PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PERIPHERAL NERVE DISEASES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 91 records · Page 5Linked to original sources
PubMed2001

Magnetic resonance neurography: magnetic resonance imaging of peripheral nerves.

With advances in modern MR imaging, direct MR visualization of many peripheral nerves is now possible. MR nerve imaging can detect and delineate the extent of neural tumors, demonstrate nerve continuity in cases of traumatic injury, and demonstrate abnormal enlargement and abnormal signal in diseased peripheral nerves. This ability to image peripheral nerves has the potential to dramatically change the diagnosis and treatment of peripheral nerve disease. This article describes the techniques for peripheral nerve imaging and provides a brief overview of a broad spectrum of peripheral nerve abnormalities.

Humans↗
PubMed1980

Peripheral nerve conduction in Fabry disease.

Peripheral nerve conduction was studied in 34 members, aged 3 to 54 years, from three separate kindreds with Fabry disease. Nerve conduction velocity was prolonged in one-third (11 of 34) of the study group. Of the 9 control family members with normal plasma alpha-galactosidase levels, 8 had normal velocity. A 6-year-old girl with normal plasma and leukocyte alpha-galactosidase levels and absent corneal deposits had slightly lower than normal nerve conduction velocity. One of the 3 obligate female carriers and 1 of 10 suspected carriers of Fabry disease had prolonged conduction velocity but normal distal latency. On the other hand, 8 of 12 males affected with Fabry disease demonstrated slow nerve conduction velocity while 4 of the 8 had prolonged distal latency. Frequently, only one of the two nerves studied showed abnormalities. These abnormalities were not related to patient age. Interfamilial variations in the abnormalities were present.

Adolescent↗
PubMed2007

[Pathophysiology of pain].

Clinically relevant pain states are usually characterized as either inflammatory or neuropathic. While inflammatory pain results from tissue injury or damage, neuropathic pain results from damage or disease of nerve fibers. In either pain state, both the peripheral and the central nociceptive system contribute significantly to the generation of pain. During inflammation peripheral nociceptors ("pain fibers") are sensitized (peripheral sensitization), and upon nerve injury or nerve disease peripheral nerve fibers develop ectopic discharges originating from the site of the nerve lesion or the cell body of damaged fibers. As a consequence a complex neuronal response is evoked in the spinal cord where neurons become hyperexcitable (central sensitization).Central sensitization is a neuronal process that amplifies the activity from the periphery. Numerous molecular mechanisms are involved in peripheral and central nociceptive processes including rapid functional changes of signaling (increase of excitability) and long-term regulatory changes such as upregulation of mediator/receptor systems. The conscious pain is generated by thalamocortical networks that produce both sensory discriminative and affective components of the pain response.

Animals↗
PubMedDate not supplied

Diseases of peripheral nerves as seen in the Nigerian African.

The anatomical and aetiological diagnoses of peripheral nerve disease excluding its primary benign and malignant disorders, as seen in 358 Nigerians are presented. There is a male preponderance and the peak incidence is in the fourth decade. Sensori-motor neuropathy was the commonest presentation (50%). Guillain-Barré syndrome was the commonest identifiable cause (15.6%), accounting for half of the cases with motor neuropathy. Peripheral neuropathy due to nutritional deficiency of thiamine and riboflavin was common (10.1%) and presented mainly as sensory and sensori-motor neuropathy. Diabetes mellitus was the major cause of autonomic neuropathy. Isoniazid was the most frequent agent in drug-induced neuropathy. Migraine (20%) was not an uncommon cause of cranial neuropathy although malignancies arising from the reticuloendothelial system or related structures of the head and neck were more frequent (26%). In 26.5% of all the cases, the aetiology of the neuropathy was undetermined. Heredofamilial and connective tissue disorders were rare. Some of the factors related to the clinical presentation and pathogenesis of the neuropathies are briefly discussed.

Adolescent↗
PubMed1970

Peripheral nerve function in chronic liver disease.

Peripheral nerve function has been studied in 50 patients with chronic liver disease. An increase in the latency or a reduction in the response amplitude of the evoked sensory potential of the median nerve was detected in 34 of the 50 subjects. This was in striking contrast to the paucity of neurological signs and symptoms suggestive of peripheral nerve damage seen in these patients. There was no evidence to show that alcohol was responsible for the neuropathy. Abnormalities in the excitability changes of sensory nerve during ischaemia were detected in seven of the 16 subjects whose distal sensory latencies were within normal limits. A critical evaluation of the hypotheses which have been postulated to account for the increased resistance of peripheral nerve to inactivation by ischaemia has been made. It is concluded that an increase of the permeability of the periaxonal diffusion barrier to K offers the most acceptable explanation for this phenomenon.

Adult↗