Neurosurgery
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Brain hypoxia (BH) can aggravate outcome after severe traumatic brain injury (TBI). Whether BH or reduced brain oxygen (Pbto(2)) is an independent outcome predictor or a marker of disease severity is not fully elucidated. ⋯ Brain hypoxia is associated with poor short-term outcome after severe traumatic brain injury independently of elevated ICP, low CPP, and injury severity. Pbto(2) may be an important therapeutic target after severe traumatic brain injury.
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The ventralis intermedius (VIM) nucleus of the thalamus is the primary surgical target for treatment of tremor. Most centers rely on indirect targeting based on atlas-defined coordinates rather than patient-specific anatomy, making intraoperative physiological mapping critical. Detailed identification of this target based on patient-specific anatomic features can help optimize the surgical treatment of tremor. ⋯ Analysis of DTI and FA maps on widely available 1.5-T magnetic resonance imaging yields clear identification of various structures key to neurosurgical targeting. Prospective evaluation of integrating DTI into neurosurgical planning may be warranted.
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Hemodynamic treatment of subarachnoid hemorrhage-induced vasospasm is associated with a number of systemic and cerebral risks. However, hypertensive encephalopathy has rarely been reported in the setting of induced hypertension. Recognition of this complication is nonetheless critical because failure to lower blood pressure may lead to worsening of deficits and even permanent injury. ⋯ This is the first reported case of unilateral PRES in the setting of subarachnoid hemorrhage. It likely occurred because right-sided vasospasm attenuated ipsilateral distal perfusion pressures, leaving the left hemisphere vulnerable to the consequences of induced hypertension. Hypertensive encephalopathy should be considered in patients with unilateral or asymmetric vasospasm when neurological worsening occurs in the contralateral hemisphere during induced hypertension and/or the patient paradoxically worsens despite raising blood pressure.
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Biography Historical Article
History of the vertebral venous plexus and the significant contributions of Breschet and Batson.
Before the 18th century, the vertebral venous plexus (VVP) received scant mention, had no clinical relevance, and was largely ignored by anatomists, most likely because of its location and nondistensible nature. Gilbert Breschet in 1819 provided the first detailed anatomic description of the VVP, describing it as a large plexiform valveless network of vertebral veins consisting of 3 interconnecting divisions and spanning the entire spinal column with connections to the cranial dural sinuses distributed in a longitudinal pattern, running parallel to and communicating with the venae cavae, and having multiple interconnections. More than a century passed before any work of significance on the VVP was noted. ⋯ With his seminal work, Batson reclassified the human venous system to consist of the caval, pulmonary, portal, and vertebral divisions. Further advances in imaging technology confirmed Batson's results. Today, the VVP is considered part of the cerebrospinal venous system, which is regarded as a unique, large-capacitance, valveless plexiform venous network in which flow is bidirectional that plays an important role in the regulation of intracranial pressure with changes in posture and in venous outflow from the brain, whereas in disease states, it provides a potential route for the spread of tumor, infection, or emboli.
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Small-animal models have been used in traumatic brain injury (TBI) research to investigate the basic mechanisms and pathology of TBI. Unfortunately, successful TBI investigations in small-animal models have not resulted in marked improvements in clinical outcomes of TBI patients. ⋯ LPR and Pbto(2) can be utilized as serial nonterminal secondary markers in our injury model for neuropathology, and as evaluation metrics for novel interventions and therapeutics in the acute postinjury period. This translational model bridges a vital gap in knowledge between TBI studies in small-animal models and clinical trials in the pediatric TBI population.