Skinner, John A.

Objectives The aim of this study was to create and validate a 3-dimensional (3D) ultrasound model with normal and abnormal pediatric hip joint anatomy that is comparable to a pediatric hip joint in appearance and anatomy and replicates sonographic characteristics of a pediatric hip joint. Methods A 3D rendering of the bone and soft tissue was created from a computed tomography pelvic scan of a pediatric patient. This rendering was modified to include a unilateral joint effusion. The bone was 3D printed with a photopolymer plastic, whereas the soft tissue was cast with a silicone mixture in a 3D-printed mold. The effusion was simulated by injecting saline into the soft tissue cavity surrounding the bone. The ultrasound model was validated by pediatric point-of-care ultrasonographers at an international pediatric ultrasound conference. Results A pediatric hip ultrasound model was developed that simulates both normal and abnormal pediatric hip joint anatomy, each with an appropriately sized, measurable joint effusion. Validation by pediatric point-of-care ultrasonographers showed that the key aspects of a normal pediatric hip joint (femoral physis, sloped femoral neck, and adequate soft tissue) with an identifiable and measurable effusion were included in the ultrasound model. Conclusions In this study, we successfully created a cost-effective, reusable, and reproducible 3D pediatric hip ultrasound model. The majority of pediatric point-of-care ultrasonographers who evaluated the model agreed that this model is comparable to a pediatric patient for the purpose of teaching ultrasound skills and joint space measurement.

Snapping elbow is a well‐known condition where elbow flexion and extension elicits a painful, popping sensation. The most frequent etiology is anterior dislocation of the ulnar nerve over the medial epicondyle. Four patients (3 females and 1 male) presented with complaints of a popping sensation in the elbow, pain over the medial aspect of the forearm, and ulnar neuritis. All patients underwent preoperative dynamic ultrasound and surgical exploration of the medial elbow. Intraoperatively, snapping of the MABC over the medial epicondyle was discovered in all four patients. In three patients, there was abnormal displacement of the medial triceps and ulnar nerve: in two of these, both structures dislocated over the medial epicondyle and in one patient both structures subluxated. In each case, the MABC was decompressed (n = 1) and transposed (n = 3), and in three cases, the medial triceps and ulnar nerve were addressed as well. Symptomatic improvement was achieved in all cases. Retrospective review of the ultrasound revealed the snapping MABC, though it was less effective prospectively in the cases when snapping MABC was not suspected. In conclusion, snapping of the MABC broadens the spectrum of disorders that results in snapping elbow. To our knowledge, we are unaware of prior reports of this entity. Clin. Anat. 28:872–877, 2015. © 2015 Wiley Periodicals, Inc.

Background We describe a patient with tardy ulnar neuropathy and cubitus valgus deformity found to have an intracapsular ulnar nerve. Methods An 89-year-old woman presented with severe neuropathic pain in the ulnar digits of the hand, advanced degenerative arthritis of the elbow, and tardy ulnar nerve palsy. Her pain was exacerbated with elbow movement, particularly flexion. She had paralysis of ulnar nerve innervated muscles, hypersensitivity with absence of two-point discrimination in her ulnar 1–1/2 digits, and a fixed ulnar claw deformity. She also had a grossly unstable elbow. Results Plain films revealed a cubitus valgus deformity (38°), an absent radial head, a dislocated proximal radioulnar joint and advanced arthritic changes. Ultrasonography revealed an indistinct ulnar nerve within the cubital tunnel which penetrated the joint. Electrophysiological studies revealed evidence of a severe ulnar neuropathy at the level of the elbow. Intraoperatively, an attenuated 2 cm length of the retrocondylar ulnar nerve was observed to be incorporated into the joint capsule tethered by a fibrous/synovial band which was released. A large effusion was drained. The ulnar nerve was transposed subcutaneously. The capsular rent was repaired in layers. She noted immediate and sustained (2 year follow-up) pain relief and regained moderate function in her interossei. Conclusions We believe that the chronic cubitus valgus deformity and secondary degenerative elbow joint changes led to an altered course of the nerve and attenuation of the medial joint capsule such that the ulnar nerve spontaneously buttonholed itself intra-articularly.

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.

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.