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At least 307 records · Page 17Linked to original sources
PubMed1992

Spasmodic torticollis: severe compression neuropathy in rami dorsales of cervical nerves C1-6.

In 28 patients with spasmodic torticollis dorsal branches of the cervical nerves C1-6, and in 25 of these patients fascicles of the contralateral accessory nerve were investigated by light and electron microscopy. Significant changes were noted in 15 patients. The alterations were not seen or were less prominent in the 5 control cases studied for comparison. Semiquantitative evaluation of light microscopic findings revealed in 12 cases prominent and numerous Renaut bodies; in 9 cases evidence of regeneration (in 3 of these postoperatively); and in 11 cases disproportionately thin myelin sheaths in relation to axon calibers. In conjunction with endoneurial edema and thickening of the perineurium, these changes were suggestive of compression neuropathy. Whether these changes were the cause, or a side effect of the abnormal muscle contractions in spasmodic torticollis could not be elucidated. Peripheral nerve compression, however, may trigger abnormal activity in the peripheral part of the involved interneuronal circuits and may, thus, be considered as one of the many possible causes of spasmodic torticollis.

Adult↗
PubMed1980

Electron microscopic study of the early changes proximal to a constriction in myelinated nerve.

An ultrastructural study has been carried out of the changes observed proximal to a nerve constriction in rabbits. The lesion was experimentally produced with a silk ligature. Specimens were examined 24 h after ligation. Significant alterations of the ultra structure were found in sections taken at approximately 1 mm above the constriction. Examination revealed swelling of the nerve fibres due to failure of axoplasmic flow, a marked increase in the number of mitochondria, most of which showed degenerative changes and degenerative changes in the myelin sheath.

Animals↗
PubMed1981

Electromyographic findings in patients after recovery from peripheral nerve lesions and poliomyelitis.

Electromyography was performed in 10 patients 14 to 50 years after acute poliomyelitis and in 12 patients 6 to 16 years after a peripheral nerve lesion. All patients had made an almost complete recovery from initially severe paresis. In the poliomyelitis group the main finding was an increased mean action potential duration in all patients. In the patients with peripheral nerve lesions an increased frequency of spontaneous activity could be seen in 8 out of 10 and an increased mean action potential duration in 7 out of 9 patients during the initial phase. Six to 16 years later the main pathological results were a prolonged mean action potential duration (9 out of 12 patients) whilst increased spontaneous activity was detectable only in 3 out of 12 patients. In two patients all EMG findings were normal.

Adolescent↗
PubMed1976

Morton's metatarsalgia. Light and electron microscopic observations and their relation to entrapment neuropathies.

The dissected plantar nerves of 105 patients with clinical symptoms of Morton's disease were examined under light and electron microscopy. Of the 105 cases, 75 showed characteristic neuronal lesions; in the others different pathologic substrates responsible for the clinical symptoms could be demonstrated. The nervous lesions are characterized by: 1. Thickening of the walls of the endoneurial vessels produced by multiple layers of basement membranes. 2. Edema and sclerosis of the endoneurium. In the electron microscope the endoneurium was filled by deposits of fibrils with a tubular substructure and a diameter of 100-110 A. 3. Thickening of the perineurium. 4. Degeneration of the nerve fibers without signs of wallerian degeneration or obvious reactive Schwann's cell hyperplasia. The possible pathogenetic mechanisms of Morton's disease and some clinical problems are discussed.

Adult↗
PubMed1996

The effect of immediate decompression on the optic nerve in retrobulbar hematoma.

We produced retrobulbar hematoma in both orbits of 10 pigs in order to assess the effects of blood elements and pressure created by the hematoma on the optic nerves. Ten other pigs were used as a control group. Following decompression in the right orbits, ocular movements, fundi, and intraocular pressure were evaluated for 6 weeks. At the end of the 6th week the optic nerves of 20 pigs were dissected bilaterally for measurements of ATP-ase activity and ultrastructural examination. The results of the ultrastructural examination of the optic nerves of the control group were normal. Optic nerves with decompressed retrobulbar hematoma showed minimal degeneration, whereas the nerves subjected to retrobulbar hematoma with no decompression showed significant degenerative changes. For all groups ATP-ase activities were measured and evaluated. Na+, K+ ATP-ase activities decreased, while Ca+2, Mg+2 ATP-ase activities increased with the extent of degeneration. Optic nerve damage can develop after trauma. Decompression procedures are not among the causes of optic nerve degeneration but retrobulbar hematoma can result in optic neuropathy caused by the compression from the hematoma and the direct effect of blood waste products on the optic nerve.

Animals↗
PubMed1993

Orbital pain and unruptured carotid-posterior communicating artery aneurysms: the role of sensory fibers of the third cranial nerve.

Intact aneurysms of the carotid siphon at the point of take-off of the posterior communicating artery may exhibit orbital pain, whether associated with oculomotor palsy or not as a warning symptom prior to rupture. In order to explain this symptom the hypothesis of a sensory pathway within the third cranial nerve, which is liable to compression by the enlarging aneurysm sac, has been investigated. Data from human autopsy material show evidence of sensory ganglion cells within the rootlets of the oculomotor nerve; furthermore, studies in animals prove that the third nerve contains sensory fibers which run proximally along the nerve bundles, enter the brainstem and reach the spinal trigeminal nucleus. These fibers come from the ophthalmic division of the fifth nerve and join the third nerve at the level of the lateral wall of the cavernous sinus. Although a number of questions remain to be solved, the presence of a sensory pattern within the third nerve could account for fronto-orbital pain from enlarging aneurysms impinging on the third nerve itself.

Animals↗
PubMed2008

[Megadolichobasilar anomaly causing acute deafness with vertigo].

Megadolichobasilar anomaly, a dilatant arteriopathy of the basilar artery attributable to chronic arterial hypertension, can cause cranial nerve compression syndromes of the cerebellopontine angle or infarcts of the vertebrobasilar circulation. In this paper, we report on a patient with known megadolichobasilar anomaly and a partially thrombosed fusiform aneurysm of the basilar artery, who presented with acute-onset vertigo and subsequent deafness due to thromboembolic occlusion of the labyrinthine artery. Because of the vascular origin of the patient's symptoms, his vertigo disappeared over time while the deafness persisted.

Acute Disease↗
PubMed2003

Sonographic evaluation of brachial plexus pathology.

Pre-operative US examinations of the brachial plexus were performed with the purpose of exploring the potential of this technique in recognizing lesions in the region and defining their sonographic morphology, site, extent, and relations to adjacent anatomic structures, and comparing them to the surgical findings to obtain maximal confirmation. Twenty-eight patients with clinical, electro-conductive, and imaging findings suggestive of brachial plexus pathology were included in this study. There were four main etiology groups: post-traumatic brachial plexopathies; primary tumors (benign and malignant); secondary tumors; and post irradiation injuries. Twenty-one of the 28 patients underwent surgery. Advanced imaging (mostly MRI) served as an alternative gold standard for confirmation of the findings in the non-surgically treated group of patients. The US examinations were performed with conventional US units operating at 5- to 10-MHz frequencies. The nerves were initially localized at the level of the vertebral foramina and then were followed longitudinally and axially down to the axillary region. Abnormal US findings were detected in 20 of 28 patients. Disruption of nerve continuity and focal scar tissue masses were the principal findings in the post-traumatic cases. Focal masses within a nerve or adjacent to it and diffuse thickening of the nerve were the findings in primary and secondary tumors. Post-irradiation changes presented as nerve thickening. Color Doppler was useful in detecting internal vascularization within masses and relation of a mass to adjacent vessels. The eight sonographically negative cases consisted either of traumatic neuromas smaller than 12 mm in size and located in relatively small branches of posterior location or due to fibrotic changes of diffuse nature. Sonography succeeded in depicting a spectrum of lesions of traumatic, neoplastic, and inflammatory nature in the brachial plexus. It provided useful information regarding the lesion site, extent, and anatomic relationships; thus, the principal aims of the study were therefore met. Once the technique of examination is mastered, sonography should be recommended as part of the pre-operative evaluation process post-ganglionic brachial plexus pathology. Most disadvantages are related to the restricted field of view and inability to overcome bonny obstacles particularly in evaluating pre-ganglionic region. As sonography is frequently employed for investigation of the supraclavicular region, awareness of the radiologist to the findings described may enable the early recognition of pathologies involving or threatening to involve the brachial plexus.

Adult↗
PubMed1996

Occurrence of epidermal nerve endings in glabrous and hairy skin of the rat foot after sciatic nerve regeneration.

The occurrence and distribution of intraepidermal nerve endings in hairy and glabrous skin of the rat foot was examined in normal cases and three months after sciatic neurotomy/suture or a crush lesion. The nerve endings were visualized in cryostate sections with antibodies against protein gene product 9.5. Normal glabrous skin exhibited 23.3 endings/mm length. Neurotomy/suture cases had 6.1 endings/mm. In rats with nerve crush injury the occurrence was normal, but the intraepidermal nerve endings tended to be abnormally short and occurred mainly in the basal layer of the epidermis. In sections from hairy skin countings were not possible. Subjective evaluation indicated that the occurrence of dermal and epidermal axon profiles usually was very deficient after neurotomy/suture and essentially normal after crush. Skin samples from the contralateral side of operated animals showed a normal occurrence and distribution of nerve endings. We also noted that cases subjected to neurotomy/suture showed increased numbers of protein gene product 9.5-immunoreactive intraepidermal cells and an abnormally thin epidermis. We suggest that a highly deficient occurrence of intraepidermal nerve endings may be one factor behind the unsatisfactory restitution of the sensory function of the hand typically seen in patients subjected to neurotomy and suture.

Animals↗
PubMed1999

Effect of acrylamide on neurological recovery following spinal cord injury in rats.

Acrylamide (ACR) is a cumulative neurotoxin which causes axonal degeneration in animals and man. Industrial workers exposed to ACR have been reported to suffer from a variety of central and peripheral neuropathological symptoms including numbness of hands and feet, skin peeling and muscular weakness of legs. These reports suggest that the body burden of ACR may be a risk factor in recovery patterns following neurotrauma. The present study was designed to assess the effect of ACR on neurological recovery following spinal cord injury (SCI) in rats. Male Sprague-Dawley rats weighing 200-230 g were anaesthetised with chloral hydrate and laminectomy was performed at T 7-8 level leaving the dura intact. A compression plate (2.2 x 5.0 mm) loaded with a weight of 35 g was placed on the exposed cord for 5 minutes. Animals were divided into seven groups of eight rats each. The animals in Group 1 served as control whereas rats in Group 2 underwent laminectomy alone (sham). The rats in Group 3 to 6 were subjected to SCI as mentioned above. Animals in Groups 4, 5 and 6 also received ACR in the doses of 10 mg/kg, 20 mg/kg and 40 mg/kg, i.p., respectively in addition to SCI, whereas the rats in Group 7 received ACR alone at a dose of 40 mg/kg body weight. The first dose of ACR was given 30 minutes before SCI, followed by daily administration of drug for 7 days. Post traumatic neurological recovery was recorded daily for 10 days using a modified Tarlov score, inclined plane test and sensory and vocal score. Electrophysiological changes were assessed using somatosensory and corticomotor evoked potentials. The animals were sacrificed at different time intervals and the injured site of the spinal cord was analysed for lipid hydroperoxides (LPH), conjugated dienes (CD) and glutathione (GSH). Neuropathological changes in the spinal cord were assessed using light microscopy. The rats exposed to compression injury alone showed a maximum neurological deficit at 24 hr and then a gradual recovery was observed over a period of 10 days. The rats treated with ACR along with SCI showed poor or no recovery over a period of 10 days. Our electrophysiological and histopathological studies also confirmed that concomitant exposure to ACR produces a significant deleterious effect on the recovery from SCI. SCI induced increase in oxidative stress (increase in LPH and CD and decrease in GSH) is also exacerbated by ACR suggesting a role of free radicals. The results of this study suggest that increased body burden of ACR may retard the recovery from neurotrauma or even lead to permanent disability.

Acrylamide↗
PubMed2004

Functional and morphological changes of lumbar nerve roots induced by mechanical compression or the nucleus pulposus in contact with the root: analysis of fiber size-dependent vulnerability in rabbits.

The variation in symptoms of spinal nerve root damage may be caused by the difference of the size of damaged nerve fiber or difference between the mechanical influence and some chemical factors. We studied the relative vulnerability of small versus large myelinated fibers to a focal compression and/or an application of nucleus pulposus. We prepared the mechanical compression model by clipping the nerve root and the nucleus pulposus model by applying autologous nucleus pulposus on the nerve root in a rabbit and evaluated nerve root damage with respect to its fiber diameter. Nerve conduction velocity (NCV) of large myelinated nerve fiber was reduced significantly in every group compared with a sham operation group (sham) after 1 day in compression, but in the nucleus pulposus group (NP) the velocity was reduced significantly compared with sham only after 7 days. Histologic examination revealed that the number of damaged large fibers increased significantly in the compression group compared with sham after 3 days, but there was no difference in NP. NCV of small myelinated nerve fibers was reduced significantly in both the compression and NP groups compared with sham after 7 days. Histologic study showed the number of damaged small fibers increased significantly in the compression group compared with sham after 7 days. However, in the NP group the number of damaged fibers did not increase compared with sham. In conclusion, large myelinated nerve fiber was damaged earlier than small myelinated nerve fiber by compression, while nerve fiber damage caused by only the nucleus pulposus had no relation to nerve fiber size.

Action Potentials↗
PubMed2005

MRI detection of early bone metastases in b16 mouse melanoma models.

Bone metastasis causes significant morbidity in cancer patients, including bone pain, pathologic fractures, nerve compression syndrome, and hypercalcemia. Animal models are utilized to study the pathogenesis of skeletal metastases and to evaluate potential therapeutic agents. Previously published methods for imaging bone metastasis in rodent models have focused on identifying advanced stage metastasis using simple X-rays. Here we report MRI as a method for detecting early bone metastases in mouse models in vivo. B16 mouse melanoma cells were injected into the left cardiac ventricle of C57BL/6 mice and magnetic resonance (MR) images were obtained of the left leg following the development of metastatic disease, when tumor associated bone destruction was histologically present but not visible by X-ray. T1 and T2 relaxation times of bone marrow were measured in healthy control mice and B16 melanoma tumor-bearing mice. Mean T2 values for normal marrow were 28 ms (SD 5) and for diseased bone marrow were 41 ms (SD 3). T2 relaxation time of diseased bone marrow is significantly longer than that of normal bone marrow (P < 0.0001) and can be used as a marker of early bone metastases. These studies demonstrate that MR imaging can detect bone marrow metastases in small animals prior to development of cortical bone loss identified by X-ray.

Animals↗
PubMed1988

Echocardiographic abnormalities in the mucopolysaccharide storage diseases.

The mucopolysaccharide storage diseases express themselves clinically with a wide variety of abnormalities, including growth and mental retardation, skeletal abnormalities, clouded corneas, nerve compression syndromes, upper airway obstruction and cardiovascular involvement, to name the most common. In most cases the cause of early death is cardiorespiratory failure secondary to cardiovascular involvement and upper airway obstruction. The findings of cardiac ultrasound examination in 29 children, adolescents and young adults are presented. In addition to the previously well-described abnormalities of the mitral and aortic valves in several types of mucopolysaccharide storage disease, we report patchy involvement in some cases, 3 instances of asymmetric septal hypertrophy not previously reported in mucopolysaccharide storage diseases, cardiac involvement in half of our patients with Sanfilippo syndrome and a lack of age-related severity of cardiac involvement even within the specific syndromes.

Adolescent↗
PubMed1990

Endoneurial microenvironment and acute nerve crush injury in the rat sciatic nerve.

In severe peripheral nerve ischemia in the rat, serial nerve blood flow (NBF) measurements have identified evidence of 'no reflow', a mechanism of continued fiber damage during reperfusion. It has been postulated that 'no reflow' also occurs in nerve compression due to direct mechanical or ischemic (if compression is prolonged) injury of microvessels, resulting in continuing nerve fiber damage. To address this question, we measured endoneurial blood flow (NBF), oxygen tension and pH at the site of an acute nerve crush injury. In further sets of experiments, NBF and endoneurial oxygen tension were examined before and after prolonged epochs of crush. NBF and MR (microvascular resistance) were not appreciably different than values obtained in control animals without intervening brief nerve crush. NBF was slightly higher and MR slightly lower 2 h after injury, but the difference was not statistically significant. No evidence of significant endoneurial hypoxia or acidosis was observed. Similarly, after more prolonged crush there was no significant oligemia or hypoxia. The studies provide no evidence that 'no reflow' occurs in crush injury even if the injury is maintained for a period of time known to induce 'no reflow' with severe ischemia. We suggest that nerve damage in crush, and possibly compression, more likely arises from direct mechanical injury of fibers.

Animals↗
PubMed1990

The venous drainage of nerves; anatomical study and clinical implications.

The venous drainage of the peripheral nerves was studied in the upper and lower limbs of two human fresh cadaver subjects after total body perfusion with a radio-opaque lead oxide mixture. Four patterns of extraneural drainage were identified in which the venae nervosa drained: directly to the venae comitantes of the neurovascular bundle; indirectly via nearby veins, derived usually from muscles; to the periarterial venous plexus; or, in the case of the cutaneous nerves, to the perivenous plexus. The various patterns of the drainage along the length of the radial, median, ulnar, sciatic, anterior and posterior tibial nerves were identified. A rich longitudinal plexus of veins exists on and within the nerve which appears to be mainly free of valves. The large venae nervosa usually contained valves, whereas the tiny veins draining the nerves were valveless or exhibited a sentinel valve at their entry point into a larger venous channel. The clinical implications of these results are discussed in relation to the mobilisation of nerves, the use of island nerve flaps, possible donor sites for free arteriolised neurovenous flaps and the compressive nerve syndromes.

Brachial Plexus↗