Extensive Loss of Tibialis Anterior Tendon: Surgical Repair With Split Tendon Transfer of Tibialis Posterior Tendon: A Case Report.

Extensive damage of the tibialis anterior tendon is rare and mainly caused by trauma. Surgical treatment of these injuries can become challenging owing to the limited availability of autogenous graft resources for reconstruction of the defect. In the present case report, we describe a large defect in the midfoot soft tissue after a traffic injury, which included complete loss of the tibialis anterior tendon. The tendon was reconstructed by split tendon transfer of the tibialis posterior tendon without sacrificing function, which was confirmed by the follow-up examination at 6 years after injury. We believe split tendon transfer of the tibialis posterior tendon can be one of the treatment options for patients with extensive disruption of the tibialis anterior tendon.

Second lumbrical-interossei nerve test predicts clinical severity and surgical outcome of carpal tunnel syndrome.

The purpose of this study was to examine the utility of the second lumbrical-interossei nerve (2L-IN) test in the diagnosis of carpal tunnel syndrome (CTS). We examined 65 patients with suspected unilateral CTS using the 2L-IN test, in addition to the standard electrophysiological test. The operative cases were divided into three classes of severity based on Padua's neurophysiological classification: extreme CTS (absence of median motor and sensory response); severe CTS (absence of sensory response, abnormal distal motor latency [DML]); and moderate CTS (abnormal sensory nerve conduction velocity, abnormal DML). With the 2L-IN test, the extreme CTS group could be further subdivided into extreme CTS-A (both abductor pollicis brevis [APB]- compound muscle action potential [CMAP] and 2L-CMAP not recordable) and extreme CTS-B (2L-CMAP recordable, APB-CMAP not recordable). Patients with extreme CTS and severe CTS were older, had chronic symptoms, and poorer outcome compared with the moderate CTS patients. Patients of the moderate CTS group were almost all satisfied with the results of surgery. The electrodiagnostic severity correlated with the clinical outcome. Severe strangulation of the thenar muscle branch was identified in patients in the extreme CTS-B group, requiring decompression of the thenar muscle branch rather than conventional simple transverse ligament detachment.

Additional method for diagnosis of carpal tunnel syndrome: value of the second lumbrical-interossei test (2L-INT).

We examined 57 hands referred with suspected carpal tunnel syndrome (CTS) using the second lumbrical-interossei nerve test (2L-INT) as well as standard test. Sensory nerve conduction velocity (SCV) was detectible in 67% of patients (38/57), the abductor pollicis brevis-compound muscle action potential (APB-CMAP) in 84% (48/57), 2L-CMAP in 96% (55/57) and the first interossei palmares muscle (INT-CMAP) in 100% (57/57). ABP-CMAP was not recorded in patients in whom severe atrophy of the abductor pollicis brevis muscle was evident. As 2L-CMAP is maintained even in the most severe cases of CTS, the 2L-INT method is a valuable test for improving the accuracy of preoperative diagnosis in the electrophysiological diagnosis of CTS.

A large neurinoma originating from the anterior interosseous nerve.

We report an interesting case of a neurinoma originating from the anterior interosseous nerve. Magnetic resonance (MR) images showed an egg-shaped, well-circumscribed mass on the volar side of the forearm. On the enhanced three-dimensional computer tomography (3D-CT), it was clearly demonstrated that the tumour had arterial feeding from the anterior interosseous artery. The enhanced 3D-CT angiography was useful in the pre-operative diagnosis and surgical planning of peripheral neurinomas.

Apoptosis of neurons and oligodendrocytes in the spinal cord of spinal hyperostotic mouse (twy/twy): possible pathomechanism of human cervical compressive myelopathy.

INTRODUCTION: Cervical compressive myelopathy is the most serious complication of cervical spondylosis or ossification of the posterior longitudinal ligament (OPLL) and the most frequent cause of spinal cord dysfunction. There is little information on the exact pathophysiological mechanism responsible for the progressive loss of neural tissue in the spinal cord of such patients. In this study, we used the spinal hyperostotic mouse (twy/twy) as a suitable model of human spondylosis, and OPLL to investigate the cellular and molecular changes in the spinal cord. Mutant twy/twy mouse developed ossification of the ligamentum flavum at C2-C3 and exhibited progressive paralysis. MATERIALS AND METHODS: The mutant twy/twy mice, aged 16 and 24 weeks, were used in the present study. The cervical spinal cord was analyzed histologically and immunohistochemically. RESULTS: We observed that a significant correlation between the proportion of apoptotic oligodendrocytes in the compressed area of the spinal cord and the magnitude of cord compression. Immunohistochemical analysis indicated overexpression of TNFR1, CD95, and p75NTR in the twy/twy mice, which was localized by the immunofluorescence in the neurons and oligodendrocytes. CONCLUSION: The expression of such factors seems to play at least some role in the apoptotic process, which probably contributes to axonal degeneration and demyelination in the twy/twy mice spinal cords with severe compression.

Tumor necrosis factor-alpha and its receptors contribute to apoptosis of oligodendrocytes in the spinal cord of spinal hyperostotic mouse (twy/twy) sustaining chronic mechanical compression.

STUDY DESIGN.: To examine the distribution of apoptotic cells and expression of tumor necrosis factor (TNF)-alpha and its receptors in the spinal hyperostotic mouse (twy/twy) with chronic cord compression using immunohistochemical methods. OBJECTIVE.: To study the mechanisms of apoptosis, particularly in oligodendrocytes, which could contribute to degenerative change and demyelination in chronic mechanical cord compression. SUMMARY OF BACKGROUND DATA.: TNF-alpha acts as an external signal initiating apoptosis in neurons and oligodendrocytes after spinal cord injury. Chronic spinal cord compression caused neuronal loss, myelin destruction, and axonal degeneration. However, the biologic mechanisms of apoptosis in chronically compressed spinal cord remain unclear. METHODS.: The cervical spinal cord of 34 twy mice aged 20 to 24 weeks and 11 control animals were examined. The apoptotic cells were detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) staining. The expression and the localization of TNF-alpha, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2) were examined using immunoblot and immnohistochemical analysis. RESULTS.: The number of TUNEL-positive cells in the white matter increased with the severity of compression, which was further increased bilaterally in the white matter of twy/twy mice. Double immunofluorescence staining showed that the number of cells positive for TUNEL and RIP, a marker of oligodendrocytes, increased in the white matter with increased severity of cord compression. Immunoblot analysis demonstrated overexpression of TNF-alpha, TNFR1, and TNFR2 in severe compression. The expression of TNF-alpha appeared in local cells including microglia while that of TNFR1 and TNFR2 was noted in apoptotic oligodendrocytes. CONCLUSION.: Our results suggested that the proportion of apoptotic oligodendrocytes, causing spongy axonal degeneration and demyelination, correlated with the magnitude of cord compression and that overexpression of TNF-alpha, TNFR1, and TNFR2 seems to participate in apoptosis of such cells in the chronically compressed spinal cord.

Visualization of intraneural edema using gadolinium-enhanced magnetic resonance imaging of carpal tunnel syndrome.

BACKGROUND: In general, carpal tunnel syndrome (CTS) is diagnosed based mainly on clinical findings and electrophysiology. However, the pathological state of the compressed median nerve could not be shown on imaging. Gadolinium-enhanced magnetic resonance (MR) imaging may give us an idea about the status of the blood-nerve barrier of peripheral nerves. Therefore, detecting intraneural edema may be a way of diagnosing entrapment neuropathy. The present study investigated the diagnostic role of gadolinium-enhanced MR imaging of CTS. METHODS: The subjects were 23 patients (34 hands) with idiopathic CTS. To serve as control subjects, 12 wrists of asymptomatic volunteers were studied. Using the spin-echo method, T1- and T2-weighted axial MR images were obtained. Intravenously injected gadolinium was used to obtain enhanced images. We studied the relation between nerve enhancement and the symptomatology. RESULTS: After intravenous injection of gadolinium, there was no enhancement of the unaffected nerves in the carpal tunnels of the control group. Gadolinium enhancement was found in only 87% of patients with CTS who visited the hospital at an early stage and therefore had no nerve deficiency on electrophysiological studies (39%). Based on this finding, during the early stages when the nerve is in a state of neuropraxia, gadolinium-enhanced MR imaging of the median nerve might prove to be the most sensitive modality for detecting early nerve dysfunction. MR imaging also revealed a higher frequency of enhancement in the advanced stage of CTS with muscle atrophy. CONCLUSIONS: We conclude that gadolinium-enhanced MR imaging can detect not only morphological changes but also pathological changes of the median nerve in patients with CTS. Currently, gadolinium-enhanced-MR imaging is probably most commonly used to image patients who have ambiguous electrodiagnostic studies and clinical examination in an early stage of CTS.

Target muscles for retrograde gene delivery to specific spinal cord segments.

Targeted retrograde gene delivery into the injured spinal cord is less invasive for the damaged tissue. One of the advantages of this approach is the possible selection of target organs according to the level of spinal cord injury. We evaluated nine candidate target organs for retrograde delivery of an adenovirus vector carrying beta-galactosidase (AdV-LacZ) gene to cervical, thoracic and lumbar spinal cord segments. One week after vector injection into each muscle, we assessed the LacZ gene expression in the spinal cord by X-gal staining. The most appropriate target organs with high transduction efficacy were the sternomastoid and clavotrapezius muscles for cervical spinal cord, tibialis anterior and the gastrocnemius muscles for the lumbar spinal cord. Retrograde gene delivery to the thoracic spinal cord was inefficient probably due to the small number of anterior horn neurons in the region. Gene expression was mainly identified over the anatomical area of innervation and not into other body organs. Our results suggested that retrograde delivery of adenovirus genome to the cervical and lumbar spinal cord segments seems feasible by injection of an adenoviral vector into the appropriate target organ. Adenovirus vector is an efficient retrograde tracer since it can deliver the carried gene to a wide area of the spinal cord and not to other body organs.

Adenovirus-mediated retrograde transfer of neurotrophin-3 gene enhances survival of anterior horn neurons of twy/twy mice with chronic mechanical compression of the spinal cord.

Chronic mechanical compression of the spinal cord causes neural tissue damage, including loss of anterior horn cells around the level of injury. Exogenous delivery of neurotrophins to neuronal cells could provide neuroprotection to a spinal cord subjected to mechanical injury. We investigated the efficacy of retrograde gene delivery of adenoviral vector (AdV) carrying neurotrophin-3 (NT-3) gene into twy (twy/twy) mouse spinal cord anterior horn neurons with chronic and progressive mechanical compression at C1-C2 level. AdV-NT-3 was used for retrograde delivery via the sternomastoid muscle to the cervical spinal accessory motoneurons in 16-week-old adult twy mice with relatively mild spinal cord compression. Four weeks after the AdV-NT-3 or AdV-beta-galactosidase cDNA (LacZ) as a marker gene injection, the compressed cervical spinal cord was examined histologically, immunohistologically, and by immunoblot analysis. Immunoreactivity to NT-3 was significantly enhanced in the AdV-NT-3-injected twy mice compared with the AdV-LacZ-injected mice. The numbers of anterior horn neurons of Nissl-, choline acetyltransferase (ChAT)-, and trkC-stained and wheat germ agglutinin-horseradish peroxidase (WGA-HRP)-labeled neurons at the spinal cord level with maximum compression were significantly higher in AdV-NT-3-transfected than in AdV-LacZ-transfected twy mice. Retrograde NT-3 gene transfer to twy mouse anterior horn neurons increased neurite axonal length and arborization of WGA-HRP-labeled neurons. Our results suggest that targeted retrograde NT-3 gene delivery is feasible in the intact animal and that it enhances neuronal survival even under chronic mechanical compression of the spinal cord.

Motion analysis of the wrist joints in patients with rheumatoid arthritis.

We investigated the characteristics of the wrist joint motion in patients with rheumatoid arthritis (RA), using a biaxial flexible goniometer. Wrist joint range of motion and velocity were measured on the dominant hand in RA patients (n = 22) and normal individuals (n = 5). We investigated flexion-extension (FE) task, radial-ulnar deviation (RUD) task, and functional motion tasks, such as writing letters or unscrewing the lid of a jar. In normal individuals, there was cooperative coupling of FE and RUD during wrist movement, and this coupling motion was essential for normal wrist movements. On the other hand, in RA patients, wrist joint range of motion was restricted at various degrees, with reduced joint motion velocity that was severe on RUD. Functional wrist motion tasks indicated circumductive movement with both FE and RUD in normal individuals, whereas the direction of movement was limited in RA patients, and results revealed failure of cooperative coupling of FE and RUD. Our results indicate that disturbed coupling of FE and RUD results in difficulties in the cooperative movements and have great influence on the daily activities in RA wrist joint.

Rescue of rat anterior horn neurons after spinal cord injury by retrograde transfection of adenovirus vector carrying brain-derived neurotrophic factor gene.

We investigated the efficacy of retrograde gene delivery via the sternomastoid muscle of recombinant adenovirus vector (AdV) carrying brain-derived neurotrophic factor (BDNF) gene for the rescue of injured rat spinal cord. One hundred-thirty five adult Sprague-Dawley rats were used in the study with a standard weight-compression technique to produce spinal cord injury. AdV-BDNF gene or AdV-beta-galactosidase (AdV-LacZ) gene was injected into the sternomastoid muscle immediately after traumatic C4 segment spinal cord injury. AdV-BDNF was successfully appeared in the injured cervical spinal cord following injection into the sternomastoid muscle. BDNF expression in the anterior horn neurons of the cervical spinal cord reached peak levels at 1-2 weeks; and the expression persisted at significant levels for approximately 4 weeks after injury. AdV-BDNF transfection was associated with increased numbers of intact neurons as confirmed by Nissl, cholineacetyltransferase (ChAT), and acetylcholine esterase (AChE) staining especially from 2 weeks after injury, compared with the AdV-LacZ injected rats. Our results suggest that in vivo targeted retrograde AdV-BDNF-gene delivery may enhance neuronal survival following traumatic injury of the spinal cord.