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PubMed1982

Possible enhancement of vincristine neuropathy by VP-16.

Eleven consecutive patients with small cell carcinoma of the lung treated intensively with a combination chemotherapy regimen cyclophosphamide, Adriamycin, VP-16, and vincristine experienced peripheral neuropathy. Four of the 11 patients had severe (Grade III) neuropathy, leaving them virtually bedridden; the remaining seven patients had mild to moderate neuropathy. Only 8 of the 14 patients treated less intensively with vincristine and VP-16 had Grade I and II neuropathy. Predisposing factors for severe neuropathy included advanced age and preexisting peripheral neuropathy. All patients' performance status declined and all lost much weight before developing neuropathy. From accumulated treatment experience of small cell carcinoma with vincristine alone or with vincristine, Adriamycin, cyclophosphamide combinations, the authors feel that the severe neuropathy observed was due to an interaction of vincristine and VP-16. This conclusion is supported by electron microscopic observation of electronopaque granular degeneration of the myelin lamellae of affected nerve fibers.

Aged↗
PubMed2002

Immunosuppressive treatment for multifocal motor neuropathy.

BACKGROUND: Multifocal motor neuropathy is a distinct clinical entity characterised by progressive, predominantly distal, asymmetrical limb weakness and minimal sensory abnormality. The pathognomonic feature of this condition is the presence of multiple partial motor nerve conduction blocks. Controlled trials have demonstrated the efficacy of regular intravenous immunoglobulin infusions. Immunosuppressive agents have been used as primary, second-line or adjunctive agents for its treatment. This review was undertaken to identify and review systematically randomised controlled trials of immunosuppressive agents. The use of intravenous immunoglobulin will be the subject of a separate review. OBJECTIVES: To provide the best available evidence from randomised controlled trials on the role of immunosuppressive agents for the treatment of multifocal motor neuropathy. SEARCH STRATEGY: The Cochrane Neuromuscular Disease Group register was searched for all trials of multifocal motor neuropathy published, using 'multifocal motor neuropathy' OR 'chronic inflammatory demyelinating polyradiculoneuropathy' OR ' conduction block' OR ' motor neuropathy' AND 'immunosuppressive agents', 'immunosuppressants', 'corticosteroids', 'plasma exchange', 'azathioprine', 'cyclophosphamide', 'cyclosporin', 'methotrexate', and 'mycophenolate', 'immunomodulatory agents', 'interferon', 'total lymphoid irradiation' or 'bone marrow transplantation' as search terms. In addition we searched MEDLINE, EMBASE for 2000 and 2001 and CINAHL, LILACS for all years. SELECTION CRITERIA: All randomised controlled trials and quasi-randomised clinical trials in which allocation was not random but was intended to be unbiased (e.g. alternate allocation) were to have been selected. Since no such trials were discovered, all prospective and retrospective case series were included in 'background' or 'discussion' sections of the review. DATA COLLECTION AND ANALYSIS: All studies on multifocal motor neuropathy or lower motor neuron weakness with conduction block and no sensory abnormality were scrutinized for data on patients treated with any form of immunosuppressive agents besides intravenous immunoglobulin. The information on the outcome of treatment was then collated and summarised. MAIN RESULTS: We found no randomised controlled trials of any immunosuppressive agents for multifocal motor neuropathy. We summarised the results of retrospective and prospective case series in the discussion of the review. REVIEWER'S CONCLUSIONS: There are no randomised controlled trials to indicate whether immunosuppressive agents are beneficial in multifocal motor neuropathy.

Humans↗
PubMed2005

Immunosuppressant and immunomodulatory treatments for multifocal motor neuropathy.

BACKGROUND: Multifocal motor neuropathy is a distinct clinical entity characterised by progressive, predominantly distal, asymmetrical limb weakness and minimal sensory abnormality. The diagnostic feature of this condition is the presence of multiple partial motor nerve conduction blocks. Controlled trials have demonstrated the efficacy of regular intravenous immunoglobulin infusions. Immunosuppressive agents have been used as primary, second-line or adjunctive agents for its treatment. This review was undertaken to identify and review systematically randomised controlled trials of immunosuppressive agents. The use of intravenous immunoglobulin will be the subject of a separate review. OBJECTIVES: To provide the best available evidence from randomised controlled trials on the role of immunosuppressive agents for the treatment of multifocal motor neuropathy. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group trials register for all trials of multifocal motor neuropathy published, using 'multifocal motor neuropathy' OR 'chronic inflammatory demyelinating polyradiculoneuropathy' OR ' conduction block' OR ' motor neuropathy' AND 'immunosuppressive agents', 'immunosuppressants', 'corticosteroids', 'plasma exchange', 'azathioprine', 'cyclophosphamide', 'cyclosporin', 'ciclosporin', 'methotrexate', and 'mycophenolate', 'immunomodulatory agents', 'interferon', 'total lymphoid irradiation' or 'bone marrow transplantation' as search terms. In addition we searched MEDLINE, EMBASE for 2000 and 2001 and CINAHL, LILACS for all years. We updated the register search in February 2004 and searched MEDLINE (January 1966 to end May 2004) and EMBASE (January 1980 to end May 2004). SELECTION CRITERIA: All randomised controlled trials and quasi-randomised clinical trials in which allocation was not random but was intended to be unbiased (e.g. alternate allocation) were to have been selected. Since no such trials were discovered, all prospective and retrospective case series were included in the 'background' or 'discussion' sections of the review. DATA COLLECTION AND ANALYSIS: All studies on multifocal motor neuropathy or lower motor neuron weakness with conduction block and no sensory abnormality were scrutinised for data on patients treated with any form of immunosuppressive agents besides intravenous immunoglobulin. The information on the outcome of treatment was then collated and summarised. MAIN RESULTS: We found no randomised controlled trials of any immunosuppressive agents for multifocal motor neuropathy. We summarised the results of retrospective and prospective case series in the discussion of the review. AUTHORS' CONCLUSIONS: There are no randomised controlled trials to indicate whether immunosuppressive agents are beneficial in multifocal motor neuropathy.

Humans↗
PubMed2004

Exercise for people with peripheral neuropathy.

BACKGROUND: Peripheral neuropathies are a wide range of diseases affecting the peripheral nerves. Demyelination or axonal degeneration gives rise to a variety of symptoms including reduced or altered sensation, pain, muscle weakness and fatigue. Secondary disability arises and this may result in adjustments to psychological and social function. Exercise therapy, with a view to developing strength and stamina, forms part of the treatment for people with peripheral neuropathy, particularly in the later stages of recovery from acute neuropathy and in chronic neuropathies. OBJECTIVES: The primary objective was to examine the effect of exercise therapy on functional ability in the treatment of people with peripheral neuropathy. In addition, secondary outcomes of muscle strength, endurance, broader measures of health and well being, as well as unfavourable outcomes were examined. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group register (July 2002 and updated February 2004) and MEDLINE (from January 1966 to June 2004), EMBASE (from January 1980 to June 2004), CINAHL (from January 1982 to July 2002) and LILACS (from January 1982 to July 2002) electronic databases. Bibliographies of all selected randomised controlled trials were checked and authors contacted to identify additional published or unpublished data. SELECTION CRITERIA: Any randomised or quasi-randomised controlled trial comparing the effect of exercise therapy with no exercise therapy or drugs or an alternative non-drug treatment on functional ability (or disability) in people with peripheral neuropathy at least eight weeks after randomisation was included. DATA COLLECTION AND ANALYSIS: Two reviewers independently selected eligible studies, rated the methodological quality and extracted data. MAIN RESULTS: Only one trial fully met the inclusion criteria. An additional two trials assessed outcomes less than eight weeks after randomisation and were also included. Methodological quality was poor for several criteria in each study. Data used in the three studies could not be pooled due to heterogeneity of diagnostic groups and outcome measures. The results of the included trials failed to show any effect of strengthening and endurance exercise programmes on functional ability in people with peripheral neuropathy. However, there is some evidence that strengthening exercise programmes were moderately effective in increasing the strength of tested muscles. REVIEWERS' CONCLUSIONS: There is inadequate evidence to evaluate the effect of exercise on functional ability in people with peripheral neuropathy. The results suggest that progressive resisted exercise may improve muscle strength in affected muscles.

Exercise Therapy↗
PubMed2007

Peripheral neuropathy associated with leflunomide: is there a risk patient profile?

PURPOSE: (i) To monitor the potential clinical neurotoxic symptoms in patients treated with leflunomide in daily practice and (ii) to describe the characteristics of patients presenting with this peripheral nervous system symptoms. METHOD: All patients treated with leflunomide between May 2000 and April 2003 and followed in the rheumatology department of the University Hospital participated in the study. Data concerning treatment patterns with leflunomide, demographic and disease characteristics were obtained from clinical charts. Neuropathy was diagnosed with nerve conduction study (NCS). Cases of neuropathy were described and then compared to other patients using univariate analyses. RESULTS: One hundred and thirteen patients were included in the study. M/F sex ratio was 0.45. Mean age at start of treatment was 55.6 years (range = 27-81). During the study period, eight incident cases of peripheral neuropathy and two cases of worsening of preexisting neuropathy were reported (incidence: 9.8%). Compared with other patients, neuropathy cases were older (69 vs. 54 years, p = 0.0006), more often diabetic (30% vs. 2.9%, p = 0.009) and more often treated with potentially neurotoxic drugs (20% vs. 1.9%, p = 0.039). At least one risk factor (potentially neurotoxic drug or diabetes) was found in 50% of patients with neuropathy versus 4% of patients without neuropathy (56% PPV, 96% NPV). CONCLUSION: Cases of toxic neuropathy have been observed during treatment of rheumatoid arthritis with leflunomide. Their occurrence seems to be associated with known risk factors. Careful monitoring of the patient's neurological status during leflunomide treatment is therefore mandatory.

Adult↗
PubMed1995

Thalidomide-induced neuropathy and genetic differences in drug metabolism.

A pharmacogenetic predisposition to thalidomide-induced neuropathy has been investigated. Differences of drug metabolism were examined in 16 patients with severe orogenital ulceration, who were treated with thalidomide (< or = 200 mg/day) for 0.3-5.0 years. Eight had evidence of early peripheral neuropathy according to nerve conduction studies. Rates of C-hydroxylation, N-acetylation, and conjugation reactions with sulphate, glucuronide and glycine, were tested with the probe compounds debrisoquine, sulphadimidine, paracetamol and aspirin, respectively. Urinary drug metabolites were analysed by high pressure liquid chromatography. Results were compared with 16 healthy age- and sex-matched volunteers. Of the patients 6.25% and 13.3% of the controls had a poor Debrisoquine Hydroxylator Ratio (DMR); none of the patients with neuropathy had a poor DMR as compared to 12.5% without neuropathy. Of the patients 40.0% and 35.7% of the controls were slow acetylators; 28.6% with neuropathy were slow acetylators as opposed to 50% without neuropathy. Similarly, there were no significant differences in rates of conjugation between groups. All unaffected patients were active smokers, whereas only two of those with neuropathy smoked. Cumulative dose or duration of therapy were unrelated to risk of neuropathy. In conclusion, changes of nerve conductivity are a frequent and unpredictable adverse effect of thalidomide (< or = 200 mg/day), although smoking may have a protective action against their development. Nerve conduction studies are required before and during treatment, irrespective of the prescribed dose.

Acetylation↗
PubMed1995

Autonomic neuropathy and prolongation of QT interval in human immunodeficiency virus infection.

Autonomic neuropathy has been reported in human immunodeficiency virus positive (HIV+) patients. Since alterations in cardiac innervation may determine QT interval prolongation, this interval was studied in a group of HIV+ subjects to evaluate if it is prolonged and to compare this measurement with other diagnostic tests for autonomic neuropathy. Fifty-seven HIV+ and 23 human immunodeficiency virus negative (HIV-) subjects were studied. Autonomic function was tested by noninvasive cardiovascular reflex tests, and the QT interval on the electrocardiogram was measured at rest, at maximum tachycardia during Valsalva manoeuvre, and afterwards at maximum bradycardia. QT intervals were corrected for heart rate according to Bazzett's formula (QTc). Autonomic neuropathy was found in 37 HIV+ subjects: 25 had moderate autonomic neuropathy (HIV+/mAN) and twelve had severe autonomic neuropathy (HIV+/sAN). The 23 HIV- and 20 HIV+ (HIV+/AN-) patients did not have autonomic neuropathy. QTc intervals were significantly longer in HIV+/sAN and HIV+/mAN than in HIV- at rest; in HIV+/sAN than in HIV- at maximum tachycardia; in HIV+/sAN and HIV+/mAN than in HIV+, in HIV+/sAN and HIV+/mAN than in HIV+/AN- and in HIV+/sAN than in HIV+/mAN at maximum bradycardia. QTc was > or = 440 ms in 24 out of 37 (64.8%) patients with autonomic neuropathy and in five out of 20 (25%) HIV+/AN- patients (sensitivity 65%, specificity 75%). A significant correlation was observed between scores of autonomic involvement and QTc interval prolongation. This study confirms that the QTc measurement is a reliable parameter indicating the presence of autonomic neuropathy. Since QT prolongation may determine ventricular arrhythmias, such patients must be followed because they may be at increased risk of sudden death.

Adult↗
PubMed1995

Prevalence of pudendal neuropathy in fecal incontinence. Results of a prospective study.

PURPOSE: A prospective study was made of the prevalence and associations of pudendal neuropathy in 96 patients with fecal incontinence (72 females and 24 males). METHODS: Clinical exploration, perineal level measurement, anorectal manometry, and electrophysiologic evaluations (pudendal nerve terminal motor latency (PNTML) and external sphincter fiber density (FD)) were performed. RESULTS: Pudendal neuropathy (defined as PNTML > 2.2 ms or FD > 1.65) was found in 67 patients (69.8 percent) and was more common in females (75 percent) than in males (50 percent; P = 0.05). Pudendal neuropathy was also more frequent in patients with pathologic perineal descent (85 percent vs. 55 percent; P < 0.01) or exhibiting risk factors such as difficult labor or excessive defecatory straining (P < 0.01). Perineal level at staining correlated inversely with both PNTML and FD (P < 0.01). Manometric findings suggested greater external anal sphincter damage in patients with pudendal neuropathy than in those suffering fecal incontinence but no neuropathy (P < 0.05). Pressure caused by the striated anal sphincter was also inversely correlated to PNTML. Pudendal neuropathy was encountered in 37 of 33 (58.7 percent) patients with sphincter injury vs. in 31 of 33 (93.9 percent) patients with idiopathic fecal incontinence (P < 0.01). CONCLUSIONS: Pudendal neuropathy is an etiologic or associated factor often present in patients with fecal incontinence. In this sense, clinical, perineometric, and manometric findings correlate with pudendal neuropathy, though such explorations do not suffice to detect it.

Adolescent↗
PubMed1996

Unilateral pudendal neuropathy. Impact on outcome of anal sphincter repair.

PURPOSE: Our purpose was to study the effect of unilateral pudendal neuropathy on the results of anal sphincter repair. METHOD: Fifteen female patients who underwent external sphincter repair for fecal incontinence were studied. In all instances, incontinence was the result of obstetric delivery injury. Anal manometry and neurophysiologic investigations to document sphincter defects and pudendal neuropathy were performed in all patients. Sphincter repair was performed using an overlapping suture technique. RESULTS: All patients had anterior sphincter defects. Seven patients (47 percent) had pudendal neuropathy: six (85 percent) had unilateral neuropathy, and one (15 percent) had bilateral neuropathy. Six patients (40 percent) had excellent results; three (20 percent) had good results; four (27 percent) were improved; two (13 percent) experienced no improvement after sphincter repair. All patients with excellent results had normal pudendal nerve terminal motor latency on both sides. Of the three patients with good results, one patient had unilateral pudendal neuropathy. The patients in the remaining two groups (improved and failed) had unilateral (six patients) or bilateral (one patient) pudendal neuropathy. CONCLUSION: We conclude that both pudendal nerves must be intact to achieve normal continence after sphincter repair. Patients with unilateral pudendal neuropathy are more likely to have poor than to have good postoperative function.

Adult↗
PubMed2002

Chemotherapy-induced peripheral neuropathy.

The induction of peripheral neuropathy is a common factor in limiting therapy with chemotherapeutic drugs. Little is known about the mechanisms responsible for the development of neuropathy. Depending on the substance used, a pure sensory and painful neuropathy (with cisplatin, oxaliplatin, carboplatin) or a mixed sensorimotor neuropathy with or without involvement of the autonomic nervous system (with vincristine, taxol, suramin) can ensue. Neurotoxicity depends on the total cumulative dose and the type of drug used. In individual cases neuropathy can evolve even after a single drug application. A general predisposition for developing a chemotherapy-induced neuropathy has been observed in nerves previously damaged by diabetes mellitus, alcohol or inherited neuropathy. The recovery from symptoms is often incomplete and a long period of regeneration is required to restore function. Up to now, no drug is available to reliably prevent or cure chemotherapy-induced neuropathy.

Antineoplastic Agents↗
PubMed2005

[The role of the immune system in hereditary demyelinating neuropathies].

Hereditary neuropathies, e.g., Charcot-Marie-Tooth (CMT) disease, are inherited diseases of the peripheral nervous system causing chronic progressive motor and sensory dysfunction. Most neuropathies are due to mutations in myelin genes such as PMP22, P0, and the gap junction protein Cx32. Myelin mutant mice are regarded as suitable animal models for several forms of hereditary neuropathies and are important neurobiological tools for the evaluation of pathogenetic and therapeutic concepts in hereditary neuropathies. Using these animal models we could recently show that the immune system is involved in the pathogenesis of hereditary neuropathies. Due to the phenotypic similarities we also consider the immune system important for human inherited neuropathies, in particular since several case reports demonstrate a beneficial effect of immune therapies in patients with hereditary neuropathies. In this review we compare findings from animal models and human disease to elucidate the role of the immune system in hereditary neuropathies.

Animals↗
PubMed2003

Expression of matrix metalloproteinases in vasculitic neuropathy.

The aim of this study was to investigate the expression pattern and cellular source of matrix metalloproteinases (MMP) in vasculitic neuropathy. Matrix metalloproteinases are endopeptidases degrading components of extracellular matrix proteins, and they have been implicated in the pathogenesis of inflammatory demyelination. They are induced by cytokines, secreted by inflammatory cells, and enhance T cell migration. Vasculitic neuropathy occurs as a component of systemic vasculitis or as an isolated angiitis of the peripheral nervous system, and T cell-mediated inflammation is detected in its pathogenesis. Nerve biopsy sections of eight patients with nonsystemic vasculitic neuropathy (NSVN) and four with systemic vasculitic neuropathy were examined for the presence of CD4+, CD8+, and CD68+ cells and immunohistochemically for MMP-2 and MMP-9 expression. Nerve biopsies of eight patients with noninflammatory neuropathy were used as a control group. Semiquantitative polymerase chain reaction analysis was performed to detect MMP-2 and MMP-9 mRNA. The predominant cells were CD8+ and CD68+ T cells. Expression of MMP-9, but not MMP-2, was increased in perivascular inflammatory infiltrate in nerve tissues of vasculitic neuropathy patients. This MMP-9 expression correlated positively with immunostaining of CD8+ T cells. No difference was detected between immunostaining patterns of nonsystemic and systemic vasculitic neuropathies with the antibodies used, except in MMP-9 immunostaining, which was found to be enhanced in NSVN group. Polymerase chain reaction analysis revealed elevated mRNA levels of MMP-9 and MMP-2 compared with controls, but this did not reach statistical significance. Our results imply a pathogenic role for MMP-9 secreted from CD8+ cells in vasculitic neuropathy.

Adolescent↗
PubMed2004

Peripheral neuropathy in patients treated with leflunomide.

OBJECTIVE: Our objective was to describe the clinical features, time course, and outcome of new-onset peripheral neuropathy occurring in patients treated with leflunomide. METHODS: Case reports of peripheral neuropathy submitted to the US Food and Drug Administration in association with leflunomide use were reviewed. Data on patient demographics, underlying medical conditions and medications, details of leflunomide therapy, and treatment and outcome of the neuropathy event were abstracted. Time to neuropathy onset and time to improvement or recovery were analyzed by survival analysis. RESULTS: Of 80 reported patients, 61% were women. The patients' mean age was 62 years. Symptoms of peripheral neuropathy began after a mean of 6 months of leflunomide use (range, 3 days to 3 years). Electrodiagnostic testing in 37 patients was consistent with a distal axonal, sensory, or sensorimotor polyneuropathy in most patients. Patients who stopped leflunomide use within 30 days of neuropathy symptom onset were more likely to have improvement or recovery than those who continued taking leflunomide for a longer period (P <.001). CONCLUSION: Leflunomide use is associated with peripheral neuropathy in some patients. This neuropathy is usually axonal in nature, affecting multiple sensory or motor nerves of distal extremities. Patients who stopped leflunomide use within 30 days of symptom onset were more likely to have improvement of symptoms or complete recovery than were patients who continued to use the drug for longer periods of time.

Adverse Drug Reaction Reporting Systems↗
PubMed2005

[Peripheral neuropathies: the rational diagnostic process].

PURPOSES: Neuropathies are defined as dysfunction of peripheral nerves, which may show motor, sensory and autonomic symptoms. Although most neuropathies are symmetric, it is important to distinguish a polyneuropathy from a mononeuropathy, a multiple mononeuropathy or a polyradiculoneuropathy. Electrophysiological procedures are helpful in determining the pathological process which may be either an axonopathy, a myelinopathy or a neuronopathy. MAIN POINTS: Major progresses have been made in the ten past years in the management and diagnostic approaches of peripheral neuropathy. The history and the physical examination are the first steps to the evaluation of patients with peripheral neuropathy. Electrodiagnostic studies and then laboratory tests are the next step in the diagnostic procedures of peripheral neuropathies. These will lead to a proper identification of the cause of neuropathy, allowing to develop a specific treatment for the patient. However, even after a careful work-up of a patient with neuropathy, 25 to 40% of patients with polyneuropathies remain undiagnosed. PERSPECTIVES: Further development are focused in better understanding the pathogenesis and molecular mechanisms of peripheral nerve diseases in order to provide a specific and adequate treatment for each neuropathy.

Biopsy↗
PubMed1993

Peripheral neuropathies associated with monoclonal proteins.

Peripheral neuropathies associated with monoclonal proteins have received considerable attention as a clinically important group of chronic late-onset neuropathies. When a monoclonal protein is found in patients with peripheral neuropathy of unknown cause, as occurs in 10% of such cases, usually no associated disease is discovered; hence MGUS. Less often, disorders such as multiple myeloma, AL amyloidosis, Waldenström's macroglobulinemia, osteosclerotic myeloma, and lymphoma are found. Demyelinating neuropathies associated with MGUS of all classes, but particularly IgM, Waldenström's macroglobulinemia, and osteosclerotic myeloma typically follow an indolently progressive course, and frequently respond to treatments aimed at interfering with putative underlying immune mechanisms. By contrast, axonal neuropathies associated with MGUS, multiple myeloma, and AL amyloidosis have generally shown no response to therapy. Recently, IgM monoclonal and polyclonal antibodies directed against human peripheral nerve antigens including MAG and various glycolipids such as GM1 ganglioside have been found in patients with specific neuropathy syndromes. Anti-MAG antibodies occur in predominantly sensory demyelinating neuropathies, whereas elevated titers of anti-GM1 ganglioside antibodies are associated with lower motor neuron syndromes with multifocal motor conduction block. Although the evidence for autoimmune mechanisms in some monoclonal protein-associated neuropathies is mounting, a causal connection between monoclonal proteins and these neurologic syndromes has yet to be established.

Amyloidosis↗
PubMed2000

Does autonomic neuropathy influence spinal cord stimulation therapy success in diabetic patients with critical lower limb ischemia?

BACKGROUND: Spinal cord stimulation (SCS) improves microcirculatory blood flow and relieves diabetic neuropathic and ischemic pain, reducing the amputation rate in patients with peripheral arterial occlusive disease (PAOD). The purpose of this study was to evaluate whether the presence of autonomic neuropathy in diabetic patients with PAOD influences the success of SCS therapy. METHODS: Sixty consecutive diabetic patients (15 with early and 13 with definite and/or combined autonomic neuropathy) with an ankle/brachial systolic pressure index (ABI) less than 0.20 +/- 0.08, underwent spinal cord stimulation after failed conservative or surgical treatment. The neuropathic status of the patients was evaluated before implantation and pedal TcpO2 measurements on the dorsum of the foot were performed. RESULTS: Limb salvage and pain relief >75%, evaluated with the visual analogue scale, were achieved in 35 patients, whereas in 12 a partial success with pain relief >50% and limb salvage for at least 6 months were obtained. In 13 patients the method failed and the ischemic limbs were amputated. Among the 28 diabetic patients with autonomic neuropathy the treatment failed or resulted in only partial success in 25, whereas in all 32 patients without neuropathy limb salvage and pain relief >75% were achieved (p < 0.0001). Partial success in 10 patients with early neuropathy and in two with definite was achieved (p = 0.008), whereas in 11 patients with definite neuropathy and in two with early the method failed (p < 0.001). The stage of the neuropathy was inversely related to the success of SCS therapy, independent of the stage of the disease. The method's success was related to the presence of adequate paraesthesias and warm feeling in the painful area with size reduction of the trophic lesions. CONCLUSIONS: Diabetic patients with peripheral arterial occlusive disease presenting with intractable pain may be successfully treated with spinal cord stimulation unless they have associated severe autonomic neuropathy.

Aged↗
PubMed2003

Acquired peripheral neuropathy.

The element of time is a crucial factor in the electrodiagnostic presentation of PN. The characteristic changes seen in various neuropathies evolve over time. If testing is performed very early in the course of the disease, abnormalities may not yet be present, in part, because the range of normal values for NCS parameters is broad. In addition, if the process is asymmetric, the affected nerves may not be sampled. Very late in the course of the disease, a multifocal process may appear diffuse and symmetric as the areas of focal involvement coalesce. A primarily, demyelinating process may begin to demonstrate secondary axonal involvement. In very severe neuropathies, it may become difficult to evoke any NCS responses to characterize the neuropathy. It is essential to place the electrodiagnostic findings within the context of the clinical progression to avoid drawing erroneous conclusions. Sometimes, the true nature of the neuropathy is clear only after sequential testing. The etiologic diagnoses of acquired polyneuropathy are vast. A well-crafted electrodiagnostic evaluation can categorize neuropathies into more specific diagnostic groups by identifying the descriptive diagnosis, significantly narrowing the list of possible etiologic diagnoses. Electrodiagnostic testing, which always starts with a pertinent history and physical examination, should always be viewed as a continuation and quantification of the physical examination. Only by knowing the extent and pattern of the clinical involvement is it possible to formulate a thorough electrodiagnostic evaluation. This knowledge is especially important in cases in which the presentation is multifocal, because the neuropathy can be missed entirely if the affected nerves are not evaluated. When evaluating a neuropathy, there are three important questions to answer: (1) Is the process diffuse or multifocal? (2) Is it demyelinating or axonal? (3) Does it predominantly involve the motor or sensory nerves? By assessing the neuropathy along these three axes, the large number of possible etiologic diagnoses becomes much more manageable.

Diagnosis, Differential↗
PubMed2001

Mitochondrial alterations with mitochondrial DNA depletion in the nerves of AIDS patients with peripheral neuropathy induced by 2'3'-dideoxycytidine (ddC).

The 2'3'-dideoxycytidine (ddC), a nonazylated dideoxynucleoside analog used for the treatment of AIDS, causes a dose-dependent, painful, sensorimotor axonal peripheral neuropathy in up to 30% of the patients. To investigate the cause of the neuropathy, we performed morphological and molecular studies on nerve biopsy specimens from well-selected patients with ddC-neuropathy and from control subjects with disease, including patients with AIDS-related neuropathy never treated with ddC. Because ddC, in vitro, inhibits the replication of mitochondrial DNA (mtDNA), we counted the number of normal and abnormal mitochondria in a 0.04 mm(2) cross-sectional area of the nerves and quantified the copy numbers of mtDNA by competitive PCR in all specimens. A varying degree of axonal degeneration was present in all nerves. Abnormal mitochondria with enlarged size, excessive vacuolization, electron-dense concentric inclusions and degenerative myelin structures were prominent in the ddC-neuropathy and accounted for 55% +/- 2.5% of all counted mitochondria in the axon and Schwann cells, compared with 9% +/- 0.7% of the controls (p < 0.001). Significantly (p < 0.005) reduced copy numbers, with as high as 80% depletion, of the mtDNA was demonstrated in the nerves of the ddC-treated patients compared with the controls. We conclude that ddC induces a mitochondrial neuropathy with depletion of the nerve's mtDNA. The findings are consistent with the ability of ddC to selectively inhibit the gamma-DNA polymerase in neuronal cell lines. Toxicity to mitochondria of the peripheral nerve is a new cause of acquired neuropathy induced by exogenous toxins and may be the cause of neuropathy associated with the other neurotoxic antiretroviral drugs or toxic-metabolic conditions.

Acquired Immunodeficiency Syndrome↗