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  • Author or Editor: Robert L. Tiel x
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Robert J. Spinner, John L. D. Atkinson and Robert L. Tiel

Object. Based on a large multicenter experience and a review of the literature, the authors propose a unifying theory to explain an articular origin of peroneal intraneural ganglia. They believe that this unifying theory explains certain intriguing, but poorly understood findings in the literature, including the proximity of the cyst to the joint, the unusual preferential deep peroneal nerve (DPN) deficit, the absence of a pure superficial peroneal nerve (SPN) involvement, the finding of a pedicle in 40% of cases, and the high (10–20%) recurrence rate.

Methods. The authors believe that peroneal intraneural lesions are derived from the superior tibiofibular joint and communicate from it via a one-way valve. Given access to the articular branch, the cyst typically dissects proximally by the path of least resistance within the epineurium and up the DPN and the DPN component of the common peroneal nerve (CPN) before compressing nearby SPN fascicles. The authors present objective evidence based on anatomical, clinical, imaging, operative, and histological data that support this unifying theory.

Conclusions. The predictable clinical presentation, electrical studies, imaging characteristics, operative observations, and histological findings regarding peroneal intraneural ganglia can be understood in terms of their origin from the superior tibiofibular joint, the anatomy of the articular branch, and the internal topography of the peroneal nerve that the cyst invades. Understanding the controversial pathogenesis of these cysts will enable surgeons to perform operations based on the pathoanatomy of the articular branch of the CPN and the superior tibiofibular joint, which will ultimately improve clinical results.

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Robert J. Spinner, Robert L. Tiel and David G. Kline

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Robert J. Spinner, John L. D. Atkinson, Bernd W. Scheithauer, Michael G. Rock, Rolfe Birch, Thomas A. Kim, Michel Kliot, David G. Kline and Robert L. Tiel

Object. The peroneal nerve is the most common site of intraneural ganglia. The neurological deficit associated with these cysts is often severe and the operation to eradicate them is difficult. The aims of this multicenter study were to collate the authors' experience with a relatively rare lesion and to improve clinical outcomes by better understanding its controversial pathogenesis.

Methods. Part I of this paper offers a description of 24 patients with peroneal intraneural ganglia who were treated by surgeons aware of the importance of the peroneal nerve's articular branch. Part II offers a description of three more patients who were seen after earlier operations in which the ganglion was excised, but the articular branch was not identified (all reportedly gross-total resections). Twenty-six of the 27 patients presented with clinical, electrophysiological, and imaging evidence of a common peroneal nerve (CPN) lesion, predominantly affecting the deep peroneal nerve (DPN) division, and one patient presented with a painful mass of the CPN that was not accompanied by a neurological deficit.

In all 24 patients in Part I there was magnetic resonance (MR) imaging evidence of a connection between the cyst and the superior tibiofibular joint, including one patient in whom high-resolution (3-tesla) MR neurography demonstrated the pathological articular branch itself. At the operation, the communication proved to extend through the articular branch of the CPN in all cases. The operation consisted of drainage of the cyst and ligation of the articular branch. At a minimum follow-up period of 1 year, these patients experienced significant improvements in their neuropathic pain, but only mild improvements in their functional deficits. In none of the 24 patients was there evidence of an intraneural recurrence. In three patients, however, extraneural ganglia developed: two patients with symptoms subsequently underwent resection of the superior tibiofibular joint without further recurrence and one patient with no symptoms was followed clinically after the recurrence was detected incidentally on 1-year postoperative imaging. As predicted, in Part II all three patients in whom the articular branch had not been ligated experienced early intraneural recurrence; both postoperative MR images and original studies, which were retrospectively examined, demonstrated a connection with the superior tibiofibular joint.

Conclusions. The clinical presentation, electrical studies, imaging characteristics, and operative observations regarding peroneal intraneural ganglia are predictable. Treatment must address the underlying pathoanatomy and should include decompression of the cyst and ligation of the articular branch of the nerve. To avoid extraneural recurrence, resection of the superior tibiofibular joint may also be necessary, but indications for this additional procedure need to be defined. These recommendations are based on the authors' belief that intraneural peroneal ganglia arise from the superior tibiofibular joint and are connected to it by the articular branch.