Video-Assisted Thoracoscopic Surgery for Re-Collapse of Vertebrae after Percutaneous Vertebral Augmentation (PVA).

INTRODUCTION: Due to the increase in osteoporosis accompanying the aging society in Japan, osteoporotic vertebral fractures (OVFs) are increasing. Percutaneous vertebral augmentation (PVA) has been widely used for OVFs because it reduces pain immediately with less invasiveness. Re-collapse of vertebral body after PVA is a rare, but important, complication. Once the re-collapse has occurred, patients should undergo an additional invasive salvage surgery. METHODS: We treated 5 patients with re-collapse after PVA in our hospital. For re-collapse after PVA, we performed anterior column reconstruction with video-assisted thoracoscopic surgery (VATS), posterior fixation with percutaneous pedicle screws (PPSs) and minimally invasive spine stabilization (MISt). RESULTS: The mean postoperative follow-up was at 62.8 months. At the final follow-up, the patients were free of low back pain, and bony union was achieved in all cases. The postoperative correction loss was 6 degrees. Perioperative complications included aspiration pneumonia in one patient and bone fracture of an adjacent vertebral body in two patients. There were no reoperation cases. CONCLUSIONS: We perform minimally invasive combined anterior and posterior surgery with VATS for re-collapse after PVA. This procedure is useful in elderly patients with less reserve capacity.

The protective effect and mechanism of COA-Cl in acute phase after spinal cord injury.

Spinal cord injury (SCI) induces severe motor and sensory dysfunction. We previously showed the neuroprotective effects of COA-Cl, a novel synthesized adenosine analog, in a rat stroke model. In this study, we evaluated the neuroprotective effects of COA-Cl in acute phase of SCI. SCI was induced in rats at the T9 vertebra by using a drop device. Rats were divided into acute and subacute groups. A 5-day dose of 6 mg/kg COA-Cl in saline was given to the acute group immediately after SCI and the subacute group 4 days after SCI. Motor function assessed by Basso-Beattie-Bresnahan scoring and inclined plane test improved significantly in the acute group while the subacute group did not. Histological evaluation and TUNEL staining revealed that both the cavity volume and apoptosis were significantly decreased in the acute group compared with the subacute group. In addition, pERK/ERK was increased in the acute group 7 days after SCI. These results suggest that COA-Cl exerts neuroprotective effects via the ERK pathway when administered in the acute phase after SCI, resulting in the recovery of motor function. COA-Cl could be a novel therapeutic agent for the acute phase of SCI.

Very Early Initiation Reduces Benefits of Poststroke Rehabilitation Despite Increased Corticospinal Projections.

Background. Although the effect of rehabilitation is influenced by aspects of the training protocol, such as initiation time and intensity of training, it is unclear whether training protocol modifications affect the corticospinal projections. Objective. The present study was designed to investigate how modification of initiation time (time-dependency) and affected forelimb use (use-dependency) influence the effects of rehabilitation on functional recovery and corticospinal projections. Methods. The time-dependency of rehabilitation was investigated in rats forced to use their impaired forelimb immediately, at 1 day, and 4 days after photothrombotic stroke. The use-dependency of rehabilitation was investigated by comparing rats with affected forelimb immobilization (forced nonuse), unaffected forelimb immobilization (forced use), and a combination of forced use and skilled forelimb training beginning at 4 days after stroke. Results. Although forced use beginning 1 day or 4 days after stroke caused significant functional improvement, immediate forced limb use caused no functional improvement. On the other hand, a combination of forced use and skilled forelimb training boosted functional recovery in multiple tasks compared to simple forced use treatment. Histological examination showed that no treatment caused brain damage. However, a retrograde tracer study revealed that immediate forced use and combination training, including forced use and skilled forelimb training, increased corticospinal projections from the contralesional and ipsilesional motor cortex, respectively. Conclusions. These results indicate that although both very early initiation time and enhanced skilled forelimb use increased corticospinal projections, premature initiation time hampers the functional improvement induced by poststroke rehabilitation.

Effects of intravesicular loading of a Ca2+ chelator and depolymerization of actin fibers on neurotransmitter release in frog motor nerve terminals.

Ca2+ -induced Ca2+ release (CICR) via type-3 ryanodine receptor enhances neurotransmitter release in frog motor nerve terminals. To test a possible role of synaptic vesicle in CICR, we examined the effects of loading of EGTA, a Ca2+ chelator, into synaptic vesicles and depolymerization of actin fibers. Intravesicular EGTA loading via endocytosis inhibited the ryanodine sensitive enhancement of transmitter release induced by tetanic stimulation and the associated rises in intracellular-free Ca2+ ([Ca2+ ]i : Ca2+ transients). Latrunculin A, a depolymerizer of actin fibers, enhanced both spontaneous and stimulation-induced transmitter release, but inhibited the enhancement of transmitter release elicited by successive tetanic stimulation. The results suggest a possibility that the activation of CICR from mobilized synaptic vesicles caused the enhancement of neurotransmitter release.

Improvement of motor function induced by skeletal muscle contraction in spinal cord-injured rats.

BACKGROUND: The involvement of neurotrophic factors such as brain-derived neurotrophic factor (BDNF) in functional recovery after spinal cord injury (SCI) by treadmill training has been suggested. The precise mechanism is poorly understood. However, muscle-derived bioactive molecules (myokines) are known to be produced by muscle contraction. Although BDNF is a myokine and is considered to be a potential mediator of neuroplasticity following exercise, its contribution to motor function recovery after SCI has not yet been described in detail. PURPOSE: To investigate the role of muscle contraction in motor function recovery after SCI, with a focus on BDNF. STUDY DESIGN: Male Sprague-Dawley rats (aged 8-9 weeks) were used to establish the SCI model. Percutaneous electrical muscle stimulation (10 mA, 2 Hz, 10 minutes) was applied to both hindlimbs of the rats immediately after SCI. The stimulation was performed once per day for 4 weeks. The sham, SCI only (SCI), and SCI with electrical muscle stimulation (SCI+ES) groups were compared. METHODS: Spinal cord injury was induced by dropping a 20 g rod with an apex diameter of 2 mm from a height of 25 mm onto the spine of an anesthetized rat at the T9 level. Motor function was assessed using the Basso-Beattie-Bresnahan Locomotor Scale, inclined plane test, and rotarod test. One week after injury, terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells were counted at the injury epicenter, and the level of BDNF was measured in both the spinal cord and the anterior tibial muscle. Four weeks after injury, the cavity volume of the epicenter and the level of phosphorylated growth-associated protein 43 in the spinal cord were measured. RESULTS: Significantly improved Basso-Beattie-Bresnahan scores and inclined plane test results were observed in the SCI+ES group compared with those in the SCI group at 4 weeks post-SCI. We also observed a decrease in the cavity volume and an increase in phosphorylated growth-associated protein 43 levels in the SCI+ES group. Electrical muscle stimulation decreased the numbers of terminal deoxynucleotidyl transferase dUTP nick end labeling-positive cells in the epicenter and increased the levels of BDNF in the spinal cord and lower limb muscles at 1 week post-SCI. CONCLUSIONS: Electrical muscle stimulation improved motor function and increased BDNF levels in both the muscles and the spinal cords of rats subjected to SCI. Muscle contraction-induced BDNF expression might be involved in motor recovery during rehabilitation. CLINICAL RELEVANCE: Our study provides experimental evidence for a possible therapeutic role of peripheral electrical muscle stimulation to enhance motor recovery after SCI.

Constraint-induced movement therapy improves efficacy of task-specific training after severe cortical stroke depending on the ipsilesional corticospinal projections.

Descending spinal pathways (corticospinal, rubrospinal, and reticulospinal) are believed to contribute to functional recovery resulting from rehabilitative training after stroke. However, the contribution of each pathway remains unclear. In the current study, we investigated rehabilitation-induced functional recovery and remodelling of the descending spinal pathways after severe cortical stroke in rats followed by 3 weeks of various rehabilitation [constraint-induced movement therapy (CIMT), skilled forelimb reaching, rotarod, and treadmill exercise]. Following photothrombotic stroke, 96% of corticospinal neurons in the ipsilesional motor cortex were destroyed. Despite the preservation of 82% of total spinal projection neurons (e.g. rubrospinal and reticulospinal projection neurons), rats showed persistent and severe disability, especially in skilled motor function. In this severe stroke model, only CIMT promoted functional recovery, associated with increased corticospinal projections from the peri-infarct motor cortex. Rehabilitation-induced recovery was reversed when the restored corticospinal neurons were destroyed by a second stroke. These data indicate that training-induced functional recovery is dependent on ipsilesional corticospinal projections, which highlights the importance of using strategies to enhance survival, axonal remodelling, or regeneration of corticospinal neurons to effectively restore function in severely affected stroke patients.

Radiculopathy Contralateral to the Side of Disc Herniation -Microendoscopic Observation.

INTRODUCTION: There are patients with lumbar disc herniation (LDH) having contralateral sciatic symptoms although the mechanisms of this clinical feature are still not well understood. The purpose of this study was to investigate these mechanisms by microendoscopic findings. METHODS: Patients were performed microendoscopic surgery using over-the-top approach (ME-OTT), with laminoplasty, extirpation of herniation, and observation of the contralateral nerve root. The over-the-top approach was applied through the same incision from the herniation side. Clinical results were assessed according to the clinical scoring system established by the Japanese Orthopedic Association (JOA) score. RESULTS: This study consisted of five patients, with the average age of 55.6 years old. The mean preoperative JOA score was 13 points. Three cases were Grade II and two were Grade III degrees of disc herniation. Levels of herniation were one at L3-4 and four at L4-5. Remission of sciatic symptoms was obtained in all cases after surgery. The average and percent improvements (%IP) of JOA scores at 2 months after surgery were 27.8 points and 92%, respectively. By the approach from the herniation side using ME-OTT, image around the contralateral nerve root was obtained without radical intervention. By ME-OTT, redness of the nerve root and fibrosis around the symptomatic nerve root were identified, whereas inflammatory changes were not apparent on the ipsilateral nerve root. CONCLUSIONS: Operative treatment of LDH with contralateral symptoms by ME-OTT was a useful procedure for decompression and observation of the affected nerve root. Asymptomatic disc herniation, "silent disc herniation," was considered at the herniation side since there were less inflammatory changes around the ipsilateral nerve root. In contrast, compression of dura toward the opposite side by disc herniation could have led to mechanical stress against the contralateral nerve root and triggered inflammation at lateral recess, resulting in radicular pain.

Rehabilitative skilled forelimb training enhances axonal remodeling in the corticospinal pathway but not the brainstem-spinal pathways after photothrombotic stroke in the primary motor cortex.

Task-specific rehabilitative training is commonly used for chronic stroke patients. Axonal remodeling is believed to be one mechanism underlying rehabilitation-induced functional recovery, and significant roles of the corticospinal pathway have previously been demonstrated. Brainstem-spinal pathways, as well as the corticospinal tract, have been suggested to contribute to skilled motor function and functional recovery after brain injury. However, whether axonal remodeling in the brainstem-spinal pathways is a critical component for rehabilitation-induced functional recovery is not known. In this study, rats were subjected to photothrombotic stroke in the caudal forelimb area of the primary motor cortex and received rehabilitative training with a skilled forelimb reaching task for 4 weeks. After completion of the rehabilitative training, the retrograde tracer Fast blue was injected into the contralesional lower cervical spinal cord. Fast blue-positive cells were counted in 32 brain areas located in the cerebral cortex, hypothalamus, midbrain, pons, and medulla oblongata. Rehabilitative training improved motor performance in the skilled forelimb reaching task but not in the cylinder test, ladder walk test, or staircase test, indicating that rehabilitative skilled forelimb training induced task-specific recovery. In the histological analysis, rehabilitative training significantly increased the number of Fast blue-positive neurons in the ipsilesional rostral forelimb area and secondary sensory cortex. However, rehabilitative training did not alter the number of Fast blue-positive neurons in any areas of the brainstem. These results indicate that rehabilitative skilled forelimb training enhances axonal remodeling selectively in the corticospinal pathway, which suggests a critical role of cortical plasticity, rather than brainstem plasticity, in task-specific recovery after subtotal motor cortex destruction.

[Anesthetic management of posterior lumbar spinal fusion in a patient suspected of having acute exacerbation of chronic interstitial pneumonia].

A patient complicated with interstitial pneumonia required emergency posterior lumbar spinal fusion. The blood gas analysis showed relatively benign values (PaO2 81 torr, PaCO2 44 torr, under room air), but the honeycombing lungs were noted in the bilateral lung fields on CT, and the KL-6 level was high (1,000 U x ml(-1)), for which the acute exacerbation of interstitial pneumonia was suspected. Sivelestat sodium administration was initiated during the surgery and continued postoperatively. During surgery, setting the FIO2 at 0.34, the P/F ratio and intra-airway pressure could be maintained at 500 and 25 mmHg, respectively. To reduce postoperative respiratory complication, anesthesia was maintained with desflurane, which is dissipated easily, and 0.5% ropivacaine 15 ml was subcutaneously injected to the surgical field at the time of wound closure to reduce the total doses of intraoperative fentanyl and postoperative analgesics. After the completion of surgery, the endotracheal tube was removed with head elevated position, and the patient was transported back to the ward. No acute exacerbation occurred thereafter, and the patient was discharged 67 days after surgery. The prediction of acute exacerbation of interstitial pneumonia is difficult. Moreover, there is no established preventive method, although the mortality is high. Therefore, physicians should be thoroughly informed about the currently available evidence, including developmental factors.