TL;DR: Representation of these cholinergic pathways within a 3D MRI volume helped to identify white matter lesion sites that could interfere with the corticopetal flow of cholinergy pathways.
Abstract: All sectors of the human cerebral cortex receive dense cholinergic input. The origin of this projection is located in the Ch4 cell group of the nucleus basalis of Meynert. However, very little is known about the location of the pathways which link the cholinergic neurons of the nucleus basalis to the human cerebral cortex. This question was addressed in whole-hemisphere sections processed for the visualization of multiple cholinergic markers. Two highly organized and discrete bundles of cholinergic fibres extended from the nucleus basalis to the cerebral cortex and amygdala and were designated as the medial and lateral cholinergic pathways. These bundles contained acetylcholinesterase, choline acetyltransferase and nerve growth factor receptors, confirming their cholinergic nature and origin within the basal forebrain. The medial pathway joined the white matter of the gyrus rectus, curved around the rostrum of the corpus callosum to enter the cingulum and merged with fibres of the lateral pathway within the occipital lobe. It supplied the parolfactory, cingulate, pericingulate and retrosplenial cortices. The lateral pathway was subdivided into a capsular division travelling in the white matter of the external capsule and uncinate fasciculus and a perisylvian division travelling within the claustrum. Branches of the perisylvian division supplied the frontoparietal operculum, insula and superior temporal gyrus. Branches of the capsular division innervated the remaining parts of the frontal, parietal and temporal neocortex. Representation of these cholinergic pathways within a 3D MRI volume helped to identify white matter lesion sites that could interfere with the corticopetal flow of cholinergic pathways.
TL;DR: The delay in serotonin innervation of the suprachiasmatic nucleus, striatum, and middle cortical layers long after the axons have reached these structures suggests that the formation of serotonin axon terminals is dependent on maturation of other elements in local neuronal circuitry.
TL;DR: The ability to stain the cerebral microvessels and demonstrate the finer points of their patterns in sections and microradiographs has enabled us to resolve some long-standing questions about vascular connections and directions.
Abstract: In an ongoing study of brain microvasculature in humans at autopsy, we had the opportunity to analyze the overall scheme of this vascular supply. The native endothelial membrane enzyme, alkaline phosphatase, is used to precipitate black lead sulfide salt in the vessel wall, rendering the brain microvasculature visible by both light microscopy and microradiography. There are six distinct patterns of intraparenchymal afferent blood supply to the supratentorial brain: short arterioles from a single source (e.g., those in the cortex); short- to intermediate-length arterioles, single source (anterior two-thirds of the corpus callosum); short- to intermediate length arterioles and arteries, dual source (subcortical U fibers); intermediate-length arterioles and arteries, triple source (extreme/external capsule and claustrum); long arteries and arterioles, single source (centrum semiovale); and large, long muscular arteries, single source (thalamus and basal ganglia). The nature of this arrangement offers some protection to certain regions of the cerebrum from circulatory challenges such as hypotension, while leaving other areas vulnerable. The distal arterioles supplying two of these protected regions, the U-fiber area and the extreme/external capsule and claustrum area, also exhibit the feature of interdigitation, which can offer additional collateral potential from one arteriolar territory to the next. Aging, hypertension, diabetes mellitus, and atherosclerosis can have a significant impact on brain microcirculation. The way in which vascular patterns dictate the distribution of these effects is discussed. The ability to stain the cerebral microvessels and demonstrate the finer points of their patterns in sections and microradiographs has enabled us to resolve some long-standing questions about vascular connections and directions.(ABSTRACT TRUNCATED AT 250 WORDS)
TL;DR: DTI was able to detect differences in FA between VLBW adolescents and controls in several white matter areas at risk of periventricular leucomalacia in V LBW newborns, indicating that perinatal injury of white matter tracts persist with clinical significance in adolescence.
Abstract: Very low birth weight (VLBW) children are at high risk of perinatal white matter injury, which, when subtle, may not be seen using conventional magnetic resonance imaging. The relationship between clinical findings and fractional anisotropy (FA) measurements in white matter of adolescents born prematurely with VLBW was studied in 34 subjects (age = 15 years, birth weight =1500 g) and 47 age-matched controls born at term, who were examined both clinically and with diffusion tensor imaging (DTI). Perceptual and cognitive functions were evaluated by visual motor integration (VMI) with supplementary tests and sub-tests from WISC-III, motor function by movement ABC and Grooved Pegboard test and psychiatric symptoms by the schedule for affective disorders and schizophrenia for school-age children semistructured interview, the Autism Spectrum Screening Questionnaire and attention deficit hyperactivity disorder (ADHD) rating scale IV. Overall functioning was scored on the children's global assessment scale. DTI scans were performed for calculation of FA maps and areas of significant differences in mean FA values between subjects and controls were compared with their clinical data. The VLBW children had reduced FA values in the internal and external capsule, corpus callosum and superior, middle superior and inferior fasciculus. Within this group of children, visual motor and visual perceptual deficits were associated with low FA values in the external capsule, posterior part of the internal capsule and in the inferior fasciculus. Children with low IQ had low FA values in the external capsule and inferior and middle superior fasciculus. Fine motor impairment was related to low FA values in the internal and external capsule and superior fasciculus. Eight VLBW children with inattention symptoms or a diagnosis of ADHD had significantly lower FA values in several areas. Mild social deficits correlated with reduced FA values in the external capsule and superior fasciculus. We conclude that DTI was able to detect differences in FA between VLBW adolescents and controls in several white matter areas at risk of periventricular leucomalacia in VLBW newborns. Our results show that low FA values in these areas were associated with perceptual, cognitive, motor and mental health impairments. These conclusions indicate that perinatal injury of white matter tracts persist with clinical significance in adolescence.
TL;DR: This study demonstrates that TBSS provides an observer-independent method of identifying white matter abnormalities in the preterm brain at term equivalent age in the absence of focal lesions.