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At least 19 recordsLinked to original sources
PubMed1979

Lipoma of the corpus callosum.

A case of corpus callosum lipoma with presumptive diagnosis is presented. Review of the literature disclosed 84 cases with such diagnoses. Lipoma of the corpus callosum is a rare intracranial lesion, perhaps congenital and often asymptomatic, but can present with seizure disorder, headache, mental changes, paresis or paralysis. Twenty-one patients had been operated upon. Surgical treatment seems to be of no value in this disease.

Adolescent↗
PubMed1978

Agenesis of corpus callosum in calves.

Agenesis of the corpus callosum is a rare brain defect in cattle, and was described in two calves. It was characterized by the total absence of the corpus callosum, septum pellucidum and hippocampal commissure. Fornices were present but separated. Both calves also had moderate internal hydrocephalus, micrencephaly and a CSF-filled cyst in the longitudinal fissure dorsal to the thalamus. Clinical signs were not specific. Etiology and pathogenesis are unknown. No evidence of inflammation or inheritance was found as cause of the defect.

Agenesis of Corpus Callosum↗
PubMed1979

Traumatic lesions of the corpus callosum.

We investigated the mechanism of damage to the corpus callosum in a study of 46 brains obtained at the autopsies of patients with head injuries. After correlating the gross findings with the site of impact on the head, we think that such lesions in the corpus callosum are caused by stretching of callosal fibers and/or shearing forces in cases in which lateral movement or twisting of the brain occurs. This mechanism of the dynamic development of callosal injuries is also supported by the retraction bulb formation of axons found histologically in the corpus callosum.

Axons↗
PubMed1979

Importance of corpus callosum for visual receptive fields of single neurons in cat superior colliculus.

1. Section of the posterior two-thirds of the corpus callosum eliminates almost completely the response of superior colliculus (SC) neurons to stimulation of the contralateral eye in split-chiasm cats. On the contrary, the responsiveness of SC neurons to stimulation of the contralateral eye is not abolished by a transection of the posterior and tectal commissures leaving the corpus callosum intact. The callosal section also reduces the number of SC receptive fields abutting the vertical meridian in the ipsilateral eye of split-chiasm cats. 2. In cats with intact optic pathways, a similar callosal section abolishes the SC representation of the ipsilateral visual field in the ipsilateral eye and also reduces the number of receptive fields adjoining the vertical meridian in the same eye. In the contralateral eye, the SC representation of the ipsilateral visual field is reduced in extension to about one-fifth of that seen in cats with intact commissures. 3. The results suggest that the corpus callosum is the main pathway for cross-midline communication of visual information at not only the cortical, but also the midbrain level. The corpus callosum may subserve this function because it contains uninterrupted crossed corticotectal projections or because it transmits visual information from one hemisphere to contralateral cortical areas projecting ipsilaterally to SC. The latter hypothesis is more likely but, in any case, the findings imply that the lack of interhemispheric transfer of visual learning in cats with a chiasmatic and callosal section may depend on a midline disconnection of both subcortical and cortical visual centers. 4. The corpus callosum is also responsible for the representation of the ipsilateral visual field of the ipsilateral eye in the cat SC. The SC representation of the ipsilateral visual field in the contralateral eye is due, in minimal part, to direct retinotectal connections from temporal retina and, for the largest part, to the corpus callosum. 5. Finally, the corpus callosum contributes to the representation of the contralateral visual field near the vertical meridian of the temporal retina in both split-chiasm and normal cats. This is probably due to the scarcity of direct retinotectal projections from this part of the retina and to their supplementation by corticotectal neurons influenced by the callosal afferents.

Animals↗
PubMed1978

Radioautographic investigation of gliogenesis in the corpus callosum of young rats. II. Origin of microglial cells.

Microglial cells are absent from the corpus callosum of newborn rats. In the hope of finding out when and how microglial cells appear with age, 3H-thymidine was given intraperitoneally as single or three shortly spaced injections to 5-day-old rats weighing about 15 g; and these animals were sacrificed at various time intervals from 2 hours to 35 days later. Pieces of corpus callosum were taken near the superior lateral angle of the lateral ventricles; and semithin sections were radioautographed and stained with toluidine blue. The corpus callosum of 5-day-old rats is composed of loosely arranged unmyelinated fibers and scattered cells. Among these cells, microglia are rare; there are a few astrocytes, many immature glial cells, rare pericytes, and 6--7% of phagocytic "ameboid cells" consisting of a few monocytes and many macrophages. In the animals sacrificed two hours after 3H-thymidine administration, label is present only in immature cells and "ameboid cells." As time elapses and the fibers of corpus callosum become myelinated, oligodendrocytes and, later, microglial cells appear. At the age of 12 days, microglial cells are present in substantial number; and by 19 days, the number doubles to reach a plateau. Many of the new microglial cells are labeled, e.g., 78.1% in 12-day-old animals (7 days after 3H-thymidine administration). The labeled microglial cells must have come from the transformation of cells that acquired label early, that is, from the immature cells or the "ameboid cells." The height of the peaks of labeling--59.8% at nine days for immature cells and 77.8% at 12 days for "ameboid cells"--points to the latter as precursors of the highly labeled microglial cells. Furthermore, the "ameboid cells" disappear as microglial cells appear and there are transitional elements between these two cell types. Cell counts suggest that about a third of the "ameboid cells" transform into microglial cells, while the others degenerate and die. Thus, the microglial cells which appear in the corpus callosum during the first three weeks of life result from transformation of the "ameboid cells"--a group of macrophages showing various stages of transition from monocytes. As for the occasional microglial cell appearing after the third week or in the adult, they presumably come directly from monocytes. In either case, monocytes would be the initial precursors.

Aging↗
PubMed1978

Structure and ultrastructure of cultivated glial cells from Corpus callosum.

1. Explants and dissociated cells from Corpus callosum (c. c.) of rats and rabbits were cultivated in Petri dishes and Rose chambers. 2. Different types of glial cells were found in the cultivated Corpus callosum (c. c.) explanted from 12 days old rats: a) adendritic glial cells, typical for migrating oligodendroglial cells, b)-migrating large, nondifferentiated astrocytes with pronounced phagocytosing activity, c) macro- and microglial cells which differentiated during cultivation. 3. The population of differentiated glial cells is mostly composed of oligodendroglia, less of astrocytes and microglial cells are rare. 4. Differentiation of dissociated cells from c. c. in homogenous and mixed population was studied. The appearance of first processes of macroglial cells is postponed to 6 to 10 days of cultivation. No substantial difference was observed between homogenous and mixed population. A higher incidence of macrophages was observed in the later. 5. Glial cells differentiate surrounded by degenerated nerve fibers and myelin, exhibiting phagocytoses and cleaning reaction.

Animals↗
PubMed1978

Radioautographic investigation of gliogenesis in the corpus callosum of young rats. I. Sequential changes in oligodendrocytes.

The corpus callosum of young rats was examined to clarify the behavior of the three subtypes of oligodendrocytes (the large organelle-rich "light oligodendrocytes," the smaller and more densely stained cells referred to as "medium oligodendrocytes," and the even smaller and denser "dark oligodendrocytes"). It was hoped to find out whether cells of the three subtypes undergo division and how they are related to one another. 3H-thymidine was given intraperitoneally as single or three shortly spaced injections to a first group of 19- to 20-day old rats weighing about 40 g, and to a second group of 25-day old rats weighing about 80 g. The animals were sacrificed at various time intervals from 2 hours to 35 days after 3H-thymidine administration. Pieces of corpus callosum were taken near the superior lateral angle of the lateral ventricles; and semithin sections were radioautographed and stained with toluidine blue. Two hours after 3H-thymidine injection, label is virtually absent from light, medium and dark oligodendrocytes, from microglia, and probably from astrocytes, but is present in about 10% of the immature glial cells, which include the poorly differentiated glioblasts and the partially differentiated oligodendroblasts and astroblasts. Hence, the cells undergoing DNA synthesis and mitosis in the corpus callosum are these three types of immature cells. During the week that follow the administration of 3H-thymidine, label appears in oligodendrocytes and astrocytes, which presumably have arisen from the initially labeled immature cells. The oligodendrocytes acquire label in a sequential manner: the light cells show label first and their labeling index reaches a peak at the seven-day interval; the medium oligodendrocytes become labeled next with a labeling peak toward the 14- and 21-day intervals and, finally, the dark oligodendrocytes with a peak around the 28-day interval. Analysis by the method of Zilversmit et al. ('42-'43) provides precise details on the sequence: immature cells presumed to be oligodendroblasts give rise to light oligodendrocytes which, after four to seven days, transform into medium oligodendrocytes which, after another 11 to 18 days, transform into dark oligodendrocytes. The dark cells may persist indefinitely or turn over at a very slow rate. It is concluded that oligodendrocytes arise from the last division of oligodendroblasts and develop in three main periods: a light stage lasting less than a week, a medium stage lasting about two weeks, and a very long lasting dark stage.

Animals↗
PubMed1979

Lysophosphatidyl choline-induced focal demyelination in the rabbit corpus callosum. Light-microscopic observations.

The local application of lysophosphatidyl choline (LPC) by microinjection into the region of the corpus callosum of the rabbit produced demyelinating lesions. The lesions were assessed histologically using the Luxol fast blue myelin stain and the Holmes silver nitrate stain for the axis cylinders. Survival times for the animals ranged from 7 to 14 days. The center of the lesion was marked by infiltration of macrophages and necrosis, but the major area of the lesion was characterized by demyelination. By consideration of anatomical factors influencing LPC diffusion and of the appropriate placement of the injection, the entire vertical extent (about 0.5 mm) of the corpus callosum could be demyelinated with minimal amounts of necrosis. Since focal demyelination was possible in the fine caliber axons of the corpus callosum which are anatomically representative of many forebrain fiber systems, and since this fiber system is amenable to chronic physiological investigation, the corpus callosum may serve as an experimental model for morpho-physiological studies of mammalian central demyelinating pathways.

Animals↗
PubMed1979

The effect of dibutyryl cyclic AMP on cultivated glial cells from corpus callosum of 30-day-old rats.

1) Fragments of corpus callosum of 30-day-old rats were cultivated in Rose chambers. Mature astrocytes and predominantly differentiated oligodendroglial cells are present in the corpus callosum of rats at this age. 2) In vitro, astrocytes dedifferentiated into epithelial--like flattened cells, which highly adhered to the surface. Cells exhibited signs of phagocytosis, and their ultrastructure differed from differentiated cells, especially by the absence of microtubules and microfilaments. 3) After dibutyryl cyclic AMP (db-c-AMP) application, epithelial--like cells became rounded and multipolar. Cells were less liable to adhere to the surface. Bundles of microfilaments and microtubules appeared in cell perikarya and their processes. 3--4 hour after application, the morphological changes were well developed and disappeared after 24--48 hours. 4) It is being suggested that the increased intracellular concentration of db-c-AMP induced the formation of microfilamentous structures. The formation of the cyto-skeleton has a direct influence on the shape of cells and appearance of processes and cell adhesivity. 5) These results have demonstrated the high structural plasticity of mature astrocytes, their dedifferentiation in vitro and convertion into mature cells after db-c-AMP application.

Animals↗
PubMed1975

[Tumours of the corpus callosum in the anglogram (author's transl)].

On account of the median location of tumours of the corpus callosum, serial angiography reveals displacements only at an advanced stage. In many cases there is no lateral displacement of the anterior cerebral artery and a lateral angiogram of the pericallosal artery does not reveal tumours of the corpus callosum, especially if they are associated with a vascular pattern characteristic of arteriosclerosis or hydrocephalus. The deep mid-line veins are not consistently displaced. A differentiation of the vascular pattern associated with small tumours of the corpus callosum from normal variations may be problematic. The inner veins cannot be visualised sometimes on account of increased intracranial pressure and a slowing of the circulation.

Astrocytoma↗
PubMed1979

Transformation of monocytes into amoeboid microglia in the corpus callosum of postnatal rats, as shown by labelling monocytes by carbon particles.

Two successive intravenous doses of carbon suspension were given at 24 hourly intervals into six days old rats. These animals were killed at intervals ranging from 1 to 9 days after the second injection. The corpus callosum and neighbouring structures were examined for cells containing ingested colloidal carbon particles in their cytoplasm. Twenty four hours after the second injection, a variable number of carbon-labelled monocytes were adherent to the luminal wall of blood vessels in the corpus callosum. Numerous carbon-labelled cells appeared to have left the lumen and entered the brain tissue surrounding the vessels. These perivascular carbon-labelled monocytes in the neuropil displayed a large pale nucleus with fine chromatin granules. The phagocytic amoeboid microglia in the corpus callosum were unlabelled at first, although a few cells of a similar nature in the cavum septi pellucidi did show carbon particles in their cytoplasm. Four or five days after the second carbon injection perivascular carbon-labelled monocytes were rare, but carbon particles were now present in the amoeboid microglia. At 8 days amoeboid microglia were virtually absent from the corpus callosum but carbon particles now appeared in cells which closely resembled microglia (flattened nucleus, coarse chromatin, scanty cytoplasm at one pole). The sequential appearance of carbon particles in monocytes, amoeboid microglia, and microglia, suggests that monocytes transform into microglia by way of an amoeboid microglial stage.

Aging↗
PubMed1979

[Abnormal corpus callosum and epilepsy--a catamnestic report].

A catamnestic account is given of a case of corpus callosum deficiency. The clinical symptoms and para-clinical findings could not be interpreted with the syndrome. A short reference is made to the importance of the corpus callosum deficiency.

Agenesis of Corpus Callosum↗