Mental status changes and stroke.

OBJECTIVE: To determine the frequency with which an acute confusional state is caused by a stroke and to evaluate the usefulness of obtaining computed tomography scans in this setting. DESIGN: Retrospective analysis. SETTING: Tertiary referral center. PATIENTS: The authors reviewed 127 neurology consultations requested for patients presenting with acute and apparently isolated mental status changes. The mean age was 62 years. RESULTS: Nine (7%) of the 127 patients were thought to have suffered mental status changes as a result of an acute stroke: one subarachnoid hemorrhage, and eight ischemic strokes. There was no intracerebral hemorrhage. The locations of the infarcts were: right frontoparietal (four patients), bilateral occipital (two patients), bilateral frontal (two patients), and right pontine (one patient, for whom the causality of the stroke was uncertain). Of those nine stroke patients presenting with isolated mental symptoms, six (66%) had some focal abnormality on neurologic examination. Only three (2.7%) of the 109 patients with no focal findings were ultimately diagnosed as having strokes, and one of these had a subarachnoid hemorrhage. CONCLUSIONS: Stroke was a relatively rare cause of acute confusional syndrome. The neurologic examination had a very high negative predictive value (97%) and was reliable in selecting patients who should undergo an imaging study.

Mental status changes and stroke.

A retrospective analysis at a tertiary referred center was done to determine the frequency with which an acute confusional state is caused by a stroke and to evaluate the usefulness of performing computed tomography in this setting. We reviewed 127 neurology consultations requested for patients presenting with acute and apparently isolated mental status changes. The mean age was 62. Nine of 127 (7%) were thought to have suffered mental status changes as a result of an acute stroke: one subarachnoid hemorrhage and eight ischemic strokes. There was no intracerebral hemorrhage. The locations of the infarcts were right frontoparietal (four patients), bilateral occipital (two patients), bilateral frontal (two patients), and right pontine (one patient, in whom the causality of the stroke was uncertain). Of those nine strokes presenting with isolated mental symptoms, six (66%) had some focal abnormality on neurological examination. Only three of the 109 patients (2.7%) with no focal findings were ultimately diagnosed as strokes, and one of these had a subarachnoid hemorrhage. Stroke was a relatively rare cause of acute confusional syndrome. The neurological examination had a very high negative predictive value (97%) and was reliable in selecting patients who should undergo an imaging study.

Dexamethasone induces chondrogenesis in organoid culture of cell mixtures from mouse embryos.

The effect of dexamethasone on morphogenesis and differentiation of cells obtained from mouse embryos grown at high density in vitro was investigated. Cells from decapitated mouse embryos of day 10 to day 13 were isolated by enzymatic treatment and grown at high density at the medium/air interface in organoid culture. After 28 days in culture, organoid-like structures such as vesicles, gland-like structures and cell aggregates had developed, dependent on the stage of the embryos. After the addition of 10(-7) M dexamethasone, cartilage had formed in cultures of cells from day-10, -11 and -12 embryos. It was maximal in cultures of day-11 cells and rare in day-10 cells. No cartilage was found in cultures of day-13 cells. Cartilage induction was similar in cultures treated with 10(-6) and 10(-7) M dexamethasone, but clearly less in cultures treated with 10(-8) M. Only minute amounts of cartilage were detectable after dexamethasone treatment of cells obtained from decapitated embryos (day-11 and -12) whose limb buds had been cut off. In organoid cultures of pure limb bud cells, 10(-7) M dexamethasone had no influence on chondrogenesis. The results indicate that the cells inducible to form cartilage by dexamethasone originate from the limb buds. Glucocorticoid induction of chondrogenesis has not been described in vivo. The dependency of both chondrogenesis and expression of glucocorticoid receptor on cell density in vitro may be the cause for this effect.