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At least 19 recordsLinked to original sources
PubMed2005

Surgical relief of causalgia with an artificial nerve guide tube: Successful surgical treatment of causalgia (Complex Regional Pain Syndrome Type II) by in situ tissue engineering with a polyglycolic acid-collagen tube.

Two patients with causalgia associated with allodynia and finger contracture were treated surgically with a bioresorbable nerve guide tube made from polygycolic acid and collagen: the injured segment of the digital nerve was resected and the resulting gap (25 and 36mm) was bridged with the tube. In both cases, a neuroma was found on the injured nerve and many sprouting branches were. After reconstruction, the causalgia and allodynia disappeared and movement of the fingers recovered during the following 6 months. Functional recovery was objectively identified for 1 year and 9 months. Both patients regained full use of their finger and were free of discomfort for up to 24 and 18 months, respectively. Since the first description of causalgia in 1864, there has been no definitive treatment for this intractable burning pain. Our experience shows that at least some types of causalgia can be resolved successfully by surgery.

Adult↗
PubMed1989

An unusual case of causalgia. Relevance to recent hypothesis on mechanism of causalgia.

Intravenous regional sympathetic block with guanethidine caused only limited improvement in a patient with longstanding causalgia. Lumbar sympathetic block with phenol also had little direct effect on the pain but completely abolished associated allodynia and vasomotor signs. Following sympathectomy the response to subsequent guanethidine blocks was enhanced. This improvement persisted even after 8 months when there was some return of the previous allodynia and vasomotor signs (to involve a smaller area than previously). The case would appear to have implications for a recently proposed hypothesis concerning the mechanism of pain in causalgia.

Autonomic Nerve Block↗
PubMed1986

Mechanisms of causalgia and related clinical conditions. The role of the central and of the sympathetic nervous systems.

The definition of causalgia as a pain state following peripheral nerve injury has been accepted since the term was introduced by Weir Mitchell over a century ago. In the present paper, problems of nomenclature and nosology are discussed, and attention is drawn to the fact that the same clinical features can occur spontaneously, in nontraumatic nerve lesions, in the absence of a part as in phantom limb states, and in diseases confined to the central nervous system. Attention is also drawn to the lack of correlation of pain with the effects mediated by catecholamines in the sympathetic nervous system and with the response to sympathetic blockade. Concerning mechanisms, a number of peripheral mechanisms have been postulated. These are reviewed, and while they might be correct when causalgia arises from peripheral nerve damage, they cannot provide adequate explanation for at least some instances of causalgia. The relevance of the neuroma as a model for chronic pain in general, and causalgia, is questioned. Also questioned is the view that causalgia is a state that depends on peripheral involvement of the sympathetic nerve supply. Certain authors in the past considered that the central nervous system (CNS) played an important part in causalgia, and current evidence supporting this view is assessed. Involvement of the CNS is suggested by the development of causalgia in diseases confined to the CNS and in phantom pain states; the unusual distribution of pain sometimes experienced; the paradoxical development of widespread pain that can occur after damage to the sympathetic nervous system; the effects of peripheral sympathetic blockade even when the cause lies centrally; and central interactions with motor, sensory and psychological phenomena. Reservations concerning the role of catecholamines in causalgia are outlined, and the possibility is considered that nonadrenergic substances may be implicated.

Adult↗
PubMed2003

Causalgia: a meta-analysis of the literature.

BACKGROUND: Causalgia is not familiar to most physicians whose training and experience are limited to civilian practice. HYPOTHESIS: Through a thorough review of the literature, we attempted to determine the boundaries of causalgia and separate it from other sympathetically related disorders. DATA SOURCES: Database search for English-language articles in MEDLINE and Index Medicus up to the year 2000 as both keyword and subject under causalgia. STUDY SELECTION: References that described any new cases referred to as "causalgia" by their authors were included in a meta-analysis. DATA SYNTHESIS: One hundred ten articles contained a total of 1528 cases of causalgia. High-velocity missiles caused at least 77% of the injuries. In 72% and 90% of the cases reported, the time from injury to onset of pain was within 1 week and 1 month, respectively. Median nerve alone or in combination with other nerves (56%) and sciatic trunk injury (60%) were the most common nerves involved. In 92%, the nerve injury was incomplete. The most prominent clinical manifestations included burning pain in 86%, increased sweating in 73%, relief with application of cold in 62%, warmth in 50%, paresthesias in 96%, absence of anesthesia in 81%, and sensitivity to stimuli in 98%. Response to sympathetic blocks was observed in 88%. Finally, a total of 94% of the patients undergoing sympathectomy were cured. CONCLUSIONS: Cases of causalgia are easy to recognize and treat, with excellent results. Causalgia always follows a somatic nerve injury, usually partial, and is associated with near-constant, very severe pain distal to the injury in the extremity, varied in nature but characteristically with a predominantly burning quality. An effective anesthetic block of the appropriate part of the sympathetic chain frequently immediately relieves the pain. Most cases are cured by surgical sympathectomy.

Causalgia↗
PubMed2000

Sympathectomy for causalgia: experience with military injuries.

BACKGROUND: Causalgia is a rare disease in civilian practice, and most reports regarding causalgia in the literature are from major extended wars. To increase awareness of this syndrome, our wartime experience with this disease is presented. METHODS: The charts of patients with causalgia referred to two university hospitals for treatment from 1985 to 1989 were retrospectively studied. Characteristics of the cause, clinical manifestations, and the response to therapy were evaluated. RESULTS: Among 1,564 patients with peripheral nerve injuries, there were 54 cases (3.4%) of causalgia. All of the patients, except five, were injured in battle by high-velocity bullets or missiles. Upper extremities were involved in 28 patients (52 %) and lower extremities in 26 patients (48%). The most common presenting symptoms were as follows: burning pain, 100%; wet extremity, 100%; cold extremity, 93%; sensitivity to cold, 89%; paresthesia, 78%; and color changes in the extremities, 55%. In 48 patients (89%), pain was relieved by sympathetic block (3 patients had permanent cure). Six patients had no response to the blocks (11%). Of 45 patients who had temporary relief, all underwent sympathectomy. All of these patients had complete relief of symptoms in the immediate postoperative period and for follow-up from 1 to 6 years. CONCLUSION: Causalgia is essentially a war casualty disease. The condition is associated with burning pain, hyperesthesia, and symptoms of sympathetic overactivity. Sympathectomy is effective and the treatment of choice, particularly for patients who respond temporarily to sympathetic blocks.

Adolescent↗
PubMed1988

[Postoperative treatment of phantom pain and causalgias with calcitonin].

Results of IV calcitonin treatment in patients suffering from postoperative phantom limb pain (n = 12) or causalgia following peripheral nerve lesions (n = 4) are reported. All patients were complained of severe pain after a traumatic event or amputation, with disturbed sleep in many cases. After only 1-2 infusions 10 patients with phantom limb pain (83%) were discharged from hospital pain-free. Pain was effectively reduced by up to 5 infusions in 2 patients (17%). A follow-up for maximally 24 months showed a recurrence of pain in only 4 patients with obvious stump problems or reamputations. Three patients with causalgia also profited from a remarkable but transitory pain reduction; in 1 patient therapy was ineffective. Recurrent pain due to causalgia could not be improved by repeated calcitonin infusion, although this was effective for phantom limb pain. The administration of calcitonin IV can be recommended as a valuable treatment for phantom limb pain and causalgias in the early postoperative period. Therapy was effective with negligible side-effects, and long-term follow-up revealed a long-lasting effect.

Arm↗
PubMed1984

Iatrogenic causalgia. Classification, clinical findings, and legal ramifications.

Eleven patients had causalgia that resulted from surgical procedures or improperly placed injections. It is the intense, unremitting, burning quality of the pain that distinguishes causalgia from other nerve injury sequelae. The mode of injury, as well as the symptoms and signs and their duration, suggests that the recent tendency to divide causalgia into "major" and "minor" forms on the basis of its occurrence during war or peace, with or without autonomic dysfunction, is improper. Most of these patients have sought legal redress. All cases for which the legal issues are complete have been settled in favor of the plaintiffs.

Adult↗
PubMed1999

Causalgia and reflex sympathetic dystrophy: does the sympathetic nervous system contribute to the generation of pain?

The striking response of causalgia and reflex sympathetic dystrophy (RSD) to sympatholytic procedures together with signs of autonomic nervous system abnormalities suggest that the sympathetic efferent system can generate or enhance pain (sympathetically maintained pain, SMP). This concept is supported by human and animal experiments indicating that sympathetic activity and catecholamines can activate primary afferent nociceptors. Some clinical evidence, however, calls the SMP concept into question and alternative explanations have been advanced. In this review, we describe the clinical features of causalgia and RSD and the evidence for sympatholytic efficacy. The major barrier to proving the SMP concept is that all available sympatholytic procedures are problematic. We conclude that, although the weight of current evidence supports the SMP concept and its relevance to causalgia and RSD, it remains unproven by scientific criteria. More careful adherence to diagnostic criteria and well-controlled trials of sympatholysis are needed to finally settle the issue.

Animals↗
PubMed1990

Comparison of sympathetic neurons in orofacial and upper extremity nerves: implications for causalgia.

This study compared nerves of the orofacial region with nerves frequently associated with causalgia to determine if there is a significant difference in the proportion of sympathetic neurons within these nerves, which may account for the lower incidence of orofacial causalgia. Three orofacial and two upper extremity nerves were examined. Each nerve was transected and labeled with horseradish peroxidase to identify the cell bodies of neurons contributing axons to the nerve. The study included two trials per nerve, for a total of 10 trials in eight cats. The trigeminal and dorsal root ganglia, containing sensory neurons (SN), and the stellate, middle, and superior cervical ganglia, containing postganglionic sympathetic neurons (PGSN), were sectioned and reacted with tetramethyl benzidine to visualize the labeled neurons. The total number of labeled PGSN and SN were counted and the ratio (PGSN:SN) determined for each of the five nerves. The average PGSN:SN ratio from upper extremity nerves (0.40) is 2 1/2 times greater than the ratio determined for branches of the trigeminal nerve (0.16). The lower proportion of sympathetic neurons within the trigeminal nerves provides an anatomic explanation for the lower incidence of orofacial causalgia consistent with the currently accepted etiology.

Animals↗
PubMed1981

Causalgia: redefinition as a clinical pain syndrome.

In this report, the following criteria were used for the diagnosis of causalgia: (a) the presence of continuous, burning pain distal to a site of injury; (b) hyperalgesia and allodynia in the painful area; and (c) a traumatic event occurring proximal in the painful area and within weeks prior to the onset of pain. The McGill pain questionnaire was used to test the selected pain population for homogeneity. The scores were similar among the patients and different from the scores in other pain syndromes. It is concluded that the above criteria are sufficient to make the diagnosis of causalgia. In addition, it appears that a central nervous system abnormality best accounts for the clinical features of causalgia.

Adult↗
PubMed1984

Abnormal and collateral innervations of sympathetic and peripheral sensory fields associated with a case of causalgia.

A 41-year-old female developed spontaneous burning pain (causalgia) and stimulus-induced dysesthesia (allodynia) of the dorso-lateral part of her right foot following trauma. An L3 and L4 sympathectomy eliminated the spontaneous burning pain for only 1 year, but did not affect the stimulus-induced dysesthesia. We evaluated her two years post-sympathectomy with grouped sequential anesthetic blocks and sensory testing. Sympathetic blocks at L1 and L2 eliminated the burning pain and normalized heat perception from baseline hyperalgesia, indicating that the causalgia had been reactivated via more rostral sympathetic ganglia. Anesthetic block of the sural nerve eliminated both the burning pain and the stimulus-induced dysesthesia. During the sural nerve block, perception of touch and pin, but not heat, was preserved in the sural distribution. All perception was lost following subsequent block of the peroneal branches. When the peroneals were blocked first, perception of touch, pin and heat remained in the sural distribution. With peroneal block the burning pain was eliminated, but the stimulus-induced dysesthesia remained, even in the anesthetic peroneal territory. When sural block was added to the peroneal block the stimulus-induced dysesthesia was eliminated, and sensation in the sural distribution was lost. We conclude that the sural distribution received overalapping innervation for touch and pin-prick perception, but that heat perception, burning pain and the stimulus-induced dysesthesia were sural nerve dependent. Further, we were able to dissociate causalgia pain from allodynia in this patient.

Adult↗
PubMed1996

Lumbar sympathectomy for causalgia secondary to lumbar laminectomy.

BACKGROUND: This study reviews 12 patients (15 limbs) who underwent lumbar sympathectomies (LS) (after a series of chemical sympathetic blocks) for causalgia following a lumbar laminectomy (LL). To our knowledge, using LS to treat causalgia after LL has only been reported once before in the English literature. PATIENTS AND METHODS: Patients were classified (Drucker) as Stage I, II, or III. Sympathetic block results were graded as excellent, fair, or poor. Early and late responses to LS were classified as complete relief, partial relief (patient satisfied or unsatisfied), or no relief. RESULTS: The mean duration between LL and the first sympathetic block was 8.4 months, with a mean of 9.5 months to LS. There were no operative deaths; however, 13% of limbs (2/15) had transient postoperative sympathetic neuralgia. Eighty percent (12 limbs) had an early satisfactory outcome after LS, and 73% (11 limbs) had a late satisfactory outcome. Stage II patients were more likely to have satisfactory early and late outcomes (92% and 85%) than Stage III patients (0%, P<0.01). Limbs with an excellent response to sympathetic block were more likely to have satisfactory early and late surgical outcomes (11/11, 100%). The time among LL and sympathetic block and L was shorter in patients who had satisfactory early and late surgical outcomes (P<0.0001). A multivariate analysis demonstrated that the most important independent factor in determining early and late outcomes of sympathectomy was the time between LL and LS (P=0.01). CONCLUSIONS: LS for causalgia following LL should be confined to Stage II patients who have had an excellent response to sympathetic block.

Adult↗
PubMed1995

Capsaicin and the cause of causalgia.

From self-experimentation, I propose that the pain which occurs after application of capsaicin is causalgia and that this "capsaicin causalgia" is due to actual or functional depletion of neuropeptides such as substance P. This idea could provide an objective definition of the causalgic syndromes and improve the means of diagnosis. The analogy with capsaicin causalgia could also be extended to the pain of epidermal necrolysis, solar and thermal burns, and leprosy. The concept could lead to a better treatment of these causalgic syndromes by modulation of neuropeptide concentration or responsivity, or by mitigation of the consequences of its depletion.

Capsaicin↗
PubMed1993

The causalgia-dystonia syndrome.

We report 18 patients (16 women and two men) with causalgia and dystonia, triggered by peripheral injuries in 15 cases and occurring spontaneously in three. The injury was often trivial, and did not cause overt peripheral nerve lesions. The mean age at presentation was 28.5 years. None had a family history of dystonia. The leg was affected initially in 12 patients, the arm in the remaining six cases. All had burning pain, allodynia and hyperpathia, along with vasomotor, sudomotor and trophic changes. All developed dystonic muscle spasms in the affected part. Dystonia always appeared at the same time or after the causalgia. The spasms were typically sustained, producing a 'fixed' dystonic posture, in contrast to the mobile spasms characteristics of idiopathic torsion dystonia. There was spread of the causalgia and of the dystonia from its initial site both in the affected limb and to other extremities, the latter in hemiplegic, transverse and triplegic distribution. All investigations were normal. All modes of conventional treatment failed to relieve either the pain or the dystonia, but two patients recovered spontaneously. At present it is impossible to decide whether this distressing syndrome is a true functional disorder of the central nervous system, or is of psychogenic origin.

Adolescent↗
PubMed1990

T2-ganglionectomy via limited costotransversectomy for minor causalgia.

T2-ganglionectomy via limited costotransversectomy is a safe and effective method to produce sympathetic denervation of the upper extremity. It provides prompt and lasting relief of the complex array of symptoms associated with minor causalgia. Four patients with minor causalgia treated by this procedure are presented. All patients were seen by multiple physicians before a correct diagnosis was made. Pain and trophic changes resolved in all cases. No instances of Horner's syndrome or pneumothorax were encountered. Preoperative response to temporary stellate ganglion block is essential to both diagnosis and treatment. Consideration of early surgical intervention should be given in cases involving significant disability. A fundamental problem surrounding the appropriate management of minor causalgia has been and continues to be accurate recognition of the diagnosis.

Adult↗
PubMed1976

Pain mechanisma in causalgia.

A study of the clinical features of causalgia and the central neuronal effects of injuries to peripheral nerves suggests that causalgia is the functional expression of the intensity of the retrograde neuronal reaction in which pools of dorsal horn neurones become converted into foci of abnormal activity. These foci initiate a chain reaction along transmission pathways as far centrally as the cortex, causalgia being the terminal effect of this disorderly activity on the sensorium. This is the basis of the 'turbulance hypothesis' introduced to account for the pain.

Causalgia↗