The Painful Sequeæ of Injuries to Peripheral Nerves

Sunderlannd, S.; Kelly, Michael

doi:10.1111/j.1445-2197.1948.tb06343.x

Cited by 24 publications

(6 citation statements)

References 80 publications

(1 reference statement)

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“…The allodynia and hyperpathia of causalgia cannot be explained solely on the basis of ephaptic or ectopic transmission at the site of nerve injury (Nystrom and Hagbarth, 1981). Also the pain of causalgia may not be abolished by deafferentation and may persist even in an anaesthetized limb (Appenzeller and Bicknell, 1969;Sunderland, 1978;Noordenbos and Wall, 1981). This implies that an intact peripheral sensory nerve supply is not essential for some types of persistent causalgic pain.…”

Section: Discussionmentioning

confidence: 99%

The causalgia—dystonia syndrome

Bhatia

Bhatt

Marsden

1993

Brain

197

121

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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.

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Section: Discussionmentioning

confidence: 99%

The causalgia—dystonia syndrome

Bhatia

Bhatt

Marsden

1993

Brain

197

121

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“…Of importance to understanding the incidence of causalgia are data from Sunderland and Kelly,8 and Nathan,9 also from World War II, who described an incidence of 12.0% and 13.8% respectively out of a total 442 nerve injury cases involving primarily median and sciatic nerves. These are almost 2 to 3 times the incidence of causalgia reported by other observers but may reflect the higher proportion of sympathetic fibers in these 2 nerves.…”

Section: A Prologuementioning

confidence: 99%

CRPS: what’s in a name? Taxonomy, epidemiology, neurologic, immune and autoimmune considerations

Stanton‐Hicks

2019

Reg Anesth Pain Med

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This account of the condition now termed complex regional pain syndrome (CRPS) spans approximately 462 years since a description embodying similar clinical features was described by Ambroise Paré in 1557. While reviewing its historical origins, the text describes why it became necessary to change the taxonomies of two clinical syndromes with similar pathophysiologies to one which acknowledges this aspect but does not introduce any mechanistic overtones. Discussed at length is the role of the sympathetic component of the autonomic nervous system (ANS) and why its dysfunction has both directly and indirectly influenced our understanding of the inflammatory aspects of CRPS. As the following article will show, our knowledge has expanded in an exponential fashion to include musculoskeletal, immune, autoimmune, central and peripheral nervous system and ANS dysfunction, all of which increase the complexity of its clinical management. A burgeoning literature is beginning to shed light on the mechanistic aspects of these syndromes and the increasing evidence of a genetic influence on such factors as autoimmunity, and its importance is also discussed at length. An important aspect that has been missing from the diagnostic criteria is a measure of disease severity. The recent validation of a CRPS Severity Score is also included.

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“…Sunderland, alone, 20 and with Kelly, 21 tried to describe the missing pathological basis for Livingston's theory and proposed the 'turbulence hypothesis'. After damage to a peripheral nerve, the distal portion degenerates completely, while the proximal portion may undergo retrograde changes that can affect the structure and function of parent cell bodies.…”

Section: Hypotheses On the Mechanisms Underlying Crpsmentioning

confidence: 99%

Complex regional pain syndrome type I

Kemler¹

2001

Pain Reviews

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Complex regional pain syndrome type I (CRPS) is a painful and disabling syndrome of unknown pathophysiology that may occur spontaneously or after trauma or surgery to a limb. Over the last two decades, the theories about the cause and treatment of CRPS have been based increasingly on evidence from controlled trials instead of being in uenced by anecdotal case reports.The literature on CRPS was reviewed. With regard to treatment, the review was based on controlled studies reported during the period 1979-1999. At present, there is still only limited understanding of the pathophysiology of CRPS. However, the key to its causes is likely to be that, in certain individuals, peripheral nerve injury leads to the development of maladaptive compensatory changes in both the peripheral and central nervous systems. Recent studies have indicated that speci c human leucocyte antigen alleles are associated with CRPS, suggesting that certain individuals may be at risk of its development. On the other hand, the incidence of CRPS after trauma can be reduced by supplementation with vitamin C. Treatment is based on physiotherapy together with medication that reduces neuropathic pain. Blocking the sympathetic nervous system is ineffective in most patients. In chronic cases, electrical stimulation of the nervous system (transcutaneous or direct stimulation of peripheral nerves or the spinal cord) effectively reduces pain in more than half of those patients in whom alternative therapies have failed.There has at last been some progress in our understanding of the pathophysiology and treatment of CRPS. Currently, however, prevention (vitamin C after trauma) still seems the best option.

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The Painful Sequeæ of Injuries to Peripheral Nerves

Cited by 24 publications

References 80 publications

The causalgia—dystonia syndrome

The causalgia—dystonia syndrome

CRPS: what’s in a name? Taxonomy, epidemiology, neurologic, immune and autoimmune considerations

Complex regional pain syndrome type I

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