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PubMed2002

Electrodiagnostic approach to the patient with suspected mononeuropathy of the lower extremity.

Lower extremity mononeuropathies are less common than those affecting the upper limb. Yet, they are often challenging and more difficult to diagnose. The electrodiagnostic (EDX) studies play a pivotal role in diagnosis. Well planned and executed studies are very useful, although limiting factors such as age, foot swelling or prior lumbar spine surgery may hinder making a definite diagnosis. In this section, the author emphasizes the EDX studies of most lower extremity mononeuropathies and discusses, briefly, their anatomical and clinical aspects.

Diagnosis, Differential↗
PubMed2004

Simvastatin-induced mononeuropathy multiplex: case report.

The association between the use of statins and neuromuscular disease is currently being intensely discussed. We relate a 63 years old man with possible case of statin-induced neuropathy in a patient with dislipidemia in use of simvastatina at high doses. The electrophysiologic studies disclosed findings compatible with mononeuropathy multiplex, suggested by clinical prescutation of asymmetrical numbness and weakness. More common causes of mononeuropathy multiplex were excluded and the patient improved after the discontinuation of the drug.

Humans↗
PubMed2005

Intercostal nerve mononeuropathy: study of 14 cases.

This retrospective study describes 14 cases of intercostal nerve mononeuropathy (INM) found in 5,560 electromyography (EMG) exams performed between January 1991 and June 2004 in our University Hospital. Medical charts of all patients with history of thoracic pain and EMG diagnosis of intercostal mononeuropathy were reviewed. INM was detected in 14 patients; etiology was thoracic surgery in 6 (43%), post-herpetic neuropathy in 4 (28%), probable intercostal neuritis in 2 (14%), lung neoplasia in 1 (7%), and radiculopathy in 1 (7%). From this study, trauma and infection were the main etiologies in intercostal neuropathic pain development. Tricyclic antidepressants and anticonvulsants were the most common therapeutic drugs used.

Electromyography↗
PubMed2001

[Multiple mononeuropathy and inflammatory syndrome manifested in Lyme disease].

Meningo-radiculitis is the most common peripheral nerve system involvement of Lyme disease. We report the observation of a 73 year-old woman presenting a subacute multiple mononeuropathy and a severe inflammatory syndrome. Diagnosis of Lyme disease was confirmed by a lymphocytic meningitis with positive serologic results in the cerebrospinal fluid. Nerve biopsy showed inflammatory cells spreading along the endoneurium. This case report emphasizes that Lyme disease may present as a multiple mononeuropathy mimicking a vasculitic neuropathy.

Aged↗
PubMed2005

Mononeuropathy of the suprascapular nerve: study of 3 South American cases.

In this work 3 new cases of suprascapular nerve mononeuropathy are described. ENMG diagnosis criteria were: a) normal sensory conduction studies of the ipsolateral ulnar, median and radial nerves; b) bilateral suprascapular nerve latencies with bilateral compound muscle action potential, obtained from the infraspinatus muscle with symmetrical techniques; and c) abnormal neurogenic infraspinatus muscle electromyographic findings, coexisting with normal electromyographical data of the ipsolateral deltoideus and supraspinatus muscles. These 3 cases of suprascapular mononeurpathy were found in 6,080 ENMG exams from our University Hospital. For us this mononeuropathy is rare with a 0.05% occurrence.

Adult↗
PubMed1996

Nonsystemic vasculitic mononeuropathy multiplex, cryoglobulinemia, and hepatitis C.

A 39-year-old man developed sequential acute mononeuropathies involving both median, both ulnar, and the right radial and left peroneal nerves. Electrophysiology demonstrated an asymmetric sensorimotor axonal polyneuropathy; nerve biopsy confirmed a vasculitis. Laboratory evaluation revealed a mixed cryoglobulinemia and active hepatitis C infection. The patient stabilized with prednisone/cyclophosphamide/interferon-alpha. Hepatitis C should be considered in the differential diagnosis of mononeuropathy multiplex. Accurate diagnosis is important, as interferon-alpha may prevent transition to chronic hepatitis/cirrhosis.

Adult↗
PubMed1998

Detection of hereditary neuropathy with liability to pressure palsies among patients with acute painless mononeuropathy or plexopathy.

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal dominant disorder characterized by recurrent mononeuropathies or brachial plexopathies, commonly associated with a chromosome 17p11.2-12 deletion encompassing the peripheral myelin protein-22 (PMP22) gene. We tried to identify criteria distinguishing HNPP among patients with acute painless mononeuropathy/plexopathy. We investigated by pulsed-field gel electrophoresis the presence of the deletion in 27 patients with isolated or recurrent acute painless mononeuropathy or brachial plexopathy, and no obvious cause of neuropathy. Eight patients carried the deletion, whereas 19 had neither the deletion nor mutations in the PMP22 gene. Age at onset, presenting modality, precipitating events, and rate of recovery did not significantly differ in the two groups. Family history was informative for HNPP diagnosis in 3 cases only. HNPP patients more often showed recurrent episodes, brachial plexopathy, and clinical or electrophysiologic involvement of other nerves. Non-HNPP patients more frequently had peroneal palsy, recent weight loss, and normal electrophysiologic examination in other nerves. Signs of generalized neuropathy and evidence of disease in other family member are often subtle in HNPP and must be thoroughly investigated in patients with acute painless mononeuropathy/plexopathy.

Action Potentials↗
PubMed1990

Embolic mononeuropathy in subacute bacterial endocarditis.

A 49-year-old man presented with temperature up to 39.5 degrees C, a sudden peroneal nerve lesion, and a cardiac murmur. The peroneal nerve lesion was likely caused by an embolic occlusion of an artery supplying the nerve. Until now, six cases of embolic mononeuropathy in endocarditis have been reported in the literature. Embolic mononeuropathy is a very rare manifestation of subacute bacterial endocarditis and quite often complicates, as do other more common embolic manifestations, the correct diagnosis.

Embolism↗
PubMedDate not supplied

AAEE case report #12: Common peroneal mononeuropathy at the fibular head.

Common peroneal mononeuropathies, usually located at the fibular head, are one of the many causes of foot-drop, a condition often evaluated in the electromyography laboratory. If appropriate nerve conduction studies are performed and particular muscles studied on needle myography, a satisfactory diagnosis can almost always be provided for what may be a perplexing problem clinically. With all peroneal mononeuropathies, the compound muscle action potential amplitude of the peroneal motor tibialis anterior nerve conduction studies, stimulating distal to the fibular head, is a semi-quantitative measure of the number of viable fibers supplying the tibialis anterior and allows for accurate prognostication regarding the foot-drop.

Diagnosis, Differential↗
PubMed1993

Influence of an experimental peripheral mononeuropathy on the responses of medial bulboreticular neurons to noxious skin stimulation and the modulation of the responses by an alpha 2-adrenoceptor agonist in the rat.

A peripheral mononeuropathy was induced in rats by the placement of four loose ligatures around the right sciatic nerve. After the development of mechanical hyperalgesia in the neuropathic limb, the responses of medial bulboreticular neurons to noxious skin stimulation were determined, and the attenuation of the responses was attempted by administering systemically medetomidine, a highly specific alpha 2-adrenoceptor agonist. The neuronal responses to noxious stimulation of the sciatic nerve area or the saphenous nerve area in the hyperalgesic limb were of a magnitude equal to that of the responses from the corresponding areas in the intact limb of neuropathic or control rats. Also the spontaneous activity of bulboreticular neurons in neuropathic rats was of a magnitude equal to that in intact rats. The dose-dependent (50-200 micrograms/kg) suppression of the evoked responses by medetomidine was equal in intact and neuropathic animals. It is concluded that the medial bulboreticular neurons are not involved in the development of hyperalgesia in rats with an experimental mononeuropathy.

Adrenergic alpha-Agonists↗
PubMed2000

Peroneal mononeuropathy: predisposing factors, and clinical and neurophysiological relationships.

The most common mononeuropathy in the lower extremity involves the nerve. We retrospectively evaluated the etiological predisposing factors and clinical-neurophysiological features of 36 patients affected by peroneal mononeuropathy (PM). In 30 patients, a clear predisposing factor was identified. PM was more frequently perioperative (11 cases), associated with axonal involvement. Unexpectedly, PM was not only due to surgery close to the peroneal region, but was mostly associated with hip surgery and, rarely, with thoracic-abdominal surgery. A postural predisposing factor of PM was also frequently observed, usually associated with a pure conduction block. Conversely, most patients with bedridden predisposing factor presented axonal involvement, which was rarely associated with conduction block. In 25 of 36 PM cases, a long-term follow-up lead to an improvement (12 cases) or to good recovery (13 cases) of PM. In conclusion, our study shows that: (1) in most PM cases it is possible to identify a predisposing factor; (2) there is a good correlation between predisposing factor and neurophysiological involvement, and (3) PM usually has usually a good prognosis.

Adolescent↗
PubMed1992

Intrathecal MK-801 and local nerve anesthesia synergistically reduce nociceptive behaviors in rats with experimental peripheral mononeuropathy.

The hyperalgesia and spontaneous pain that occur following peripheral nerve injury may be related to abnormal peripheral input or altered central activity, or both. The present experiments investigated these possibilities by examining the effects of MK-801 (a non-competitive N-methyl-D-aspartate, NMDA, receptor antagonist) and bupivacaine (a local anesthetic agent) on thermal hyperalgesia and spontaneous nociceptive behaviors in rats with painful peripheral mononeuropathy. Peripheral mononeuropathy was produced by loosely ligating the rat's common sciatic nerve, a procedure which causes chronic constrictive injury (CCI) of the ligated nerve. The resulting hyperalgesia to radiant heat and spontaneous nociceptive behaviors was assessed by using a foot-withdrawal test and a spontaneous pain behavior rating method, respectively. CCI rats receiving 4 daily intraperitoneal (i.p.) MK-801 injections (0.03, 0.1, 0.3 mg/kg) beginning 15 min prior to nerve ligation exhibited less hyperalgesia (i.e., longer foot-withdrawal latencies) on days 3, 5, 7, 10, and 15 after nerve ligation as compared to those receiving saline injections. Thermal hyperalgesia also was reduced when a single MK-801 injection was given intrathecally (i.t.) onto the spinal cord lumbar segments on Day 3 after nerve ligation. This effect of postinjury MK-801 treatment was dose-dependent (2.5-20 nmol) and lasted for at least 48 h after injection. Moreover, i.t. injection of MK-801 (10 nmol) reliably lowered spontaneous pain behavior rating scores in CCI rats compared to those in the saline group. The spinal site of MK-801 action is situated within the caudal (probably lumbar) spinal cord, since i.t. injection of MK-801 (10 nmol) onto the spinal cord thoracic segments did not affect thermal hyperalgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Local↗
PubMed1996

Increased delayed type hypersensitivity in rats subjected to unilateral mononeuropathy is mediated by neurokinin-1 receptors.

An animal model or peripheral mononeuropathy was utilized in the present study to investigate the potential role of substance P (SP) in modifying immune responses associated with chronic pain conditions. Animals subjected to unilateral sciatic ligation and sham-operated animals were sensitized with keyhole limpet hemocyanin (KLH) and subsequently challenged in the ipsilateral or contralateral hind paw to produce a delayed-type hypersensitivity (DTH) response. Subcutaneous microdialysis and radioimmunoassay were used to measure interstitial fluid SP levels in the challenged tissue prior to and following immune challenge in control and neuropathic animals. Following immune challenge, there was a significant increase in the concentration of SP in tissue dialysate samples from the challenged paw of both sham-operated and neuropathic animals. However, tissue SP levels in neuropathic animals were more than two-fold higher than those obtained from sham-operated controls following challenge. SP concentration remained elevated for 2.5 h following immune challenge in neuropathic animals compared to 90 min in sham-operated animals. Compared with controls, neuropathic animals also exhibited an increased DTH response that was reversed, in a dose-related fashion, by the non-peptide NK-1 receptor blocker L-703,606. The same antagonist had no effect in sham-operated animals. These data suggest that the increased DTH response in animals subjected to unilateral mononeuropathy involves SP and NK-1 receptors present in the challenged tissue.

Animals↗
PubMed1995

The clinically tested N-methyl-D-aspartate receptor antagonist memantine blocks and reverses thermal hyperalgesia in a rat model of painful mononeuropathy.

This study tested the prophylactic and therapeutic efficacy of memantine (1-amino-3,5-dimethyl-amandate), a clinically tested N-methyl-D-aspartate (NMDA) antagonist on thermal hyperalgesia in a rat model of painful mononeuropathy. Persistent hyperalgesia induced by chronic constrictive injury (CCI) to the sciatic nerve was significantly reduced for up to 14 days by prophylactic administration of memantine (3.0 mg/kg) via i.p. implanted osmotic micropumps for a period of 7 days. Therapeutic i.p. injections of memantine (10 mg/kg) given on post-injury days 7 and 14 completely reversed existing hyperalgesia for a short period of 1 h. These results provide evidence that memantine produces long-term prophylactic and short-term therapeutic effects on thermal hyperalgesia in a model of painful mononeuropathy.

Animals↗
PubMed1994

Chronic pain and immunity: mononeuropathy alters immune responses in rats.

In order to investigate the possible relationship between chronic pain and the immune system, delayed-type hypersensitivity (DTH) and humoral immunity were assessed in Sprague-Dawley rats subjected to unilateral peripheral mononeuropathy induced by sciatic ligation. Paw withdrawal latency (PWL) time was measured twice during the experiment in animals subjected to sciatic nerve ligation or sham surgery. Sciatic nerve-ligated animals showed hyperalgesia in the leg subjected to neural ligation when compared to the contralateral leg. No differences in PWL times existed in sham-operated animals. In order to exclude possible alterations in immune response due to the surgical procedure or to the hyperalgesia testing, a group of control animals, not subjected to surgical procedures or hyperalgesia testing, was also included in the experiment. Three days post-sciatic ligation or sham surgery, both experimental and control animals were sensitized to keyhole limpet hemocyanin (KLH). A secondary sensitization followed 1 week after the initial immunization. Fourteen days after the initial sensitization, KLH was injected into the hind foot pad and vehicle into the contralateral foot pad in order to assess DTH. One group of rats subjected to sciatic nerve ligation was tested for DTH in the hind foot pad ipsilateral to the ligated nerve, while another group was tested in the contralateral foot pad. Twenty-four hours following foot pad injections, the thickness of both paws was measured and animals were bled to test for anti-KLH immunoglobulins. Animals in which mononeuropathy was induced, but not sham-operated or control animals, exhibited an enhanced DTH response to KLH.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

The calcitonin gene-related peptide antagonist CGRP8-37 increases the latency to withdrawal responses bilaterally in rats with unilateral experimental mononeuropathy, an effect reversed by naloxone.

The present study was performed in rats with experimental mononeuropathy after left common sciatic nerve constriction. A bilateral decrease in hindpaw withdrawal latency to thermal and mechanical stimulation was observed after unilateral ligation of the left common sciatic nerve; however, it was more pronounced on the lesioned side. Compared with sham-operated rats, the content of calcitonin gene-related peptide-like immunoreactivity was significantly decreased in the left dorsal horn of the spinal cord and left dorsal root ganglia in rats with mononeuropathy. Blocking the receptor of calcitonin gene-related peptide, by intrathecal injection of 5 or 10 nmol of calcitonin gene-related peptide (8-37), induced a significant bilateral increase in hindpaw withdrawal latency to both thermal and mechanical stimulation which, however, was significantly less pronounced in mononeuropathic rats than in intact rats. The effect of calcitonin gene-related peptide (8-37) was reversed by intrathecal administration of the opioid antagonist naloxone. The contribution of calcitonin gene-related peptide and its receptors to transmission of presumed nociceptive information appears to be reduced in the sciatic nerve constriction model. The decrease in reflex responsiveness induced by calcitonin gene-related peptide (8-37) was counteracted by naloxone, indicating that opioids control the net effect of excitation in the spinal cord circuitry induced by calcitonin gene-related peptide and possibly other co-released neurotransmitters.

Animals↗
PubMed2004

Acute ocular motor mononeuropathies: prospective study of the roles of neuroimaging and clinical assessment.

The role for immediate neuroimaging in patients 50 years of age or older with acute isolated third, fourth, and sixth nerve palsies is controversial. We prospectively evaluated 66 patients, aged 50 years and older (median 67 years, range 50-85), with acute isolated ocular motor mononeuropathies. Our purpose was to evaluate both the role of neuroimaging and the role of clinical assessment in determining etiology. We found that clinical features, including time to maximal diplopic symptoms, were not predictive of etiology (median 2 days to maximal diplopic symptoms for both peripheral microvascular and other etiologies). The presence of any common vascular risk factor, including diabetes mellitus, hypertension, hypercholesterolemia, or coronary artery disease, was significantly associated with peripheral microvascular etiology in this cohort (p=0.0004, Fisher's exact test). Despite the high prevalence of peripheral microvascular ischemia as an etiology in this age group, other causes were identified by magnetic resonance imaging (MRI) or computed tomography (CT) scanning in 14% of patients. Diagnoses included brainstem and skull base neoplasms, brainstem infarcts, aneurysms, demyelinating disease, and pituitary apoplexy. Neuroimaging procedures may have a role in the initial evaluation of patients 50 years of age or older with acute ocular motor mononeuropathies.

Abducens Nerve Diseases↗
PubMed1997

Cytokine and growth factor immunohistochemical spinal profiles in two animal models of mononeuropathy.

Nerve injury leads to central neuroimmunologic responses that may be integral to the development and maintenance of chronic neuropathic pain in humans. Recent data have demonstrated that cytokines and growth factors may be strongly implicated in the generation of pain states at both peripheral and central nervous system sites. We utilized immunohistochemical methods to investigate this phenomenon in rat models of neuropathic pain. Specifically, we employed well-characterized models of neuropathy that result in behaviors suggestive of neuropathic pain in humans; a freeze lesion of the sciatic nerve, termed sciatic cryoneurolysis, and a chronic constriction sciatic nerve injury. We used immunohistochemistry to examine spinal localization of the cytokines, interleukin-1beta (IL-1beta), tumor necrosis factor-alpha (TNF-alpha) and the growth factors, basic fibroblast growth factor (bFGF), and transforming growth factor-beta1 (TGF-beta) at 3, 14, and 35 days following sciatic cryoneurolysis or 6 days following chronic constriction injury as compared with normal, unoperated rats. There was minimal, diffuse cytokine/growth factor staining in lumbar spinal tissue from the normal group. However, cell profile quantification demonstrated increases in lumbar spinal IL-1beta-, TNF-alpha- and TGF-beta-like immunoreactivity (LI) in both mononeuropathy models studied. At 3 days following sciatic cryoneurolysis, intense bFGF LI was present in the ipsilateral dorsal and ventral horn. By 14 days bFGF LI was also observed in contralateral dorsal and ventral horns. In contrast, we found no obvious staining differences in lumbar spinal cord following the chronic constriction injury. This study demonstrated increased specific cytokine and growth factor-like expression in the spinal cord following peripheral nerve injuries. It also showed a differential expression of bFGF in two distinct mononeuropathy models. These results provide further evidence that central cytokine production via a neuroimmune cascade may be involved in the development and maintenance of behaviors that mimic neuropathic pain following nerve injury.

Animals↗