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PubMedDate not supplied

[Peripheral nerve diseases disclosing Horton's disease (2 cases)].

Peripheral nerves are rarely involved in Horton's disease, and when peripheral neuropathy predominates in the clinical complex it is sometimes a source of diagnostic errors. We report two cases of giant cell arteritis revealed by peripheral neuropathy.

Aged↗
PubMed1999

A skin blister method to study epidermal nerves in peripheral nerve disease.

Skin is a reservoir of sensory and autonomic nerve fibers that are potential indicators of peripheral nerve disease. Biopsies of skin have shown that sensory nerves in the most superficial layer of skin, the epidermal nerve fibers (ENFs), are reduced in patients with polyneuropathy. This report describes a minimally invasive skin blister method to isolate, image, and obtain quantitative analysis of ENFs. Blisters are made by applying a suction capsule to skin. The epidermal roof of the blister is excised, immunostained, whole mounted, and analyzed for ENF number and distribution. A reduction in number and abnormal distribution of ENFs are early indicators of peripheral nerve disease. Illustrations of skin blister and skin biopsy specimens from patients with different types of peripheral nerve disorders are included. These patients were chosen because their findings demonstrate the complementary information obtained by the blister and biopsy methods and the potential of the blister procedure to evaluate single nerve lesions and polyneuropathy and to follow the progress of ENF degeneration and regeneration.

Adult↗
PubMed2000

Clinicopathologic analysis of 124 biopsy-proven peripheral nerve diseases.

We reviewed dinical, histological and ultrastructural findings of 124 cases of sural nerve biopsy specimens to delineate the trends of peripheral nerve diseases in our institute. Eighty-one were men and 43 were women. We categorized them into five groups: specific diagnosis (66 cases, 53.2%), axonal degeneration type (47 cases, 37.9%), demyelinating type (4 cases, 3.2%), mixed axonal degeneration-demyelinating type (6 cases, 4.8%) and normal (1 case, 0.9%). Cases with specific diagnosis included 21 inflammatory demyelinating polyneuropathy (15 chronic inflammatory demyelinating polyradiculoneuropathy, 6 Guillain-Barre disease), 13 hereditary motor and sensory neuropathy (7 Charcot-Marie-Tooth type I, 6 Charcot-Marie-Tooth type II), 10 vasculitis, 6 toxic neuropathy, 4 leprosy, 3 diabetic neuropathy, 2 alcoholic neuropathy, 1 Fabry's disease and other specific diseases (5 cases). In our cases, the proportion of specific diagnoses was higher, while the proportion of demyelinating peripheral neuropathies and normal were lower than those of Western series. The results of this study indicate that 1) a dose clinicopathologic correlation is important to make a precise diagnosis of peripheral nerve biopsy, 2) Biopsy under strict indication may reduce unnecessary histologic examination, 3) There is no difference in disease pattern of peripheral neuropathy between Western people and Koreans.

Adult↗
PubMed1979

Subperineurial space of the sural nerve in various peripheral nerve diseases.

The size of the subperineurial space of the sural nerve has been evaluated quantitatively in 69 cases of various peripheral nerve diseases and in controls. A significant increase was found in beriberi neuropathy (6 cases) and idiopathic polyradiculoneuropathy (9 cases) as compared with the control (8 cases). On electron microscopy a few macrophages, fibroblast processes, collagen fibrils with a diameter of 50 nm, microfibrils with a diameter of 8 nm, and amorphous material were observed in both the enlarged subperineural space and the endoneurial intercellular space. They were less frequently observed in controls. No significant correlation was found between the size of subperineurial space and the density of myelinated fibers.

Adolescent↗
PubMed2004

Acquired spinal cord and peripheral nerve disease.

Acquired spinal cord diseases in ruminants result most commonly from infectious, traumatic, metabolic/nutritional, or toxic causes and rarely from neoplasia. Clinical signs of spinal cord disease depend on the neuroanatomic location of the lesion. Acquired spinal cord diseases including vertebral osteomyelitis/spinal abscess, cauda-equina disease, enzootic ataxia, lymphosarcoma,polyradiculoneuritis, and degenerative myeloencephalopathy are discussed. Acquired peripheral nerve disease in cattle most often is a result of injury, and most commonly only one limb is involved. Peripheral nerve injuries frequently occur secondary to myopathy in recumbent adult cattle. In small ruminants, peripheral nerve injury seems less common, most likely due to their smaller size,but may occur from predator wounds or iatrogenically following intramuscular drug administration. Injury to the brachial plexus and radial, suprascapular, sciatic, femoral, and obturator nerves is discussed.

Animals↗
PubMed1982

Abnormalities of axonal transport: are they a cause of peripheral nerve disease?

Applications of pulse-labeling techniques to the study of axonal transport have provided new insights into certain types of peripheral nerve disease. In normal neurons, many of the newly synthesized proteins that are rapidly transported to distal parts of the cell eventually undergo a process of "turnaround," after which they are carried back to the cell bodies for degradation. This turnaround is selectively impaired in rat nerves early in the course of streptozotocin-induced diabetes and of experimental neuropathies induced by exposure to acrylamide, zinc pyridinethione, or p-bromophenylacetylurea. In the neuropathy of p-bromo-phenylacetylurea, depression of turnaround precedes the clinical signs of neurologic dysfunction, is later proportional to the severity of the disability, and may account for the characteristic accumulation of debris in preterminal axons.

Acrylamides↗
PubMed2004

[Neuromuscular diseases (NME). I. Spinal muscular atrophy, peripheral nerve diseases, congenital myasthenia gravis].

Among the group of clinically and genetically heterogeneous spinal muscular atrophies(SMA), the autosomal recessive proximal types I-III are the most frequent. They are caused by mutations of the telomeric copy of the survival motor neuron gene (SMN1) on chromosome sq while loss of the centromeric copy (SMN2) does not lead to SMA. The conservation of exon 7 in the SMN2 copy seems to be crucial for possible causal therapy options. The genetic defect is also known for spinal muscular atrophy with respiratory distress. Hereditary polyneuropathies are caused by mutations in several genes on different chromosomes. Genetic and phenotypic heterogeneity must be considered. Data on clinical symptoms, inheritance, and neurophysiology are obligatory for the most effective molecular analysis. Hereditary congenital myasthenic syndromes are clinically, genetically, and pathogenetically heterogeneous. The diagnostic significance of molecular genetic analyses is still increasing. Therapeutic options include oral medication and assisted ventilation as needed.

Humans↗
PubMed1993

Autonomic dysfunction in peripheral nerve disease.

Autonomic dysfunction is a common complication of peripheral neuropathies. Frequently, it is of little clinical importance, but in some conditions there may be profound disturbance of autonomic function, including orthostatic hypotension, impairment of heart rate and bladder control, and impotence. Some autonomic neuropathies are of acute onset, but most are chronic and of gradual onset. Diseases that primarily affect small fibers in peripheral nerves or cause acute demyelination of small myelinated fibers are those most likely to cause autonomic dysfunction. Conditions that cause severe autonomic dysfunction include acute dysautonomia, familial and primary amyloidosis, Guillain-Barré syndrome, diabetes, porphyria, Chagas' disease, and some hereditary sensory and autonomic neuropathies. Management consists of treating the underlying cause and symptomatic therapy.

Autonomic Nervous System↗
PubMed1996

Intrathecal synthesis of anti-sulfatide IgG is associated with peripheral nerve disease in acquired immunodeficiency syndrome.

Peripheral nervous system involvement in the acquired immunodeficiency syndrome (AIDS) can take the form of an acute or chronic inflammatory demyelinating polyneuropathy, polyradiculopathy, mononeuropathy multiplex, or autonomic neuropathy. There is no widely held consensus on the etiology of PNS or other neurological complications associated with HIV infection. We report here that PNS disease in HIV-infected individuals is associated with intrathecal synthesis of an antibody directed against sulfatide, a major component of myelin. The anti-sulfatide antibody is also present nonspecifically in serum. The antibody requires the presence of the 3-O-sulfogalactosyl residue for binding and recognizes preferentially the hydroxy fatty acid-containing form of sulfatide. Anti-sulfatide antibodies are therefore one of the humoral factors responsible for demyelinating diseases in AIDS patients.

Acquired Immunodeficiency Syndrome↗