Complex regional pain syndrome (CRPS) is the current consensus-derived name for a syndrome usually triggered by limb trauma. Required elements include prolonged, disproportionate distal-limb pain and microvascular dysregulation (e.g., edema or color changes) or altered sweating. CRPS-II (formerly "causalgia") describes patients with identified nerve injuries. CRPS-I (formerly "reflex sympathetic dystrophy") describes most patients who lack evidence of specific nerve injuries. Diagnosis is clinical and the pathophysiology involves combinations of small-fiber axonopathy, microvasculopathy, inflammation, and brain plasticity/sensitization. Females have much higher risk and workplace accidents are a well-recognized cause. Inflammation and dysimmunity, perhaps facilitated by injury to the blood-nerve barrier, may contribute. Most patients, particularly the young, recover gradually, but treatment can speed healing. Evidence of efficacy is strongest for rehabilitation therapies (e.g., graded-motor imagery), neuropathic pain medications, and electric stimulation of the spinal cord, injured nerve, or motor cortex. Investigational treatments include ketamine, botulinum toxin, immunoglobulins, and transcranial neuromodulation. Nonrecovering patients should be re-evaluated for neurosurgically treatable causal lesions (nerve entrapment, impingement, infections, or tumors) and treatable potentiating medical conditions, including polyneuropathy and circulatory insufficiency. Earlier impressions that CRPS represents malingering or psychosomatic illness have been replaced by evidence that CRPS is a rare complication of limb injury in biologically susceptible individuals.

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Internal Medicine HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Internal Medicine journal

Department of Neurology, Massachusetts General Hospital, Boston, MA 02114, USA. Tel.: +1 617 724 3992; fax: +1 617 726 6991. E-mail: [email protected]

Neuropathic pain is initiated or caused by damage or dysfunction of the peripheral or central nervous systems in various disorders, each having pain-related symptoms and signs thought secondary to common pain mechanisms. Ancillary testing may demonstrate associated nervous system abnormalities, however its specificity is inadequate at present, as it makes inferential conclusions from indirect data. Symptom assessment and physical findings remain paramount in the diagnosis of neuropathic pain.

In this double-blind, placebo-controlled trial, researchers administered botulinum toxin type A (Botox) to patients with chronic regional neuropathic

Purpose of review Recent dramatic increases in the incidence and prevalence of diabetes make an understanding of chronic symmetric sensorimotor diabetic polyneuropathy, the most common and problematic of chronic diabetic complications, essential for a wide range of medical practitioners. Recent findings The demonstration of neuropathic dysfunction in patients with prediabetes or impaired glucose tolerance emphasizes the susceptibility of peripheral nerve fibers, especially small A delta fibers and C fibers, to relatively mild, short-duration hyperglycemia. New testing can reveal peripheral nerve dysfunction prior to clinical neuropathic symptoms and signs. In the absence of effective medications to halt or reverse nerve damage or promote nerve regeneration, early diagnosis of diabetic polyneuropathy, followed by tight glycemic control with diet and exercise, offers the best opportunity to prevent progressive symptoms of sensory loss, pain, autonomic dysfunction, ulcerations, and amputations. Some patients with impaired glucose tolerance have a reversal of neuropathic features with tight glycemic control. Nonpharmacologic therapies for neuropathic pain in diabetic polyneuropathy appear promising. Summary Tight glycemic control, especially early in diabetes, is the best approach to minimizing the prevalence and severity of diabetic polyneuropathy and makes research into the deleterious effects of even mild hyperglycemia imperative.

Most neuropathic pain conditions are caused by damage to peripheral nociceptive neurons known as “small-fibers.” Examination of punch skin biopsies immunolabeled with pan-axonal markers has identified degeneration of distal nociceptive axons as a pathological hallmark of most neuralgias including numerous polyneuropathies, postherpetic neuralgia, and complex regional pain syndrome. Similar axonopathy is present in several rodent models of neuralgia (chronic constriction injury and spared nerve injury). Here we have measured the density of distal cutaneous small-fiber axons in rats with persistent mechanical allodynia caused by the sciatic inflammatory neuropathy (SIN), a model of painful neuritis. We have evaluated whether perineural immune activation sufficient to cause evoked-pain behaviors is also associated with loss of distal epidermal innervation.SIN was created in adult male Sprague-Dawley rats by perineural zymosan administration using established methods. Unoperated rats provided controls. Two weeks of sensory testing established the presence of static mechanical allodynia. Full-thickness punches were then collected from ipsilesional sural-innervated plantar hindpaw skin. These were immunolabeled against PGP9.5 using standard methods, and the density of epidermal neurites quantitated microscopically by a single examiner who was unaware of rats' experimental group. Neurite densities were similar in SIN and control samples (P = 0.96), suggesting that mechanical allodynia can occur from inflammation near a nerve, without distal small-fiber degeneration.

(2005). Venipuncture-Induced Nerve Injury. Journal of Neuropathic Pain & Symptom Palliation: Vol. 1, No. 1, pp. 109-114.

Muscle & NerveVolume 31, Issue 4 p. 415-417 Editorial What happens when cutaneous nerves are injured during venipuncture? Steven H. Horowitz MD, Corresponding Author Steven H. Horowitz MD [email protected] Nerve Injury Unit, Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USANerve Injury Unit, Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USASearch for more papers by this author Steven H. Horowitz MD, Corresponding Author Steven H. Horowitz MD [email protected] Nerve Injury Unit, Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USANerve Injury Unit, Department of Neurology, Massachusetts General Hospital, 55 Fruit Street, Boston, Massachusetts 02114, USASearch for more papers by this author First published: 09 February 2005 https://doi.org/10.1002/mus.20287Citations: 9Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article.Citing Literature Volume31, Issue4April 2005Pages 415-417 RelatedInformation

Inferior alveolar nerve blockade is one of the most common, yet technically difficult local procedures performed. Inadvertent injury to the inferior alveolar or lingual nerve, resulting in persistent anesthesia, paresthesias, loss of taste, or pain in the distribution of these nerves, is more common than once thought. We report on two cases of lingual nerve injury during routine inferior alveolar nerve blockade. These cases are consistent with the hypotheses that direct nerve trauma, whether by nerve-needle contact or compression by anesthetic bolus, and the neurotoxic effects of specific anesthetic preparations may produce long term nerve damage. When this damage occurs to the pain-sensing A-delta and C-fibers, symptoms may resemble those seen in complex regional pain syndrome.

Hereditary neuropathy with liability to pressure palsy (HNPP) is characterised by recurrent mononeuropathies following minor trauma. We describe a case of fulminant HNPP beginning on the first day of military physical training. Protracted weakness, muscle atrophy, hand contractures, and multifocal sensory loss developed during a further three weeks of basic training. Nerve conduction changes were typical of HNPP, but without segmental slowing. Electromyographically, there was prominent acute denervation in muscles of the hands and right shoulder. Sural nerve biopsy demonstrated tomaculae and remyelination. Genetic testing revealed PMP-22 gene deletion. This case report demonstrates that HNPP can present with rapidly progressive peripheral nerve dysfunction and electrophysiological evidence of focal axonal loss.

Muscle & NerveVolume 30, Issue 2 p. 247-247 Book Review Textbook of diabetic neuropathy, edited by F.A. Gries, N.E. Cameron, P.A. Low, and D. Ziegler, 394 pp., ill., Stuttgart, Thieme, 2003 Steven H. Horowitz MD, Steven H. Horowitz MDSearch for more papers by this author Steven H. Horowitz MD, Steven H. Horowitz MDSearch for more papers by this author First published: 14 June 2004 https://doi.org/10.1002/mus.20061Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume30, Issue2August 2004Pages 247-247 RelatedInformation