Prediction of psychosis onset in Alzheimer disease: The role of cognitive impairment, depressive symptoms, and further evidence for psychosis subtypes.

BACKGROUND: Psychotic symptoms in Alzheimer disease (AD+P) identify a heritable phenotype associated with more rapid cognitive decline. The authors have proposed that AD+P is itself a composite of a misidentification and a paranoid subtype with increased cognitive impairment restricted to the misidentification type. Most prior studies of the clinical correlates of AD+P have been limited, however, by the inclusion of prevalent cases. METHODS: Subjects with possible or probable AD or mild cognitive impairment (MCI) without psychosis at study entry were assessed at the time of initial presentation and then annually. Psychotic symptoms were assessed using the CERAD Behavioral Rating Scale. Survival analyses used Cox proportional hazard models with time-dependent covariates to examine the predictors of psychosis onset. RESULTS: A total of 288 subjects completed at least one follow-up examination. Mean duration of follow-up was 22.1 months. The incidence of psychosis was 0.19 per person-year. Cognitive impairment was associated with onset of psychosis, largely as a result of its association with onset of the misidentification, but not the paranoid, subtype. Including psychotropic medication use in the model revealed an association of antidepressant use with the onset of psychosis. This latter association appeared to arise from an underlying association between depression and the risk of psychosis onset rather than from antidepressant treatment. CONCLUSION: These findings are consistent with the hypothesis that the misidentification and the paranoid subtypes each define a more biologically homogeneous group than AD+P as a whole. Further exploration of the relationship between depressive symptoms and psychosis in patients with AD is warranted.     

Development of the New Lung Allocation System in the United States

This article reviews the development of the new U.S. lung allocation system that took effect in spring 2005. In 1998, the Health Resources and Services Administration of the U.S. Department of Health and Human Services published the Organ Procurement and Transplantation Network (OPTN) Final Rule. Under the rule, which became effective in 2000, the OPTN had to demonstrate that existing allocation policies met certain conditions or change the policies to meet a range of criteria, including broader geographic sharing of organs, reducing the use of waiting time as an allocation criterion and creating equitable organ allocation systems using objective medical criteria and medical urgency to allocate donor organs for transplant. This mandate resulted in reviews of all organ allocation policies, and led to the creation of the Lung Allocation Subcommittee of the OPTN Thoracic Organ Transplantation Committee. This paper reviews the deliberations of the Subcommittee in identifying priorities for a new lung allocation system, the analyses undertaken by the OPTN and the Scientific Registry for Transplant Recipients and the evolution of a new lung allocation system that ranks candidates for lungs based on a Lung Allocation Score, incorporating waiting list and posttransplant survival probabilities.     

Entrapment of the C2 root and ganglion by the atlanto-epistrophic ligament: clinical syndrome and surgical anatomy

Two cases of progressive, occipital lancinating pain and dysesthesias associated with a sensory deficit of the C2 dermatome are presented. Symptoms were relieved, and C2 sensory function restored by releasing a hypertrophied atlanto-epistrophic ligament entrapping the C2 root and ganglion. The normal anatomy and abnormal surgical findings are described. C2 entrapment by the atlanto-epistrophic ligament is discussed in reference to other C2 lesions causing occipital pain. We conclude that some patients whose progressive occipital pain is accompanied by a C2 sensory deficit are suffering from entrapment of the C2 root and ganglion amenable to surgical decompression.     

Hypothermia differentially affects tuning curves generated by forward and by simultaneous masking.

In the gerbil maintained at euthermic (37.5 degrees C) conditions, forward masking produces a compound action potential tuning curve (CAP TC) which is less sensitive but more sharply tuned than that which is generated by simultaneous masking. These differences between forward- and simultaneously-masked CAP TCs are minimized at hypothermic (30 degrees C) conditions. The unmasking effect occurs at both temperatures, suggesting that hypothermia does not exert these changes by eliminating two-tone suppression.