Limbic encephalitis may occur as an infectious, paraneoplastic, or autoimmune phenomenon. One such cause of limbic encephalitis is voltage gated potassium channel antibodies (VKGC). Hyponatremia with new cognitive decline may be one of the presenting symptoms. The exact mechanism of hyponatremia is unknown though findings consistent with syndrome of inappropriate antidiuretic hormone (SIADH) are observed. We retrospectively reviewed all cases admitted to an academic medical center with a diagnosis of limbic encephalitis (848 adults between 2004 to 2010) and found six cases of VGKC antibody associated limbic encephalitis. Three of the six cases had SIADH that completely or partially resolved with a combination of water restriction and immunotherapy. The reversibility of hyponatremia and limbic encephalitis with immunomodulation suggests an antibody-mediated cause. We further review available literature for association of hyponatremia and VGKC limbic encephalitis and propose mechanisms of for the hyponatremia in autoimmune encephalitis.
Background: Induced mild hypothermia (MIH) is generally an effective intervention for reducing intracranial pressure (ICP) in patients with severe traumatic brain injury (TBI). Unfortunately, MIH also influences brain tissue oxygenation (PbtO2). The significance of the PbtO2 change is unknown. We report a patient with severe traumatic brain injury (TBI) with refractory intracranial hypertension requiring MIH which resulted in a decrease in his PbtO2 values. Case report:The patient presented in a coma following an altercation. He was found to have a large left subdural hemorrhage with significant mass effect requiring craniectomy. He subsequently developed refractory intracranial hypertension requiring medically induced coma and MIH. As temperature decreased, his PbtO2 values decreased from 23-35 mmHg to 6-10 mmHg. There was a significant reduction in PbtO2 values as temperature decreased (p<0.001). ICP did not change with a decrease in temperature and remained elevated (p=0.78). Conclusion:PbtO2 significantly decreased linearly with the decrease in body temperature. Future studies should evaluate the clinical significance of the reduction in PbtO2 in patients with severe TBI and refractory intracranial hypertension requiring MIH. Recognizing expected changes in PbtO2 monitoring with MIH is important for managing neurocritically ill patients.
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