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Nerve Disorders (nerve + disorders)
Kinds of Nerve Disorders Selected AbstractsBiopsy of the posterior interosseous nerve: a low morbidity method for assessment of peripheral nerve disordersDIABETIC MEDICINE, Issue 1 2009N. O. B. Thomsen Abstract Aims The sural nerve is the commonest peripheral nerve biopsied to help in the diagnosis of peripheral neuropathy of unknown cause. However, associated complications limit its use. The aim was, as an alternative, to asses biopsy of the terminal branch of the posterior interosseous nerve (PIN) in the forearm. Methods PIN pathology was morphometrically quantified in 10 male patients with Type 2 diabetes and compared with six PIN biopsy specimens taken post mortem from male cadavers with no history of neuropathy or trauma. Results The PIN biopsy procedure provides a long (approximately 3 cm) mono- or bifascicular nerve biopsy with generous epineurial tissue and adjacent vessels. Our results show a significantly lower myelinated fibre density in subjects with diabetes [5782 (3332,9060)/mm2] compared with autopsy control material [9256 (6593,12 935)/mm2, P < 0.007]. No postoperative discomfort or complications were encountered. Conclusions A reduction in myelinated fibre density has previously been shown to be a clinically meaningful measure of neuropathy in diabetic patients. We demonstrate similar findings using the PIN biopsy. The PIN biopsy procedure fulfils the criteria for nerve biopsy and was well tolerated by the patients. It may be a possible alternative to sural nerve biopsy to allow for diagnosis of neuropathy. [source] Diagnosis of motor neuropathyEUROPEAN JOURNAL OF NEUROLOGY, Issue 3 2001J. -M. Motor neuropathy is a clinical entity which leads to consideration of a wide spectrum of peripheral nerve disorders. Firstly, it may be distinguished from other causes of peripheral motor involvement such as muscle diseases and disorders of the neuromuscular junction. Secondly, it may be discussed in two different forms: acute and chronic. Acute chronic neuropathies are mainly observed in Guillain-Barré syndrome, in which electrophysiological studies allow us to recognize the classical demyelinating form and the axonal form. The other causes of acute motor neuropathy are mainly poliomyelitis and porphyrias. Chronic motor neuropathies are mainly observed in motor neuron diseases, mainly amyotrophic lateral sclerosis, but also Kennedy's disease and other lower motor neuron diseases which may be inherited or acquired. The other causes are multifocal motor neuropathy and the predominantly motor forms of chronic inflammatory demyelinating polyneuropathy. The characterization of these different types of chronic neuropathy is of major importance because of the therapeutic consequences which may lead to the proposal of specific treatments. [source] Usefulness of muscle denervation as an MRI sign of peripheral nerve pathologyJOURNAL OF MEDICAL IMAGING AND RADIATION ONCOLOGY, Issue 6 2007DA Lisle Summary Peripheral nerve disorders may be classified into compressive or entrapment neuropathies and non-compressive neuropathies. Muscle denervation recognized on MRI may be a useful sign in the diagnosis of peripheral nerve disorders. Acute or subacute denervation results in prolonged T2 relaxation time, producing increased signal in skeletal muscle on short tau inversion-recovery and fat-suppressed T2-weighted images. Chronic denervation produces fatty atrophy of skeletal muscles, resulting in increased muscle signal on T1-weighted images. This review will outline and illustrate the various ways that muscle denervation as seen on MRI may assist in the diagnosis and localization of peripheral nerve disorders. [source] Abstracts of the 8th Meeting of the Italian Peripheral Nerve Study Group: 21JOURNAL OF THE PERIPHERAL NERVOUS SYSTEM, Issue 1 2003R Bianchi Erythropoietin (EPO) has neurotrophic and neuroprotective effects and its efficacy and safety has been demonstrated in patients with ischemic stroke. We investigated its efficacy in preventing and reversing established nerve disorders in streptozotocin (STZ) diabetes. After STZ injection (60 mg/kg/ip), EPO (5000 units/kg b.w. i.p. three times a week) was started in a group of rats and continued for five weeks (prevention schedule). In another group of diabetic rats, EPO was started six weeks after STZ, continued for five weeks (therapeutic schedule). Groups of non-diabetic control rats were similarly treated. Antidromic nerve conduction velocity (NCV) in the tail was assessed at five weeks for all groups and at 11 weeks for the therapeutic schedule. Compared to non-diabetic rats, NCV was 21% lower (P < 0.001) at five weeks in the STZ group, EPO partially prevented this decrease (14% lower than with non-diabetic controls), with a significant difference from the untreated-diabetic group (P < 0.01). After six weeks of uncontrolled diabetes, at the beginning of therapeutic EPO, NCV was reduced by 23% and after 11 weeks by 40%, EPO efficacy was confirmed. Thermal (hot plate method) and mechanical (Randall-Selitto method) nociceptive thresholds were monitored weekly throughout the study. In addition, in all groups, the density of intra-epidermal nerve fibers, which reflects possible degeneration of somatic unmyelinated fibers, was assessed in the hindpaw using protein-gene-product 9.5 immunostaining. Rats developed mechanical hyperalgesia within two weeks after STZ injection. Both the prevention and therapeutic schedules of EPO reduced diabetic hyperalgesia after two weeks of treatment, reaching statistical significance at fur, and five weeks of treatment, with no such effect in non-diabetic controls. Hindpaw thermal response latencies were significantly (P < 0.001) increased in untreated diabetic rats compared with untreated controls. EPO had no effect on these latencies in control rats but partially prevented the increase in diabetic rats, so the values were still different from controls, but significantly different from untreated diabetics at four and five weeks in both the prevention and therapeutic studies (P < 0.05). These observations extend the therapeutic utility of EPO and highlight its potential for treating established diabetic neuropathies. [source] The utility of magnetic resonance imaging in evaluating peripheral nerve disordersMUSCLE AND NERVE, Issue 3 2002Gerald A. Grant MD Abstract The evaluation of peripheral nerve injuries has traditionally relied primarily on information gained from the clinical history, physical examination, and electrodiagnostic testing. Taken together, all of this clinical and diagnostic information often allows one to determine the location and severity of the underlying peripheral nerve problem. However, it may not be sufficient in diagnosing a focal entrapment neuropathy superimposed upon a more generalized peripheral neuropathy; localizing a focal lesion along a long segment of nerve which may be difficult to assess accurately with electrodiagnostic sutdies; distinguishing early between an axonotmetic grade of injury, which can recover through axonal regeneration, and a neurotmetic grade which cannot and therefore may benefit from a surgical exploration and repair procedure; and noninvasively diagnosing and determining the surgical resectability of peripheral nerve mass lesions such as tumors. The goal of this review is to illustrate how standard and evolving magnetic resonance imaging techniques can provide additional information in dealing with some of these problems. © 2002 Wiley Periodicals, Inc. Muscle Nerve 25: 000,000, 2002 DOI 10.1002/mus.10013 [source] Historical perspective: Neurological advances from studies of war injuries and illnesses,ANNALS OF NEUROLOGY, Issue 4 2009Douglas J. Lanska MD Early in the 20th century during the Russo-Japanese War and World War I (WWI), some of the most important, lasting contributions to clinical neurology were descriptive clinical studies, especially those concerning war-related peripheral nerve disorders (eg, Hoffmann-Tinel sign, Guillain-Barré-Strohl syndrome [GBS]) and occipital bullet wounds (eg, the retinal projection on the cortex by Inouye and later by Holmes and Lister, and the functional partitioning of visual processes in the occipital cortex by Riddoch), but there were also other important descriptive studies concerning war-related aphasia, cerebellar injuries, and spinal cord injuries (eg, cerebellar injuries by Holmes, and autonomic dysreflexia by Head and Riddoch). Later progress, during and shortly after World War II (WWII), included major progress in understanding the pathophysiology of traumatic brain injuries by Denny-Brown, Russell, and Holbourn, pioneering accident injury studies by Cairns and Holbourn, promulgation of helmets to prevent motorcycle injuries by Cairns, development of comprehensive multidisciplinary neurorehabilitation by Rusk, and development of spinal cord injury care by Munro, Guttman, and Bors. These studies and developments were possible only because of the large number of cases that allowed individual physicians the opportunity to collect, collate, and synthesize observations of numerous cases in a short span of time. Such studies also required dedicated, disciplined, and knowledgeable investigators who made the most out of their opportunities to systematically assess large numbers of seriously ill and injured soldiers under stressful and often overtly dangerous situations. Ann Neurol 2009;66:444,459 [source] Common cranial nerve disorders in dogs and cats 2.AUSTRALIAN VETERINARY JOURNAL, Issue 10 2003CN VII No abstract is available for this article. [source] Prevalence of HSV-1 LAT in Human Trigeminal, Geniculate, and Vestibular Ganglia and Its Implication for Cranial Nerve SyndromesBRAIN PATHOLOGY, Issue 4 2001Diethilde Theil Herpes simplex virus type 1 (HSV-1) enters sensory neurons and can remain latent there until reactivation. During latency restricted HSV-1 gene expression takes place in the form of latency-associated transcripts (LAT). LAT has been demonstrated to be important not only for latency but also for reactivation, which may cause cranial nerve disorders. Tissue sections of the trigeminal ganglia (TG), geniculate ganglia (GG), and the vestibular ganglia (VG) from seven subjects were examined for the presence of LAT using the in situ hybridization technique. LAT was found on both sides in all TG (100%), on both sides of five subjects (70%) in the GG, and in none of the VG. Using a second more sensitive detection method (RT-PCR), we found LAT in the VG of seven of ten other persons (70%). This is the first study to demonstrate viral latency in the VG, a finding that supports the hypothesis that vestibular neuritis is caused by HSV-1 reactivation. The distribution of LAT in the cranial nerve ganglia indicates that primary infection occurs in the TG and GG and subsequently spreads along the faciovestibular anastomosis to the VG. [source] | ||||||||||