Tumours of cranial and peripheral nerves

2010 ◽  
pp. 474-481
Author(s):  
George Samandouras

Chapter 8.17 covers tumours of cranial and peripheral nerves, including vestibular schwannoma (VS), neurofibroma, and malignant peripheral nerve tumours (MPNSTs).

Author(s):  
Dina V. Rusanova ◽  
Oleg L. Lakhman ◽  
Galina M. Bodienkova ◽  
Irina V. Kudaeva ◽  
Natalya G. Kuptsova

Introduction. There is a lack of knowledge of the pathophysiological mechanisms that form peripheral nerve disorders in mercury lesions of professional origin. The study aims to reveal the mechanisms underlying peripheral nerve damage in the long-term post-contact period of chronic mercury intoxication (CMI). Materials and methods. Fifty-one people had the diagnosis of a long-term period of CMI. The post-contact period was 8.5±2.6 years. The authors compared the results with a control group of 26 healthy men who had no contact with toxic substances. Stimulating electroneuromyography was performed. We studied the body systems that could contribute to the formation of disorders in the peripheral nerves. Changes in peripheral hemodynamics were studied using reovasography. The content of autoantibodies, neuron-specific enolase, serotonin, histamine, catecholamines (epinephrine, dopamine), metanephrine, and neurotrophin-3 was reviewed. The content of ceruloplasmin, secondary products of lipid peroxidation processes, reduced glutathione, the activity of superoxide dismutase and the content of nitric oxide levels were determined. Results. The study established pathogenetic structural links of peripheral nerve disorders. The autoimmune process's role was to increase the range of antibodies to the MAG protein and increase the level of antibodies to DNA. Violations of elastic-tonic properties of peripheral vessels could be associated with the functional state of motor axons. The increased content of neurotransmitters is related to the state of peripheral blood circulation; the most pronounced changes were on the legs, which could contribute to the occurrence and maintenance of vasoconstriction. The role of oxidative stress in the formation of demyelinating disorders in patients' peripheral nerves in the long-term period of CRI is possible. Conclusion. Neuroimmunological processes has an essential role in the development of peripheral nerve demyelination was shown, which consists in an increase in the content of antibodies to the MAG protein expressed on Schwann cells of peripheral nerves and in an increase in the level of antibodies to DNA involved in the formation of demyelinating changes when exposed to metallic mercury. The revealed pathological changes in the state of the peripheral blood circulation, characterized by a violation of the vessels' elastic-tonic properties, leading to demyelination of motor axons in patients in the long-term period of CMI. The increased content of neurotransmitters in the examined is of great importance in the state of peripheral circulation. Pronounced changes in blood circulation are established on the lower extremities, which may be associated with the predominance of α-adrenergic receptors in the arterial bed and may contribute to the occurrence and maintenance of vasoconstriction in the legs. The relationship between changes in indicators of oxidative stress, consisting of a decrease in the value of superoxide dismutase and reduced glutathione, and the formation of demyelinating disorders of peripheral nerves in patients in the long-term period of CMI has been proved.


2021 ◽  
Vol 10 (8) ◽  
pp. 1613
Author(s):  
Alessandro Crosio ◽  
Giulia Ronchi ◽  
Benedetta Elena Fornasari ◽  
Simonetta Odella ◽  
Stefania Raimondo ◽  
...  

As a consequence of trauma or surgical interventions on peripheral nerves, scar tissue can form, interfering with the capacity of the nerve to regenerate properly. Scar tissue may also lead to traction neuropathies, with functional dysfunction and pain for the patient. The search for effective antiadhesion products to prevent scar tissue formation has, therefore, become an important clinical challenge. In this review, we perform extensive research on the PubMed database, retrieving experimental papers on the prevention of peripheral nerve scarring. Different parameters have been considered and discussed, including the animal and nerve models used and the experimental methods employed to simulate and evaluate scar formation. An overview of the different types of antiadhesion devices and strategies investigated in experimental models is also provided. To successfully evaluate the efficacy of new antiscarring agents, it is necessary to have reliable animal models mimicking the complications of peripheral nerve scarring and also standard and quantitative parameters to evaluate perineural scars. So far, there are no standardized methods used in experimental research, and it is, therefore, difficult to compare the results of the different antiadhesion devices.


1992 ◽  
Vol 421 (4) ◽  
pp. 331-338 ◽  
Author(s):  
Sibylle Haraida ◽  
Andreas G. Nerlich ◽  
Karl Bise ◽  
Irmgard Wiest ◽  
Erwin Schleicher

Author(s):  
Alexander Scarborough ◽  
Robert J MacFarlane ◽  
Michail Klontzas ◽  
Rui Zhou ◽  
Mohammad Waseem

The upper limb consists of four major parts: a girdle formed by the clavicle and scapula, the arm, the forearm and the hand. Peripheral nerve lesions of the upper limb are divided into lesions of the brachial plexus or the nerves arising from it. Lesions of the nerves arising from the brachial plexus are further divided into upper (proximal) or lower (distal) lesions based on their location. Peripheral nerves in the forearm can be compressed in various locations and by a wide range of pathologies. A thorough understanding of the anatomy and clinical presentations of these compression neuropathies can lead to prompt diagnosis and management, preventing possible permanent damage. This article discusses the aetiology, anatomy, clinical presentation and surgical management of compressive neuropathies of the upper limb.


1990 ◽  
Vol 15 (1) ◽  
pp. 25-34
Author(s):  
D. MARSH

Erik Moberg pioneered the idea of validating measures of sensory function following peripheral nerve suture by correlating their results with those of functional tests. However it is important that powerful prior variables (age at suture, time elapsed since suture and delay between injury and suture) be controlled. Failure to do this may result in spurious correlations, as illustrated by analysis of two sets of data, one collected by the author and the other given in the classic paper of Önne (1962).


1956 ◽  
Vol 185 (1) ◽  
pp. 217-229 ◽  
Author(s):  
Samuel Gelfan ◽  
I. M. Tarlov

The reversible conduction block produced by maintained mechanical pressure around small segments of spinal cord, nerve root or peripheral nerve (dog) is due to mechanical deformation of the neuronal tissue and not to lack of O2. The compressed segment, although ischemic, is not anoxic; O2 from adjacent nonischemic tissue reaches it, presumably by diffusion. The entire pattern of modification of neuronal responses by compression and the postdecompression recovery pattern are distinctly different from the patterns observed during anoxia and recovery from the latter, indicating the difference in mechanisms by which mechanical deformation and O2 lack block conduction. The largest fibers in dorsal columns, roots and peripheral nerves are most susceptible to pressure and the smallest ones are relatively most resistant. Secondary neurons are less vulnerable than the primary afferent ones to light and moderate, but suprasystolic, circumferential spinal cord pressure. All components of the composite spinal cord potential are blocked at about the same time by larger compressive forces. Anoxia, on the other hand, always inactivates secondary neurons before dorsal column fibers and blocks smaller A fibers in peripheral nerves before the larger ones. The latency for complete blocking in each neuronal structure is specific and irreducible in the case of anoxia, whereas in compression it varies over a wide range, depending upon the magnitude of the compressive force.


2021 ◽  
Author(s):  
Brendan Zotter ◽  
Or Dagan ◽  
Jacob Brady ◽  
Hasna Baloui ◽  
Jayshree Samanta ◽  
...  

ABSTRACTPeripheral nerves are organized into discrete cellular compartments. Axons, Schwann cells (SCs), and endoneurial fibroblasts (EFs) reside within the endoneurium and are surrounded by the perineurium - a cellular sheath comprised of layers of perineurial glia (PNG). SC secretion of Desert Hedgehog (Dhh) regulates this organization. In Dhh nulls, the perineurium is deficient and the endoneurium is subdivided into small compartments termed minifascicles. Human Dhh mutations cause a peripheral neuropathy with similar defects. Here we examine the role of Gli1, a canonical transcriptional effector of hedgehog signaling, in regulating peripheral nerve organization. We identify PNG, EFs, and pericytes as Gli1-expressing cells by genetic fate mapping. Although expression of Dhh by SCs and Gli1 in target cells is coordinately regulated with myelination, Gli1 expression unexpectedly persists in Dhh null EFs. Thus, Gli1 is expressed in EFs non-canonically i.e., independent of hedgehog signaling. Gli1 and Dhh also have non-redundant activities. In contrast to Dhh nulls, Gli1 nulls have a normal perineurium. Like Dhh nulls, Gli1 nulls form minifascicles, which we show likely arise from EFs. Thus, Dhh and Gli1 are independent signals: Gli1 is dispensable for perineurial development but functions cooperatively with Dhh to drive normal endoneurial development. During development, Gli1 also regulates endoneurial extracellular matrix production, nerve vascular organization, and has modest, non-autonomous effects on SC sorting and myelination of axons. Finally, in adult nerves, induced deletion of Gli1 is sufficient to drive minifascicle formation. Thus, Gli1 regulates the development and is required to maintain the endoneurial architecture of peripheral nerves.SIGNIFICANCE STATEMENTPeripheral nerves are organized into distinct cellular/ECM compartments: the epineurium, perineurium and endoneurium. This organization, with its associated cellular constituents, are critical for the structural and metabolic support of nerves and their response to injury. Here, we show Gli1 - a transcription factor normally expressed downstream of hedgehog signaling - is required for the proper organization of the endoneurium but not the perineurium. Unexpectedly, Gli1 expression by endoneurial cells is independent of, and functions non-redundantly with, Schwann Cell-derived Desert Hedgehog in regulating peripheral nerve architecture. These results further delineate how peripheral nerves acquire their distinctive organization during normal development and highlight mechanisms that may regulate their reorganization in pathologic settings including peripheral neuropathies and nerve injury.


2019 ◽  
Vol 6 (7) ◽  
pp. 2634
Author(s):  
Shipra Singhal ◽  
Sufian Zaheer ◽  
Rashmi Arora

Schwannomas are benign peripheral nerve sheet tumours that may arise almost anywhere in the body but are commonly seen in the head, neck region and in the extremities. They may be associated with variable clinical presentations depending on their location. The peripheral nerves are closely related to vascular tissues morphologically and physiologically and therefore schwannomas may be associated with vascular changes like vascular hyperplasia and vascular dilation. Here authors represent one such case where a 38-year-old patient presented with a cervical swelling which on histopathology was diagnosed as vascular schwannoma.


1987 ◽  
Vol 165 (4) ◽  
pp. 1218-1223 ◽  
Author(s):  
V H Perry ◽  
M C Brown ◽  
S Gordon

Using mAbs and immunocytochemistry we have examined the response of macrophages (M phi) after crush injury to the sciatic or optic nerve in the mouse and rat. We have established that large numbers of M phi enter peripheral nerves containing degenerating axons; the M phi are localized to the portion containing damaged axons, and they phagocytose myelin. The period of recruitment of the M phi in the peripheral nerve is before and during the period of maximal proliferation of the Schwann cells. In contrast, the degenerating optic nerve attracts few M phi, and the removal of myelin is much slower. These results show the clearly different responses of M phi to damage in the central and peripheral nervous systems, and suggest that M phi may be an important component of subsequent repair as well as myelin degradation.


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