Background: Anatomical localization remains integral to neurosurgery, particularly in the posterior fossa where neuronavigation is less reliable. There have been many attempts to define the location of the transverse- sigmoid sinus junction (TSSJ) using anatomical landmarks, to aid in the placement of the “strategic burr hole” during a retrosigmoid approach. There is a paucity of research allowing direct comparison of such techniques. Methods: Using high-resolution contrast-enhanced cranial computed tomography images, we constructed three-dimensional virtual cranial models. Fifty models (100 sides) were created from a retrospective sample of images performed in a New Zealand population. Ten methods of anatomical localization were applied to each model allowing qualitative and quantitative comparisons. The “key point” was defined as the point on the outer surface of the skull that directly overlaid the junction of the posterior fossa dura, transverse sinus (TS), and sigmoid sinus (SS). The proximity of each method to this “key point” was compared quantitatively, in addition to other descriptive observations. TSSJ localization methods analyzed included: (1) asterion; (2) emissary foramen; (3) Lang and Samii; (4) Day; (5) Rhoton; (6) Avci; (7) Ribas; (8) Tubbs; (9) Li; and (10) Teranishi. Results: Mean distance to the “key point” showed two tiers of accuracy, those <10 mm, and those >10 mm: Li (6.3 mm), Ribas (6.6 mm), Tubbs (6.8 mm), Teranishi (7.8 mm), Day (8.4 mm), emissary foramen (12.0 mm), Avci (13.0 mm), asterion (13.9 mm), Lang and Samii (15.6 mm), and Rhoton (17.4 mm). The asterion would most frequently overlie the TS (63%) and was often supratentorial (14%). Conclusion: Each method has a unique profile of dura or sinus exposure. There are significant differences in the accuracy of localization of the TSSJ among anatomical localization methods.

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Skin sympathetic nerve activity (SSNA) controls skin blood flow and sweat release, and acute noxious stimulation of skin has been shown to cause a decrease in SSNA in the anaesthetised or spinal cat. In awake human subjects, acute muscle pain causes a transient rise in SSNA, but the impact of long-lasting (tonic) stimulation of muscle nociceptors on skin sympathetic outflow, blood flow and sweat release is unknown. We tested the hypothesis that tonic stimulation of muscle nociceptors causes a sustained increase in sympathetic outflow to the skin. SSNA was recorded from the common peroneal nerve of 10 awake human subjects. Tonic muscle pain was induced by infusing hypertonic saline (7 %) into the tibialis anterior muscle over ~40 min, titrated to achieve a constant level of muscle pain. SSNA initially increased following the onset of the infusion, reaching a peak of 164 % of baseline within 5 min, but then showed a prolonged and sustained decrease, reaching a nadir of 77 % in 20 min. Conversely, skin blood flow (and vascular conductance) initially decreased, followed by a progressive increase; there were no consistent changes in sweat release. In 9 of 10 subjects, SSNA and skin blood flow were inversely related. We conclude that sympathetic outflow to the skin exhibits a biphasic response to long-lasting stimulation of muscle nociceptors: an initial increase presumably related to the 'arousal' or 'alerting' component of pain, characterised by increased SSNA and decreased skin blood flow, followed by a prolonged decrease in SSNA and increased skin blood flow. The latter may be a purposeful response that contributes to wound healing.

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