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Results for “Nerve Compression Syndromes”

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At least 361 records · Page 20Linked to original sources
PubMed1998

Distal nerve entrapment following nerve repair.

Failure of nerve repair or poor functional outcome after reconstruction can be influenced by various causes. Besides improper microsurgical technique, fascicular malalignment and unphysiologic tension, we found in our clinical series that a subclinical nerve compression distal to the repair site can seriously impair regeneration. We concluded that the injured nerve, whether from trauma or microsurgical intervention, could be more susceptible to distal entrapment in the regenerative stage because of its disturbed microcirculation, swelling and the increase of regenerating axons followed by increased nerve volume. In two cases we found the regenerating nerve entrapped at pre-existing anatomical sites of narrowing resulting in impaired functional recovery. In both cases the surgical therapy was decompression of the distal entrapped nerve and this was followed by continued regeneration. Thorough clinical and electrophysiologic follow-up is necessary to detect such adverse compression effects and to distinguish between the various causes of failed regeneration. Under certain circumstances primary preventive decompression may be beneficial if performed at the time of nerve coaptation.

Adult↗
PubMed2003

Recurrent arachnoid cyst of Meckel's cave mimicking a brain stem ischaemia. Report of a rare case.

UNLABELLED: A 44-years old man developed TIA-like symptoms with dysaesthesia around the mouth, vertigo and diplopia. MRI revealed a cystic space-occupying lesion on the right Meckel's cave, which spread out into cerebellopontine angle in a further examination. Therefore surgical exploration was performed using a suboccipital approach. An arachnoidal cyst was found and removed including its wall. About three months later the patient suffered again from dysaesthesias of the right side of the face and a new MRI revealed a recurrence of the lesion, with extension into the cerebellopontine angle, too. Surgical revision was done using the same approach and the recurrent cyst was removed. Postoperatively, there were a transient hypaesthesia in the distribution area of the right trigeminal nerve and a light pulmonary embolism occurred as a complication. No symptoms have returned during an observation period of 15 months. CONCLUSION: An arachnoidal cyst must be considered as a rare cause, when a lesion is found at the Meckel's cave with intermittent clinical symptoms of a trigeminal nerve affection. As surgical treatment we favour fenestration and cyst wall resection.

Adult↗
PubMed2004

Structural and functional regeneration of muscle-related axons after transection and repair of the rat sciatic nerve using nonvascularized autologous fascia as a barrier between tibial and peroneal nerve fascicles.

Aberrant reinnervation of target organs caused by misdirected axonal growth at the repair site is a major reason for the poor functional outcome usually seen after peripheral nerve transection and repair. This study investigates whether the criss-crossing of regenerating rat sciatic nerve axons between tibial and peroneal nerve fascicles can be reduced by using non-vascularized autologous fascia as a barrier. The left sciatic nerve was transected and repaired at midthigh as follows: epineurialy sutures (Group A); fascicular repair of tibial and peroneal nerve fascicles (Group B); fascicular repair of tibial and peroneal nerve fascicles separating the two fascicles by non-vascularized autologous fascia (Group C). In the control Group D, only the left tibial fascicle was transected and repaired. Five months postoperatively, the outcome of regeneration was evaluated by histology, by retrograde tracing, and by assessment of the contraction force of the gastrocnemius and tibial anterior muscles. The tracing experiments showed that muscle reinnervation was less abnormal in Group C than in Groups A and B. However, muscle contraction force was not better in Group C than in Groups A and B. With respect to the peroneal nerve innervated muscle, the contraction force in Group C was significantly lower than in Group B. The histologic picture indicated that this inferior result in Group C was due to nerve compression caused by fibrotic scar tissue at the site of the fascia graft. Results of this study show that a non-vascularized autologous fascial graft used as a barrier between two sutured nerve fascicles in adjacency reduces criss-crossing of regenerating axons between the fascicles, but causes significant nerve compression.

Animals↗
PubMed2007

[Recurrent facial paresis with facial neurinoma].

PATIENT: A clinical case of a 49-year-old man is described who presented with a right facial paresis for 4 weeks. The patient had undergone a decompression of facial nerve and a radical mastoidectomy elsewhere in 1998 because of a facial paresis and acute mastoiditis. In the following years a complete right facial paresis occurred several times improving with prednisolone. In addition to topognostic examinations a high resolution computed tomography of the temporal bone was made. CT showed a mass in the right tympanic cavity with close contact to the ossicular chain. Diagnostic tympanotomy disclosed a tumor of the tympanic segment of the facial nerve. Pathological examination indicated a diagnosis of neurinoma with an Antoni B architecture. In a second operation the tumor was resected totally and a facial nerve reconstruction was performed by a greater auricular nerve interposition graft. Seven month postoperative beginning nerve reinnervation was seen proceeding continually until the control examination after 1 1/2 year. DISCUSSION: Facial neurinoma are a rare course of facial paresis. There are no specific symptoms. That's why the diagnosis is difficult. But it is necessary to think of with differential diagnosis of facial paresis.

Cranial Nerve Neoplasms↗
PubMed1998

Nerve wrapping with vein grafts in a rat model: a safe technique for the treatment of recurrent chronic compressive neuropathy.

The surgical outcome in recurrent chronic nerve compression remains unsatisfactory. Clinically, it has been reported that vein grafts can be used to wrap the nerve, following nerve decompression, to improve the functional recovery of the nerve. In order to determine the safety and feasibility of the technique of vein wrapping of nerve, this study assessed the effect of vein-graft wrapping around normal nerve. In each of 30 rats, a segment of femoral vein was wrapped around the sciatic nerve. Functional, electrophysiologic, and histologic testing was performed at 9, 12 and 15 weeks postoperatively, and the results showed no significant differences between the experimental and control groups. Neither scar tissue between the nerve and the vein graft, nor demyelinization or degeneration of the nerve fibers were identified histologically. The study demonstrated that autogenous vein-graft wrapping did not result in any pathologic nerve entrapment. The technique of vein wrapping of nerve appears to be safe, feasible, and reliable. The results supported further study for the use of vein-graft wrapping in the surgical management of recurrent chronic nerve compression.

Action Potentials↗
PubMed1988

Human ulnar neuropathy at the elbow: clinical, electrical, and morphometric correlations.

This study explored and compared clinical, electrodiagnostic, and morphometric observations on bilateral ulnar nerves obtained at necropsy in a patient with severe bilateral ulnar compression neuropathy at the elbow. There was excellent correlation among all three evaluation techniques. On the patient's more symptomatic side, there was significant slowing of conduction velocity across the elbow, with sensory conduction unobtainable in the little finger. Morphometric results demonstrated loss of myelin, decreased nerve fiber diameter, and reduction in percent of neural tissue present in the compressed elbow segment of the ulnar nerve.

Aged↗
PubMedDate not supplied

[The effect of cytokines on regeneration results of compressed nerve roots and transsected peripheral nerves].

The possible beneficial effect of Interleukin-1 (IL-1) on nerve regeneration was studied using clinical, neurophysiological and histomorphological methods. The sciatic nerves of Wistar rats were transsected and the severed ends abutted, sewn together and covered with fibrin adhesive. In a second group the lumbar-sacral nerve roots were exposed, IL-1 was injected and compression of the nerve roots was carried out. The region surrounding the lesion was infused with either saline (controls) or IL-1 (treatment group) in both groups. Compared to the controls, the treated animals showed a significant improvement of nerve regeneration as measured by clinical and neurophysiological parameters. After 3 months of observation, the total number of myelinated axons distal to the site of lesion was increased, while the fiber diameter distribution was unchanged. It is likely that cloned IL-1 will soon become available for human treatment. The present results indicate that it may be worthwhile to investigate its usefulness in the treatment of peripheral nerve injury in primates and humans.

Animals↗
PubMedDate not supplied

[Synovial cytokines facilitate the development of spontaneous nerve root activity following compression].

The nerve roots of Wistar rats were studied electrophysiologically following exposure to synovial cytokines. A total of 12 rats was examined. In the experimental series a preparation of synovial cytokines (50 microliters, 250 micrograms protein) was injected into the S1 nerve root of 6 Wistar rats. Six animals served as controls and were injected with a similar solution lacking cytokines. Forty-eight hours after this procedure the S1 nerve root was compressed by a force of 0.2 N for 1 hour. EMG recordings at mid-gastrocnemius levels were performed during, and 3 hours after, compression. The neurophysiological testing performed 3 hours after compression showed a significantly higher level of compression-induced muscle activity in the cytokine group compared to the control.

Animals↗
PubMed1990

[Acute progressive paralysis caused by intraneural ganglion--a neurosurgical emergency].

Intraneural ganglia, particularly of the peroneal and ulnar nerves may produce rapidly progressive paresis after minor trauma, for instance, following a sport injury. The chance of recovery of nerve function depends on the timing of surgical treatment. A patient with a ganglion of the peroneal nerve is reported in order to stress the relevance of intraneural ganglia, the danger of missing the lesion and the importance of early treatment. It is stressed that in the presence of rapidly progressing paralysis and the clinical suspicion of an intraneural ganglion, early decompression offers the best prognosis for recovery.

Adult↗
PubMed1989

Resistance to axonal degeneration after nerve compression in experimental diabetes.

To determine the effect of diabetes on the development of axonal degeneration after acute nerve compression, the mobilized peroneal nerves of rats with streptozotocin-induced diabetes and of control rats were compressed at 150 mmHg (1 mmHg = 133 Pa) for 30 min by using specially devised cuffs. At three intervals after compression--3 days, rats diabetic for 31 wk; 14 days, diabetic for 6 wk; and 24 days, diabetic for 31 wk--groups of nerves were studied to assess numbers and sizes of fibers above, at, and below the cuff and to assess frequency of fiber degeneration in teased fibers from nerve distal to the cuff. Teased fibers with pathologic abnormalities were more frequent in nerves from controls than in nerves from diabetic rats in all three groups but the difference was statistically significant only at 3 and 14 days after compression. The lack of significant difference at 24 days may be explained by higher rates of disappearance of degenerating products and of fiber regeneration at 24 than at 3 and 14 days. This study provides evidence that in addition to delaying the reported functional deficit of vibratory detection threshold and conduction block during nerve compression, diabetes also may partially prevent axonal injury. Low nerve myo-inositol concentration did not predispose diabetic nerve to acute compression injury. If these results also apply to human diabetes and if repeated acute compression is involved in the genesis of fiber degeneration in entrapment, then a higher frequency of entrapment neuropathy among diabetics might be due to mechanisms other than increased susceptibility of fibers to acute compression--e.g., possibly to greater constriction of nerve due to pathologic alterations of the carpal ligament.

Animals↗
PubMed1990

Structural alterations of nerve during cuff compression.

Whether compression nerve injury is due to ischemia, direct mechanical injury, or both remains unsettled. To assess structural changes of nerve during compression, peroneal nerves of rats were compressed at various pressures for different times, and the structural alterations were stopped by simultaneous in situ and perfusion fixation. The structural changes observed during a few minutes of compression cannot be explained by ischemic injury because the pathologic alterations characteristic of ischemia take many hours to develop and in any case are different from the ones found here. The pressure- and time-related structural changes observed in the present study under the cuff were (i) decrease in fascicular area and increase in fiber density due to expression of endoneurial fluid; (ii) compression and expression of axoplasm, sometimes to the point of fiber transection; (iii) lengthening of internodes; and (iv) obscuration of nodes of Ranvier due to cleavage and displacement of myelin and overlapping of nodes by displaced loops of myelin. At the edges of the cuff the changes were (i) increase of fascicular area probably from expressed endoneurial fluid; (ii) widening of nodal gaps, perhaps mainly from translocated axonal fluid; and (iii) disordered structure of axoplasm. We suggest that the process of paranodal demyelination and axonal transection are linked, occur during the act of compression, and are due to shear forces. The initial event is expression of endoneurial fluid, followed by compression and expression of axoplasm and cleavage and displacement of layers of myelin. Conceivably, with prolonged cuff compression ischemic injury might be found to be superimposed on mechanical injury.

Animals↗
PubMed2004

A mild acute compression induces neurapraxia in rat sciatic nerve.

The pressure that induces neurapraxia in rat remains unrevealed. To determine the appropriate force to induce neurapraxia, two types of clips were applied to the sciatic nerve and were evaluated with functional, electrophysiological, and histological examinations. With a compression of 60 g/mm2, walking track analysis showed complete sciatic nerve paralysis one day postoperatively, but became normal in 14 days. Electrophysiologically, complete conduction block occurred one day post operatively, whereas the motor conduction velocity (MCV) below the compression site remained normal. Histologically, only limited signs of Wallerian degeneration were seen. The model in this study exhibited the features of neurapraxia.

Animals↗
PubMed1983

Hand injuries and disorders. Principles of management for the family physician.

Hand injuries and disorders constitute a major cause of disability and time lost from work. Viewed as relatively minor, they are often neglected until permanent disability and restriction of function occur. The first physician to evaluate and treat an injured hand often determines the ultimate outcome of the patient's hand function. Skillful diagnosis and appropriate treatment are necessary. Neglected or mistreated injury may result in significant impairment in a person whose livelihood depends on the skillful, integrated function of both hands.

Burns↗
PubMed1999

Effect of compression on the cochlear nerve: a short- and long-term electrophysiological and histological study.

The short- and long-term effects of static compression of the cochlear nerve were studied in dogs. The nerve was exposed in the cerebellopontine angle and a modified aneurysm clip was applied to reduce the diameter of the nerve trunk to 50%, 40%, 30% or 20% of normal (designated respectively as 50%, 60%, 70%, and 80% compression). Brainstem auditory evoked potentials (BAEPs) were monitored intraoperatively and post-operatively. The animals were sacrificed between 5 and 119 days after nerve compression and temporal bones were examined histologically. In the 50% compression group, all peaks except peak I disappeared immediately after nerve compression. After release of the clip, however, peak II and subsequent components recovered and prolonged interpeak latency (IPL) between peaks I and IV normalized within 7 days. In the 60% compression group, recovery was incomplete for as long as 49 days after compression. Significant histological changes were not always reflected in the electrophysiological recordings, as shown by the finding of multiple cavitations at the compressed portion of the cochlear nerve in cases in which conduction block of cochlear nerve impulses was reversible. In the 70% compression group, peak IV did not reappear for more than 1 week, and histological examination revealed severe damage to all cochlear nerve fibers except those from the apical turn, which lie in the center of the cochlear nerve trunk. Severe injury occurred to the cochlear nerve fibers that are situated more superficially in the nerve, which are tonotopically responsible for the perception of high-frequency sound and the generation of BAEPs. This means that the BAEP changes due to cochlear nerve compression would be detectable by BAEP monitoring, although changes in the apical region of the cochlea are not fully detectable by BAEP monitoring. In the 80% compression group, all peaks except peak I were lost permanently and the amplitude of peak I, which had been preserved in the acute phase, gradually decreased. Reversibility of impaired cochlear nerve impulse conduction was related to the severity of compression, and at some level of compression between 70% and 80% the nerve fibers generating BAEPs permanently lost the ability to conduct electrical impulses proximal to the site of compression. In the 70% and 80% compression groups, the amplitude of peak I gradually decreased over the first 30 days after compression and did not change significantly thereafter. Histologically, the branches of the internal auditory artery were resilient to compression, although they are easily avulsed due to stretch force. Furthermore, retrograde degeneration of cochlear neurons triggered by compression at the cisternal portion of the cochlear nerve was apparent. Such slowly progressive degeneration of nerve fibers may play a part in development of the delayed postoperative hearing disturbance.

Animals↗
PubMed2005

Induction of activating transcription factor 3 (ATF3) by peripheral nerve compression.

Nuclear translocation of activating transcription factor 3 (ATF3), used as a marker for neuronal injury, was studied by immunocytochemistry in sensory neurons in dorsal root ganglia and locally along the sciatic nerve after severe chronic nerve compression in rats. In compressed nerves (application of a narrow silicone tube), ATF3 immunoreactivity was seen in the nucleus of sensory neurons and in Schwann cells below the compression at two and four weeks. Removal of the silicone tube (decompression) at two weeks did not affect the number of ATF3-positive cell nuclei in dorsal root ganglia. No ATF3 immunoreactivity was found in undamaged nerves on the other side. Functional variables (toe spreading and muscle force) were impaired at two weeks, with partial improvement at four weeks. Nerve compression induces nuclear translocation of ATF3, a transcription factor associated with survival and regeneration of sensory neurons. The response is related to duration of compression and partly correlated to function.

Activating Transcription Factor 3↗