the results of a controlled study using dermal lidocaine patch.MethodsWithin the skin area of maximal pain QST (thermotest) and QCART (histamine iontophoresis and laser Doppler flowmetry) were performed prospectively in 18 PHN patients. A controlled study using cutaneous lidocaine (lidocaine 5% patch, IBSA) followed.ResultsSix patients (group I, sensitised nociceptors) had no sensory loss. Heat pain thresholds were equal or lower than on the contralateral side. Histamine–induced flare and axon reflex vasodilatation were not different on both sides. Histamine evoked pain increased. In 12 patients (group II, nociceptor impairment) heat pain thresholds were higher than contralateral. Histamine–induced flare was impaired or abolished. Histamine did not induce any sensation. Lidocaine was efficacious in the entire group of patients. Subgroup analysis revealed that patients with impairment of nociceptor function had significantly greater pain reduction under lidocaine vs placebo. Patients with preserved and sensitised nociceptors demonstrated no significant pain relief.ConclusionsPHN patients differ concerning their cutaneous nociceptor function: In the group I pain is caused by pathologically sensitised nociceptors. In subset II there is a loss of function of cutaneous C–nociceptors within the allodynic skin. Patients responded well to topical lidocaine even if the skin was completely deprived of nociceptors. Different underlying mechanims of lidocaine action in nociceptor–deprived skin are discussed.
Pain | 2002
Gunnar Wasner; Jörn Schattschneider; Ralf Baron
&NA; Complex regional pain syndrome type I (CRPS I) is a chronic painful disease of one extremity that may develop as a disproportionate consequence of a trauma affecting the limbs without overt nerve injury. It is clinically characterized by sensory, motor and autonomic symptoms including vascular abnormalities. Previously, we have reported that pathophysiological alterations of the ongoing sympathetic activity play a crucial role in vasomotor disturbances (Brain 124 (2001) 587). As a companion article, the aim of this study was to evaluate the diagnostic value of skin temperature side differences in consideration of the spontaneous sympathetic vasoconstrictor activity. Twenty‐five patients with CRPS I were studied. Fifteen patients with painful limbs of other origin and 20 healthy individuals served as controls. Controlled thermoregulation was performed to change cutaneous sympathetic vasoconstrictor activity by the use of a thermal suit: skin sympathetic vasoconstrictor neurones were activated by whole‐body cooling and nerve activity was abolished by whole‐body warming. Skin temperature at the affected and unaffected limbs (infra‐red thermometry) was measured under resting conditions and continuously monitored during controlled modulation of sympathetic activity. The results showed only minor skin temperature asymmetries between both limbs under resting conditions in most CRPS patients. However, during controlled thermoregulation temperature differences between both sides increased dynamically and were most prominent at a high to medium level of vasoconstrictor activity. In both control groups, there were only minor side differences in temperature both in rest and during thermoregulatory changes of sympathetic activity. When comparing the diagnostic value of skin temperature asymmetries in CRPS I, sensitivity was only 32% under resting conditions, but increased up to 76% during controlled alteration of sympathetic activity. Specificity was 100% at rest and 93% at controlled thermoregulation. We concluded that the degree of unilateral vascular disturbances in CRPS I depends critically on spontaneous sympathetic activity. Taking this into consideration, skin temperature differences in the distal limbs are capable of reliably distinguishing CRPS I from other extremity pain syndromes with high sensitivity and specificity.
Neurologic Clinics | 1998
Gunnar Wasner; Misha-Miroslav Backonja; Ralf Baron
Complex regional pain syndromes (CPRS) may develop as a disproportionate consequence of a trauma affecting the limbs without (CRPS I, reflex sympathetic dystrophy) or with (CRPS II, causalgia) obvious nerve lesions. The clinical picture of CRPS consists of asymmetrical distal extremity pain, swelling, and autonomic (sympathetic) and motor symptoms. Changes in the peripheral and central somatosensory, autonomic and motor processing, and a pathologic interaction of sympathetic and afferent systems are discussed as underlying pathophysiologic mechanisms. Therapeutic strategies include pharmacologic pain relief, sympatholytic interventions, and rehabilitation.
Neuroreport | 2001
Ralf Baron; Katja Schwarz; Anne Kleinert; Jörn Schattschneider; Gunnar Wasner
Physiologically, itch and pain are transmitted in separate specific peripheral C-units and central afferent pathways. Some neuropathic pain patients with intact but sensitized (irritable) primary C-nociceptors have spontaneous pain, heat hyperalgesia, static and dynamic mechanical hyperalgesia. The question was whether cutaneous histamine application induces pain in these patients. For comparison histamine was applied into normal skin experimentally sensitized by capsaicin. Histamine application in the capsaicin-induced primary or secondary hyperalgesic skin did not change the intensity and quality of capsaicin pain. Itch was profoundly inhibited. Conversely, histamine application in neuropathic skin induced severe increase in spontaneous burning pain but no itch. In neuropathies irritable nociceptors may express histamine receptors or induce central sensitization to histaminergic stimuli so that itch converts into pain.
Drugs & Aging | 2008
Robert W. Johnson; Gunnar Wasner; Patricia Saddier; Ralf Baron
Herpes zoster (HZ) results from reactivation of varicella-zoster virus (VZV) that has been persistent and clinically dormant in spinal ganglia or cranial sensory nerves since primary infection with VZV. The most common reason for reactivation is a decline in zoster-specific cell mediated immunity as a result of aging (immunosenescence). More than two-thirds of HZ cases occur in people ≥60 years of age. HZ incidence is higher in persons who are immunocompromised as a result of disease (e.g. malignancies such as lymphoma, HIV/AIDS, diabetes mellitus) or treatments such as chemotherapy and radiotherapy. HZ incidence is also increased by therapeutic immune suppression following organ transplantation and in patients taking high-dose corticosteroids. However, HZ may occur in otherwise healthy young people. Although serious and life-threatening complications sometimes occur, the most common complication is postherpetic neuralgia (PHN), which may persist for months or years and is significantly resistant to treatment despite substantial advances in the understanding of its pathological mechanisms. The medical and social costs of HZ and PHN are high, particularly in older patients. Prevention of PHN in patients with HZ is unsatisfactory although antiviral drugs reduce the duration of pain after HZ. A live attenuated vaccine has been shown to reduce the incidence of HZ and PHN as well as the burden of illness in subjects aged ≥60 years. In view of the increasing numbers of elderly persons in the population and the poor outcomes of PHN treatment, vaccination against HZ at approximately 60 years of age appears to be an appropriate strategy.
Journal of Neurology | 2004
Jörn Schattschneider; Andre Bode; Gunnar Wasner; Andreas Binder; Günther Deuschl; Ralf Baron
Abstract.ObjectivesNeurophysiological studies have shown an impairment of temperature perception in secondary and idiopathic restless legs syndrome (RLS). It is unclear whether these deficits are caused by peripheral nerve fibre damage or by central impairment of somatosensory processing. The aim of the present study was (1) to determine the frequency of thermal hypaesthesia in a large population of secondary and idiopathic RLS patients; (2) to differentiate between a peripheral and central disturbance of somatosensory processing and (3) to correlate these findings with the clinical manifestation of the disease.MethodsFrom the results of clinical examination, nerve conduction studies and blood samples the patients were divided into secondary and idiopathic RLS groups. The severity of RLS symptoms was assessed by standardized questionnaires. Quantitative sensory testing (QST) assessing temperature perception was performed in all patients. The peripheral function of small nerve fibres was evaluated by the quantitative nociceptor axon reflex test (QNART).Results22 secondary and 20 idiopathic RLS patients participated in the study. Impairment of temperature perception (QST) was found in 72% of the secondary RLS patients and in 55% of idiopathic RLS patients. The peripheral C–fibre function (QNART) was normal in idiopathic RLS patients. In contrast it was significantly impaired in secondary RLS patients compared with idiopathic RLS patients and age matched controls. There was no correlation between the results obtained in QST and clinical scores.ConclusionImpairment of temperature perception is present in a high percentage of RLS patients. In secondary RLS the sensory deficits are at least in part caused by small fibre neuropathy. In idiopathic RLS a functional impairment of central somatosensory processing is present.