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We produced unilateral photochemical infarcts in the hindlimb sensorimotor neocortex of 186 rats by intravenous injection of the fluoroscein derivative rose bengal and focal illumination of the intact skull surface. Infarcted rats showed specific, long-lasting deficits in tactile and proprioceptive placing reactions of the contralateral limbs, mostly the hindlimb. Placing deficits were most prominent during transition to immobility and/or when independent limb movements were required. Administration of flunarizine, a Class FV calcium antagonist, 30 minutes after infarction resulted in marked sparing of sensorimotor function in 30 rats. In contrast to 20 vehicle-treated rats, which remained deficient for at least 21 days, 15 (75%) of the rats treated with 1.25 mg/kg i.v. flunarizine showed normal placing on Day 1 after infarction, whereas the remaining five (25%) recovered within 5 days. Oral treatment of 10 rats with 40 mg/kg flunarizine was also effective. Neocortical infarct volume and thalamic gliosis, assessed 21 days after infarction, did not differ between 30 flunarizine-and 30 vehicle-treated rats. However, when 4-hour-old infarcts were measured in 16 rats, posttreatment with intravenous flunarizine reduced infarct size by 31%. In combination with appropriate behavioral analyses, photochemical thrombosis may constitute a relevant stroke model, in which flunarizine preserved behavioral function during a critical period, corresponding to the spread of ischemic damage. {Stroke 1989;20:1383-1390) W hen the fluorescein derivative rose bengal is intravenously injected into rats and the intact skull surface is focally illuminated, cerebral blood vessels in a confined area sustain photochemical injury. Singlet oxygen molecules generated by the dye/light interaction cause peroxidation of endothelial cell membranes and occlusive platelet aggregation. Subsequent thrombus formation, vascular stasis, extravasation, and cytotoxic edema lead to cerebral infarction and necrosis. 1-2 This photochemical model of thrombotic stroke is virtually noninvasive, allows for reproducible infarct size and location, and includes endothelial damage/platelet aggregation interactions in a cascade of stroke-like ischemic events. In this model, the time course of changes in cerebral

Eighty-two children underwent polysomnography (PSG) for symptoms suggestive of obstructive sleep apnea (OSA). Symptoms reported included snoring, witnessed apneic episodes, daytime somnolence, mouth breathing, and enuresis. Tonsillar size, nasal airway patency, and percentile weight were recorded. OSA was diagnosed on PSG when obstructive events were noted and apnea + hypopnea index was five or more per hour. The overall predictive accuracy of clinical suspicion of OSA was 25 (30%) of 82. Predictive accuracies (as a percentage of those with symptoms/signs who have OSA) and prevalences (as a percentage of those with OSA who have the symptom/sign), respectively, were for moderate snoring 29% (12 of 41), 48%; loud snoring 31% (11 of 35), 44%; witnessed apneas 32% (22 of 69), 88%; enuresis 46% (11 of 24), 44%; 2+ tonsillar size 37% (21 of 57), 84%; 3+ tonsillar size 33% (3 of 9), 12%; 90th percentile weight or greater 26% (7 of 27), 28%; 10th percentile weight or less 33% (5 of 15), 20%. Multiple regression analysis did not reveal a significant association between clinical parameters and the presence of OSA as defined by PSG.

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Recently developed agents specifically acting on different 5-hydroxytryptamine (5-HT) receptor populations were used to analyze the functional role of 5-HT2 receptor subtypes in the sleep-wakefulness cycle of the rat. The 5-HT2 receptor antagonist ritanserin injected intraperitoneally (IP) (0.04-2.5 mg/kg) induced an increase in deep slow wave sleep (SWS2) duration at the expense of wakefulness (W), light slow wave sleep (SWS1) and paradoxical sleep (PS). The stimulation of 5-HT2 receptors by 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) produced a dose-related increase in W and a dose-dependent decrease in both SWS2 and PS. Pretreatment with ritanserin (0.16-2.5 mg/kg) or with cinanserin (2.5-5 mg/kg), another 5-HT2 receptor antagonist, dose-dependently reversed the W enhancement and the SWS2 deficit produced by DOM, but not the PS deficit. Sleep-wakefulness alterations (increase in W and SWS1 combined with a suppression of SWS2 and PS) observed after IP injection of two putative 5-HT1 receptor agonists, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) (2.5 mg/kg) and 5-methoxy-3-(1,2,3,6-tetrahydro-4-pyridinyl)-1H-indole (RU 24969) (0.63 mg/kg), were not modified by ritanserin pretreatment (0.16-2.5 mg/kg). These results further support the hypothesis that the serotonergic system plays an active role in the regulation of the sleep-wakefulness cycle in the rat and that 5-HT2 receptors are involved in this action. In addition, it is suggested that 5-HT1 receptor subtypes are unlikely to interact with 5-HT2 receptors in the sleep-wakefulness modulation mediated through 5-HT2 receptors.

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