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Study Design: Retrospective review of the practice of 3 surgeons in a single centre during a 1-year period. Objective: We aimed to investigate our adherence to the Society of British Neurological Surgeons (SBNS) guidelines regarding intra-operative imaging during lumbar surgery and to determine if this has any impact on length of surgery or complications rates, in particular rates of wrong-level surgery. Background: The SBNS recommends three x-rays for intra-operative spinal localisation – one prior to incision, the second after exposure of the laminae and before the commencement of decompression, and the third at the end of the operation to confirm the adequacy of decompression. At our centre, surgeon A performs x-rays 1 and 3 routinely, and x-ray 2 in cases where the anatomy is uncertain, surgeon B performs x-ray 2 only, and the practice of surgeon C varies depending on the complexity of cases. Method: We reviewed the surgical logbooks of 3 consultant neurosurgeons in our centre for the 1-year period between October 2015 and October 2016. Our study included 301 patients who had undergone lumbar decompression or lumbar discectomy during this period. Results: There were no cases of wrong-level surgery. The incorrect spinal level was initially exposed in 13 cases (4.3%). 10 of these had x-ray 2 only, 1 had x-ray 1, 1 had x-rays 1 and 2, and 1 had all 3 x-rays. Surgeon B performed 8 of these cases, four were performed by surgeon C, and 1 by surgeon A. The median duration of surgery was 80 minutes for lumbar decompression and 67.5 minutes for lumbar discectomy. The median duration of surgery in patients in whom the wrong level was initially exposed was 85 minutes for lumbar decompression and 80 minutes for lumbar discectomy. Conclusion: Performance of the 3 recommended x-rays may increase the identification of wrong-level exposures before the commencement of decompression and may reduce the length of surgery. [ABSTRACT FROM AUTHOR]

Presents a study which focused on small groups of symphathetic neurons in the superior cervical ganglion (SCG) of the rat. Neurotrophin expression in target tissues; Neurotrophin receptor expression in subpopulations of SCN neurons; Experimental procedures.

Nociceptive dorsal root ganglion (DRG) cells can be divided into three main populations, namely (1) small diameter non-peptide-expressing cells, (2) small-diameter peptide-expressing (calcitonin gene related peptide (CGRP), substance P) cells, and (3) medium-diameter peptide-expressing (CGRP) cells. The properties of these cell populations will be reviewed, with a special emphasis on the expression of the vanilloid (capsaicin) receptor VR1 and its regulation by growth factors. Cells in populations 1 and 2 express VR1, a nonselective channel that transduces certain nociceptive stimuli and that is crucial to the functioning of polymodal nociceptors. Cells in population 1 can be regulated by glial cell line derived neurotrophic factor (GDNF) and those in populations 2 and 3 by nerve growth factor (NGF). In vivo, DRG cells express a range of levels of VR1 expression and VR1 is downregulated after axotomy. However, treatment with NGF or GDNF can prevent this downregulation. In vitro, DRG cells also show a range of VR1 expression levels that is NGF and (or) GDNF dependent. Functional studies indicate that freshly dissociated cells also show differences in sensitivity to capsaicin. The significance of this is not known but may indicate a difference in the physiological role of cells in populations 1 and 2. [ABSTRACT FROM AUTHOR]

Glial cell line-derived neurotrophic factor (GDNF) is a trophic factor with an established role in sensory neuron development. More recently it has also been shown to support adult sensory neuron survival and exert a neuroprotective effect on damaged sensory neurons. Some adult small-sized dorsal root ganglion (DRG) cells that are GDNF-sensitive sensory neurons express the inhibitory peptide somatostatin (SOM). Thus, we tested the hypothesis that prolonged GDNF administration would regulate SOM expression in sensory neuron cell bodies in the dorsal root ganglia (DRG) and activity-induced release of SOM from axon terminals in the dorsal horn. Continuous intrathecal delivery of GDNF for 11–13 days significantly increased the number of small DRG cells that expressed SOM. Furthermore, GDNF treatment evoked SOM release in the isolated dorsal horn following electrical stimulation of the dorsal roots that was otherwise undetectable in control rats. Conversely capsaicin-induced release of SOM (EC[sub 50] 50 nm) was not modified by GDNF treatment. These results show that GDNF can regulate central synaptic function in SOM-containing sensory neurons. [ABSTRACT FROM AUTHOR]

Spinal renal cell metastases are a common insidious pathological manifestation of the oncological process but less common are intramedullary and intraneural spinal metastases. The differential diagnosis of such pathological features can be difficult in the presence of conflicting radiological evidence. In the present case report, we have detailed the clinical, diagnostic, surgical, and therapeutic progression of a 54-year-old man diagnosed with metastatic renal cell carcinoma. After the initial presentation and treatment, he had presented with symptomatic right lower limb radiculopathy. Magnetic resonance imaging identified a well-defined cystic lesion expanding in the right exit foramina at L5-S1, suggestive of a benign schwannoma. After a multidisciplinary review, he was treated symptomatically and imaging surveillance for a 19-month period, with static lesion findings. Failure of symptomatic management resulted in operative intervention and subsequent histological diagnosis of the metastatic deposit. To the best of our knowledge, the present report is the first documented case of intraneural metastatic deposits from renal cell carcinoma that showed benign radiographic features and demonstrated a stable appearance on surveillance imaging studies for a significant period. These findings suggest that clinicians should have a high index of suspicion for a metastatic process in symptomatic patients with a known renal cell cancer regardless of the lesion's radiographic or temporal characteristics. [ABSTRACT FROM AUTHOR]