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  • Journal of Neurosurgery Publishing Group (JNSPG)  (3)
  • Medicine  (3)
  • 1
    Online Resource
    Online Resource
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2003
    In:  Journal of Neurosurgery Vol. 99, No. 2 ( 2003-08), p. 319-329
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 99, No. 2 ( 2003-08), p. 319-329
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0022-3085
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    RVK:
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2003
    detail.hit.zdb_id: 2026156-1
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  • 2
    Online Resource
    Online Resource
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2011
    In:  Journal of Neurosurgery Vol. 114, No. 1 ( 2011-01), p. 217-224
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 114, No. 1 ( 2011-01), p. 217-224
    Abstract: The mechanism responsible for exceptional examples of intraneural ganglia with extensive longitudinal involvement has not been understood. Such cases of intraneural cysts, seemingly remote from a joint, have been thought not to have articular connections. Decompression and attempted resection of the cyst has led to intraneural recurrence and poor neurological recovery. The purpose of this report is not only to clarify the pathogenesis of these cysts, but also to discuss their treatment based on modern concepts of intraneural ganglia. Methods Two examples of extreme longitudinal propagation of intraneural ganglia are presented. Results A patient with a moderate tibial neuropathy was found to have a tibial intraneural ganglion. Prospective interpretation of the MR imaging study demonstrated the cyst's origin from the posterior portion of the superior tibiofibular joint (STFJ), with proximal extension within the sciatic nerve to the lower buttock region. Communication between the STFJ and the cyst was confirmed with direct knee MR arthrography. The tibial intraneural cyst was treated successfully by a relatively limited exposure in the distal popliteal fossa: the cyst was decompressed, the articular branch disconnected, and the STFJ resected. Postoperatively, the patient improved neurologically and there was no evidence of recurrent cyst on postoperative MR imaging. A second patient, previously reported by another group, was reexamined 22 years after surgery. This patient had an extensive peroneal intraneural ganglion that extended into the sciatic nerve from the knee to the buttock; no joint connection or recurrent cyst had initially been described. In this patient, the authors hypothesized and established with MR imaging the presence of both: a joint connection to the anterior portion of the STFJ from the peroneal articular branch as well as recurrent cyst within the peroneal and tibial nerves. Conclusions This paper demonstrates that extreme intraneural cysts are not clinical outliers but represent extreme examples of other more typical intraneural cysts. They logically obey the same principles, previously described in the unified articular (synovial) theory. The degree of longitudinal extension is probably due to high intraarticular pressures within the degenerative joint of origin. The generalizability of the mechanistic principles is highlighted by the fact that these 2 cases, involving the tibial and the peroneal nerve respectively, both extended well distant (that is, to the buttock) from the STFJ via their respective articular branch of origin. These extensive intraneural cysts can be treated successfully by disconnecting the affected articular branch and by resection of the joint of origin, rather than by a more aggressive operation resecting the cyst and cyst wall.
    Type of Medium: Online Resource
    ISSN: 0022-3085 , 1933-0693
    RVK:
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    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2011
    detail.hit.zdb_id: 2026156-1
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  • 3
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 107, No. 2 ( 2007-08), p. 296-307
    Abstract: 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.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    RVK:
    RVK:
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2007
    detail.hit.zdb_id: 2026156-1
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