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Recent years have seen the emergence of the S100 calcium-binding protein B (S100B) biomarker used in the initial management of minor traumatic brain injury (TBI) patients. S100B has been found to reduce cerebral computed tomography (CT-C) scans and was recently implemented in the Scandinavian Neurotrauma Committee (SNC) guidelines. In a clinical setup, we retrospectively investigated the use of the S100B biomarker in relation to the SNC guidelines in the respective year before and after implementation. Accordingly, minor TBI patients with the International Classification of Diseases, Tenth Revision diagnostic code of S06.0 commotio cerebri were included in 2018 (n = 786) and 2019 (n = 709) for comparison of emergency department time (EDT) and CT-Cs. In 2019, we included all patients with an S100B sample (n = 547; 348/199 male:female; median age, 52 years). We found an S100B sensitivity of 92% and negative predictive value (NPV) of 99% (cutoff, 0.10 µg/L) regardless of SNC guideline compliance. With strict SNC guideline management, sensitivity and NPV increased to 100%, even at a 0.20-µg/L cutoff that increased the specificity from 49% to 76%. After S100B implementation, we found the median EDT to significantly increase from 196 min (interquartile range [IQR] = 127-289) in 2018 to 216 min (IQR = 134.0-309.5) in 2019 (p = 0.0148), which may have resulted from poor guideline compliance (53.9%). Contrarily, the proportion of CT-C scanned patients decreased from 70% to 56.3% equal to a relative 27.5% decrease of scanned patients (p < 0.0001). Conclusively, our study supported the safe and efficient clinical use of the S100B biomarker, albeit with a minor EDT increase. S100B combination with the SNC guidelines improved clinical potential.

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Background: Deep brain stimulation (DBS) of the dorsal subthalamic nucleus (STN) is a validated neurosurgical treatment of Parkinson's Disease (PD). To investigate the mechanism of action, including potential DBS induced neuroplasticity, we have previously used a minipig model of Parkinson's Disease, although the basal ganglia circuitry was not elucidated in detail. Aim: To describe the cortical projections from the primary motor cortex (M1) to the basal ganglia and confirm the presence of a cortico-striatal pathway and a hyperdirect pathway to the subthalamic nucleus, respectively, which is known to exist in primates. Materials and Methods: Five female Göttingen minipigs were injected into the primary motor cortex (n = 4) and adjacent prefrontal cortex (n = 1) with the anterograde neuronal tracer, Biotinylated Dextran Amine (BDA). 4 weeks later the animals were sacrificed and the brains cryosectioned into 30 µm thick coronal sections for subsequent microscopic analysis. Results: The hyperdirect axonal connections from the primary motor cortex were seen to terminate in the dorsolateral STN, whereas the axonal projections from the prefrontal cortex terminated medially in the STN. Furthermore, striatal tracing from the motor cortex was especially prominent in the dorsolateral putamen and less so in the dorsolateral caudate nucleus. The prefrontal efferents were concentrated mainly in the caudate nucleus and to a smaller degree in the juxtacapsular dorsal putamen, but they were also found in the nucleus accumbens and ventral prefrontal cortex. Discussion: The organization of the Göttingen minipig basal ganglia circuitry is in accordance with previous descriptions in primates. The existence of a cortico-striatal and hyperdirect basal ganglia pathway in this non-primate, large animal model may accordingly permit further translational studies on STN-DBS induced neuroplasticity of major relevance for future DBS treatments.

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