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PubMed2003

Positive salivary gland biopsy, Sjögren syndrome, and neuropathy: clinical implications.

The relationship between neuropathy and Sjögren syndrome has been predicated largely on sicca symptoms or serological abnormalities rather than salivary gland pathology. We reviewed consecutive neuropathy patients who had had a lip biopsy to identify features of the neuropathy that were associated with a positive lip biopsy suggesting Sjögren syndrome. Twenty of 54 neuropathy patients were biopsy positive; 13 had a painful or nonspecific sensory neuropathy and only 4 were ataxic. Sicca symptoms were not associated with a positive biopsy (P = 0.14). Serological abnormalities were found more often in the biopsy-positive group (P = 0.008), but anti-Sjögren syndrome A or B (anti-SSA or SSB) antibodies were detected in only 30%. There were no other clinical or electromyographic (EMG) features associated with a positive biopsy. From this experience, we conclude that: (1). most patients with neuropathy and a positive lip biopsy for Sjögren syndrome have a painful, distal, sensory axonal neuropathy; (2). there are no clinical or EMG features that are predictive of a positive lip biopsy; (3). ataxic neuropathy is uncommon; and (4). the lack of sicca symptoms or anti-SSA or SSB antibodies in patients with neuropathy does not exclude Sjögren syndrome based upon salivary gland pathology.

Adult↗
PubMed1989

Reversible axonal neuropathy from the treatment of AIDS and related disorders with 2',3'-dideoxycytidine (ddC).

A total of 20 patients with acquired immune deficiency syndrome (AIDS) or AIDS-related complex (ARC) received the anti-retroviral drug 2',3',dideoxycytidine in a phase I study at doses ranging from 0.03 mg/kg every 8 hours to 0.25 mg/kg every 8 hours. Of the 11 patients who participated in the study for more than 5 weeks, 9 developed symptoms and signs of a mainly sensory painful neuropathy that was confirmed by electromyography to be mixed sensory and motor neuropathy of axonal type. The neuropathy which developed on dideoxycytidine occurred between 9 and 12 weeks of treatment. One patient, who had the drug stopped at 3 weeks owing to thrombocytopenia, developed a similar clinical picture of a sensory peripheral neuropathy after 2 weeks off dideoxycytidine. However, he did not have electromyographic evidence of a neuropathy, and he subsequently returned to normal clinically while taking a lower dose of dideoxycytidine in an alternating regimen. Five patients were withdrawn from the study because of the neuropathy. The pattern of this neuropathy was different from that of the slowly progressive painful neuropathy of AIDS, in that there was (1) a sudden onset of intense burning discomfort in both feet sparing the hands at about the tenth week (mean 10.4 weeks) of treatment, (2) there was motor involvement in some patients without progression, and (3) onset of the neuropathy was temporally related to the administration of dideoxycytidine and began to resolve 3-5 weeks after its discontinuation. We believe that dideoxycytidine can be an axonal toxin, especially when given in high dose continuous regimens.(ABSTRACT TRUNCATED AT 250 WORDS)

AIDS-Related Complex↗
PubMed1993

Interactions between neuropathy target esterase and its inhibitors and the development of polyneuropathy.

This paper combines new and old data in order to offer a modified perspective of the mechanism of organophosphate-induced delayed polyneuropathy. Neuropathy target esterase (NTE) is though to be the molecular target and neuropathy to be initiated with a two-step mechanism: progressive inhibition of NTE and aging of the phosphorylated enzyme. When neuropathic organophosphates modify more than 70% of NTE in this way, neuropathy develops 2 weeks later. Other chemicals producing an inhibited NTE, which is incapable of aging, were thought to be not neuropathic. When given before a challenging dose of a neuropathic organophosphate they protect animals from neuropathy. However, recent evidence indicates that aging may not always be essential in causing neuropathy. In fact, mipafox and methamidophos as well as certain classic protective inhibitors such as carbamate and sulfonyl fluoride form an inhibited NTE which apparently does not age and yet produces neuropathy. We propose that all NTE inhibitors may have the potential to cause neuropathy. In analogy with pharmacological models of drug-receptor interactions, NTE inhibitors might have variable intrinsic activities to initiate neuropathy once attached to the protein. Strong neuropathic chemicals require about 70% inhibition of NTE, others 80-90%, and the least potent almost 100%. These differences have been amplified by means of promotion. Different levels of NTE inhibition as caused by different compounds were promoted by the same dose of phenylmethanesulfonyl fluoride to similar degrees of ataxia. Conversely nearly complete NTE inhibitions obtained in chicks with different chemicals were promoted to varying severities of ataxia. Protection from delayed polyneuropathy by the least neuropathic inhibitors can be explained by their weak intrinsic activity: occupying NTE, they prevent the binding of more neuropathic compounds. Methamidophos represents a particular example because it is protective at lower doses and neuropathic at high doses. Moreover, the levels of NTE inhibited by methamidophos which can be promoted to neuropathy are lower than those required for classic protective chemicals and higher than those of classic neuropathic OPs. This suggests that methamidophos has an intermediate position between the most and the least neuropathic NTE inhibitors.

Animals↗
PubMed2001

Neuropathy and malignancy: a retrospective survey.

Peripheral neuropathy is a common condition with a variety of causes. In some cases the neuropathy is the first symptom of an underlying malignancy. The frequency of occult cancer in patients with neuropathy is of importance in planning the investigations and follow-up of these patients. This retrospective study examined the incidence of cancer-related neuropathy among patients originally diagnosed with idiopathic peripheral neuropathy. Between 1981-1995 our department discharged 187 patients with the diagnosis of idiopathic peripheral neuropathy. Their names were cross-matched with the Norwegian Cancer Registry, and the medical records of the patients with known cancer were reviewed. In 14 patients (7.5%) we found cancer as the probable cause of the peripheral neuropathy originally classified as idiopathic. In eight of the patients the neuropathic symptoms preceded the tumour. In six cancer was already diagnosed when the neuropathic symptoms developed, but in three of these the neuropathy heralded a tumour recurrence. Idiopathic progressive neuropathy should always raise the suspicion of an underlying malignancy, especially if there are atypical accompanying symptoms and signs.

Adult↗
PubMed2004

Optical coherence tomography can measure axonal loss in patients with ethambutol-induced optic neuropathy.

PURPOSE: To map and identify the pattern, in vivo, of axonal degeneration in ethambutol-induced optic neuropathy using optical coherence tomography (OCT). Ethambutol is an antimycobacterial agent often used to treat tuberculosis. A serious complication of ethambutol is an optic neuropathy that impairs visual acuity, contrast sensitivity, and color vision. However, early on, when the toxic optic neuropathy is mild and partly reversible, the funduscopic findings are often subtle and easy to miss. METHODS: Three subjects with a history of ethambutol (EMB)-induced optic neuropathy of short-, intermediate-, and long-term visual deficits were administered a full neuro-ophthalmologic examination including visual acuity, color vision, contrast sensitivity, and fundus examination. In addition, OCT (OCT 3000, Humphrey-Zeiss, Dublin, CA) was performed on both eyes of each subject using the retinal nerve fiber layer (RNFL) analysis protocol. OCT interpolates data from 100 points around the optic nerve to effectively map out the RNFL. RESULTS: The results were compared to the calculated average RNFL of normal eyes accumulated from four prior studies using OCT, n=661. In all subjects with history of EMB-induced optic neuropathy, there was a mean loss of 72% nerve fiber layer thickness in the temporal quadrant (patient A, with eventual recovery of visual acuity and fields, 58% loss; patient B, with intermediate visual deficits, 68% loss; patient C, with chronic visual deficits, 90% loss), with an average mean optic nerve thickness of 26+/-16 microm. There was a combined mean loss of 46% of fibers from the superior, inferior, and nasal quadrants in the (six) eyes of all three subjects (mean average thickness of 55+/-29 microm). In both sets (four) of eyes of the subjects with persistent visual deficits (patients B and C), there was an average loss of 79% of nerve fiber thickness in the temporal quadrant. CONCLUSIONS: The OCT results in these patients with EMB-induced optic neuropathy show considerable loss especially of the temporal fibers. This is consistent with prior histopathological studies that show predominant loss of parvo-cellular axons (or small-caliber axons) within the papillo-macular bundle in toxic or hereditary optic neuropathies. OCT can be a valuable tool in the quantitative analysis of optic neuropathies. Additionally, in terms of management of EMB-induced optic neuropathy, it is important to properly manage ethambutol dosing in patients with renal impairment and to achieve proper transition to a maintenance dose once an appropriate loading dose has been reached.

Aged↗
PubMed1996

Coexistent entrapment neuropathies in patients with amyotrophic lateral sclerosis.

OBJECTIVE: To determine the incidence of entrapment neuropathy in patients with amyotrophic lateral sclerosis (ALS). Although it is well known that patients with motor neuron disease may have coexisting focal neuropathies, their prevalence has not been previously determined. METHODS: Electrophysiologic studies (EMG/NCS) were reviewed from 126 patients with ALS seen at a university-affiliated hospital from 1991 to 1994. Every patient had an EMG/ NCS consistent with motor neuron disease (i.e., active and chronic denervation in at least 3 body regions). RESULTS: Forty-three percent (54 patients) had evidence of a neuropathy. Abnormalities included median neuropathy at the wrist in 15 (12%), ulnar neuropathy at the elbow in 18 (14%), nonlocalized ulnar neuropathy in 10 (8%), and peroneal neuropathy at the fibular head in 2 (2%). Furthermore, 9 patients (7%) had a superimposed polyneuropathy. Of these 54 patients, 7 (13%) had clinical symptoms of their neuropathy. CONCLUSIONS: Coexistent focal or generalized neuropathies in ALS are not uncommon. Careful attention to these abnormalities may decrease morbidity in these patients.

Adult↗
PubMed1998

The distribution of CD1 molecules in inflammatory neuropathy.

The CD1 molecules have been shown to present non-protein antigens, such as complex lipids to Mycobacteria, and may be important in presenting glycolipids which are involved in inflammatory neuropathies. To study the expression of CD1 molecules in peripheral nerve, we examined nerve biopsies from two patients with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), five with acute axonal neuropathy, six with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), nine with chronic axonal neuropathy, six with vasculitic neuropathy and three with no histological abnormality. Immunocytochemical studies showed strong labelling of CD1b on endoneurial macrophages (CD68+) and on myelinated nerve fibres in both AIDP patients, but it was rarely observed in the other patients. Weaker staining was seen on endoneurial macrophages and/or other endoneurial cells in some of the patients with other peripheral neuropathies, but none of the control nerves. CD1a had a weaker, but similar pattern. There was endoneurial infiltration of CD4+ and CD8+ T cells in the AIDP and CIDP nerves and sometimes in the other peripheral neuropathy nerves, but not in the normal nerves. Most T cells had alpha beta+ T cell receptors (TCR), but gamma delta+ TCR T cells were found in the nerves of both AIDP patients and sometimes in the nerves of other patients with peripheral neuropathy. Staining for mannose receptor was almost universal, being more intense in AIDP, chronic axonal neuropathy and vasculitis patients. We conclude that CD1 molecule expression is upregulated in peripheral neuropathy, especially in association with inflammation.

Aged↗
PubMed2001

[Peripheral neuropathy and hepatitis C virus infection: more than cryoglobulinemia].

PURPOSE: To study characteristics of peripheral neuropathies associated with hepatitis C virus infection. METHODS: A study of two groups of four patients with peripheral neuropathy and infected with hepatitis C virus, and a literature review. RESULTS: We observed four cases of peripheral neuropathy in patients with hepatitis C virus infection with persistent negativity of mixed cryoglobulinemia, and with no purpura, rheumatoid factor, or low C4 level. Neuropathy improved with treatment in three patients between 8 and 28 months after treatment was begun. We report four other observations of peripheral neuropathy with mixed cryoglobulinemia. Worsening of peripheral neuropathy was observed 2 to 13 weeks after initiation of interferon alpha despite improvement of hepatic parameters. After stopping interferon, peripheral neuropathy worsened (one case), stabilized (one case), or improved (two cases). DISCUSSION: In patients infected with hepatitis C virus, peripheral neuropathy can be due to mixed cryoglobulinemia, periarteritis nodosa, and perhaps hepatitis C virus itself as suggested by our first observations. Low doses of interferon alpha may worsen peripheral neuropathy in patients with mixed cryoglobulinemia, as suggested in our later observations.

Adult↗
PubMed2001

Epidemiology and clinical features of HIV-1 associated neuropathies.

Peripheral neuropathy is common in human immunodeficiency virus type-1 (HIV-1) infection. Peripheral neuropathies complicate all stages of the HIV-1 disease and cause considerable morbidity and disability in HIV-1 infected individuals and acquired immunodeficiency syndrome (AIDS) patients. Whereas symptomatic neuropathies occur in approximately 10% to 15% of HIV-1-infected patients overall, pathologic evidence of peripheral nerve involvement is present in virtually all end-stage AIDS patients. There are 6 major clinical types of HIV-associated neuropathies that are regularly seen in large HIV-1 clinics. Distal sensory polyneuropathy (DSP) is the most common among the HIV-1-associated neuropathies. DSP generally occurs in later stages of HIV-1 infection and it follows an indolent and protracted clinical course. The dominant clinical features in DSP include distal pain, paresthesia and numbness in a typical length-dependent fashion with proximal to distal gradient. Whereas toxic neuropathies--secondary to certain antiretroviral agents--are clinically similar to DSP, their temporal relation to neurotoxic medication helps distinguish them from other HIV-1-associated neuropathies. DSP and toxic neuropathy may coexist in a single patient. Acute and chronic inflammatory demyelinating polyradiculoneuropathies (AIDP and CIDP) produce global limb weakness. AIDP may occur at seroconversion and it can therefore be the initial manifestation of HIV-1 infection. CIDP generally occurs in the mid to late stages of HIV-1 infection. Progressive polyradiculopathy (PP) occurs in patients with advanced immunodeficiency and is generally caused by the opportunist cytomegalovirus (CMV) infection. Mononeuropathy multiplex (MM) in early stages of HIV-1 infection is immune mediated, whereas in advanced AIDS it is caused by the CMV infection. Finally, subclinical autonomic nervous system involvement is common in all stages of HIV-1 infection. Because HIV-1-associated neuropathies are diverse in their etiology and pathogenesis, a precise clinical diagnosis is required to formulate a rational therapeutic intervention.

HIV Infections↗
PubMed1996

A prospective study of suramin-induced peripheral neuropathy.

Suramin is an investigational drug that has shown therapeutic activity in hormone-refractory metastatic prostate cancer in Phase I/II trials. Dose-limiting neurotoxicity remains the most serious complication of suramin treatment. We performed a prospective study to define the incidence, severity, characteristics, and dose relationships of suramin-induced peripheral neuropathy. Twenty-two patients who received suramin in a Phase-I trial underwent baseline and serial follow-up neurological evaluations consisting of history, examination, nerve conduction studies and quantitative sensory testing (QST). Suramin was administered intravenously in escalating dosages by using a 5-day schedule (repeated monthly), with the dose, determined by a population pharmacokinetic model, to accomplish 30-min post-infusion concentrations of 300 micrograms ml-1 (cohort I), 350 micrograms m-1 (cohort II) and 400 micrograms ml-1 (cohort III). Twelve patients developed a mild, axonal, length-dependent, sensory-motor poly-neuropathy. Three other patients developed a subacutely progressive, functionally disabling, demyelinating neuropathy; sural nerve biopsy in two patients showed lymphocytic inflammation. These three patients improved after drug discontinuation and plasmapheresis. Although there was no apparent correlation between the cumulative dose and the severity of the neuropathy, no patient from cohort I, but 88% of patients from cohorts II and III, developed neuropathy. We conclude that when suramin is used at peak concentrations of > or = 350 micrograms ml-1 its administration is associated with two patterns of neuropathy, a distal axonal neuropathy and an inflammatory demyelinating neuropathy that is partially reversible. Neurological monitoring for development of neuropathy will improve the safety of suramin use in future clinical studies.

Aged↗
PubMed2004

Calpain inhibition protects against Taxol-induced sensory neuropathy.

Taxol is a highly effective anticancer agent that causes peripheral neuropathy as its major toxic side effect. The neuropathy is characterized by degeneration of sensory axons that may be severe enough to be dose limiting. Axonal degeneration involves the activation of the calcium-activated proteases calpains, and here we tested whether systemic inhibition of calpains with the peptide alpha-ketoamide calpain inhibitor AK295 can reduce the clinical and pathological effects of Taxol in a rodent model of Taxol neuropathy. In mice with Taxol neuropathy, AK295 reduced the degree of axonal degeneration in sensory nerve roots, and improved clinical measures of neuropathy, including behavioural and electrophysiological function. These findings were consistent for both 3- and 6-week models of neuropathy. In vitro, Taxol caused activation of both calpains and caspases in PC12 cells. AK295 inhibited the activation of calpains but did not interfere with the antimitotic effects of Taxol on microtubules, nor did it inhibit caspase-mediated cell death. These data implicate calpains in the pathogenesis of Taxol neuropathy, and demonstrate that AK295 can prevent axonal degeneration and clinical neuropathy in mice. In addition, AK295 did not interfere with the primary antineoplastic effects of Taxol on microtubules and cell death, suggesting that systemic calpain inhibition may be a good strategy for preventing neuropathy in patients being treated with Taxol.

Animals↗
PubMed1994

Lower-extremity motor neuropathy associated with surgery performed on patients in a lithotomy position.

BACKGROUND: Motor neuropathy of a lower extremity is well-recognized as a potential complication of procedures performed on patients in a lithotomy position. Most of this awareness is based on anecdotal reports, however, and the incidence and risk factors for this complication have not been reported. METHODS: We retrospectively reviewed the perioperative courses of 198,461 consecutive patients who underwent 1 of 56 surgical procedures historically performed on patients in a lithotomy position at the Mayo Clinic, Rochester, Minnesota, from 1957 to 1991 inclusive. The medical diagnoses of patients who had procedures in a lithotomy position were scanned for 26 diagnoses associated with neuropathy. Persistent neuropathy of the lower extremity was defined as a motor deficit of at least 3 months' duration. Risk factors anecdotally associated with persistent neuropathy were analyzed by comparing identified cases of neuropathy to controls in a 1:3 case-control study. RESULTS: Persistent neuropathies after procedures performed on patients in a lithotomy position were identified in 55 cases for a rate of 1 per 3,608. Multivariate risk factors for development of a persistent neuropathy of a lower extremity included duration in lithotomy of 4 h or longer, a body mass index (kilograms per squared meter) of 20 or less, and a history of smoking within 30 days of the procedure. Regional anesthetic techniques were not found to be associated with an increased risk of neuropathy. Of the 53 patients who lived at least 1 yr after their procedure, 24 (45%) required either prosthetic or ambulatory support for persistent foot drop or leg weakness. CONCLUSIONS: These data suggest that prolonged duration in lithotomy and patient risk factors, including very thin body habitus and smoking in the preoperative period, are associated with the development of a lower-extremity neuropathy after procedures performed on patients in a lithotomy position. A reduction of time in the lithotomy position may be particularly worthwhile for patients with these risk factors.

Adolescent↗
PubMed2003

Familial auditory neuropathy.

OBJECTIVES/HYPOTHESIS: Auditory neuropathy is a sensorineural hearing disorder characterized by absent or abnormal auditory brainstem responses and normal cochlear outer hair cell function as measured by otoacoustic emission recordings. Many risk factors are thought to be involved in its etiology and pathophysiology. Four Chinese pedigrees with familial auditory neuropathy were presented to demonstrate involvement of genetic factors in the etiology of auditory neuropathy. STUDY DESIGN: Probands of the above-mentioned pedigrees, who had been diagnosed with auditory neuropathy, were evaluated and followed in the Department of Otolaryngology-Head and Neck Surgery, China People Liberation Army General Hospital (Beijing, China). Their family members were studied, and the pedigree maps established. METHODS: History of illness, physical examination, pure-tone audiometry, acoustic reflex, auditory brainstem responses, and transient evoked and distortion-product otoacoustic emissions were obtained from members of these families. Some subjects received vestibular caloric testing, computed tomography scan of the temporal bone, and electrocardiography to exclude other possible neuropathic disorders. RESULTS: In most affected patients, hearing loss of various degrees and speech discrimination difficulties started at 10 to 16 years of age. Their audiological evaluation showed absence of acoustic reflex and auditory brainstem responses. As expected in auditory neuropathy, these patients exhibited near-normal cochlear outer hair cell function as shown in distortion product otoacoustic emission recordings. Pure-tone audiometry revealed hearing loss ranging from mild to profound in these patients. Different inheritance patterns were observed in the four families. In Pedigree I, 7 male patients were identified among 43 family members, exhibiting an X-linked recessive pattern. Affected brothers were found in Pedigrees II and III, whereas in pedigree IV, two sisters were affected. All the patients were otherwise normal without evidence of peripheral neuropathy at the time of writing. CONCLUSION: Patients with characteristics of nonsyndromic hereditary auditory neuropathy were identified in one large and three smaller Chinese families. Pedigree analysis suggested an X-linked, recessive hereditary pattern in one pedigree and autosomal recessive inheritances in the other three pedigrees. The phenotypes in the study were typical of auditory neuropathy; they were transmitted in different inheritance patterns, indicating clinical and genetic heterogeneity of this disorder. The observed inheritance and clinical audiological findings are different from those previously described for nonsyndromic low-frequency sensorineural hearing loss. This information should facilitate future molecular linkage analyses and positional cloning for the relative genes contributing to auditory neuropathy.

Adolescent↗
PubMed2004

IgM paraproteinaemic neuropathies.

PURPOSE OF REVIEW: To conduct a critical review of recent studies on the pathogenesis and treatment of IgM paraproteinaemic neuropathies and analyse their implication for patient management. RECENT FINDINGS: A better definition and classification of IgM monoclonal gammopathies has led to recommendations on therapeutic strategies for these patients, particularly for those with the asymptomatic form of Waldenström macroglobulinemia. Studies on the pathogenetic role of IgM paraprotein in neuropathy have led to the identification of a novel antibody reactivity against trisulfated heparin disaccharide, which was associated with painful, predominantly sensory, axonal distal neuropathy. Pathological studies on patients with axonal polyneuropathy and no antibody reactivity of the IgM paraprotein have shown that vasculitis may play an important role in this form of neuropathy, as possibly confirmed by its positive response to steroids. A number of open pilot trials have addressed the effect in IgM paraproteinaemic neuropathies of the humanized monoclonal antibody (rituximab) directed against the CD20 antigen. Even if the results of these studies are less promising than initially hoped, they provide evidence that rituximab may be effective in some patients with this neuropathy. SUMMARY: New insights into the pathogenesis of axonal forms of IgM paraproteinaemic neuropathy have derived from the identification of novel antibody reactivity and of vasculitis. The latter finding may justify the use of steroids, otherwise ineffective in IgM paraproteinaemic neuropathy. Rituximab has opened the way to more selective and apparently safer immune therapies for this neuropathy, but its efficacy needs to be confirmed by randomized controlled trials.

Antibodies, Monoclonal↗
PubMed2004

Relationship between loss of pedal sensibility, balance, and falls in patients with peripheral neuropathy.

: The purpose of this study was to describe the relationship between balance and foot sensibility in a population of patients with impaired lower extremity sensation. The hypothesis was that increasing impairment of sensation correlates with impaired balance. To date, no report has investigated the relationship between loss of balance with the degree of sensibility in the foot in a population with neuropathy. Ten control subjects and 35 patients with sensory abnormalities and balance problems related to a neuropathy were evaluated. The MatScan Measurement System was used to measure their ability to stand still, maintaining their balance with their eyes open and then with their eyes shut. The degree to which the person moves while attempting to stand still is defined as "sway," which was recorded for normal and neuropathy patients. Sensibility of the foot was measured with the Pressure-Specified Sensory Device, which is noninvasive and nonpainful. The 1- and 2-point static touch thresholds are measured for the pulp of the big toe, medial heel, and the dorsum of the foot. Loss of 2- or 1-point sensation was recorded as sensibility score and compared with controls. Statistical analysis of data and their comparisons for the 2 groups was completed. There were 55% females in control and 64% in neuropathy patients, whereas average age was 50 and 62 years, respectively. Neuropathy was the result of diabetes in 64.5%, hypothyroidism in 19.3%, their combination in 13%, and of unknown etiology in the remaining 19% of patients. Controls had significantly lower mean sway than neuropathy patients (22.9 +/- 9% vs. 189.5 +/- 180%, P = 0.006). Likewise, sensibility score for normal and neuropathy patients was also significantly different (31.4 +/- 9% vs. 232.8 +/- 59%, P <0.0001). When compared with the controls, 99% upper limit of confidence, sensibility in the neuropathy group at the hallux pulp was abnormal at a level consistent with axonal loss in 52% and was completely absent in the remaining 48%. Similarly, at the heel, sensibility was normal in 6.5%, abnormal at a level consistent with axonal loss in 71%, and absent in the remaining 22.5%. The correlation coefficient between sway and sensibility score was 0.36. The results of this investigation for the first time document the intuitive relationship between increasing loss of foot sensibility and increasing loss of balance. These measurements can now be used prospectively to evaluate whether restoration of sensation to patients with neuropathy, through peripheral nerve decompression, can improve balance and reduce falls/fractures in this patient population.

Accidental Falls↗
PubMed2005

Multifocal motor neuropathy.

PURPOSE OF THIS REVIEW: To conduct a critical review of recent studies on the clinical and therapeutic aspects of multifocal motor neuropathy, and to analyse their implications for patient management. RECENT FINDINGS: Recent studies have contributed to defining the specific position of multifocal motor neuropathy within the spectrum of chronic immune-mediated polyneuropathies. One study compared features of this condition with multifocal acquired demyelinating sensory and motor neuropathy, while others have focused on pathological alterations at the site of conduction blocks. A further study described six new cases of multifocal acquired motor neuropathy, which should be considered as a variant of multifocal motor neuropathy. Several Cochrane reviews and review articles have shown evidence of the efficacy of intravenous immunoglobulins in the treatment of multifocal motor neuropathy. The issue of long-term intravenous immunoglobulins in multifocal motor neuropathy, however, has yielded controversial results. Two studies have shown progressive motor deterioration in most patients, correlated with electrophysiological signs indicative of axonal degeneration, while a third study found signs of sustained clinical and electrophysiological improvement after a mean follow up of 7.25 years. SUMMARY: Multifocal motor neuropathy is a distinct clinical entity that differs from chronic inflammatory demyelinating polyradiculoneuropathy and multifocal acquired demyelinating sensory and motor neuropathy, although they share some electrophysiological characteristics. Although the aetiology remains unsolved, frequent association with high-titer antibodies against ganglioside GM1, together with an often positive response to intravenous immunoglobulins further support an autoimmune mechanism. New therapeutic strategies are required, however, that focus on the effects and the costs of treatment over long-term follow up.

Humans↗
PubMed1982

Benign monoclonal gammopathy and peripheral neuropathy.

Peripheral neuropathy has been described in malignant plasma cell dyscrasias such as multiple myeloma and Waldenstöm's macroglobulinaemia. Since it is not known whether the neuropathy is related to the plasma cell disorder or is a paramalignant phenomenon, 21 consecutive out-patients with benign monoclonal gammopathy (BMG) were analysed for peripheral neuropathies. Eleven patients had noticed slight motor and/or sensory extremity symptoms. Clinical examination, electromyographic and electroneurographic studies of the upper and lower extremities were performed. In five patients all results indicated a neuropathy, six other patients had clinical signs of neuropathy and four additional patients had positive electromyographic and/or electroneurographic results compatible with neuropathy. There were no significant differences in haematological parameters between the group where all results indicated a neuropathy and the totally negative group or between the two groups with and without clinical neuropathy. Thus, the benign form of plasma cell dyscrasias seems also to be associated with mild clinical or subclinical peripheral neuropathy.

Adult↗
PubMed1992

Peripheral neuropathy in essential mixed cryoglobulinaemia.

The prevalence of various forms of peripheral neuropathy has not been previously assessed in large series of patients with essential mixed cryoglobulinaemia (EMC). Clinical and electrophysiological signs of peripheral neuropathy were observed in 21 of 37 EMC patients, consisting of polyneuropathy in 19, mononeuropathy or multiple mononeuropathy in eight, and both in six. The various forms of peripheral neuropathy occurred differently in the subgroups of EMC. Isolated polyneuropathy was more common with type II (eight of 10) than type III EMC (two of eight). Multifocal neuropathy, in association with polyneuropathy, was the most common form in type III EMC (five of eight). Patients with peripheral neuropathy and type II EMC were significantly older than type II EMC patients without neuropathy, regarding present age and age of onset of EMC. Patients with peripheral neuropathy and type III EMC tended to have higher values of ESR and IgM than type III EMC patients without neuropathy. Electrophysiological findings and sural nerve biopsy specimens (nine cases) showed prominent axonal changes. Vascular changes included vasculitis and alterations of the endoneurial microvessels in type II and type III EMC. Our findings suggest that distinct pathogenic factors are implicated in the subgroups of cryoglobulinaemic neuropathy, possibly inducing different types of vascular changes underlying polyneuropathy or, respectively, mononeuropathy and multiple mononeuropathy.

Adult↗