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PubMed2006

Peripheral neuropathy exacerbation associated with topical 5-fluorouracil.

Peripheral neuropathy secondary to 5-flourouracil and capecitabine (Xeloda) has been reported. We report the first case of exacerbation of peripheral neuropathy related to topical 5-flourouracil (Efudex). A 70-year-old Caucasian male with a history of actinic keratosis for 15 years was treated intermittently with topical application of 5-flourouracil. He also developed sensory peripheral neuropathy around the same time, but extensive work-up disclosed no clear etiology. In early 2005, he developed an exacerbation of his peripheral neuropathy following a 21-day course of topical 5-flourouracil for actinic keratosis, especially pain and parasthesias. Dihydropyrimidine dehydrogenase activity was evaluated in the peripheral mononuclear cells both by radioassay and by [2-C] uracil breath test. Dihydropyrimidine dehydrogenase activity was within the normal range by both methods. Stopping topical 5-flourouracil resolved the symptoms to baseline. Instead of topical 5-flourouracil, topical imiquimod was used which did not exacerbate his neuropathy. He was not re-challenged with topical 5-flourouracil. Topical 5-flourouracil has been known to cause mainly dermatological adverse effects, but systemic effects because of absorption are possible, especially in dihydropyrimidine dehydrogenase-deficient patients. As our patient had no other cause responsible for his neuropathy, the onset of symptoms coincided historically with topical application of 5-flourouracil and the 5-flourouracil usage preceded an exacerbation of sensory symptoms, we conclude that this drug was responsible for his polyneuropathy.

Aged↗
PubMed2007

Vasculitic neuropathies: an update.

BACKGROUND: Systemic vasculitis has been classically categorized as a primary disorder, such as polyarteritis nodosa, Churg-Strauss syndrome, and Wegener granulomatous, or as a secondary process, representing a complication from a connective tissue disorder (eg, rheumatoid vasculitis), infection, medication, or malignancy. Peripheral neuropathy is a well-recognized consequence of systemic vasculitis due to peripheral nerve infarction with Wallerian degeneration. Rarely, neuropathy is the sole manifestation of vasculitis, referred to as nonsystemic vasculitic neuropathy (NSVN). These conditions are defined pathologically by tissue biopsy demonstrating disruption or destruction of the vessel wall with inflammatory cell infiltrates. REVIEW SUMMARY: The diagnosis of vasculitic neuropathy is straightforward in patients with an established diagnosis of systemic vasculitis and classic features of mononeuritis multiplex. Most patients have clinical features of a subacute, progressive, generalized but asymmetric, painful, sensorimotor polyneuropathy. Laboratory tests often indicate features of systemic inflammation, such as an elevated sedimentation rate or positive anti-neutrophil cytoplasmic antibody, and electrodiagnostic evaluation shows multiple mononeuropathies or a confluent, asymmetric axonal neuropathy. Nerve biopsy is necessary to establish the diagnosis in most cases, particularly in patients with NSVN. This review summarizes the current treatment of vasculitic neuropathy. CONCLUSION: Long-term immunosuppressive therapy is required in most cases. High-dose prednisone combined with intravenous pulse or oral daily cyclophosphamide is standard initial therapy. In those with NSVN, cyclophosphamide also should be used if prednisone monotherapy is ineffective or the patient relapses with tapering. Other agents, such as azathioprine, methotrexate, intravenous immunoglobulin, mycophenolate mofetil, plasma exchange, and rituximab can be offered to patients who are intolerant or have a contraindication to cyclophosphamide. However, evidence for the benefit of these agents is limited to case reports and small case series.

Humans↗
PubMed2003

Recent developments in the HIV neuropathies.

PURPOSE OF REVIEW: With the introduction of highly active antiretroviral therapy peripheral neuropathies have become the most common neurological complications in HIV infection. The frequency and spectrum of these neuropathies are changing, as the various toxic and immune factors are modified by new treatment strategies. Recent studies have provided a better understanding of the risk factors, markers and relevant pathogenic mechanisms, and a thorough review of these is critical for an improved understanding of this important and increasingly common complication. RECENT FINDINGS: The combined use of dideoxynucleosides, in association with immune-mediated mechanisms triggered by HIV infection, are critical in the development of distal sensory polyneuropathy. Valuable markers of neuropathy such as intraepidermal nerve fiber density from skin biopsies have been validated and promise to be a valuable tool in the detection and monitoring of distal sensory polyneuropathy. Markers of virological activity have also been associated with the severity of neuropathic pain in distal sensory polyneuropathy. In some instances, the enhanced viral suppression from antiretroviral agents may actually improve or decrease the frequency of certain types of neuropathy. New evidence supports mitochondrial toxicity as a principal mechanism for dideoxynucleoside-associated sensory neuropathy, and questions arise about enhanced risk with pre-existing mitochondrial defects. Confirmed treatments are limited to the reduction of symptoms, with a need for the further investigation of corrective therapies. SUMMARY: Increased and improved surveillance for HIV-associated neuropathy will allow earlier interventions to improve quality of life and prevent severe toxicities. A better understanding of the prevailing mechanisms will allow for more effective interventions.

Biomarkers↗
PubMed2005

New developments in diabetic neuropathy.

PURPOSE OF REVIEW: Diabetic neuropathy is a debilitating consequence of type 1 and 2 diabetes. Hyperglycemia disrupts the normal function of neurons and their supporting glia at multiple levels. The complexity of this complication, combined with difficulties of delivering therapy to sensory, sympathetic and parasympathetic neurons, contributes to the intractability of this serious diabetic complication. This review summarizes recent reviews examining the state of research on and treatment of diabetic neuropathy and highlights areas of clinical and basic research that may yield new diagnostic and treatment options. RECENT FINDINGS: Recent reviews summarize the effects of hyperglycemia on the peripheral nervous system as well as diagnosis and treatment of patients with diabetic neuropathy. Advances in the analysis of intraepidermal fiber densities could shorten the time course of clinical trials and extend data analyses to include sympathetic as well as sensory information. Unchecked glucose-mediated oxidative stress and advanced glycation endproduct signaling through receptors for advanced glycation endproducts are implicated in diabetic neuropathy and may serve as new therapeutic targets. SUMMARY: The best efforts of countless investigators have yet to find effective treatments either to stop the progression of axonal degeneration and cell death or regrow damaged axons. Basic research into the prevention of oxidative stress caused by excess glucose as well as the prevention of advanced glycation endproduct/receptor for advanced glycation endproduct signaling may offer new therapeutic targets. The use of skin biopsies may aid in early detection of both sensory and autonomic neuropathy, and perhaps in the case of patients with type 2 diabetes, diagnose neuropathy prior to the onset of symptoms.

Animals↗
PubMed2006

Recent advances in HIV neuropathy.

PURPOSE OF REVIEW: To describe recent advances in HIV neuropathy. RECENT FINDINGS: Epidemiologic studies since highly active antiretroviral therapy was introduced have shown that the incidence of HIV-associated distal sensory polyneuropathy is reduced. Studies have also shown the relationship between distal sensory polyneuropathy and the use of neurotoxic antiretroviral drugs. Skin punch biopsy for assessment of epidermal nerve fiber density is valuable both for diagnosis of distal sensory polyneuropathy and as a predictor of the condition occurring in the future. An in-vitro model of antiretroviral toxic neuropathy showed that dideoxynucleoside analogues that cause neuropathy exert direct mitochondrial toxicity that is not mediated indirectly through the inhibition of DNA polymerase-gamma. HIV envelope protein gp120 exerts axonal toxicity directly or indirectly via perineuronal Schwann cells. A feline model of HIV, infection of neonatal cats with the feline immunodeficiency virus, showed development of peripheral neuropathy characterized by loss of epidermal innervation. SUMMARY: While epidemiological studies of HIV-associated peripheral neuropathy continue to provide useful information, pathogenic studies are moving forward. Animal models of the disease will allow researchers to 'manipulate' the system. It is hoped that these types of studies will translate to an improved understanding of the pathogenesis of HIV-associated neuropathies leading to better treatments.

Antiretroviral Therapy, Highly Active↗
PubMed2006

Anti-myelin-associated glycoprotein neuropathy.

PURPOSE OF REVIEW: The anti-myelin-associated glycoprotein (MAG) neuropathy is an antibody-mediated demyelinating neuropathy. The clinical picture is characterized by a distal and symmetric, mostly sensory neuropathy. Monoclonal immunoglobulin M anti-MAG antibodies are uniquely found in this condition and are believed to be pathogenic. This review focuses on recent progress in understanding the mechanisms of this neuropathy and discusses new therapeutic advances. RECENT FINDINGS: Different electrophysiological parameters have been demonstrated to distinguish the anti-MAG-associated polyneuropathy from chronic inflammatory demyelinating polyneuropathy. The electrophysiological findings generally indicate a predominantly demyelinating neuropathy with a distal accentuation of conduction slowing. Analyses of pathology in nerve tissue from anti-MAG patients using classical nerve biopsy or skin biopsy tissue demonstrated immunoglobulin M deposits at the site of MAG localization, demyelination and axonal degeneration. MAG is a Schwann cell-based glycoprotein and has been implicated as a mediator of an outside-in signaling cascade influencing the cytoskeletal integrity of axons. SUMMARY: Therapy in patients with anti-MAG neuropathy is directed at reducing the antibody concentration, blocking the effector mechanisms and depleting the monoclonal B cells. The recent availability of rituximab, a monoclonal antibody suppressing B-cell clones, which is not myelosuppressive and does not cause secondary malignancies, allows for early targeted intervention.

Animals↗
PubMed2006

Expression of capsaicin receptor immunoreactivity in human peripheral nervous system and in painful neuropathies.

We describe the expression of the capsaicin receptor (TRPV1) in human peripheral nervous system (PNS) and its changes in sural nerve and skin nerve fibers of patients with painful neuropathy. Dorsal root ganglion (DRG), root, and spinal cord autopsy specimens from subjects without PNS diseases were immunoassayed with anti-TRPV1 antibodies. Bright-field and confocal microscope studies using anti-TRPV1, protein gene product 9.5 (PGP 9.5), and unique-beta-tubulin (TuJ1) antibodies were performed in skin biopsies from 15 healthy subjects and 10 painful neuropathies. The density of intraepidermal nerve fiber (IENF) labeled by each antibody was quantified. Sural nerve biopsies from three patients with painful, one patient with nonpainful diabetic neuropathy, and two patients with multifocal motor neuropathy used as controls were immunoassayed with anti-TRPV1 antibodies and investigated by immunoelectron microscopy. TRPV1 strongly labeled laminae I and II of dorsal horns, most small-size and some medium-size DRG neurons, and small-diameter axons of dorsal roots. In sural nerve, TRPV1 was expressed within the cytoplasm of most unmyelinated and some small myelinated axons, in the muscular lamina of epineural vessels, and in the endothelium of endoneurial vessels. The density of IENF labeled by TRPV1, PGP 9.5, and TuJ1 did not differ. TRPV1 colocalized with TuJ1 in all IENF and dermal nerve bundles. Painful neuropathies showed a diffuse loss of TRPV1-positive axons both in the sural nerve and in the skin. Our findings demonstrated that TRPV1 is normally expressed throughout the nociceptive pathway of PNS and that TRPV1-positive peripheral nerve fibers degenerate in painful neuropathies.

Adult↗
PubMed2007

Linezolid-induced optic neuropathy: a mitochondrial disorder?

We report a case of bilateral mitochondrial optic neuropathies secondary to long-term linezolid treatment, show the nature of recovery, review the findings in the literature and propose a potential mitochondrial mechanism for linezolid-induced mitochondrial optic neuropathy. This is an observational case report and literature review with presentation of the clinical course of linezolid mitochondrial optic neuropathies through clinical and psychophysical documentation. Main outcome measures included: visual acuity, funduscopical examinations and peripapillary retinal nerve fibre layer (PRNFL) optical coherence tomography (OCT). A 6-year-old boy presented with bilateral optic neuropathies secondary to 1 year of linezolid treatment for osteomyelitis of the mandible. On presentation, visual acuities were 20/400 in both eyes, with considerable optic disc oedema, hyperaemia and PRNFL swelling confirmed by OCT. 2 weeks after the discontinuation of linezolid, visual acuities returned to 20/25 in both eyes, with reduction in the optic disc oedema, hyperaemia and PRNFL swelling. 3 months after the discontinuation of linezolid treatment, visual acuities were stable at 20/20 in both eyes, with a marked decrease in PRNFL swelling confirmed by OCT, and the development of mild temporal optic disc pallor in both eyes. Doctors should be aware of impairments of vision among patients on long-term linezolid treatment and promptly discontinue treatment to prevent irreversible vision loss. The development and resolution of bilateral optic neuropathies with considerable PRNFL swelling in this patient provide insight into the more general rubric of mitochondrial optic neuropathies.

Acetamides↗
PubMed2000

Reversal of dysthyroid optic neuropathy following orbital fat decompression.

AIMS: To document the successful treatment of five patients with dysthyroid optic neuropathy by orbital fat decompression instead of orbital bone decompression after failed medical therapy. METHODS: Eight orbits of five patients with dysthyroid optic neuropathy were selected for orbital fat decompression as an alternative to bone removal decompression. Treatment with systemic corticosteroids and/or orbital radiotherapy was either unsuccessful or contraindicated in each case. All patients satisfied clinical indications for orbital bone decompression to reverse the optic neuropathy. High resolution computerised tomographic (CT) scans were performed in all cases and in each case showed signs of enlargement of the orbital fat compartment. As an alternative to bone decompression, orbital fat decompression was performed on all eight orbits. RESULTS: Orbital fat decompression was performed on five patients (eight orbits) with optic neuropathy. Optic neuropathy was reversed in all cases. There were no cases of postoperative diplopia, enophthalmos, globe ptosis, or anaesthesia. All patients were followed for a minimum of 1 year. CONCLUSIONS: In a subset of patients with an enlarged orbital fat compartment and in whom extraocular muscle enlargement is not the solitary cause of optic neuropathy, fat decompression is a surgical alternative to bony decompression.

Adipose Tissue↗
PubMed1994

IgM ganglioside GM1 antibodies in patients with autoimmune disease or neuropathy, and controls.

AIMS: To compare the titre of anti-ganglioside antibodies (AGA) to GM1 ganglioside in patients with central and peripheral neurological disease and pure motor and sensorimotor neuropathy, in patients with classic autoimmune diseases, and controls. METHODS: AGA to GM1 were measured using an enzyme linked immunosorbent assay (ELISA) technique, highly purified bovine GM1 ganglioside, and sequential dilution of control and test sera. Antibody titre was calculated using the optical density readings of three consecutive serum dilutions multiplied by the dilution factor. RESULTS: A considerable overlap was evident in the titre of AGA to GM1 in control and test sera. High antibody titres were most frequent in patients with multifocal motor neuropathy with conduction block (MMNCB). Low AGA titre were observed in several patient groups. Compared with the controls, the median titre of AGA to GM1 was significantly higher in patients with multiple sclerosis, rheumatoid arthritis, primary Sjögren's syndrome and systemic lupus erythematosus. In contrast, the median titre in patients with diabetic peripheral neuropathy, motor neurone disease, sensorimotor neuropathy and chronic inflammatory demyelinating polyneuropathy was no different from that in normal control subjects. CONCLUSIONS: Estimation of AGA to GM1 may be helpful in the diagnosis of MMNCB in patients with a pure motor neuropathy but in few other conditions. Low titre AGA to GM1 are evident in several autoimmune conditions. The pathogenetic importance of AGA to GM1 in patients with neuropathy is not clear.

Arthritis, Rheumatoid↗
PubMed2004

Neurofibromatous neuropathy in neurofibromatosis 1 (NF1).

BACKGROUND: Neurofibromatosis 1 (NF1) is a common, autosomal dominant, neurocutaneous disease that is clinically and genetically distinct from the rare condition neurofibromatosis 2 (NF2). Neurofibromatous neuropathy has been regarded as a common feature of NF2, but is an unusual and unexplained complication of NF1. The clinical and histological features of the NF1 neuropathy are distinct from those encountered in NF2. We describe eight patients with a symmetrical polyneuropathy, which has been called neurofibromatous neuropathy. METHODS: Clinical assessments, laboratory investigations, neuroimaging, and neurophysiology were undertaken in eight individuals with neurofibromatous neuropathy. None were referred because of neuropathic symptoms. Two subjects underwent sural nerve biopsy and three agreed to mutational analysis. RESULTS: The patients had an indolent symmetrical predominantly sensory axonal neuropathy and unusually early development of large numbers of neurofibromas. The biopsied nerves showed diffuse neurofibromatous change and disruption of the perineurium. Two patients developed a high grade malignant peripheral nerve sheath tumour. Disease causing mutations were detected in two individuals and molecular studies did not reveal any whole gene deletions. CONCLUSIONS: Neurofibromatous neuropathy occurred in 1.3% of 600 patients with NF1. Its cause may be a diffuse neuropathic process arising from inappropriate signalling between Schwann cells, fibroblasts, and perineurial cells.

Adult↗
PubMed2004

Axonal sensorimotor neuropathy in patients with beta-thalassaemia.

OBJECTIVE: The purpose of this study was to investigate the prevalence of peripheral neuropathy in patients with beta-thalassaemia. METHODS: Thirty six patients with a mean age of 29.2+/-8.2 years and 17 healthy controls with a mean age of 27.6+/-9.1 were included in this study. Measurements included the neuropathy symptoms score (NSS), the neuropathy disability score (NDS) as well as nerve conduction studies of two motor (ulnar and peroneal) and two sensory (ulnar and sural) nerves of the right limbs. RESULTS: A mainly sensory axonal polyneuropathy was present in 19 out of 36 patients (52.7%). Eight out of these 19 patients also had abnormal NDS values. The neuropathy correlated significantly with the age of the patients and the hematocrit. However, it did not correlate with the presence of antibodies against HCV, the ferritin levels, or with a history of transfusions, desferrioxamine treatment, or splenectomy. CONCLUSIONS: This study showed a high prevalence of a predominantly sensory neuropathy in patients with beta-thalassaemia. The electrophysiological data suggest that the underlying pathology is an axonopathy. Chronic hypoxia of the nerves resulting from severe anaemia may contribute to the pathogenesis of this neuropathy.

Adolescent↗
PubMed1972

Peripheral neuropathy in chronic liver disease: clinical, electrodiagnostic, and nerve biopsy findings.

In a prospective study of 70 unselected patients with chronic liver disease, clinical signs of a peripheral neuropathy were observed in 13 patients. Abnormal nerve conduction was demonstrated in nine of these and in one further patient who had no abnormal neurological signs. The occurrence of a neuropathy (in patients with cryptogenic cirrhosis, haemochromatosis, active chronic hepatitis as well as in alcoholic cirrhosis) could not be related to liver function, although it was associated with higher IgA and IgM values. Clinical diabetes was present in six of the 14 patients with neuropathy but there was no relation in the non-diabetic patients between neuropathy and minor impairment of carbohydrate tolerance. Those with neuropathy had a significantly higher incidence of oesophageal varices and there was also a relationship to a history of previous encephalopathy. Sural nerve biopsy was carried out on 14 patients, eight of whom had clinical or electrodiagnostic evidence of neuropathy. Single nerve fibres were examined by teasing and in all nerves histological evidence was found of an indolent process which had damaged whole Schwann cells and which resulted in demyelination and remyelination. Diabetic angiopathy was not seen and axonal degeneration, which was never severe, was found in all disease groups equally.

Adolescent↗
PubMed1993

Tibial nerve somatosensory evoked potentials at various stages of peripheral neuropathy in insulin dependent diabetic patients.

To determine whether central nervous conduction deficits are related to the degree of peripheral neuropathy somatosensory evoked potentials (SEP) were measured after tibial nerve stimulation in 51 healthy subjects aged 39.3 (SE 2.0, (range 21-71) years and 100 insulin dependent diabetic patients aged 37.3 (1.5, 18-73) years. Five criteria were used for staging of peripheral neuropathy: nerve conduction; thermal discrimination threshold; vibration perception threshold; tendon reflexes; and neuropathic symptoms. Thirty seven patients had fewer than two abnormalities among the first four criteria and no symptoms (stage 0 = no neuropathy), 37 had 2 or more abnormalities but no symptoms (stage 1 = subclinical neuropathy); 26 had 2 or more abnormalities in conjunction with symptoms (stage 2 = symptomatic neuropathy). Multiple regression analysis was used to define the age and height dependent limits of normal of SEP at the 97.5th and 2.5th centiles. In five patients with stage 1, seven patients with stage 2, but no patient with stage 0 the individual SEP components were unrecordable. The relative frequencies of abnormally prolonged or non-evokable popliteal N8 latency as well as cortical N33 latency and N33/P40 amplitude increased significantly from stage 0 (3-30%) to stage 1 (22-62%) and stage 2 (46-84%) (p < 0.05 for each component and stage). The numbers and percentages of abnormal recordable spinal N22-30 and supraspinal N30-33 interpeak latencies were two (6.3%) and four (11.8%) in patients with stage 0, but these rates did not increase in subjects with stage 1 or 2. The components of SEP were significantly associated with the indices of peripheral and autonomic function tests. There were no major relations between the latencies of SEP and duration of diabetes or prevailing glycaemic control. These findings suggest that the degree of dysfunction along the somatosensory afferent pathways in insulin dependent diabetic patients depends on the stage of peripheral neuropathy; is not related to the degree of glycaemic control or duration of diabetes; and can be characterized mainly by an alteration of the cortical sensory complex and peripheral transmission delay, while spinal and supraspinal conduction deficits are detected infrequently.

Adult↗
PubMed1993

Anti-sulphatide antibodies in peripheral neuropathy.

A study was carried out on 135 patients with chronic idiopathic neuropathy (63), neuropathy associated with monoclonal gammopathy (51, including eight with anti-MAG antibody activity) and the Guillain-Barré syndrome (GBS) (21). Serum IgM, IgG and IgA anti-sulphatide antibody titres were compared with titres in 304 patients with other neurological or immunological diseases and in 50 normal subjects. Titres were presented a) as the highest serum dilution at which reactivity could be detected, and b) in the linear region of the optical density curve. A substantial number of patients with neurological or immunological diseases had higher titres than normal subjects. Compared with normal and disease controls, five patients with neuropathy associated with IgMk monoclonal gammopathy had raised titres of IgM anti-sulphatide antibodies and one patient with GBS had raised IgM, IgG and IgA anti-sulphatide antibodies in the acute phase of the disease. Two patients had a predominantly axonal sensory neuropathy with presenting symptoms of painful paresthesiae and minimal neurological deficit. Three patients had a predominantly demyelinating sensorimotor neuropathy associated with anti-MAG antibody activity. The patient with GBS had extensive sensory loss and antibody titres returned to normal within three weeks. Raised titres of anti-sulphatide antibodies occurred in several types of neuropathy, but all had some degree of sensory impairment and associated immunological abnormality.

Adult↗
PubMed2005

Association of Paclitaxel pharmacokinetics with the development of peripheral neuropathy in patients with advanced cancer.

PURPOSE: The shortening of infusion time from 3 to 1 hour decreases the systemic exposure (area under the curve, AUC) of total and unbound paclitaxel but increases the AUC of its vehicle Cremophor EL, whereas the time above total paclitaxel concentrations of 0.05 micromol/L (T >0.05) remains almost constant. As both Cremophor EL and paclitaxel are neurotoxic, we evaluated their pharmacodynamic effects on the development of peripheral neuropathy as the most important nonhematologic toxicity. EXPERIMENTAL DESIGN: Patients with advanced cancer of different origin were randomized to receive a maximum of 12 weekly-given 1- or 3-hour infusions of 100 mg/m2 paclitaxel (Taxol). Twenty-four patients were assessable for both pharmacokinetics and peripheral neuropathy development evaluated by a clinical scoring system including sensory symptoms, strength, tendon reflexes, and vibratory sense. RESULTS: Patients with peripheral neuropathy development (n=14) received more weeks of therapy (P=0.056) and showed significantly higher T(>0.05) (P=0.022) and overall systemic drug exposures (weeks of therapy x AUC) for total paclitaxel (P=0.002) and unbound paclitaxel (P=0.003) than those without peripheral neuropathy. In Kaplan-Meier analyses, T(>0.05) > or = 10.6 hours (P=0.023), AUC of total paclitaxel > or = 4.7 microg/mL x hour (P = 0.047), and AUC of unbound paclitaxel > or = 0.375 microg/mL x hour (P = 0.095) were identified as being potential factors for peripheral neuropathy development. In a Cox regression analysis, only T(>0.05) > or = 10.6 hours remained as an independent risk factor (relative risk, 18.43; P = 0.036) after adjusting for prior vincamycin (relative risk, 11.28; P = 0.038). CONCLUSIONS: From the results obtained in this study, it is concluded that exposure to paclitaxel but not Cremophor EL is associated with peripheral neuropathy development.

Adult↗
PubMedDate not supplied

The role of autonomic neuropathy in the genesis of intradialytic hypotension.

BACKGROUND: Intradialytic hypotension is a frequent complication of hemodialysis. Some authors have pointed to autonomic neuropathy as a major cause of intradialytic hypotension. However, other authors have found no such association. METHODS: Tilt-table test and time-domain measures of heart rate variation were used to determine autonomic function. Conventional nerve conduction studies (NCS) were also performed to assess whether intradialytic hypotension is associated with polyneuropathy and autonomic neuropathy. RESULTS: The incidences of polyneuropathy confirmed by standard NCS were similar for the intradialytic hypotensive and normotensive subjects, implying that polyneuropathy is not strongly related to intradialytic hypotension. However, heart rate variation decreased significantly in intradialytic hypotensive subjects, suggesting that isolated autonomic neuropathy plays a major role in the pathogenesis of intradialytic hypotension. One of 9 intradialytic hypotensive subjects had normal autonomic tests and 2 of 18 normotensive subjects had abnormal autonomic function, implying that intradialytic hypotension is not caused by autonomic neuropathy alone. CONCLUSION: Autonomic neuropathy plays an important role in the genesis of intradialytic neuropathy. Tilt-table is easily performed and time-domain measures for heart rate variation are easily determined. Tilt-table test and time-domain measures provide useful information concerning autonomic function.

Adult↗
PubMed1981

Anterior ischemic optic neuropathy. VI. In juvenile diabetics.

3 cases of acute optic neuropathy in juvenile diabetics are reported. The neuropathy included initially optic disc edema (ODE), usually with prominent, dilated and frequently telangiectatic vessels over the disc, and later, generally, development of optic disc-related visual field defects. On resolution of the neuropathy, the disc was normal in all eyes except for a mild pallor in one, and the visual acuity and fields recovered to normal. 2 of the patients also had early diabetic retinopathy. The nature of the optic neuropathy is discussed. We feel the available evidence indicates that the condition most likely represents a mild or subclinical anterior ischemic optic neuropathy (AION) despite the youth of the patient. It is pertinent to note that AION can vary widely not only in severity (from subclinical to severe) but also in age distribution (from juvenile to elderly), and the subject is discussed. The clinical significance of early detection of this optic neuropathy, and the dangers of confusing it with proliferative diabetic retinopathy or ODE due to other causes, are stressed.

Adolescent↗