Image-guided thoracoscopic resection of thoracic dumbbell nerve sheath tumors.

BACKGROUND: Surgical removal of dumbbell nerve sheath tumors (NSTs) remains challenging because these neoplasms occupy ≥ 2 spinal and extraspinal spaces. The presence of intraspinal extension, tumor dimension, and/or its location within the thoracic cavity have previously made the resection of these types of neoplasms difficult. OBJECTIVE: To describe the feasibility of performing minimally invasive thoracoscopic surgery, as facilitated by an image guidance system (IGS), to achieve gross total resection of select dumbbell NSTs located in the thoracic spine. METHODS: The 3 cases presented here contained small intraspinal or foraminal components. Preoperative symptoms included Horner syndrome and back and chest wall pain. We used IGS to help guide the complete thoracoscopic resection of select dumbbell NSTs, consisting of extradural, intraforaminal, and paravertebral tumor components, which previously would have been challenging with only a thoracoscopic approach. RESULTS: IGS provided continuous intraoperative anatomic orientation to achieve gross total resection in all 3 cases. All surgical and postsurgical outcomes were satisfactory; preoperative symptoms improved or resolved; and no adverse events were observed. CONCLUSION: Thoracic dumbbell NSTs that have small intraspinal or foraminal components could be resected thoracoscopically when facilitated by IGS. Image-guided thoracoscopic resection of such dumbbell tumors may not only improve the precision of resection, reduce recurrence, and avoid the need for spinal reconstruction but also obviate the need for more invasive or simultaneous posterior procedures. The IGS enhances the accuracy and safety of 2-dimensional thoracoscopic surgery and may reduce its learning curve.

Cervicothoracic junction kyphosis: surgical reconstruction with pedicle subtraction osteotomy and Smith-Petersen osteotomy. Presented at the 2009 Joint Spine Section Meeting. Clinical article.

OBJECT: Sagittal plane deformities can be subdivided into kyphotic and lordotic forms and further characterized according to their global or regional (focal) presentation. Regional deformities of a significant magnitude constitute a gibbous deformity. Pedicle subtraction osteotomy (PSO) and interlaminar Smith-Petersen osteotomies have been used to correct sagittal plane deformities in the cervical, thoracic, and lumbar spine. By resecting a portion of the vertebral body and closing in the gap of this vertebra, the spine is placed in local lordosis and kyphosis is corrected. These osteotomies have generally been carried out in the lumbar or less frequently in the thoracic area. While PSO has been performed in the mid and lower thoracic spine, there have been no case series of patients undergoing PSO at the CTJ. Specifically, a PSO approach that addresses the challenges of the CTJ is needed. Here, the authors review their case series of PSOs performed in the CTJ. Their goal in the treatment of these patients was to correct the regional CTJ kyphosis, restore forward gaze, and reduce the pain associated with the deformity. METHODS: Eight patients (5 males and 3 females, mean age 63 years) underwent PSO for the correction of CTJ kyphosis. Pedicle subtraction osteotomy was performed at C-7 or the upper thoracic vertebrae and was facilitated by a computer-guided intraoperative monitoring system. Surgical indications included postlaminectomy kyphosis, spinal cord tumor resection, posttraumatic kyphosis, and degenerative cervical spondylosis. RESULTS: The mean follow-up was 15.3 months (range 12-20 months), and the mean preoperative CTJ kyphosis was 38.67° (range 25°-60°). Clinically satisfactory correction of the regional deformity was accomplished in all patients, achieving a mean correction of 35.63° (range 15°-66°) at the CTJ, with restoration of forward gaze and significant reduction in pain. CONCLUSIONS: A CTJ deformity is a distinctive form of kyphosis that presents as a variable local deformity and requires complex spinal reconstructive techniques to restore sagittal balance and forward gaze. Pedicle subtraction osteotomy allows for significant correction through one spinal segment, and it can be used safely to correct the regional sagittal alignment of the cervical spine and head in relation to the pelvis. Pedicle subtraction osteotomy can be used alone or in combination with other techniques as some patients may require multistage procedures with anterior and posterior spinal reconstruction to obtain stable sagittal correction. All deformities in these patients were kyphotic in nature with only mild elements of scoliosis or coronal plane deformity. This is unlike lumbar and thoracic curves where the kyphosis is frequently associated with scoliosis.

The rare case of an intramedullary cervical spinal cord teratoma in an elderly adult: case report and literature review.

STUDY DESIGN.: Case report and literature review. OBJECTIVES.: To report the very rare case of a mature intramedullary teratoma with exophytic extension localized to the uppermost cervical spinal level in a 65-year-old woman and review the pertinent medical literature. SUMMARY OF BACKGROUND DATA.: Cervical intramedullary teratomas are extremely rare in adults, especially in patients older than 50 years. METHODS.: The patient presented with progressive ataxia, mild bilateral kinetic hand tremors, and dizziness. Magnetic resonance imaging revealed an intramedullary 1.7 x 1.3 x 2.3 cm mass at C1 with exophytic extension. A C1-C2 laminectomy and a partial suboccipital craniotomy were performed, followed by a subtotal microscopic resection of the tumor. Pathology was consistent with a mature teratoma. RESULTS.: After surgery, the patient's ataxia, tremor, and dizziness resolved almost immediately. CONCLUSION.: This report presents the very rare case of a mature intramedullary teratoma located in the upper cervical spine of an elderly patient, possibly the oldest patient documented with this type of lesion. The authors recommend a conservative subtotal surgical resection of cervical intramedullary tumors because it may improve symptoms that relate to direct mechanical cord compression and avoid further harm from a gross resection.

Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition.

Brain-derived neurotrophic factor (BDNF) has been shown to mediate the effects of exercise on synaptic plasticity and cognitive function, in a process in which energy metabolism probably plays an important role. The purpose of the present study was to examine the influence of exercise on rat hippocampal expression of molecules involved in the regulation of energy management and cognitive function, and to determine the role of BDNF in these events. One week of voluntary exercise that enhanced learning and memory performance elevated the expression of molecular systems involved in the metabolism of energy [AMP-activated protein kinase (AMPK), ubiquitous mitochondrial creatine kinase (uMtCK) and uncoupling protein 2] and molecules that work at the interface of energy and synaptic plasticity [BDNF, insulin-like growth factor I (IGF-I) and ghrelin]. The levels of BDNF mRNA were associated with the mRNA levels of AMPK, uMtCK, IGF-I and ghrelin. Inhibiting the action of BDNF during exercise abolished an exercise-mediated enhancement in spatial learning and increased the expression of all of the molecular systems studied. BDNF blocking also disrupted the association between learning speed and levels of AMPK, uMtCK, ghrelin and IGF-I mRNAs. These findings suggest that the effects of exercise on synaptic plasticity and cognitive function involve elements of energy metabolism, and that BDNF seems to work at the interface between the two processes as a metabotrophin.

Microvascular decompression for intractable singultus: technical case report.

OBJECTIVE: Intractable singultus is a rare but significantly disruptive clinical phenomenon that often accompanies other diseases but can present in isolation due entirely to intracranial pathology. We report a case of intractable singultus that improved after microvascular decompression and present a comprehensive review of singultus by discussing its similarity to other cases of microvascular decompression, its history and etiology, and its evolutionary basis. CLINICAL PRESENTATION: The patient exhibited intractable singultus for 15 years, resistant to multiple medical regimens. INTERVENTION: Microvascular decompression to relieve pressure on the tenth cranial nerve and medulla oblongata resulted in near total resolution of the singultus. CONCLUSION: Neurovascular compression should be considered a potentially reversible cause of intractable singultus, a significantly disabling clinical phenomenon.

Exercise affects energy metabolism and neural plasticity-related proteins in the hippocampus as revealed by proteomic analysis.

Studies were conducted to evaluate the effect of a brief voluntary exercise period on the expression pattern and post-translational modification of multiple protein classes in the rat hippocampus using proteomics. An analysis of 80 protein spots of relative high abundance on two-dimensional gels revealed that approximately 90% of the proteins identified were associated with energy metabolism and synaptic plasticity. Exercise up-regulated proteins involved in four aspects of energy metabolism, i.e. glycolysis, ATP synthesis, ATP transduction and glutamate turnover. Specifically, we found increases in fructose-bisphosphate aldolase C, phosphoglycerate kinase 1, mitochondrial ATP synthase, ubiquitous mitochondrial creatine kinase and glutamate dehydrogenase 1. Exercise also up-regulated specific synaptic-plasticity-related proteins, the cytoskeletal protein alpha-internexin and molecular chaperones (chaperonin-containing TCP-1, neuronal protein 22, heat shock 60-kDa protein 1 and heat shock protein 8). Western blot was used to confirm the direction and magnitude of change in ubiquitous mitochondrial creatine kinase, an enzyme essential for transducing mitochondrial-derived ATP to sites of high-energy demand such as the synapse. Protein phosphorylation visualized by Pro-Q Diamond fluorescent staining showed that neurofilament light polypeptide, glial fibrillary acidic protein, heat shock protein 8 and transcriptional activator protein pur-alpha were more intensely phosphorylated with exercise as compared with sedentary control levels. Our results, together with the fact that most of the proteins that we found to be up-regulated have been implicated in cognitive function, support a mechanism by which exercise uses processes of energy metabolism and synaptic plasticity to promote brain health.

Revenge of the "sit": how lifestyle impacts neuronal and cognitive health through molecular systems that interface energy metabolism with neuronal plasticity.

Exercise, a behavior that is inherently associated with energy metabolism, impacts the molecular systems important for synaptic plasticity and learning and memory. This implies that a close association must exist between these systems to ensure proper neuronal function. This review emphasizes the ability of exercise and other lifestyle implementations that modulate energy metabolism, such as diet, to impact brain function. Mechanisms believed to interface metabolism and cognition seem to play a critical role with the brain derived neurotrophic factor (BDNF) system. Behaviors concerned with activity and metabolism may have developed simultaneously and interdependently during evolution to determine the influence of exercise and diet on cognition. A look into our evolutionary past indicates that our genome remains unchanged from the times of our hunter-gatherer ancestors, whose active lifestyle predominated throughout almost 100% of humankind's existence. Consequently, the sedentary lifestyle and eating behaviors enabled by the comforts of technologic progress may be reaping "revenge" on the health of both our bodies and brains. In the 21st century we are confronted by the ever-increasing incidence of metabolic disorders in both the adult and child population. The ability of exercise and diet to impact systems that promote cell survival and plasticity may be applicable for combating the deleterious effects of disease and ageing on brain health and cognition.

Exercise differentially regulates synaptic proteins associated to the function of BDNF.

We explored the capacity of exercise to impact select events comprising synaptic transmission under the direction of brain-derived neurotrophic factor (BDNF), which may be central to the events by which exercise potentiates synaptic function. We used a specific immunoadhesin chimera (TrkB-IgG) that mimics the BDNF receptor, TrkB, to selectively block BDNF in the hippocampus during 3 days of voluntary wheel running. We measured resultant synapsin I, synaptophysin, and syntaxin levels involved in vesicular pool formation, endocytosis, and exocytosis, respectively. Synapsin I is involved in vesicle pool formation and neurotransmitter release, synaptophysin, in the biogenesis of synaptic vesicles and budding, and syntaxin, in vesicle docking and fusion. Exercise preferentially increased synapsin I and synaptophysin levels, without affecting syntaxin. There was a positive correlation between synapsin I and synaptophysin in exercising rats and synapsin I with the amount of exercise. Blocking BDNF abrogated the exercise-induced increases in synapsin I and synatophysin, revealing that exercise regulates select properties of synaptic transmission under the direction of BDNF.

License to run: exercise impacts functional plasticity in the intact and injured central nervous system by using neurotrophins.

Exercise has been found to impact molecular systems important for maintaining neural function and plasticity. A characteristic finding for the effects of exercise in the brain and spinal cord has been the up-regulation of brain-derived neurotrophic factor (BDNF). This review focuses on the ability of exercise to impact brain circuitry by promoting neuronal repair and enhance learning and memory by increasing neurotrophic support. A paragon for the role of activity-dependent neurotrophins in the CNS is the capacity of BDNF to facilitate synaptic function and neuronal excitability. The authors discuss the effects of exercise in the intact and injured brain and spinal cord injury and the implementation of exercise preinjury and postinjury. As the CNS displays a capacity for plasticity throughout one's lifespan, exercise may be a powerful lifestyle implementation that could be used to augment synaptic plasticity, promote behavioral rehabilitation, and counteract the deleterious effects of aging.

Hippocampal BDNF mediates the efficacy of exercise on synaptic plasticity and cognition.

We found that a short exercise period enhanced cognitive function on the Morris water maze (MWM), such that exercised animals were significantly better than sedentary controls at learning and recalling the location of the platform. The finding that exercise increased brain-derived neurotrophic factor (BDNF), a molecule important for synaptic plasticity and learning and memory, impelled us to examine whether a BDNF-mediated mechanism subserves the capacity of exercise to improve hippocampal-dependent learning. A specific immunoadhesin chimera (TrkB-IgG), that mimics the BDNF receptor, TrkB, to selectively bind BDNF molecules, was used to block BDNF in the hippocampus during a 1-week voluntary exercise period. After this, a 2-trial-per-day MWM was performed for 5 consecutive days, succeeded by a probe trial 2 days later. By inhibiting BDNF action we blocked the benefit of exercise on cognitive function, such that the learning and recall abilities of exercising animals receiving the BDNF blocker were reduced to sedentary control levels. Inhibiting BDNF action also blocked the effect of exercise on downstream systems regulated by BDNF and important for synaptic plasticity, cAMP response-element-binding protein (CREB) and synapsin I. Specific to exercise, we found an association between CREB and BDNF expression and cognitive function, such that animals who were the fastest learners and had the best recall showed the highest expression of BDNF and associated CREB mRNA levels. These findings suggest a functional role for CREB under the control of BDNF in mediating the exercise-induced enhancement in learning and memory. Our results indicate that synapsin I might also contribute to this BDNF-mediated mechanism.

Exercise induces BDNF and synapsin I to specific hippocampal subfields.

To assess the relationship between brain-derived neurotrophic factor (BDNF) and synapsin I in the hippocampus during exercise, we employed a novel microsphere injection method to block the action of BDNF through its tyrosine kinase (Trk) receptor and subsequently measure the mRNA levels of synapsin I, using real-time TaqMan RT-PCR for RNA quantification. After establishing a causal link between BDNF and exercise-induced synapsin I mRNA levels, we studied the exercise-induced distribution of BDNF and synapsin I in the rodent hippocampus. Quantitative immunohistochemical analysis revealed increases of BDNF and synapsin I in CA3 stratum lucidum and dentate gyrus, and synapsin I alone in CA1 stratum radiatum and stratum laconosum moleculare. These results indicate that exercise induces plasticity of select hippocampal transsynaptic circuitry, possibly comprising a spatial restriction on synapsin I regulation by BDNF.