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PubMed2001

Optic neuropathy in uremia: an interdisciplinary emergency.

Optic neuropathy in uremia is rare. Although the consequences of optic neuropathy-blindness or substantial loss of vision-are devastating, only a few cases have been reported by way of single case reports and case series studies. The reported patients are heterogeneous with regard to the cause of neuropathy. We report the case of a patient with uremic optic neuropathy and summarize the other cases reported in the literature so far. Based on the data available from these reports, we propose a classification system, which includes nonischemic neurotoxic uremic optic neuropathy; ischemic optic neuropathy, more specifically anterior ischemic optic neuropathy; and optic neuropathy as a result of drug side effects, benign intracranial hypertension, and optic neuritis. The immediate institution of dialysis and corticosteroid therapy and correction of anemia and relative hypotension can optimize the chances of visual recovery for these patients. Close collaboration among nephrologists, ophthalmologists, and neurologists is important in this interdisciplinary emergency.

Anti-Inflammatory Agents↗
PubMed2001

Unipedal stance testing in the assessment of peripheral neuropathy.

OBJECTIVE: To define further the relation between unipedal stance testing and peripheral neuropathy. DESIGN: Prospective cohort. SETTING: Electroneuromyography laboratory of a Veterans Affairs medical center and a university hospital. PATIENTS: Ninety-two patients referred for lower extremity electrodiagnostic studies. MAIN OUTCOME MEASURES: A standardized history and physical examination designed to detect peripheral neuropathy, 3 trials of unipedal stance, and electrodiagnostic studies. RESULTS: Peripheral neuropathy was identified by electrodiagnostic testing in 32%. These subjects had a significantly shorter (p <.001) unipedal stance time (15.7s, longest of 3 trials) than the patients without peripheral neuropathy (37.1s). Abnormal unipedal stance time (<45s) identified peripheral neuropathy with a sensitivity of 83% and a specificity of 71%, whereas a normal unipedal stance time had a negative predictive value of 90%. Abnormal unipedal stance time was associated with an increased risk of having peripheral neuropathy on univariate analysis (odds ratio = 8.8, 95% confidence interval = 2.5--31), and was the only significant predictor of peripheral neuropathy in the regression model. Aspects of the neurologic examination did not add to the regression model compared with abnormal unipedal stance time. CONCLUSIONS: Unipedal stance testing is useful in the clinical setting both to identify and to exclude the presence of peripheral neuropathy.

Adult↗
PubMed2002

The clinical identification of peripheral neuropathy among older persons.

OBJECTIVE: To identify simple clinical rules for the detection of a diffuse peripheral neuropathy among older outpatients. DESIGN: Observational, blinded, controlled study. SETTING: A tertiary-care electrodiagnostic laboratory and biomechanics laboratory. PARTICIPANTS: One hundred research subjects, 68 with electrodiagnostic evidence of peripheral neuropathy, between the ages of 50 and 80 years. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASUREMENTS: One examiner, unaware of the results of electrodiagnostic testing, evaluated Achilles' and patellar reflexes, Romberg testing, semiquantified vibration, and position sense at the toe and ankle in all subjects, and unipedal stance time and the Michigan Diabetes Neuropathy Score in a subset of subjects. RESULTS: Significant group differences were present in all clinical measures tested. Three signs, Achilles' reflex (absent despite facilitation), vibration (128Hz tuning fork perceived for <10s), and position sense (<8/10 1-cm trials) at the toe, were the best predictors of peripheral neuropathy on both univariate and logistic regression (pseudo R(2)=.744) analyses. The presence of 2 or 3 signs versus 0 or 1 sign identified peripheral neuropathy with sensitivity, specificity, and positive and negative predictive values of 94.1%, 84.4%, 92.8%, and 87.1%, respectively. Values were similar among subgroups of subjects with and without diabetes mellitus. When other clinicians applied the technique to 12 more subjects, excellent interrater reliability regarding the presence of peripheral neuropathy (kappa=.833) and good to excellent interrater reliability for each sign (kappa range,.667-1.00) were shown. CONCLUSION: Among older persons, the presence of 2 or 3 of the 3 clinical signs strongly suggested electrodiagnostic evidence of a peripheral neuropathy, regardless of etiology. Age-related decline in peripheral nerve function need not be a barrier to the clinical recognition of a diffuse peripheral neuropathy among older persons.

Achilles Tendon↗
PubMed2005

Medication and toxin-induced peripheral neuropathy.

Medication and toxin-induced neuropathies, although uncommon, are important to identify because of potential reversibility. Numerous medications and toxins are implicated with neuropathy, but objective proof is lacking for many. Chemotherapeutic agents, nucleoside analogs, and other medications and toxins have clear causative links with neuropathy, but many agents have only rare temporal associations. Neuropathies are being recognized from new medications approved for use and other medications, which have expanded indications. Some established associations with neuropathy are less widely known while others are overestimated. Peripheral neuropathy from chronic drug exposure is more problematic to determine. Axonal pathology is most common, but some agents cause demyelination and even conduction block, mimicking immune-mediated neuropathies. Multiple and varied toxic mechanisms are implicated. Neuropathy is a dose-limiting complication of some critical treatments and preventative agents are being actively pursued.

Anti-Bacterial Agents↗
PubMed2006

Rituximab therapy in monoclonal IgM-related neuropathies.

Monoclonal IgM-related neuropathies constitute a heterogeneous group of disorders, which are generally poorly responsive to treatment. Rituximab, a chimeric monoclonal antibody against the CD20 molecule, has been used with success in patients with neuropathy and monoclonal IgM with anti-MAG or anti-GM1 ganglioside activity. Based on this observation, four patients were treated with IgM-related neuropathy with rituximab. Between January 1999 - December 2000, four patients with IgM-related neuropathy (one with chronic inflammatory demyelinating polyneuropathy (CIDP) and three with sensorimotor demyelinating neuropathy) were treated with rituximab. Rituximab was administered at a standard dose of 375 mg m(-2) iv weekly for a consecutive 4 weeks; 3 months later, four additional weekly courses were administered to patients who did not experience deterioration of their neuropathy symptoms. Neurological evaluation was performed before each rituximab infusion and at 1 week and 2 months after last infusion and every 6 months the following years; including motor (MRC in six muscle groups, 9-hole peg test, 10 m walk, hand grip strength), sensory neuropathy (vibration threshold and sensory subjective score) assessment. Neurophysiological parameters were also assessed (MNCV, SNCV, CMAP, SNAP). Strength improved in three of four patients; including the patient with CIDP. This patient developed a significant worsening of her weakness 3 weeks after the initiation of rituximab. This phenomenon coincided with a serum monoclonal IgM flare and resolved spontaneously 1 week later. Her improvement is ongoing for more than 5 years. Considering neurophysiological parameters, two patients showed a slight improved regarding conduction velocities and CMAP (10%) and the patient with IgM flare had a transient worsening of conduction velocities followed by improvement. In conclusion, rituximab is a safe and well-tolerated treatment which may be effective in some patients with IgM-related neuropathy.

Adult↗
PubMed2003

Neuropathy in arsenic toxicity from groundwater arsenic contamination in West Bengal, India.

Large number of people from 9 out of 18 districts of West Bengal, India are endemically exposed to arsenic contaminated groundwater due to drinking of tubewell water containing arsenic level above World Health Organization's maximum permissible limit of 50 microg/L. From our ongoing studies on neurological involvement in patients of arsenicosis from different districts of West Bengal, we report our findings in a total of 451 patients of three districts (Murshidabad, Nadia, and Burdwan), comprising 267 males and 184 females with age ranging from 11 to 79 years. They all had arsenical skin lesions, positive biomarkers and identified source of arsenic contaminated water drinking. Peripheral neuropathy was the predominant neurological complication in these patients affecting 154 (37.3%) of 413 patients of Group 1 and 33 (86.8%) of 38 patients of Group 2. Other possible causes and alternative explanations of neuropathy were excluded. The temporal profile in most of the cases (154 of Group 1) were of chronic affection while the 33 patients of Group 2 developed both neuropathy and dermopathy subacutely. Subacutely affected Group 2 patients had much higher incidence of neuropathy. Paresthesias and pains in the distal parts of extremities were much higher in incidence in Group 2 (73.7% and 23.7% respectively) than in Group 1 (18.4% and 11.1%). Distal limb weakness or atrophy was evident in 7.3% in Group 1 and 10.5% in Group 2. Overall, sensory features were more common than motor features in patients of neuropathy and sensory neuropathy was diagnosed in 30% and 76.3% and sensorimotor in 7.3% and 10.5% respectively in Group 1 and Group 2 subjects. Nerve conduction and electromyographic studies performed in 88 cases revealed dysfunction of sensory nerve in 45% and 27% and of motor nerve in 20% and 16.7% of patients with moderate degree and mild degree of clinical neuropathies respectively. Evoked potential studies performed in 20 patients were largely normal except for two instances each of abnormal visual evoked potential and brainstem auditory evoked potential findings. Prognosis was favorable in mild and early diagnosed cases of neuropathy whereas most of the other more severe and late diagnosed cases showed slow and partial recovery or even deterioration. Outcome in neuropathic patients of arsenicosis and long term toxic neurologic effects yet unexplored and unknown remain as matters of future concern requiring close monitoring.

Adolescent↗
PubMed2000

Expression of accessory molecules for T-cell activation in peripheral nerve of patients with CIDP and vasculitic neuropathy.

Vasculitic neuropathy and chronic inflammatory demyelinating polyneuropathy (CIDP) are neuropathies characterized by a T-lymphocyte infiltrate in the peripheral nerves. The microenvironment in which these T cells become activated, and the molecules and cells that play a role in this process are incompletely understood. Using immunohistochemical analysis, we studied the effect of the presence of adhesion, costimulatory and antigen-presenting molecules on different cell types as a precondition for local T-cell activation in human sural nerve biopsies of seven patients with CIDP, three patients with vasculitic neuropathy and three healthy controls. In biopsies from CIDP and vasculitic neuropathy patients, but not in those from healthy controls, Schwann cells expressed the adhesion/T-cell stimulatory molecule CD58 (LFA-3). The CD58 molecule was also present on endothelial cells of all vasculitic neuropathy patients and one CIDP patient. In biopsies from normal controls and patients, CD54 (ICAM-1) expression was detectable on microvascular endothelial cells. In addition, expression of the costimulatory molecule CD86 was detected on vascular tissue in patients with vasculitic neuropathy. Although macrophages were always present in all subjects, expression of the major histocompatibility complex (MHC)-like molecule CD1a by macrophages was restricted to biopsies from two CIDP patients and one vasculitic neuropathy patient. Unexpectedly, Schwann cells of a single vasculitis patient strongly expressed CD1b, a molecule involved in the presentation of self-glycolipids to T cells. Schwann cells in biopsies from patients and normal controls expressed high levels of the invariant chain, CD74, a molecule involved in the intracellular sorting of MHC class II molecules. There was no evidence for the presence of dendritic cells in sural nerve biopsies. These findings support a model in which T-cell activation can be initiated and/or perpetuated locally in sural nerve biopsies of patients with CIDP and vasculitic neuropathy, and predict an important role for Schwann cells and endothelial cells.

Adult↗
PubMed2003

Gastric emptying time and the effect of cisapride in cirrhotic patients with autonomic neuropathy.

GOALS To investigate the relationships between gastric emptying and autonomic dysfunction in hepatic cirrhosis and to assess the effects of cisapride on gastric emptying in cirrhotic patients. STUDY Twenty-four cirrhotic patients (8 patients in each Child-Pugh classification) and 25 healthy controls were enrolled. All the patients had viral (B or C) hepatitis. Patients with DM, alcoholic cirrhosis, active peptic ulcer, gastric malignancy and pyloric obstruction were excluded by esophagogastroduodenoscopy. Parasympathetic and sympathetic functions were assessed by the criteria set forth by Ewing and Clark. Drugs affecting GI motility and smoking were discontinued 48 hours and 12 hours prior to the study respectively. A solid-phase of gastric emptying study was conducted by scintigraphic method for the calculation of gastric half-emptying time (GET1/2). RESULTS The study revealed that 9 patients with Child-Pugh B and C cirrhosis had autonomic neuropathy and none of Child-Pugh A cirrhosis had autonomic neuropathy. Prolonged GET1/2 was noted in cirrhotics compared with the control group (p < 0.05). However, there was significant difference between 9 patients (Child B-C) with autonomic neuropathy compared with patients 15 patients without autonomic neuropathy. Again there was a significant difference in GET1/2 between Child A cirrhotic and Child B-C cirrhotic whether they had autonomic neuropathy or not. Cisapride decreased GET1/2 significantly in cirrhotic patients (Child B-C cirrhotic). Clearly, patients with autonomic neuropathy in Child B-C cirrhosis had significantly reduced GET1/2 after cisapride administration. Even though cisapride decreased GET1/2 in patients with Child B-C cirrhosis without autonomic neuropathy, this was not significant. CONCLUSION Autonomic neuropathy in advanced cirrhosis from viral hepatitis may cause prolonged gastric emptying. Cisapride can shorten gastric emptying time in such patients.

Administration, Oral↗
PubMed1997

Autoimmune ataxic neuropathies (sensory ganglionopathies).

Autoimmune ataxic neuropathies are a subset of the sensory ataxic neuropathies which are characterized by ataxia as the dominant presenting feature. The major known causes of autoimmune ataxic neuropathies include sensory variants of the Guillain-Barré syndrome, including Miller-Fisher syndrome, subsets of immunoglobulin M paraproteinaemic neuropathy, paraneoplastic neuropathy and the neuropathy associated with Sjögren's syndrome. Identified antigens as targets for autoantibodies include gangliosides, myelin associated glycoprotein, Hu antigen and extractable nuclear antigens. Some recent studies support the pathogenic role of anti-GD1b ganglioside antibody in autoimmune ataxic neuropathies. The major site of pathology in autoimmune ataxic neuropathies is the dorsal root ganglion, but dorsal roots and peripheral nerve myelin and axons may also be affected.

Antibodies, Antinuclear↗
PubMed2004

Non-systemic vasculitic neuropathy.

PURPOSE OF REVIEW: This article reviews the literature on non-systemic vasculitic neuropathy, with emphasis on recent advances, summarizing the clinical presentation, diagnosis, pathology, treatment, and outcome of this condition, and speculating on its nosological status vis-à-vis the systemic vasculitides. RECENT FINDINGS: A new cohort of non-systemic vasculitic neuropathy patients was recently reported. Analysis of the clinical characteristics of this cohort demonstrated a higher incidence of painful, asymmetric, overlapping deficits than in previous studies. Extended follow-up revealed a high relapse rate, low risk of systemic spread, high incidence of chronic pain, relatively good neurological outcome, and low mortality rate. Analysis of therapeutic responses showed better outcomes with combination therapy than corticosteroid monotherapy. Another recent report proposed a role for magnetic resonance angiography in the diagnosis and follow-up of non-systemic vasculitic neuropathy. Recent pathological studies implicated proinflammatory cytokines and matrix metalloproteinase-9 in the mediation of vascular and axonal damage in non-systemic vasculitic neuropathy. SUMMARY: Non-systemic vasculitic neuropathy is one of many localized vasculitides, with involvement restricted to nerves and (possibly) muscles. Inclusion and exclusion criteria differ between reported cohorts. All require a nerve biopsy diagnostic of or suspicious for vasculitis and no extra-neuromuscular involvement. Patients typically present subacutely with a painful, multifocal/asymmetric, distal-predominant neuropathy. In the absence of clinical or laboratory evidence of systemic vasculitis or a condition predisposing to such, prognosis with treatment is good. Pathological data are supportive of a primary T-cell-mediated immunopathogenesis. Some patients classified as having non-systemic vasculitic neuropathy have a systemic vasculitis presenting with neuropathy; in others, the disease is organ-specific.

Anti-Inflammatory Agents↗
PubMed1995

Risk factors for dideoxynucleoside-induced toxic neuropathy in patients with the human immunodeficiency virus infection.

Dideoxynucleosides induce a dose-related toxic neuropathy; however, there is a paucity of information on whether other risk factors influence the development of neuropathy. We reviewed the records of 103 patients at an AIDS Clinical Trials Unit who were taking didanosine and/or zalcitabine to determine the risk factors for dideoxynucleoside-induced toxic neuropathy. Most were homosexual or bisexual (85%) men with a mean age of 39 years. The median CD4+ lymphocyte count was 59 cells/mm3, and 35% had a previous diagnosis of AIDS. Toxic neuropathy was more common in patients taking zalcitabine compared with those taking didanosine (14 of 51 versus seven of 55, p = 0.08). In the patients who took zalcitabine, those who had a low baseline serum cobalamin level, a history of heavy ethanol consumption, or a history of symptoms of peripheral nerve dysfunction were more likely to develop a toxic neuropathy (10 of 14 versus 12 of 37, p = 0.01). Conversely, there were no factors associated with the development of didanosine-induced toxic neuropathy. Dideoxynucleoside-induced toxic neuropathy is a common problem that can be disabling but is usually reversible. A history of symptoms of peripheral nervous system disease, heavy ethanol consumption, or a low serum cobalamin level may be useful in distinguishing patients at higher risk of developing zalcitabine-induced toxic neuropathy.

Acquired Immunodeficiency Syndrome↗
PubMed2005

Mitochondrial haplogroups and peripheral neuropathy during antiretroviral therapy: an adult AIDS clinical trials group study.

OBJECTIVE: HIV nucleoside reverse transcriptase inhibitors (NRTI) can cause peripheral neuropathy that is a result of mitochondrial injury. Polymorphisms in the mitochondrial genome define haplogroups that may have functional implications. The objective of this study was to determine if NRTI-associated peripheral neuropathy is associated with European mitochondrial haplogroups. DESIGN: Case-control study of Adult AIDS Clinical Trials Group (ACTG) study 384 and ACTG Human DNA Repository participants. METHODS: ACTG study 384 was a treatment strategy trial of antiretroviral therapy with didanosine (ddI) plus stavudine (d4T) or zidovudine plus lamivudine given with efavirenz, nelfinavir, or both. Subjects were followed for up to 3 years. Peripheral neuropathy was ascertained based on signs and symptoms. For this analysis, polymorphisms that define European mitochondrial haplogroups were characterized in a majority of ACTG 384 participants, and associations with peripheral neuropathy were assessed using logistic regression. RESULTS: A total of 509 subjects were included in this analysis of whom 250 (49%) were self-identified as white, non-Hispanic. Mitochondrial haplogroup T was more frequent in subjects who developed peripheral neuropathy. Among 137 white subjects randomized to receive ddI plus d4T, 20.8% of those who developed peripheral neuropathy belonged to mitochondrial haplogroup T compared to 4.5% of control subjects (odds ratio, 5.4; 95% confidence interval, 1.4-25.1; P = 0.009). Independent predictors of peripheral neuropathy were randomization to receive ddI plus d4T, older age, and mitochondrial haplogroup T. CONCLUSIONS: A common European mitochondrial haplogroup may predict NRTI-associated peripheral neuropathy. Future studies should validate this relationship, and evaluate non-European mitochondrial haplogroups and other NRTI toxicities.

Adolescent↗
PubMed2005

Small fibre neuropathies.

PURPOSE OF REVIEW: To summarize the recent advances in aetiology, diagnostic assessment, and treatment of small fibre neuropathies. RECENT FINDINGS: New causes of small fibre neuropathy have been recognized and advances in neurophysiologic and neuropathologic techniques for investigating small fibres have been made, increasing the interest in this field. In particular, skin biopsy proved to be a sensitive method to diagnose small fibre neuropathy. It allows the detection of subclinical abnormalities of peripheral nerve function in patients with diabetes and tongue denervation in patients with burning mouth syndrome. This technique has also been used to demonstrate the neuroprotective effect of erythropoietin in experimental models of neuropathy. Among nonconventional neurophysiologic techniques for investigating small fibres, laser-evoked potential and contact heat-evoked potential stimulators have been developed and deserve particular interest. Several trials on neuropathic pain that is a typical feature of small fibre neuropathies have been performed and guidelines have recently been published. SUMMARY: Detection of small fibre impairment allows earlier diagnosis of neuropathy and could be used as an outcome measure in future regenerative neuropathy trials. Standardization of skin biopsy can have an important impact on clinical practice and research. Further studies are needed to assess the reliability of current neurophysiologic techniques for testing small fibre function in peripheral neuropathies and the correlation with well established neuropathologic examination.

Animals↗
PubMed2005

Large and small fiber neuropathy in chronic alcohol-dependent subjects.

The aim of the present study was to evaluate the occurrence of large and small fiber neuropathy among alcohol-dependent subjects and to correlate neuropathy with the pattern of alcohol abuse, age of the subjects, nutritional status, and biochemical parameters. The study sample comprised 98 consecutive alcohol-dependent subjects without signs of malnutrition treated for detoxification voluntarily in the specialized unit of the Athens University Psychiatric Clinic in an inpatient basis. Polyneuropathy (PN) was graded using the neuropathy symptoms score and neurologic disability score, conduction velocity studies, and quantitative sensory tests. Seventy-seven men and 21 women aged 27-70 years took part in the study. PN was diagnosed in 57 subjects (58.2%). PN of both large and small fibers was found in 25 patients (25.5%); exclusively small fiber neuropathy was observed in 12 (12.2%) and exclusively large fiber neuropathy in 20 patients (20.4%). Neuropathy was significantly correlated with the age of the subjects, duration of alcohol abuse, liver dysfunction, macrocytosis, and blood sugar levels upon admission. PN was significantly more frequent in males than in females. The two groups of exclusively large and exclusively small fiber neuropathy did not differ significantly in any clinical and laboratory parameter. Subclinical neuropathy (stage 1) was observed in 11.2%, which also did not differ significantly in any clinical and laboratory parameter from the stage 2 PN group subjects. Our findings indicate the direct toxic effect of alcohol on peripheral nerve fibers as the main etiologic factor of alcoholic PN. Long-standing hyperglycemia may be another contributing factor. Impaired vitamin B(12) utilization may be also involved.

Adult↗
PubMed2005

Treatment of immune-mediated, dysimmune neuropathies.

This review focuses on the actual status and recent advances in the treatment of immune-mediated neuropathies, including: Guillain-Barre syndrome (GBS) with its subtypes acute inflammatory demyelinating polyradiculoneuropathy, acute motor axonal neuropathy, acute motor and sensory axonal neuropathy, Miller Fisher syndrome, and acute pandysautonomia; chronic inflammatory demyelinating polyneuropathy (CIDP) with its subtypes classical CIDP, CIDP with diabetes, CIDP/monoclonal gammopathy of undetermined significance (MGUS), sensory CIDP, multifocal motor neuropathy (MMN), multifocal acquired demyelinating sensory and motor neuropathy or Lewis-Sumner syndrome, multifocal acquired sensory and motor neuropathy, and distal acquired demyelinating sensory neuropathy; IgM monoclonal gammopathies with its subtypes Waldenstrom's macroglobulinemia, myelin-associated glycoprotein-associated gammopathy, polyneuropathy, organomegaly, endocrinopathy, M-protein, skin changes syndrome, mixed cryoglobulinemia, gait ataxia, late-onset polyneuropathy syndrome, and MGUS. Concerning the treatment of GBS, there is no significant difference between intravenous immunoglobulins (IVIG), plasma exchange or plasma exchange followed by IVIG. Because of convenience and absent invasiveness, IVIG are usually preferred. In treating CIDP corticosteroids, IVIG, or plasma exchange are equally effective. Despite the high costs and relative lack of availability, IVIG are preferentially used. For the one-third of patients, who does not respond, other immunosuppressive options are available. In MMN IVIG are the treatment of choice. Inadequate response in 20% of the patients requires adjunctive immunosuppressive therapies. Neuropathies with IgM monoclonal gammopathy may respond to various chemotherapeutic agents, although the long-term effects are unknown. In addition, such treatment may be associated with serious side effects. Recent data support the use of rituximab, a monoclonal antibody against the B-cell surface-membrane-marker CD20.

Adrenal Cortex Hormones↗
PubMed1990

Anterior ischaemic optic neuropathy and intraocular pressure.

Anterior ischaemic optic neuropathy is a stroke syndrome of the distal optic nerve, characterised by disc oedema and optic nerve dysfunction--loss of central vision, loss of colour vision, a relative afferent pupillary defect, and nerve fibre layer field loss. We prospectively evaluated the changes of intraocular pressure throughout the day in 16 patients with non-arteritic anterior ischaemic optic neuropathy and 15 normal control subjects of similar age and race. The peak intraocular pressure exceeded 21 mm Hg in five of the ischaemic optic neuropathy patients but none of the controls. The mean peak intraocular pressure was 19.9 mm Hg for the ischaemic optic neuropathy group versus 17.6 mm Hg for controls (p = 0.034). The range of intraocular pressure was also greater for the ischaemic optic neuropathy group (p = 0.030). Eight of 16 ischaemic optic neuropathy patients had a range of intraocular pressure of 6 mm Hg or more, compared with three of 15 control subjects. The intraocular pressure exceeded 21 mm Hg during a subsequent visit in two additional patients in whom the hourly determined intraocular pressure peaked at less than 21 mm Hg. Thus, seven of 16 of our ischaemic optic neuropathy group had an intraocular pressure exceeding 21 mm Hg during the study period. Raised intraocular pressure may be a predisposing factor in some patients who develop anterior ischaemic optic neuropathy.

Aged↗
PubMed2004

Neurophysiological testing correlates with clinical examination according to fibre type involvement and severity in sensory neuropathy.

OBJECTIVE: To investigate a comprehensive battery of neurophysiological tests for objective evaluation of sensory neuropathies including fibre type involvement and severity, and to determine the relation between neurophysiological data and clinical examination. METHODS: 45 patients referred for sensory neuropathy were studied using a standardised clinical evaluation of large and small fibre symptoms and an original neurophysiological battery. Clinical evaluation included: assessment of tactile, vibratory, and pin sensation; tendon reflexes; toe position sense; ataxia score; pain level; and presence of trophic, vasomotor, or sudomotor abnormalities. The neurophysiological battery included: recording of large fibre and small fibre components of the sural sensory nerve action potential; somatosensory evoked cortical potentials and soleus H reflex following tibial nerve electrical stimulation; laser evoked potentials following Nd:YAG laser stimulation of the foot; and plantar sympathetic skin response to median nerve stimulation. Neuropathy was classified according to the predominantly affected fibre type, and a severity score was established based on clinical and neurophysiological abnormalities. RESULTS: On clinical examination there were 22 patients with large fibre sensory neuropathy (LFSN), 18 with mixed sensory neuropathy (MSN), and five with small fibre sensory neuropathy (SFSN). Neurophysiological classification identified 25 patients with LFSN, 13 with MSN, and seven with SFSN. Clinical and neurophysiological classifications and severity scores were correlated, whatever the type of neuropathy. CONCLUSIONS: The correlation between clinical examination and the results of an original neurophysiological test battery offers a comprehensive clinical and neurophysiological approach to the objective assessment of peripheral neuropathies according to fibre type involvement and overall severity.

Adult↗
PubMed2005

Should coeliac disease be considered in the work up of patients with chronic peripheral neuropathy?

OBJECTIVE: To investigate whether there is an association between chronic peripheral neuropathy and coeliac disease. METHODS: The cause of chronic peripheral neuropathy was first investigated in a group of 478 patients. Published reports were then examined systematically for an association between chronic peripheral neuropathy and coeliac disease. Cases were divided into two groups: group A, polyneuropathy preceding duodenal biopsy and controls undergoing duodenal biopsies; group B, coeliac disease preceding polyneuropathy. Patients with cerebellar ataxia, small fibre neuropathy, or a cause for their neuropathy were excluded. RESULTS: In 425 of the 478 patients, a cause other than coeliac disease was established. In the patients with no determined cause for neuropathy, one had abnormally increased IgA antigliadin antibodies but duodenal biopsy was normal. Ten previous studies of patients with chronic peripheral neuropathies were reviewed. The incidence of biopsy proven coeliac disease in patients with polyneuropathy did not differ from the controls (group A). In patients with a proven coeliac disease (group B), polyneuropathy could not be diagnosed more often than in the general population. CONCLUSIONS: The results of both the clinical study and the literature review suggest that it is unlikely that chronic peripheral neuropathy without other neurological signs is associated with coeliac disease.

Antibodies, Anti-Idiotypic↗