Emission tomography of positron or gamma emitting inert gases allows calculation of regional cerebral blood flow (rCBF) in cross-sectional slices of human brain. An algorithm is presented for rCBF calculations from a sequence of time averaged tomograms using inhaled 133Xe. The approach is designed to avoid loss of information in brain areas with low flow rates. It is based on linearizing and scaling the early isotope distribution picture (recorded from 0 to 2 min) in rCBF units of ml/100 g/min. This is done by calculating the time constant ki for pixels with high count rate using the entire sequence of four 1 min pictures and using a fixed value for the brain:blood partition coefficient, lambda. The method is essentially based on the bolus distribution principle, and it allows the estimation of blood flow in ischemic areas. Application to positron emission tomography is discussed.

Cerebral Infarction↗

PubMed1981

Perstimulatory adaptation as measured by reaction time: asymmetry between 400 and 500 kc/s.

The finger-withdrawal reaction time (RT) of 22 normal-hearing young adults was measured to 40 presentations of test tones of .5 kc/s and of .4 kc/s at 50 db SPL. An adapting tone of .4 or .5 kc/s at 50 db SPL was then presented, and after 7 min, RTs were collected to a series of 40 test tones as in the pre-adaptation procedure. The adapting tone-test tone order of .4-.5 kc/s, respectively, and the reverse order, were counterbalanced among Ss. In this study, as reported previously (Davis and Weiler, Brit. J. Audiol., 1976, 10, 102-106), RT changes were significant as a function of adaptation, but only in the order .5-.4 kc/s. Further study would be required to determine whether cochlear or more central processes are responsible for adaptation at .5 kc/s affecting RT at .4 kc/s, but for adaptation at .4 kc/s not significantly affecting RT at .5 kc/s.

Acoustic Stimulation↗

PubMed1977

Platelet and plasma amine oxidase inhibition and urinary amine excretion changes during phenelzine treatment.

The treatment of depressed patients with the monoamine oxidase (MAO)-inhibiting antidepressant, phenelzine, was found to be accompanied by an 82 per cent reduction in platelet MAO activity and a 91 per cent reduction in plasma amine oxidase activity. Maximum reductions in enzyme activity occurred after 7 to 14 days of treatment; recovery of enzyme activity posttreatment required an average of 14 days for the platelet MAO and greater than 6 weeks for the plasma enzyme. Marked elevations in urinary tryptamine excretion occurred in conjunction with MAO inhibition during phenelzine treatment, but the magnitidue of urinary tryptamine change in individual patients was not closely correlated with the magnitude of enzyme activity reduction. Changes in platelet serotonin content serotonin content and in urinary catecholamine metabolites also occurred in response to phenelzine treatment.

Blood Platelets↗