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At least 109 records · Page 6Linked to original sources
PubMed1998

Alcoholism, peripheral neuropathy (PNP) and cardiovascular autonomic neuropathy (CAN).

In contrast to diabetic autonomic neuropathy, cardiovascular autonomic neuropathy (CAN) in long-term alcoholics has been studied rarely. Using both standardized bedside tests and computer-assisted analysis of heart rate variability (HRV), we prospectively compared autonomic neurocardial function between 35 strictly selected, detoxified alcoholics (DSM-III-R), and 80 well matched healthy controls. Evidence for a potential CAN was found in 25.7% of all the alcoholics studied and in 41% of those with clinically manifest PNP (n=22). Overall, our results demonstrated a significant association between the presence of a CAN and peripheral neuropathy (PNP) amongst chronic alcoholics (chi-square test P<0.05); there was no evidence of a CAN in any of the alcoholics without a clinically manifest PNP. The CAN was characterized by a dissociated appearance of parasympathetic and sympathetic disorders. Our findings provide reason to suspect that the total lifetime dose of alcohol and the duration of alcohol dependence are the most important factors contributing to the pathogenesis of both PNP and sympathetic dysfunction. As is the case with diabetics, computer-assisted measurements of HRV including spectral analysis appear to be far superior to conventional bedside tests for detecting evidence of cardiovagal dysfunction in long-term alcoholics.

Adult↗
PubMed1999

Acute motor axonal neuropathy and acute motor-sensory axonal neuropathy share a common immunological profile.

Griffin and colleagues (Griffin JW, Li CY, Ho TW, Tian M, Gao CY, Xue P, Mishu B, Cornblath DR, Macko C, McKhann GM, Asbury AK. Pathology of motor-sensory axonal Guillain-Barré syndrome. Ann Neurol 1996;39:17-28 [4]) proposed that acute motor axonal neuropathy (AMAN) and acute motor-sensory axonal neuropathy (AMSAN) are part of the spectrum of a single type of immune attack on the axon. In contrast, IgG anti-GM1 antibody is associated closely with AMAN, but whether other IgG anti-ganglioside antibodies are associated with this neuropathy is not clear. We investigated whether IgG anti-ganglioside antibodies can be used as immunological markers to differentiate AMAN from acute inflammatory demyelinating polyneuropathy (AIDP) and whether these autoantibodies are present in AMSAN. The frequencies of anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies in 21 AMAN patients were significantly higher than in 19 AIDP patients. Anti-GM1b and anti-GD1a IgG, as well as anti-GM1 IgG antibodies, therefore are immunological markers for AMAN. The patients with AMSAN had anti-GM1, anti-GM1b, and anti-GD1a IgG antibodies, indicative that AMAN and AMSAN share a common immunological profile.

Adolescent↗
PubMed2004

[Leber's optic neuropathy presenting as an alcohol- and tobacco-related optic neuropathy].

The authors report a case of a 70-year-old man presenting a recent unilateral decrease in visual acuity, appearing in a context of alcohol and tobacco intoxication. Diagnosis of Leber's optic neuropathy was evoked after elimination of other causes of a visual acuity decrease such as giant cell arteritis and compressive or inflammatory optic neuropathy. The authors emphasize that Leber's optic neuropathy must be evoked in a recent decrease in visual acuity, even if it appears in an unusual context.

Aged↗
PubMed2004

Early parasympathetic neuropathy associated with elevated fasting plasma C-peptide concentrations and late parasympathetic neuropathy with hyperglycaemia and other microvascular complications.

AIMS: To examine the relationship between parasympathetic neuropathy, hyperinsulinaemia, glycaemic control (HbA(1c)), and future diabetic complications. METHODS: We assessed parasympathetic nerve function [expiration/inspiration (E/I) ratio], glomerular filtration rate (GFR), glycaemic control (HbA(1c)), fasting plasma (f-p-) C-peptide in 82 Type 2 diabetic patients (age 61 +/- 1 years) 5 and 12-15 years after diagnosis. Diabetic retinopathy was assessed 15 years after diagnosis. RESULTS: High HbA(1c) values in the first study were associated with retinopathy (with 8.6 +/- 2.0 vs. without retinopathy 6.2 +/- 1.9%; P < 0.0001) and disturbed parasympathetic nerve function (low E/I ratio; r(s) = -0.41; P = 0.0061) in the second study, as well as with deteriorations in GFR between the first and second study (r(s) = 0.62; P < 0.0001). Patients with parasympathetic neuropathy in the first study had significantly higher f-p-C-peptide concentrations than those without 3 years (1.20 +/- 0.43 vs. 0.86 +/- 0.40 nmol/l; P = 0.0015) and 5 years (1.20 +/- 0.44 vs. 0.82 +/- 0.33 nmol/l; P < 0.0001), but not 15 years after diagnosis. CONCLUSION: High HbA(1c) values 5 years after diagnosis of Type 2 diabetes were associated with retinopathy, disturbed parasympathetic nerve function, and deterioration in GFR 7-10 years later. Parasympathetic neuropathy 5 years after diagnosis was associated with high C-peptide concentrations. Parasympathetic nerve function has to be considered when beta-cell function is evaluated. Hyperglycaemia is an important factor for the development of complications in Type 2 diabetes.

Autonomic Nervous System Diseases↗
PubMed2004

Progressive auditory neuropathy in patients with Leber's hereditary optic neuropathy.

OBJECTIVE: To investigate auditory neural involvement in patients with Leber's hereditary optic neuropathy (LHON). METHODS: Auditory assessment was undertaken in two patients with LHON. One was a 45 year old woman with Harding disease (multiple-sclerosis-like illness and positive 11778mtDNA mutation) and mild auditory symptoms, whose auditory function was monitored over five years. The other was a 59 year old man with positive 11778mtDNA mutation, who presented with a long standing progressive bilateral hearing loss, moderate on one side and severe to profound on the other. Standard pure tone audiometry, tympanometry, stapedial reflex threshold measurements, stapedial reflex decay, otoacoustic emissions with olivo-cochlear suppression, auditory brain stem responses, and vestibular function tests were undertaken. RESULTS: Both patients had good cochlear function, as judged by otoacoustic emissions (intact outer hair cells) and normal stapedial reflexes (intact inner hair cells). A brain stem lesion was excluded by negative findings on imaging, recordable stapedial reflex thresholds, and, in one of the patients, olivocochlear suppression of otoacoustic emissions. The deterioration of auditory function implied a progressive course in both cases. Vestibular function was unaffected. CONCLUSIONS: The findings are consistent with auditory neuropathy-a lesion of the cochlear nerve presenting with abnormal auditory brain stem responses and with normal inner hair cells and the cochlear nucleus (lower brain stem). The association of auditory neuropathy, or any other auditory dysfunction, with LHON has not been recognised previously. Further studies are necessary to establish whether this is a consistent finding.

Audiometry, Evoked Response↗
PubMed1992

"Chronic sensory demyelinating neuropathy": chronic inflammatory demyelinating polyneuropathy presenting as a pure sensory neuropathy.

The clinical electrophysiological and histological features of 10 cases of "chronic sensory demyelinating neuropathy" (CSDN) are reported. This entity is characterised by: 1) subacute or chronic progression; 2) pure sensory neuropathy; 3) high spinal fluid protein in the majority of cases; 4) electrophysiological evidence of demyelination affecting motor as well as sensory nerve fibres; 5) demyelination on sural nerve biopsy and 6) good response to immunotherapy in progressive phase. It is believed that this entity represents chronic inflammatory demyelinating polyneuropathy (CIDP) presenting as pure sensory neuropathy.

Aged↗
PubMed1998

[Uremic neuropathy--I. Is uremic neuropathy related to patient age, duration of nephropathy and dialysis treatment?].

The aim of the study was to analyse the relationship between clinical and electrophysiological features of uremic neuropathy and age of patients, duration of kidney disease, renal failure and dialysis treatment. 51 patients with end-stage renal failure without diabetes were examined. Apart from a basic neurological examination, conduction velocities in the sural and tibial nerves were determined, and in order to assess the function of the autonomic nervous system, R-R interval variation and sympathetic skin response were tested. In majority of patients, symptoms and signs of sensorimotor neuropathy were found, and about 50% of them had dysautonomia. A negative correlation between age and R-R interval variation was observed. No relationship was found between neuropathy and the duration of nephropathy, duration of renal nor dialysis treatment.

Adult↗
PubMed1998

[Uremic neuropathy--II. Is pruritus in dialyzed patients related to neuropathy?].

The problem of pruritus in dialyzed patients remains unsolved. The aim of this study was to analyse the relationship between pruritus and clinical symptoms and signs, and electrophysiological aspects of peripheral neuropathy, both somatic and autonomic. 51 patients with end-stage renal failure undergoing hemodialysis were examined. Diabetics were excluded. Apart from taking history and physical examination, conduction velocities in peripheral nerves were determined, and R-R interval variation (RRIV: assessment of vagal function) and sympathetic skin response (SSR) tests were performed. Pruritus was present in about 63% of patients. In majority of them, symptoms and sings of neuropathy were also found. A significant relationship between pruritus and paresthesia was noted. This indicates a possible relationship between pruritus and secondary neuropathy.

Adult↗
PubMedDate not supplied

[Neuropathies and sensory neuropathies].

INTRODUCTION: In the recent years several clinical syndromes have been recognized that are purely sensory in character and therefore the site of lesion is seemingly restricted to nerve cell bodies in the posterior root ganglia. Collectively, these disorders are referred to as sensory neuronopathies. Although they may present as distinct clinical entities with different etiologies, the severity of the clinical manifestations and outcomes varies and may overlap with those of sensory neuropathy. This similarities are better understood in the case of toxic sensory neuropathies where a dose-dependent response has been clearly demonstrated; experimentally, low doses of pyridoxine induce sensory neuropathy whereas higher doses cause neuronopathy.

Acute Disease↗
PubMed1999

Sympathetic skin responses in hereditary sensory and autonomic neuropathy and familial amyloid neuropathy are different.

We compared the clinical and electrophysiological findings in seven patients with familial amyloid polyneuropathy (FAP) and six with hereditary sensory and autonomic neuropathy type I (HSAN). Both groups had progressive loss of pain and temperature appreciation, beginning distally in the feet. In HSAN, the median sensory nerve action potentials (SNAP) were lost early, but the sympathetic skin responses (SSR) were always preserved. In FAP, the SSR were lost at an early stage. The SSR may thus help to distinguish between these two causes of small-fiber neuropathy early in the course of the disorder.

Action Potentials↗
PubMed1996

Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the Ischemic Optic Neuropathy Decompression Trial.

OBJECTIVE: To describe the baseline clinical characteristics of patients in the Ischemic Optic Neuropathy Decompression Trial (IONDT). DESIGN: The IONDT is a single-masked, multicenter, randomized clinical trial. SETTINGS: Twenty-five US clinical centers. PATIENTS: Eligibility criteria for randomization to either optic nerve sheath decompression surgery or careful follow-up included a diagnosis of acute unilateral nonarteritic anterior ischemic optic neuropathy (NAION), a visual acuity of 20/64 or worse and better than no light perception, and an age of 50 years or older. Patients who were eligible except for having visual acuity better than 20/64 were not randomized, but were followed up. METHODS: Each patient underwent a standardized history and examination by certified study personnel within 14 days of the onset of symptoms. Masked personnel performed outcome measurements. RESULTS: Of 420 patients with NAION, 258 were randomized, and 162 were not randomized and are being followed up. Sixty-two percent of the patients were men and 95% were white. The mean +/- SD age at onset was 66.0 +/- 8.7 years. Hypertension was reported in 47% of the patients in the IONDT, and 24% of the patients had diabetes mellitus. Forty-two percent of the patients recalled the onset of visual symptoms to be within 2 hours of awakening. Initial visual acuities in the study eye ranged from 20/20 or better to light perception, with 49% of the patients seeing better than 20/64 and 34% of the patients seeing 20/200 or worse. The mean Westergren sedimentation rate was 18.4 mm/h, with 9% of the patients having a rate greater than 40 mm/h. The nonrandomized patients (visual acuity better than 20/64) were younger, 72% were male, and they had a lower prevalence of hypertension and diabetes mellitus. CONCLUSION: Although our baseline findings are derived from a selected population of patients with NAION who were eligible for the IONDT, they provide the first description of NAION from a large prospective study that used a standard definition of NAION and only included patients who were identified within 2 weeks of the onset of symptoms.

Aged↗
PubMed2001

Hereditary motor and sensory neuropathy-russe: new autosomal recessive neuropathy in Balkan Gypsies.

A novel peripheral neuropathy of autosomal recessive inheritance has been identified in Balkan Gypsies and termed hereditary motor and sensory neuropathy-Russe (HMSN-R). We investigated 21 affected individuals from 10 families. Distal lower limb weakness began between the ages of 8 and 16 years, upper limb involvement beginning between 10 and 43 years, with an average of 22 years. This progressive disorder led to severe weakness of the lower limbs, generalized in the oldest subject (aged 57 years), and marked distal upper limb weakness. Prominent distal sensory loss involved all modalities, resulting in neuropathic joint degeneration in two instances. All patients showed foot deformity, and most showed hand deformity. Motor nerve conduction velocity was moderately reduced in the upper limbs but unobtainable in the legs. Sensory nerve action potentials were absent. There was loss of larger myelinated nerve fibers and profuse regenerative activity in the sural nerve. HMSN-R is a new form of autosomal recessive inherited HMSN caused by a single founder mutation in a 1 Mb interval on chromosome 10q.

Adolescent↗
PubMed1994

Relationship between diabetic autonomic neuropathy and peripheral neuropathy as assessed by power spectral analysis of heart rate variations and vibratory perception thresholds.

To investigate the relationship between diabetic autonomic and peripheral neuropathies, we carried out power spectral analysis (PSA) of heart rate variations and determined the vibratory perception threshold (VPT) in diabetic subjects (DM). The VPT, measured with a Suzuki-Matsuoka Vibrometer (SMV-5), was greater in diabetic subjects than in controls. The low frequency (LF) component of the PSA which represents sympathetic nervous activity and the high frequency (HF) component of the PSA which indicates parasympathetic nervous activity were significantly decreased in diabetic subjects when compared to values in the controls. In addition, there were significant inverse correlations between the LF and HF components of the PSA of heart rate variations and the VPT. These results suggest that the PSA of heart rate variations and the measurement of VPT are useful tools for evaluating diabetic autonomic and peripheral neuropathies.

Autonomic Nervous System↗
PubMed2000

[Amiodarone-associated optic neuropathy: an independent syndrome? Three patients with bilateral optic neuropathy].

BACKGROUND: Optic neuropathy has been reported to occur during antiarrhythmic therapy with amiodarone. Whether or not there is a causal relationship has been discussed controversely. PATIENTS: Three patients presented with a visual impairment three to seven months after starting amiodarone therapy. In all three patients both optic discs were swollen and showed hemorrhages on the margin. After discontinuing amiodarone, the vision improved and the swelling of the optic discs resolved. CONCLUSION: The bilateral occurrence at the same time, the close time correlation with the amiodarone application and the improvement after discontinuing amiodarone suggest that our three patients suffered from a toxic effect of amiodarone rather than an incidental other disease, as for instance ischemic optic neuropathy.

Aged↗
PubMed1987

Hereditary sensory neuropathy with neurotrophic keratitis. Description of an autosomal recessive disorder with a selective reduction of small myelinated nerve fibres and a discussion of the classification of the hereditary sensory neuropathies.

A Kashmiri family with 3 members affected by a congenital sensory and autonomic neuropathy and corneal opacification is described. The 3 affected cases were offspring of consanguinous marriages in two generations; autosomal recessive inheritance is therefore probable. Pain and temperature sensation was lost in the limbs with a resulting mutilating acropathy. Sudomotor function was also impaired. Motor function, tendon reflexes, kinaesthetic sensation and sensory nerve action potentials were normal. Sural nerve biopsy showed a selectively reduced small myelinated nerve fibre population. Corneal histology revealed neurotrophic keratitis. The classification of the hereditary sensory and autonomic neuropathies is discussed. This family represents a previously unrecognized variant.

Adult↗
PubMed2004

Charcot-Marie-Tooth disease (hereditary motor sensory neuropathies) and hereditary sensory and autonomic neuropathies.

BACKGROUND: Since the description of Charcot-Marie-Tooth disease over a century ago. it has now been recognized that these conditions are not caused by generalized metabolic defects but rather have various discrete genetic origins. These disorders can also have variable phenotypes due to dysfunction of peripheral nerve axons or their myelin due to the genetic defects that affect the formation of specific nerve proteins. REVIEW SUMMARY: This article summarizes the clinical presentation of various phenotypes of the hereditary motor sensory neuropathies and the hereditary sensory and autonomic neuropathies, genetic mutations, and their relevant protein products. Proper identification of the genetic defects provides the opportunity for better genetic counseling and hopefully therapies in the future.

Charcot-Marie-Tooth Disease↗
PubMed2006

A rare genetic disorder in the differential diagnosis of the entrapment neuropathies: hereditary neuropathy with liability to pressure palsies.

Hereditary neuropathy with liability to pressure palsies (HNPP) is an autosomal-dominant, slowly progressive neuromuscular disorder, which is characterized by recurrent acute peripheral nerve palsies. Electrophysiological studies show decreased motor and sensory conduction velocities in both clinically affected and unaffected nerves. Focal thickening of myelin sheath with sausage-like formation, also called tomacula, is seen in nerve biopsies. In genetic studies, 1.5-Mb deletion on chromosome 17p11.2 is detected in approximately 85% of HNPP cases and point mutations are determined in some cases. We describe a 26-year-old man who had a 6-month history of paresthesia in the little fingers of his hands. He was diagnosed with HNPP by neurologic examination, and electrophysiological and histopathologic studies. Studies in his mother and one brother also showed entrapment neuropathy. However, no deletions or point mutations were determined in this family. Other genetic defects apart from the known ones might be present in this disease. The most frequent entrapment syndrome, carpal tunnel syndrome, is also seen in this disease, so physicians dealing with musculoskeletal problems should be alert about this subject. Awareness of HNPP may help avoid unnecessary operative interventions.

Adult↗
PubMed1993

Prevalence of QT prolongation in a type 1 diabetic population and its association with autonomic neuropathy. The Neuropathy Study Group of the Italian Society for the Study of Diabetes.

The prevalence of QT prolongation in a large random sample of Type 1 diabetic patients in Piemonte, Italy and its association with autonomic neuropathy were assessed. Three hundred and seventy-nine Type 1 diabetic patients (age 15-59) with (94, DAN+) and without (280, DAN-) autonomic neuropathy and 118 non-diabetic control subjects participated in the study. QT interval was measured on an ECG recorded at rest and QTc calculated according to Bazett's formula. QTc was greater than 0.440 s in 7.6% (95% CI 2.9-12.3) of control subjects, 25.6% (21.0-30.0) of diabetic patients, 30.8% (21.5-40.1) of DAN+, 23.9% (18.9-28.9) of DAN-. QTc was greater than 0.460 s (mean + 2SD of QTc in control subjects) in 11.7% (8.5-14.9) of diabetic patients, 18.1% (10.3-25.9) of DAN+, 9.6% (6.2-13.0) of DAN-. QT was above the 95% upper limit for the control subjects in the plot of measured QT against RR interval in 21.4% (17.3-25.5) of diabetic patients, 26.6% (17.7-35.5) of DAN+, 19.3% (14.7-23.9) of DAN-. No correlation was found between QT interval and age or disease duration. The prevalence of QT prolongation was higher in diabetic patients than in control subjects and in DAN+ than in DAN-.

Adolescent↗