Hyperglycemia and Hypoglycemia-Related Chorea in an 83-Year-Old Man.

We report a case of a patient who first presented with hyperglycemic chorea, and subsequently with hypoglycemic chorea. The patient's hypoglycemia was thought to be iatrogenic, highlighting the importance of careful glucose management following glycemia- related chorea. Presumably secondary to the patient's chorea, the patient also suffered from new onset shoulder pain, which was managed with gabapentin. Unfortunately, due to the patient's renal failure, the gabapentin, combined with infection, led to encephalopathy in this patient. This report presents and offers useful tips on the management of a unique patient who suffered from hyperglycemic chorea, hypoglycemic chorea, and encephalopathy, all within a few weeks.

On the Ethics of Mandatory Reporting of Positive Drug Tests in Newborns and Pregnant Parents at the Time of Delivery.

The opioid epidemic has renewed debate about how to structure laws, agency policies and hospital protocols for mandatory reporting of illicit substances during pregnancy. This paper analyzes the ethics of Rhode Island's approach to mandatory reporting - in particular, reporting of positive maternal and newborn drug tests at time of delivery. Given that state intervention is generally perceived by pregnant people as punitive and threatening to their family, we consider how four elements often used to justify punitive action by the state - retribution, deterrence, rehabilitation, and incapacitation (societal protection) - apply to Rhode Island's policy and approach to prenatal substance use. In addition, the paper considers the equity implications of Rhode Island's approach. It concludes that, given the potential for the policy to do more harm than good, investment of resources would be better spent on clinical and community services that support substance using parents and their newborns.

Tau PET following acute TBI: Off-target binding to blood products, tauopathy, or both?

Repeated mild Traumatic Brain Injury (TBI) is a risk factor for Chronic Traumatic Encephalopathy (CTE), characterized pathologically by neurofibrillary tau deposition in the depths of brain sulci and surrounding blood vessels. The mechanism by which TBI leads to CTE remains unknown but has been posited to relate to axonal shear injury leading to release and possibly deposition of tau at the time of injury. As part of an IRB-approved study designed to learn how processes occurring acutely after TBI may predict later proteinopathy and neurodegeneration, we performed tau PET using 18F-MK6240 and MRI within 14 days of complicated mild TBI in three subjects. PET radiotracer accumulation was apparent in regions of traumatic hemorrhage in all subjects, with prominent intraparenchymal PET signal in one young subject with a history of repeated sports-related concussions. These results are consistent with off-target tracer binding to blood products as well as possible on-target binding to chronically and/or acutely-deposited neurofibrillary tau. Both explanations are highly relevant to applying tau PET to understanding TBI and CTE. Additional study is needed to assess the potential utility of tau PET in understanding how processes occurring acutely after TBI, such as release and deposition of tau and blood from damaged axons and blood vessels, may relate to development CTE years later.

Greater specificity for cerebrospinal fluid P-tau231 over P-tau181 in the differentiation of healthy controls from Alzheimer's disease.

Cerebrospinal fluid (CSF) measures of phosphorylated-tau (P-tau) 231 and P-tau181 are two biomarkers for the identification of tau pathology as related to Alzheimer's disease (AD). While both are pathologically validated, their relative diagnostic performances are not well known. This cross-sectional diagnostic study of 87 normal (NL) subjects and 28 AD subjects compared CSF P-tau231 with CSF P-tau181. Logistic regression modeling demonstrated that the P-tau231 was superior to the P-tau181 in the diagnostic classifications. At a fixed 85% sensitivity cutoff, the ROC analysis shows that P-tau231 has greater overall specificity than P-tau181. While both P-tau analytes demonstrated equivalent negative predictive accuracies, P-tau231 yielded significantly fewer false positives. Moreover, P-tau231, but not P-tau181, demonstrated sensitivity to the E4 genotype. A postmortem validation with 9 AD subjects confirmed the superiority of the CSF P-tau231 specificity. This study suggests that P-tau231 has the potential to improve the CSF tau biomarker diagnosis of AD.