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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cause of the neuropathic pain that is experienced by some patients with diabetic neuropathy remains to be established. Early neuropathological reports, based on comparisons between diabetic patients and non-diabetic control subjects, emphasised associations between pathological changes in specific classes of peripheral nerve fibre and the presence of pain. By making comparisons with more appropriate control subjects, namely diabetic patients without neuropathic pain, more recent studies have found that there are few clear morphological correlates for this type of pain. To investigate this further, we have conducted a detailed morphometric study of sural nerve biopsies from six diabetic patients, four with active acute painful neuropathy and two with recent remission from the same condition. Normal values for the neuropathological parameters were obtained from six non-diabetic control subjects. Teased fibre analysis showed that similar axonal and Schwann cell abnormalities were present in both groups of diabetic patients. Electron microscopical studies revealed that evidence of both myelinated and unmyelinated fibre degeneration and regeneration was also present in the nerves of all diabetic patients, irrespective of whether they had pain. Within the constraints of interpreting results from small numbers of patients, our observations suggested that remission from pain might be associated with a less abnormal axon/Schwann cell calibre ratio, more successful myelinated fibre regeneration and less active unmyelinated fibre regeneration. However, the inescapable finding of this study was, in fact, the similarity in the nerve fibre pathology in diabetic patients with active and remitting painful neuropathy. We conclude that the occurrence of nerve fibre degeneration and regeneration is in itself unlikely to be sufficient to account fully for diabetic neuropathic pain. However, it is conceivable that events occurring during certain stages in the pathological cycle of degeneration and regeneration create the necessary circumstances which lead to pain.
Pain 1992 Mar
PMID:Acute and remitting painful diabetic polyneuropathy: a comparison of peripheral nerve fibre pathology. 159 58

The syndromes of painful diabetic neuropathy and painless foot ulceration are distinct clinical entities. To investigate whether there is a pattern of nerve fibre involvement that could clearly discriminate between them, we have studied three groups of diabetic patients, 19 with painful neuropathy, 14 with painless foot ulceration, and 19 with no clinical neuropathy. Large somatic nerve fibre function was assessed by nerve conduction studies and vibration thresholds, small somatic nerve function by cooling and warming thresholds, the parasympathetic system by heart-rate dependent cardiac autonomic reflexes, and the sympathetic system by postural drop in blood pressure and plasma noradrenaline (supine and erect). Normal ranges were obtained from 25 age-matched healthy subjects. Painful neuropathy was characterized by uniform dysfunction of small somatic fibres and preserved sympathetic nerve activity (plasma noradrenaline) with a wide range of large somatic fibre and autonomic reflex abnormalities. By contrast, in painless foot ulceration there was universal severe dysfunction of all nerve fibre populations. Discriminant analysis identified peroneal motor conduction velocity as the best single variable for distinguishing between painful and painless neuropathy (81% of cases). A combination of peroneal motor conduction velocity with vibration threshold and plasma noradrenaline discriminated completely between the two clinical syndromes. These findings suggest that the key differences between painful and painless diabetic neuropathy are in large somatic and sympathetic fibre function.
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PMID:Discrimination between painful and painless diabetic neuropathy based on testing of large somatic nerve and sympathetic nerve function. 160 Jul 8

In a phase I trial, 12 patients with GD2 antigen-positive metastatic melanoma received the murine anti-GD2 monoclonal antibody 14G2a. The monoclonal antibody was administered in four doses over an 8-day period with total dose ranging from 10 to 120 mg. All patients receiving greater than 10 mg of 14G2a experienced transient abdominal/pelvic pain during the antibody infusion. Five patients had a delayed extremity pain syndrome following the third and fourth antibody infusion. Four of the five patients developed neurological toxicity, including two patients with significant although reversible motor neuropathy. Two of the patients developed hyponatremia secondary to a syndrome of inappropriate antidiuretic hormone. All 12 patients developed high levels of human anti-14G2a antibody. The plasma half-life of 14G2a was 42 +/- 6 (SD) h. One patient each had a partial response, mixed response, and stable disease, respectively. The very modest antitumor activity accompanied by dose-limiting neurological toxicity at total doses greater than 80 mg may restrict the clinical utility of murine 14G2a.
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PMID:Phase I trial of the murine monoclonal anti-GD2 antibody 14G2a in metastatic melanoma. 164 31

Two cases are reported in which patients presented with complaints of foot pain, and a clinical suspicion of radiculopathy was supported by current perception threshold testing. Chiropractic manipulation of the lumbar spine resulted in alleviation of the lower extremity symptoms. Current perception threshold testing is a valuable neurologic testing modality that is noninvasive, nonaversive, and highly reliable for evaluation of sensory nerves where neuropathy is suspected. This technology has been described for evaluation of diabetic neuropathy, uremic screening, and alcohol and chemical toxicity. Additionally, current perception threshold is useful for evaluation of other neuropathies, such as carpal tunnel syndrome and other entrapment neuropathies. The authors encourage further investigation of this modality in the diagnosis and evaluation of peripheral neuropathy and unexplained foot pain secondary to spinal nerve impingement.
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PMID:Current perception threshold in evaluating foot pain. Two case presentations. 164 17

1. Neurogenic inflammation, mediated by nociceptor C fibres, is part of the acute neurovascular response to injury producing the axon reflex flare. Laser Doppler flowmetry was used to measure the flare response induced by the electrophoresis, at various current strengths, of a ring of acetylcholine solution into dorsal foot skin. 2. Nineteen control subjects and 52 long-duration insulin-dependent (Type 1) diabetic patients of similar age (20 without complications; 19 with laser-treated retinopathy; 13 with reduced vibration perception and retinopathy) were studied in order to investigate the possible attenuation of this defence mechanism in diabetes. 3. The maximal (1 mA) flare response [control median (interquartile range): 1.55 (1.16-2.06) arbitrary units] was reduced greatly in neuropathic patients [0.37 (0.24-0.66) arbitrary units; P less than or equal to 0.001 with respect to all other groups], especially those with a previous history of foot ulceration. The flare was also reduced in some patients with retinopathy alone [1.06 (0.56-1.27) arbitrary units; P less than 0.005 with respect to control subjects]. 4. No rightward shift of the curve of hyperaemic response plotted against current strength was found, suggesting that the abnormal response was due to axonal loss rather than to dysfunction. 5. Neurogenic inflammation, mediated by small pain fibres, was markedly impaired in a group of diabetic patients at risk of foot ulceration. Furthermore, impairment of this nociceptor C fibre response can develop before clinical large-fibre neuropathy and could itself predispose to foot complications.
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PMID:Early loss of neurogenic inflammation in the human diabetic foot. 164 24

The main component of the compound sensory action potential reflects the activity of large myelinated sensory fibers with diameters of greater than 9 micron(s). By recording the averaged potential using a needle electrode placed close to the nerve, small late components can be measured. The latency of these late components can be used to calculate minimum conduction velocity (CV); in normal subjects, average minimum CV is 15 m/s, corresponding to conduction in fibers of about 4 micron(s) in diameter. Minimum CV was measured in median, ulnar, and sural nerves of 187 patients with mild to severe neuropathic symptoms. A reduction in minimum CV was a sensitive measure of peripheral nerve dysfunction, often showing abnormalities when measures derived from the main component were normal. Patients with isolated abnormalities in minimum CV tended to have neuropathic symptoms but no signs of neuropathy. In addition, reduced minimum conduction velocity has implications for the pathology of different types of neuropathy. Slowing conducting potentials may originate from regenerating fibers, which may be of particular relevance in patients with neuropathic pain.
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PMID:Slowly conducting myelinated fibers in peripheral neuropathy. 164 97

When symptoms of peripheral neuropathy appear, the possibility that they have been induced by drugs should be considered. A large number of drugs of all kinds, several of which are considered indispensable, have been implicated in peripheral neuropathy. A list of some of these drugs is provided. Neuropathy is a universal and dose-limiting factor during treatment with vinca alkaloids, but is otherwise a rare complication of drug therapy. Drug-induced peripheral neuropathy is almost always due to a dose-dependent primary axonal degeneration caused either by toxic reactions or by metabolic changes in neurons or their surroundings. The use of drugs should be restricted, especially in patients with a risk for development of neuropathy or with already existing neuropathy, e.g. patients with hepatic or renal failure, diabetes mellitus, or malnutrition. Patients should be given vitamins, prophylactically or therapeutically, which will sometimes allow a treatment to be continued. In other cases of drug-induced neuropathy the drug should be stopped. Reversal depends on the severity of the neuropathy, intensity and duration of the treatment and existence of causative cofactors, but generally the prognosis is good. While waiting for recovery physiotherapy is of importance, and when paraesthesia and pain are troublesome the patient should be treated with carbamazepine, imipramine or lidocaine (lignocaine).
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PMID:Prevention and management of drug-induced peripheral neuropathy. 165 73

This article has reviewed recurrent carpal tunnel syndrome, epineural fibrous fixation, and traction neuropathy of the median nerve. The problems surrounding the diagnosis and treatment of recurrent CTS have been discussed at length. The percent of failures from traditional open ligament surgery is observed to be high, and will become more prevalent as more casual treatments are carried out. This article makes a positive statement with reference to mobilization of the median nerve and anatomic restoration of the transverse carpal ligament. Fibrous fixation of the median nerve is a product of life and function. All cases are different, reflecting the strength, abilities, and personalities of the patients. A bottom line is drawn on these patients, where the summation of the problems of life become symptomatic and disabling. Epineural fibrous fixations induce median nerve traction, governed by hand, wrist, and forearm movements. Traction and tension suggest the intermittent disturbance of nerve nutrition and nerve conduction as the elastic limits of the nerve are approached. These factors accumulate and, in time, cause traction neuropathies with pain. This is followed by a reduced work capability. This impairment can be reversed by surgical nerve mobilization followed by functional nerve gliding therapy. A background history injury to the hand and wrist may be significant, as well as factors such as overuse and misuse of the hand and extremity. Prior to surgery, the careful application of diagnostic stress tests are essential, for the differential diagnosis of fixation traction and positional peripheral neuropathies. Nerve mobilization supported by magnification and the techniques of hand surgery has been successful by the methods discussed and has permitted, importantly, the restoration of the anatomic retinaculum for the flexor tendon system. This can be restored in carpal tunnel surgery and reconstructed with basic ligament material in recurrent carpal tunnel surgery.
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PMID:Recurrent carpal tunnel syndrome, epineural fibrous fixation, and traction neuropathy. 165 11

Small nerve fibre sensory function was assessed by psychophysical estimates of cutaneous thermal thresholds in 30 patients who presented with the symptoms of painful burning feet. Thresholds were abnormal in 12 and normal in 18 patients although symptoms in the two groups were very similar. Various hypotheses for the mechanism of pain in small fibre neuropathy have been proposed previously and these are discussed, but the cause of symptoms in patients with normal thresholds, is unknown. The possibility exists that these patients have a neuropathic disorder which affects only those unmyelinated fibres involved with pain.
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PMID:Cutaneous thermal thresholds in patients with painful burning feet. 166 May 31

Primary lumbosacral plexus neuropathy (LSPN) is a well-defined syndrome characterized by pain, weakness and atrophy in the distribution of the lumbosacral plexus. Previous reports of LSPN have stressed the benign nature of the syndrome. Patients generally have a nearly complete recovery in months to years following the initial event. Two patients presenting with a relapsing form of LSPN are reported. The diagnosis of LSPN was based on clinical and electromyographic features, and no underlying cause was found on initial evaluation or subsequent follow-up over a 6- to 8-year period. We suggest that these patients represent a clinically and possibly pathologically distinct subgroup of LSPN.
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PMID:Relapsing lumbosacral plexus neuropathy. Report of two cases. 166 76


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