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PubMed1995

Spinal cord stimulation in animal models of mononeuropathy: effects on the withdrawal response and the flexor reflex.

Spinal cord stimulation (SCS) is efficacious for pain due to injury of peripheral nerves, and therefore models of mononeuropathy appear to be particularly suitable for an experimental approach to the study of mechanisms underlying the clinical effect of this mode of treatment in chronic neuropathic pain. Virtually all previous experimental studies on SCS have utilized acute and nociceptive types of peripheral pain stimuli to explore the attenuating effects of SCS. In the present study we made use of the two models of supposedly painful neuropathy developed by Bennett and Xie (1988) and Seltzer et al. (1990) to explore the effect of SCS applied with stimulus parameters similar to those used in clinical practice. In rats subjected to ligatures of the sciatic nerve according to these two methods, SCS was applied via chronically implanted electrodes, or acutely via a laminectomy in the lower thoracic region. In awake, freely moving animals SCS produced a marked increase of the withdrawal thresholds to innocuous mechanical stimuli in the form of von Frey filaments. This threshold elevation lasted for up to 40 min after 10 min of SCS. In about one-half of the animals there was also a moderate, but short-lasting increase in the intact leg. The degree and duration of the withdrawal threshold elevation was clearly related to the intensity of SCS which was kept below the level of which a response in the thoracic or leg musculature was produced. In a second series of experiments the effect of SCS, applied acutely via a laminectomy, on the early component (latency: 8-12 msec) of the flexor reflex was studied. As a result of nerve ligation with either of the methods used, the thresholds for evoking the early as well as the late component in the nerve-ligated leg were significantly lower than in the intact one. SCS resulted in a marked and long-lasting increase of the threshold of the early component in the nerve-ligated leg. On the intact side only a slight and short-lasting increase was observed. The late, C fibre-mediated component was not influenced by SCS. The first component of the flexor reflex is conceivably mediated by A beta-fibre activation and it presumably corresponds to the withdrawal response induced by innocuous mechanical stimuli. The lack of effect of SCS on the late reflex component indicates that it selectively influences transmission of A-fibre activity. (ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Extra-territorial pain in rats with a peripheral mononeuropathy: mechano-hyperalgesia and mechano-allodynia in the territory of an uninjured nerve.

The abnormal pain sensations that accompany peripheral neuropathies are sometimes found in a distribution that does not coincide with the territories of nerves or posterior roots. This 'extra-territorial' pain is one of the lines of evidence that has been advanced to support the proposal that these patients suffer from a psychogenic disorder. In the present experiments, rats were prepared with a unilateral chronic constriction injury (CCI) to the sciatic nerve. Beginning on the first postoperative day and continuing for at least 18 days, exaggerated withdrawal reflexes to pinprick stimulation, indicative of mechano-hyperalgesia, were seen on the side of nerve injury in the hindpaw territories of both the injured sciatic nerve and the uninjured saphenous nerve. Beginning on postoperative day 4 and continuing for at least the next 3 weeks, the withdrawal responses to von Frey hair stimulation on the nerve-injured side occurred at a significantly lower threshold, indicating the presence of mechano-allodynia. The severity and time course of the mechano-allodynia were similar in both nerve territories. When tested 18 days after the CCI, mechano-allodynia in the saphenous territory was abolished by an acute saphenous transection, but unaffected by sciatic transection. Conversely, mechano-allodynia evoked from the mid-plantar sciatic territory was abolished by acute sciatic transection, but unaffected by saphenous transection. These results show that rats with an experimental painful peripheral mononeuropathy have extra-territorial pain like that seen in man. Extra-territorial pain may be partly or entirely due to a peripheral nerve injury-evoked dysfunction of pain processing neurons in the central nervous system.

Animals↗
PubMed1995

Evidence for a peripheral component in the enhanced antinociceptive effect of a low dose of systemic morphine in rats with peripheral mononeuropathy.

In a rat model of peripheral mononeuropathy produced by moderate constriction of the sciatic nerve, we have shown that various i.v. doses of morphine and selective opioid agonists produce potent and long-lasting antinociceptive effects on the vocalization threshold to paw pressure. For all the opioids, the antinociceptive effects were more marked for the paw on the nerve-injured side (nerve-injured paw) than for the sham-operated paw. One contributory mechanism could be a peripheral action of the opioid agonists in the nerve-injured paw. This hypothesis was tested in the present study, using systemic morphine and low doses of local naloxone or its quaternary salt naloxone methiodide, exhibiting peripherally acting antagonist properties. The effects of escalating doses of naloxone (0.5-2 microgram injected i.v. or intraplantar into the nerve-injured paw) or naloxone methiodide (5-30 micrograms into the nerve-injured paw) on the antinociceptive effect of morphine (1 mg/kg i.v.) were evaluated using the vocalization threshold to paw pressure in neuropathic rats at two weeks after placing ligatures, a time when the behavioural pain-related disorders have reached a maximum.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesics↗
PubMed1996

Peripheral mononeuropathy affects hypothalamic and splenocyte beta-endorphin levels but not immune function in the rat.

Beta-endorphin and substance P levels were measured in the hypothalamus of rats 14 days after chronic constriction injury of right sciatic nerve. Furthermore, beta-endorphin concentrations in splenocytes, phytoemoagglutinin-induced proliferation of splenocytes, and natural killer activity were assessed. We observed a significant increase of beta-endorphin and substance P hypothalamic levels, and a significant decrease of beta-endorphin concentrations in the immune cells. In contrast, the peripheral mononeuropathy did not affect the immune function. This study presents a picture of central and peripheral peptide changes consistent with a painful condition, but different from what previously observed in rats which underwent peripheral nerve deafferentation or stressful conditions.

Animals↗
PubMed2005

Mononeuropathies of the radial nerve: clinical and neurographic findings in 91 consecutive cases.

Retrospective features of 91 consecutive cases (68 men, 23 women; mean age 44.4 years) of radial mononeuropathy diagnosed over the last 8 years in two electromyography (EMG) services are reported to define the clinical and electrophysiological findings of radial neuropathies in relation to traumatic and non-traumatic causes and site of injury. The occurrence of radial neuropathy was 0.65 x 100 first electromyographic examinations. The most frequent site of damage was the main trunk at the spiral groove of the humerus (36%); the most frequent cause was nerve trauma (70%) due to fracture (36%). In neuropathies of the main trunk and posterior interosseous (PI) nerve, "complete nerve injury" was observed in 36% of cases, conduction motor block in 33% and motor conduction velocity slowing in 46%. At least one of these findings was present in 51%, whereas motor neurography was normal in 13% of cases. Sensory action potential (SAP) anomalies were observed in 51% of cases. In neuropathy of the superficial radial nerve, no SAP was detected in 30% of cases; in all others except one, SAP was reduced in amplitude. Non-traumatic neuropathies showed severer conduction block and less severe anomalies of SAP than traumatic neuropathies. No differences were found between men and women. EMG is essential for confirming the site of injury and neurographic study may be helpful for diagnosis, providing information about lesion type and severity.

Adult↗
PubMed1998

Painful mononeuropathy in C57BL/Wld mice with delayed wallerian degeneration: differential effects of cytokine production and nerve regeneration on thermal and mechanical hypersensitivity.

Wallerian degeneration with macrophage influx and production of proinflammatory cytokines is a critical factor in the development of hyperalgesia in animal models of neuropathic pain. We hypothesized that in the mouse strain with delayed Wallerian degeneration, the C57BL/Wld mouse, the temporal course of mechanical allodynia and thermal hyperalgesia as well as the temporal profile of cytokine expression after nerve injury would differ from normal mice. Here we used the model of chronic constriction injury of the sciatic nerve (CCI) to study the correlation of pain related behavior with peripheral nerve de- and regeneration and concomitant cytokine production. Indeed, after CCI, C57BL/Wld mice showed markedly reduced thermal hyperalgesia compared to normal C57BL/6 mice, temporally related to the delayed recruitment of hematogeneous macrophages to the injured nerve. Endoneurial tumor necrosis factor-alpha (TNF)-like immunoreactivity increased rapidly in normal mice but did so with a delayed time course in C57BL/Wld mice. In addition, the duration of mechanical allodynia was significantly prolonged in C57BL/Wld mice as compared to C57BL/6 mice, in accordance with the delay in regeneration of sensory nerve fibers in these mice. These results suggest that macrophage invasion and production of TNF may influence the development of thermal hyperalgesia and that regenerative activity is linked to mechanical allodynia in peripheral mononeuropathy.

Animals↗
PubMed2000

Interactions of galanin and morphine in the spinal antinociception in rats with mononeuropathy.

The increased hind-paw withdrawal latency (HWL) to thermal stimulation and hind-paw withdrawal threshold (HWT) to mechanical stimulation induced by morphine were attenuated by intrathecal injection of 1 or 3 nmol, but not 0.3 nmol of the selective galanin antagonist galantide. The result indicated a possible interaction between galanin and opioids in the transmission of presumed nociceptive information in the spinal cord of rats with mononeuropathy.

Analgesics, Opioid↗
PubMed1997

Painful small-fibre multifocal mononeuropathy and local myositis following influenza B infection.

A 47-year-old man experienced multifocal mononeuropathy and putative ganglionopathy associated with influenza B infection, characterized by aching and dysesthesia in the right arm and left leg with normal deep sense. He displayed muscle atrophy in the affected limbs, which might have resulted from local myositis or a disorder similar to neuralgic amyotrophy. Sural nerve biopsy revealed a severe loss of unmyelinated and thinly myelinated fibres, consistent with a small fibre neuropathy, without evidence of angiopathy or inflammation. We could not detect any other cause of the neuropathy except influenza B. In this case, it may be inferred that small-diameter neurons in the dorsal root ganglia and thinly- or nonmyelinated fibres were selectively involved through a post-infectious immune process. To our knowledge, small fibre neuropathy following influenza B has never been reported.

Humans↗
PubMed1984

Papilloedema in diabetes: an ischaemic optic mononeuropathy.

Five diabetic patients had acute visual impairment due to papilloedema, which was bilateral in two patients. The clinical features and subsequent course were compatible with ischaemic optic mononeuropathy presumed to result from ischaemia in a posterior ciliary artery. This cause should always be considered in the differential diagnosis of papilloedema in a diabetic patient to avoid the instigation of inappropriate and invasive investigations. In general the condition has a good prognosis.

Adult↗
PubMed1999

Idiopathic sciatic mononeuropathy.

Sciatic nerve lesions are usually painful and secondary to compression, trauma, infarction or part of a systemic illness. The etiology is usually defined by radiographic or blood studies, or by exploratory surgery. In rare cases, as the one being presented, there is clear clinical and electrophysiological evidence for a lesion of the sciatic nerve, but no morphological correlate or defined etiology. These idiopathic sciatic mononeuropathies seem to occur in the nerves of the legs in young adults.

Adult↗
PubMed2000

MRI in unexplained mononeuropathy.

Four young patients with severe unexplained progressive mononeuropathy are described. None had a history of known trauma to the affected limb. In addition to the standard neurologic examination and electrophysiologic studies (nerve conduction studies and electromyography), all underwent neuroimaging of the involved extremity. In three patients, magnetic resonance imaging revealed intrinsic abnormalities of the appropriate nerve. The pattern or absence of magnetic resonance imaging changes directly influenced decisions about surgical exploration of the nerve in all four patients. With the advent of more sophisticated technology, magnetic resonance neurography has become a potent diagnostic tool in the evaluation of disorders of peripheral nerve and muscle.

Adolescent↗
PubMed2002

The active metabolite of leflunomide, an immunosuppressive agent, reduces mechanical sensitivity in a rat mononeuropathy model.

Recent work has supported a key role for spinal cytokines and glial activation in the development and maintenance of persistent neuropathic pain after peripheral nerve injury. This study was undertaken to determine whether the active metabolite of leflunomide (A77 1726), an anti-inflammatory and immunosuppressive agent, could attenuate persistent mechanical allodynia in a rodent L5 spinal nerve transection model. A77 1726 was administered daily intraperitoneally (0.01 to 10 mg/kg) beginning 1 day before nerve transection. In a separate experiment, A77 1726 was administered daily intrathecally (0.001 to 10 microg in 40 microL) beginning 1 hour before nerve transection. Both systemic and centrally administered A77 1726 significantly reduced mechanical allodynia across the time course of the study (P < .05). A77 1726 attenuated glial activation on day 10 after transection at doses that reduced mechanical sensitivity. In addition, central A77 1726 administration decreased spinal expression of major histocompatibility complex class II. Spinal interleukin-6 levels were unaffected by A77 1726 treatment. This study provides further evidence implicating a contribution of spinal glial activation in the development and maintenance of persistent neuropathic pain. Furthermore, this study reports that systemic and central administration of the active metabolite of leflunomide, an immunosuppressive agent used for the treatment of rheumatoid arthritis, produces an antiallodynic action in a rodent mononeuropathy model.

Journal Article↗
PubMed1990

Diabetic oculomotor mononeuropathy: involvement of pupillomotor fibres with slow resolution.

The third and sixth cranial nerves are most frequently affected in diabetic extraocular mononeuropathies. In diabetic oculomotor involvement the pupil is undisturbed. Of the 21 patients of diabetic oculomotor paralysis 4 patients (19 percent) had dilated unreactive pupil suggestive of pupillomotor involvement. No other cause could be attributed to oculomotor paralysis. These patients showed complete but slow resolution as compared to those without pupil involvement.

Blood Glucose↗
PubMed1998

Sensory mononeuropathies.

The clinical neurologist frequently encounters patients with a variety of focal sensory symptoms and signs. This article reviews the clinical features, etiologies, laboratory findings, and management of the common sensory mononeuropathies including meralgia paresthetica, cheiralgia paresthetica, notalgia paresthetica, gonyalgia paresthetica, digitalgia paresthetica, intercostal neuropathy, and mental neuropathy.

Humans↗
PubMed1987

[Hereditary neuropathy with liability to pressure palsies. A contribution to the differential diagnosis of multiplex mononeuropathy].

Hereditary neuropathy with liability to pressure palsies could be diagnosed in two families. This little-known, dominantly inherited disorder is clinically characterised by recurring, spontaneously regressive palsies of peripheral nerves, mostly after minimal mechanical compression of the nerve concerned. It can be clearly differentiated from mononeuropathies of different pathogenesis even in clinically not involved nerves, by means of pathological neurographic findings and by the detection of pathognomonic myelinic thickenings in nerve biopsies. Prognosis is favourable if recurrences are avoided. This means that counselling of the patients and their families is of prophylactic significance.

Adult↗
PubMed1979

Mononeuropathy in diabetes mellitus: a phenomenon easily overlooked.

In patients with diabetes, a carefully taken history and meticulously performed neurologic examination enable the clinician to separate superimposed mononeuropathy from more generalized symmetric polyneuropathy. Recognition of mononeuroparhy is important, since often it is reversible.

Carpal Tunnel Syndrome↗