The signal decay with increasing b‐factor at fixed echo time from brain tissue in vivo has been measured using a line scan Stejskal–Tanner spin echo diffusion approach in eight healthy adult volunteers. The use of a 175 ms echo time and maximum gradient strengths of 10 mT/m allowed 64 b‐factors to be sampled, ranging from 5 to 6000 s/mm2, a maximum some three times larger than that typically used for diffusion imaging. The signal decay with b‐factor over this extended range showed a decidedly non‐exponential behavior well‐suited to biexponential modeling. Statistical analyses of the fitted biexponential parameters from over 125 brain voxels (15 × 15 × 1 mm3 volume) per volunteer yielded a mean volume fraction of 0.74 which decayed with a typical apparent diffusion coefficient around 1.4 µm2/ms. The remaining fraction had an apparent diffusion coefficient of approximately 0.25 µm2/ms. Simple models which might explain the non‐exponential behavior, such as intra‐ and extracellular water compartmentation with slow exchange, appear inadequate for a complete description. For typical diffusion imaging with b‐factors below 2000 s/mm2, the standard model of monoexponential signal decay with b‐factor, apparent diffusion coefficient values around 0.7 µm2/ms, and a sensitivity to diffusion gradient direction may appear appropriate. Over a more extended but readily accessible b‐factor range, however, the complexity of brain signal decay with b‐factor increases, offering a greater parametrization of the water diffusion process for tissue characterization. Copyright © 1999 John Wiley & Sons, Ltd.

The response to cerebral hypoxia/ischemia may be different in the neonate compared to other age groups. An in vivo model was developed in the rat to determine whether there are age-dependent differences in the effects of hypoxia on electroencephalographic (EEG) activity. EEG recordings were obtained from Long Evans hooded rats deprived of oxygen at five ages: postnatal days 5 to 7, 10 to 12, 15 to 17, 25 to 27, and 50 to 60. Oxygen concentration was varied from 0, 2, 3, and 4% between animals. EEGs were recorded in all animals before, during, and at 1 hour after exposure to the hypoxic condition and at 1 to 7 days afterward in a subset of animals. All animals were deprived of oxygen until the onset of apnea and bradycardia to 20 to 40% of baseline heart rate values. Hypoxia resulted in isoelectric EEG significantly more frequently in the animals deprived of oxygen at postnatal days 25 to 27 and 50 to 60 than in the younger age groups. A highly significant effect was that the animals deprived at postnatal days 5 to 17 revealed a high incidence of epileptiform EEG activity during hypoxia. In contrast, the older animals exhibited only rare isolated EEG spikes before reaching an isoelectric EEG. The severity of hypoxia-induced epileptiform EEG changes was highest in the animals subjected to moderately hypoxic conditions (3% and 4% oxygen) at postnatal days 10 to 12. Furthermore, epileptiform changes persisted for hours to days following prolonged episodes of hypoxia in the younger animals. This study demonstrates a unique response of the immature brain to exhibit epileptiform activity during hypoxia.

Alzheimer disease represents an insidious impairment of intellect and emotional well-being. However, recent advances in biochemical pathology and human genetics offer promise that effective therapeutic agents may soon be developed.