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PubMed2003

Mononeuropathy multiplex in association with livedoid vasculitis.

Livedoid vasculitis is a chronic dermatological disorder associated with petechiae and recurrent, unusually shaped ulcers that heal to form hyperpigmentated areas and atrophie blanche. This condition is more correctly termed a vasculopathy, rather than a vascultis, and is often associated with an underlying hypercoagulable disorder. We report a patient with livedoid vasculitis and mononeuropathy multiplex. We propose that peripheral nervous system involvement arises from multifocal areas of ischemia due to fibrin and thrombin deposition within both the wall and lumen of vasa nervorum.

Adult↗
PubMed2004

Transthyretin amyloidosis presenting with multifocal demyelinating mononeuropathies.

We describe a patient with transthyretin amyloidosis who presented with multifocal mononeuropathies with features of demyelination on nerve conduction studies, a constellation of findings not previously described in amyloid polyneuropathy. Genetic testing revealed a valine122isoleucine mutation in the coding region of the transthyretin gene, a mutation that generally presents with late-onset cardiac amyloidosis. Our patient was also unusual in that she was 34 years old at the time of presentation and had no cardiac involvement.

Adult↗
PubMed2005

Exogenous interleukin-6 increases cold allodynia in rats with a mononeuropathy.

Interleukin-6 (IL-6) is a pleiotropic cytokine, signaling intracellularly via its unique membrane-bound receptor IL-6R and gp130. In peripheral nerve injury models, IL-6 and IL-6R are increased at the injured nerve and the respective dorsal root ganglion. IL-6 is increased at the ipsilateral dorsal and ventral horn of the spinal cord. IL-6 is known to affect neuronal survival, differentiation and regeneration. It is involved in synaptic plasticity and hyperexitability and induces the synthesis or release of other substances with known neuroprotective or neuromodulatory effects. In this study, intrathecal administration of recombinant rat IL-6 to rats with a chronic constriction injury of the sciatic nerve, induced a logarithmic dose-dependent increase in cold allodynia with a threshold of 10 pg IL-6 and a maximal effect at 100 ng IL-6. Intrathecal administration of saline or denaturated IL-6 was without effect. In rats with a chronic constriction injury, systemic administered IL-6 did not induce a hyperalgesic effect, illustrating that IL-6 acts at the level of the dorsal root ganglion or the spinal cord. Intraplantar injection of 100 ng IL-6 in the operated hind paw resulted in an increased cold allodynia. This study demonstrates that the sensitivity to exogenous intrathecal or peripheral IL-6 increases in rats with a mononeuropathy.

Animals↗
PubMed2004

Continuous perfusion with morphine of the orbitofrontal cortex reduces allodynia and hyperalgesia in a rat model for mononeuropathy.

Recent imaging reports demonstrate the activation of the orbitofrontal cortical (OFC) area during acute and chronic pain. The aim of this study was to compare the effects of chronic perfusion of this area with morphine on nociception in control rats and in rats subjected to mononeuropathy. Chronic perfusion of morphine, using miniosmotic pumps, produced significant and naloxone-reversible depression of tactile and cold allodynias and thermal hyperalgesia, observed in neuropathic rats, while it produced significant elevation and naloxone insensitive increase of acute nociceptive thresholds in control rats. The observed results support the idea that this area is a component of a flexible cerebral network involved in pain processing and perception.

Analgesics, Opioid↗
PubMed2000

Possible role of inflammatory mediators in tactile hypersensitivity in rat models of mononeuropathy.

Peripheral hypersensitivity (hyperalgesia and allodynia) are common phenomena both in inflammatory and in neuropathic pain conditions. Several rat models of mononeuropathy (Bennett, Seltzer and Gazelius models) display such symptoms following partial injury to the sciatic nerve. Using immunohistochemistry and behavioral tests, we investigated inflammatory cell and cytokine responses in the sciatic nerve 14 days after injury created in these different models as well as after axotomy. Tactile hypersensitivity ('allodynia') was present in all Gazelius model rats whereas only 38 and 29% of the Bennett and Seltzer models, respectively, displayed this sign of neuropathy. The inflammatory reactions in rats with and without tactile allodynia were compared. Monocytes/macrophages (ED-1), natural killer cells, T lymphocytes, and the pro-inflammatory cytokines tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), were significantly upregulated in all nerve injured rats in comparison to sham-operated controls. Interestingly, ED-1-, TNF-alpha- and IL-6-positive cells increased more markedly in allodynic Bennett and Seltzer rats than in non-allodynic ones. The magnitude of the inflammatory response does not seem to relate to the extent of damage to the nerve fibers because axotomized rats displayed much lower upregulation. Our findings indicate that the considerable increase in monocytes/macrophages induced by a nerve injury results in a very high release of IL-6 and TNF-alpha. This may relate to the generation of tactile allodynia/hyperalgesia, since there was a clear correlation between the number of ED-1 and IL-6-positive cells and the degree of allodynia. It is possible that measures to reduce monocyte/macrophage recruitment and the release of pro-inflammatory interleukins after nerve damage could influence the development of neuropathic pain.

Animals↗
PubMed2003

Paw withdrawal thresholds and persistent hindlimb flexion in experimental mononeuropathies.

Hypersensitivity of the foot produced by a number of sciatic mononeuropathies was assessed and compared. A new tool was used, the strain-gauge algometer, that delivers a noxious stimulus and gives a direct measurement of the force for paw withdrawal. In addition, we report observations of another alteration of the flexion reflex, persistent hindlimb flexion. The mean mechanical threshold for naive rats was 5.9 +/- 0.97 centinewton (standard deviation). A superficial surgical procedure had no effect on mechanical sensitivity. Sham surgeries and a surgery in which a silicone pellet was glued to the sciatic nerve produced moderate increases in mechanical sensitivity. Interventions that produced the greatest reductions in thresholds were carrageenan neuritis, complete Freund's adjuvant neuritis, and the chronic constriction injury (CCI) model. Mechanical thresholds returned to baseline in 2 weeks in all groups. Neuropathic behaviors (licking and holding the paw after the stimulus) were observed more frequently in the CCI group. Persistent hindlimb flexion was only observed in the CCI group. The results support that midaxonal inflammation is sufficient to induce hyperalgesia. The strain-gauge algometer proved to be efficient and reliable, and calculations support that used as described in this report one can demonstrate changes in paw withdrawal thresholds as small as 15%.

Animals↗
PubMed2000

Intraneural nerve metastasis with multiple mononeuropathies.

Although cancer is a frequent condition, neoplastic involvement of the peripheral nervous system is rare. The mechanisms are heterogeneous and include lesions within the cerebrospinal fluid (CSF) space, local invasion (e.g. brachial plexus), compression, rarely direct infiltration, perineurial spread and even rarer intranerval metastasis. A 47-year-old woman had been treated for a carcinoid 10 years earlier and had received axillar irradiation. At presentation she suffered from weakness of the biceps brachii and was experiencing pain radiating from the axilla into the forearm and thumb. MR scans of the brachial plexus were negative and her symptoms were primarily considered to stem from a postradiation brachial plexopathy, Because of increasing pain, the brachial plexus was explored and a metastasis in the left musculocutaneous nerve was resected. Several months later, numbness and pain appeared in the ulnar nerve and another intrafascicular metastasis in the ulnar nerve was discovered. Resection with preservation of remaining fascicles was performed. This rare case report demonstrates that multiple mononeuropathies, resembling multiplex neuropathy, may be caused by intranerval metastasis.

Brachial Plexus Neuropathies↗
PubMed2005

Mononeuropathy multiplex and chylothorax as earlier manifestations of pulmonary tuberculosis.

Mononeuropathy multiplex (MNM) and chylothorax are rare clinical disorders. The concurrence of these two disorders with Mycobacterium tuberculosis infection has not been reported. We herein report a patient who was initially diagnosed with fever of unknown origin and MNM, and then developed chylothorax. Pulmonary tuberculosis was proved 1 month after chylothorax appeared. With low-dose prednisolone 15 mg day(-1) and anti-tuberculosis drugs, all these disorders completely resolved 1 year later.

Aged↗
PubMed2005

Ca2+/calmodulin-dependent protein kinase II in the spinal cord contributes to neuropathic pain in a rat model of mononeuropathy.

Ca2+/calmodulin-dependent protein kinase II (CaMKII) is known to subserve activity-dependent neuronal plasticity in the central nervous system. To examine in vivo the implication of spinal CaMKII activity in the generation and development of neuropathic pain after peripheral nerve injury, we used an animal model of mononeuropathy, the chronic constriction injury (CCI) model, in the rat. We found that, 3 days after CCI, the total CaMKII (tCaMKII) immunoreactivity increased in the superficial laminae of the spinal cord and this increase continued for up to 14 days. The immunoreactivity of phosphorylated CaMKII showed an increase from 1 day after CCI, which preceded the up-regulation of tCaMKII. A non-selective N-methyl-d-aspartate receptor antagonist, MK801, significantly attenuated the increase of tCaMKII and phosphorylated CaMKII. Moreover, intrathecal administration of an inhibitor of CaMKII, KN93, before the CCI surgery attenuated the development of thermal hyperalgesia and mechanical allodynia. In addition, KN93 significantly reduced the nociceptive behavior in phase II of the formalin test. These findings demonstrate that the activity of CaMKII in spinal neurons is elevated after peripheral nerve injury and may be involved in central sensitization. The alteration of CaMKII is considered to be a neuroplastic change that occurs in spinal neurons that contributes to neuropathic pain, suggesting the potential for the development of novel therapeutics for neuropathic pain that target CaMKII.

Animals↗
PubMed2003

Idiopathic thrombocytopenic purpura and mononeuropathy multiplex.

Peripheral neuropathy is an uncommon complication of idiopathic thrombocytopenic purpura (ITP). We report a 61-year-old man with ITP who developed acute-onset mononeuropathy multiplex. An electrophysiologic study revealed active axonal degenerative alteration, and a sural nerve biopsy showed axonal degeneration. Intraneural hemorrhage was suggested to be the most likely cause.

Acute Disease↗
PubMedDate not supplied

Confluent peripheral multiple mononeuropathy associated to acute hepatitis B: a case report.

A thirty three year-old, male patient was admitted at the Hospital of the São Paulo University School of Medicine, at the city of São Paulo, Brazil, with complaint of pains, tingling and decreased sensibility in the right hand for the last four months. This had progressed to the left hand, left foot and right foot, in addition to a difficulty of flexing and stretching in the left foot. Tests were positive for HBeAg, IgM anti-HBc and HBsAg, thus characterizing the condition of acute hepatitis B. The ALT serum level was 15 times above the upper normal limit. Blood glucose, cerebral spinal fluid, antinuclear antibodies (ANA) and anti-HIV and anti-HCV serum tests were either normal or negative. Electroneuromyography disclosed severe peripheral neuropathy with an axon prevalence and signs of denervation; nerve biopsy disclosed intense vasculitis. The diagnosis of multiple confluent mononeuropathy associated to acute hepatitis B was done. This association is not often reported in international literature and its probable cause is the direct action of the hepatitis B virus on the nerves or a vasculitis of the vasa nervorum brought about by deposits of immune complexes.

Acute Disease↗
PubMed2000

Peroneal mononeuropathy in pediatric Hodgkin's disease.

A 12-year-old boy with Hodgkin's disease developed left peroneal nerve palsy during combination therapy with chemotherapy and low-dose irradiation. The palsy occurred twice; around 1-2 weeks after the second administration of vincristine in the second and third COPP (cyclophosphamide, vincristine, prednisolone, and procarbazine) regimens. Without any treatment, the peroneal neuropathy completely resolved clinically three months and electromyographically six months after the onset. He used to play television games for more than 6 hours a day with the legs crossed while sitting on the bedside. Compared to adult patients, little is known about the relationship between peroneal neuropathy and systemic malignant diseases in pediatric patients. This case shows for the first time that habitual leg crossing during potentially neurotoxic chemotherapy could induce peroneal mononeuropathy in a pediatric cancer patient.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

Multiple mononeuropathy due to vasculitis associated with anticardiolipin antibodies: a case report.

This report illustrates a case of peripheral nerve vasculitis associated with elevated anticardiolipin antibodies. A 49-year-old female with a history of seven spontaneous abortions initially complained of pain and numbness in her right calf that later spread to the left foot and ankle. Over the next few months, she developed a Raynaud phenomenon and livedo reticularis. Clinical examination revealed signs of multiple mononeuropathy. Right sural nerve biopsy performed two months after the beginning of the disease revealed active necrotizing arteritis of the epineural arteries with transmural inflammatory infiltrate and thrombosis. Vasculitis is a rare finding in sural nerve biopsies, usually in patients with systemic vasculitis or autoimmune connective tissue diseases. However, vasculitis restricted to the peripheral nerves has also been described. Our patient had no clinical or laboratory features of any autoimmune disorder and also no signs of systemic vasculitis. We discuss the potential role of anticardiolipin antibodies in the pathogenesis of vasculitis.

Abortion, Spontaneous↗
PubMed1984

Clinical characteristics and prognosis of vasculitic mononeuropathy multiplex.

The initial appearance and course of 19 patients with mononeuropathy multiplex due to systemic vasculitis were evaluated. Neuropathy first occurred within one year of the onset of systemic vasculitis in all patients and within one year of the onset of rheumatoid arthritis in four of nine patients. Concurrent cutaneous arteritic lesions and elevated ESRs occurred more frequently in patients with rheumatoid arthritis than in those without it. The overall six-month and five-year survival rates were approximately 80% and 60%, respectively. Significant nerve improvement was noted in 86% of surviving patients after one year. There were no factors at initial appearance predictive of outcome.

Adult↗
PubMed1988

Proximal ulnar mononeuropathy caused by conduction block at Erb's point.

We describe a young man with classic symptoms of isolated ulnar mononeuropathy, whose nerve conduction studies showed a severe conduction block of the ulnar nerve between the stimulation at the axilla and Erb's point. His clinical and electrophysiologic abnormalities resolved completely in eight weeks.

Action Potentials↗
PubMed1993

Idiopathic, progressive mononeuropathy in young people.

We describe six young patients with insidiously progressive, painless weakness in the distribution of a single major lower extremity nerve. No cause could be found despite extensive evaluation, including surgical exploration. At the time of diagnosis, all patients had weakness and three patients had sensory loss. In all cases, electromyography revealed a chronic axonal mononeuropathy without conduction block or focal conduction slowing. Magnetic resonance, computed tomographic, and ultrasound imaging studies did not identify a region of nerve swelling, mass, or compression. At surgical exploration, the nerve appeared atrophic in two patients, indurated in one patient, and normal in two patients. Biopsy specimens obtained from two abnormal nerves revealed either wallerian degeneration or endoneurial fibrosis. The clinical features of these patients comprise an unusual clinical entity with no known cause or treatment.

Action Potentials↗
PubMed1996

Frequency of median mononeuropathy in patients with mild diabetic neuropathy in the early diabetes intervention trial (EDIT). Tolrestat Study Group For Edit (Early Diabetes Intervention Trial)

We used electrophysiologic criteria to identify median mononeuropathy (MM) at the nondominant wrist among 414 patients enrolled in a multicenter study of patients with mild diabetic neuropathy according to consensus recommendations. Patients with absent sural or peroneal responses or greater than mild symptoms of carpal tunnel syndrome were ineligible. Ninety-five of 414 participants (23%) fulfilled criteria for MM, independent of diabetes type. Patients with MM had a longer duration of diabetes than remaining patients, independent of age, and patients with MM and type II diabetes were more likely to be female (34% vs. 19%; P = 0.008), shorter (165.7 vs. 172.7 cm; P = 0.001), and have a higher body mass index (32.5 vs. 29.1; P = 0.0008) than remaining type II patients. Sural or peroneal conduction abnormalities did not influence the frequency of MM. These results suggest that patients with diabetic neuropathy require special consideration with regard to the evaluation of suspected carpel tunnel syndrome.

Adult↗