Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neuropathy”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources
PubMed2006

Development of neuropathy in patients with myeloma treated with thalidomide: patterns of occurrence and the role of electrophysiologic monitoring.

PURPOSE: Peripheral neuropathy frequently limits the duration of treatment with thalidomide for patients with multiple myeloma. We assessed the time course of occurrence, possible predictive factors, and the utility of serial nerve electrophysiological studies (NES) for detecting onset of neuropathy. PATIENTS AND METHODS: Seventy-five patients with relapsed/refractory myeloma were enrolled onto a multicenter trial of dose-escalating thalidomide with or without interferon. Patients underwent clinical assessment plus NES at baseline and every 3 months. Time to development of neuropathy according to clinical or NES criteria was compared. Patient and treatment-related factors were compared as predictors of neuropathy. RESULTS: Thirty-nine percent had some NES abnormalities at baseline. Patients received thalidomide at a median dose-intensity of 373 mg/d. Thirty-one of 75 patients (41%) developed neuropathy during thalidomide treatment; 11 patients (15%) discontinued treatment with thalidomide due to neuropathy. The actuarial incidence of neuropathy increased from 38% at 6 months to 73% at 12 months, with 81% of responding patients developing this complication. Serial NES did not reliably predict the imminent development of clinical neuropathy requiring thalidomide cessation, nor were patient age, sex, or prior therapy predictive. Patients who developed neuropathy had a longer duration of thalidomide exposure (median, 268 v 89 days; P = .0001). Cumulative dose or dose-intensity received was not predictive. CONCLUSION: The majority of patients will develop peripheral neuropathy given sufficient length of treatment with thalidomide. To minimize the risk of neurotoxicity, therapy should be limited to less than 6 months. Electrophysiologic monitoring provides no clear benefit versus careful clinical evaluation for the development of clinically significant neuropathy.

Aged↗
PubMed2005

Evaluation of a clinical screening tool for HIV-associated sensory neuropathies.

OBJECTIVE: To evaluate the performance characteristics of a brief clinical neuropathy screening tool for use in sensory neuropathies complicating HIV infection. METHODS: The authors assessed 80 patients using the Brief Peripheral Neuropathy Screen (BPNS). Patients were defined as having neuropathy if they had both symptoms and signs consistent with this diagnosis. All subjects underwent sensory threshold testing and lower limb epidermal nerve fiber quantification using punch skin biopsy as objective measures. RESULTS: Individuals defined as having neuropathy using the BPNS (n = 37) performed less well on sensory threshold testing than other HIV-infected individuals (p < 0.0001 for warming, cooling, and vibration) and also had lower distal calf epidermal nerve fiber densities (p < 0.0001). Individuals who had symptoms but no neuropathic signs (n = 13) did not perform differently on any objective testing compared with neuropathy-free individuals, supporting the decision to require signs as well as symptoms as an operational criterion for the diagnosis of neuropathy. Of the symptoms listed in the screening tool, the presence of numbness had the greatest diagnostic efficiency for identifying those with neuropathy. CONCLUSION: The Brief Neuropathy Screening Tool (and the chosen definition of neuropathy) accurately detects those HIV-infected individuals with the greatest degree of peripheral nerve dysfunction and pathology. This is a valid neuropathy screening tool for use in the context of HIV infection, and is simple enough to be applicable in resource-limited settings.

Adult↗
PubMed2006

Advances in understanding drug-induced neuropathies.

Many commonly used medications have neurotoxic adverse effects; the most common of these is peripheral neuropathy. Neuropathy can be a dose-limiting adverse effect for many medications used in life-threatening conditions, such as malignancy and HIV-related disease. Epidemiological evidence supports previous case reports of HMG-CoA reductase inhibitors (or 'statins') causing an axonal sensorimotor neuropathy or a purely small-fibre neuropathy in some patients. The neuropathy improves when the medication is withdrawn. Despite the association between HMG-CoA reductase inhibitors and neuropathy, the risk is low compared with the significant vascular protective benefits. Oxaliplatin, a new platinum chemotherapy agent designed to have fewer adverse effects than other such agents, has been shown to cause a transient initial dysaesthesia in addition to an axonal polyneuropathy. Thalidomide, an old therapy currently being utilised for new therapeutic indications (e.g. treatment of haematological malignancies), is associated with a painful, axonal sensorimotor neuropathy that does not improve on withdrawal of the drug. Nucleoside reverse transcriptase inhibitors are important components of highly active antiretroviral therapy, but are associated with a sensory neuropathy that is likely to be due to a direct effect of these drugs on mitochondrial DNA replication. New research demonstrates that lactate levels may help discriminate between neuropathy caused by nucleoside analogues and HIV-induced neuropathy. Understanding the mechanism of drug-induced neuropathy has led to advances in preventing this disabling condition.

Antineoplastic Agents↗
PubMed2000

[Paraneoplastic neuropathies].

RARE AND INAUGURAL: Paraneoplastic neuropathies (PN) are rare, affecting approximately 4-5% of patients with cancer. Their diagnosis is difficult because the clinical picture is nonspecific and because the neuropathy precedes the discovery of the cancer in a majority of patients. SUBACUTE SENSORY NEUROPATHY (SSN): Initially described by Denny-Brown, subacute sensory neuropathy is characterized by a severe inflammatory loss of the dorsal roots ganglia. The clinical hallmark is a severe, asymmetric sensory neuropathy progressing over a few weeks to months until the patient is bedridden. The underlying cancer is most often a small-cell lung cancer (SCLC) and the presence of anti-Hu antibodies is almost specific of SSN associated with SCLC. MOTOR NEURON DISEASES: Motor neuron diseases are rarely of paraneoplastic origin save for subacute sensory neuropathy associated with Hodgkin's disease. SENSORIMOTOR NEUROPATHIES: Sensorimotor neuropathies are the most frequent PN but constitute a hetereogeneous group. Acute Guillain-Barré syndrome occurs in patients with Hodgkin's syndrome. Paraneoplastic chronic inflammatory demyelinating polyneuropathy probably exists during lymphomas and carcinomas but a fortuitous association has not been formally excluded. Paraneolastic peripheral nerve microvasculitis often presents as mononeuritis multiplex and complicates mainly lymphoma and SCLC. Other PN are generally of the chronic and axonal type. Among them are the so-called "terminal neuropathies" which are linked to weight loss. AUTONOMIC NEUROPATHIES: Autonomic neuropathis occur during SCLC or Hodgkin's disease. Their most frequent clinical presentation is a pseudo-obstruction which is rarely isolated but which generally occurs as part of diffuse encephalomyelitis.

Diagnosis, Differential↗
PubMed2001

Neuropathy in rheumatoid arthritis.

BACKGROUND: Paucity of Indian literature on rheumatoid neuropathy creates a lacuna in the critical evaluation and discussion of the subject. We did this study to find out the incidence and pattern of neuropathy and to correlate it with disease parameters and other extra-articular involvement. MATERIAL AND METHODS: We studied 31 patients of rheumatoid arthritis (RA) classified by ACR criteria. Electromyography and nerve conduction studies (EMG/NCV) were done in all the patients apart from routine laboratory and radiological investigations. Electrocardiograph (ECG), pulmonary function tests (PFT) and ophthalmological examination were also carried out to ascertain extra-articular involvement. RESULTS: Ten out of 31 RA patients had neuropathy of which five each were overt and subclinical respectively. Only one patient had entrapment neuropathy. Four of the ten patients had pure motor neuropathy whereas the other six were sensori-motor neuropathies. Four patients had mononeuritis multiplex and five had symmetrical peripheral neuropathy. Nine of the ten neuropathic patients had RA for more than 2 years. Seven patients had other extra-articular features along with neuropathy. CONCLUSIONS: One-third of patients with RA have evidence of neuropathy. Disease parameters such as activity, rheumatoid factor and functional and radiological grade do not correlate with neuropathy. Non-entrapment sensori-motor type of neuropathy is the most common type.

Adult↗
PubMed2001

[The dawn of neuroprotective therapy for glaucomatous optic neuropathy].

BACKGROUND: Neuroprotective therapy for glaucoma can be defined as treatment of the recalcitrant disease via direct modification of the molecular mechanism involving retinal ganglion cell death. I and my collaborators, at the dawn of the neuroprotective era, elaborated and conducted the following investigations in order to pursue our final goal, i.e., substantial improvement of the quality of life of glaucoma patients. METHODS AND RESULTS: 1. Investigation of in traocular pressure (IOP) independent prognostic factors in glaucomatous optic neuropathy. Clinical investigation along with multivariate analyses revealed that some IOP-independent factors including optic disc hemorrhage and compromised retrobulbar hemodynamics are associated with the development and progression of glaucomatous optic neuropathy. 2. Glaucoma therapy other than ocular hypotensive therapy. A long-term follow-up study demonstrated that calcium-channel blockers are efficacious in stabilizing the visual field in normal-tension glaucoma. 3. Establishment of animal models for glaucomatous optic neuropathy. Experimental animal models were created to conduct neuroprotective research for glaucomatous optic neuropathy: an IOP elevation model and an optic nerve crush model in the rat. In addition, a system was constructed for electrophysiological study in the rat to quantitatively investigate neuroprotective effect on the retina and the optic nerve. 4. Neuroprotective effects of several agents on experimental optic neuropathies. Several agents were studied for their neuroprotective effects on optic neuropathies induced in the rat. Some apoptosis-modifying agents were found to possess neuroprotective effects against optic neuropathy. CONCLUSIONS: IOP-independent prognostic factors exist in glaucomatous optic neuropathy. Glaucomatous optic neuropathy can be stabilized by IOP-unrelated therapy like calcium-channel blockers, at least in a subset of the disease. Modification of the apoptosis mechanism can protect retinal ganglion cells from damage caused by optic neuropathy in the rat models. All of the present studies suggest that neuroprotective therapy will probably become the treatment of choice in the near future for glaucomatous optic neuropathy.

Animals↗
PubMed2004

[Peculiarities of the investigation, clinics and treatment of stylohyoid syndrome and glossopharyngeal neuropathy].

UNLABELLED: The aim of the study was to investigate the causes and the clinics of stylohyoid syndrome and its tendency to convert into glossopharyngeal nerve neuropathy; to investigate clinical peculiarities of glossopharyngeal neuropathy; to estimate differential diagnosis criteria for the glossopharyngeal neuropathy and stylohyoid syndrome; as well as to propose optimal treatment of the neuropathy. MATERIAL AND METHODS: Sixty-five patients with stylohyoid syndrome and 53 patients with glossopharyngeal neuropathy have been treated on. The diagnosis was estimated according to the data of clinical and X-ray investigation. For the localization of affected zone we performed modified facial straight plain radiograms of the patients in open bite position, facial oblique contact radiograms, orthopantomograms and cervical spondylograms. RESULTS: The majority of the patients were females; they comprised 61.5% of patients with stylohyoid syndrome and 56.6% of glossopharyngeal neuropathy sufferers. Older persons had neuropathy, younger--stylohyoid syndrome. The mean age of neuropathy patients was 63.8 years, and of stylohyoid syndrome--57.1 years. Seven years and longer duration of disease was observed in 73.3% of glossopharyngeal neuropathy patients, while duration of 7 and more years was observed in only 3.1% of stylohyoid syndrome patients. The mean duration of glossopharyngeal neuropathy was 10.9 years, and of stylohyoid syndrome--2.6 years. The analysis of etiological factors showed they are the same for both diseases. CONCLUSIONS: The core of the glossopharyngeal neuropathy pathogenesis is destruction at the glossopharyngeal nerve or at the perivascular plexus of carotid artery, because of elongation or dislocation of styloid processus in case of neck osteochondrosis and compression by ossified styloid ligament. In case of stylohyoid syndrome, inflammatory processes occur at the above-mentioned nervous elements.

Anticonvulsants↗
PubMed2005

[Clinical and neurophysiological features of 700 patients with diabetic peripheral neuropathy].

OBJECTIVE: To study the clinical and electrophysiological features of diabetic peripheral neuropathy in 700 patients to elucidate the relationships between them and evaluate the value of electromyography in the diagnosis of diabetic peripheral neuropathy. METHODS: Standard sensory and motor nerve conduction studies were performed in the 700 patients, sensory nerve conduction velocity (SCV), amplitude of sensory nerve action potential (SNAP), distal motor latency (DML) and amplitude of compound muscle action potential (CMAP) of median nerve, ulnar nerve, posterior tibial nerve and common peroneal nerve were studied simultaneously. Needle electromyogram (EMG) test was performed in 239 patients. RESULTS: (1) The most common symptoms of peripheral neuropathy were numbness and pain in limbs, while impaired or lost tendon reflexes were the most common abnormal signs in lower limbs. (2) The abnormal rate of nerve conduction studies was 72.4% in the 700 patients. Slow SCV, prolonged DML and decreased amplitude of SNAP and CMAP were detected. (3) More severe abnormal nerve conduction was found in lower limbs than in upper limbs. The abnormal degree was more severe in sensory nerve than in motor nerve and severity was more in amplitude than in conduction velocity (P < 0.05). (4) Abnormal motor and/or sensory nerve conduction was detected in 67.3% of the patients with clinical manifestations of neuropathy and 5.1% patients without signs or symptoms of neuropathy, while motor or sensory nerve conduction was normal in 27.6% patients with manifestations of neuropathy. Needle EMG showed neurogenic lesion in 4.6% of the patients with normal motor and sensory nerve conduction. (5) polyneuropathy is the most common type of diabetic neuropathy and carpal tunnel syndrome the next. CONCLUSIONS: The most common clinical and electrophysiological manifestation of diabetic neuropathy is sensory disturbance, which is more severe in lower limbs. The electrophysiological changes are not always accordant with clinical manifestations. Subclinical diabetic peripheral neuropathy can be detected by electrophysiological tests, which are useful to verify the range and extent of the nerve lesion involved in the early stage of diabetic peripheral neuropathy. Needle EMG is not recommended for screening diabetic neuropathy.

Adolescent↗
PubMed1997

Peripheral neuropathy after bone marrow transplantation.

Peripheral neuropathy after bone marrow transplantation can produce motor disability with significant morbidity and mortality, particularly when the neuropathy occurs within the first few months of the transplant. Most of these severe neuropathies have demyelinating features on electrophysiologic tests and histopathology, characteristic of immunologically-mediated neuropathies. The specific immune mechanism is uncertain. It is possible that cyclosporin, FK-506, and interferon-alpha may all trigger immunologically mediated neuropathies in rare patients. Transplants in patients with pre-existing demyelinating neuropathy may result in abrupt exacerbation of the neuropathy. Other causes of severe neuropathies include high-dose cytosine arabinoside and critical illness polyneuropathy. Less severe neuropathies with primarily sensory deficits may result from etoposide conditioning, thalidomide treatment for graft-versus-host disease, and the chemotherapeutic agents cisplatin and paclitaxel when used at high-dose with peripheral stem cell support. When encountering patients with disabling motor neuropathies, transplant physicians must identify (with the aid of nerve conduction tests) those neuropathies that are likely to be immunologically mediated and then empirically add or alter immunosuppressant therapies. Unfortunately, experience has been too limited to suggest specific regimens or the optimal sequence of immunosuppressant therapies.

Bone Marrow Transplantation↗
PubMed1993

Symptoms of sensory neuropathy in adults with NIDDM in the U.S. population.

OBJECTIVE: To ascertain the prevalence and determinants of sensory neuropathy symptoms through structured interview of a representative sample of people with diabetes in the U.S. population. RESEARCH DESIGN AND METHODS: The 1989 National Health Interview Survey consisted of a representative sample of 84,572 persons in the U.S. > or = 18 yr of age. A household respondent identified all people in the household believed to have diabetes (n = 2829). Subjects who could not be personally interviewed (n = 129) and individuals who stated they did not have diabetes (n = 295) were excluded. A detailed questionnaire was administered to 99.3% of the remaining 2405 subjects. Questions on symptoms of sensory neuropathy included whether during the past 3 mo the subjects had experienced numbness or loss of feeling, pain or tingling, or decreased ability to feel hot or cold. The neuropathy questions were also administered to a representative sample of 20,037 subjects who were not known to have diabetes. RESULTS: Prevalence of symptoms of sensory neuropathy was 30.2% among people with IDDM. This prevalence was 36.0% for men with NIDDM and 39.8% for women with NIDDM, compared with 9.8 and 11.8% for nondiabetic men and women, respectively. In logistic regression, factors independently related to symptoms of sensory neuropathy in people with NIDDM included duration of diabetes, hypertension, hyperglycemia, and glycosuria. Long duration of NIDDM (> or = 20 yr) was associated with a twofold increased risk of symptoms of sensory neuropathy compared with those with 0-4 yr of diabetes. Hypertension was associated with a 60% higher likelihood of symptoms. Diabetic individuals whose blood glucose was high all or most of the time or whose urine tests showed glucose all of the time were > 2 times as likely to have symptoms of sensory neuropathy than those who did not report hyperglycemia or glycosuria. Age, sex, ethnicity, cigarette smoking, and height were not determinants of sensory neuropathy. CONCLUSIONS: Symptoms of sensory neuropathy affect 30-40% of diabetic patients in the U.S. Men and women are affected equally. Prevalence of these symptoms increases with longer duration of diabetes; hypertension and hyperglycemia predispose to symptoms of sensory neuropathy.

Adolescent↗
PubMed1993

Neuropathies associated with diabetes.

Diabetic neuropathy is the most frequent complication of diabetes and the leading cause of polyneuropathy in the Western world. A distal symmetric predominantly sensory polyneuropathy is the most common of the diverse neuropathies that occur secondary to diabetes. Pain is often the most bothersome and difficult to treat symptom of diabetic neuropathy. Autonomic neuropathy is a frequent feature of diabetic neuropathy and the source of many significant problems including postural hypotension, gastroparesis, diarrhea, constipation, neurogenic bladder, and male impotence. Physicians need to be familiar with the multiple, less common forms of diabetic neuropathy, as these often mimic other medical or neurologic conditions. The cause of diabetic neuropathy is not determined, but abundant evidence suggests that both metabolic and ischemic nerve injury are likely factors. These should not be considered mutually exclusive causes of diabetic neuropathy as both factors likely operate to different degrees to produce the clinical spectrum of neuropathies that are seen in diabetes. Although no effective treatment exists to cure diabetic neuropathy, improvement is possible with glycemic control and symptomatic therapy.

Blood Glucose↗
PubMed2003

Impairment of cerebral autoregulation in diabetic patients with cardiovascular autonomic neuropathy and orthostatic hypotension.

AIMS: Impaired cerebrovascular reactivity and autoregulation has been previously reported in patients with diabetes mellitus. However, the contribution of cardiovascular diabetic autonomic neuropathy and orthostatic hypotension to the pathogenesis of such disturbances is not known. The purpose of this study was to evaluate cerebral blood flow velocity in response to standing in patients with diabetes and cardiovascular autonomic neuropathy with or without orthostatic hypotension. METHODS: We studied 27 patients with diabetes--eight had cardiovascular autonomic neuropathy and orthostatic hypotension (age 46.4 +/- 13.5 years, diabetes duration 25.0 +/- 11.0 years), seven had autonomic neuropathy without hypotension (age 47.3 +/- 12.7 years, diabetes duration 26.4 +/- 12.1 years), and 12 had no evidence of autonomic neuropathy (age 44.1 +/- 13.8 years, diabetes duration 17.1 +/- 10.2 years)-and 12 control subjects (age 42.6 +/- 9.7 years). Flow velocity was recorded in the right middle cerebral artery using transcranial Doppler sonography in the supine position and after active standing. RESULTS: Cerebral flow velocity in the supine position was not different between the groups studied. Active standing resulted in a significant drop of mean and diastolic flow velocities in autonomic neuropathy patients with orthostatic hypotension, while there were no such changes in the other groups. The relative changes in mean flow velocity 1 min after standing up were -22.7 +/- 16.25% in patients with neuropathy and orthostatic hypotension, +0.02 +/- 9.8% in those with neuropathy without hypotension, -2.8 +/- 14.05% in patients without neuropathy, and -9.2 +/- 15.1% in controls. CONCLUSIONS: Patients with diabetes and cardiovascular autonomic neuropathy with orthostatic hypotension show instability in cerebral blood flow upon active standing, which suggests impaired cerebral autoregulation.

Adolescent↗
PubMed2002

Incidence and risk factors for thalidomide neuropathy: a prospective study of 135 dermatologic patients.

Thalidomide is effective in several cutaneous diseases. Peripheral neuropathy is the most important adverse event limiting its use. Its incidence rate and its relation to thalidomide doses remain unclear. We prospectively monitored 135 patients treated with thalidomide for various dermatologic diseases for 2 y in order to estimate the annual incidence rate and risk factors for neuropathy. Patients underwent standardized neurologic examination and nerve conduction studies prior to, and regularly during treatment. Risk factors for neuropathy were assessed using a Cox proportional-hazards model. Clinical and electrophysiologic evidence of a thalidomide-induced neuropathy were present in 25.2% of the patients; however, when considering all potential cases, this rate reached 55.6%. The incidence rate was maximal during the first year of treatment (20%). The risk of neuropathy was related to the daily dose whatever the duration of treatment (p<10-3). Considering a daily dose < or =50 mg per day as reference, the relative risk for thalidomide neuropathy was 8.2 for a daily dose comprised between 50 and 75 mg per day and 20.2 for a daily dose >75 mg per day (p<10-3). No neuropathy occurred for daily doses < or =25 mg per day. The neuropathy was subclinical in nearly a quarter of patients with such an adverse event. These data confirm the high rate of thalidomide neuropathy and identify the daily dose as the main risk factor. The risk of neuropathy seems to be negligible for doses less than 25 mg per day, whatever the duration of therapy.

Adult↗
PubMed2001

Continuous delivery of neurotrophin 3 by gene therapy has a neuroprotective effect in experimental models of diabetic and acrylamide neuropathies.

Neurotrophic factors (NFs) are promising agents for the treatment of peripheral neuropathies such as diabetic neuropathy. However, the value of treatment with recombinant NF is limited by the short half-lives of these molecules, which reduces efficiency, and by their potential toxicity. We explored the use of intramuscular injection of a recombinant adenovirus encoding NT-3 (AdNT-3) to deliver sustained low doses of NT-3. We assessed its effect in two rat models: streptozotocin (STZ)-induced diabetes, a model of early diabetic neuropathy characterized by demyelination, and acrylamide experimental neuropathy, a model of diffuse axonal neuropathy which, like late-onset human diabetic neuropathy, results in a diffuse sensorimotor neuropathy with dysautonomy. Treatment of STZ-diabetic rats with AdNT-3 partially prevented the slowing of motor and sensory nerve conduction velocities (p < 0.01 and p < 0.0001, respectively). Treatment with AdNT-3 of acrylamide-intoxicated rats prevented the slowing of motor and nerve conduction velocities (p < 0.001 and p < 0.0001, respectively) and the decrease in amplitude of compound muscle potentials (p < 0.0001), an index of denervation. Acrylamide-intoxicated rats treated with NT-3 had higher than control levels of muscle choline acetyltransferase activity (p < 0.05), suggesting greater muscle innervation. In addition, treatment of acrylamide-intoxicated rats with AdNT-3 significantly improved behavioral test results. Treatment with AdNT-3 was well tolerated with minimal muscle inflammation and no detectable general side effects. Therefore, our results suggest that NT-3 delivery by adenovirus-based gene therapy is a promising strategy for the prevention of both early diabetic neuropathy and axonal neuropathies, especially late axonal diabetic neuropathy.

Acrylamides↗
PubMed2004

Hereditary sensory neuropathies.

PURPOSE OF REVIEW: The hereditary sensory neuropathies, also known as the hereditary sensory and autonomic neuropathies, are a clinically and genetically heterogeneous group of disorders. As they are not as common as Charcot-Marie-Tooth disease, they do not receive the same level of attention, but there have been major advances in the identification of the causative genes in the past decade. Certain forms of hereditary sensory and autonomic neuropathy, especially hereditary sensory and autonomic neuropathy type I, which has minimal autonomic involvement and is more accurately termed hereditary sensory neuropathy type I, can present in a very similar fashion to certain forms of Charcot-Marie-Tooth disease (Charcot-Marie-Tooth type 2B, see below), and therefore it is important that clinicians who regularly manage patients with neuropathy are familiar with the latest developments in the hereditary sensory and autonomic neuropathies. This review will concentrate on the recent genetic advances in hereditary sensory and autonomic neuropathy, and especially on those forms that overlap clinically with Charcot-Marie-Tooth disease, hence the title of the review 'Hereditary sensory neuropathies' rather than hereditary sensory and autonomic neuropathies.

Acyltransferases↗
PubMed1994

Peripheral neuropathy as a presenting feature of type 2 diabetes: a case-controlled study.

The characteristics and outcome of 68 newly diagnosed Type 2 diabetic patients who presented with clinically evident peripheral neuropathy were compared with matched controls who had no neuropathy at diagnosis. All subjects (34 male) whose median age was 68 (range 47-89) yr were identified from a computerized diabetes register and presented in 1982-1990. The groups were compared at diagnosis for haemoglobin A1, body mass index, blood pressure, smoking, and alcohol consumption, and for co-existent coronary and peripheral vascular disease. Mortality and morbidity were recorded to March 1991. Significantly more patients with neuropathy had co-existent peripheral vascular disease: 24(35%) compared to 6(9%) controls (p = 0.0021). Twenty (30%) of those with neuropathy and no controls had retinopathy at diagnosis, which was sight-threatening in 10. Seven (10%) with neuropathy but no controls presented with foot ulcers, one requiring limited amputation. Two more patients with neuropathy and one control subsequently developed foot ulcers resulting in one or more amputation in each group. Twenty-one (31%) of those with neuropathy and 14 (21%) controls died (p = 0.2109). In conclusion more diabetic patients with clinically evident peripheral neuropathy at diagnosis have peripheral vascular disease than matched patients without neuropathy. It is likely that macrovascular disease either exacerbates or causes the neuropathy in this group of patients. They are at high risk of developing foot ulceration and high priority should be given to foot care in planning their management.

Aged↗
PubMed1993

Erythromycin induces supranormal gall bladder contraction in diabetic autonomic neuropathy.

Gall bladder motor function is impaired in some patients with diabetes. It has been suggested that the abnormalities of gall bladder motility are confined to those patients with autonomic neuropathy. Erythromycin, a motilin receptor agonist, causes gall bladder contraction in both normal subjects and patients with gall stones with impaired gall bladder emptying. The effect of erythromycin on gall bladder motility in seven patients with diabetes with an autonomic neuropathy, six patients with diabetes without autonomic neuropathy, and 17 normal subjects was studied using ultrasound. There was no significant difference in gall bladder fasting volume between the three groups, but the patients with diabetes with autonomic neuropathy had impaired postprandial gall bladder emptying compared with normal subjects (percentage emptied (SEM) 40 (10.3)% v 64 (2.8)%, p < 0.01) and those with autonomic neuropathy (48 (7.7)%, NS). Erythromycin produced a dramatic reduction in gall bladder fasting volume in patients with diabetes with an autonomic neuropathy, compared with either normal subjects or patients with diabetes without autonomic neuropathy (percentage reduction 62 (4.6)% in patients with autonomic neuropathy, v 37 (17.6)% in those without autonomic neuropathy, and 26 (7.3)% in the normal subjects, (p < 0.02) and returned gall bladder emptying to normal in all patients with impaired emptying. The pronounced effect of erythromycin in diabetic autonomic neuropathy suggests denervation supersensitivity and that the action of erythromycin on the gall bladder is neurally modulated.

Adult↗
PubMed1993

Mechanisms of arterial hypotension after therapeutic dose of subcutaneous insulin in diabetic autonomic neuropathy.

To assess whether a therapeutic, subcutaneous injection of insulin exerts hemodynamic effects in subjects with IDDM, 0.2 U/kg regular insulin was injected subcutaneously in 17 IDDM subjects: 6 without autonomic neuropathy, 7 with autonomic neuropathy and othostatic hypotension, and 4 with autonomic neuropathy but without orthostatic hypotension. Plasma glucose was maintained at approximately 8.5 mM throughout the studies. Mean blood pressure, plasma norepinephrine concentration, forearm vascular resistances, and calf venous volume were measured before and 120 min after subcutaneous insulin, in the supine position and 5 min after standing. Supine plasma volume ([125I]albumin and [131I]albumin) was measured before and after subcutaneous injection of insulin. In all three groups, subcutaneous insulin activated the sympathetic nervous system (approximately 30% increase in norepinephrine concentration). In subjects with IDDM but without autonomic neuropathy, standing forearm vascular resistance increased approximately 70% less after subcutaneous insulin, but supine or standing mean blood pressure did not decrease. In contrast, in subjects with IDDM with autonomic neuropathy and orthostatic hypotension, subcutaneous insulin decreased supine mean blood pressure (from 99 +/- 3 to 94 +/- 5 mmHg) and exaggerated the standing decrement in mean blood pressure (24 +/- 3 vs. 19 +/- 2 mmHg) (P < 0.05). This was associated with a decrease in forearm vascular resistance. Similarly, in subjects with IDDM with autonomic neuropathy without orthostatic hypotension, subcutaneously injected insulin decreased supine mean blood pressure (from 95 +/- 2 to 89 +/- 2 mmHg) and standing mean blood pressure by 8 +/- 1 mmHg (P < 0.05). Calf venous volume was not affected by subcutaneous insulin in any of the three groups. Plasma volume did not change after subcutaneous insulin in subjects with IDDM without autonomic neuropathy, whereas it decreased in those with autonomic neuropathy and orthostatic hypotension from 1.692 +/- 0.069 to 1.610 +/- 0.064 L/m2, without orthostatic hypotension from 1.631 +/- 0.027 to 1.593 +/- 0.024 L/m2, P < 0.05). No hemodynamic effects were observed when subjects with IDDM were restudied in a control experiment where placebo (distilled water), not insulin, was injected subcutaneously. In conclusion, therapeutic doses of subcutaneous insulin activate the sympathetic nervous system; decrease blood pressure in subjects with IDDM with autonomic neuropathy, but not in those without, primarily by decreasing arterial vascular resistances and plasma volume; and have no effects of capacitance vessels. Thus, in subjects with IDDM without autonomic neuropathy, greater activation of sympathetic nervous system after subcutaneous injection of insulin prevents orthostatic hypotension.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗