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Nine patients with a peripheral nerve lesion (six intrinsic and three extrinsic) were evaluated with computerized tomography (CT). In all but one instance, the CT scans gave useful information regarding the anatomical location, size, and relationship of the lesion to surrounding structures. These cases illustrate the usefulness of CT as a diagnostic tool in the evaluation of peripheral nerve lesions.
Although much progress has been made, current treatments of peripheral nerve injury often result in only partial recovery. Many methods have been used to improve the surgical exploration for injured nerve repair. However, much less is known about the involvement of complex neurochemical interactions. Several neurotrophic factors have been shown to play an essential trophic role in the development, maintenance, and regulation of neuronal function. These include nerve growth factor (NGF) and several recently identified members of the NGF family. In this article we give an overview of the process of peripheral nerve injury and regeneration, review the roles of Schwann cells and neurotrophic factors, and summarize perspectives on how gene therapy with viral vectors and cell-mediated DNA strand technology may be used to improve treatment of peripheral nerve injuries.
1. Myeline proteins in bovine peripheral nerve migrated as two main band-(BF and BR protein) and one faint middle band (BM protein) on sodium dodecyls sulfate-polyacrylamide gel electrophoresis. The relative mobility of these two main bands differed from those of myelin proteins in the central nervous system. 2. The acid extract of the myelin fraction from bovine peripheral nerve was separated into one main peak and two minor peaks on a Sephadex G-75 column. The major component of the second minor peak was the BM protein; the major component of the main peak was the BF protein. The BR protein was not extractable by acid solution. 3. Molecular weights of the BF, the BM and the BR protein were determined as around 13 000, 20 000 and 28 000, respectively, by sodium dodecylsulfate-polyacrylamide gel electrophoresis. 4. The amino acid composition of the BF protein was quite different from the encephalitogenic protein and the Folch-Lees type proteolipid protein in the central nervous system. However the BM protein showed similar amino acid composition to the encephalitogenic protein. 5. The tryptic peptide maps of the BF protein and of the encephalitogenic protein were quite different. The results suggested that the amino acid sequences of these two proteins are different and that they contain no common tryptophan-containing peptide.
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This article reviews the epidemiology and classification of traumatic peripheral nerve injuries, the effects of these injuries on nerve and muscle, and how electrodiagnosis is used to help classify the injury. Mechanisms of recovery are also reviewed. Motor and sensory nerve conduction studies, needle electromyography, and other electrophysiological methods are particularly useful for localizing peripheral nerve injuries, detecting and quantifying the degree of axon loss, and contributing toward treatment decisions as well as prognostication.
To study the fascicular anatomy of peripheral nerves, three different groups of retrograde axonal tracers were evaluated: fluorophores, horseradish peroxidase conjugated to subunit B of cholera toxin (CT-HRP), and adeno-associated virus (AAV). The hindlimb nerves in rats served as a model to identify the most efficient tracer in regard to labeling axons within peripheral nerves. The rat's tibial and common peroneal nerves were injected with the different tracers and the sciatic nerve was subsequently examined for evidence of labeled axons. The CT-HRP clearly provided the best results in this rat model. Subsequently, CT-HRP was injected into the recurrent laryngeal nerve (RLN) of two horses in order to identify the location and distribution pattern of the RLN axons within the course of the cervical vagus nerve trunk. No labeling could be observed in either of the two horses.
BACKGROUND: Malignant peripheral nerve sheath tumors are rare tumor entities that originate from peripheral nerve sheaths and have an unfavorable prognosis. Metastatic spread to the cerebral parenchyma is absolutely rare. This case report describes the clinical course in a 60-year-old man whose tumor came to medical attention because of a seizure. CASE PRESENTATION: Magnetic resonance imaging demonstrated two intracerebral lesions. The symptomatic lesion was removed microneurosurgically and histology demonstrated a metastasis from a malignant peripheral nerve sheath tumor. Postoperatively, whole-brain irradiation was performed. The primary tumor was identified in the area of the sciatic nerve on the right. Follow-up 14 months after resection showed that there was no progression of the intracerebral lesions but an increase in size and number of distant metastases. CONCLUSION: There are no generally accepted guidelines for the treatment of malignant peripheral nerve sheath tumors with cerebral metastases. This case report presents and discusses one possible therapeutic approach. Due to the poor overall prognosis, the least invasive therapy should be chosen.
The Bennett and Xie model of peripheral nerve injury was used to study the effects of aging on the onset and progression of sciatic nerve ligation (SNL)-induced thermal hyperalgesia and tactile-evoked allodynia in young, mature, and aged Fischer 344 FBNF1 male rats (4-6, 14-16, and 24-26 months old, respectively). A plantar analgesia meter and calibrated von Frey pressure filaments were employed as the analgesiometric assays. In the absence of nerve injury, aged rats were found to be more sensitive than younger animals to noxious thermal stimuli. Following the SNL surgery, thermal hyperalgesia was observed in all three age groups within 3 days. On post-SNL day 35, the paw-withdrawal latency values of the young and mature animals returned to presurgical baseline levels, while the aged rats continued to exhibit thermal hyperalgesia. Tactile-evoked allodynia was apparent within 3 days following peripheral nerve injury in the oldest cohort, but was delayed in the younger animals. On post-SNL days 0 (control), 3, 21, and 35, young, mature, and aged rats were sacrificed and high-performance liquid chromatography and electrochemical detection (HPLC/ECD) methods were used for neurochemical analyses of spinal serotonin (5-HT), norepinephrine (NE), and 5-hydroxyindoleacetic acid (5-HIAA). Spinal 5-HT and NE levels were not significantly altered by the aging process, nor were they affected by peripheral nerve injury. However, spinal 5-HT turnover from the aged animals was greater than that detected in spinal tissue from the younger counterparts. Differences in spinal 5-HT turnover may contribute to age-related variability in spinal nociceptive processing.
Malignant peripheral nerve sheath tumors of the nose and paranasal sinuses are extremely uncommon. We report the case of a 65-year-old woman who presented with a rapid emergence of "nasal polyps" that completely obstructed her nasal passages. Six years earlier she had been assessed elsewhere for nasal polyps. At presentation, the patient exhibited gross polyposis, with lesions protruding from both nostrils. Histology confirmed a diagnosis of a malignant peripheral nerve sheath tumor This case demonstrates that symptoms of nasal obstruction are not always secondary to simple causes. We discuss the clinical picture of nasal and paranasal malignant peripheral nerve sheath tumor, its pathology, and its treatment.
Abnormalities of peripheral nerve Na+ and K+ channels result in clinical manifestations unrelated to axonal degeneration or demyelination. Na+ channel blockade causes weakness and sensory loss associated with slowed conduction and decreased motor and sensory action potential amplitudes. K+ channel abnormalities result in high frequency repetitive action potentials (e.g., myokymia). Ion channel abnormalities may also play an important role in electrophysiologic changes seen in demyelinating disorders.
Peripheral nerve sheath tumors rarely occur in the oral cavity and include neurofibroma, schwannoma, and palisaded encapsulated neuroma. We report a rare case of benign peripheral nerve sheath tumor of the tongue. This tumor was a 0.8 X 0.5 cm sized, firm mass on the left lateral surface of the tongue. Histologically, this mass was composed of well- circumscribed variable sized nodules, which consisted of moderately cellular spindle cells with vague nuclear palisading and a small amount of fibrous tissue. Most of the tumor cells were strongly positive for S-100 protein, but negative for epithelial membrane antigen on immunohistochemistry. No axons were found by immunostaining for neurofilament and Bodian stains. In addition, the surrounding, compressed, fibrous tissue showed rare EMA- positive cells. The present case might be a rare case of neurofibroma arising in the tongue, although immunohistochemical and special stains did not support such a diagnosis.
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To analyze the peripheral nerve pathological abnormalities in familial amyloid polyneuropathy, a correlative pathological study was carried out on the spinal nerve roots, proximal sciatic nerves, sural nerves, and brachial plexuses from 3 patients with the disease in Japan. The spinal nerve roots appeared to be unaffected except for amyloid deposition on the epineurium. In sciatic nerves and brachial plexuses the nerve lesions had a multifocal distribution, showing prominent interstitial edema in the endoneurium frequently adjacent to deposits of amyloid; in these regions the nerve fibers were severely depleted. A teased-fiber study revealed that segmental demyelination was the predominant type of nerve fiber abnormality. However, these findings were not seen in the sural nerves; instead a diffuse fiber loss with axonal degeneration was observed. It is suggested that multifocal lesions in the proximal portions of the long extremity nerves could summate distally to produce a symmetrical polyneuropathy in the disease. In addition to a space-occupying effect of amyloid deposits in the endoneurium, severe endoneurial edema associated with amyloid deposition in blood vessels and the endoneurial interstitium may induce ischemia in nerve fibers, thus causing the progressive polyneuropathy in this disorder.
Extensive mobilization of injured peripheral nerves is often required to allow a tension-free repair. The purpose of this study was to determine the effect of surgical mobilization and division on intraneural blood flow and oxygen tension in a rat sciatic nerve model. The right and left sciatic nerves were exposed in male Lewis rats Four experimental groups were studied: 1) nerve in situ/intact (n=7); 2) nerve mobilized and intact (n=7); 3) nerve in situ/divided (n=7); and 4) nerve mobilized and divided (n=7). Intraneural oxygen tension and blood flow were measured postoperatively. Mean oxygen tension (mmHg) in mobilized/intact nerves (17.47+/-4.79) was significantly lower than in in situ/intact nerves (38.32+/-5.16) [p < 0.05]. Mean oxygen tension in mobilized/divided nerves (3.10+/-1.25) was significantly lower than in in situ/divided nerves (30.30+/-6.36) [p < 0.005]. Laser Doppler flow (ml/min/100 g) in mobilized divided nerves (11.31+/-1.81) was significantly lower than in in situ/divided nerves (25.60+/-3.31) [p < 0.05]. Laser Doppler flow in mobilized/intact nerves was not statistically significantly different from in situ/intact nerves. Mobilization of the extrinsic blood supply was shown to significantly lower intraneura) oxygen tension and laser Doppler flow in mobilized intact and divided rat peripheral nerves.
To investigate the pressure threshold for peripheral nerve dysfunction in compression syndromes (carpal tunnel and compartment syndromes), carpal canal pressure was elevated to 40, 50, 60, and 70 mm Hg in normal volunteers. Motor and sensory latencies and amplitudes of the median nerve were evaluated before compression, after 30-240 minutes of compression, and during the postcompression recovery phase. Although some functional loss occurred at 40 mm Hg, motor and sensory responses were completely blocked at a threshold tissue fluid pressure of 50 mm Hg, measured by the wick catheter. In one subject in whom diastolic blood pressure was significantly higher than in other subjects, the threshold pressure was raised slightly. The Semmes-Weinstein monofilament test and the 256-cycle vibratory test were more sensitive than two-point discrimination tests for evaluating peripheral nerve function in this compression model. These results indicate that between 40 mm Hg and 50 mm Hg there exists a critical pressure threshold at which peripheral nerve is acutely jeopardized. Compartment decompression may not be indicated when interstitial pressures are below this level.
Hypersensitivity to cold is a relatively frequent sequel of peripheral nerve injuries but its mechanism is not well understood. We suggested that incomplete recovery of diameter of regenerated fibers is one of the factors involved in cold intolerance after nerve damage. Conduction velocity is correlated to fiber diameter, and is slowed down by cold. In normal subjects, cold does not desynchronize the volleys of sensory impulses sufficiently to change the intelligibility of the peripheral 'messages'. Sensory perceptions remain accurate although they acquire a characteristic numbness. On the other hand, post-traumatic reduction in fiber diameters causes a permanent distortion of the messages. We considered that when the distortion is severe, the resulting messages may be perceived by the centers as containing nociceptive components. We further hypothesized that, even in cases of moderate permanent distortion, cold acts by increasing the post-traumatic abnormalities of impulse synchronization. In winter, decompensation is observed when a threshold of desynchronization is reached. We constructed a model of peripheral nerve messages in an attempt to represent and quantitate the desynchronizations produced by cold and crush damage lesions in peripheral nerve messages. A number of parameters concerning fiber anatomy, exposure to cold, and type of nerve damage were taken into consideration. Four elementary types of desynchronization could be recognized by considering the times of arrival of pairs of impulses at the nervous centers. The difference between a normal and a distorted message could be expressed by eight variables. Thus, although our model was quite simple, a large amount of data was obtained and a preliminary statistical study was necessary in order to orient the final analysis. Then, we used factor analysis in an attempt to obtain a satisfactory interpretation of the data. The results indicated that peripheral desynchronization might explain, at least in part, the painful sensations experienced in winter by many patients after peripheral nerve injury.
Although somatostatin receptors have been detected in many normal and neoplastic tissues, little is known of their expression and function in peripheral nerve tumors. In the present study, we examined the expression of all 5 somatostatin receptor subtypes (sst1-5) in 3 normal peripheral nerves, 3 traumatic neuromas, 27 schwannomas, 18 neurofibromas, and 177 malignant peripheral nerve sheath tumors (MPNSTs) by immunohistochemistry as well as by Western blot and reverse transcriptase-polymerase chain reaction investigations in 2 normal peripheral nerves, one neurofibroma, 5 schwannomas, and 5 MPNSTs. Immunoreactive somatostatin receptors were not detectable in normal peripheral nerve and in nonneoplastic Schwann cell proliferations. In contrast, sst2A mRNA and protein was present in 89% of schwannomas. This receptor subtype was less frequently detected in neurofibromas (22%) and MPNSTs (15%). Interestingly, sst4 was seen in 32% of MPNSTs and was almost exclusively expressed in this malignant tumor type. In support of a role in Schwann cell tumor growth control by somatostatin was the observation of induced internalization of sst2A and inhibition of cell proliferation in an NF1-associated MPNST cell line. Moreover, administration of an sst2A-selective agonist resulted in induction of MPNST cell apoptosis. We conclude that peripheral nerve sheath tumors often express at least one functional somatostatin receptor. Furthermore, our findings suggest a potential clinical role for somatostatin receptor agonists in tumor imaging and/or treatment of schwannomas and MPNSTs.
Malignant peripheral nerve sheath tumors are usually Schwann cell derived. Differentiation along mesenchymal lines is uncommon. Herein we present an example with smooth muscle differentiation occurring in the left distal forearm of a 62-year-old male with neurofibromatosis type I. Incisional biopsy of the slowly growing mass demonstrated a low-grade malignant peripheral nerve sheath tumor with strong S-100 protein immunoexpression as well as focal smooth muscle actin staining in atypical neoplastic cells. Immunostains for epithelial membrane antigen, neurofilament protein, glial fibrillary acidic protein, CD57, desmin, and myogenin were negative. The MIB-1 labeling index was 5.4%. Electron microscopy revealed arrays of microfilaments (actin myofilaments) variably associated with fusiform dense bodies, plasmalemmal micropinocytotic vesicles, and foci of external lamina (basement membrane) consistent with smooth muscle differentiation. Smooth muscle should be added to the spectrum of differentiation exhibited by malignant peripheral nerve sheath tumors. Its recognition requires exclusion of the alternative diagnosis of leiomyosarcoma.