Sixteen children with active hydrocephalus were studied using the Pressure Volume Index (PVI) technique to characterize neural axis compliance and the resistance to CSF absorption (Ro). Intracranial pressure for the series was 16.2 +/- 6.2/13.3 +/- 6.1 mm Hg. Measured PVI was twice that predicted for each child, indicating abnormally compliant systems. Ro was 7.8 +/- 1.7 mm Hg/ml/min, a three-fold increase above normal. There was no correlation between PVI and ventricular size. These studies indicate that the biomechanical properties of the brain and its coverings are altered by the hydrocephalic process in a way that encourages further accumulation of volume.

Biomechanical Phenomena↗

PubMedDate not supplied

Pial microcirculation in subarachnoid hemorrhage.

Microsurgical and microscopic methods were employed in guinea pigs to expose, observe, and measure response characteristics of cerebral cortical pial microvessels and microcirculation to traumatic and nontraumatic experimental subarachnoid hemorrhage. Bleeding produced by vascular micropuncture was associated with a 44.3% arteriolar constriction. Topical application of homologous blood alone produced a 33.2% vasoconstriction. Observed microcirculatory flow characteristics subsequent to such microvascular changes were consistent with those known to be associated with cerebral cortical infarction. These changes could be prevented or reversed by topical application of the alpha adrenergic blocker, phenoxybenzamine. Topical pretreatment with the beta adrenergic blocker, propranolol, prevented blood-induced spasm, but did not reverse such spasm once it had been established. A chemo-mechanical mechanism is suggested as underlying the vasoconstriction association with rupture of pial microvessels. It is thought that consideration of such microvascular characteristics, in conjunction with those known to be associated with larger intracranial vessels, adds to current knowledge of the pathophysiology of subarachnoid hemorrhage and may be extrapolated to bear future clinical import.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

Breaststroker's knee: pathology, etiology, and treatment.

Twenty-three breaststroke swimmers (ranging in age from 6 to 30 years old) with painful knees were examined. Underwater movies of these swimmers were taken. Eighteen swimmers had tenderness under the medial facet of the patella and over the medial femoral intercondylar ridge. Five of these 18 swimmers also had tenderness along the tibial collateral ligament. Five swimmers had tenderness just along the tibial collateral ligament. The onset of knee pain usually occurred within 3 years of the swimmers' beginning the breaststroke. Initially, the knees were only symptomatic when the swimmers performed the whipkick. As the swimmer continued the breaststroke, in spite of discomfort, the knees became symptomatic during other athletic and nonathletic activity. Breaststroke who had been using the whipkick for more than 8 years had clinical evidence of patellofemoral osteoarthritis. The site of pain in the knee was related to the way in which the whipkick was performed. Breaststroke without knee pain used a whipkick with characteristics that were consistently different than those of the symptomatic swimmers. Treatment of breaststroke's knee should be directed toward correcting the swimmer's whipkick. This approach is most likely to be successful if applied as soon as the swimmer becomes symptomatic.

Adolescent↗