Circulating intercellular adhesion molecule-1 and E-selectin in acute ischemic stroke.

Exposure of endothelia to hypoxia followed by reperfusion, results in increased leukocyte activation and extravasation. These leukocytes potentiate ischemic neuronal damage. Extravasation of leukocytes is guided by adhesion molecule interactions on inflammatory and endothelial cells. Circulating adhesion molecules rapidly appear in peripheral blood. Commercially available ELISA kits were used to determine serum levels of E-selectin and intercellular adhesion molecule-1 (ICAM-1) in 36 patients at 1, 3, and 14 days after acute ischemic stroke. E-selectin levels were nonsignificantly increased at day 1, and decreased thereafter, reaching significantly lower values at day 14 in the stroke patients. ICAM-1 levels were similar in stroke patients at each sampling period, and did not differ from those of controls. Our data on ICAM-1 are in line with those of a recently published study. The decreasing circulating E-selectin may stem from endothelial cell damage, alterations in cytokine interactions, or unknown factors.

Treatment of acute ischemic stroke with piracetam. Members of the Piracetam in Acute Stroke Study (PASS) Group.

BACKGROUND AND PURPOSE: Piracetam, a nootropic agent with neuroprotective properties, has been reported in pilot studies to increase compromised regional cerebral blood flow in patients with acute stroke and, given soon after onset, to improve clinical outcome. We performed a multicenter, randomized, double-blind trial to test whether piracetam conferred benefit when given within 12 hours of the onset of acute ischemic stroke to a large group of patients. METHODS: Patients received placebo or 12 g piracetam as an initial intravenous bolus, 12 g daily for 4 weeks and 4.8 g daily for 8 weeks. The primary end point was neurologic outcome after 4 weeks as assessed by the Orgogozo scale. Functional status at 12 weeks as measured by the Barthel Index was the major secondary outcome. CT scan was performed within 24 hours of the onset of stroke but not necessarily before treatment. Analyses based on the intention to treat were performed in all randomized patients (n = 927) and in an "early treatment" population specified in the protocol as treatment within 6 hours of the onset of stroke but subsequently redefined as less than 7 hours after onset (n = 452). RESULTS: In the total population, outcome was similar with both treatments (the mean Orgogozo scale after 4 weeks: piracetam 57.7, placebo 57.6; the mean Barthel Index after 12 weeks: piracetam 55.8, placebo 53.1). Mortality at 12 weeks was 23.9% (111/464) in the piracetam group and 19.2% (89/463) in the placebo group (relative risk 1.24, 95% confidence interval, 0.97 to 1.59; P = .15). Deaths were fewer in the piracetam group in those patients in the intention-to-treat population admitted with primary hemorrhagic stroke. Post hoc analyses in the early treatment subgroup showed differences favoring piracetam relative to placebo in mean Orgogozo scale scores after 4 weeks (piracetam 60.4, placebo 54.9; P = .07) and Barthel Index scores at 12 weeks (piracetam 58.6, placebo 49.4; P = .02). Additional analyses within this subgroup, confined to 360 patients with moderate and severe stroke (initial Orgogozo scale score < 55), showed significant improvement on piracetam in both outcomes (P < .02). CONCLUSIONS: Piracetam did not influence outcome when given within 12 hours of the onset of acute ischemic stroke. Post hoc analyses suggest that piracetam may confer benefit when given within 7 hours of onset, particularly in patients with stroke of moderate and severe degree. A randomized, placebo-controlled, multicenter study, the Piracetam Acute Stroke Study II (PASS II) will soon begin.

Complications of the chronic subdural hematoma.

Eighty three chronic subdural hematomas, obtained by surgery or by necropsy, were examinated. The patient age distribution curve of the non-complicated operative cases showed the highest incidence in the first year of life and also a moderate increase in the elderly group. Recurrent hemorrhage in the walls and in the cavity, was observed in twenty of the seventy three non-complicated cases of chronic subdural hematoma. In five cases the membranes and the subdural sac were invaded by leucemic cells and in the five remaining ones the hematoma was transformed in a subdural empyema. All these complicated subdural hematomas showed evidence of recurrent bleeding, suggesting that the leucemic cells or the infectious agent had spread to the subdural space by this way.