Neurosurgery
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Review Case Reports
Brainstem dysfunction in chiari malformation presenting as profound hypoglycemia: presentation of four cases, review of the literature, and conjecture as to mechanism.
We report four patients whose cases resulted in our observation that profound hypoglycemia resulting from intermittent hyperinsulinism plays a significant role in patients with brainstem dysfunction from Chiari I or II malformations who have intermittent autonomic dysfunction ("blue spells"). ⋯ Patients with severe intermittent brainstem dysfunction after decompression of Chiari I or Chiari II malformations should have laboratory studies of glucose levels performed at the time of the episodes to rule out hypoglycemia.
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Laboratory studies have identified numerous potential therapeutic interventions that might have clinical application for the treatment of human traumatic brain injury. Many of these therapies have progressed into human clinical trials in severe traumatic brain injury. Numerous trials have been completed, and many others have been prematurely terminated or are currently in various phases of testing. ⋯ In this review, we summarize the current status of human traumatic brain injury clinical trials, as well as the animal laboratory studies that led to some of these trials. We summarize criteria for conducting clinical trials in severe traumatic brain injury, with suggestions for future improvements. We also attempt to identify factors that might contribute to the discrepancies between animal and human trials, and we propose recommendations that could help investigators avoid certain pitfalls in future clinical trials in traumatic brain injury.
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An alternative endovascular treatment to conventional transarterial embolization of cerebral arteriovenous malformations (AVMs) is proposed. ⋯ Instead of relying on access to an AVM nidus from the arterial side (with its usual complexity), TRENSH would require retrograde access to the lesion via much larger and anatomically simpler draining veins. Retrograde permeation of the AVM nidus may then be possible with a liquid sclerosant (to effect a "chemical embolization") provided that the arterial inflow is reduced sufficiently by temporary controlled systemic hypotension, with or without the aid of temporary balloon occlusion of the main arterial feeder(s). Retrograde spread of sclerosant within the nidus that falls short of filling arterial feeders and their branches to normal brain tissue may then be possible. Angioarchitectural and hemodynamic considerations are addressed, as are the potential role and limitations of TRENSH in the management of cerebral pial AVMs. Future implementation of this new technique in some specific selected cases in which the anatomic configuration of the AVM and its draining veins might be favorable could prove to be a potentially useful addition to the armamentarium of AVM therapies, which currently includes microsurgery, radiosurgery, and transarterial embolotherapy. Experimental studies directed at assessing the feasibility of TRENSH before potential future clinical application seem justified.