Symptomatic spinal stenosis is a very common problem, and decompression surgery has been shown to be superior to nonoperative treatment in selected patient groups. However, performing an instrumented fusion in addition to decompression may avoid revision and improve outcomes. The aim of the SpInOuT feasibility study was to establish whether a definitive randomized controlled trial (RCT) that accounted for the spectrum of pathology contributing to spinal stenosis, including pelvic incidence-lumbar lordosis (PI-LL) mismatch and mobile spondylolisthesis, could be conducted. As part of the SpInOuT-F study, a pilot randomized trial was carried out across five NHS hospitals. Patients were randomized to either spinal decompression alone or spinal decompression plus instrumented fusion. Patient-reported outcome measures were collected at baseline and three months. The intended sample size was 60 patients.Aims
Methods
Traumatic central cord syndrome (CCS) typically follows a hyperextension injury and results in motor impairment affecting the upper limbs more than the lower, with occasional sensory impairment and urinary retention. Current evidence on mortality and long-term outcomes is limited. The primary aim of this study was to assess the five-year mortality of CCS, and to determine any difference in mortality between management groups or age. Patients aged ≥ 18 years with a traumatic CCS between January 2012 and December 2017 in Wales were identified. Patient demographics and data about injury, management, and outcome were collected. Statistical analysis was performed to assess mortality and between-group differences.Aims
Methods
In this investigation, we administered oxidative stress to nucleus pulposus cells (NPCs), recognized DNA-damage-inducible transcript 4 (DDIT4) as a component in intervertebral disc degeneration (IVDD), and devised a hydrogel capable of conveying small interfering RNA (siRNA) to IVDD. An in vitro model for oxidative stress-induced injury in NPCs was developed to elucidate the mechanisms underlying the upregulation of DDIT4 expression, activation of the reactive oxygen species (ROS)-thioredoxin-interacting protein (TXNIP)-NLRP3 signalling pathway, and nucleus pulposus pyroptosis. Furthermore, the mechanism of action of small interfering DDIT4 (siDDIT4) on NPCs in vitro was validated. A triplex hydrogel named siDDIT4@G5-P-HA was created by adsorbing siDDIT4 onto fifth-generation polyamidoamine (PAMAM) dendrimer using van der Waals interactions, and then coating it with hyaluronic acid (HA). In addition, we established a rat puncture IVDD model to decipher the hydrogel’s mechanism in IVDD.Aims
Methods
We aimed to retrospectively assess the accuracy and safety of
CT navigated pedicle screws and to compare accuracy in the cervical
and thoracic spine (C2-T8) with (COMB) and without (POST) prior
anterior surgery (anterior cervical discectomy or corpectomy and
fusion with ventral plating: ACDF/ACCF). A total of 592 pedicle screws, which were used in 107 consecutively
operated patients (210 COMB, 382 POST), were analysed. The accuracy
of positioning was determined according to the classification of
Gertzbein and Robbins on post-operative CT scans.Aims
Patients and Methods
There are many causes of paraspinal muscle weakness which give rise to the dropped-head syndrome. In the upper cervical spine the central portion of the spinal cord innervates the cervical paraspinal muscles. Dropped-head syndrome resulting from injury to the central spinal cord at this level has not previously been described. We report two patients who were treated acutely for this condition. Both presented with weakness in the upper limbs and paraspinal cervical musculature after a fracture of C2. Despite improvement in the strength of the upper limbs, the paraspinal muscle weakness persisted in both patients. One ultimately underwent cervicothoracic fusion to treat her dropped-head syndrome. While the cause of the dropped-head syndrome cannot be definitively ascribed to the injuries to the spinal cord, this pattern is consistent with the known patho-anatomical mechanisms of both injury to the central spinal cord and dropped-head syndrome.
