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PubMedDate not supplied

Further investigation of the negative association between hypertension and peripheral neuropathy in the elderly: an Oklahoma Physicians Resource/Research Network (OKPRN) Study.

BACKGROUND: In a previous cross-sectional study of age-associated peripheral neuropathy (AAPN), we found that a history of hypertension was protective. The purpose of this study, conducted in the same cohort, was to investigate further this association in the same subjects and in a comparison group of older subjects with diabetes mellitus. METHODS: Baseline data from 584 subjects involved in a longitudinal study of primary care patients 65 years of age and older, with no history of 10 medical conditions known to cause peripheral neuropathy, were analyzed for associations between peripheral neuropathy by examination and history of hypertension, number of antihypertensive medications, systolic blood pressure, diastolic blood pressure, pulse pressure, and orthostatic hypotension. In addition, we examined associations between neuropathy at baseline and use of specific classes of antihypertensive medications and non-steroidal anti-inflammatory agents (NSAIDs) in year 3. The analyses were repeated in 110 subjects with diabetes mellitus. RESULTS: History of hypertension, but not the other hypertension-related variables, was negatively associated (OR, 0.60; 95% CI: 0.40 to 0.90) with AAPN after controlling for age and body mass index (BMI). In 287 subjects evaluated in the 3rd year of the study, beta-blocking agents (OR, 3.56; 95% CI: 1.58 to 8.03) and NSAIDs (OR, 2.65; 95% CI: 1.37 to 5.10) were positively associated with AAPN. In subjects with diabetes mellitus, a history of hypertension was again protective, but current pulse pressure (OR, 1.03; 95% CI: 1.00 to 1.05) was a positive predictor of peripheral neuropathy. There were interesting interactions between pulse pressure and military service and pulse pressure and BMI in diabetic patients. CONCLUSIONS: The negative association between hypertension and AAPN remains unexplained. The positive association between pulse pressure and neuropathy in diabetic subjects supports findings from previous studies and suggests that AAPN and the neuropathy of diabetes may be distinct entities. The incidental finding of an association between NSAIDs and AAPN is concerning and should be investigated further.

Adrenergic beta-Antagonists↗
PubMed1999

[Antiganglioside antibodies in the pathogenesis of autoimmune neuropathies].

Antiganglioside antibodies are frequently detected in sera from patients with autoimmune neuropathies, such as Guillain-Barré syndrome, Miller Fisher syndrome, IgM paraproteinemic neuropathy, chronic inflammatory demyelinating polyneuropathy, and multifocal motor neuropathy. In the acute phase sera from GBS patients, antiganglioside antibodies are detected in 60-70%. Ganglioside antigens recognized by serum antibodies are varied from case to case. IgG antibody against GQ1b ganglioside is specifically raised in sera from patients with Miller Fisher syndrome and Guillain-Barré syndrome with ophthalmoplegia. That antibody may bind to the paranodal myelin of oculomotor, trochlear and abducens nerves, where GQ1b ganglioside is specifically localized, to cause ophthalmoplegia. IgM M-protein which recognizes the disialosyl residue of GD1b is specifically associated with sensory ataxic neuropathy. The IgM M-protein may bind to the primary sensory neurons, where GD1b ganglioside is localized, to cause sensory disturbance. After we confirmed the localization of GD1b in the rabbit primary sensory neurons, we sensitized rabbits with GD1b and induced sensory ataxic neuropathy in them. This is the first established animal model of autoimmune neuropathy induced by sensitization with ganglioside. Some antiganglioside antibodies may determine the clinical phenotype of neuropathy by binding specifically to the ganglioside antigens which have unique localization.

Animals↗
PubMedDate not supplied

Cardiac autonomic neuropathy and its correlation with QTc dispersion in type 2 diabetes.

This study was conducted on 50 patients of diabetes mellitus type 2 and 20 healthy controls to correlate severity of diabetic cardiac autonomic neuropathy with QTc interval and QTc dispersion. Five standard cardiovascular response tests were carried out (i.e. Valsalva ratio, expiration-inspiration ratio, immediate heart rate response to standing, fall of systolic blood pressure on standing and sustained hand grip test) to determine the severity of cardiac autonomic neuropathy by scoring system. QTc dispersion was determined by subtracting heart rate-corrected minimum QTc interval (QTc min) from maximum QT interval (QTc max) from standard electrocardiogram. Severity of cardiac autonomic neuropathy strongly correlated with QTc dispersion (r = 0.760; p = 0.0001). Correlation of severity of cardiac autonomic neuropathy with QTc max and QTc mean was also found but weaker than with QTc dispersion (r = 0.663, r = 0.542, p = 0.0001 each) and no correlation was found with QTc min (r = 0.177; p = 0.17). This shows that QTc dispersion is a better predictor of cardiac autonomic neuropathy than any of above three QTc intervals. QTc max, QTc mean and QTc dispersion were significantly higher (p < 0.001) in diabetics with autonomic neuropathy (450 +/- 23, 423 +/- 22 and 57 +/- 12 msec; n = 30) than without neuropathy (407 +/- 14, 397 +/- 15 and 20 +/- 7 msec; n = 20) and control subjects (408 +/- 20, 399 +/- 19 and 19 +/- 7 msec; n = 20) but QTc min remained same in the three groups (393 +/- 21, 387 +/- 12, 388 +/- 19 msec, respectively) (p > 0.05). Correlation of QTc dispersion was stronger with QTc max (r = 0.781; p < 0.001) than QTc mean (r = 0.625; p = 0.001) but not with QTc min (r = 0.097; p = 1.0) which suggests that regional increase in QT interval due to regional autonomic denervation leads to increased QTc dispersion. Thus, QTc dispersion is a sensitive, non-invasive, simple and cost-effective predictor of cardiac dysautonomia.

Adult↗
PubMedDate not supplied

[Peripheral neuropathy in systemic lupus erythematosus].

INTRODUCTION: Systemic lupus erythematosus (SLE) is the connective tissue disorder in which neuropsychiatric complications are most often seen. The prevalence of peripheral neuropathy varies from 5 to 27% depending on the series of cases described, with subclinical forms being most frequent. OBJECTIVES: To determine the prevalence of subclinical peripheral neuropathy in a group of patients with SLE, define their characteristics, and investigate any possible associations with clinico analytical parameters of the disease. PATIENTS AND METHODS. 32 patients with SLE were diagnosed in an Internal Medicine Outpatient Clinic and followed up for at least a year. They were studied prospectively and consecutively by clinical examination, laboratory test and neurophysiological studies (electroneurogram). RESULTS: Neurophysiological study showed peripheral neuropathy to be present in 50% of the patients, who were mainly asymptomatic (75%) and found to be normal on neurological examination (81.2%). The most frequent type of neuropathy was polyneuropathy (37.5%) which was predominantly axonal symmetrical and sensomotor followed by isolated mono neuropathy (6.2%) and multiple mononeuritis (6.2%). No clinical or analytical parameter was significantly associated with the development of peripheral neuropathy. CONCLUSIONS: The considerable frequency of subclinical peripheral neuropathy in patients with SLE and the absence of associated clinical or analytical parameters makes it necessary to carry out neurophysiological studies in these patients to detect its presence and establish the precise extent of the disorder.

Adolescent↗
PubMedDate not supplied

Electrodiagnostic patterns in MGUS neuropathy.

Monoclonal gammopathies of undetermined significance (MGUS) are frequently associated with neuropathies, particularly in the elderly. To better characterize the electrodiagnostic findings in MGUS-associated neuropathies, we analyzed electrodiagnostic data from 35 patients with MGUS-associated neuropathies (mean age 70.6; 12 IgM, 19 IgG, 4 IgA) who had no other cause for their neuropathies. Data was also analyzed for 29 age-matched patients (mean age 69.8) with diabetic neuropathies. Using electrodiagnostic criteria, studies were classified as being consistent with demyelination; 9 patients had findings consistent with axonal injury; and, in 3 patients, criteria for both demyelination and axonal injury were present. However, 24 of the 35 patients with MGUS-associated neuropathies had dyssummetric findings. In contrast, only 4 of the 29 patients with only diabetes had a dyssymmetric process (p < 0.0001). In MGUS-associated neuropathies, dyssymmetry is the most common, definable abnormal electrodiagnostic pattern.

Aged↗
PubMed2002

Neuropathies associated with IgG and IgA monoclonal gammopathy.

Neuropathy has been frequently reported in patients with monoclonal gammopathy, particularly those with monoclonal gammopathy of undetermined significance (MGUS). While the neuropathy associated with IgM-MGUS is well characterized and is often associated with a reactivity of the monoclonal protein with neural antigens, the relationship between the neuropathy and IgG and IgA MGUS is less clear. We review here the clinical, electrophysiological and pathogenetic features of neuropathies associated with IgG and IgA M-proteins in order to determine whether they represent distinct clinical entities and, most importantly, whether the finding of an IgG or IgA monoclonal gammopathy in a patient with neuropathy should led to different diagnostic or therapeutical approaches. This review will mainly focus on neuropathies associated with MGUS since the disclosure of a malignant monoclonal gammopathy, including multiple or osteosclerotic myeloma, lymphoma or primary amyloidosis, in a patient with neuropathy usually divert the therapeutical decisions to the hematologist for an appropriate therapy of the underlying life threatening condition.

Humans↗
PubMed2002

[Disulfiram neuropathy. Report of 3 cases].

Disulfiram is widely used for aversive treatment of alcoholism. Although it is well tolerated in most patients, one in 15,000 patients will develop peripheral neuropathy every year, which is frequently misdiagnosed as alcoholic neuropathy. Disulfiram neuropathy can be mild or severe, depending on diverse factors such as time of exposure and the dosage. Most patients will present with a motor-sensory neuropathy of the lower limbs, which tends to improve as disulfiram administration ceases, however some cases may remain with permanent sequelae. We report the clinical, laboratory and electrophysiological features of three patients who developed disulfiram neuropathy during treatment of alcoholism. Recovery was incomplete at 8 weeks after treatment cessation in all of them. No other findings justified the clinical features described in these patients. Considering the incidence of alcoholism and the wide use of disulfiram treatment in Chile, we suggest that disulfiram neuropathy is being underdiagnosed. We also stress the fact that disulfiram neuropathy could be avoided by using lower doses.

Adult↗
PubMed2002

[Sensory neuropathy and primary biliary cirrhosis].

Primary biliary cirrhosis (PBC) may associate an axonal neuropathy, a somatic and autonomic neuropathy and a very infrequently sensory neuropathy (with or without xanthomata). The aim of this paper is to describe the case of a 46 year old man diagnosed with PBC in stage I-II and a progressive sensory neuropathy (axonopathy) confined to his upper limbs with distal predominance. It had progressed slowly an began asymmetrically. A complete clinical study excluded other causes of neuropathy. We followed him clinically and electromyographically and he remains stable after two years evolution. The sensory neuropathy in this case, a primary biliary cirrhosis, is compatible with an assymetric sensory neuropathy limited to the upper limbs with assymmetric beginning.

Electromyography↗
PubMed1992

Neuropathy in chronic obstructive pulmonary disease: a multicentre electrophysiological and clinical study.

The incidence and type of neuropathy in patients with chronic obstructive pulmonary disease (COPD) were assessed. In a selected group of 89 patients, abnormal nerve conduction studies were found in 44%. Electrophysiological signs of a generalized peripheral neuropathy were found in 5-18%, depending on diagnostic criteria. Lesions which were thought to be due to compression or other forms of trauma were present in a further 24%. In the patients with peripheral neuropathy, the changes were distally predominant, affected mainly sensory fibres, and were consistent with an axonal type of neuropathy. There was a significant correlation between age and the incidence of peripheral neuropathy. Electrophysiological evidence of neuropathy was three times as common as clinical evidence. Much of the variation in the reported incidence of neuropathy in COPD is probably due to imprecise diagnostic criteria.

Adult↗
PubMed2003

[Bilateral optic neuropathy in a case of primary Gougerot Sjögren's syndrome].

INTRODUCTION: Primary Sjögren's syndrome is frequently characterized by a sicca syndrome without associated connective tissue disease. Association with an optic neuropathy is uncommon. CASE REPORT: We report a case of optic neuropathy in a 59-year-old woman known to have primary Sjögren's syndrome confirmed clinically and histologically 2 years ago. She suddenly presented an initial bilateral visual loss. The ophthalmological exam noted a visual acuity of 1/10 in the right eye and limited to light perception in the left eye, with bilateral optic ischemic neuropathy more developed in the left eye. Fluorescein angiography showed, signs of ischemic neuropathy. The diagnosis of Horton disease was suspected, but subnormal blood velocity and a negative biopsy of the temporal artery confirmed the diagnosis of optic neuropathy associated with primary Sjögren's syndrome. General steroid therapy improved optic neuropathy in the right eye but was ineffective in the left eye. CONCLUSION: Optic neuropathy associated with Sjögren's syndrome is rare but must be considered the most common ophthalmological manifestation of the disease. Visual prognosis depends on the rapidity of diagnosis and therapy.

Anti-Inflammatory Agents↗
PubMed2004

[Contribution of autoantibodies to the diagnosis of peripheral neuropathies].

The identification of autoantibodies associated with dysimmune neuropathies was a major contribution to the characterisation of peripheral nerve disorders, the understanding of their pathophysiology, and the clinical diagnosis of neuropathies. This review focuses essentially on the interest of these antibodies in clinical practice. The methods used for their detection, their specificity and sensitivity is the first point to take into account. The second is the aim of the antibody detection, pathophysiological or diagnostic. The last is to adapt the search for antibodies to the clinical characteristics of the neuropathy. Antibodies directed to GM1, GQ1b and disyalilated gangliosides, and anti-MAG antibodies are very useful in the diagnosis of acute or chronic motor or sensory-motor neuropathies with or without monoclonal IgM. Anti-onconeural anti-Hu and anti-CV2/CRMP antibodies allow when they are detected the diagnosis of paraneoplastic neuropathies. Neuropathies also occur in the setting of systemic diseases. Detection of antibodies associated with these diseases such as ANCA, soluble nuclear antigens, gliadin, or mitochondry may be helpful in the diagnosis of neuropathies.

Autoantibodies↗
PubMedDate not supplied

[Diabetic peripheral neuropathy].

Peripheral neuropathy is a very frequent consequence of diabetes mellitus. Its clinical expression is quite variable. A specific therapy is sometimes necessary. Early diagnosis of diabetic neuropathy is a cornerstone of patient's follow-up. Differential diagnosis of diabetic neuropathy is sometimes difficult from another type of neuropathy or a focal, even systemic, disease. It is mandatory to know how a diabetic neuropathy may express. Pathophysiological mechanisms involved in diabetic neuropathy are complex and interrelated. Hyperglycaemia alone, even mild or moderate, vascular disorders and dysimmune factors may be combined to induce axonal injury. Glycaemic control is the cornerstone of effective treatment for neuropathy associated with diabetes. Specific pain control and therapies of autonomic disturbances are regularly required.

Diabetes Complications↗
PubMed1976

Neurophysiological aspects of peripheral neuropathies.

1. Eighty-eight intrafascicular neural recordings were obtained in 10 normal subjects, 5 patients with axonal degeneration and 11 patients with demyelinating neuropathy. 2. Stimulus levels required for perception and fibre activation were higher in neuropathic subjects. Fibres transmitting touch perception had significantly lower conduction velocities in both patient groups, but were very much lower in the group with demyelinating neuropahty than the group with axonal degeneration. Maximum electrical stimulation evoked dispersed fibre responses in the axonal degeneration group and more dispersed, slowly conducting fibre potentials in the demyelinating group. In patients with hypertrophic Charcot-Marie-Tooth disorder, usually only a small group of slowly conducting low amplitude potentials was recorded. 3. Delivery of a train of supramaximal stimuli caused prolongation of latency and dispersion of fibre potentials in all microneurographic recordings. The changes were significantly greater in the axonal neuropathy group than in normals, and recovery was slower. The demyelinating neuropathies showed significantly greater changes than both the normal and the axonal neuropathy groups, and post-tetanic conduction slowing became even more marked after limb temperature was raised. 4. Surface SAP recordings showed normal refractory period in chronic axonal neuropathy but significant latency prolongation occurred in demyelinating neuropathy. 5. It is concluded that both receptor and nerve fibre abnormalities contribute to sensory dysfunction in degenerative and demyelinating neuropathies.

Action Potentials↗
PubMed1990

Nutritionally induced peripheral neuropathies.

The authors have presented a discussion of some of the more common nutritional deficiency syndromes. A discussion of the etiology, clinical manifestation, diagnosis, and prognosis has been provided. Special attention has been given to the relationship between nutritional deficiency and the development of peripheral neuropathies. When patients suffering from peripheral neuropathy present, the possibility of a nutritional deficiency should be considered. The diagnosis of a nutritional deficiency neuropathy is rarely established. This may not merely be the result of a low incidence of the problem. The prompt diagnosis and treatment may afford dramatic results. The more protracted the course for diagnosis, the less favorable the prognosis. It is often difficult to pinpoint the exact nutritional deficiency present. Various methods have been discussed in this article; however, often multiple deficiencies are present simultaneously. The treatment with pharmacologic supplementation is usually very innocuous. It often proves beneficial to administer pharmacologic supplementation for a short period. This will aid in the differential diagnosis. Often prescribing a patient large doses of the B-complex vitamins for a limited time will allow the physician to determine if a nutritional neuropathy is present. It should also be remembered that just because a patient is suffering from a peripheral neuropathy from a metabolic disease or secondary to medication, they may also be suffering from a nutritional deficiency simultaneously. We believe that the podiatric physician is well trained to extend comprehensive treatment of pedal manifestations of peripheral neuropathies. Podiatric physicians have a large armamentarium at their disposal to treat the pedal manifestations of the disease sufficiently. These treatments may be conservative or surgical in nature, as previously discussed. We hope that this discussion will increase the awareness of the physician to the various ramifications of nutritionally induced neuropathies as well as the provision of insight into the most efficacious means available for appropriate management.

Alcoholism↗
PubMed1989

[Carcinomatous neuropathy: clinical and pathologic findings of sural nerve biopsy in 7 cases].

Sural nerve biopsy was done 7 cases of cancer patients associated with peripheral neuropathy. There were 3 cases of lung carcinoma and one each of pancreas adenoma, seminoma, sigmoid carcinoma and chondrosarcoma of the femur. The neurological features manifested themselves with sensory pattern of neuropathy associated with ataxia in one case, sensorimotor neuropathy in 3 cases, and idiopathic polyneuropathy, peripheral neuropathy with proximal myopathy and neuropathy with paraneoplastic cerebellar syndrome each in one case, 6 patients showed neuropathy before malignancy was discovered and only one patient had neuropathy after the onset of carcinoma. Sural nerve biopsy studied in all the 7 patients with light and electron microscope revealed no infiltration of carcinomatous cells in the sural nerve fascicles. There was severe loss of myelinated fibers and severely axonal degeneration in one patient. Another patient showed segmental demyelination (5.03 x 10(3)/mm2). There was evidence of both axonal degeneration and demyelination associated with moderate reduction in the number of the myelinated fiber density ranging from 1.02 to 4.35 x 10(3)/mm2. In 6 cases, mononuclear cells were seen in nerve fascicles under the electron microscope. The characteristic pathological findings, their relation with the duration and onset of the cancer and some ideas regarding the pathogenesis are discussed.

Adult↗
PubMed1985

Distal sensory nerves of the lower extremity in peripheral neuropathy: comparison of medial dorsal cutaneous and sural nerve abnormalities.

This study investigates the sensitivity and usefulness of medial dorsal cutaneous nerve (MDCN) conduction studies in patients with peripheral neuropathy. Two hundred twenty-three patients with clinical signs and symptoms of peripheral neuropathy in their lower extremities were evaluated. Nerve conduction velocity studies of the MDCN were compared to those of the sural and peroneal motor nerves. Fifty-eight percent of the patients had no measurable sensory nerve action potential (SNAP) from either the MDCN or sural nerve or both, indicating moderate to severe neuropathy. Of the remaining patients with mild neuropathy, 12% had a normal sural nerve and an abnormal MDCN, whereas 7% had a normal MDCN and an abnormal sural nerve. Fifty-one percent of the mild cases had normal peroneal motor nerve studies. It is concluded that the MDCN is equal to the sural nerve as a sensitive indicator in all stages of peripheral neuropathy; in mild or early neuropathy approximately 12% of patients will have normal sural nerve studies; and it is important to examine both distal sensory nerves of the leg. Addition of the MDCN study to the standard sural study increases diagnostic accuracy in mild peripheral neuropathy from 88% to nearly 100%.

Action Potentials↗
PubMed1981

Norepinephrine therapy of ischemic optic neuropathy.

Two monocular normotensive patients with nonarteritic ischemic optic neuropathy and retinal ischemia unresponsive to steroid therapy were treated with intravenous norepinephrine. In both patients, improvement in vision began within minutes after moderate hypertension was produced. A third patient showed no response to this therapy in one eye with established ischemic optic neuropathy, but had prompt recovery of vision in the second eye early in the course of ischemic optic neuropathy. This patient returned with recurrent ischemic optic neuropathy more than 1 year later. At that time she was found to have essential hypertension. One patient could not be weaned from the norepinephrine infusion without recurrent visual loss. In the second patient, controlled hypertensive therapy restored visual acuity to 20/30 during two separate recurrences of ischemic optic neuropathy. Therapy of a later episode of ischemic optic neuropathy was delayed for 2 days, and vision did not improve with norepinephrine infusion. This eye subsequently became painful and required enucleation. Histopathological evaluation showed combined arterial and venous occlusions within the optic nerve and evidence of previous peripapillary choroidal vascular occlusion. Selected normotensive patients with ischemic optic neuropathy and retinal ischemia may benefit from controlled hypertensive therapy induced by norepinephrine infusion.

Aged↗
PubMed1980

Misonidazole peripheral neuropathy: its relationship to plasma concentration and other drugs.

The data from 44 patients with documented glioblastoma who received 1.5 g/m2 of misonidazole twice weekly in conjunction with whole brain radiotherapy (total dose 6000 rad) was analyzed for factors associated with the development of peripheral neuropathy. The average total cumulative dose of misonidazole was 16.9 g/m2 and mild to moderate reversible peripheral neuropathy developed in 18% of patients. Peripheral neuropathy was positively associated with: 1) evidence of residual misonidazole in pretreatment plasma samples (> 10 microgram/ml), 2) elevated plasma concentrations of misonidazole on the day following treatment (> 25% of 4-hour plasma concentration), and 3) a prolonged plasma half-life (an average of 25% greater in patients developing peripheral neuropathy). The use of corticosteriods was negatively associated with the development of peripheral neuropathy and appeared to confer some protection. Age, sex, total dose of misonidazole, 4-hour plasma concentration (namely, at the time of radiotherapy), or the receipt of phenytoin or barbiturates was not related to the development of peripheral neuropathy. Monitoring of plasma misonidazole concentrations during treatment in conjunction with careful examination of the patient may result in a reduction of the incidence or severity of peripheral neuropathy.

Adrenal Cortex Hormones↗