SPINAL-CORD COMPRESSION DUE TO PAGETIC SPINAL STENOSIS WITH INVOLVEMENT OF EXTRADURAL SOFT-TISSUES - A CASE-REPORT

Although Paget's disease of the spine may cause neurological dysfunction by bone hypertrophy or collapse, it is very rare for the disease process to extend into the soft tissues of the spinal canal. We report a case of Paget's disease causing ossification of the ligamentum flavum and extradural fat, thus causing spinal cord compression. Decompressive laminectomy was carried out, resulting in neurological improvement. In such cases surgical decompression should be followed by therapy with calcitonin

Preliminary Evaluation of a Novel Intraparenchymal Capacitive Intracranial Pressure Monitor

Object Intracranial pressure (ICP) monitors are currently based on fluid-filled, strain gauge, or fiberoptic technology. Capacitive sensors have minimal zero drift and energy requirements, allowing long-term implantation and telemetric interrogation; their application to neurosurgery has only occasionally been reported. The aim of this study was to undertake a preliminary in vitro and in vivo evaluation of a capacitive telemetric implantable ICP monitor. Methods Four devices were tested in air- and saline-filled pressure chambers; long-term capacitance-pressure curves were obtained. Devices implanted in a gel phantom and in a piglet were placed in a 3-T MR unit to evaluate MR compatibility. Four devices were implanted in a piglet neonatal hydrocephalus model; output was compared with ICP obtained through fluid-filled transduction and a strain-gauge ICP monitor. Results The capacitance-pressure relationship was constant over 4 weeks, suggesting minimal zero drift during this period. There were no temperature changes around the monitor. Signal loss at the sensor was minimal in both the phantom and the piglet. Over 114,000 measurements were obtained; the difference between mean capacitive ICP and fluid-transduced ICP was 1.8 ± 1.42 mm Hg. The correlation between ICP from the capacitive sensor and fluid-filled transducer (r = 0.97, p &lt; 0.0001) or strain-gauge monitor (r = 0.99, p &lt; 0.0001) was excellent. In vivo monitoring was restricted to 48 hours due to problems with robustness in the clinical environment. Conclusions This preliminary study demonstrates minimal long-term zero drift in vitro, good MR compatibility, and good correlation with other methods of ICP monitoring in vivo in the short term. Further long-term in vivo study is required.</jats:sec

The cytotoxic action of lymphokine activated killer cells upon the human glioma cell line U251 is stimulated by bispecific monoclonal antibody (MoAb) constructs.

The ability of IL-2 stimulated mononuclear cells to kill the human glioblastoma cell line U251 has been investigated. Highest cytotoxic activity was generated in low cell density cultures incubated for 15 days with 250-1000 U/ml IL-2. Sub-optimal killing was noted, with cells only exposed to IL-2 for three days. Under the latter conditions, bispecific monoclonal antibodies (MoAbs) of either anti-CD3 or anti-CD16 and an anti-NCAM MoAb stimulated LAK cell activity markedly. Anti-CD16 conjugates were found more effective than anti-CD3 and (Fab')2 constructs more efficacious than those made with whole Ig molecules. Maximal stimulation of LAK cell activity was noted with bispecific MoAbs. Little effect was observed with either single or mixtures of monomeric MoAbs. Furthermore, no effect of bispecific MoAbs was observed when target cells lacked expression of NCAM. These results could be of clinical importance as it is not always feasible to screen LAK cells for optimal activity before administration to patients. Whilst bispecific MoAbs have no effect on optimally stimulated LAK cells, they are not inhibitory and can stimulate killing under sub-optimal IL-2 stimulation