We conducted a double-blind pilot study of 8 patients with established cerebral infarction to evaluate the effect of a single dose of amphetamine on recovery of motor function using the Fugl-Meyer scale. Four patients received amphetamine; the rest were given placebo. All underwent a session of physical therapy. Patients treated with amphetamine obtained greater increments in motor scores than the controls. Along with animal studies, these findings may allow the development of a pharmacological approach to stroke rehabilitation.

Species differences in the distribution of beta-adrenergic receptors in the hippocampal and retrohippocampal regions of rats and guinea pigs were examined using in vitro autoradiographic techniques. beta 1-receptors were found in the hippocampal area CA1 of both species, although guinea pigs had significantly lower receptor densities in comparison to rats. In guinea pigs, beta 2-adrenergic receptors were predominant in hippocampal area CA1. Hippocampal area CA3 had very low levels of beta 1- and beta 2-receptors in both species. The retrohippocampal area was also found to have a distinct topographic distribution of beta-receptors. In rats, the subiculum and parasubiculum (layers II-III) were heavily labeled for beta 1-receptors; in contrast, guinea pigs had few receptors in these regions. beta 2-receptors were particularly prominent in the parasubicular region in rats. The entorhinal cortex laminae was found to contain beta-receptors in both rats and guinea pigs. Immunohistochemical techniques were used to compare the pattern of catecholaminergic innervation with the receptor distribution within each hippocampal subregion. Despite the general lack of beta-receptors in area CA3, abundant catecholamine immunoreactive fibers were observed in CA3 of rat and guinea pig hippocampus. Significant species differences were found in the distribution of hippocampal beta-adrenergic receptor subtypes, and moreover, in both species the distribution of beta-adrenergic receptors did not coincide with the pattern of hippocampal adrenergic innervation.

A patient who sustained closed head injury demonstrated brachial diplegia and intact leg strength, a case of man-in-the-barrel syndrome. Extensive hemorrhagic contusion was seen in the inferior frontal lobes bilaterally. Although aptly descriptive, the syndrome is neither predictive of an exact anatomical substrate nor representative of a specific etiology.

Proton nuclear magnetic resonance spectroscopy is a unique method to monitor noninvasively the concentrations of cerebral metabolites. JV-Acetyl-L-aspartate, the concentration of which is assumed to be stable during hypoxia, has been used to form ratios with lactate. To determine the stability of the signal from iV-acetyl-L-aspartate, we used a model of graded hypoxia in rats to monitor the percentage changes from baseline of the peak heights for lactate, lipids, and A'-acetyl-L-aspartate. Anesthetized adult rats were exposed sequentially to 15% and 10% O 2 while proton nuclear magnetic resonance spectra were collected with a surface coil in a 7-T 89-mm-bore spectrometer. Brain lactate concentration was either increased by feeding or infusion of glucose (n=9) or lowered by fasting (n=7). After death the brains were removed and frozen, and the water-and lipid-solublc compounds were extracted to identify the origin of the signals. We analyzed the data both as the percentage change from baseline for heights of the lactate (1.33 ppm), lipids (1.5 ppm), and iV-acetyl-L-aspartate (2.02 ppm) peaks and as the ratios of heights of the 1.33 and 2.02 and the 1.5 and 2.02 ppm peaks. Both hypoxic episodes caused a 45% decrease from baseline in the 2.02 ppm peak. During the second hypoxic episode, the 1.33:2.02 ppm peak height ratio increased significantly in hyperglycemic rats (p<0.05) but was unchanged in hypoglycemic rats. However, the 1.5:2.02 ppm peak height ratio increased during the second hypoxic episode in both hyperglycemic and hypoglycemic rats (/7<0.05). We conclude that the 2.02 ppm peak is unstable and that it contains signals from compounds that are affected by hypoxia in addition to N-acetyl-L-aspartate. (Stroke 1991^2:73-79)