Purpose: The study aimed to investigate the clinical outcomes and limitations after vertebroplasty with posterior spinal fusion (VP+PSF) without neural decompression for osteoporotic vertebral collapse.
Methods: We conducted a prospective multicenter study including 45 patients (12 men and 33 women, mean age: 77.0 years) evaluated between 2008 and 2012. Operation time, blood loss, visual analog scale (VAS) of back pain, neurological status, kyphosis angle in the fused area, and vertebral union of the collapsed vertebra were evaluated.
Results: The mean operation time was 162 min and blood loss was 381 mL. The postoperative VAS score significantly improved, and the neurological status improved in 35 patients (83 %), and none of the remaining patients demonstrated a deteriorating neurological status at two years post-operatively. The mean kyphosis angle pre-operatively, immediately post-operatively, and two years post-operatively was 23.8°, 10.7°, and 24.3°, respectively, and there was no significant difference between the angles pre-operatively and two years post-operatively. The extensive correction of kyphosis >16° was a risk factor for a higher correction loss and subsequent fracture. Union of the collapsed vertebra was observed in 43 patients (95 %) at two years post-operatively.
Conclusions: The present study suggests that spinal stabilization rather than neural decompression is essential to treat OVC. Short-segment VP+PSF can achieve a high union rate of collapsed vertebra and provide a significant improvement in back pain or neurological status with less invasive surgery, but has a limit of kyphosis correction more than 16°.
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http://dx.doi.org/10.1007/s00264-016-3222-3 | DOI Listing |
BMC Med Educ
January 2025
Department of Neurology, the First Affiliated Hospital of Shenzhen University, Shenzhen, Guangdong, 518000, China.
In the modern medical education system, teaching of clinical neurology in outpatient settings is crucial for training future neurologists. The neurology outpatient clinic is a pivotal setting for both initial consultations and follow-up visits. It plays a significant role in the prevention, diagnosis, treatment, and ongoing monitoring of neurological disorders, and is a critical platform for clinical education.
View Article and Find Full Text PDFCalcif Tissue Int
January 2025
Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy.
Rett syndrome (RS) is a rare neurodevelopmental disorder primarily caused by mutations in the X-linked methyl-CpG binding protein 2 (MECP2) gene, responsible for encoding MECP2 which plays a pivotal role in regulating gene expression. The neurological and non-neurological manifestations of RS vary widely in severity depending on the specific mutation type. Bone complications, mostly scoliosis but also osteoporosis, hip displacement, and a high rate of fractures, are among the most prevalent non-neurological comorbidities observed in girls with RS.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Boston University Alzheimer's Disease Research Center, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Background: Alzheimer's disease (AD) has both genetic and environmental risk factors. Gene-environment interaction may help explain some missing heritability. There is strong evidence for cigarette smoking as a risk factor for AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
School of Public Health, University of Pittsburgh, Pittsburgh, PA, USA.
Background: Cognitive decline represents a significant and gradual clinical manifestation in individuals affected by Alzheimer's disease (AD). Currently, there is a lack of effective treatments to delay its progression. Quantitative genome-wide association studies (GWAS) have yielded limited insights into progression traits.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Laboratory of Behavioral Neuroscience, National Institute on Aging, Intramural Research Program, Baltimore, MD, USA.
Background: While immune function is known to play a mechanistic role in Alzheimer's disease (AD), whether immune proteins in peripheral circulation influence the rate of amyloid-b (Aβ) progression remains unknown.
Method: Using the Baltimore Longitudinal Study of Aging (BLSA; n = 196; mean follow-up: 5 years/4 scans), we identified immune-related proteins in plasma (candidate proteins) related to rates of change in cortical Aβ levels, as measured by C-PiB PET. Along with identifying genetic variants that contributed to candidate protein associations, characterizing their relationships with tau-PET and changes in ADRD biomarkers (Aβ, NfL, GFAP, pTau-181), and assessing their expression patterns in human microglia, we leveraged data from the Atherosclerosis Risk in Communities (ARIC) study to determine if changes in candidate protein levels precede Ab = β onset (n = 272), and whether they predict 20-year dementia risk during mid-life (n = 11,596) and 8-year dementia risk during late-life (n = 4,288).
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