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Background: Cubitus varus has long been considered merely a cosmetic deformity. The purpose of this paper is to demonstrate a causal relationship between cubitus varus and instability of the elbow.Methods: In twenty-four patients (twenty-five limbs) with a cubitus varus deformity following a pediatric distal humeral fracture or resulting from a congenital anomaly (three limbs of two patients), tardy posterolateral rotatory instability of the elbow developed approximately two to three decades after the deformity occurred. All patients presented with lateral elbow pain and recurrent instability. The average varus deformity was 15 degrees (range, 0 degrees to 35 degrees ). Surgery was performed in twenty-one patients (twenty-two limbs). Treatment consisted of reconstruction of the lateral collateral ligament and osteotomy in seven limbs, ligament reconstruction alone in ten, osteotomy alone in four, and total elbow arthroplasty in one.Results: In three patients, the triceps muscle was dynamically stimulated intraoperatively to contract while resisting extension of the elbow. This produced posterolateral rotatory subluxation of the elbow, which was reversed by corrective osteotomy and lateral transposition of a portion of the medial head of the triceps that originally had been attached to the elongated, deformed medial aspect of the olecranon. At an average of three years (minimum, one year) after the operation, the result was good or excellent for nineteen of the twenty-two limbs that had undergone an operation; three limbs had persistent instability.Conclusions: With cubitus varus, the mechanical axis, the olecranon, and the triceps line of pull are all displaced medially. The repetitive external rotation torque on the ulna permitted by these deformities can stretch the lateral collateral ligament complex and lead to posterolateral rotatory instability. Thus, cubitus varus deformity secondary to supracondylar malunion or congenital deformity of the distal part of the humerus may not always be a benign condition and may have important long-term clinical implications. Operative correction can relieve symptoms of instability. The indications for preventive corrective osteotomy remain to be determined. [ABSTRACT FROM AUTHOR]

Malignant melanotic nerve sheath tumors are uncommon pigmented tumors of Schwann cell origin, most often found along the spinal nerves. Although well-described in the literature, the tumors are quite rare, making up <1% of nerve sheath tumors. Physicians are, therefore, often unfamiliar with both the appearance and the optimal treatment of such tumors. Morphologically, many imaging features overlap with schwannomas and neurofibromas. Nevertheless, the malignant melanotic nerve sheath tumors are crucial to identify. They can be extremely aggressive, and the management of these tumors is considerably different from their benign counterparts. In this radiology-pathology review, we will highlight the imaging appearance, histologic features, surgical resection, and subsequent therapeutic strategies in a patient with a lumbar malignant melanotic nerve sheath tumor., (© 2022 by American Journal of Neuroradiology.)

We report the case of a patient who presented with right arm and shoulder pain due to compression of the infraclavicular brachial plexus due to benign metastasizing leiomyomatosis (BML). She was initially and had been repeatedly misdiagnosed as having neurofibromatosis type 1 (NF 1). The diagnosis of BML was not obvious due to its rare nature, the patient's not detailing the specifics of her gynecologic history of having undergone resection of a large uterine leiomyoma and followed by disseminated pelvic leiomyomatous nodules, histologic misinterpretation of an extrauterine lesion of the spine and the brachial plexus as a neurofibroma and the radiologic diagnosis of lung nodules as being "non-specific" in nature. In addition and importantly, no clinical, radiographic or histologic features of NF 1 were present. Although a rare condition, BML should be considered in the differential diagnosis of NF and in patients having a history of uterine leiomyoma. The remarkable, selective involvement of the brachial plexus in this case is unexplained.

We postulate an iatrogenic cause for snapping of the medial head of the triceps. A patient whose ulnar nerve and triceps did not dislocate over the medial epicondyle preoperatively had snapping of a portion of the medial triceps after submuscular transposition of the ulnar nerve. We believe that release of the brachial fascia and excision of the medial intermuscular septum removed the restraint to anterior translation of the medial aspect of the triceps, permitting dislocation of a portion of the medial head of the triceps with elbow flexion in this case. Previous reports of snapping of the triceps resulting after ulnar nerve transposition occurred in patients whose ulnar nerve dislocated preoperatively; in these cases, the triceps was thought to have dislocated preoperatively (along with the ulnar nerve) but was not recognized. Careful intraoperative assessment of the triceps after ulnar nerve transposition should prevent medial triceps instability as a postoperative concern.

Medial and lateral snapping (dislocation) of the distal triceps over the epicondyle during elbow flexion has been reported but is frequently misdiagnosed and is not well understood. In this study a mathematical model was designed to simulate the effect that bony abnormalities at the distal humerus and soft tissue variations of the distal triceps have on the line of pull of the triceps. The predictions were then tested on prefabricated and fabricated plastic elbow models, as well as 8 cadaveric elbows. When the bony alignment was altered, varus angulation had the greatest effect: 30 degrees varus malalignment of the distal humerus displaced the centroid of the triceps vector medially by approximately 2.0 cm. Valgus malalignment had a lesser effect: 30 degrees valgus displaced it laterally by 1.5 cm. Negligible effects on the triceps line of pull were seen with internal or external malrotation and with flexion or extension malalignment. Of the soft tissue alterations, displacement of the triceps insertion had a greater effect than movement of the triceps origin. The triceps vector was displaced by approximately 70% of the amount of translation of the triceps insertion. The relationship between the triceps line of pull and the bony alignment is represented by the triceps (T) angle. Our use of the T angle to understand snapping triceps is analogous to the use of the quadriceps (Q) angle for patellar subluxation/dislocation. Treatment should aim to restore normal triceps biomechanics with soft tissue or bony procedures.

Because of the poor clinical results in achieving hand function in patients with complete brachial plexus root avulsion with other nerve transfers, we evaluated 111 patients prospectively to evaluate the technique of the hemi-contralateral C7 transfer to the median nerve. The transfer was performed as a primary procedure in 62 patients and as a secondary procedure in additional 49 patients. Twenty-one of the 62 patients in the primary group had sufficient follow-up (at least 3 years) to assess the motor and sensory recovery in the median nerve. The adverse effects of the operation were also analyzed in all 111 patients. Six of the 21 (29%) patients obtained M3 and 4 (19%) experienced M2 recovery of the wrist and finger flexors. Ten (48%) patients obtained S3 and 7 (33%) had S2 recovery in the median nerve area. The rate of the advancing Tinel's sign was markedly different between those achieving M3 function and the remaining patients. Although the age of the patient did not correlate with outcome, patients aged 18 and younger had the best motor recovery (ie, achieving M3 function in 3 of 6 cases). There was no correlation between the timing of the surgery after the initial injury, medical comorbidities, and clinical outcome. After surgery 108 of 111 (97%) patients experienced temporary paresthesia in the median nerve area, which resolved by an average of 2.8 months. Three (3%) patients had motor weakness of the donor limb; this resolved completely in 2 patients and left a mild deficit in wrist extension in 1 patient.

The practice of neurological surgery at the Mayo Clinic began as early efforts were undertaken by Drs. Charles Mayo and Emil Beckman, and surgical procedures were performed for trauma, infection, tumor, epilepsy, and hemorrhage. In 1919, the Section of Neurologic Surgery was established, with Alfred W. Adson as its first chair. Subsequently, Drs. Winchell McK. Craig, J. Grafton Love, Collin S. MacCarty, Ross H. Miller, and Thoralf M. Sundt, Jr., followed as eminent chairmen. Beginning with a modest number of cases per year, the neurosurgical service at the Mayo Clinic has grown to become one of the largest in North America. Under the current leadership of Dr. David G. Piepgras, approximately 3200 surgical procedures spanning the spectrum of subspecialties are performed each year by a staff of 10 neurosurgeons. This article traces neurosurgery at the Mayo Clinic, including several persons who contributed to its achievements over the past century.

Diagnosis of piriformis syndrome is difficult and its precise definition is highly controversial. In this article, the authors present the case of a patient who had clinical features suggestive of piriformis syndrome. During surgery the patient was found to have a rare variation in anatomical structures, in which the peroneal nerve was displaced by the piriformis muscle. Surgical decompression did not alleviate the patient's symptoms.

A study was conducted to determine the incidence of ulnar and peripheral neuropathy in patients with rheumatoid arthritis undergoing total elbow arthroplasty and the effect it has on ulnar nerve function after surgery. Preoperative and postoperative clinical and electrodiagnostic examinations were completed in 10 patients. Before surgery 4 patients had clinical and electrophysiologic evidence of a neuropathy (2 each with a peripheral neuropathy and an ulnar neuropathy). One patient had subclinical evidence of a chronic T-1 radiculopathy. After surgery 2 patients showed neurologic improvement (1 had ulnar neuropathy and 1 had diabetic neuropathy). One patient who had normal test results before surgery developed transient ulnar sensory symptoms after surgery. An electrodiagnostic study confirmed an ulnar neuropathy that was not detected on physical examination; the electrodiagnostic findings improved 4 months later. We found that a large percentage of patients (40%) with rheumatoid arthritis had evidence of ulnar or peripheral neuropathy before surgery. The presence of an ulnar or peripheral neuropathy did not predispose patients to develop postoperative ulnar nerve dysfunction either clinically or electrophysiologically. Preoperative and postoperative physical and electrodiagnostic examination results correlated in 9 of the 10 patients., (Copyright 2000 by the American Society for Surgery of the Hand.)

Different theories have evolved to explain the pathogenesis and the cell of origin of intraneural ganglion cysts. Reportedly only three cases of intraneural ganglion of the tibial nerve have been located within the popliteal fossa, and all of these were thought to arise within the nerve. The authors report a case of a recurrent tibial intraneural ganglion in which a connection to the proximal tibiofibular joint was demonstrated on magnetic resonance (MR) images and at surgery. Surgical ligation of the articular branch and evacuation of the cyst led to symptomatic relief, and an MR image obtained 1 year after surgery documented no recurrence. This case reinforces the fact that surgeons need to consider and search for an articular connection in all cases of intraneural ganglia, especially in those that have recurred.

Object: Failed surgical treatment for ulnar neuropathy or neuritis due to dislocation of the ulnar nerve presents diagnostic and therapeutic challenges. The authors of this paper will establish unrecognized dislocation (snapping) of the medial portion of the triceps as a preventable cause of failed ulnar nerve transposition., Methods: Fifteen patients had persistent, painful snapping at the medial elbow after ulnar nerve transposition, which had been performed for documented ulnar nerve dislocation with or without ulnar neuropathy. The snapping was caused by a previously unrecognized dislocation of the medial portion of triceps over the medial epicondyle. Seven of the 15 patients also had persistent ulnar nerve symptoms. The correct diagnosis of snapping triceps was delayed for an average of 22 months after the initial ulnar nerve transposition. An additional surgical procedure was performed in nine of the 15 cases and, in part, consisted of lateral transposition or excision of the offending snapping medial portion of the triceps. Of the four patients in this group who had persistent neurological symptoms, submuscular transposition was performed in the two with more severe symptoms and treatment of the triceps alone was performed in the two with milder neurological symptoms. Excellent results were achieved in all surgically treated patients. Six patients declined additional surgery and experienced persistent snapping and/or ulnar nerve symptoms., Conclusions: Failure to recognize that dislocation of both the medial portion of the triceps and the ulnar nerve can exist concurrently may result in persistent snapping, elbow pain, and even ulnar nerve symptoms after a technically successful ulnar nerve transposition.

We have developed an experimental model for brachial plexus injuries in the rat that closely simulates the characteristics of human injury. This model produces avulsion injuries in a noninvasive manner. A prototype apparatus was designed that allowed a force to be transmitted to a restrained limb by passive acceleration. Reproducible results were obtained in 32 rats. A significant correlation was found between the test weight and the number of roots avulsed (r = 0.92; P < 0.05). The amount of force also correlated to the pattern of avulsion injury: a 230-g weight produced either C6 (54%), C7 (15%), or C6 and C7 (31%) avulsions; a 330-g weight produced C6 (18%), C7 (9%), or C6 and C7 (73%) avulsions; a 530-g weight produced C5 through C8 (75%) or C6 through T1 (25%) avulsions. This model of brachial plexus injury may be useful to further our understanding of the cellular response to this incapacitating injury and to develop therapeutic strategies with behavioral correlates., (Copyright 2000 Wiley-Liss, Inc.)

We describe two patients who had episodic elbow snapping and ulnar nerve dysesthesias only after weightlifting. These symptoms would disappear soon afterward. The episodic nature of their complaints and findings led to misdiagnosis. We documented by repeated clinical examinations and magnetic resonance imaging that the presence of these symptoms correlated directly with the finding of intermittent, activity-related snapping of the medial triceps. In both patients, the symptoms disappeared when the medial portion of the triceps migrated medially but did not dislocate over the medial epicondyle with elbow flexion. Thus, a minor change in the configuration of the medial portion of the triceps (fluid accumulation) in the same individual at different times can cause intermittent dislocation of the medial triceps. Previous papers dealing with patients with snapping of the medial triceps describe symptoms exacerbated by athletic activities, but the constant finding of snapping on sequential examinations.

Five patients with cubitus varus deformities from malunited childhood fractures had dislocation (snapping) of both the medial portion of the triceps and the ulnar nerve over the medial epicondyle. In addition to snapping, these patients had medial elbow pain or ulnar nerve symptoms. Cubitus varus shifts the line of pull of the triceps more medial, which can cause anteromedial displacement of the medial portion of the triceps during elbow flexion. The ulnar nerve is concomitantly pushed or pulled anteromedially by the triceps, and ulnar neuropathy may result from friction neuritis or from dynamic compression by the triceps against the epicondyle. Recognition of both the dislocating ulnar nerve and the snapping medial triceps is crucial in the successful treatment of this pathologic finding. In symptomatic individuals, we recommend either corrective valgus osteotomy of the distal humerus or partial excision or lateral transposition of the snapping medial triceps, or a combination of both. Alternatively, medial epicondylectomy can also eliminate the snapping. Transposition of the ulnar nerve can be performed for ulnar nerve symptoms and/or ulnar nerve instability. Using this approach, correction of the snapping and/or ulnar nerve symptoms was achieved in all cases.

We describe a patient with a preexisting posttraumatic brachial plexopathy who had a complete high median nerve palsy due to rupture of the pectoralis major to biceps transfer near its distal insertion at the elbow region.

We present a patient with translocation (snapping) of a portion of the triceps over the lateral epicondyle with elbow flexion. This condition is in many ways analogous to its counterpart at the medial aspect of the elbow, snapping of the medial head of the triceps, a clinical entity that is being increasingly recognized.

This 4 1-year-old man presented with a 2-year history of symptoms and signs of sciatic nerve compression. Imaging studies revealed a large ossified fragment within the biceps muscle of the thigh abutting the sciatic nerve at the level of the lesser trochanter. The bony fragment resulted from an unrecognized apophyseal avulsion fracture of the ischial tuberosity, which the patient had sustained while sprinting 27 years earlier. External neurolysis of the sciatic nerve and excision of the mass led to a successful outcome.