A complex regional pain syndrome characterized by burning pain and marked sensitivity to touch (HYPERESTHESIA) in the distribution of an injured peripheral nerve. Autonomic dysfunction in the form of sudomotor (i.e., sympathetic innervation to sweat glands), vasomotor, and trophic skin changes may also occur. (Adams et al., Principles of Neurology, 6th ed, p1359)
The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.
A syndrome characterized by severe burning pain in an extremity accompanied by sudomotor, vasomotor, and trophic changes in bone without an associated specific nerve injury. This condition is most often precipitated by trauma to soft tissue or nerve complexes. The skin over the affected region is usually erythematous and demonstrates hypersensitivity to tactile stimuli and erythema. (Adams et al., Principles of Neurology, 6th ed, p1360; Pain 1995 Oct;63(1):127-33)
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.

Causalgia, pathological pain, and adrenergic receptors. (1/28)

Control of expression of molecular receptors for chemical messengers and modulation of these receptors' activity are now established as ways to alter cellular reaction. This paper extends these mechanisms to the arena of pathological pain by presenting the hypothesis that increased expression of alpha-adrenergic receptors in primary afferent neurons is part of the etiology of pain in classical causalgia. It is argued that partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable by sympathetic activity and adrenergic substances. This excitation is mediated by alpha-adrenergic receptors and has a time course reminiscent of experimental denervation supersensitivity. The change in neuronal phenotype is demonstrable after lesions of mixed nerves or of the sympathetic postganglionic supply. Similar partial denervations also produce a substantial increase in the number of dorsal root ganglion neurons evidencing the presence of alpha-adrenergic receptors. The hypothesis proposes the increased presence of alpha-adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies. These additional adrenergic receptors are suggested to make nociceptors and other primary afferent neurons excitable by local or circulating norepinephrine and epinephrine. For central pathways, the adrenergic excitation would be equivalent to that produced by noxious events and would consequently evoke pain. In support, evidence is cited for a form of denervation supersensitivity in causalgia and for increased expression of human alpha-adrenergic receptors after loss of sympathetic activity.  (+info)

The clinical efficacy of neuroendoscope in surgical treatment for deafferentation pain. (2/28)

Spinal cord stimulation (SCS) is one of the most minimally invasive and effective treatments for intractable pain. We report the efficacy of a very small diameter neuroendoscope on setting the electrode to the proper site in the epidural space. Our cases include thalamic hemorrhage, and each patient had unilateral intractable pain on L1 or less as the main complaint. They had been treated for over two years in other hospitals, but no significant relief was achieved. Because each patient had been given frequent epidural blocks, the adhesion in the epidural space was expected. In Group A (3 cases), we used very small diameter neuroendoscope to dissect adhesion in the epidural space and to make optimal space for lead placement under direct vision. Conventional lead placement under fluoroscopy was performed in Group B (3 cases). Medtronic's PISCES lead system was used for SCS. In Group A, stimulation and pain regions matched in all cases, and good pain relief was also achieved. In Group B, however, stimulation and pain regions matched incompletely and the increase in stimulation caused stimulation on the pain-free side.  (+info)

Receptor subtype-specific pronociceptive and analgesic actions of galanin in the spinal cord: selective actions via GalR1 and GalR2 receptors. (3/28)

Galanin is a 29-aa neuropeptide with a complex role in pain processing. Several galanin receptor subtypes are present in dorsal root ganglia and spinal cord with a differential distribution. Here, we describe a generation of a specific galanin R2 (GalR2) agonist, AR-M1896, and its application in studies of a rat neuropathic pain model (Bennett). The results show that in normal rats mechanical and cold allodynia of the hindpaw are induced after intrathecal infusion of low-dose galanin (25 ng per 0.5 microl/h). The same effect is seen with equimolar doses of AR-M1896 or AR-M961, an agonist both at GalR1 and GalR2 receptors. In allodynic Bennett model rats, the mechanical threshold increased dose-dependently after intrathecal injection of a high dose of AR-M961, whereas no effect was observed in the control or AR-M1896 group. No effect of either of the two compounds was observed in nonallodynic Bennett model rats. These data indicate that a low dose of galanin has a nociceptive role at the spinal cord level mediated by GalR2 receptors, whereas the antiallodynic effect of high-dose galanin on neuropathic pain is mediated by the GalR1 receptors. Thus, a selective GalR1 agonist may be used to treat neuropathic pain.  (+info)

Sympathectomy for complex regional pain syndrome. (4/28)

BACKGROUND: With the easier and earlier recognition of complex regional pain syndrome (CRPS), a reappraisal of its therapy, particularly the role and timing of sympathectomy, is warranted. PATIENTS AND METHODS: Over a 9-year period, 42 patients with CRPS type II of the upper extremity were referred for sympathectomy. Patients were categorized according to the duration of the symptoms (group I, <3 months; group II, >3 months). All patients underwent initial medical treatment; stellate ganglion blocks were performed when symptoms persisted beyond 6 weeks. Patients were referred for thoracoscopic sympathectomy on persistence of the pain syndrome. A visual linear analogue scale was used to evaluate outcome of sympathectomy. RESULTS: Thoracoscopic dorsal sympathectomy was successfully undertaken in 32 patients. In the remaining 10 patients, thoracoscopy was not technically feasible and open sympathectomy was performed. There was an overall improvement in all 42 patients undergoing sympathectomy (P <.001, Wilcoxon signed rank test). The outcome in group I was significantly better than in group II (P <.003, Mann-Whitney U test). The diagnosis of sympathetically mediated pain with stellate blockade did not correlate with clinical outcome. Patients undergoing thoracoscopic sympathectomy had a better outcome than those undergoing open sympathectomy. There were no complications, and the hospital stay was shorter in the thoracoscopic group. CONCLUSION: Early recognition of CRPS and prompt recourse to surgical sympathectomy is a useful option in the management of CRPS.  (+info)

Rho-kinase inhibition enhances axonal plasticity and attenuates cold hyperalgesia after dorsal rhizotomy. (5/28)

Dorsal rhizotomy results in primary deafferentation of the dorsal horn with concomitant sprouting of spared intraspinal monoaminergic axons. Because descending monoaminergic systems are thought to mitigate nociceptive transmission from the periphery and because dorsal rhizotomy can result in neuropathic pain, we sought to determine whether the rhizotomy-induced sprouting response could be further augmented. Because myelin-derived molecules mask endogenous plasticity of CNS axons and because myelin-inhibitory signaling occurs through the Rho-GTPase pathway, we inhibited Rho-pathway signaling after cervical dorsal rhizotomy in rats. An increase in the density of serotonergic- and tyrosine hydroxylase-positive fibers was seen in the dorsal horn 1 week after septuple rhizotomy, and axon density continued to increase for at least 1 month. One week after septuple rhizotomy, administration of intrathecal Y-27632, an antagonist of Rho-kinase (ROCK), increased the density of both fiber types over vehicle-treated controls. To examine behavioral effects of both cervical rhizotomy and ROCK inhibition, we examined responses to evoked pain: mechanical and thermal allodynia and cold hyperalgesia in the forepaw were examined after single, double, and quadruple rhizotomies of dorsal roots of the brachial plexus. The most notable behavioral outcome was the development of cold hyperalgesia in the affected forepaw after rhizotomies of the C7 and C8 dorsal roots. Application of Y-27632 both attenuated cold hyperalgesia and induced monoaminergic plasticity after C7/8 rhizotomy. Thus, inhibition of Rho-pathway signaling both promoted the sprouting of intact supraspinal monoaminergic fibers and alleviated pain after dorsal rhizotomy.  (+info)

Tail-flick latency and self-mutilation following unilateral deafferentation in rats. (6/28)

Unilateral deafferentation induced by transection of the C(4)-C(8) dorsal roots of spinal cord, followed by a complex of abnormal self-mutilating behavior, is interpreted as an animal model of chronic nociception. The objective of our study was to test the differences in tail-flick latency between intact control and unilaterally deafferented animals and to assess the changes in their acute nociceptive sensation. The initial hypothesis was that deafferentation-induced painful sensation might cause stress-induced analgesia that should be manifested as prolonged tail-flick latency. The experiment was carried out on 11 male and 10 female adult Wistar rats. The tail-flick latency was repeatedly measured over a period of 10 consecutive weeks both in the preoperative baseline period and following multiple cervical dorsal rhizotomy. Contrary to our hypothesis, unilateral deafferentation was followed by a significant shortening of the tail-flick latency both in males and females. In deafferented animals, compared to the controls, variations of tail-flick latency were reduced. In individual animals after deafferentation, concurrent dynamic changes were observed in self-mutilating behavior, in a loss and regaining of body weight, and in tail-flick latency. Our data suggest that changes in tail-flick latency may be interpreted in terms of central sensitization and that tail-flick latency might be considered as a useful marker of chronic nociception.  (+info)

Microcoagulation of junctional dorsal root entry zone is effective treatment of brachial plexus avulsion pain: long-term follow-up study. (7/28)

AIM: To analyze long-term clinical results of coagulation lesions of the dorsal root entry zone (DREZ) in patients with deafferentation pain due to brachial plexus avulsion and to correlate the pain relief after DREZ coagulation with pain duration before the DREZ coagulation. METHODS: Twenty-six patients with intractable deafferentation pain after brachial plexus avulsion lesion were treated for pain at the Department of Neurosurgery. Junctional coagulation lesion was made with bipolar forceps along the DREZ. The patients assessed post-operative analgesic effect using a visual analog scale at 1 week, 1 year, 3 years, and 5 years after the surgery. RESULTS: The greatest pain relief was reported immediately after the DREZ procedure. Over the 5-year follow-up period, the pain relief effect gradually and significantly decreased. There were no significant differences between the pain relief evaluated at 1 week and after 1 year and between the pain relief evaluated at 1 week and after 3 years. There was a correlation between the pain duration before the surgery and pain relief after the surgery, with best correlation found between pain duration before surgery and pain relief 5 years after DREZ procedure (r = 0.623, P = 0.007). CONCLUSION: The long-term follow up showed that the pain relief gradually decreased over 5 years after surgery. However, the pain relief still did not significantly decrease after 3 years.  (+info)

Transcutaneous electrical nerve stimulation for the management of neuropathic pain: the effects of frequency and electrode position on prevention of allodynia in a rat model of complex regional pain syndrome type II. (8/28)

BACKGROUND AND PURPOSE: Complex regional pain syndrome type II (CPSII) is a painful condition that develops following a nerve injury. Although transcutaneous electrical nerve stimulation (TENS) relieves the pain of CPSII, the stimulation parameters that would best prevent the development of the condition are not known. The purpose of this study was to compare the ability of several different stimulation strategies to reduce the development of allodynia. SUBJECTS: Sprague-Dawley rats were used in the study. METHODS: A chronic constriction injury (CCI) to the right sciatic nerve was used to induce allodynia. Two groups of CCI rats received high-frequency TENS to the lumbar paravertebral region with electrodes positioned on the skin overlying either the right or left paraspinal musculature. Two additional groups of CCI rats received low-frequency TENS to acupuncture points in the right or left hind limbs. A fifth group of CCI rats received no TENS intervention. Thermal and mechanical pain thresholds were assessed in the right hind paw before and 12 days after the CCI surgery. The TENS was delivered 1 hour per day beginning on the day of surgery. RESULTS: Daily high-frequency TENS reduced the development of mechanical allodynia in CCI rats, and low-frequency TENS reduced the development of thermal allodynia, but only when TENS was delivered on the left side. DISCUSSION AND CONCLUSION: The results indicate that TENS delivered contralateral to a nerve injury best reduces allodynia development. Comprehensive reduction of allodynia development would require a combination of high- and low-frequency TENS intervention.  (+info)

Causalgia is a type of complex regional pain syndrome (CRPS) that occurs after a nerve injury. It is characterized by severe, persistent burning pain, sensitivity to touch, and changes in skin color, temperature, and swelling in the affected limb. These symptoms are often disproportionate to the severity of the initial injury.

Causalgia was originally described as a symptom of nerve injuries sustained during wartime, but it can also occur after trauma, surgery, or other types of nerve damage. The exact cause of causalgia is not fully understood, but it is thought to involve abnormalities in the nervous system's processing of pain signals.

Treatment for causalgia typically involves a combination of medications, physical therapy, and other therapies to manage pain and improve function. In some cases, more invasive treatments such as nerve blocks or spinal cord stimulation may be recommended.

Sympathectomy is a surgical procedure that involves interrupting the sympathetic nerve pathways. These nerves are part of the autonomic nervous system, which controls involuntary bodily functions such as heart rate, blood pressure, sweating, and digestion. The goal of sympathectomy is to manage conditions like hyperhidrosis (excessive sweating), Raynaud's phenomenon, and certain types of chronic pain.

There are different types of sympathectomy, including thoracic sympathectomy (which targets the sympathetic nerves in the chest), lumbar sympathectomy (which targets the sympathetic nerves in the lower back), and cervical sympathectomy (which targets the sympathetic nerves in the neck). The specific type of procedure depends on the location of the affected nerves and the condition being treated.

Sympathectomy is usually performed using minimally invasive techniques, such as endoscopic surgery, which involves making small incisions and using specialized instruments to access the nerves. While sympathectomy can be effective in managing certain conditions, it carries risks such as nerve damage, bleeding, infection, and chronic pain.

Reflex Sympathetic Dystrophy (RSD), also known as Complex Regional Pain Syndrome (CRPS), is a chronic pain condition that most often affects a limb after an injury or trauma. It is characterized by prolonged or excessive pain and sensitivity, along with changes in skin color, temperature, and swelling.

The symptoms of RSD/CRPS are thought to be caused by an overactive sympathetic nervous system, which controls involuntary bodily functions such as heart rate, blood pressure, and sweating. In RSD/CRPS, the sympathetic nerves are believed to send incorrect signals to the brain, causing it to perceive intense pain even in the absence of any actual tissue damage.

RSD/CRPS can be classified into two types: Type 1, which occurs after an injury or trauma that did not directly damage the nerves, and Type 2, which occurs after a distinct nerve injury. The symptoms of both types are similar, but Type 2 is typically more severe and may involve more widespread nerve damage.

Treatment for RSD/CRPS usually involves a combination of medications, physical therapy, and other therapies such as spinal cord stimulation or sympathetic nerve blocks. Early diagnosis and treatment can help improve outcomes and reduce the risk of long-term complications.

Neuralgia is a type of pain that occurs along the pathway of a nerve, often caused by damage or irritation to the nerve. It is typically described as a sharp, stabbing, burning, or electric-shock like pain that can be severe and debilitating. Neuralgia can affect any nerve in the body, but it most commonly occurs in the facial area (trigeminal neuralgia) or in the nerves related to the spine (postherpetic neuralgia). The pain associated with neuralgia can be intermittent or constant and may be worsened by certain triggers such as touch, temperature changes, or movement. Treatment for neuralgia typically involves medications to manage pain, as well as other therapies such as nerve blocks, surgery, or lifestyle modifications.

Causalgia syndrome. Causalgia syndrome is a pain syndrome caused by damage to the peripheral nerve and irritation of its ...
Causalgia or Complex Regional Pain Syndrome is a rare pain syndrome related to partial peripheral nerve injuries. Severe cases ... Do you have Causalgia Pain? Let your Causalgia Management Specialist Handle It. Request An Appointment Here Appointment Request ... Causalgia - Complex Regional Pain Syndrome. Although pain is characterized in many ways, some diagnoses are not so obvious. One ...
In 1959, Noordenbos observed in causalgia patients that "the damage of the nerve is always partial." Misuse of the terms, as ... Richards RL (January 1967). "The term causalgia". Medical History. 11 (1): 97-99. doi:10.1017/s0025727300011789. PMC 1033672 ... "causalgia". However, this term was actually coined by Mitchells friend Robley Dunglison from the Greek words for heat and for ... with causalgia and RSD as subtypes. The National Institute of Neurological Disorders and Stroke (NINDS), a part of the National ...
ClinicalTrials.gov: Causalgia (National Institutes of Health) * ClinicalTrials.gov: Complex Regional Pain Syndromes (National ...
CRPS; RSDS; Causalgia - RSD; Shoulder-hand syndrome; Reflex sympathetic dystrophy syndrome; Sudeck atrophy; Pain - CRPS ...
Genito-femoral causalgia. Can Med Assoc J. 1945. 53:213-6. *. Magee RK. Genito-femoral causalgia. Can Med Assoc J. 1942. 46:326 ...
Genito-femoral causalgia. Can Med Assoc J. 1945. 53:213-6. *. Magee RK. Genito-femoral causalgia. Can Med Assoc J. 1942. 46:326 ...
Genito-femoral causalgia. Can Med Assoc J. 1945. 53:213-6. *. Magee RK. Genito-femoral causalgia. Can Med Assoc J. 1942. 46:326 ...
SEE ALSO: causalgia. SYN: shoulder-hand syndrome, sympathetic reflex d.. Reis-Bücklers corneal d. an autosomal dominant ...
Genito-femoral causalgia. Can Med Assoc J. 1945. 53:213-6. *. Magee RK. Genito-femoral causalgia. Can Med Assoc J. 1942. 46:326 ...
Causalgia. JEWELL AH Jr. JEWELL AH Jr. Q Bull Northwest Univ Med Sch. 1949;23(4):458-64. Q Bull Northwest Univ Med Sch. 1949. ...
causalgia Causality, Causes, and Causal Inference Causality, Divine Causality, Primary and Secondary ...
Complex Regional Pain Syndrome (CRPS), Reflex Sympathetic Dystrophy (RSD), or causalgia. Contraindications ...
1979) Causalgia and other reflex sympathetic dystrophies. in Proceedings of the 2nd World Congress on Pain. Advances in pain ... 1999) Causalgia and reflex sympathetic dystrophy: does the sympathetic nervous system contribute to the generation of pain? ... Earlier this century, others noted that there were patients with a similar but less severe condition that resembled causalgia ... The French surgeon Leriche had already noted that the limbs of patients with causalgia showed features that he thought ...
Sympathetic reflex dystrophy and causalgia].. Baron R; Binder A; Ulrich W; Maier C. Schmerz; 2003 Jun; 17(3):213-26. PubMed ID ... Reflex sympathetic dystrophy and causalgia].. Baron R; Binder A; Ulrich W; Maier C. Nervenarzt; 2002 Apr; 73(4):305-18; quiz ... 3. Traumatic neuralgias: complex regional pain syndromes (reflex sympathetic dystrophy and causalgia): clinical characteristics ...
Usually occurring after nerve injury to a hand, foot, arm or leg, causalgia and RSD may be triggered by any minor injury, by a ... This was the first observation of the chronic constriction injury model: the rat with symptoms similar to causalgia or RSD. ... Bennett and Xie recognized the characteristic guarding action of a causalgia or RSD patient. Excitedly, they tested various non ... The classic neuropathic pain disorders are the agonizing conditions known as causalgia -- the most terrible of all tortures, ...
... and type II was known as causalgia. Both types occur most often in young adults and are 2 or 3 times more common among women. ...
... has been recognized since the Civil War when it was called causalgia, a name chosen to describe intense, burning extremity pain ... According to the IASP, CRPS II (also known as causalgia) is diagnosed as follows:. *. The presence of continuing pain, ...
Causalgia / drug therapy Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Mitchell coined the term causalgia, meaning burning pain. The most striking feature described by Mitchell was that the pain ... causalgia,complex regional pain syndrome Reflex sympathetic dystrophy - learn about the onset, symptoms and treatment options ...
Additionally, many patients report maddening pruritus and/or causalgia. Finally, some patients experience flexion contractures ...
CRPS; RSDS; Causalgia - RSD; Shoulder-hand syndrome; Reflex sympathetic dystrophy syndrome; Sudeck atrophy; Pain - CRPS. ...
Nervous System: Abnormal thinking, agitation, amnesia, anxiety, causalgia, circumoral paresthesia, confusion, depression, ...
This condition was previously known as reflex sympathetic dystrophy, Sudecks atrophy, shoulder-hand syndrome, or causalgia. ...
Causalgia is usually caused by brachial plexus injuries, involving nerves that run from the neck to the arm. The disruption of ... NB…Causalgia is a rare pain syndrome related to partial peripheral nerve injuries. The peripheral nervous system encompasses ...
" = "G56.4 Causalgia" "G568" = "G56.8 Other mononeuropathies of upper limb" "G569" = "G56.9 Mononeuropathy of upper limb, ...
CAUSALGIA Expand A syndrome of sustained burning pain, allodynia, and hyperpathia after a traumatic nerve lesion, often ... These were formerly labeled Reflex Sympathetic Dystrophy and Causalgia, and the discussion of Sympathetically Maintained Pain ...
... causalgia, or intractable angina.1 An SCG block can also be performed to treat patients with vasospasm (eg, primary or ...
Many names have been used to describe this syndrome such as; Reflex Sympathetic Dystrophy, causalgia, algodystrophy, Sudecks ...
  • Causalgia is technically known as complex regional pain syndrome type II (CRPS II). (carolinapainscrambler.com)
  • Two types exist: CRPS Type 1, previously referred to as Reflex Sympathetic Dystrophy, and CRPS Type 2, previously referred to as causalgia. (wikipedia.org)
  • CRPS is also known as reflex sympathetic dystrophy or causalgia. (medtronic.com)
  • CRPS type I was previously known as reflex sympathetic dystrophy (see also Complex Regional Pain Syndrome: Treatment Guidelines ), and type II was known as causalgia. (msdmanuals.com)
  • CRPS II (caused by damage to a nerve) was previously called causalgia . (eorthopod.com)
  • CRPS er en kompleks, smertefuld, invaliderende og i mange tilfælde kronisk sygdom, der primært afficerer ekstremiteterne. (ugeskriftet.dk)
  • CRPS debuterer oftest i forbindelse med en operation eller et fysisk traume. (ugeskriftet.dk)
  • CRPS er en klinisk diagnose, der kan understøttes af parakliniske undersøgelser som måling af hudtemperatur og anvendelse af knoglescintigrafi [14]. (ugeskriftet.dk)
  • Der er ikke udarbejdet en dansk guideline eller en national klinisk retningslinje for udredning og behandling af CRPS. (ugeskriftet.dk)
  • Proclaim TM DRG Neurostimulation System, which targets the dorsal root ganglion nerves near the spinal cord, to relieve pain of the lower limbs due to complex regional pain syndrome (CRPS) and nerve damage called causalgia. (abbott.com)
  • This injection is typically ordered by your doctor for pain located in the head, neck, chest or arm caused by sympathetically maintained pain (reflex sympathetic dystrophy), causalgia (nerve injury), herpes zoster (shingles), or intractable angina (pain related to decreased blood flow to the heart). (umms.org)
  • Causalgia is an intense burning pain accompanied by local vasomotor, trophic, and motor disorders. (medic-journal.com)
  • Mitchell referred to the cluster of symptoms he noticed in some of the Civil War soldiers who were under his care as 'causalgia. (psychiatrictimes.com)

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