Intraneural Pressure Research Articles

Immediate Effects of Median Nerve Mobilization on Nerve Conduction Velocities, Upperlimb Strength and Bimanual CoOrdination in Normal Healthy Subjects

Background and Objectives: - Neural tissue mobilization is a manipulative technique by which tissues are moved and stretched either by movement relative to surrounding structures or tension development. Mobilization of neural structures dependently or independently improves patient’s signs and symptoms. Nervous system adapts to lengthening through increase in intraneural or intramural pressures. Thus the continuum of the nervous system serve its ability to move either alone or through surrounding tissue interface to relieve contributing neural tension to patient’s symptoms. This Study assesses the immediate effects of neural tissue mobilization on the Nerve Conduction Velocities, the Bimanual Coordination and the Upper limb Grip Strength in normal healthy individuals. Materials and Method:- The participants in the study were normal healthy subjects. These subjects were assessed for their Upper limb Grip Strength, Bimanual coordination and the Nerve Conduction Velocities of the Median Nerve before and immediately after the Median Nerve Mobilization and analysis was done for the same. Result: - Data was analyzed by statistical means, standard deviation and students t- test and the results showed significant changes in terms of the nerve conduction velocity, upper limb strength and bimanual co-ordination in normal healthy subjects on an immediate basis. Conclusion: - This study concludes that immediate effects of median nerve mobilization on Nerve Conduction Velocities, Bimanual Coordination and Upper Limb Strength in normal healthy subjects are statisticaly significant. Hence immediate relief of discomfort through neural mobilization on these parameters can be obtained.

Ultrasound elastography in the evaluation of peripheral neuropathies: a systematic review of the literature.

Peripheral neuropathy is associated with an increase in intraneural pressure, and hence ultrasound elastography seems to be an ideal method to detect early stages of this condition based on changes in the affected nerve stiffness. The aim of this systematic review was to analyse the applicability of strain elastography (SE) and shear wave elastography (SWE) in the evaluation of peripheral nerves in patients with neuropathy of various aetiologies. Published evidence shows clearly that ultrasound elastography can accurately diagnose many types of peripheral neuropathies (carpal tunnel syndrome and other entrapment neuropathies, diabetic peripheral neuropathy and peripheral neuropathy associated with other systemic diseases), sometimes at the stages at which the condition is still asymptomatic. However, it is still unclear whether elastographic changes within the nerves precede functional anomalies detectable on nerve conduction studies. Also, relatively little is known about the relationship between the stiffness of peripheral nerves and the severity of peripheral neuropathy and its underlying condition. Based on the reproducibility data, SWE seems to be superior to SE. Nevertheless, the sources of heterogeneity in the peripheral nerve stiffness in healthy persons need to be identified, and the sets of reference values for specific peripheral nerves need to be determined. Finally, the potential confounding effect of hardening artefacts, such as bones, on the stiffness of peripheral nerves needs to be verified. After addressing all these issues, elastographic evaluation of peripheral nerve stiffness might become a reliable, easily accessible, and convenient diagnostic test performed routinely in patients with various peripheral neuropathies.

Preferential peroneal nerve injury after acetabular fracture and reconstruction

Background: Sciatic nerve dysfunction typically involving the peroneal division infamously plagues acetabular reconstruction through a posterior exposure. Competing explanations include mechanical compression from retractor placement at the hip versus overstretch. In an effort to improve the current care paradigm, we asked what underlying mechanisms of injury lead to preferential injury to the peroneal division of the sciatic nerve. Methods: A cadaver model was established to measure both sciatic nerve strain and intraneural pressure generated during simulated retraction performed during acetabular reconstruction. The tibial and peroneal divisions were studied independently using a micro differential variable reluctance transducer (DVRT) to quantify strain and an angiocatheter to measure intraneural pressure. Measurements were recorded at both the hip and knee. Results: Both divisions of the sciatic nerve experienced significantly more pressure at the hip than at the knee. Knee flexion reduced intraneural pressure of the peroneal division at the hip by approximately 30%. Intraneural pressure at the knee was significantly greater in the peroneal versus tibial nerve during knee extension, yet was reduced with knee flexion. Conclusions: Our results suggest that direct compression of the peroneal nerve during hip retraction has the most potential to cause iatrogenic sciatic nerve injury. Knee flexion was beneficial for decreasing nerve stretch and pressure. The peroneal division, however, is vulnerable to dysfunction because of the higher intraneural pressures experienced by the tethering effect of the fibular tunnel at the knee.

Pressure Monitoring of Intraneural an Perineural Injections Into the Median, Radial, and Ulnar Nerves; Lessons From a Cadaveric Study

Background:Nerve damage after regional anesthesia has been of great concern to anesthetists. Various modalities have been suggested to recognize and prevent its incidence. An understudied area is the measurement of intraneural pressure during peripheral nerve blockade. Previous investigations have produced contradicting results with only one study being conducted on human cadavers.Objectives:The purpose of this investigation was to systematically record intraneural and perineural injection pressures on the median, ulnar, and radial nerves exclusively as a primary outcome.Materials and Methods:Ultrasonography-guided injections of 1 mL of 0.9% NaCl over ten seconds were performed on phenol glycerine embalmed cadaveric median, ulnar, and radial nerves. A total of 60 injections were performed, 30 intraneural and 30 perineural injections. The injections pressure was measured using a controlled disc stimulation device. Anatomic dissection was used to confirm needle placement.Results:Intraneural needle placement produced significantly greater pressures than perineural injections did. The mean generated pressures in median, radial, and ulnar nerves were respectively 29.4 ± 9.3, 27.3 ± 8.5, and 17.9 ± 7.0 pound per square inch (psi) (1 psi = 51.7 mmHg) for the intraneural injections and respectively 7.2 ± 2.5, 8.3 ± 2.5, and 6.7 ± 1.8 psi for perineural injections. Additionally the intraneural injection pressures of the ulnar nerve were lower than those of the median and radial nerves.Conclusions:Obtained results demonstrate significant differences between intraneural and perineural injection pressures in the median, ulnar, and radial nerves. Intraneural injection pressures show low specificity but high sensitivity suggesting that pressure monitoring might be a valuable tool in improving the safety and efficacy of peripheral nerve blockade in regional anesthesia. Peripheral nerves “pressure mapping” hypothetically might show difference amongst various nerves depending on anatomic location, histologic structure, and ultrasonographic appearance.

Sindromi compressive dei nervi cutanei alla fascia della gamba

Entrapment syndromes are a group of peripheral nerves disorders characterized by neurological signs or vascular symptoms, due to chronic injury to the nerve as it travels from one body segment to the next. The two leading causes of this pathology are work postures and sports activities, the latter more and more common also in the elderly population. Nerve entrapment is generally caused by localized mechanical pressure from inelastic structures such as an osseoligamentous tunnel or by estrinsic compressions due to neoplasms or anatomic variations.Nerve damage is classified as neurapraxia and symptoms don’t often correlate with nerve damage or histological features. Repetitive injury to a nerve may initially result in microvascular (ischemic) changes in perineural venous system (vasa nervorum) leading to endoneurial edema formation, increase in intraneural pressures and further interference of endoneurial microcirculation with subsequent ipoxia. Injury to the outside layers of the nerve (myelin sheath) leads to perineural fibrosis and, in more advanced stages, focal segmental demyelination related to sclerosis at the area of compression. The diagnosis is made with a thorough clinical examination, allowing to identify the nerve involved in this painful condition and the area of compression and to define the severity of the disease. EMG and, rarely, MRI or echography complete the diagnostic pathway.Operative treatment is reserved for those patients in whom conservative treatment has been unsuccessful. Timing for surgery is dependent on knowing the different anatomical entrapment sites and their specific clinical presentations. Surgical treatment in the early stages of the disease is preferable, before chronic ischemic lesions lead to permanent sensory and motor impairment.

Entrapment neuropathies: pathophysiology and pathogenesis

A number of theories of pathogenesis of entrapment neuropathy, due to repeated loading, have been proposed and these theories are being actively explored with animal models. Tubes placed loosely around peripheral nerves cause delayed onset, chronic pain and changes in nerve morphology including nerve sprouting. Balloons placed around or adjacent to the nerve and inflated to low pressures, rapidly produce endoneurial edema and a persistent increase in intraneural pressure. The same models demonstrate long-term changes such as demyelination and fibrosis. The applied pressure causes a decrement in nerve function and abnormal morphology in a dose-dependent manner that appears to be linked to the amount of endoneurial edema. A new model involving involuntary, repetitive fingertip loading for 6 h per week for 4 weeks has caused slowing of nerve function at the wrist similar to that seen in patients with carpal tunnel syndrome. These models have the potential to reveal the mechanisms of injury at the cellular and biochemical level and address questions about the relative importance of various biomechanical factors (e.g. peak force, mean force, force rate, duty cycle, etc.). In addition, these models will allow us to evaluate various prevention, treatment and rehabilitation protocols.

Effect of various nerve decompression procedures on the functions of distal limbs in streptozotocin-induced diabetic rats: further optimism in diabetic neuropathy.

It is known that diabetic neuropathy is the result of endoneurial edema caused by various biochemical reactions triggered by hyperglycemia. This sequence of events can cause cessation of circulation at the perineurial level, or the tough layer, which is not resilient enough to spread intraneural pressure. Internal and external limiting structures create a double crush phenomenon to the nerve structure. Decompression of the nerve trunk at separate levels is one of the adjuncts to the overall treatment plan for diabetic neuropathy. In this study, the right sciatic nerves of 30 rats with streptozotocin-induced diabetes were used; three groups were created. In the control group, the sciatic nerves were explored and dissected only. In group II, tarsal tunnel release was performed and accompanied by epineurotomy of the sciatic nerve and its peroneal and tibial extensions. In group III, in addition to the procedures performed in group II, perineural sheaths, exposed through the epineurotomy sites at both the peroneal and tibial nerves, were incised for decompression of the fascicles. Improvement in diabetic neuropathy was evaluated by using footprint parameters. The last print length values, estimated according to the 38-month measurements, were 26.1 +/- 0.12 mm in the control group, 23.2 +/- 0.07 mm in group II, and 22.2 +/- 0.1 mm in group III. The toe spread and intermediate toe spread values of the groups were parallel to improvements in print lengths throughout the study. The best improvement was observed in the perineurotomy group. Finally, an electron microscopic study revealed variable degenerative changes in all groups, but they were milder in groups II and III. This experimental study reveals that adding internal decompression to external release doubled the effect in reducing derangement in the sciatic nerves of the rats and, in the authors' opinion, offers cause for further optimism in the treatment of diabetic neuropathy.

Intraneural sciatic nerve pressures relative to the position of the hip and knee: a human cadaveric study.

To determine the effects of ipsilateral hip and knee position on intraneural sciatic nerve pressures. Intraneural sciatic nerve pressures measured in intact, fresh cadaveric specimens relative to ipsilateral hip and knee positions. Medical school anatomy laboratory. Randomly acquired adult cadavers. Pressure transducer placed within the sciatic nerve distal to the femoral attachment of the gluteus maximus. Intraneural pressures measured with the hip placed in 0, 45, and 90 degrees of flexion while the knee was positioned in 90, 45, and 0 degrees of flexion. Tissue fluid pressures within the sciatic nerve relative to the position of the ipsilateral hip and knee. Tissue fluid pressure within the sciatic nerve exceeded previously defined critical thresholds for alteration of neural microcirculation and function. Although increased intraneural pressures were realized as the hip was positioned in greater flexion and the knee was extended, clinically relevant pressures were realized only when the hip was flexed to 90 degrees and the knee was fully extended. Pressures with the limbs in these positions were fifty-five millimeters of mercury (range 38 to 74 millimeters of mercury). With the hip held flexed to 90 degrees, statistically significantly increased intraneural pressures were measured as the knee was extended from 90 to 45 degrees of flexion (p = 0.048) and again from 45 to 0 degrees of flexion (p < or = 0.01). With the knee positioned in 45 degrees of flexion, statistically significantly increased intraneural pressures were measured as the hip was flexed from 45 to 90 degrees (p < or = 0.0062). When the knee was held fully extended, statistically significantly increased intraneural pressures were measured as the hip was flexed from 0 to 45 degrees of flexion (p = 0.0006) and again when the hip was brought from 45 to 90 degrees of flexion (p < or = 0.01). Intraneural sciatic nerve pressures are influenced by the position of the ipsilateral hip and knee. The magnitude of the pressure elevation appears to be related to the excursion of the nerve as the linear distance between the greater sciatic notch and the distal aspect of the leg increases. Intraneural tissue fluid pressures measured within a localized section of the sciatic nerve appeared to exceed published critical thresholds for alterations of blood flow and neural function only when the hip was flexed to 90 degrees and the knee was fully extended.

Facial Paralysis: Diagnosis and Management

Facial paralysis is a condition frequently seen in otology and audiology clinics. Its most common etiologies are idiopathic, trauma and infection. This article deals with the pathophysiology of facial paralysis, diagnostic technique and treatment modalities illustrated with case studies. The section on pathophysiology includes a discussion of the classification of nerve injury: neuropraxia that may be associated with a compressional injury, axonotmesis associated with an interruption of the myelin layer and axon and neurotmesis involving a complete transection. Among diagnostic techniques, evoked facial electromyography or electroneuronography and needle EMG are discussed and compared. Needle EMG in particular is useful in cases with complete facial paralysis and an evoked EMG reduction of 90% or more. Among patients with idiopathic facial paralysis approximately 71% recover completely and approximately 16% remain with serious sequelae. In terms of treatment, corticosteroids and antiviral medications may be used. Surgical decompression may be used in selected cases to relieve intraneural pressure.

Changes in interstitial pressure and cross-sectional area of the cubital tunnel and of the ulnar nerve with flexion of the elbow. An experimental study in human cadavera.

The purpose of this study was to determine the relationship between the ulnar nerve and the cubital tunnel during flexion of the elbow with use of magnetic resonance imaging and measurements of intraneural and extraneural interstitial pressure. Twenty specimens from human cadavera were studied with the elbow in positions of incremental flexion. With use of magnetic resonance imaging, cross-sectional images were made at each of three anatomical regions of the cubital tunnel: the medial epicondyle, deep to the cubital tunnel aponeurosis, and deep to the flexor carpi ulnaris muscle. The cross-sectional areas of the cubital tunnel and the ulnar nerve were calculated and compared for different positions of elbow flexion. Interstitial pressures were measured with use of ultrasonographic imaging to allow a minimally invasive method of placement of the pressure catheter, both within the cubital tunnel and four centimeters proximal to it, at 10-degree increments from 0 to 130 degrees of elbow flexion. As the elbow was moved from full extension to 135 degrees of flexion, the mean cross-sectional area of the three regions of the cubital tunnel decreased by 30, 39, and 41 per cent and the mean area of the ulnar nerve decreased by 33, 50, and 34 per cent. These changes were significant in all three regions of the cubital tunnel (p < 0.05). The greatest changes occurred in the region beneath the aponeurosis of the cubital tunnel with the elbow at 135 degrees of flexion. The mean intraneural pressure within the cubital tunnel was significantly higher than the mean extraneural pressure when the elbow was flexed 90, 100, 110, and 130 degrees (p < 0.05). With the elbow flexed 130 degrees, the mean intraneural pressure was 45 per cent higher than the mean extraneural pressure (p < 0.001). Similarly, with the elbow flexed 120 degrees or more, the mean intraneural pressure four centimeters proximal to the cubital tunnel was significantly higher than the mean extraneural pressure (p < 0.01). Relative to their lowest values, intraneural pressure increased at smaller angles of flexion than did extraneural pressure, both within the cubital tunnel and proximal to it. With the numbers available, we could not detect any significant difference in intraneural pressure measured, either at the level of the cubital tunnel or four centimeters proximal to it, after release of the aponeurotic roof of the cubital tunnel.

Intraneural ulnar nerve pressure changes related to operative techniques for cubital tunnel decompression

To evaluate the effect of critical anatomic structures on the ulnar nerve after cubital tunnel decompression, we determined the intraneural ulnar nerve pressure in 50 fresh cadavers after the following surgical procedures: simple decompression, medial epicondylectomy, subcutaneous transposition, and submuscular transposition by the Learmonth and by the musculofascial lengthening technique. Intraneural pressure was measured in 0°, 30°, 60°, and 90° elbow flexion at locations that were proximal, within, and distal to the cubital tunnel. Statistical analysis compared the mean change in intraneural pressure between the “postoperative” and the baseline “preoperative” pressure measurements for the different surgical strategies. While both the simple decompression and the medial epicondylectomy had significantly lower intraneural pressures than the Learmonth or the subcutaneous transposition, each of these four techniques resulted in elevated intraneural pressures. The musculofascial lengthening technique for submuscular transposition was the only surgical strategy that reduced intraneural ulnar pressure at each site of measurement and for all degrees of elbow flexion, this reduction of pressure being significant in comparison with the other surgical techniques.

末梢神経急性圧迫損傷に対する薬物療法の有効性に関する実験的研究 第三報： 神経外膜とステロイドの有効性について

Experiments in our laboratory have shown that steroid therapy commenced immediately before the operation prevents the functional deficit caused by silicone cuffs applied to intact sciatic nerves in rats. A further study showed that epineurectomy alone caused no significant functional deficit. In this experiments when compression was applied after removal of the epineurium the same dose of steroid used in our previous experiments proved unable to prevent the functional deficit.In intact nerves, it is probable that the trauma of cuff application caused edema of the intraneural pressure in the segment under the cuff and thus neuronal injury. The maximum injury and edema would occur in the epineurium, which can be prevented by steroid administration. Following epineurectomy edema of the perineurium and endoneurium resulted in a similar pressure increase that was not prevented by the steroids.

Anatomically selective peripheral nerve ablation using intraneural ricin injection

Anatomically selective destruction of sensory and motor neurons based upon which nerve contains the corresponding axons can be accomplished by intraneural pressure microinjection of the toxic lectin, ricin. Ricin is taken up by axons at the injection site and axonally transported to perikarya resulting in destruction of the neurons. In the present report, we describe a reliable procedure for making such lesions using pressure microinjection of ricin into nerve trunks. Consistent, complete lesions restricted to the appropriate sensory and motor neurons are documented after injection of the vagus, hypoglossal, phrenic and sciatic nerves and the superior cervical ganglion. Complete vagal ablations could be achieved with 100 ng or less of ricin; whereas, 1–3 μg was required to obtain similar results with hypoglossal and sciatic nerves. Although most neurons are dead within 24 h after the injection, survival times of 10–14 days may be necessary for complete disappearance of poisoned neurons. This technique can be valuable in making highly selective lesions for anatomical, neurochemical and neurophysiological experiments.

Évaluation des pressions canalaires et sous-épineurales dans les syndromes de souffrance du nerf médian lépreux au poignet

The authors measured the carpal tunnel and intraneural pressures with a soft catheter in fifteen cases of leprous neuritis of the median nerve at the wrist. In the carpal tunnel, the pressure was about 40 mm of mercury, while within the nerve, the pressure was about 25 mm of mercury. In five healthy male volunteers, the same pressures were measured: the results were much lower (2 to 4 mm of mercury). The authors call attention to the high pressures found in acute leprous neuritis. They conclude that the sooner a surgical procedure (careful neurolysis) is performed, the better the results, before irreparable nerve damage occurs.

Ocular malformations in chick embryo resulting from diminished intraneural pressure.

Ocular malformations in chick embryo resulting from diminished intraneural pressure.