Kenzo Uchida

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‐β‐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.

Ganglioneuromas are benign, slow-growing tumors originating from sympathetic nerves or peripheral nerves, often associated with multiple tumor syndromes. They occasionally occur as spinal lesions and grow within the spinal canal or as paraspinal lesions. In this report, we describe a rare solitary ganglioneuroma arising from the cervical nerve root (C8) within the intervertebral foramen in adults. The tumor could be detected as a mass limited to the neuroforamen at an early stage by MR images. Unilateral microsurgical foraminotomy and en bloc resection of the tumor resulted in disappearance of the symptoms. Microsurgical resection of the relevant nerve root through limited medial foraminotomy at an intricate anatomical region of the cervico-thoracic junction was appropriate in the current case for complete resection of the tumor as well as to prevent postoperative structural weakness that could result in late segmental instability.

Object: The authors investigated the usefulness of using an expandable cage strut in anterior reconstruction after osteoporotic vertebral collapse in patients with neurological deficits.Methods: Twenty-eight patients who had undergone expandable cage strut–augmented anterior thoracolumbar reconstruction participated in a follow-up review for a mean of 4.9 years. Radiographs were reviewed for kyphosis, lateral tilt of the implant, cage subsidence, the presence of a solid fusion mass, and instrumentation failure. Changes in neurological status and visual analog scale (VAS) pain score, as well as technique-related complications, were examined.The mean angles ± the standard deviations of kyphosis correction 4 to 6 weeks after surgery and at final follow-up examination were 10.4 ± 7.6° and 5.6 ± 6.0°, respectively. The mean subsidence of the expandable cage within the adjacent vertebrae was 2.5 ± 3.0 mm at the final follow-up examination. Neurological improvement at the final follow up was more significant in patients with Type 1 (wedge-type) than Type 2 (flat-type) (p = 0.037) or Type 3 (concave-type) (p = 0.006) vertebral collapse. Follow-up VAS scores were significantly higher in patients with Type 1 than Type 3 collapse (p = 0.012). In all cases the authors observed solid union with incorporation of the cage. There were no surgery-related complications.Conclusions: An expandable titanium cage strut seems useful in vertebral body replacement in patients with osteoporotic thoracolumbar collapse. Favorable results were obtained in cases of Type 1 collapse (wedge type) in which the middle and posterior columns remained comparatively intact.

Despite the increasing number of reports on surgical treatments for thoracolumbar osteoporotic vertebral collapse with neurological deficits, the choice of surgery remains controversial. In this retrospective study, we compared the outcomes of posterior and anterior surgeries for single-level osteoporotic vertebral collapse with neurological deficit in the thoracolumbar spine. Both posterior and anterior surgical approaches were performed with a consistent procedure for a single surgical indication at one institution. Twenty-four patients treated with posterior surgery and 28 patients treated with anterior surgery were followed-up over an average of 5 years after surgery. Radiographic results (kyphotic angle, bony fusion, and instrumentation failure), neurological improvement, and surgical complications were compared between the two groups. The average correction angle after surgery was larger in the posterior group than in the anterior group (P = 0.013), but not at final follow-up (P = 0.755). The average loss of correction was also higher in the posterior group than in the anterior group (P = 0.037). There was no significant difference in neurological outcomes between anterior and posterior approaches (P = 0.080). Two-way analysis of variance (ANOVA) showed that the neurological outcome was better in wedge type than in flat type vertebral collapse, regardless of the type of surgical approach (P = 0.0093). In wedge type vertebral collapse, neurological improvement tended to be greater after anterior than after posterior surgery. In four of six cases with instrumentation failure in the anterior group, a titanium cage subsided more than 5 mm but bony fusion was eventually achieved without causing neurological problems. In the posterior group, six cases experienced instrumentation failure during the postoperative course (two cases with screws loosened from pedicles and bodies, and one case with breakage of a screw neck). None of the patients developed instrumentation-related neurological problems. Two cases in each group developed pseudoarthrosis. In single-level osteoporotic vertebral collapse with neurological deficit, anterior surgery tended to improve neurological deficit in wedge type, but not in flat type collapse, compared with posterior surgery.

Object. The authors conducted a study to examine whether high-resolution [¹⁸F]fluorodeoxyglucose (FDG)—positron emission tomography (PET) could be used to visualize deterioration of cervical spinal cord function associated with various degrees of compression and to determine its potential usefulness during assessment of compressive myelopathy. Methods. In 23 patients requiring decompressive surgery for myelopathy FDG-PET was performed. The preoperative findings of high-resolution FDG-PET were compared with the neurological scores and magnetic resonance (MR) imaging findings. The preoperative standardized uptake value (SUV) of FDG utilization rate of the cervical cord correlated with the pre- (r = 0.497, p = 0.016) and postoperative neurological scores (r = 0.595, p = 0.003), as well as with the rate of neurological improvement postoperatively (r = 0.538, p = 0.008). The FDG utilization rate did not correlate with the high signal intensity on T₂-weighted MR images. Conclusions. Analysis of these results indicates that high-resolution FDG-PET imaging provides useful qualitative and quantitative estimates of impaired metabolic activity of the compromised cervical cord that correlate closely with the severity of neurological dysfunction.

The purpose of the present study was to identify any compensatory changes at the site of chronic compression of the spinal cord and neighboring segments. For this purpose, serial immunohistochemical and immunoblot analyses were performed for the expression levels of endogenous brain-derived neurotrophic factor (BDNF), neurotrophin (NT)-3, and their receptors, trkB and trkC in 24 tip-toe walking Yoshimura mice (twy/twy) aged 12-24 weeks. The twy mouse exhibits spontaneous calcified deposits posteriorly at the C1-C2 level, compressing the spinal cord. Immunoreactivities for BDNF, NT-3, trkB and trkC were preferentially localized in the gray matter, particularly in the anterior horn cells. In 24-week-old twy mice with severe compression, expression levels of these neurotrophins at the site of maximal compression were significantly lower than at the less- or non-compressed sites. In contrast, the expression levels of BDNF, NT-3, trkB and trkC were significantly higher at the rostral and caudal sites immediately adjacent to the maximal compression site. No such changes were noted in 12-week-old twy mice or in control Institute of Cancer Research mice. Our results suggest that overexpression of BDNF, NT-3, trkB and trkC in motoneuron areas neighboring the site of mechanical compression may represent compensatory changes in response to the compromised neuronal function at the level of compression, and that these proteins possibly contribute to neuronal survival and plasticity.