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PubMed1997

[Diagnostic criteria for post-traumatic algodystrophy].

Algodystrophy (reflex sympathetic dystrophy, Sudeck's atrophy) is a clinical syndrome, developing in most cases as a consequence of trauma and characterized by pain, swelling, tenderness, vascular and sudomotor instability trophic changes of the skin and stiffness. There are several controversial issues concerning algodystrophy in the literature: incidence of the condition (from 0.03% to 95% in various studies), the value of the diagnostic tests in its recognizing and efficacy of the various methods of the treatment. The causes of these discrepancies were discussed: various diagnostic criteria, its unrestricted use by authors and specificity of the natural history of the condition were considered as the main reasons. The features of algodystrophy and its importance in recognizing of the disorder were described in detail; the diagnostic value of the radiographic, static and dynamic scintigraphic examination and diagnostic sympathetic block were also discussed. Several clinical classifications of algodystrophy were presented; the usefulness of these classifications in providing more accurate assessment of the clinical groups and in facilitating of comparison between studies were underlined.

Humans↗
PubMedDate not supplied

Ultrasound imaging for stellate ganglion block: direct visualization of puncture site and local anesthetic spread. A pilot study.

BACKGROUND AND OBJECTIVES: Stellate ganglion block (SGB) inhibits sympathetic innervation and is a common treatment for reflex sympathetic dystrophy. During the positioning of the needle, there is a risk of injury to the adjacent structures. The aim of the study was to develop an ultrasonographic imaging technique for the performance of SGB. METHODS: Twelve patients (ASA I-II) underwent SGB first by using the blind standard technique (group A: 8 mL bupivacaine 0.25%) and a second time by using an ultrasonographic imaging technique (group B: 5 mL bupivacaine 0.25%). In group B a 10 MHz ultrasound scanning probe was used to identify the anatomic structures and to guide the needle toward the transverse process of C6. RESULTS: Stellate ganglion block was satisfactory in 11 of 12 attempts by the blind technique. Ultrasonographic guidance (group B) resulted in a complete block in all patients. Onset of block was observed within 10 minutes in only 10 of 12 group A patients, while all patients in group B exhibited an adequate block after 10 minutes. During the imaging technique, the needle was inserted to an average depth of 22 +/- 3 mm and the injection of 5 mL bupivacaine resulted in an anesthetic depot with a mean diameter of 14 +/- 3 mm. Distance from the depot to the vagal nerve was 5 +/- 3 mm and 5 +/- 4 mm to the root of C6. All patients (n = 4) with a distance of < 1 mm between anesthetic depot and the root of C6 developed paresthesia within the corresponding cutaneous segment. Blind technique resulted in hematoma formation in three study patients, with no hematoma occurring during imaging technique. CONCLUSIONS: Ultrasonographic guided SGB may improve safety and allows the visualization of the local anesthetic depot. Studying the local anesthetic spread might allow the avoidance of side effects as well as typical complications of SGB.

Adult↗
PubMed1997

Sympathetic nervous system and pain: a clinical reappraisal.

The target article discusses various aspects of the relationship between the sympathetic system and pain. To this end, the patients under study are divided into three groups. In the first group, called "reflex sympathetic dystrophy" (RSD), the syndrome can be characterized by a triad of autonomic, motor, and sensory symptoms, which occur in a distally generalized distribution. The pain is typically felt deeply and diffusely, has an orthostatic component, and is suppressed by the ischemia test. Under those circumstances, the pain is likely to respond to sympatholytic interventions. In a second group, called "sympathetically maintained pain" (SMP) syndrome, the principal symptoms are spontaneous pain, which is felt superficially and has no orthostatic component, and allodynia. These symptoms, typically confined to the zone of a lesioned nerve, may also be relieved by sympathetic blocks. Since the characteristics of the pain differ between RSD and SMP, the underlying kind of sympathetic-sensory coupling may also vary between these cases. A very small third group of patients exhibits symptoms of both RSD and SMP. The dependence or independence of pain on sympathetic function reported in most published studies seems to be questionable because the degree of technical success of the block remains uncertain. Therefore, pain should not be reported as sympathetic function independent until the criteria for a complete sympathetic block have been established and satisfied.

Aged↗
PubMed1998

Partial peripheral neuropathy and denervation induced adrenoceptor supersensitivity. Functional studies in an experimental model.

Sciatic nerve ligation in rats (chronic constriction injury (CCI)) induces clinical signs and symptoms that mimic human conditions of neuropathic origin, such as reflex sympathetic dystrophy (RSD). Denervation-induced supersensitivity to (circulating) catecholamines has been implicated in sympathetic dysfunction in the CCI model as well as in RSD. In the present paper we studied functional properties of sympathetic innervation in subcutaneous resistance arteries, isolated from the hind paw of rats 3 weeks after ligation. Contractile responses to electric field stimulation of adrenergic nerves and exogenously administered cumulative doses of various adrenergic agonists were studied using a myograph. As compared to the contralateral side, subcutaneous arteries from the ligated side were less responsive to electrical field stimulation. Besides, as compared to the contralateral side, subcutaneous arteries from the ligated side showed increased sensitivity to alpha 1-adrenoceptor stimulation. This study demonstrates that sympathetic dysfunction in an experimental model of neuropathic pain consists of denervation-induced supersensitivity to catecholamines rather than of an afferently-induced increase in efferent sympathetic nerve impulses.

Adrenergic Fibers↗
PubMed1993

Morphine injected around the stellate ganglion does not modulate the sympathetic nervous system nor does it provide pain relief.

Six patients with a presumptive diagnosis of upper limb reflex sympathetic dystrophy and 1 patient with anaesthesia dolorosa had pain and sympathetic activity assessed before and after injection of bupivacaine and morphine around the stellate ganglion. Sympathetic modulation was assessed by measuring the effect of each injection on the inspiratory gasping response (IGR), a measure of central arousal, the sympathetic skin response (SSR), a measure of peripheral sudomotor activity and the plethsymographic wave (PW), a measure of peripheral vasomotor activity. There were 5 women and 2 men with a mean age of 49 years (range: 41-66 years). The duration of pain varied from 9 months to 7 years. Bupivacaine abolished the IGR and SSR and increased the amplitude of the PW in all patients without any demonstrable sensory or motor blockade in the treated limb, nor did it have any effect on the contralateral IGR or PW. Bupivacaine did provide short-term pain relief in 4 out of 7 patients. Morphine did not produce any demonstrable effect on the sympathetic nervous system nor did it provide pain relief for any patient. Thus these data do not support injection of morphine around the stellate ganglion as it neither modulated sympathetic activity nor provided pain relief.

Adult↗
PubMed1998

[Pain syndromes with causal participation of the sympathetic nervous system].

The efferent sympathetic nervous system is organized into subsystems that innervate and regulate via separate peripheral sympathic pathways the different autonomic target organs. This review discusses mechanisms through which this efferent system may be causally involved in the generation of pain. Clinical pain syndromes in which this may be the case are "complex regional pain syndromes" (CRPS) type I (previously reflex sympathetic dystrophy) and type II (recently causalgia). The "sympathetically maintained pain" (SMP) is a symptom (and not a clinical entity) that can principally also be present in other pain syndromes. An explanatory hypothesis, which may explain the clinical phenomenology of CRPS (different types of pain, swelling, autonomic, motor and trophic changes) and the mechanisms involved, is described and discussed. This hypothesis consists of different components that either have been tested and verified experimentally or which are still hypothetical. The hypothesis consists of changes in the primary afferent (nociceptive and non-nociceptive) neurones (sensitization, ectopic impulse generation) and of the neurones in the spinal cord (preferentially in the dorsal horn) which are secondary consequences of the changes in the primary afferent neurones ("central sensitization"). These changes are not specific for SMP. The centerpiece of the hypothesis is a positive feedback circuit that consists of the primary afferent neurones, spinal cord neurones, sympathic neurones and the pathologic sympathetic-afferent coupling. This coupling can occur directly via noradrenaline (or possibly another substance) at different sites of the afferent neurone (at the lesion site, remote from the lesion site in the periphery and in the spinal ganglion). The direct coupling requires that the afferent neurone expresses adrenoceptors. Indirect coupling can occur via the vascular bed or otherwise, e.g. by changes of the neurovascular transmission. The activity in the sympathetic neurones to the affected extremity can change. This change does not consist of a generalized increase of sympathetic activity but of a change of the reflexes (e.g., thermoregulatory and nociceptive reflexes). From this follows that the pathophysiologal processes operating in CRPS may occur at four levels of integration that interact with each other: effector organ, peripheral afferent and sympathetic neurone, spinal cord, supraspinal centres. Recent experimental investigations on rats show that the sympathetic nervous system is possibly also causally involved in the generation of inflammation and inflammatory pain. The mechanisms by which this occurs are different from those operating in SMP during CRPS.

Animals↗
PubMed2004

Mechanistic and clinical aspects of complex regional pain syndrome (CRPS).

Complex regional pain syndromes (CRPS, reflex sympathetic dystrophy, causalgia) are painful disorders that develop after trauma affecting a limb with (I) or without (II) nerve injury. Clinical features are pain, impairment of motor function, swelling and autonomic abnormalities (changes in sweating and blood flow). Autonomic abnormalities. The maximal skin temperature difference between the affected and unaffected extremity that occurs during a controlled thermoregulation can be used as a diagnostic tool. SMP. Sympathetic outflow to the painful extremity was experimentally activated. The intensity as well as area of spontaneous pain and mechanical hyperalgesia increased considerably in patients that had been classified as having SMP by positive sympathetic blocks. A pathological interaction between sympathetic vasoconstrictor and afferent neurons within the affected skin is the likely explanation for SMP in CRPS patients. Motor abnormalities. Kinematic analysis of target reaching as well as grip force analysis showed a pathological sensorimotor integration located in the parietal cortex. Furthermore, MEG studies demonstrated a continuous inhibition of the primary motor cortex. Neurogenic inflammation. Some features of acute CRPS (vasodilatation, swelling, pain) indicate a localized inflammatory process. Transcutaneous electrical stimulation of nociceptive C-fibre provoked protein extravasation into the interstitial fluid (microdialysis) only in CRPS patients and not in controls.

Animals↗
PubMed1989

[Treatment of reflex algoneurodystrophies by sympathetic blockade with guanethidine].

Reflex sympathetic dystrophy (RSD) can be treated by regional sympathetic blockade with guanethidine. This method was used systematically in 25 patients with post-traumatic RSD of the upper (n = 8) or lower limb (n = 17). Sixty three blocks were performed, each patient receiving 1 to 4 blocks. The results were appreciated by the effects after one month on pain, mobility and trophic changes. They were excellent in 7 cases, good in 4 cases and poor in 7 cases. The results were better in moderate RSD without psychiatric overlay. Thirteen patients were cured after 3 months. Pain decreased significantly 2 days after injection in 28 of the 63 blocks. The effects on mobility and trophic changes always occurred after the analgesic effect. No side effects were observed with the exception of one patient who had a convulsion 2 hours after the injection. These results show that regional sympathetic blockage with guanethidine is useful for the treatment of RSD, especially in its moderate stages. In view of the negligible risks and its efficacy, the authors consider it to be the first line treatment of moderate RSD.

Adult↗
PubMed1995

[Reflex sympathetic algodystrophies. Preventive and therapeutic aspects].

Deafferentation syndromes have in common the existence of a physical injury and/or of a functional impairment of a nerve, either somatosensory afferent (Phantom Limb Pain) and/or sympathetic efferent (Reflex Sympathetic Dystrophy). These progressively debilitating syndromes are the witness of the absence of self-limitation of neuronal sensitization, which is normally the evolution of any painful stimulation of spinal cord neurons. To some extent deafferentation syndromes could be defined as a maladaptive neuronal plasticity. The lack of complete understanding of underlying pathophysiological mechanisms gives account of the wide variety of proposed treatments and of their unpredictable and variable efficacy. This fact is also due in part to the lack of controlled studies of most of the therapeutic propositions, whose purported efficacy is usually based on anecdotal reports. Finally, the role of prevention must be strongly emphasized, focusing, if those syndromes are likely to occur following surgery, on the importance of pre- and postoperative efficient analgesia, and also, possibly, on the preemptive role of regional anaesthetic techniques.

Anesthesia, Conduction↗
PubMed1994

The syndrome of painful legs and moving toes.

The clinical presentation, symptoms, and signs in 20 new patients with the painful legs and moving toes syndrome are presented. Painful legs and moving toes may develop in the setting of spinal cord and cauda equina trauma, lumbar root lesions, injuries to bony or soft tissues of the feet, and peripheral neuropathy. In 4 of the 20 cases in the present study, no definite cause was found. Pain preceded the onset of toe movements in 18 cases, but in 2 the reverse sequence occurred. The pain had many of the characteristics of causalgia, but none of the patients exhibited the full picture of reflex sympathetic dystrophy, and peripheral trauma was the trigger in only 5 cases. Several patients reported that the occurrence of toe movements was closely related to the pain, although abolition of pain with lumbar sympathetic blocks was not necessarily associated with disappearance of the movements. Several features suggest a central origin for the movements. Symptoms may begin on one side and become bilateral; movements may be momentarily suppressed by voluntary action or exacerbated by changing posture; and electromyography reveals complex patterns of rhythmic activity with normal recruitment of motor units involving several myotomes. Three other patients with similar moving toes but no pain are also described. The occurrence of similar movements in the absence of pain raises the possibility that these cases represent examples at one end of a spectrum of disorders, with pain alone (causalgia) at the other end and the syndrome of painful legs and moving toes in between.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Neurogenic inflammation in an animal model of neuropathic pain.

Loose ligation of a rat sciatic nerve (chronic constriction injury (CCI) model) provokes signs and symptoms like those observed in reflex sympathetic dystrophy (RSD) patients. Primary afferent nociceptive C-fibers seem to be involved in an afferent orthodromic as well as in an efferent antidromic manner. In this study we hypothesize that consequent to development of antidromic impulses in C-nociceptive afferents, neuropeptides released from peripheral endings of these fibers, increase skin blood flow (SBF), vascular permeability, and tissue accumulation of polymorphonuclear leukocytes (PMNs). Collectively, these phenomena have been referred to as neurogenic inflammation. To investigate the presence of neurogenic inflammation in the CCI-model, we assessed skin blood flow (SBF) as well as the level of edema and accumulation of PMNs in muscle tissue obtained from the affected hindpaw. SBF was measured, by means of laser Doppler flowmetry, before ligation as well as at day 4 after ligation. At day 4, SBF measurements were performed before and after abolition of the capability of C-fibers to mediate a vasodilator response. To this end, capsaicin was applied perineurally. Increased vascular permeability was inferred from the level of edema of muscle tissue as determined by assessment of wet/dry weight ratios of muscle biopsies. PMN accumulation was investigated by enzymatic detection of myeloperoxidase (MPO) activity in muscle biopsies. Compared with preligation values, at day 4 SBF was increased more than twofold (p < 0.05). The latter response was annihilated by capsaicin application. Compared with sham operated controls, wet/dry ratios were higher in the ligated animals (1.104 vs. 1.068; p < 0.05). Likewise, when compared with sham operated controls, MPO activity was found to be increased in the ligated hindpaw (Optic Density 0.15 vs. 0.89; p < 0.001). In conclusion, the findings of this study indicate that loose ligation of a sciatic nerve induces an inflammatory response in the ipsilateral hindpaw, which most likely is mediated by release of neuropeptides from the peripheral endings of antidromically acting nociceptive C-fibres.

Animals↗
PubMedDate not supplied

[Neurological disorders in post-traumatic algodystrophy of the upper extremity].

Sensory disturbances (hypoaesthesia in fingertips and tenderness) and movement disorders (tremor, dystonia, muscle spasms, abnormal postures and inability in initiating of movement) were investigated in 80 patients with post-traumatic reflex sympathetic dystrophy (RSD) of the upper extremity. Sensory disturbances were found in 67 patients (84%): most frequently hypoaesthesia in fingertips--in 49, and tenderness of the dorsal aspect of the hand in 24; in six patients both these signs were present simultaneously. Movement disorders were found less frequently: tremor was observed in 12 patients, spasms of the flexor muscles of the forearm and hand in two, postural dystonia in one, and inability initiating of movement in the other one. Sympathetic interruptions reduced movement disturbances in two patients. Dystonia was resistant to various treatment approaches including botulinum toxin injections. Certain hypothesis explaining pathogenic background of motor and sensory disorders in RSD are discussed. The results of this study show that sensory disturbances are frequently observed in RSD, however, they usually disappear after successful treatment of the condition; movement disorders are less frequent, but much more difficult to control. Neurologists are not frequently faced with the problem of neurological disorders after trauma of the limb. Inclusion of RSD in differential diagnosis may improve recognition of the disorder and result in its faster and proper management.

Adult↗
PubMedDate not supplied

Complex regional pain syndrome type I: associated visual sensorimotor case findings.

OBJECTIVE: The objective was to present new visual sensorimotor findings in a patient with complex regional pain syndrome type I, formerly known as reflex sympathetic dystrophy. DESIGN: Clinical measurements were compared for the following visual sensorimotor tasks before and after 10 minutes of near visual stimulation: accommodation, vergence, and reading eye movements. PATIENT: The patient was a 19-year-old female university student with complex regional pain syndrome type I. RESULTS: All visual sensorimotor findings worsened dramatically after performance of the brief near visual task. In addition, the patient experienced severe dizziness, nausea, dull eye ache, and general fatigue, which persisted for 30 to 45 minutes following each test period. CONCLUSIONS: The patient manifested signs and symptoms of complex regional pain syndrome type I per the prior neurologic diagnosis, as well as the newly diagnosed accommodative infacility, accommodative insufficiency, convergence insufficiency, and deficits of saccades and pursuits, which were severely debilitating. The findings neither support nor refute the conventional notion of abnormal sympathetic mediation as a mechanism of fatigue and pain. However, the diagnoses of accommodative infacility and insufficiency suggest abnormal parasympathetic activation. Further investigation is needed to characterize the array of visual dysfunctions in a large sample of such patients, which may help elucidate the precise underlying neurologic causes of the sensorimotor deficits in these patients.

Accommodation, Ocular↗
PubMed2006

Correlation between changes in regional cerebral blood flow and pain relief in complex regional pain syndrome type 1.

OBJECTIVE: Analyzing changes in regional cerebral blood flow (rCBF) with SPECT in complex regional pain syndrome type 1 (CRPS 1), formerly known as reflex sympathetic dystrophy, is an optimal method for evaluating effective pain relief. We attempted to investigate the correlation of changes in rCBF with pain relief during treatments of sympathetic blockade and multimodal epidural pain control. CASE REPORT: We describe a patient with severe CRPS 1 in whom conventional treatment failed to relieve the pain. Combined repeated lumbar sympathetic blocks and long-term epidural morphine, bupivacaine, and ketamine administration provided satisfactory pain relief and functional activity recovery. Six normal control subjects having one Tc-99m HMPAO scan each and the patient with CRPS having 3 Tc-99m HMPAO scans (once before treatment and twice at 4 months and 6 months after treatment, respectively). The patient with CRPS showed lower rCBF than normal controls in the left thalamus and higher rCBF than normal controls in the right parietal lobe and left frontal lobe. After subsequent treatment, the subtraction images showed increased rCBF in the left thalamus and decreased rCBF in the right parietal and left frontal lobes. CONCLUSIONS: Tc-99m HMPAO SPECT showed a relationship of rCBF in the thalamus, parietal lobe, and frontal lobe with pain relief. rCBF alterations may provide an indicator for the quality of pain management for neuropathic pains. Subtraction analysis between pre- and posttreatment, by using statistical parametric mapping (version 2), can be used as an objective indicator for the effectiveness of therapy.

Adult↗
PubMed1992

Painful neuropathy: altered central processing maintained dynamically by peripheral input.

We performed sensory assessments before and during diagnostic tourniquet-cuff and local anesthetic blocks in 4 patients diagnosed with reflex sympathetic dystrophy (RSD). All patients complained of mechano-allodynia; lightly touching the skin evoked an intense pain sensation. At detection levels, electrical stimuli were perceived as painful, suggesting that the mechano-allodynia was mediated by A beta low-threshold mechanoreceptor afferents. A beta-mediated allodynia was further supported by reaction time latencies to painful electrical stimuli at threshold for A-fiber activation and, in 1 patient, by differential cuff blocks which abolished A beta function and allodynia while thermal sensation (warm and cold) were preserved. Local anesthetic block of painful foci associated with previous trauma abolished mechano-allodynia, cold allodynia, and spontaneous pain in all patients and relieved the motor symptoms in 1 patient with tonic contractures of the toes. Tactile and thermal perception in the previously allodynic area was preserved. When the local anesthetic block waned, spontaneous pain, allodynia, and motor symptoms returned. We propose a model of neuropathic pain in which ongoing nociceptive afferent input from a peripheral focus dynamically maintains altered central processing that accounts for allodynia, spontaneous pain, and other sensory and motor abnormalities. Blocking the peripheral input causes the central processing to revert to normal, abolishing the symptoms for the duration of the block. The model accounts for sympathetically maintained (SMP) and sympathetically independent (SIP) pain. The peripheral input can be independent of sympathetic activity or driven completely or in part by activity in sympathetic efferents or by circulating catecholamines. The shared final common pathway may explain the common features of SMP and SIP.

Adult↗
PubMed1996

Percutaneous radiofrequency upper thoracic sympathectomy.

Between June 1979 and May 1994, I performed 148 unilateral or bilateral sympathectomies on 247 limbs in 110 patients using a percutaneous radiofrequency technique, usually on an outpatient surgery basis. Patient ages ranged from 10 to 81 years, with 45 male and 65 female patients. Four patients had unsuccessfully undergone prior open surgical sympathectomy. Patients suffered from hyperhidrosis, vascular occlusion, Raynaud's disease or other chronic vasculopathies, painful causalgia or reflex sympathetic dystrophy, or Prinzmetal's angina. The sympathectomy technique has evolved over this 15-year period and is currently in its third phase. Changes in the procedure were based on anatomic and clinical/radiographic correlations and careful patient follow-up. Current modifications have reduced the frequency of both early and late failures. The present technique (Phase III) relies on neuroleptanalgesia with superficial local anesthesia only and does not require general anesthesia, intubation, or lung collapse. Two 18-gauge radiofrequency TIC needle electrodes (Radionics, Burlington, MA) are used. A series of three lesions is rostrocaudally made at each of the ganglion sites selected in an attempt to destroy the entire fusiform ganglion. Lesion sites are targeted by C-arm fluoroscopy and electrical stimulation, which produces a threshold of sensory awareness of > 1.0 V. Lesion effectiveness is monitored by bilateral finger plethysmography and hand skin temperature measurement. With the Phase III technique, the sympathetic activity in 96% of operated limbs after 2 years and in 91% of operated limbs after 3 years continues to be completely or largely interrupted. By comparison, I achieved similar success in 83 and 72% operated limbs with the Phase I technique and in 77 and 71% with the Phase II technique. Symptomatic pneumothorax, in six patients, has been the only serious complication. When necessary, a subsequent operation can easily be performed and is effective.

Adolescent↗
PubMedDate not supplied

Sympathetic nerve blocks: in search of a role.

OBJECTIVE: The role of sympathetic blocks in pain therapy is examined in the light of changing concepts of pain pathophysiology. A critical review of the literature also sought to develop an evidence-based analysis of outcome studies to provide recommendations for appropriate applications of sympathetic blocks, together with ideas for further clinically based research. METHODS: A focus on the pathophysiology of neuropathic and inflammatory pain disorders was used to help redefine what contribution, if any, was provided by the sympathetic system, to chronic pain states. Validation of nerve block therapies based on historical practices and these newer concepts and outcome determinations has then been used to present an overview of clinical nerve block therapies as applied to the sympathetic nervous system. RESULTS: 1. Pain Diagnosis: A reclassification of reflex sympathetic dystrophy (RSD) to the new taxonomy of complex regional pain syndromes (CRPS) is supported, with evidence that only a questionable sympathetic contribution at the dorsal root ganglion level can be ascribed etiologically to this group of disorders. Sympathetic blocks can establish whether pains may be nonresponsive or variably responsive to such blocks, but are considered inappropriate in determining a clinical diagnosis. 2. Neuropathic Pain Therapy: (a) A critical review of the literature regarding the use of sympathetic blocks in the treatment of acute herpes zoster pain and in the treatment of postherpetic neuralgia found little support for the widely held view that sympathetic blocks reduced either the incidence of long-term reduction of pain in these disorders. Further attempts to reduce PHN by the combination of blocks with aggressive drug therapies during acute herpes infection are suggested. (b) CRPS (RSD) treatments are seen as evolutionary at present, with the role of sympathetic blocks being only part of a balanced pain treatment strategy aimed at getting patients activated under cover of good analgesia and improved function. These proposals come as consensus recommendations but are not substantiated by outcome studies. 3. Ischemic Pain: Permanent sympathetic block with neurolytic or thermocoagulation techniques provides up to 50% long-term improved blood flow and reduction of pain and ulceration for patients with advanced peripheral vascular disease. This is particularly appropriate at lumbar levels in which percutaneous techniques are safe when conducted with real time imaging control. CONCLUSIONS: Changes in the understanding of CRPS disorders and the role of the sympathetic nervous system in neuropathic pain has changed both the diagnostic and management strategies for these pain states. The sensitivity and specificity of response to sympathetic blocks in establishing their value at diagnostic aids will not be fully established without further clinical study. Further use of intravenous regional blocks or diagnostic intravenous infusions remains questionable. Preventive and therapeutic use of sympathetic blocks in herpes zoster pain remains open to well-controlled study.

Animals↗
PubMed1996

Innervation of hyperalgesic skin in patients with complex regional pain syndrome.

OBJECTIVE: To look for anatomical and histochemical signs of interaction between sensory and sympathetic nerves in the hyperalgesic skin of patients with complex regional pain syndrome. SUBJECTS: Skin samples were obtained from eight patients whose condition developed after a suspected or confirmed peripheral nerve injury, and from nine patients with features of reflex sympathetic dystrophy (RSD) following a soft-tissue injury. A skin sample was also obtained from 18 control subjects of similar age and sex distribution to patients. DESIGN: In patients, skin samples were taken from an area of static mechanical hyperalgesia and from an equivalent site in the contralateral limb. In controls, skin samples were obtained from the dorsum of one hand or foot. HISTOCHEMICAL MARKERS: We used neuron-specific enolase for all classes of nerve fiber; tyrosine hydroxylase for noradrenergic fibers; vasoactive intestinal peptide for sympathetic sudomotor fibers; tyrosine hydroxylase co-existing with neuropeptide Y for sympathetic vasoconstrictor fibers; and calcitonin gene-related peptide with substance P or somatostatin for peptide-containing unmyelinated sensory fibers. RESULTS: In patients, the distribution of markers was similar in skin taken from an area of mechanical hyperalgesia and skin taken from an equivalent site contralaterally, and was unrelated to clinical features of RSD. The distribution of markers did not differ between patients and controls. Nerve tangles immunoreactive to neuron-specific enolase, but not to other markers, were detected in samples taken from four patients and two controls. The nerve tangles were present bilaterally in two patients, and only on the affected side in two other patients. The clinical condition was more fully developed in the four patients whose skin samples contained nerve tangles than in most other patients. CONCLUSIONS: A major difference in distribution or change in histochemical content of cutaneous autonomic or nociceptor fibers is unlikely to underly static mechanical hyperalgesia following a soft-tissue or peripheral nerve injury. The relevance of cutaneous nerve tangles for the pathophysiology of RSD is uncertain.

Adolescent↗