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Endoscopically assisted decompression of the suprascapular nerve in the supraspinous fossa: a cadaveric feasibility study

Laboratory investigation

R. Shane Tubbs, Marios Loukas, Mohammadali M. Shoja, Robert J. Spinner, Erik H. Middlebrooks, William R. Stetler Jr., Leslie Acakpo-Satchivi, John C. Wellons III, Jeffrey P. Blount, and W. Jerry Oakes

Object

The suprascapular nerve may become entrapped as it travels deep to the suprascapular ligament, necessitating decompression. The present study was performed to verify the feasibility of a minimally invasive, endoscopically assisted technique for decompressing the suprascapular nerve in the supraspinous fossa.

Methods

The authors performed dissection and decompression of the suprascapular ligament using an endoscopically assisted technique via a 3-cm skin incision in 10 adult cadavers (20 sides). Measurements were also made of the depth from the skin to the suprascapular ligament.

Results

A mean depth of 4 cm was necessary to reach the suprascapular ligament from the skin surface. With the authors' approach, no obvious injury occurred to the suprascapular or other vicinal neurovascular structures (such as the spinal accessory nerve and suprascapular vessels).

Conclusions

The results of this cadaveric study demonstrate that access to the suprascapular nerve can be obtained endoscopically via a small suprascapular incision. This approach obviates a large incision, entry into the glenohumeral joint, and reduces the risk of spinal accessory nerve injury in the posterior cervical triangle, or atrophy of the trapezius or supraspinatus muscles from a standard larger dissection. To the authors' knowledge an endoscopically assisted approach to decompressing the suprascapular nerve as it courses deep to the suprascapular ligament has not been reported previously.

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Colocalized cellular schwannoma and plexiform neurofibroma in the absence of neurofibromatosis

Case report

Robert J. Spinner, Bernd W. Scheithauer, Arie Perry, Kimberly K. Amrami, Ryan Emnett, and David H. Gutmann

✓ The authors report on a patient without neurofibromatosis Type 1 or 2 (NF1 or NF2) and without evidence of schwannomatosis, who was found to have an unusual combination of nerve sheath tumors—a large cellular schwannoma and multifascicular involvement of a plexiform neurofibroma arising from the same site within the radial nerve and posterior cord of the infraclavicular brachial plexus. This case broadens the spectrum of combined pathological features of nerve sheath tumors. Genetic studies revealed a combined loss of neurofibromin and merlin in both regions and chromosome arm 22q deletion within the neurofibroma component only. The latter finding supports the suggestion that these were two different clonal neoplasms, and is consistent with a collision tumor pattern.

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Dynamic phases of peroneal and tibial intraneural ganglia formation: a new dimension added to the unifying articular theory

Robert J. Spinner, Kimberly K. Amrami, Alexandra P. Wolanskyj, Nicholas M. Desy, Huan Wang, Eduardo E. Benarroch, John A. Skinner, Michael G. Rock, and Bernd W. Scheithauer

Object

The pathogenesis of intraneural ganglia has been a controversial issue for longer than a century. Recently the authors identified a stereotypical pattern of occurrence of peroneal and tibial intraneural ganglia, and based on an understanding of their pathogenesis provided a unifying articular explanation. Atypical features, which occasionally are observed, have offered an opportunity to verify further and expand on the authors' proposed theory.

Methods

Three unusual cases are presented to exemplify the dynamic features of peroneal and tibial intraneural ganglia formation.

Results

Two patients with a predominant deep peroneal nerve deficit shared essential anatomical findings common to peroneal intraneural ganglia: namely, 1) joint connections to the anterior portion of the superior tibiofibular joint, and 2) dissection of the cyst along the articular branch of the peroneal nerve and proximally. Magnetic resonance (MR) images obtained in these patients demonstrated some unusual findings, including the presence of a cyst within the tibial and sural nerves in the popliteal fossa region, and spontaneous regression of the cysts, which was observed on serial images obtained weeks apart. The authors identified a clinical outlier, a case that could not be understood within the context of their previously reported theory of intraneural ganglion cyst formation. Described 32 years ago, this patient had a tibial neuropathy and was found at surgery to have tibial, peroneal, and sciatic intraneural cysts without a joint connection. The authors' hypothesis about this case, based on their unified theory, was twofold: 1) the lesion was a primary tibial intraneural ganglion with proximal extension followed by sciatic cross-over and distal descent; and 2) a joint connection to the posterior aspect of the superior tibiofibular joint with a remnant cyst within the articular branch would be present, a finding that would help explain the formation of different cysts by a single mechanism. The authors proved their hypothesis by careful inspection of a recently obtained postoperative MR image.

Conclusions

These three cases together with data obtained from a retrospective review of the authors' clinical material and findings reported in the literature provide firm evidence for mechanisms underlying intraneural ganglia formation. Thus, expansion of the authors' unified articular theory permits understanding and elucidation of unusual presentations of intraneural cysts. Whereas an articular connection and fluid following the path of least resistance was pivotal, the authors now incorporate dynamic aspects of cyst formation due to pressure fluxes. These basic principles explain patterns of ascent, cross-over, and descent down terminal nerve branches based on articular connections, paths of diminished resistance to fluid flow within recognized anatomical compartments, and the effects of fluctuating pressure gradients.

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Dynamic phases of peroneal and tibial intraneural ganglia formation: a new dimension added to the unifying articular theory

Robert J. Spinner, Kimberly K. Amrami, Alexandra P. Wolanskyj, Nicholas M. Desy, Huan Wang, Eduardo E. Benarroch, John A. Skinner, Michael G. Rock, and Bernd W. Scheithauer

Object

The pathogenesis of intraneural ganglia has been a controversial issue for longer than a century. Recently the authors identified a stereotypical pattern of occurrence of peroneal and tibial intraneural ganglia, and based on an understanding of their pathogenesis provided a unifying articular explanation. Atypical features, which occasionally are observed, have offered an opportunity to verify further and expand on the authors' proposed theory.

Methods

Three unusual cases are presented to exemplify the dynamic features of peroneal and tibial intraneural ganglia formation.

Results

Two patients with a predominant deep peroneal nerve deficit shared essential anatomical findings common to peroneal intraneural ganglia: namely, 1) joint connections to the anterior portion of the superior tibiofibular joint, and 2) dissection of the cyst along the articular branch of the peroneal nerve and proximally. Magnetic resonance (MR) images obtained in these patients demonstrated some unusual findings, including the presence of a cyst within the tibial and sural nerves in the popliteal fossa region, and spontaneous regression of the cysts, which was observed on serial images obtained weeks apart. The authors identified a clinical outlier, a case that could not be understood within the context of their previously reported theory of intraneural ganglion cyst formation. Described 32 years ago, this patient had a tibial neuropathy and was found at surgery to have tibial, peroneal, and sciatic intraneural cysts without a joint connection. The authors' hypothesis about this case, based on their unified theory, was twofold: 1) the lesion was a primary tibial intraneural ganglion with proximal extension followed by sciatic cross-over and distal descent; and 2) a joint connection to the posterior aspect of the superior tibiofibular joint with a remnant cyst within the articular branch would be present, a finding that would help explain the formation of different cysts by a single mechanism. The authors proved their hypothesis by careful inspection of a recently obtained postoperative MR image.

Conclusions

These three cases together with data obtained from a retrospective review of the authors' clinical material and findings reported in the literature provide firm evidence for mechanisms underlying intraneural ganglia formation. Thus, expansion of the authors' unified articular theory permits understanding and elucidation of unusual presentations of intraneural cysts. Whereas an articular connection and fluid following the path of least resistance was pivotal, the authors now incorporate dynamic aspects of cyst formation due to pressure fluxes. These basic principles explain patterns of ascent, cross-over, and descent down terminal nerve branches based on articular connections, paths of diminished resistance to fluid flow within recognized anatomical compartments, and the effects of fluctuating pressure gradients.

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Peroneal and tibial intraneural ganglia: correlation between intraepineurial compartments observed on magnetic resonance images and the potential importance of these compartments

Robert J. Spinner, Kimberly K. Amrami, Diana Angius, Huan Wang, and Stephen W. Carmichael

Object

Previously the authors demonstrated that peroneal and tibial intraneural ganglia arising from the superior tibiofibular joint may occasionally extend proximally within the epineurium to reach the sciatic nerve. The dynamic nature of these cysts, dependent on intraarticular pressures, may give rise to differing clinical and imaging presentations that have remained unexplained until now. To identify the pathogenesis of these unusual cysts and to correlate their atypical magnetic resonance (MR) imaging appearance, the authors retrospectively reviewed their own experience as well as the published literature on these types of intraneural ganglia.

Methods

A careful review of MR images obtained in 22 patients with intraneural ganglia located about the knee region (18 peroneal and four tibial intraneural ganglia) allowed the authors to substantiate three different patterns: outer (epifascicular) epineurial (20 cases); inner (interfascicular) epineurial (one case); and combined outer and inner epineurial (one case). In these cases serial MR images allowed the investigators to track the movement of the cyst within the same layer of the epineurium. All lesions had connections to the superior tibiofibular joint. Nine patients were identified as having lesions with sciatic nerve extension. Seven patients harboring an outer epineurial cyst (six in whom the cyst involved the peroneal nerve and one in whom it involved the tibial nerve) had signs of sciatic nerve cross-over, with the cyst seen in the sciatic nerve and/or other terminal branches. In only two of these cases had the cyst previously been recognized to have sciatic nerve involvement. In contrast, in one case an inner epineurial cyst involving the tibial nerve ascended within the tibial division of the sciatic nerve and did not cross over. A single patient had a combination of both outer and inner epineurial cysts; these were easily distinguished by their distinctive imaging patterns.

Conclusions

This anatomical compartmentalization of intraneural cysts can be used to explain varied clinical and imaging patterns of cleavage planes for cyst formation and propagation. Compartmentalization elucidates the mechanism for cases of outer epineurial cysts in which there are primary ascent, sciatic cross-over, and descent of the lesion down terminal branches; correlates these cysts' atypical MR imaging features; and contrasts a different pattern of inner epineurial cysts in which ascent and descent occur without cross-over. The authors present data demonstrating that the dynamic phases of these intraneural ganglia frequently involve the sciatic nerve. Their imaging features are subtle and serve to explain the underrecognition and underreporting of the longitudinal extension of these cysts. Importantly, cysts extending to the sciatic nerve are still derived from the superior tibiofibular joint. Combined with the authors' previous experimental data, the current observations help the reader understand intraneural ganglia with a different, deeper degree of anatomical detail.

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Peroneal intraneural ganglia

Part I. Techniques for successful diagnosis and treatment

Robert J. Spinner, Nicholas M. Desy, Michael G. Rock, and Kimberly K. Amrami

✓The common peroneal nerve is the peripheral nerve most often affected by intraneural ganglion cysts. Although the pathogenesis of these cysts has been the subject of controversy in the literature, it is becoming increasingly evident that they are of articular origin. Recent recognition of this fact has proven to be significant in reducing recurrences and improving treatment outcomes for patients. The authors present a stepwise method of assessing and treating peroneal intraneural ganglion cysts.

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Peroneal intraneural ganglia

Part II. Lessons learned and pitfalls to avoid for successful diagnosis and treatment

Robert J. Spinner, Nicholas M. Desy, Michael G. Rock, and Kimberly K. Amrami

✓The authors describe common modes of failure in the diagnosis and treatment of patients with peroneal intraneural ganglia. Illustrated examples correlate the modes of failure and the diagnostic or surgical errors. Understanding these pitfalls reinforces the rationale behind current treatment recommendations as outlined in the companion article. Avoiding these pitfalls will ultimately improve outcomes.

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Tumoral calcinosis producing peripheral nerve compression

A report of two cases

Ziv Williams, Kimberly K. Amrami, and Robert J. Spinner

✓Tumoral calcinosis is a rare disorder that leads to diffuse calcium phosphate deposition into soft tissue and may be seen in the setting of uremia, hyperparathyroidism, or vitamin D intoxication. This lesion can produce significant local pain and can limit mobility in large joints where it tends to occur. Less commonly, it may produce neurological symptoms by compressing or encompassing adjacent neurovascular structures. Tumoral calcinosis involving nerve structures is challenging to treat, primarily because of its extensive size and propensity to infiltrate. Although surgical intervention can often provide symptomatic improvement, this lesion tends to recur in the presence of elevated calcium phosphate levels, and its management therefore requires a combined multidisciplinary surgical and medical approach. The authors describe two cases in which patients developed tumoral calcinosis producing peripheral nerve compression and discuss their respective surgical and medical management.

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Epstein–Barr virus infection as a complication of transplantation of a nerve allograft from a living related donor

Case report

Mikko Larsen, Thomas M. Habermann, Allen T. Bishop, Alexander Y. Shin, and Robert J. Spinner

✓Reconstruction of extensive nerve defects is hampered by the amount of autogenous nerve tissue available for transplantation and by donor site morbidity. Nerve allografts, being of foreign origin and potentially unlimited in supply, provide a solution to these problems. Studies have shown that nerve allotransplants require immunosuppression only until end-organ connections are made and that immunosuppressant therapy may be subsequently discontinued with no negative effect on functional outcome. Also, recent experimental and clinical focus has been on shorter periods of immunosuppression in order to reduce risk, even stopping immunosuppression after regeneration has reached the distal suture line rather than before recovery of end-organ connections. In the pediatric population, the increased disease burden and increased potential for nerve regeneration as well as the frequent availability of a living related donor make allografts all the more attractive as solutions to nerve reconstructive problems. Nevertheless, the risks of immunosuppression must not be underemphasized, and they deserve more attention in the current nerve transplantation literature.

The authors report on a child who, at the age of 1 year, received a nerve allograft from a living related donor who was positive for Epstein–Barr virus (EBV). The child quickly developed a symptomatic EBV infection concurrent with immunosuppressant drug therapy. The immunosuppression regimen was stopped prematurely, and the patient suffered only a short illness, but the EBV infection could have developed into a life-threatening posttransplant lymphoproliferative disorder (PTLD). The patient is consequently predisposed to develop PTLD and will have to be monitored for the rest of his life. This case highlights the importance of considering the potentially fatal risks associated with this elective procedure. Future studies are needed to quantify and minimize this complication. Nevertheless, it should be weighed against the potential functional benefit from using nerve allografts.

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Medial plantar nerve compression by a tibial artery schwannoma

Case report

Robert J. Spinner, Bernd W. Scheithauer, and Kimberly K. Amrami

✓ The authors describe the case of a patient with a novel cause of medial plantar symptoms due to extrinsic compression by a schwannoma arising within the adventitia of the tibial artery in the ankle region. Additionally they provide the operative, histological, and imaging findings.