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PubMed1999

Effects of intrathecal galanin on nociceptive responses in rats with mononeuropathy.

The present study was performed on rats with experimental mononeuropathy induced by left common sciatic nerve loose ligation. Unilateral sciatic nerve loose ligation induced decreases of the hindpaw withdrawal latency to the hot-plate test, cold-plate test and the Randall Selitto test. Sciatic nerve loose ligation induced hyperesponsiveness to touch at room temperature also. Intrathecal administration of either 3 or 6 nmol of galanin, but not 1 nmol, induced significant bilateral increases in hindpaw withdrawal latencies to the hot-plate test, cold-plate test and the Randall Selitto tests in rats with left mononeuropathy. The results indicate that galanin may play important roles in transmission of presumed nociceptive information in the spinal cord of mononeuropathic rats.

Animals↗
PubMed2001

Isolated Rosai-Dorfman disease presenting as peripheral mononeuropathy and clinically mimicking a neurogenic tumor: case report.

BACKGROUND: Rosai-Dorfman disease is a rare idiopathic disorder of proliferative histiocytes affecting the lymph nodes. It usually manifests as bilateral cervical lymphadenopathy and fever with concurrent polyhyperglobulinemia. Cases involving the nervous system are quite rare; most CNS lesions are located intracranially or arise from the spinal dura or leptomeninges. To our knowledge, there has been no previous report of isolated Rosai-Dorfman disease presenting as peripheral mononeuropathy. CASE REPORT: We report a 43-year-old female with isolated extranodal Rosai-Dorfman disease in the medial aspect of the right upper arm, which presented as aberrant ulnar neuropathy caused by a mass encasing the right basilic vein and the medial anteriobrachial cutaneous branch of the right ulnar nerve. Preoperative diagnosis was a neurogenic tumor. The patient underwent excision of the mass, and pathologic examination confirmed the diagnosis of Rosai-Dorfman disease. CONCLUSION: An unusual case of extranodal isolated Rosai-Dorfman disease, presenting as peripheral mononeuropathy, is reported. Clinically, it simulated a neurogenic tumor, extending the etiologic spectrum of entrapment neuropathy of the peripheral nerve.

Adult↗
PubMed1996

Photochemically induced ischaemic lesion of the rat sciatic nerve. A novel method providing high incidence of mononeuropathy.

The incidence of behavioural signs of mononeuropathy in rats subjected to chronic constriction injury (CCI) of the sciatic nerve is unpredictable and often low. In the present study, an ischaemic lesion of the rat sciatic nerve was induced photochemically using a low power laser. In these rats tactile allodynia developed with a considerably greater incidence (95%) than in control rats subjected to CCI (45%). The allodynia lasted longer and was more prominent. Responses to thermal stimulation did not markedly differ between the two groups. The ischaemic lesions displayed marked degeneration, particularly of large myelinated fibres. The results suggest that laser irradiation of a peripheral nerve inducing a local photochemical reaction followed by Wallerian degeneration may be a convenient and reproducible experimental method of producing signs of peripheral mononeuropathy.

Animals↗
PubMedDate not supplied

Severe multiple mononeuropathy in patients with major thermal burns.

Multiple mononeuropathy after thermal burns covering greater than 40% total body surface area occurred in nine of 121 of our burn center admissions for an incidence of 7.4%. The number of nerves involved per patient ranged from three to seven, with the average being 4.9. Upper-extremity nerves were more commonly involved than were lower extremity nerves (33 versus 11). All patients had burns over the involved areas. The source was believed to be due to a multiple crush syndrome, in which multiple different neuropathic factors in each patient summate to cause a multiple mononeuropathy. The outcome with conservative treatment was variable, with lower-extremity nerve lesions having a very good outcome and upper-extremity lesions not having as good an outcome, particularly when the median nerve was affected.

Burns↗
PubMed1993

Common focal mononeuropathies and their electrodiagnosis.

Common focal mononeuropathies can be produced by compression, entrapment, crush, stretch, and transection. Injuries resulting from acute or chronic repetitive external pressure produce compressive neuropathy, whereas chronic distortion or angulation of the nerve from an internal source produces entrapment neuropathy. Electrodiagnostic techniques used in the electromyographic laboratory include nerve conduction studies and the needle electrode examination. Measurement of distal latency, amplitude, conduction velocity, and identification of focal conduction block may help in the localization of focal mononeuropathies. The needle electrode examination gives further information about the distribution of nerve damage, the activity and chronicity of axon loss, and can sometimes date the onset of injury. Basic clinical features and electrodiagnostic patterns are discussed for median, ulnar, radial, and peroneal neuropathies. Differential diagnosis is provided, and illustrative cases are presented.

Diagnosis, Differential↗
PubMed1993

Spatial patterns of increased spinal cord membrane-bound protein kinase C and their relation to increases in 14C-2-deoxyglucose metabolic activity in rats with painful peripheral mononeuropathy.

1. Three-dimensional spatial patterns of changes in membrane-bound protein kinase C (PKC) were examined in the lumbar spinal cords (L1-L5) of rats with an experimental painful peripheral mononeuropathy. Painful peripheral mononeuropathy was produced by loosely ligating the rat's common sciatic nerve, resulting in chronic constrictive nerve injury (CCI). Changes in spinal cord membrane-bound PKC distribution were assayed by employing an established quantitative [3H]-phorbol-12,13-dibutyrate ([3H]PDBu) autoradiographic assay, which includes spinal cord sectioning, incubation of spinal cord sections with [3H]PDBu, production of autoradiographs, and computer-assisted image processing. 2. Sciatic nerve ligation induced demonstrable thermal hyperalgesia in response to radiant heat stimulation and spontaneous pain-related behaviors (such as lifting of the nerve-ligated hind paw) in CCI rats 3, 7, and 10 days after unilateral sciatic nerve ligation. 3. Consistent with behavioral changes, CCI rats examined 3 or 10 days after sciatic nerve ligation displayed a three-dimensional pattern of increased membrane-bound PKC in the lumbar spinal cord (L1-L5) strikingly different from that of sham-operated rats: in the dorsoventral dimension, reliable increases in membrane-bound PKC occurred mainly within spinal cord laminae I-IV and V-VI in CCI rats; in the ipsilateral-contralateral dimension, changes in membrane-bound PKC were seen on both sides of the spinal cord in CCI rats with reliably higher levels of membrane-bound PKC on the side ipsilateral than on the side contralateral to sciatic nerve ligation; in the rostrocaudal dimension, increases in membrane-bound PKC in the spinal cord dorsal horns of CCI rats extended from spinal segments L2-L5. 4. Both three-dimensional increases in spinal cord membrane-bound PKC and nociceptive behaviors (thermal hyperalgesia and spontaneous pain behaviors) in CCI rats were reliably reduced after three daily intrathecal treatments with 80 nmol GM1 ganglioside (a glycosphingolipid shown to prevent PKC translocation/activation), the first of which was given 1 h after sciatic nerve ligation. This reduction was seen 24 h but not 7 days after the last GM1 ganglioside treatment. 5. This three-dimensional increase in membrane-bound PKC in the spinal cord dorsal horn of CCI rats displayed high correlations with thermal hyperalgesia and with spontaneous pain-related behaviors in CCI rats observed both 3 and 10 days after sciatic nerve ligation. Similar correlations were observed between decreases in levels of membrane-bound PKC in the spinal cord dorsal horn and the attenuation of nociceptive behaviors in CCI rats after three daily intrathecal treatments with GM1 ganglioside.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Progressive systemic sclerosis associated with multiple mononeuropathy.

BACKGROUND: Progressive systemic sclerosis (PSS) is a chronic connective tissue inflammatory disease which commonly attacks the skin and the visceral organs, but rarely the peripheral nervous system. OBJECTIVE: The aim of this study was to investigate PSS accompanied by peripheral neuropathy clinically, electrophysiologically and pathologically from a sural nerve biopsy. METHODS: Two women suffering from PSS but without any other collagen disease were studied. Both patients developed peripheral neuropathy with multiple mononeuropathy of the limbs, and in one woman, in the trunk as well. RESULTS: A biopsy of the sural nerve revealed axonal and myelin segmental degeneration, loss of large myelinated fibers and an increase of collagen fibers, but there was no evidence of vasculitis. An electron microscopic examination revealed degenerated axons, disrupted myelin sheaths and multilayered basal lamina in the capillaries. CONCLUSION: Mononeuropathy in PSS suggests that ischemic neuropathy may be related to the immune-mediated vasculopathy.

Aged↗
PubMed1991

Mononeuropathy multiplex complicating idiopathic thrombocytopenic purpura.

Peripheral nerve hemorrhage has rarely been reported with idiopathic thrombocytopenic purpura (ITP). We describe a patient with severe ITP who developed mononeuropathy multiplex. At autopsy, multisystem hemorrhages were found, including intraneural hemorrhage, without evidence of extraneural hematoma. ITP represents an unusual cause for clinical mononeuropathy multiplex.

Humans↗
PubMed1993

Mononeuropathy multiplex with ulcerative colitis.

We describe acute mononeuropathy multiplex in a patient with chronic ulcerative colitis. The symptoms of neuropathy were well correlated with the disease activity of colitis. Both electrophysiological study and sural nerve biopsy revealed axonal degeneration. Mononeuropathy multiplex may be an extraintestinal manifestation of ulcerative colitis.

Adult↗
PubMedDate not supplied

[A case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease].

We reported a case of mononeuropathy multiplex associated with anti-GM1 and -SGLPG antibodies in a patient with ongoing Hashimoto disease. A 56-year-old woman was admitted with asymmetrical patchy sensory and motor disturbance in the extremities. Muscle atrophy and weakness in the left palm and bilateral tibialis anterior muscles were also noted. Deep tendon reflexes were normal in all the extremities. Superficial and deep sensations were reduced in the hands and feet bilaterally, and the distribution of sensory loss was irregular. Her serum was positive for antinuclear antibody, rheumatoid factor, anti-RNP antibody, and anti-SS-A antibody. Serial electrophysiological studies suggested that the predominant process was axonal degeneration of the sensorimotor nerves. On sural nerve biopsy, there were no findings of vasculitis but severe axonal degeneration was observed. Thin-layer chromatography with immunostaining revealed anti-GM1 and -SGLPG antibodies. Treatment with corticosteroids was successful. In this case, the anti-GM1 antibody may have played a role in the pathogenesis of mononeuropathy multiplex associated with autoimmune disease.

Autoantibodies↗
PubMed1997

Motor and sensory demyelinating mononeuropathy multiplex (multifocal motor and sensory demyelinating neuropathy): a separate entity or a variant of chronic inflammatory demyelinating polyneuropathy?

We report 16 patients with motor and sensory demyelinating mononeuropathy multiplex (MSDMM) or multifocal motor and sensory demyelinating neuropathy (MMSDN). These patients had the clinical pattern of motor and sensory mononeuropathy multiplex, electrophysiological evidence of demyelination including conduction block, and segmental demyelination in the sural nerve biopsy. Sixty per cent of patients had high CSF protein. Eighty per cent of patients showed good responsiveness to steroid treatment. Unlike multifocal motor neuropathy (MMN), MSDMM is characterized by a shorter course, sensory deficits and sensory nerve conduction abnormalities, absence of GM1 antibody in most patients tested, and a good response to steroid therapy. We believe that MSDMM represents a variant of chronic inflammatory demyelinating polyneuropathy (CIDP) and an intermediate link between CIDP and MMN.

Adolescent↗
PubMed2004

Small fibers peroneal mononeuropathy in a patient with Sjögren's syndrome.

Sjögren's syndrome (SS) is an autoimmune epithelitis characterized by lymphocytic infiltration of exocrine glands and epithelia in multiple sites. One third of the patients present with peripheral nervous system involvement. We describe the case of a woman aged 62 affected by a peroneal nerve mononeuropathy with painful disturbances secondary to a prevalent involvement of small fibers as demonstrated by electrophysiological investigations and skin biopsy. Asymmetric peripheral nerve involvement is not uncommon in SS, though, to our knowledge, it has never been reported of a mononeuropathy involving primarily small fibers.

Ankle↗
PubMed1991

[A case of multiple mononeuropathy associated with pustulosis palmaris et plantaris (PPP)].

A 41-year-old man with PPP since in 1982 was admitted in May, 1987, because of the progressive asymmetric sensory disturbance in the hands and feet over 4 months, accompanied by an exacerbation of PPP. On admission, eruptions of PPP were observed in the palms and soles. Asymmetric and mildly decreased sensations of touch and pain were present in the distal part of the four extremities as well as in his trunk, accompanied by paresthesia and dysesthesia. Mild to moderate weakness was noted in the hand muscles, and slight muscular atrophy was present in the right lower leg. A work-up for collagen vascular disease was within normal limits. T lymphocyte subset showed a decreased ratio of OKT 4/OKT 8. Left sural nerve biopsy showed axonal degeneration and moderate decrease of myelinated fibers, and the vasculitis was not found. The neurological signs and symptoms as well as the skin eruptions improved with methylprednisolone 40 mg/day. A causal relationship between the multiple mononeuropathy and PPP of our patient was indicated by the almost simultaneous onset of the neuropathy and the exacerbation of PPP as well as the improvement of these two conditions with corticosteroid therapy. Such combination of multiple mononeuropathy and PPP has not so far been reported.

Adult↗
PubMed1982

Hypertrophic mononeuropathy. A report of two cases and review of the literature.

Two cases of hypertrophic mononeuropathy were studied. This entity is characterized grossly by focal enlargement of a single peripheral nerve, and microscopically by loss of nerve fibers, fibrosis, and formation of numerous onion bulbs. Our cases were diagnosed by exploratory surgery, biopsy, and light microscopy. Electron microscopic evaluation was performed in one case. Recognition of this entity by the surgical pathologist is important, so that it can be distinguished from generalized forms of onion bulb neuropathies, most of which give a much less favorable long-term prognosis. Hypertrophic mononeuropathy has usually resulted in irreversible local neurologic deficit but, unlike the polyneuropathies, in all the previously reported cases (as well as in our two cases to date) it has remained a localized process.

Adolescent↗
PubMed1996

Spinal cord NMDA receptors modulate peripheral immune responses and spinal cord c-fos expression after immune challenge in rats subjected to unilateral mononeuropathy.

To characterize further the neural involvement in local immune reactions, we evaluated the effect of intrathecal NMDA-receptor blocker dizocilpine maleate (MK-801) on the peripheral immune response itself and on spinal cord c-fos expression induced by the delayed-type hypersensitivity (DTH) response. Immune challenge took place in the hind paw ipsilateral or contralateral to an injured sciatic nerve in both previously sensitized and immune-naive animals. An enhanced immune response was observed bilaterally in the hind paws of animals subjected to unilateral mononeuropathy compared with sham-operated controls. In contrast, no such enhancement was observed when neuropathic animals were challenged in the front paws. The increased DTH response was blocked successfully by the intrathecal administration of an analgesic dose of MK-801. Compared with sham-operated animals, animals subjected to unilateral mononeuropathy showed both a differential distribution and an increase in the number of c-fos-labeled neurons in the dorsal horn of the L3-L5 spinal cord segments after immune challenge. This was observed irrespective of whether the challenge took place ipsilateral or contralateral to the injured nerve. In addition to reversing the changes in immune response, intrathecal administration of MK-801 reversed the pattern of c-fos immunoreactivity in the spinal cord after immune challenge in neuropathic animals. These data suggest that select groups of spinal cord neurons participate in enhancing the peripheral immune response to a specific antigen in neuropathic animals and that this enhancement involves central NMDA receptors.

Animals↗
PubMed1995

[Mononeuropathy multiplex in a patient receiving interferon alpha therapy for chronic hepatitis C].

We report a case of mononeuropathy multiplex due to interferon alpha (IFN alpha) therapy for chronic hepatitis C. A 61-year-old man received IFN alpha (natural type 6 x 10(6) IU), every day for two weeks and three times a week for 22 weeks by intramuscular injection. Seventeen weeks after the initiation of IFN alpha therapy, he noticed painful dysesthesia, muscle weakness and muscular atrophy of the left lower extremity. Neurological examination revealed weakness of the left iliopsoas, quadriceps femoris and femoral adductor muscles, hypesthesia and dysesthesia. Electromyogram showed neuropathic change in the left vastus lateralis muscle. Muscle computed tomography showed muscular atrophy of the left lower extremity. Two months after discontinuation of the IFN alpha therapy, dysesthesia and muscle weakness of the left lower extremity improved spontaneously. He was diagnosed as mononeuropathy multiplex of the left femoral nerve and obturator nerve caused by IFN alpha therapy. Attention must be paid to dysesthesia, muscle weakness and muscular atrophy when IFN alpha therapy is initiated.

Chronic Disease↗
PubMedDate not supplied

Correlation of EMG, CMAP and SNAP amplitude decrease in mononeuropathies with axonal loss.

We retrospectively reviewed electrodiagnostic studies from 1983 to 1994 and found 48 patients who met our criteria for mononeuropathy with axonal loss (40 ulnar, 4 peroneal, 4 radial). Appropriate diagnostic criteria required bilateral studies with a normal contralateral, sensory nerve action potential (SNAP) amplitude decrease of > 50% compared to contralateral, and/or distal compound muscle action potential (CMAP) amplitude decrease of > 40% compared to contralateral, and/or presence of denervation potentials; and sufficient electrodiagnostic investigation to rule out peripheral polyneuropathy. We conclude that in the electrodiagnosis of mononeuropathy with axonal loss: 1) a significant quantitative correlation between CMAP and SNAP amplitude percentage decrease does not exist (r = 0.274, p = 0.06), 2) SNAP amplitude percentage decrease [75.3 +/- 31.8%] is greater than CMAP amplitude percentage decrease [43.9 +/- 31.3%] (paired t-test, p = 0.0001), and 3) CMAP amplitude decrease is positively correlated with the presence of denervation potentials (Xtrend2 = 6.22, p = 0.013).

Action Potentials↗
PubMed2005

Initial cutaneous manifestations consistent with mononeuropathy multiplex in Churg-Strauss syndrome.

BACKGROUND: Churg-Strauss syndrome (CSS), also known as allergic granulomatous angiitis, is a rare entity that is characterized by systemic vasculitis in patients with a history of asthma. Patients with CSS show a marked peripheral blood eosinophilia, but the pathogenesis remains unknown. OBSERVATIONS: A retrospective review was performed in 9 cases of CSS in whom cutaneous findings were present as an initial manifestation. All 9 patients had purpura and petechiae as well as severe pain and paresthesias of the lower extremities. Four patients (44%) used leukotriene receptor antagonists to treat their asthma, and 3 (75%) of them developed CSS within 3 months. Five patients (56%) were positive for perinuclear antineutrophil cytoplasmic antibodies before therapy, but in all 5 the levels of perinuclear antineutrophil cytoplasmic antibody normalized. Serum IgE levels were elevated in all patients before treatment but decreased after treatment. Histologically, all patients demonstrated leukocytoclastic vasculitis and eosinophilic infiltration. Eight biopsy specimens (73%) revealed marked eosinophilia around the nerve fibers in the dermis. Palisading granulomas in association with vessel-based changes were present in 4 (36%) of 11 biopsy specimens. CONCLUSIONS: These characteristic cutaneous clinical patterns that are consistent with the presence of mononeuropathy multiplexes in the lower extremities may help physicians establish an earlier diagnosis. Both eosinophils and IgE, as well as perinuclear antineutrophil cytoplasmic antibodies to some degree, likely participate in skin lesion development in CSS. Furthermore, there appears to be a correlation between treatment with leukotriene receptor antagonists and the onset of CSS in some cases.

Adult↗