Abstract
To the Editor, Clinical Anatomy:The basis for the articular (unified) theory for the for-mation of intraneural ganglion cysts is a capsular disrup-tion through which joint (cyst) fluid egresses into thearticular branch and then a parent nerve (Spinner et al.,2003). Trauma has been associated with intraneural gan-glion cysts. A recent meta-analysis revealed trauma beingassociated with intraneural ganglion cysts in our group (Figs. 2A–2E) showed both a neuroma in conti-12% ofcases (Desy and Spinner, 2014). Our group has describedthe pathoanatomy by which direct and indirect traumamay give rise to the most common form, fibular (pero-neal), and its rarer corollary, tibial intraneural ganglioncysts, both derived from the superior tibiofibularjoint (STFJ) (Lalezari et al., 2012; Spinner et al.,2012a,b; Cesmebasi et al., 2014). In direct trauma, therewould be a force generated near the proximal leg/kneeregion that would affect the STFJ (Ogden, 1972, 1974;Sekiya and Kuhn, 2003); in indirect trauma, forces wouldbe translated from the ankle region (such as in anklesprains or fracture) via the interosseous membrane to theproximal leg (Cesmebasi et al., 2014). A direct cause–effect relationship between traumatic injury and intraneu-ral ganglion cyst formation has yet to be definitivelyestablished.A 20-year-old man tripped off a curb and fell on his leftknee. He sustained a multi-ligamentous knee injury as aresult from a knee dislocation. He presented to an emer-gency room with exquisite pain and foot drop from a com-mon fibular nerve (CFN) palsy and was discharged afternegative plain radiographs were obtained. Several days later,he noted increasing pain and was found to have elevated legcompartment pressures for which he underwent four com-partment fasciotomies. MRI performed 7 days after the initialinjury revealed a posterolateral corner injury involving dis-ruption of the fibular collateral and posterior cruciate liga-ments, posterolateral capsule, and the musculotendinousjunction of the popliteus, lateral meniscus, and medial patel-lofemoral ligament. There was edema and thickening of theCFN extending from the fibular neck to a point just distal tothe sciatic nerve bifurcation (Figs. 1A–1C). He was referredto colleagues at our institution for definitive care of themulti-ligament injury and the CFN injury. Repeat MRI 3months after the injury confirmed the previous findingsreferable to the ligamentous injury. The CFN was markedlyenlarged in the popliteal fossa. There was anterior and lat-eral compartment musculature atrophy consistent withdenervation. Electromyography (EMG) confirmed a com-plete common fibular neuropathy. He underwent stagedreconstruction over the course of 9 months: (1) explora-tion and nerve grafting of the left CFN with 2 cable grafts(9 cm in length) using the superficial fibular nerve; (2)high tibial wedge osteotomy with allograft bone graft; and(3) multi-ligament knee reconstruction. At last follow-up,15 months post nerve grafting, he had no return of neuro-logic function but had regained a stable knee. It was rec-ommended he undergo tendon transfer for persistent footdrop. Retrospective reinterpretation of the second MRI bynuity involving the CFN as well as an unrecognized com-plex fibular intraneural cyst, which could be traced alongits articular branch to the anterior portion of the STFJ. Afracture line was noted at the STFJ extending to the originof the intraneural cyst from the joint. The cyst was notpresent on the initial MRI.Direct blunt force trauma to the knee has long beenknown to result in severe injuries to the knee causing pos-terolateral corner, multi-ligamentous knee, and CFN inju-ries. They have also been associated with instability of theSTFJ (Fallon et al., 1994; Kapur et al., 2009; Jabara et al.,2014). The resultant stretch tends to affect a long seg-ment of the CFN. Stretch injuries associated with kneedislocations are known to have poor recovery after nervesurgery (Fallon et al., 1994; Seidel et al., 2008). In ourpatient, we believe that the knee dislocation caused theimmediate clinical appearance of the foot drop involvingthe CFN. This stretch injury resulted in a lengthy neuromain continuity of the CFN. The effect of the stretch injury onthe articular branch and/or the bony injury to the STFJresulted in a capsular injury (without instability) and theegress of joint fluid (Fallon et al., 1994; Spinner et al.,2003, 2012a,b; Lalezari et al., 2012). Unfortunately, the2nd MRI was done of the knee rather than the CFN andSTFJ and did not provide full visualization of the proximalleg. In this case, despite the limitations, serial MR imagingdemonstrates a temporal relationship following kneetrauma and documents the evolution of an intraneuralganglion cyst.
Published Version
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