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PubMed1998

[An autopsied case of multiple system atrophy with remarkable cerebral atrophy].

In this paper, we report the pathological findings of a multiple system atrophy (MSA) patient with remarkable frontal lobe atrophy. The patient was a 65-year-old woman with a 13-year history of untreatable parkinsonism, dysautonomia and progressive motor aphasia. The cranial imaging study disclosed progressive atrophy of the frontal lobe, striatum and pontocerebellar system. She died of pneumonia. The brain weight was 810 g, and there was remarkable atrophy of the cerebrum predominantly in the frontal lobe, striatum, pons and cerebellum. The microscopic examination revealed a preserved cortical structure with laminar gliosis in the sixth layer of the precentral and superior frontal gyri of the frontal lobe, and postcentral gyrus and inferior parietal lobule of the parietal lobe. The cortices of these regions also revealed to be in a spongy state in the second layer, and mild cell loss was seen in the fifth and six layers. The frontal lobe white matter showed a slight pallor, a mild loss of myelinated fiber and axon, and mild gliosis. Glial cytoplasmic inclusions (GCIs) were abundantly observed in the deep layer of the cortex in the regions mentioned above, and were more abundant in the white matter of the frontal and parietal lobes, callosal body, and internal, external and extreme capsules. There were severe degenerations in the olivopontocerebellar and striatonigral systems, and GCIs in widespread regions of the brain. We could not detect any Pick bodies, Lewy bodies, ballooned neurons, senile plaques, or any significant amounts of neurofibrillary tangles. There were no vascular changes. Thus, this was a verified MSA patient with progressive aphasia and remarkable frontal lobe atrophy. We indicate a possible involvement of the cerebral lobes in MSA.

Aged↗

PubMed1975

A golgi study of the optic tectum of the tegu lizard, Tupinambis nigropunctatus.

The dendritic patterns of cells in the optic tectum of the tegu lizard, Tupinambis nigropunctatus, were analyzed with the Ramon-Moliner modification of the Golgi-Cox technique. Cell types were compared with those described by other authors in the tectum of other reptiles; particular comparisons of our results were made with the description of cell types in the chameleon (Ramń, 1896), as the latter is the most complete analysis in the literature. The periventricular gray layers 3 and 5 consist primarily of two cell types--piriform or pyramidal shaped cells and horizontal cells. Cells in the medial portion of the tectum, in an area coextensive with the bilateral spinal projection zone, possess dendrites that extend across the midline. The latter cells have either fusiform or pyramidal shaped somas. The central white zone, layer 6, contains fibers, large fusiform or pyramidal shaped cells, fusiform cells, and small horizontal cells. The central gray zone, layer 7, is composed predominately of fusiform cells which have dendrites extending to the superficial optic layers, large polygonal cells, and horizontal cells. The superficial gray and white layers, layers 8-13, contain polygonal, fusiform, stellate, and horizontal elements. Layer 14 is composed solely of afferent optic tract fibers. Several differences in the occurrence and distribution of cell types between the tegu and the other reptiles studied are noted. Additionally, the laminar distribution of retinal, tectotectal, telencephalic, and spinal projections in the tegutectum can be related to the distribution of cell types, and those cells which may be postsynaptic to specific inputs can be identified. The highly differentiated laminar structure of the reptilian optic tectum, both in regard to cell type and to afferent and efferent connections, may serve as a model for studying some functional properties of lamination common to cortical structures.

Animals↗

PubMed1987

Anatomical interpretation of MR scans of the brain.

A stereotactic method of brain localization is applied to magnetic resonance imaging for the interpretation of brain structures. This proportional grid system developed by Talairach is based on two intracerebral structures, the anterior and posterior commissures. It takes into account individual variations in brain size and shape. In an experimental study on cadavers we demonstrated that his system permitted accurate identification of cortical structures on CT scan. In this paper, we describe its application to MR. It provides, on a routine basis, a simple reliable method of anatomical interpretation. The use of this grid system is made easier by the fact that both commissures are seen on midsagittal MR scans.

Brain↗

PubMed1995

Regional distribution of lesions in the central nervous system of cats infected with feline immunodeficiency virus.

Neuropathological examination of the central nervous system of 13 naturally and 13 experimentally feline immunodeficiency virus (FIV)-infected cats revealed diffuse gliosis of gray and white matter and vacuolar myelinopathy in a large proportion of infected animals, sometimes associated with lymphocytic meningitis. Multinucleated giant cell formation, the hallmark of multifocal giant cell encephalitis in HIV infection, was never observed. Morphometric analysis confirmed a marked increase of GFAP reactivity in infected cats. Gliosis was mainly present in cortical structures of frontal, parietal, and occipital lobes. Only one naturally infected animal evidenced clinical symptoms of neurological damage. This study confirms that FIV provides an interesting model for studying HIV-induced cortical and subcortical brain pathology believed to be the cause of the neurological manifestations frequently observed in AIDS patients.

Animals↗

PubMed1997

Familial and developmental abnormalities of front lobe function and neurochemistry in schizophrenia.

structural abnormalities of the cerebral cortex in schizophrenia have been revealed by magnetic resonance imaging, although it is not clear whether these abnormalities are diffuse or local. We predicted that changes in cortical structure would result in abnormalities in biochemical markers for the glutamate system in post-mortem brain, and that the pattern of neurochemical abnormalities would be a clue to the distribution and extent of pathology. A number of studies have now reported increases in biochemical and other markers of glutamatergic cell bodies and terminals in the frontal cortex in schizophrenia. These findings are consistent with the presence of an abnormally abundant glutamatergic innervation, which may be due to an arrest in the normal developmental process of synaptic elimination. In the anterior temporal cortex and hippocampus there is evidence of an asymmetric loss of glutamate terminals, and of reduced GABA function, which may be secondary to the glutamatergic deficit. Glutamate cell body markers are spared in the temporal lobe; we argue that the loss of glutamate uptake sites may reflect the loss of an extrinsic glutamatergic innervation of the polar temporal cortex which arises from the frontal cortex. These fronto-temporal projections may be vulnerable because they arise from a cytoarchitecture which has not been stabilized by remodelling during early post-natal life. There have been several therapeutic studies of drugs with actions on brain glutamate systems. Based on the glutamate deficiency theories, one approach has been to enhance glutamatergic function using agonists of the N-methyl-D-aspartate-linked glycine site. However, there are no clear therapeutic effects, and some studies report aggravation of positive symptoms. This might be expected if, as part of our post-mortem studies suggested, there is excess glutamatergic innervation in some brain regions in schizophrenia. There is neuropsychological evidence that frontal abnormalities in schizophrenia may be genetically determined. We found that first degree relatives of schizophrenic patients were selectively impaired in tests of frontal lobe function, whereas both frontal and temporal function is impaired in patients We conclude that the genetic predisposition to schizophrenia involves impaired frontal lobe function. Psychotic symptoms develop only when a second process results in a loss of fronto-temporal projections and leads to temporal lobe dysfunction.

Antipsychotic Agents↗

PubMed1984

Blockade by frontocortical lesion of reciprocal regulation between the two nigrostriatal dopaminergic pathways.

Tritiated dopamine synthesized from tritiated tyrosine was estimated simultaneously in the two caudate nuclei and the two substantia nigra of cats anaesthesized with halothane. In control animals, the electrical stimulation of the right forelimb enhanced dopamine release in the right caudate nucleus and decreased dopamine release in the right substantia nigra. Opposite effects were observed in the contralateral structures. Left nigral application of d-amphetamine produced the same effect. However in cats with extensive lesions of the left pericruciate cortex, an increase in the release of dopamine in the left substantia nigra was the only detectable effect of these two treatments. These results suggest that the cortical structures are involved not only in the transfer of information between the two dopaminergic pathways but are also involved with regulation of the release of dopamine in the striatum originating in the substantia nigra. With regard to the role of the thalamic structures in this transfer of information, it is proposed that the thalamostriatal control of the release of dopamine previously suggested is closely dependent on cortical activity.

Animals↗

PubMed2001

Intrinsic and extrinsic factors that shape neocortical specification.

Increasing evidence points to the importance of intrinsic molecular cues in specifying the regional identity of mammalian neocortex. Few such cues, however, have been found to be restricted to individual functionally defined cortical areas before the arrival of afferent information. In contrast, thalamocortical axons are specifically targeted to individual cortical areas, raising the possibility that they can instruct some aspects of cortical areal identity. Cortical structure and function can be altered by modifying the source or pattern of activity in thalamocortical afferents. In particular, studies of cross-modal plasticity have shown that in many respects, one sensory cortical area can substitute for another after a switch of input modality during development. Afferent inputs might therefore direct the formation of their own processing circuitry, a possibility that has important implications for brain development, plasticity and evolution.

Animals↗

PubMed2000

Event-related brain potential investigations of memory and aging.

A review of the literature that examines event-related brain potentials (ERPs) and memory with respect to aging reveals some consistency in the processes that might be spared and those that might be compromised with increasing age. By and large, the ERP repetition effect, recorded during indirect memory paradigms, appears to be relatively intact with aging, suggesting spared repetition priming mechanisms and the brain substrates upon which they depend. Some age-related findings during direct (i.e. explicit) memory testing suggest that a left-sided posterior old/new effect ( approximately 500-800 ms), thought to reflect a relatively automatic retrieval of item information, is equivalent in young and old. A later, long-duration, right-sided, prefrontal old/new effect, allied with the search for and/or the retrieval of contextual information (i.e. source memory), has been found to be smaller or absent in the waveforms of the old in two of three studies, suggesting impaired source memory mechanisms in the elderly. It is argued that the data are relatively consistent with spared item retrieval mechanisms in the elderly presumably supported by medial temporal lobe structures. However, although the data are suggestive, there are too few studies at this time to reach a firm conclusion as to whether the mechanisms that support contextual retrieval, presumably mediated by prefrontal cortical structures, are impaired in the elderly.

Adult↗

PubMed1992

The reeler gene: a clue to brain development and evolution.

Reeler mutant mice are characterized by profuse anomalies of cell positioning in the telencephalic and cerebellar cortices as well as by distinct malformations in non-cortical structures such as the inferior olive, the facial nerve nucleus and other brainstem nuclei. Studies of the embryonic development of these structures reveal that the early cell patterns formed by reeler neurons is consistently affected, so that the reeler gene plays an important role in the development of nerve cell patterns. Comparative studies of cortical development in reptiles suggest further that the mammalian type of cortical architectonics has been acquired progressively during brain evolution, and reveal some similarities in early cortical organization between reeler and reptilian, particularly chelonian, embryos, most notably the presence of an inverted gradient of cortical histogenesis. These observations point to a possible role of the reeler gene in cortical evolution. Although the factors responsible for the formation of neural cell patterns are largely unknown, most data point to the importance of cell-cell interactions. Cell-interaction molecules have probably been acquired during brain evolution and the reeler gene could act by perturbing, directly or indirectly, such cell interactions. The characterization and thus the cloning of the reeler gene is therefore important for our understanding of brain development. Recent data on the fine chromosomal mapping of the mutation prior to its positional cloning are reported.

Animals↗

PubMed2000

[Positron emission tomography in diagnosis and prognosis of postanoxic cerebral dysfunctions].

Clinical signs, laboratory tests, EEG or evoked potentials only permit an indirect estimation of the extent of structural brain damage following severe global brain anoxia. Positron emission tomography (PET) permits additional insights into the extent of neuronal damage in acute and persistent postanoxic vegetative states (VS). PET documents a severe and irreversible damage of supratentorial cortical structures in postanoxic VS and allows its differential diagnosis from related disorders, e.g. the locked-in-syndrome. PET clearly distinguishes functional alterations in VS from those in non-REM sleep and documents that patients in VS are not in a sleep-like condition, but in a state closely related to deep anesthesia. Furthermore, the extent of impairment of the residual cortical glucose consumption yields information concerning the possible recovery of consciousness and neuronal function in VS. In combination with clinical, laboratory and neurophysiological findings, PET may be helpful to establish the individual prognosis in acute VS.

Coma↗

PubMed2005

Real-time dynamics of the F-actin cytoskeleton during secretion from chromaffin cells.

Transmitted light images showed an intricate and dynamic cytoplasmic structural network in cultured bovine chromaffin cells observed under high magnification. These structures were sensitive to chemicals altering F-actin-myosin and colocalised with peripheral F-actin, beta-actin and myosin II. Interestingly, secretagogues induced a Ca2+-dependent, rapid (>10 second) and transitory (60-second cycle) disassembling of these cortical structures. The simultaneous formation of channel-like structures perpendicular to the plasmalemma conducting vesicles to the cell limits and open spaces devoid of F-actin in the cytoplasm were also observed. Vesicles moved using F-actin pathways and avoided diffusion in open, empty zones. These reorganisations representing F-actin transfer from the cortical barrier to the adjacent cytoplasmic area have been also confirmed by studying fluorescence changes in cells expressing GFP-beta-actin. Thus, these data support the function of F-actin-myosin II network acting simultaneously as a barrier and carrier system during secretion, and that transmitted light images could be used as an alternative to fluorescence in the study of cytoskeleton dynamics in neuroendocrine cells.

Actins↗

PubMed1995

Curvilinear reconstruction of 3D magnetic resonance imaging in patients with partial epilepsy: a pilot study.

In an attempt to better delineate the abnormalities associated with focal cortical dysgenesis, we performed curvilinear reformatting of the cortex from 3D magnetic resonance (MR) images. Illustrative patients with partial seizures and conventional orthogonal MRI evaluation show that small regions of cortical thickening suggestive of focal dysplastic lesions may not be recognized. In three such patients the curvilinear reformatting demonstrated two additional focal abnormalities of the cortical gyri and better defined the two focal lesions found on conventional orthogonal MR images. This method promises to be a useful tool in the evaluation of epileptic patients with proven or suspected subtle structure cortical abnormalities, particularly focal neuronal migration disorders where cortical thickening, abnormal gyral pattern, and poor delineation of the gray-white matter transition are the main findings.

Brain Damage, Chronic↗

PubMed1998

Brain abnormality in schizophrenia. A systematic and quantitative review of volumetric magnetic resonance imaging studies.

BACKGROUND: Numerous in vivo brain imaging studies suggest that cerebral structure is abnormal in schizophrenia, but implicate different regions to varying extents. METHOD: We identified published MRI studies in schizophrenia with searches of the computerised literature and key journals. Reports giving the volumes of cortical structures in people with schizophrenia and controls were included. The percentage differences in volumes were calculated and the median taken as a summary measure for each brain region. RESULTS: Forty relevant studies were identified. The median percentage volume differences revealed overall reductions in the whole brain (3%), temporal lobe (6% left, 9.5% right), and the amygdala/ hippocampal complex (6.5%, 5.5%); and increases in the lateral ventricles (44%, 36%), that were greatest in the body and occipital horns. Segmentation studies suggest that grey matter is reduced but that white matter volumes may actually be increased. In men, substantial reductions were also evident in the amygdala and hippocampus, as well as the largest reductions of all in the parahippocampus (14%, 9%). Few studies gave figures for women alone. CONCLUSIONS: Several brain structures in schizophrenia are affected to a greater extent than expected from overall reductions in brain volume. Further studies are required in affected women, and to try to identify clinical and aetiological associations of these findings.

Brain↗

PubMed1999

Multiple system atrophy with remarkable frontal lobe atrophy.

The autopsy findings of a multiple system atrophy (MSA) patient with remarkable frontal lobe atrophy are described. The patient was a 65-year-old woman with a 13-year history of untreatable parkinsonism, dysautonomia and progressive motor aphasia. The brain weight was 810 g, and there was remarkable atrophy of the cerebrum predominantly in the frontal lobe, striatum, pons and cerebellum. Microscopic examination revealed a preserved cortical structure with laminar gliosis in the sixth layer of the precentral and superior frontal gyri of the frontal lobe, and postcentral gyrus and inferior parietal lobule of the parietal lobe. The second layer of the cortices of these regions were also revealed to be in a spongy state, and mild cell loss was seen in the fifth and six layers. The frontal lobe white matter showed a mild loss of myelinated fibers and axons, and mild gliosis. Glial cytoplasmic inclusions (GCIs) were abundantly observed in the deep layer of the cortex in the regions mentioned above, and were more abundant in the white matter of the frontal and parietal lobes, callosal body, and internal, external and extreme capsules. There was severe degeneration in the olivopontocerebellar and striatonigral systems, and GCIs in widespread regions of the brain. No Pick bodies, Lewy bodies, ballooned neurons, senile plaques, or significant amounts of neurofibrillary tangles were detected. There were no vascular changes. Thus, this was a verified MSA patient with progressive aphasia and remarkable frontal lobe atrophy. We indicate a possible involvement of the cerebral lobes in MSA.

Aged↗

PubMed1984

Distribution of immunoreactive beta-neo-endorphin in discrete areas of the rat brain and pituitary gland: comparison with alpha-neo-endorphin.

The distribution of immunoreactive (ir)-beta-neo-endorphin in 101 microdissected rat brain and spinal cord regions as well as in the neurointermediate lobe of pituitary gland was determined using a highly specific radioimmunoassay. The highest concentration of beta-neo-endorphin in brain was found in the median eminence (341.4 fmol/mg of protein). High concentrations of ir-beta-neo-endorphin (greater than 250 fmol/mg of protein) were found in 11 nuclei, including dorsomedial nucleus, substantia nigra, parabrachial nuclei, periaqueductal gray matter, anterior hypothalamic nucleus, and lateral preoptic areas. Moderate concentrations of the peptide (between 100 and 250 fmol/mg of protein) were found in 66 brain nuclei such as the amygdaloid and septal nuclei, most of the diencephalic structures (not including the hypothalamus), and the majority of the medulla oblongata nuclei and others. Low concentrations of ir-beta-neo-endorphin (less than 100 fmol/mg of protein) were found in 21 nuclei, e.g., cortical structures (frontal., cingulate, piriform, parietal, entorhinal, occipital), olfactory tubercle, and cerebellum (nuclei and cortex). The olfactory bulb has the lowest beta-neo-endorphin concentration (21.3 fmol/mg of protein). Spinal cord segments exhibit low peptide concentrations. The neurointermediate lobe of the pituitary gland is extremely rich in ir-beta-neo-endorphin.

Animals↗

PubMed2006

Morphological analysis of the proximal femur using quantitative computed tomography.

The anatomy of the proximal femur was studied in 35 specimens using quantitative computed tomography (QCT) and compared with anatomical sections studied by plane radiography and gross dissection. We found the primary supporting structure of the femoral head to be the primary compressive strut, which is a dense column of trabecular bone projecting from the pressure buttress of the medial femoral neck to the epiphyseal scar. Trabecular bone mushroomed from the epiphyseal scar and terminated at right angles to the cortex of the femoral head. We believe the primary compressive strut is the predominant load-bearing structure connecting the femoral head to the femoral neck, as many specimens lacked continuity of the head cortex to the femoral neck. Based on the CT number, the primary compressive strut had similar bone density to cortical structures such as the lesser trochanter, calcar femorale and posterior lateral femoral cortex. Ward's triangle lacked structural integrity in many cases, and we doubt the significance of tensile trabculae for sharing load. Surgical techniques such as femoral fracture fixation, resurfacing hip arthroplasty and allograft transplantation may benefit from this knowledge.

Adult↗

PubMed1995

Positron emission tomography in spastic diplegia.

In this study, three patients with spastic diplegia were examined with magnetic resonance imaging (MRI) and positron emission tomography (PET), using the steady state technique with 15O. Two of them had untractable seizures and mental retardation. On MRI the cortical structures were normal; increased T2 signals in the periventricular white matter in the second patient were the main findings. PET scan showed in the two patients with a seizure disorder and mental retardation a large left cortical area of decreased regional blood flow and oxygen consumption during the interictal phase. The third patient without epileptic spells had a normal PET scan examination. It is concluded that the epileptic disorder in two of our cases is due to an additional cortical lesion, while the spastic diplegia is caused by subcortical white matter destruction.

Adolescent↗

PubMed2000

The chondrocyte cytoskeleton in mature articular cartilage: structure and distribution of actin, tubulin, and vimentin filaments.

We investigated the structure of the chondrocyte cytoskeleton in intact tissue sections of mature bovine articular cartilage using confocal fluorescence microscopy complemented by protein extraction and immunoblotting analysis. Actin microfilaments were present inside the cell membrane as a predominantly cortical structure. Vimentin and tubulin spanned the cytoplasm from cell to nuclear membrane, the vimentin network appearing finer compared to tubulin. These cytoskeletal structures were present in chondrocytes from all depth zones of the articular cartilage. However, staining intensity varied from zone to zone, usually showing more intense staining for the filament systems at the articular surface compared to the deeper zones. These results obtained on fluorescently labeled sections were also corroborated by protein contents extracted and observed by immunoblotting. The observed cytoskeletal structures are compatible with some of the proposed cellular functions of these systems and support possible microenvironmental regulation of the cytoskeleton, including that due to physical forces from load-bearing, which are known to vary through the depth layers of articular cartilage.

Actins↗