Previous experiments in anesthetized or decerebrate cats showed that the vestibular system participates in adjusting blood pressure during postural changes. The present experiments tested the hypothesis that removal of vestibular inputs in awake cats would affect orthostatic tolerance. Before the lesion, blood pressure typically remained within 10 mmHg of baseline values during nose-up-pitch body rotations of up to 60 degrees in amplitude. In contrast, bilateral peripheral vestibular lesions altered the pattern of orthostatic responses in all animals, and blood pressure fluctuated >10 mmHg from baseline values during most 60 degrees nose-up tilts in five of six animals. The deficit in correcting blood pressure was particularly large when the animal also was deprived of visual cues indicating position in space. During this testing condition, either a decrease or increase in blood pressure >10 mmHg in magnitude occurred in >80% of tilts. The deficit in adjusting blood pressure after vestibular lesions persisted for only 1 wk, after which time blood pressure remained stable during tilt. These data show that removal of vestibular inputs alters orthostatic responses and are consistent with the hypothesis that vestibular signals are one of several inputs that are integrated to elicit compensatory changes in blood pressure during movement.

Intracerebral hemorrhage (ICH) is associated with a higher degree of morbidity and mortality than other stroke subtypes. Despite this burden, currently approved treatments have demonstrated limited efficacy. To date, therapeutic strategies have principally targeted hematoma expansion and resultant mass effect. However, secondary mechanisms of brain injury are believed to be critical effectors of cell death and neurological outcome following ICH. This article reviews the pathophysiology of secondary brain injury relevant to ICH, examines pertinent experimental models, and highlights emerging therapeutic strategies. Treatment paradigms discussed include thrombin inhibitors, deferoxamine, minocycline, statins, granulocyte-colony stimulating factors, and therapeutic hypothermia. Despite promising experimental and preliminary human data, further studies are warranted prior to effective clinical translation.

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We retrospectively reviewed 18 cases of primary lung abscess and 10 cases of secondary lung abscess in infants and children during a 6-year period. Among 18 patients with primary abscesses, nine were boys and nine girls, from 9 months to 20 years old, but only two of 18 were less than 5 years old. Each had a solitary abscess. Location of abscesses included the right lower lobe (8), the right upper lobe (3), the left upper lobe (1), and the left lower lobe (6). One patient had Streptococcus pneumoniae bacteremia. Other bacterial isolates were from the upper respiratory tract and of uncertain significance. All patients recovered, although lobectomy was considered necessary in five patients because of failure to respond to intravenous antibiotic therapy. Secondary lung abscesses occurred in six boys and four girls who were from 2 1/2 months to 13 years old. All 10 had solitary, right-sided lesions, seven in the right lower lobe and three in the right upper lobe. Bacteria of unclear significance were recovered from three of 10 patients, while two had documented gram-negative bacteremia. Three secondary abscess patients underwent lobectomy because of perceived inadequate response to medical therapy, including intravenous antibiotics. Based upon the literature and our experience, therapy for pulmonary abscess should include a parenteral antibiotic with gram-positive activity against both penicillinase-producing Staphylococcus aureus and anaerobes for a minimum of 3 weeks.(ABSTRACT TRUNCATED AT 250 WORDS)