Biomedical subjects
R J Spinner
Publications and source records attributed to R J Spinner.
The balloon sign: Adn M, Hamlat A, Morandi X, Guegan Y (2006) Intraneural ganglian cyst of the tibial nerve. Acta Neurochir (Wien) 148: 885-890.
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Connective tissue dysplasia in five new patients with NF1 microdeletions: further expansion of phenotype and review of the literature.
Approximately 5% of patients with neurofibromatosis type 1 (NF1) have deletions of the entire NF1 gene. The phenotype usually includes early onset, large number of neurofibromas, presence of congenital anomalies, cognitive deficiency, and variable dysmorphic features and growth abnormalities. Connective tissue abnormalities are not generally recognised as a part of NF1 microdeletion syndrome, but mitral valve prolapse, joint laxity, and/or soft skin on the palms have been reported in a few patients. We describe clinical findings in six newly diagnosed patients with NF1 microdeletions, five of whom presented with connective tissue abnormalities. A literature review of the clinical findings associated with NF1 microdeletion was also performed. Our report confirms that connective tissue dysplasia is common in patients with NF1 microdeletions. Given the potential for associated cardiac manifestation, screening by echocardiogram may be warranted. Despite the large number (>150) of patients with known NF1 microdeletions, the clinical phenotype remains incompletely defined. Additional reports of patients with NF1 microdeletions, including comprehensive clinical and molecular information, are needed to elucidate possible genotype-phenotype correlation.
Chronic immune sensory polyradiculopathy: a possibly treatable sensory ataxia.
BACKGROUND: Chronic inflammatory neuropathies can present with a sensory ataxia due to involvement of dorsal root ganglia (DRG) or sensory nerves. Selective inflammatory involvement of sensory nerve roots proximal to the DRG has been postulated. METHODS: The authors identified 15 patients with a sensory syndrome and normal nerve conduction studies. Sensory nerve root involvement was suggested by either somatosensory evoked potential (SSEP) or imaging abnormalities. CNS disease was excluded. RESULTS: All patients had gait ataxia, large fiber sensory loss, and paresthesias, and nine had frequent falls. The disease course was chronic and progressive (median duration 5 years, range 3 months to 18 years). Sural sensory nerve action potential amplitudes were preserved and SSEP abnormalities were consistent with sensory nerve root involvement. Five patients had enlargement of lumbar nerve roots on MRI with enhancement in three. The CSF protein was elevated in 13 of 14 patients tested. Three patients had lumbar sensory rootlet biopsies that showed thickened rootlets, decreased density of large myelinated fibers, segmental demyelination, onion-bulb formation, and endoneurial inflammation. Six patients who required aids to walk were treated with immune modulating therapy and all had marked improvement with four returning to normal ambulation. CONCLUSION: Based on the described clinical features, normal nerve conduction studies, characteristic somatosensory evoked potential (SSEP) abnormality, enlarged nerve roots, elevated CSF protein, and inflammatory hypertrophic changes of sensory nerve rootlet tissue, we suggest the term chronic immune sensory polyradiculopathy (CISP) for this syndrome. This condition preferentially affects large myelinated fibers of the posterior roots, may respond favorably to treatment, and may be a restricted form of chronic inflammatory demyelinating polyradiculoneuropathy.
Hemi-contralateral C7 transfer to median nerve in the treatment of root avulsion brachial plexus injury.
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.
Dislocating medial head of triceps.
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100 years of neurological surgery at the Mayo Clinic.
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.
Tardy posterolateral rotatory instability of the elbow due to cubitus varus.
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.
Failure of surgical decompression for a presumed case of piriformis syndrome. Case report.
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.
Latrogenic snapping of the medial head of the triceps after ulnar nerve transposition.
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.
Surgery for peripheral nerve and brachial plexus injuries or other nerve lesions.
The selection of patients who will benefit from peripheral nerve surgery continues to evolve. The evaluation of patients with peripheral nerve problems, and the indications and timing of surgery are reviewed. This includes patients with transections, lesions in continuity, entrapments, tumors, injection injuries, and birth palsies. The treatment outlined for patients with peripheral nerve and brachial plexus injuries is based on a comprehensive clinical and electrodiagnostic evaluation complemented by imaging studies. A systematic approach to the surgical management of these neural lesions has evolved at our institution, based in part on extensive experience with intraoperative recording of nerve action potentials (NAPs) and a resultant large number of referrals. Advanced microsurgical techniques including use of grafts have expanded the scope of peripheral nerve surgery. These advances coupled with intraoperative electrophysiologic measurements have improved outcomes.
Model for avulsion injury in the rat brachial plexus using passive acceleration.
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.
Ulnar nerve function following total elbow arthroplasty: a prospective study comparing preoperative and postoperative clinical and electrophysiologic evaluation in patients with rheumatoid arthritis.
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.
Unrecognized dislocation of the medial portion of the triceps: another cause of failed ulnar nerve transposition.
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.
Recurrent intraneural ganglion cyst of the tibial nerve. Case report.
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.
Median nerve penetration by an anomalous tendon. Case illustration.
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Predominant infraspinatus muscle weakness in suprascapular nerve compression.
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Familial trigeminal neuralgia and contralateral hemifacial spasm.
A patient was evaluated with familial trigeminal neuralgia (TN) and contralateral hemifacial spasm. The mother of the patient, 5 of 10 siblings, and 1 nephew also had TN confirmed by neurologists. The transmission of TN was suggestive of an autosomal dominant inheritance. This family provides additional evidence of a genetic basis for TN in selected cases and also provokes further speculation on a common unifying hypothesis of pathophysiology in cranial rhizopathies.