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PubMed2001

[Gabapentin for therapy of neuropathic pain].

Gabapentin, which has been approved for add-on therapy of focal seizures, is increasingly used for treatment of neuropathic pain. Its analgesic effect is supposed to be due to reduction of glutamatergic transmission, improvement of GABAergic transmission and to binding to voltage-dependent calcium channels. Experimental studies demonstrated an ameliorating effect of gabapentin on neuropathic pain. Placebo-controlled studies revealed an efficacy of gabapentin against pain in diabetic neuropathy and postherpetic neuralgia and in prophylaxis of migraine. Case reports show an analgesic effect of gabapentin in trigeminus neuralgia and in reflex sympathetic dystrophy. The main adverse events are dizziness, ataxia and somnolence. Controlled studies, which compare the efficacy of gabapentin with that of the respective reference drug, are needed to evaluate its importance in treatment of pain.

Acetates↗

PubMed1998

[Pathophysiology and diagnosis in patients with sympathetically dependent pain].

Chronic pain in a distal extremity that is accompanied by autonomic dysfunction in the same region is taken to indicate reflex sympathetic dystrophy. Typically, hyperalgesia to light touch is present in addition to the spontaneous pain. The absence of heat hyperalgesia indicates that the underlying mechanism is central rather than peripheral sensitization. This mechanism is similar to that of secondary hyperalgesia in the intact skin surrounding an injury site. Sympathetically maintained pain (SMP) is diagnosed, when these sensory symptoms are reversible under sympathetic blockade. SMP is not due to hyperactivity of sympathetic efferents but to receptor supersensitivity, probably by overexpression of alpha(1)-adrenergic receptors on nociceptive primary afferents. This way normal levels of norepinephrine can cause pathological spontaneous activity of nociceptors which maintains the central sensitization. Chronic burning pain and cutaneous hyperalgesia may also be independent of the sympathetic innervation of the skin. In this case, central sensitization is maintained by other mechanisms. A role of the sympathetic nervous system in the pathogenesis of pain cannot be deduced simply from the simultaneous presence of sensory and autonomic clinical signs and symptoms. Therefore, sympathetic blockade in a patient initially is a diagnostic procedure, aiming to demonstrate the presence of the symptom SMP. Therapeutic blockade is only indicated after this demonstration. For the substantial number of patients with sympathetically independent pain, other treatment modalities are needed which may for example attack central sensitization.

English Abstract↗

PubMed1998

[Sympathetic nervous system and pain--some open questions].

BACKGROUND: Neuropathic pain syndromes may be treated by intervention at the sympathetic nervous system. The pain in these syndromes is therefore called sympathetically maintained pain (SMP). Typical disorders with a SMP component are complex regional pain syndromes (reflex sympathetic dystrophy and causalgia), traumatic neuralgias and herpes zoster. RESULTS: Open questions are how the efferent sympathetic nervous system is capable of influencing pain sensation and which mechanisms underly the autonomic dysregulation often observed in these syndromes.(1) Somatic afferents that project through the sympathetic trunk do not exist. Therefore, a pure sympathetic block does not block afferent information arising from the affected extremity. What alternatives are possible? Under pathophysiological conditions a functional interaction of efferent sympathetic fibers and afferent nociceptive fibers could be demonstrated in patients and animal studies. The intensity of this coupling varies considerably between individual patients and is not necessary for the diagnosis of the disorder. (2) Sympathetically maintained pain and signs of autonomic dysfunction are independent clinical and pathophysiological phenomena without any causal relation. However, it is possible to treat both the SMP and the autonomic dysfunction with sympathetic blocks.

English Abstract↗

PubMed2002

Osteoporosis following chronic constriction injury of sciatic nerve in rats.

Osteopathic changes sometimes occur in patients with complex regional pain syndrome (reflex sympathetic dystrophy and causalgia). We aimed to investigate whether such osteopathic changes occurred in rats with chronic constriction injury (CCI) of the sciatic nerve. A CCI of the sciatic nerve was established in a unilateral hind limb in 39 adult Sprague-Dawley rats, which were killed 1, 2, 3, 5, or 7 weeks after the CCI procedure. Bone mineral content (BMC) and bone mineral density (BMD) in extracted tibial bones were measured using a dual-energy X-ray absorptiometer, and the number of osteoclasts in the metaphyseal regions was counted by the use of tartrate-resistant acid phosphate (TRAP) staining. BMC was significantly decreased, compared with that of the contralateral side, 1 to 7 weeks after CCI, and BMD was decreased 2 to 7 weeks after the procedure in the ipsilateral tibial bones, compared with BMD in the contralateral bones. The number of TRAP-positive multinucleated osteoclasts in the ipsilateral bones was significantly increased at 2, 3, and 5 weeks after the CCI, when compared with the number of these osteoclasts in the contralateral bones. The results of the present study demonstrate that osteopathic changes are associated with chronic constrictive injury of the sciatic nerve.

Animals↗

PubMed2004

Comparative study of nonbridging and bridging external fixators for unstable distal radius fractures.

The purpose of this study was to compare nonbridging external fixators (group NB) with bridging external fixators (group B) in the treatment for unstable distal radius fractures. The subjects consisted of 84 patients, 42 in each group. Mean patient age was 64.0 years in group NB and 59.6 years in group B. According to Saito's classification, most fractures were of the comminuted Colles type. No bone graft was made in group NB. Patients of group B showed serious reflex sympathetic dystrophy (RSD). On Saito's evaluation criteria, the proportion of patients evaluated as "good" or better was 100% in group NB and 95.6% in group B. This finding can be taken as evidence that group NB patients showed better results.

Adolescent↗

PubMed2002

Complex regional pain syndrome is a disease of the central nervous system.

Complex regional pain syndrome (CRPS) is clinically characterized by pain, abnormal regulation of blood flow and sweating, edema of skin and subcutaneous tissues, trophic changes of skin, appendages of skin and subcutaneous tissues, and active and passive movement disorders. It is classified into type I (previously reflex sympathetic dystrophy) and type II (previously causalgia). Based on multiple evidence from clinical observations, experimentation on humans, and experimentation on animals, the hypothesis has been put forward that CRPS is primarily a disease of the central nervous system. CRPS patients exhibit changes which occur in somatosensory systems processing noxious, tactile and thermal information, in sympathetic systems innervating skin (blood vessels, sweat glands), and in the somatomotor system. This indicates that the central representations of these systems are changed and data show that CRPS, in particular type I, is a systemic disease involving these neuronal systems. This way of looking at CRPS shifts the attention away from interpreting the syndrome conceptually in a narrow manner and to reduce it to one system or to one mechanism only, e.g., to sympathetic-afferent coupling. It will further our understanding why CRPS type I may develop after a trivial trauma, after a trauma being remote from the affected extremity exhibiting CRPS, and possibly after immobilization of an extremity. It will explain why, in CRPS patients with sympathetically maintained pain, a few temporary blocks of the sympathetic innervation of the affected extremity sometimes lead to long-lasting (even permanent) pain relief and to resolution of the other changes observed in CRPS. This changed view will bring about a diagnostic reclassification and redefinition of CRPS and will have bearings on the therapeutic approaches. Finally it will shift the focus of research efforts.

Central Nervous System↗

PubMed2001

Complex regional pain syndromes.

Complex regional pain syndromes (CRPS) (formerly reflex sympathetic dystrophy and causalgia) are neuropathic pain conditions that are initiated by an extremity trauma or peripheral nerve lesion. Clinical definition and scientific understanding of CRPS are still evolving; however, both the clinical picture and therapeutic options are significantly influenced by a dysfunction of the sympathetic nervous system. Recent investigations suggest functional central abnormalities and a peripheral inflammatory component in the pathophysiology of CRPS. Interdisciplinary treatment includes physical, pharmacologic, and invasive interventional therapy, as well as stimulation techniques.

Central Nervous System↗

PubMed1999

Functional Magnetic Resonance Imaging of Pain Consciousness: Cortical Networks of Pain Critically Depend on What is Implied by "Pain"

Brain imaging studies, using primarily functional magnetic resonance imaging (fMRI), are reviewed. These studies are aimed at developing imaging approaches that can be used in the clinical setting to investigate clinically relevant pain states. To this end, our recent studies indicate that by taking advantage of the temporal variations in pain perception, we are able to identify cortical regions that may be uniquely involved in pain consciousness. This procedure in turn becomes a general approach with which clinical pain states can be studied. Preliminary results are shown in patients suffering from chronic reflex sympathetic dystrophy (RSD) and chronic back pain. The review emphasizes that different experimental pain states, and chronic and acute clinical pain states, seem to involve dramatically different networks, the details of which remain to be worked out. It is concluded that these procedures need to be applied in the larger clinical setting in which multicentered studies may be conducted to begin building the brain pain network atlas.

Journal Article↗

PubMed1993

Dorsal sympathectomy and management of thoracic outlet syndrome with VATS.

Dorsal sympathectomy and the management of the thoracic outlet syndrome have been considerably improved with the use of video assistance because it affords both magnification and an improved light system. Two techniques of video assistance were employed in the group of patients described here. One involved the sympathectomy done through three ports using standard video-assisted thoracic surgical methods. The second technique involved a transaxillary incision with removal of the first rib using video-assistance magnification and light, operating either directly or secondarily while visualizing the image on the television set. (The vast majority of cases have been performed using this latter technique.) Major indications for performing dorsal sympathectomy include (1) hyperhidrosis, (2) Raynaud's phenomenon, (3) Raynaud's disease, (4) causalgia, (5) reflex sympathetic dystrophy, and (6) vascular insufficiency of the upper extremity. Except for hyperhidrosis, all of the other indications require the usual diagnostic techniques, including cervical sympathetic blockade to assess whether the symptoms are relieved by temporary blockade of the sympathetic ganglia. In 326 patients, sympathectomy, performed either alone or in conjunction with first-rib removal for relief of the thoracic outlet syndrome, has been successful. In only 6 patients has sympathetic activity recurred in less than 6 months. Initially all of them were treated conservatively. Three of the 6 required a repeat sympathectomy. Postsympathectomy neuralgia occurred in only 2 of more than 326 patients. Both cases were managed successfully in a conservative fashion. Among the patients in whom a Horner's syndrome was not deliberately induced, the syndrome developed in 2. In both, the syndrome resolved spontaneously within several months.

Autonomic Nervous System Diseases↗

PubMed1993

Mechanical hyperalgesia in streptozotocin-diabetic rats is not sympathetically maintained.

It has been suggested that the mechanism underlying the pain that occurs in patients with diabetic neuropathy may be similar to that mediating sympathetically maintained pain (SMP), such as occurs in patients with reflex sympathetic dystrophy. To evaluate this suggestion we have examined a model of diabetes mellitus, the streptozotocin-diabetic (STZ-D) rat, for features characteristic of SMP. We demonstrate that the decrease in nociceptive threshold observed in the STZ-D rat is not attenuated by chemical sympathectomy nor exacerbated by intradermal injection of norepinephrine (NE). In addition, the NE content is markedly decreased in the skin of the STZ-D rat. These results suggest that altered nociceptive thresholds associated with diabetic neuropathy are not sympathetically maintained.

Animals↗

PubMed1992

Transient osteoporosis of the hip.

Transient osteoporosis of the hip (TOH) is an uncommon but possibly underdiagnosed condition. This pattern of regional osteoporosis affects previously healthy middle-aged men, and women in the third trimester of pregnancy. Its etiology is still unclear, yet in view of similarities to regional migratory osteoporosis and reflex sympathetic dystrophy, vascular and neurologic disturbances have been proposed as the possible pathogenetic mechanisms. Pain in the hip area and functional disability of the affected limb are the main clinical signs. Diagnosis is supported by local radiological osteopenia whose gradual disappearance parallels the spontaneous recovery. Bone scintigraphy, magnetic resonance imaging, computed tomography, and other imaging methods are supplementary diagnostic tools. Exclusion of more common entities is required. The purpose of this report is to elucidate the diagnostic and therapeutic aspects of TOH and to stimulate the physician's awareness of this condition, recognition of which may prevent unnecessary invasive procedures and inadequate treatment.

Diagnosis, Differential↗

PubMedDate not supplied

Nerve pathophysiology and mechanisms of pain in causalgia.

In contrast to sensory endings in skin, muscle, etc., afferents in the mid-course of intact nerves are normally incapable of generating impulses upon slow or prolonged depolarization. However, after various types of nerve injury, including complete nerve section and local demyelination, an ectopic pacemaker capability develops. One peculiarity of such abnormal differentiated sites is chemosensitivity to alpha-adrenergic agonists and to sympathetic efferents discharge. Such ectopic chemosensitivity may well be involved in the etiology of paraesthesias and pain in reflex sympathetic dystrophies including causalgia. Specifically, it is proposed that the fundamental cause of these conditions is the development of abnormal electrogenic membrane properties in the region of demyelination and sprout outgrowth. These abnormal properties presumably include the appearance of excess inward current conductances and ectopic alpha-adrenergic receptors. Catecholamines released from sympathetic efferents in the area of injury locally depolarize damaged sensory fibers, and because of the abnormal electrogenic properties of these fibers, an abnormal afferent discharge is generated.

Adrenergic Fibers↗

PubMed1988

The proportions of sympathetic postganglionic and unmyelinated afferent axons in normal and regenerated cat sural nerves.

Electrophysiological experiments have been carried out to see if the proportions of sympathetic postganglionic and unmyelinated afferent axons in a cutaneous nerve were changed after injury and regeneration. It seemed possible that an alteration in the relative numbers of the two groups of axons could contribute to the aetiology of reflex sympathetic dystrophy, but the experiments provided no evidence for such a change. There were, however, signs of a decrease in axon numbers in the regenerated nerves.

Animals↗

PubMed1985

Effects of regional intravenous guanethidine block in posttraumatic cold intolerance in hand amputees.

In twenty-four patients with intolerance to cold after partial or complete finger amputations, lower skin temperature together with cold and vibration allodynia (allodynia = pain due to a non-noxious stimulus to neural skin) were found in the cold intolerant area compared with the corresponding area in the uninjured hand. When treated with regional intravenous guanethidine block nine patients became free from symptoms for up to twelve weeks, which is longer than would be expected from the duration of the known pharmacological effects of guanethidine. The patients had several features in common with reflex sympathetic dystrophies, and we suggest that neurogenic rather than vascular disturbances are mainly involved in the post-traumatic cold intolerance syndrome.

Adult↗

PubMed1994

Experience of the early use of technetium 99 bone scintigraphy in wrist injury.

In a retrospective study, patients with suspected scaphoid fracture had an average of three sets of scaphoid radiographs prior to scintigraphy. Scans were performed an average of 3 months after injury and many were inconclusive because of disuse changes. A prospective analysis of early scintigraphy in 35 cases over 18 months was carried out. Scans were performed at an average of 15.5 days after injury in selected cases. Patients had an average of 1.28 sets of negative radiographs prior to scanning. There were no false negative scans and in 13 with focal uptake a wrist fracture was demonstrated. Diffuse uptake was thought to be indicative of ligamentous damage or reflex sympathetic dystrophy. Early scintigraphy was found to be a sensitive, reliable and cost-effective examination in cases of suspected significant wrist injury.

Adolescent↗

PubMed1990

Cushing's syndrome from epidural methylprednisolone.

Iatrogenic Cushing's syndrome has been reported after the use of nasal, aerosol, oral, and intramuscular steroid preparations. Presented is a case of Cushing's syndrome due to an epidural injection of methylprednisolone. A 24-year-old man had left arm pain after an occupational injury. Electromyography revealed C7 radioculopathy and cervical laminectomy was performed. Postoperatively, the patient noted improvement, however, he had recurrence of his symptoms within 1 month. Significant pain in the left arm, accompanied by swelling, persisted despite non-steroidal anti-inflammatory and anti-depressant medications. Repeat electromyography showed a resolving C7 with increased polyphasic potentials. Reflex sympathetic dystrophy was diagnosed and the patient received 3 stellate ganglion blocks with relief of the swelling, but only temporary relief of pain. He then underwent epidural injection of 60 mg of methylprednisolone. A cushingoid appearance was noted approximately 1 month later. Serum cortisol was undetectable, there was no adrenal response to synthetic ACTH, and urinary-free cortisol was below normal at 12. The patient eventually underwent a second surgical procedure for his pain and required steroid coverage. His pain subsequently showed slow improvement. Urinary-free cortisol normalized 4 months after onset; however, the patient's cushingoid appearance persisted for 12 months.

Adult↗

PubMed1991

Topical application of clonidine relieves hyperalgesia in patients with sympathetically maintained pain.

Patients with reflex sympathetic dystrophy or causalgia characteristically have ongoing pain and pain to light touch (hyperalgesia). Some of these patients obtain relief of their pain following interruption of sympathetic function to the affected area and, therefore, have sympathetically maintained pain (SMP). Evidence suggests that the pain and hyperalgesia in SMP are related to activation of peripheral adrenergic receptors. We wished to determine the contribution of alpha 1- and alpha 2-adrenergic receptors in SMP and thus examined the effects of local application of adrenergic agents in patients with SMP. The alpha 2-adrenergic agonist clonidine, available as a transdermal patch, was delivered topically to the patients' hyperalgesic skin. In four patients with SMP, clonidine eliminated or substantially reduced hyperalgesia to mechanical and cold stimuli. In three of these patients the effects were confined to the skin region beneath the patch, suggesting a peripheral and not central effect. The relief of hyperalgesia was not due to a local anesthetic effect since touch thresholds were unaffected. Topical clonidine did not relieve hyperalgesia of similar severity for two other patients whose hyperalgesia and pain were unaffected by sympathetic ganglion blocks (i.e., diagnosed as having sympathetically independent pain). In two SMP patients, intradermal injection of norepinephrine or phenylephrine (a specific alpha 1-adrenergic agonist) at a site treated with clonidine evoked intense pain and rekindled the pre-clonidine hyperalgesia at that site. It is likely that clonidine locally blocks the release of norepinephrine via activation of alpha 2 receptors on the sympathetic terminals. This study suggests, therefore, that SMP is mediated via alpha 1-adrenergic receptors located in the affected tissue.

Administration, Cutaneous↗

PubMed1992

Allodynia evoked by intrathecal administration of prostaglandin F2 alpha to conscious mice.

The intrathecal administration of prostaglandin F2 alpha to conscious mice resulted in spontaneous agitation and touch-evoked agitation (allodynia) in the animals. The maximum allodynia induced by prostaglandin F2 alpha was observed at 10-15 min after intrathecal injection, and the response did not disappear by 120 min. Prostaglandin F2 alpha produced allodynia over a wide range of dosage from 0.1 pg to 2.5 micrograms/mouse. Dose dependency of prostaglandin F2 alpha for allodynia showed a skewed bell-shaped pattern, and the maximal allodynic effect was observed at 1.0 microgram. This allodynia was dose-dependently relieved by alpha 1-adrenergic (methoxamine), alpha 2-adrenergic (clonidine), and A1-adenosine (RPIA) agonists. Clonidine was 1.5 orders of magnitude more potent than methoxamine in blocking prostaglandin F2 alpha-induced allodynia. The blockade by clonidine was dose-dependently reversed by the alpha 2-adrenergic antagonist yohimbine but not by the alpha 1-adrenergic antagonist prazosin. These results demonstrate that prostaglandin F2 alpha administered intrathecally induces allodynia in conscious mice and that the allodynia involves the alpha 2-adrenergic and A1-adenosine systems. Because this allodynia has a clear resemblance to the characteristics of chronic pain in patients with causalgia and reflex sympathetic dystrophy, prostaglandin F2 alpha may be involved in allodynia observed with these disorders.

Adenosine↗