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At least 145 records · Page 8Linked to original sources
PubMed1992

Late onset Leber's optic neuropathy: a case confused with ischaemic optic neuropathy.

A case is reported of a 63-year-old man with progressive central visual loss in one eye followed 11 months later by involvement of the fellow eye. A diagnosis of chronic ischaemic optic neuropathy was considered. However, despite a negative family history, the absence of electrocardiographic abnormalities, and minimal fundus changes a diagnosis of Leber's optic neuropathy was made on the basis of magnetic resonance imaging findings and the mitochondrial DNA mutation at base pair 11778.

DNA, Mitochondrial↗
PubMed2006

A modified peripheral neuropathy scale: the Overall Neuropathy Limitations Scale.

A new peripheral neuropathy activities measure, the Overall Neuropathy Limitations Scale (ONLS), was derived by modifying the Overall Disability Sum Score (ODSS) slightly. Its inter-rater reliability was found to be high and its correlation with the ODSS (r = 0.97), 36-item Short Form Questionnaire Physical Component Summary Score, and participation and impairment measures was significant. Acceptable responsiveness (standardised response mean 0.76) was shown by the ONLS. The results obtained from the questionnaire agreed closely with those obtained from observation of the tasks on the ONLS, but were not equivalent. The simplicity of the ODSS is shared by the ONLS, but the ONLS has better content validity and less ceiling effect, which may make it more useful for clinical practice and research.

Persons with Disabilities↗
PubMed1989

Trichloroethylene cranial neuropathy: is it really a toxic neuropathy or does it activate latent herpes virus?

The mechanism of the cranial neuropathy associated with heavy exposure to trichloroethylene (or dichloroethylene) is unknown. In severe cases there is destructive spread of the neuropathic process from the Vth cranial nerve nuclei up and down the brain stem in a manner that is difficult to explain on accepted neurotoxicological principles. However, there is a close association reported of this form of trigeminal neuropathy with reactivation of orofacial herpes simplex that suggests the possibility that the chemical, which readily gains entrance into the nervous system, may be responsible for reactivating the latent virus. This novel hypothesis is discussed in the light of current understanding of latency in herpes simplex infection in nervous tissue.

Cranial Nerve Diseases↗
PubMed1997

Gene dosage effects in hereditary peripheral neuropathy. Expression of peripheral myelin protein 22 in Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies nerve biopsies.

A duplication of a 1.5-Megabase genomic region encompassing the gene for the peripheral myelin protein 22 (PMP22) is found on chromosome 17p11.2-12 in Charcot-Marie-Tooth disease type 1A (CMT1A), whereas the reciprocal deletion is associated with hereditary neuropathy with liability to pressure palsies (HNPP). Since most CMT1A patients harbor three copies of the PMP22 gene, and most HNPP patients carry only a single copy, a gene dosage effect has been proposed as a mechanism for both diseases. We have analyzed the steady-state expression of PMP22 protein in sural nerve biopsies from three CMT1A and four HNPP patients. Quantitative immunohistochemical determination showed that PMP22 protein expression relative to that of myelin protein zero and myelin basic protein was increased in all CMT1A patients and reduced in all HNPP patients, as compared with biopsy samples of patients with normal PMP22 gene expression. These data demonstrate that both neuropathies result from an imbalance of PMP22 protein expression.

Adolescent↗
PubMed1998

[New evidence of the antigenic relation between the viruses of epidemic neuropathy and the human nervous system. A study of the immune cellular response in patients with epidemic neuropathy and controls. A review of the topic].

A series of experiments was made at the Virology Department of the "Pedro Kourí" Institute of Tropical Medicine aimed at obtaining new evidences on the possible antigenic relations existing between the viruses isolated from patients with epidemic neuropathy and the structures of the human nervous system. According to the results it may be finally inferred that the persistence and/or autoimmunity may be considered as mechanisms through which the studied viruses participate in the etiopathogenesis of the epidemic neuropathy in Cuba. For future experiments it is very important to identify the possible viral epitopes involved in the molecular mimicry that are responsible for the probable autoimmune mechanisms or for the viral persistence.

Adult↗
PubMed2002

[A case of orbital myositis complicated with optic neuropathy--analysis of the pathological mechanism of optic neuropathy from magnetic resonance imaging findings].

BACKGROUND: We observed a rare case of orbital myositis involving the optic nerve. CASE: A 52-year-old woman complained of visual disturbance, lid swelling, ocular pain, and conjunctival injection in her right eye. Her corrected vision was 0.15 in the right eye and 1.2 in the left eye. Relative afferent pupillary defect(RAPD) and central scotoma in visual field test were noted in the right eye. Ocular movement of her right eye was moderately disturbed in all directions. Although laboratory data showed elevation of erythrocyte sedimentation rate, other hematological data such as thyroid function, autoimmune antibodies, and viral infection antibodies were normal. Magnetic resonance imaging(MRI) findings showed compression of the optic nerve at the orbital apex by marked thickening of the right lateral rectus muscle and superior rectus muscle, and inflammation directly invading the optic nerve. Based on the above findings, we diagnosed the case as orbital myositis complicated with optic neuropathy, and started corticosteroid therapy. Her right corrected vision improved dramatically, and the RAPD, central scotoma, and lid swelling disappeared shortly after administration. Enlargement of the extraocular muscles was still present one month after corticosteroid therapy. CONCLUSION: MRI findings suggested that optic neuropathy in this case was induced not only by mechanical compression by the enlarged extraocular muscles at the orbital apex but also by direct inflammatory infiltration from the extraocular muscles.

Female↗
PubMed1995

Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. The Ischemic Optic Neuropathy Decompression Trial Research Group.

OBJECTIVE: To assess the safety and efficacy of optic nerve decompression surgery compared with careful follow-up alone in patients with nonarteritic anterior ischemic optic neuropathy (NAION). DESIGN: The Ischemic Optic Neuropathy Decompression Trial (IONDT) is a randomized, single-masked, multicenter trial. SETTING: Twenty-five US clinical centers. PARTICIPANTS: The IONDT ceased recruitment on October 20, 1994, on the recommendation of its Data and Safety Monitoring Committee. The preliminary results presented herein are based on data as of September 8, 1994, from 244 patients with NAION and visual acuity of 20/64 or worse. One hundred twenty-five patients had been randomized to careful follow-up, and 119 had been randomized to surgery, with 91 and 95, respectively, having completed 6 months of follow-up. INTERVENTION: Patients in the surgery group received optic nerve decompression surgery and follow-up ophthalmologic examinations; those in the careful follow-up group received ophthalmologic examinations at the same times as the surgery group. MAIN OUTCOME MEASURES: Gain or loss of three or more lines of visual acuity on the New York Lighthouse chart at 6 months after randomization, as measured by a technician masked to treatment assignment. RESULTS: Patients assigned to surgery did no better when compared with patients assigned to careful follow-up regarding improved visual acuity of three or more lines at 6 months: 32.6% of the surgery group improved compared with 42.7% of the careful follow-up group. The odds ratio (OR) for three or more lines better, adjusted for baseline visual acuity and diabetes, was 0.74 (95% confidence interval [CI], 0.39 to 1.38). Patients receiving surgery had a significantly greater risk of losing three or more lines of vision at 6 months: 23.9% in the surgery group worsened compared with 12.4% in the careful follow-up group. The 6-month adjusted OR for three or more lines worse was 1.96 (95% CI, 0.87 to 4.41). No difference in treatment effect was observed between patients with progressive NAION and all others. CONCLUSION: Results from the IONDT indicate that optic nerve decompression surgery for NAION is not effective, may be harmful, and should be abandoned. The spontaneous improvement rate is better than previously reported.

Aged↗
PubMed1996

[Multifocal motor neuropathies with persistent conduction blocks: a form of inflammatory demyelinating neuropathy].

Since the first cases described in 1986, multifocal motor neuropathy with persistent conduction blocks (MMN) appears to be a well-defined nosological entity. Clinical features include male-predominant occurrence, weakness often accompanied by cramps and fasciculations; topography of the motor involvement is characterized by assymetry, upper limb predominance, relation to the distribution of individual nerves or roots. Atrophy is variable but can lack despite severe weakness. Multifocal, purely motor and persistent conduction blocks are the electrophysiological hallmark of the disease. Serum antibodies against ganglioside GM1 are frequently associated with MMN but their diagnostic sensitibity and specificity are discussed. However high level of these antibodies may be a useful immunological marker of MMN. Their pathogenic role is probable, perhaps by their interaction with ionic channels localized in node of Ranvier. Morphological findings, immunologic abnormalities and improvement with intravenous immunoglobulin therapy define MMN as a type of inflammatory demyelinating neuropathy. Their relation with CIDP are discussed.

Adult↗
PubMed1992

Hypoxic neuropathy versus diabetic neuropathy. An electrophysiological study in rats.

In the experimental rat model of diabetes a slowing of nerve conduction velocity and a resistance to ischemic conduction failure have been found as an indication of polyneuropathy. The same electrophysiological abnormalities have been demonstrated in a model in which healthy rats are kept under hypoxic conditions (10% O2) for a 10-week period. Two factors are held responsible for the development of diabetic polyneuropathy: metabolic deterioration and hypoxia. However, until now the relative roles of metabolic deterioration and hypoxia in the development of polyneuropathy have not been settled. To test both explanations further with more sophisticated electrophysiological techniques, the H-reflex (motor and sensory NVC) and the stimulated SF-EMG (measures terminal nerve branch and neuromuscular transmission) were measured in 3 groups of 10 rats, a healthy control group, a diabetic group, and a hypoxic group, every 5 weeks, for 6 months. In the control rats an age-related increase in motor and sensory conduction velocity was found, whereas in the diabetic rats as well as in the hypoxic rats a marked decrease in sensory and a slight decrease in motor nerve conduction velocity was observed. The jitter measured in the stimulated SF-EMG was significantly increased in both the diabetic and the hypoxic group. The results of the present study support the possible role of hypoxia, in addition to metabolic factors, in the development of experimental diabetic neuropathy.

Afferent Pathways↗
PubMed1997

Differences between hereditary motor and sensory neuropathy type 2 and chronic idiopathic axonal neuropathy. A clinical and electrophysiological study.

To evaluate whether chronic idiopathic axonal polyneuropathy (CIAP) should be considered as hereditary motor and sensory neuropathy type 2 (HMSN type 2), we compared the clinical features of 48 patients with CIAP with those of 47 patients with HMSN type 2. In addition, we studied electrophysiological data in 20 patients with CIAP and in 20 patients with HMSN type 2. We found, in patients with HMSN type 2, that the initial symptoms were predominantly motor and that weakness and handicap were more severe and skeletal deformities more frequent, compared with those of CIAP patients. Electrophysiologically, the tibialis anterior muscle showed more denervation in patients with HMSN type 2, consistent with the predominance of motor symptoms. There was no important effect of age of onset on clinical features in HMSN type 2 patients. We conclude that in an individual patient with a sensory or sensorimotor idiopathic axonal polyneuropathy and no family history of polyneuropathies, the diagnosis HMSN type 2 is unlikely. However, if motor symptoms predominate, the diagnosis of HMSN type 2 should be considered.

Adult↗
PubMed1993

Reproducibility of parameters for assessment of diabetic neuropathy. The French Group for Research and Study of Diabetic Neuropathy.

This study evaluated the reproducibility of nerve function assessment in a group of 132 diabetic patients with moderate peripheral polyneuropathy. Patients were investigated at the beginning and the end of the run-in period (a 1-month placebo period) of a multicentre trial of an aldose-reductase inhibitor (Ponalrestat). Reproducibility was evaluated by performing four types of tests: quantitative visual scales of symptoms, quantitative sensory assessment (vibration perception thresholds in medial malleolus and great toe, foot thermal perception threshold to hot and cold), electrophysiological investigations on the dominant side (conduction velocities and potential amplitudes of sensory and median motor nerve, sural and peroneal nerves, amplitudes of F waves of median motor and peroneal nerves) and cardiac autonomic tests (Valsalva, deep-breathing, lying-to-standing). Reproducibility was poor for symptoms, thermal sensitivity, and potential amplitudes. It was satisfactory (total coefficient of variation < 50%) for all the other parameters and even very good (total variation coefficient < 26%, intra-subject variation factors corresponding to < 56% of total variance) for velocities of sensory and median motor and peroneal nerves, the amplitudes of F waves and the three autonomic tests. For most of the parameters total variance was mainly related to inter-subject variability. However, inter-subject variability for the three cardiac autonomic tests was very low and at least one cardiac autonomic test was altered in all the patients. Inter-centre variability was low for all the parameters, except for action potential amplitudes and for F wave velocity of the median motor nerve. This study suggests those parameters that are appropriate for the assessment of diabetic neuropathy and for therapeutic trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldehyde Reductase↗
PubMed2002

[Hereditary neuropathy with pressure hypersensitivity or tomaculous neuropathy].

Hereditary neuropathy liability to pressure palsies is characterized by recurring accesses of painless paralysis at the level of various nerves likely to be compressed. This affection remains underdiagnosed because of its usually benign course, sometimes without any symptom. The diagnosis is supported by clinical and electrophysiological data associated with, in the majority of patients, a deletion of one of the alleles coding for protein PMP 22 on the level of the locus 17p11.2.

Adult↗
PubMed2005

A case report of an uncommon neuropathy: posterior femoral cutaneous neuropathy.

Isolated posterior femoral cutaneous neuropathy is rarely encountered. Electrophysiological documentation has only been made in a few cases. We present a 73 year-old male patient who underwent a coronary angiography procedure which was performed on his right femoral artery 2 months prior of referring to our electromyography (EMG) laboratory. After this event, he had an operation in order to evacuate the hematoma formed in the right inguinal region during the procedure. In the postoperative state he began to complain of a pain and numbness in his right posterior thigh; which had radiated towards his right hip and popliteal fossa. In addition to routine electrophysiological nerve conduction studies conducted in lower extremities; we performed posteriorfemoral cutaneous nerve conduction using the method described by Dumitru and Nelson. While normal response can be obtained easily on the left side; no potential could be obtained from the right.

Aged↗
PubMedDate not supplied

[Hereditary neuropathy with recurrent mononeuropathy (tomaculous neuropathy)].

Clinical and neurophysiological studies were carried out in 15 members out of 5 families affected by recurrent peripheral nerve and brachial plexus palsies. Nerve biopsy showed typical "tomacula". While in 3 families a slight development of the symptomatology was observed in the other 2 families there was an evolution toward a severe symmetric neuropathy. Motor and sensory conduction velocity were, in some cases, slowed even in clinically unaffected nerves. Electrophysiological changes were more important at entrapment sites. Such abnormalities could be found also in unaffected family members.

Adult↗
PubMed1997

Hypertrophic neuropathy: atypical appearances resulting from the combination of type I hereditary motor and sensory neuropathy and diabetes mellitus.

A nerve biopsy from a patient with type Ia hereditary motor and sensory neuropathy and diabetes mellitus showed hypertrophic changes of atypical appearance. The onion bulbs were composed of a central core of Schwann cells, with or without associated axons, embedded in concentrically arrayed layers of collagen fibrils. These were surrounded either by highly attenuated Schwann cell processes or by fibroblasts. The biopsy showed a severe loss of myelinated axons. It is suggested that it is necessary for the supernumerary Schwann cells of the onion bulbs to be stabilized by associated unmyelinated axons. If these are lost, the Schwann cells atrophy and disappear.

Adult↗
PubMed1982

Optic nerve damage in human glaucoma. III. Quantitative correlation of nerve fiber loss and visual field defect in glaucoma, ischemic neuropathy, papilledema, and toxic neuropathy.

The number and distribution of human optic nerve axons were compared with clinical measurements available the same eyes, including visual acuity, disc appearance, and visual field studies. Definite loss of axons occurs prior to reproducible visual field defects in some patients suspected of having glaucoma. In glaucoma, the superior and inferior poles of the nerve lose nerve fibers at a selectively greater rate, leading to an hourglass-shaped atrophy. Cavernous degeneration of the retrobulbar optic nerve is rarely observed in chronic glaucoma. The pattern of atrophy in examples of toxic amblyopia, ischemic optic neuropathy and chronic papilledema differ from that of glaucoma, suggesting different mechanisms of damage in these conditions.

Adult↗
PubMed1998

Paraneoplastic demyelinating neuropathy, subacute sensory neuropathy, and anti-Hu antibodies: clinicopathological study of an autopsy case.

A patient with anti-Hu antibodies, small-cell lung carcinoma, and autopsy-proven subacute sensory neuropathy had early slowing of motor and sensory conduction velocities. In the peripheral nerves, chronic demyelinating and remyelinating lesions with axonal degeneration were associated with an inflammatory reaction consisting of CD8+ T cells and CD68+ macrophages. On immunohistochemical testing, the patient's serum did not react with normal nerve, suggesting that the Hu proteins were not the target of the inflammatory reaction in the nerve.

Aged↗
PubMed2003

Physiology of conduction block in multifocal motor neuropathy and other demyelinating neuropathies.

Conduction block is an important functional consequence of demyelination whereby nervous transmission is abolished. Its mechanism has been discussed with respect to the loss of insulation due to disruption of myelin. Recent development of threshold tracking techniques, which enabled noninvasive assessment of axonal membrane potentials and ion channels, has provided evidence that axonal excitability changes significantly and contributes to conduction failure. This view, based upon axo-glial interaction, clarifies the mechanism of muscle fatigue and fasciculation associated with peripheral demyelination and possibly explains selective motor involvement in multifocal motor neuropathy.

Demyelinating Diseases↗