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PubMed1975

Allometry in primates, with emphasis on scaling and the evolution of the brain.

Allometry should be defined broadly as the study of size and its consequences, not narrowly as the application of power functions to the data of growth. Variation in size may be ontogenetic, static or phyletic. Errors of omission and treatment have plagued the study of allometry in primates. Standard texts often treat brain size as an independent measure, ignoring its allometric relation with body size - on this basis, gracile australopithecines have been accorded the mental status of gorillas. Intrinsic allometries of the brain/body are likewise neglected: many authors cite cerebral folding as evidence of man's mental superiority, but folding is a mechanical correlate of brain size itself. Confusion among types of scaling heads errors of treatment in both historical primacy [Dubois' ontogenetic inferences from interspecific curves] and current frequency. The predicted parameters of brain-body plots differ greatly for ontogenetic, intrapopulational, interspecific and phyletic allometries. I then discuss basic trends in bivariate allometry at the ordinal level for internal organ weights, skeletal dimensions, lifespan and fetal weight. In considering the causes of basic bivariate allometries, I examine the reason for differences among types of scaling in brain-body relationships. The interspecific exponent of 0.66 strongly suggests a relationship to body surfaces, but we have no satisfactory explanation for why this should be so. The tripartite ontogenetic plot is a consequence of patterns in neuronal differentiation. We do not know why intraspecific exponents fall between 0.2 and 0.4; several partial explanations have been offered. Multivariate techniques have transcended the pictorial representation of transformed coordinates and offer new, powerful approaches to total allometric patterns. Allometry is most often used as a 'criterion for subtraction'. In order to assess the nature and purpose of an adaptation, we must be able to identify and isolate the aspect of its form that depends both upon its size and the size of the body within which it resides. Cranial indices and limb lengths are misinterpreted when authors apply no correction for body size. The search for a criterion of subtraction has been most diligently pursued in studies of the brain. Clearly, brain size must be assessed by comparison with a 'standard' animal of the same body size. But how shall size be measured, especially in fossils; and how shall a standard animal be construed. I discuss and criticize three methods recently used: RADINSKY'S foramen magnum criterion; Jerison's minimum convex polygons and cephalization quotients; and the indices of progression in comparison with 'basal' insectivores' of BAUCHOT, Stephan and their colleagues.

Animals↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. III. Light and electron microscopic findings in the rat caudoputamen.

The caudate nucleus and putamen belong to the selectively vulnerable brain regions which incur neuronal damage in clinical and experimental settings of both hypoglycemia and ischemia. We have previously documented the density and distribution of the hypoglycemic damage in rat caudoputamen, but the evolution of the injury, i.e., the sequence of structural changes, has not been assessed. Therefore, in the present study we analyze the light and electron microscopic alterations in the caudoputamen of rats exposed to standardized, pure insults of severe hypoglycemia with isoelectric EEG for 10-60 min, or in rats which, following insults of 30 or 60 min, were allowed to recover for periods from 5 min to 6 months. The hypoglycemic insult produced severe nerve cell injury in the dorsolateral caudoputamen. Immediately after the insult abnormal light neurons with clearing of the peripheral cytoplasm were present. These cells disappeared early in the recovery period, as they do in the cerebral cortex. Dark neurons were also present, but unlike those in the cerebral cortex they did not appear until recovery was instituted. Their number increased for a couple of hours and they became acidophilic within 4-6 h. At this stage, electron microscopy revealed severe clumping of the nuclear chromatin and cytoplasm as well as incipient fragmentation of cell membranes, all these changes indicating an irreversible injury. Within 24 h flocculent densities appeared in the mitochondria and by day 2-3 of recovery the great majority of the medium-sized neurons had undergone karyorrhexis and cytorrhexis, their remnants being subsequently removed by macrophages. After some weeks only large and a few medium-sized neurons remained amidst reactive astrocytes and numerous macrophages. The delay in the appearance of dark, lethally injured medium-sized neurons until the recovery was instituted suggests an effect that does not become apparent until the substrate supply and energy production are restored. Furthermore, it points out again the selectivity of the hypoglycemic nerve cell injury with respect to the type (metabolic characteristics?) and topographic location of the neurons.

Animals↗
PubMed1995

Relationship between diffusion-weighted MR images, cerebral blood flow, and energy state in experimental brain infarction.

The regional evolution of brain infarction was studied in Wistar rats submitted to remotely controlled thread occlusion of the middle cerebral artery. Occlusion was performed in the magnet of an NMR tomography system to allow continuous recording of diffusion-weighted images. After 30 min (n = 6) or 2 h (n = 9), cerebral blood flow was measured by [14C] iodoantipyrine autoradiography while the regional distribution of ATP, glucose, lactate, and pH was imaged using pictorial bioluminescence and fluoroscopic methods. In diffusion-weighted images, the hemispheric lesion area (HLA) at the level of caudate-putamen amounted to 54.2 +/- 10.9% after 30 min and to 67.0 +/- 5.9% after 2 h vascular occlusion. These areas corresponded to the regions exhibiting tissue acidosis (60.8 +/- 9.3% and 70.4 +/- 4.5%), but were clearly larger than those in which ATP was depleted (22.3 +/- 20.8% and 49.6 +/- 12.9% after 30 min and 2 h, respectively). The threshold of blood flow for the increase of signal intensity in diffusion-weighted images increased between 30 min and 2 h occlusion from 34 to 41 ml/100 g per minute, the threshold of acidosis from 40 to 47 ml/100 g per minute, and the threshold for ATP depletion from 13 to 19 ml/100 g per minute. Our study demonstrates that diffusion-weighted imaging detects both the core and the penumbra of the evolving infarction but is not able to differentiate between the two parts. It further shows that the ischemic lesion grows during the initial 2 h of vascular occlusion, and that the size of the infarct core increases more rapidly than that of the penumbra.

Adenosine Triphosphate↗
PubMed1976

Newborn: adult brain ratios in hominid evolution.

The ratio of newborn to adult brain size varies widely in primates. These variations provide an index of the different degrees of postnatal brain growth in the different members of the primate order. The uniquely low figure for Homo sapiens indicates a greater degree of postnatal brain growth and therefore postnatal dependence and also a greater need and opportunity for social organisation. An attempt is made to determine the newborn adult brain ratio in a proto-human population, Australopithecus africanus. Two possible causes of the reduction of the ratio in hominid evolution are discussed. The first is the limiting confines of the maternal pelvis adapted primarily for orthograde progression rather than parturition. The second concerns the resultant of a set of three paired variables between the members of each pair of which there exists an allometric relationship. These are the relation between brain and body size in the adult, feto-maternal weight allometry and the relation between newborn brain-size and birth weight.

Adult↗
PubMed1991

A progressive deposition of paired helical filaments (PHF) in the brain characterizes the evolution of dementia in Alzheimer's disease. An immunocytochemical study with a monoclonal antibody against the PHF core.

Using the monoclonal antibody (mAb) 6.423 which recognizes epitopes of the pronase-resistant core of paired helical filaments (PHF), we studied postmortem frontal cortex from Alzheimer's disease (AD) patients with short (Group II) and long (Group III) histories of clinical dementia. Four cases with clinically unconfirmed dementia and a postmortem diagnosis of AD (Group I) were also studied. In Group I, the 6,423 mAb was negative whereas in Group II, the antibody recognized primarily neurofibrillary tangles (NFT). In contrast, brains in Group III contained a dense network of 6,423-immunoreactive (IR) thread-like structures ("ghost" neurites) and plaque-like structures with granular appearance, in addition to NFT. The number of 6,423-IR structures appeared to be related to the duration of clinical dementia and the age of onset. Furthermore, "ghost" neurites were more abundant in young AD cases. The possible significance of the 6,423-IR pattern in the pathogenesis of AD is discussed.

Adult↗
PubMed1981

Postischemic hypervascularity of infancy: a stage in the evolution of ischemic brain damage with characteristic CT scan.

One to 2 weeks after severe brain ischemia, four infants developed an unusual vascular lesion with a characteristic appearance on computed tomography that has not been reported previously. Restricted areas (most frequently the basal ganglia and thalamus) displayed increased attenuation, which enhanced further upon infusion of contrast medium. Autopsy of one infant revealed that the CT abnormality corresponded to an extremely dense neovascular network which had almost completely replaced the parenchyma in that region. We postulate that this pathological change is a stage in the organization of ischemic brain damage reflecting the infant's vascular plasticity. Thus, hypoxia induces marked capillary proliferation in regions of normally high metabolism and capillary density. The CT pattern may prove useful in predicting the location and extent of sequelae to perinatal asphyxia.

Asphyxia Neonatorum↗
PubMed1995

Mechanisms and evolution of the brain damage in neonatal post-hemorrhagic hydrocephalus.

There are three main mechanisms of poor outcome in children with post-hemorrhagic hydrocephalus: (1) brain injuries due to ventricular dilatation, (2) shunt-related complications, and (3) primary cerebral hypoxic-ischemic and hemorrhagic lesions. The authors give a short up-to-date report, focusing mainly on the third mechanism, with reference to personal studies.

Brain Injuries↗
PubMed1985

The temporal evolution of hypoglycemic brain damage. I. Light- and electron-microscopic findings in the rat cerebral cortex.

In the course of a study on the pathogenesis of neuronal necrosis in severe hypoglycemia, the morphological characteristics reflecting reversible and irreversible neuronal lesions were examined as a function of time following normalization of blood glucose. To that end, closely spaced time intervals were studied in the rat cerebral cortex before, during, and up to 1 year after standardized pure hypoglycemic insults of 30 and 60 min of cerebral isoelectricity. Both the superficial and deep layers of the cerebral cortex showed dark and light neurons during and several hours after the insult. By electron microscopy (EM) the dark neurons were characterized by marked condensation of both karyoplasm and cytoplasm, with discernible, tightly packed cytoplasmic organelles. The light neurons displayed clustering of normal organelles around the nucleus with clearing of the peripheral cytoplasm. Some cells, both dark neurons and neurons of normal electron density, contained swollen mitochondria with fractured cristae. Light neurons disappeared from the cerebral cortex by 4 h of recovery. Some dark neurons in the superficial cortex and almost all in the deep cortex evolved through transitional forms into normal neurons by 6 h recovery. Another portion of the dark neurons in the superficial cortex became acidophilic between 4 and 12 h, and by EM they demonstrated karyorrhexis with stippled electron-dense chromatin. The plasma membrane was disrupted, the cytoplasm was composed of amorphous granular debris, and the mitochondria contained flocculent densities. These definitive indices of irreversible neuronal damage were seen as early as 4-8 h recovery. Subsequently, the acidophilic neurons were removed from the tissue, and gliosis ensued. Thus, even markedly hyperchromatic "dark" neurons are compatible with survival of the cell, as are neurons with conspicuous mitochondrial swelling. Definite nerve cell death is verified as the appearance of acidophilic neurons at which stage extensive damage to mitochondria is already seen in the form of flocculent densities, and cell membranes are ruptured. Our previous results have shown that hypoglycemic neocortical damage affects the superficial laminae, chiefly layer 2. The present results demonstrate that, following the primary insult, this damage evolves relatively rapidly within the first 4-12 h. We have obtained no evidence that additional necrotic neurons are recruited after longer recovery periods.

Animals↗
PubMed1982

The evolution of a brain abscess the complementary roles of radionuclide (RN) and computed tomography (CT) scans.

Serial Tc-99m glucoheptonate brain scans demonstrated a brain abscess in a patient from the earliest phase of acute focal encephalitis (cerebritis) through the capsule formation and the recovery phase. The role of the RN and CT scans in the diagnosis of the early stage of cerebritis and the complementary nature of RN and CT scans in intracranial infections, particularly abscesses, are discussed. Guidelines for the use of RN and CT scans are suggested.

Brain Abscess↗
PubMed1984

Experimental anaerobic brain abscess. Computerized tomographic and neuropathological correlations.

The neuropathological progression of brain abscess formation induced by a mixed anaerobic culture of Bacteroides fragilis and Staphylococcus epidermidis was studied experimentally in dogs. Histological findings were correlated with computerized tomographic (CT) brain scans. The evolution of brain abscess formation could be divided into three stages based on histological criteria: early cerebritis (Days 1 to 3); late cerebritis (Days 4 to 9); and capsule formation (Day 10 and later). Capsule formation could not be divided into early and late stages because encapsulation was delayed compared with a previously reported model of alpha-Streptococcus brain abscess. Histologically, there was evidence for a very virulent infection. Leptomeningitis was significant even in the late stages. Early ventricular rupture occurred in 25% of the animals. A pattern of extensive purulent encephalitis was seen in 25% of the animals. In the early cerebritis stage, blood vessels near the necrotic center were engorged and were surrounded by hemorrhage and/or protein-rich fluid. Cerebral edema was extensive. Although fibroblasts appeared in late cerebritis, there was marked delay of capsule formation. Three-week-old lesions still had areas of incomplete capsule formation and foci of uncontrolled infection. In the cerebritis stages, CT scans showed an area of ring enhancement which was incomplete on early scans (at 5 minutes after injection of contrast material) but partially filled in and thickened on delayed scans (at 20 to 45 minutes). On even later delayed scans there was no decrease in intensity of ring enhancement. Lesions in which capsule formation occurred also showed ring enhancement, but delayed scans showed a decrease in the intensity of enhancement. The lesions that ruptured into the ventricular system showed atypical CT findings, with either lack of contrast enhancement (histologically there was minimal cerebritis adjacent to the abscess cavity) or a marked delay in contrast enhancement (cerebritis was more extensive and corresponded to the width of ring of enhancement). This study suggests that Bacteroides fragilis is a virulent organism in the brain. The developing abscesses enlarged quickly, were prone to early ventricular rupture, and showed incomplete and delayed encapsulation.

Animals↗