Somatotopic mismatch of hand representation following stroke: is recovery possible?

Well-organized somatotopic representation of the hand is required to interpret input from cutaneous mechanoreceptors. Previous reports have identified patients with various distortions of somatotopic representation after stroke. Importantly, those patients were investigated years after the stroke, indicating that afferent signal regained access to the cortical circuits; however, further plastic changes, which would re-establish somatotopic order and ability to correctly localize tactile stimuli, did not follow. Thus, it was not known whether somatotopic organization could be restored in such patients and whether there is a potential for new rehabilitation strategies. This is the first case report demonstrating normalization of somatotopic representation.

Local anaesthetic sympathetic blockade for complex regional pain syndrome.

BACKGROUND: This is an update of the original Cochrane review published in The Cochrane Library, 2005, Issue 4, on local anaesthetic blockade (LASB) of the sympathetic chain used to treat complex regional pain syndrome (CRPS). OBJECTIVES: To assess the efficacy of LASB for the treatment of pain in CRPS and to evaluate the incidence of adverse effects of the procedure. SEARCH METHODS: We updated searches of the Cochrane Pain, Palliative and Supportive Care Group Specialised Register, the Cochrane Central Register of Controlled Trials (CENTRAL) on the Cochrane Library (Issue 11 of 12, 2012), MEDLINE (1966 to 22/11/12), EMBASE (1974 to 22/11/12), LILACS (1982 to 22/11/12), conference abstracts of the World Congresses of the International Association for the Study of Pain (1995 to 2010), and various clinical trial registers (inception to 2012). We also searched bibliographies from retrieved articles for additional studies. SELECTION CRITERIA: We considered for inclusion randomised controlled trials (RCTs) that evaluated the effect of sympathetic blockade with local anaesthetics in children or adults with CRPS. DATA COLLECTION AND ANALYSIS: The outcomes of interest were reduction in pain intensity levels, the proportion who achieved moderate or substantial pain relief, the duration of pain relief, and the presence of adverse effects in each treatment arm. MAIN RESULTS: We included an additional 10 studies (combined n = 363) in this update. Overall we include 12 studies (combined n = 386). All included studies were assessed to be at high or unclear risk of bias.Three small studies compared LASB to placebo/sham. We were able to pool the results from two of these trials (intervention n = 23). Pooling did not demonstrate significant short-term benefit for LASB (in terms of the risk of a 50% reduction of pain scores).Of two studies that investigated LASB as an addition to rehabilitation treatment, the only study that reported pain outcomes demonstrated no additional benefit from LASB.Eight small randomised studies compared sympathetic blockade to another active intervention. Most studies found no difference in pain outcomes between sympathetic block and other active treatments.Only five studies reported adverse effects, all with minor effects reported. AUTHORS' CONCLUSIONS: This update has found similar results to the original systematic review. There remains a scarcity of published evidence to support the use of local anaesthetic sympathetic blockade for CRPS. From the existing evidence it is not possible to draw firm conclusions regarding the efficacy or safety of this intervention but the limited data available do not suggest that LASB is effective for reducing pain in CRPS.

Influence of deep brain stimulation and levodopa on sensory signs in Parkinson's disease.

To examine the effects of levodopa (L-dopa) and deep brain stimulation of the subthalamic nucleus (STN-DBS) on sensory symptoms and signs in Parkinson's disease (PD). Seventeen patients with PD were included. (1) Presence of sensory symptoms and (2) effects of L-dopa and STN-DBS on sensory symptoms and signs [assessed by quantitative sensory testing (QST)] were examined 6 months after starting STN-DBS. In addition, in 12 of these patients, presence of sensory symptoms prior and post STN-DBS was compared. Pain was most frequently nociceptive. In about 30-40%, pain and sensory symptoms were associated with PD motor symptoms. In most of these cases, pain responded to L-dopa. Intensity of pain was reduced post STN-DBS compared to pre STN-DBS. L-Dopa had no influence on detection thresholds, whereas STN-DBS improved thermal detection thresholds. However, thermal and mechanical pain thresholds were uninfluenced by L-dopa or STN-DBS. Although some patients reported an improvement of pain with STN-DBS or L-dopa, objectively pain sensitivity as assessed by QST was not altered by STN-DBS or L-dopa suggesting that there is no evidence for a direct modulation of central pain processing by L-dopa or STN-DBS.

Vasomotor disturbances in complex regional pain syndrome--a review.

Complex regional pain syndromes (CRPS) are characterized by vascular disturbances primary affecting the microcirculation in the distal part of the involved extremity. In the acute stage inhibited sympathetic vasoconstriction and exaggerated neurogenic inflammation driven by central and peripheral mechanisms, respectively, seem to be the major pathophysiological mechanisms inducing vasodilation. During the chronic course of the disease as well as early in some patients vasoconstriction dominates the clinical picture induced by changes in the microcirculation itself such as endothelial dysfunction or vascular hyperreactivity, whereas sympathetic vasoconstrictor activity returns and neurogenic inflammation is less severe. It can be suggested that the interaction between different mechanisms underlying vasomotor disturbances as well as the severity of each single mechanism in the individual patient have a great impact on the variety of the overall clinical picture in CRPS. Irrespective of the underlying pathophysiology, measurements of skin temperature differences between the affected and the contralateral extremity can serve as a diagnostic tool in CRPS, in particular when sensitivity and specificity is increased by considering dynamic alterations in skin temperature asymmetries.

Central pain syndromes.

Central pain is a chronic neuropathic pain disorder that develops as a direct consequence of a lesion within the central nervous system. The most common causes for central pain are vascular lesions to the brain and the spinal cord, multiple sclerosis, and spinal cord injury. Clinically, central pain typically develops with a delay after the lesion. The pain typically is localized in an area of abnormal sensitivity corresponding to the preceding central lesion. Spontaneous pain and also evoked pains can be found. Pathophysiologically, ectopic neural activity and hyperexcitability are driven by pathological facilitatory and disinhibitory processes. In addition to medical history and clinical examination, diagnosis of central pain is based on imaging and electrophysiological techniques, including quantitative sensory testing, to confirm a central lesion and for identification of the underlying disease. Management of central pain mainly based on pharmacological treatment still is a great challenge, but evidence points to efficacy of antidepressants, anticonvulsants, and opioids.

Dynamic posturography and posturographic training for Parkinson's disease in a routine clinical setting.

BACKGROUND: Postural instability in Parkinson's disease (PD) often is ill-responsive to drugs and DBS. Physiotherapy is recommended but practicability and cost effectiveness are debatable. RESEARCH QUESTION: Can a simple 'plug and play' posturography system produce clinically meaningful measures and elicit postural motor learning in PD patients? METHODS: 40 moderately affected PD patients in a general neurology outpatient clinic who complained of postural instability were included to practice shifts and stabilization of the center of pressure (COP) in a low intensity (once weekly 20-25 minutes over 6 weeks) dynamic posturographic training using the Biodex balance systemTM. Average deviations from mean COP position and from the center of the base of support (BOS) with different degrees of visual feedback in static and dynamic posturographic tasks other than the training tasks, the Berg-Balance-Scale (BBS) and patient self-ratings (FES-I, ABC scale) were assessed before and after training. RESULTS: Posturographic performance was significantly better with eyes open than closed and more so with explicit visual feedback of COP position (p < 0.005). Only with this latter type of feedback and only the deviation form the BOS in dynamic and static posturography was significantly correlated with BBS and UPDRS III (p < 0.001). The deviation from the BOS under explicit visual feedback significantly improved after training (p < 0.005) whereas BBS, FES-I and ABC-scale did not. SIGNIFICANCE: Our posturography procedures were well applicable as a routine clinical tool. They yielded clinically valid measures when COP position was visible and directional shifts from the BOS centre were quantified. Our training was effective for this posturographic measure only. Its significance as a predictor for clinical efficacy of higher intensity and longer term training schedules is hypothesized and warrants further studies.

Residual spinothalamic tract pathways predict development of central pain after spinal cord injury.

Central neuropathic pain following lesions within the CNS, such as spinal cord injury, is one of the most excruciating types of chronic pain and one of the most difficult to treat. The role of spinothalamic pathways in this type of pain is not clear. Previous studies suggested that spinothalamic tract lesions are necessary but not sufficient for development of central pain, since deficits of spinothalamic function were equally severe in spinal cord injured people with and without pain. The aim of the present study was to examine spinothalamic tract function by quantitative sensory testing before and after activation and sensitization of small diameter afferents by applying menthol, histamine or capsaicin to the distal skin areas where spontaneous pain was localized. Investigations were performed in matched groups each of 12 patients with and without central pain below the level of a clinically complete spinal cord injury, and in 12 able-bodied controls. To test peripheral C fibre function, axon reflex vasodilations induced by histamine and capsaicin applications were quantified. In eight patients with pain, sensations of the same quality as one of their major individual pain sensations were rekindled by heat stimuli in combination with topical capsaicin (n = 7) or by cold stimuli (n = 1). No sensations were evoked in pain-free patients (P < 0.01). Capsaicin-induced axon reflex vasodilations were significantly larger in pain patients with heat- and capsaicin-evoked sensations in comparison to pain patients without capsaicin-provoked sensations. These results suggest that intact thermosensitive nociceptive afferents within lesioned spinothalamic tract pathways distinguish people with central pain from those without. The ability to mimic chronic pain sensations by activation of thermosensory nociceptive neurons implies that ongoing activity in these residual spinothalamic pathways plays a crucial role in maintaining central pain. We propose that processes associated with degeneration of neighbouring axons within the tract, such as inflammation, may trigger spontaneous activity in residual intact neurons that act as a 'central pain generator' after spinal cord injury.

Sensitized vasoactive C-nociceptors: key fibers in peripheral neuropathic pain.

INTRODUCTION: Multiple mechanisms are involved in the development and persistence of neuropathic pain. Some patients with nerve damage will remain painless and develop a "loss of function" phenotype, whereas others develop painful neuropathies. OBJECTIVES: The aim of this study is to investigate the role of a peripheral nervous system sensitization by analyzing patients with and without pain. METHODS: The topical application of capsaicin was investigated in peripheral nociceptors. Two groups of patients (painful vs painless) with length-dependent neuropathies and small-fiber impairment were tested. Quantitative sensory testing was assessed before and after topical application of 0.6% capsaicin in the affected skin. In addition, blood perfusion measurements and an axon reflex flare assessment were performed. RESULTS: Quantitative testing revealed that heat hyperalgesia was induced in all patients and volunteers (P < 0.01) without observing any significant differences between patient groups. By contrast, the extent of the axon reflex flare reaction (P < 0.01) as well as the blood perfusion (P < 0.05) was significantly greater in patients with pain than in neuropathy patients not experiencing pain. CONCLUSION: Hyperexcitable vasoactive nociceptive C fibers might contribute to pain in peripheral neuropathies and therefore may serve as a key player in separating into a painless or painful condition.

Neuroimaging Of Cold Allodynia Reveals A Central Disinhibition Mechanism Of Pain.

PURPOSE: Allodynia refers to pain evoked by physiologically innocuous stimuli. It is a disabling symptom of neuropathic pain following a lesion within the peripheral or central nervous system. In fact, two different pathophysiological mechanisms of cold allodynia (ie, hypersensitivity to innocuous cold) have been proposed. The peripheral sensitization of nociceptive neurons can produce cold allodynia, which can be induced experimentally by a topical application of menthol. An alternative mechanism involves reduced inhibition of central pain processing by innocuous cold stimuli. A model to induce the latter type of allodynia is the conduction block of peripheral A-fiber input. PATIENTS AND METHODS: In the presented study, functional MRI was used to analyze these two different experimental models of cold allodynia. In order to identify the underlying cerebral activation patterns of both mechanisms, the application of menthol and the induction of a mechanical A-fiber blockade were studied in healthy volunteers. RESULTS: The block-induced cold allodynia caused significantly stronger activation of the medial polymodal pain processing pathway, including left medial thalamus, anterior cingulate cortex, and medial prefrontal cortex. In contrast, menthol-induced cold allodynia caused significantly stronger activity of the left lateral thalamus as well as the primary and secondary somatosensory cortices, key structures of the lateral discriminative pathway of pain processing. Mean pain intensity did not differ between both forms of cold allodynia. CONCLUSION: Experimental cold allodynia is mediated in different cerebral areas depending on the underlying pathophysiology. The activity pattern associated with block-induced allodynia confirms a fundamental integration between painful and non-painful temperature sensation, ie, the cold-induced inhibition of cold pain.

Determinants of thermal pain thresholds in normal subjects.

OBJECTIVE: Measurement of thermal pain thresholds is an essential part of quantitative sensory testing (QST). However, databases of QST show limitations due to large inter-individual variations including unreasonably low thresholds for thermal pain, lack of data on intra-individual variations over time and on the subjects' perception at threshold. This study sought to reduce inter-individual variations, investigated the reproducibility of measurements of thermal pain thresholds and included evaluation of thermally induced perceptions. METHODS: Thermal pain thresholds were investigated in 20 healthy subjects over three weeks using two protocols, one of which differed in making the subjects familiar with the likely range of applied temperatures beforehand. Both protocols included subjective ratings of pain and temperature perception at the pain thresholds. RESULTS: Data obtain using both protocols showed large inter-individual variations, but small intra-individual variations of pain thresholds over time as well as good feasibility and reproducibility of subjects' ratings at threshold. CONCLUSIONS: Previous experience of test stimuli has no influence on the variability of thermal pain thresholds. However, measurement of thermal pain thresholds showed good reproducibility over time. Evaluation of perception at thresholds provided further reproducible data. SIGNIFICANCE: Further approaches are needed to reduce variability of thermal pain thresholds; however, good reproducibility of thermal pain thresholds and thermally induced perceptions warrants consideration of their use in larger longitudinal studies.

Herpes zoster and postherpetic neuralgia: optimizing management in the elderly patient.

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 >or=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 >or=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.

The effect of menthol on cold allodynia in patients with neuropathic pain.

OBJECTIVE: Cutaneous application of menthol in healthy subjects induces cold allodynia via sensitization of cold-sensitive nociceptors. We investigated the effects of menthol on preexisting cold allodynia in patients to test whether the allodynia was exacerbated. DESIGN: In eight neuropathic pain patients (six of peripheral, two of central origin), 40% menthol was applied topically to an area of preexisting cold allodynia. Mirror-image skin areas and aged-matched healthy subjects served as controls in patients with unilateral and bilateral neuropathic pain, respectively. Prior to and after menthol, cold pain thresholds were measured using a thermotest device. RESULTS: Menthol induced significant cold allodynia in control areas. However, in neuropathic areas, results were more heterogeneous. Overall, preexisting cold allodynia was not aggravated by topical menthol and was attenuated in 6/8 patients. CONCLUSIONS: These results suggest that, unlike in controls, menthol is not more hyperalgesic, but may be analgesic in some patients with peripheral and central neuropathic pain.

Pain in oxaliplatin-induced neuropathy--sensitisation in the peripheral and central nociceptive system.

BACKGROUND: This study aimed to determine the somatosensory characteristics and pain types in patients with acute oxaliplatin-induced neuropathy and to relate this profile to the hereby detected underlying pathophysiological mechanisms. PATIENTS AND METHODS: Sixteen patients treated with oxaliplatin for cancer were characterised with neurological assessment and a standardised and validated set for quantitative sensory testing (QST). Patients were allocated to two groups depending on the presence or absence of pain symptoms of acute neuropathy. RESULTS: Comparison with normative data revealed in patients with pain symptoms a characteristic somatosensory profile of cold and mechanical hyperalgesia. Group-to-group analysis revealed additional heat hyperalgesia and warm hypoesthesia. CONCLUSION: Pain symptoms of acute oxaliplatin-induced neuropathy are related to signs of sensitisation within the peripheral (cold and heat hyperalgesia) and central nervous nociceptive system (mechanical hyperalgesia). This strengthens the rationale for treatment with anticonvulsants and antidepressants and fosters research on ion channel and receptor related mechanisms.

Effects of subthalamic nucleus stimulation and levodopa on the autonomic nervous system in Parkinson's disease.

Dysfunctions of the autonomic nervous system (ANS) are common in Parkinson's disease (PD). Regarding motor disability, deep brain stimulation of the subthalamic nucleus (STN) is an effective treatment option in long lasting PD. The aims of this study were to examine whether STN stimulation has an influence on functions of the ANS and to compare these effects to those induced by levodopa. Blood pressure (BP) and heart rate (HR) during rest and orthostatic conditions, HR variability (HRV) and breathing-induced cutaneous sympathetic vasoconstriction (CVC) were tested in 14 PD patients treated with STN stimulation during "ON" and "OFF" condition of the stimulator. The effects of a single dose of levodopa on ANS were tested in 15 PD patients without DBS. STN stimulation had no influence on cardiovascular ANS functions, whereas CVC was significantly increased. In contrast, levodopa significantly lowered BP and HR at rest and enhanced orthostatic hypotension. Further, HRV, skin perfusion and temperature increased after administration of levodopa. Our results suggest that in contrast to levodopa, STN stimulation has only minor effects on autonomic functions. Since less pharmacotherapy is needed after STN stimulation, reduced levodopa intake results in relative improvement of autonomic function in deep brain stimulated PD patients.

Mechanisms of adrenosensitivity in capsaicin induced hyperalgesia.

UNLABELLED: It is well known that iontophoresis of norepinephrine in capsaicin treated skin is followed by an increase in thermal hyperalgesia. It is unclear if this action on nocicepitive afferents involves the release of prostaglandins. The aim of the present study was to determine: (1) the effect of norepinephrine iontophoresis on spontaneous and evoked pain in the human skin after topical application of capsaicin; (2) the effect of cyclooxygenase (COX) inhibition on changes in pain perception induced by norepinephrine application. METHODS: Ten volunteers were included in the study. Iontophoresis of norepinephrine or saline was performed in a randomized cross over design on the volar aspect of the forearm after topical application of capsaicin. In the second part of the study single iv. injections of saline or acetylsalicylic acid were performed in a randomized double blind cross over design. After the injection norepinephrine iontophoresis was performed on the skin treated with topical capsaicin. Spontaneous pain, mechanical hyperalgesia as well as warm and heat pain thresholds were measured before and after each iontophoresis. RESULTS: Norepinephrine did enhance spontaneous pain and mechanical and thermal hyperalgesia in capsaicin treated skin. Inhibition of COX I and II had no effect on the norepinephrine induced changes in pain perception. CONCLUSION: The results do not support the assumption that in human skin sensitized by topical capsaicin application of norepinephrine acts on nociceptive afferents via the release of prostaglandins. Thus, a direct action of norepinephrine on adrenergic receptors in the membrane of the afferent fibers is most likely.

Short Report: TRPV1-polymorphism 1911 A>G alters capsaicin-induced sensory changes in healthy subjects.

BACKGROUND: C-fibers express transient receptor potential (TRP) channels. These high-voltage gated channels function as integrators of different physical stresses (e.g. heat, protons, ATP). Additionally channel activation can be induced by capsaicin. Topically applied, capsaicin elicits burning pain, heat and mechanical hyperalgesia and serves as a human surrogate model for pain. It was suggested that the TRPV1-variant rs8065080 (1911A>G) plays a pivotal role in patients with neuropathic pain syndromes. We investigated the effect of this TRPV1-SNP on thermal sensitivity and superficial skin perfusion in 25 healthy subjects. METHODS AND FINDINGS: Nine subjects being homozygous TRPV1 wild type (AA), 8 heterozygous (AG) and 8 homozygous variant (GG) carriers were selected out of a pool of genotyped healthy individuals. Under physiological conditions (no capsaicin application), there was no statistical significant difference in thermal thresholds or skin perfusion between carriers of different TRPV1 1199A>G genotypes. However, intra-individual calculations (Δ% pre vs. post capsaicin) revealed (1) less warm-detection in AA/AG (-82.1%) compared to GG (-13.1%) and (2) a gain of heat pain sensitivity in AA/AG (+22.2%) compared to GG carriers (+15.6%) after adjustment for perfusion measurements ((1)p = 0.009, (2)p = 0.021). CONCLUSION: Presence of homozygous variant TRPV1 genotype (GG) demonstrated less capsaicin-induced warm hypoesthesia in warm-detection and less capsaicin-induced heat pain sensitivity suggesting an altered channel function. This demonstrates not only the functional influence of TRPV1 rs8065080 polymorphism itself; it further more underpins the relevance of genotyping-based approaches in both patients and surrogate models of neuropathic pain in healthy volunteers.

No adrenergic sensitization of afferent neurons in painful sensory polyneuropathy.

INTRODUCTION: The aim of the present study was to determine (1) if an adrenergic sensitivity of afferent neurons is present in patients with painful polyneuropathy as compared with non-painful polyneuropathy and (2) if there is a correlation between adrenergic sensitisation and the severity of afferent and sympathetic small fiber damage. METHODS: 10 patients with painful and non painful polyneuropathy and 10 healthy controls were included. The function of small afferent and efferent sympathetic neurons was evaluated. Adrenergic sensitivity of afferent neurons was assessed by cutaneous iontophoresis of norepinephrine. Spontaneous pain, mechanical hyperalgesia as well as warm and heat pain thresholds were measured. RESULTS: Iontophoresis of norepinephrine did not induce or enhance spontaneous pain or mechanical allodynia, either in painless or painful polyneuropathies. There was no difference in norepinephrine-induced heat hyperalgesia between both neuropathy groups and healthy controls. The response of afferent neurons to norepinephrine was not correlated with the severity of damage to afferent small fibers or efferent sympathetic vasoconstrictor neurons. CONCLUSION: The results do not support the assumption that in painful polyneuropathies afferent neurons acquire an adrenergic sensitivity after nerve injury and that adrenergic stimulation leads to an exacerbation of spontaneous pain and thermal and mechanical hyperalgesia.

Complex regional pain syndromes: the influence of cutaneous and deep somatic sympathetic innervation on pain.

OBJECTIVES: Complex regional pain syndromes (CRPS) can be relieved by sympathetic blockade. Different sympathetic efferent output channels innervate distinct effector organs (ie, cutaneous vasoconstrictor, muscle vasoconstrictor. and sudomotor neurons, as well as neurons innervating deep somatic tissues like bone, joints, and tendons). The aim of the present study was to elucidate in CRPS patients the sympathetically maintained pain (SMP) component that exclusively depends on cutaneous sympathetic activity compared with the SMP depending on the sympathetic innervation of deep somatic tissues. METHODS: The sympathetic outflow to the painful skin was modulated selectively in awake humans. High and low cutaneous vasoconstrictor activity was produced in 12 CRPS type 1 patients by whole-body cooling and warming (thermal suit). Spontaneous pain was quantified during high and low cutaneous vasoconstrictor activity. By comparing the cutaneous SMP component with the change in pain that was achieved by modulation of the entire sympathetic outflow (sympathetic ganglion block), the SMP component originating in deep somatic structures was estimated. RESULTS: The relief of spontaneous pain after sympathetic blockade was more pronounced than changes in spontaneous pain that could be induced by selective sympathetic cutaneous modulation. The entire SMP component (cutaneous and deep) changes considerably over time. It is most prominent in the acute stages of CRPS. CONCLUSIONS: Sympathetic afferent coupling takes place in the skin and in the deep somatic tissues, but especially in the acute stages of CRPS, the pain component that is influenced by the sympathetic innervation of deep somatic structures is more important than the cutaneous activation. The entire sympathetic maintained pain component is not constant in the course of the disease but decreases over time.

Harlequin Syndrome After Thoracic Paravertebral Block.

Harlequin syndrome is characterized by the sudden onset of unilateral facial flushing and sweating, often preceded by exercise, excessive heat, or, rarely, regional anesthesia. Although the exact mechanism remains unclear, it is often referred to as transient or permanent interruption of the sympathetic nervous system. We present a case of Harlequin syndrome without Horner syndrome in a patient with unilateral right-sided facial flushing that started shortly after a left-sided thoracic paravertebral nerve block for a mastectomy. We discuss the interruption of the sympathetic and parasympathetic nervous system and the levels of spinal nerve block associated with a thoracic paravertebral nerve block.

Postherpetic neuralgia: topical lidocaine is effective in nociceptor-deprived skin.

OBJECTIVES: Topical 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. METHODS: Within 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. RESULTS: Six 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. CONCLUSIONS: PHN 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 mechanisms of lidocaine action in nociceptor-deprived skin are discussed.