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Biomedical subjects

R L Friede

Publications and source records attributed to R L Friede.

At least 109 records · Page 6Linked to original sources
PubMed1978

Gliofibroma. A peculiar neoplasia of collagen forming glia-like cells.

A tumor of highly unusual composition was found in the lower medulla oblongata of a 3 year, 9 months old girl. Light microscopy of the lesion showed an intimate intermingling of astroglial processes with collagen fibers, both projecting congruent to the pattern of preexisting fiber tracts. Electronmicroscopy disclosed a mosaic formed by the intimate apposition of collagen bundles, of glial processes filled with glial fibrils, and of scattered myelinated fibers, all abutting upon each other, often without intervening basement membranes. This well differentiated mass within the medulla adjoined a dedifferentiated endophytic extension of the tumor into the fourth ventricle which had seeded into the cerebellar cortex and the cauda equina. The dedifferentiated portion of the neoplasm also displayed intimate apposition of collagenous and glial elements. The tumor was tentatively identified as a gliofibroma or a desmo-plastic glioma.

Brain Neoplasms↗
PubMed1978

Uncommon syndromes of cerebellar vermis aplasia. I: Joubert syndrome.

Necropsy findings are reported for a case of Joubert syndrome (familiar aplasia of cerebellar vermis with episodic hyperpnea, abnormal eye-movements, ataxia and retardation). The findings consisted of an almost total aplasia of the cerebellar vermis; dysplasias and numerous heterotopias of cerebellar nuclei; an almost total absence of pyramidal decussation; and anomalies in the structure of the inferior olivary nuclei, the descending trigeminal tract, solitary fascicle and of the dorsal column nuclei. The lesion resembled the Dandy-Walker malformation or simple aplasia of the cerebellar vermis in some of its aspects, but there were numerous others to set it apart--at least tentatively--as a distinct nosologic entity.

Cerebellar Ataxia↗
PubMed1978

Uncommon syndromes of cerebellar vermis aplasia. II: Tecto-cerebellar dysraphia with occipital encephalocele.

Two new cases are reported of a rare syndrome of malformation consisting of occiptal encephalocele, aplasia of the vermis and deformity of the tectum. Less consistent components are aplasia of mammillary bodies, fusion of thalami, anomalies of cerebral gyral patterns, bifid atlas or bifid occipital squame, elevation of torcular, and cervical hydromyelia. One of the present cases had survived to the age of eight years with a ventricular shunt. This syndrome, of which five cases are known, is thought to be a tandem malformation in which either an occipital dysraphia or an encephalocele induces aplasia of the vermis. A classification of aplasias of the cerebellar vermis is proposed.

Brain Stem↗
PubMed1978

Midline hyperplasia with malformation of the fornical system.

A physically and intellectually normally developed boy had a resection of a lumbar myelomeningocele shortly after birth and a shunt was inserted for hydrocephalus. He died at age 12 years after a traffic accident. Autopsy disclosed a hyperplasia of the cerebellar vermis. An abnormal median-sagittal triangular fiber tract ran on the dorsal surface of the corpus callosum and contained more than 3 million fibers, most of them very thin and myelinated. The tract was identified as a hyperplastic fornix dorsalis. The complex malformation was attributed to hyperplasia of midline structures.

Agenesis of Corpus Callosum↗
PubMed1978

The origin of subdural neomembranes. I. Fine structure of the dura-arachnoid interface in man.

A method for the in situ fixation of human meninges for electron microscopic examination is described. It was found that the cranial meninges of humans do not include a subdural space. Instead there is a complex, tight layer of cells, the interface layer, composed in the innermost portion of the dura mater (the dural border cells) and the outermost portion of the arachnoid (the arachnoid barrier layer). The fusion of these components within the interface layer is much more intimate than is either the attachment of the dural border cells to the dura proper or that of the arachnoid barrier layer to the rest of the arachnoid. The fine structural characteristics of these layers are defined. The erroneous macroscopic impression of a subdural space results from an extraordinary lack of cohesion within the dura-arachnoid interface layer conditioned by a) a complete absence of a collagenous reinforcement within this zone, b) the presence of large extracellular cisterns between the dural border cells, and c) a paucity of intercellular contacts within that latter layer. An understanding of the fine structural organization of the interface layer is essential to any consideration of the pathogenesis of subdural lesions: these form within a sheet of torn dural border cells and not within a preexistent tissue compartment.

Arachnoid↗
PubMed1978

The origin ofsubdural neomembranes. II. Fine structural of neomembranes.

A comparison of the fine structure of subdural neomembranes with the fine structural organization of the normal human dura-arachnoid interface discloses that neomembranes are not de novo proliferations of tissue from a smooth inner dural surface. Rather, a neomembrane is the result of proliferation and excessive thickening of the normal layer of dural border cells. On proliferation, the dural border cells form multilayered tiers and clusters of cells, transfixed by capillaries, with collagen fibrils and elastic fibers between them. Capillaries and collagen fibrils are absent from the normal interface layer. Pathogenetic concepts of chronic subdural hematoma need to be revised. Any pathologic condition inducing cleavage of tissue within the dural border layer at dura-arachnoid interface will be followed by proliferation of fural border cells with production of a neomembrane. There is no compelling reason to postulate that proliferation of the border cell layer is always secondary to traumatic hemorrhage.

Arachnoid↗
PubMed1977

Residual lesions of cerebral fat embolism.

Necropsy findings of a case which survived for three months after massive cerebral fat embolism are presented. The lesions are characterized by numerous patchy necroses and areas of demyelination in the white matter of cerebral and cerebellar hemispheres and brain stem, accompanied by atrophy of white matter and ventricular enlargement. Attention is drawn to the significance of these lesions for posttraumatic coma or dementia.

Accidents, Traffic↗
PubMed1977

Early stages of status marmoratus.

Basal ganglionic lesions in three young infants were found in a prospective search for early stages of status marmoratus. The lesions had formed and had passed into glial scars well before myelination of the basal ganglia commenced. The myelinating fibers crossing the scarred tissue were disoriented; however, fiber structure was normal, and the numbers of myelin lamellae did not differ significantly between scars and non-scarred tissue. There was no indication of a derangement of the process of myelin formation or of the formation of anomalous myelin sheaths around non-neuronal processes.

Basal Ganglia↗
PubMed1977

Fine structure of myomedulloblastoma.

Electronmicroscopic studies in a case of myomedulloblastoma support the concept that the medulloblastoma and the myoblastoma component of the tumor derive drom different cell lines. The myoblastoma component shows bundles of myogenic elements, whereby quite undifferentiated cells lacking myofilaments are tightly attached to differentiated elements having well organized myofilaments. These bundles are encompassed by a common basement membrane, and their cells are joined by junctions, helping the identification of the undifferentiated elements. No comparable structures were seen in the medulloblastoma component. The fine structure of the myoblastoma is reminiscent of aspects of normal fetal development of skeletal muscle.

Cell Differentiation↗
PubMed1977

Fine structure of medulloepithelioma.

A survey of published cases of medulloepitheliomas indicates that this tumor is highly malignant (average course 6 months), occurs in early childhood (average age 4,4 years) and has no sex predilection. Although it may originate in any part of the central nervous system, it is most common in the cerebral hemispheres. The first case studied with the electron microscope is reported here. The fine structure of the tumor is similar to that of the fetal neural tube in showing a primitive epithelium having uniform nuclei rich in chromatin but little cytoplasm and sparse organelles; it rests on a distinct basement membrane. The epithelial surface lacks cilia or microvilli and is covered with an irregular amorphous coat which is probably the cause of the light-microscopic misinterpretation of an inner limiting membrane. The lateral cell surfaces lack interdigitations but show extensive primitive forms of cell junctions. The case presented is also unusual in being the second case on record originating in the cerebellum and the first showing massive seeding along the spinal canal.

Cell Membrane↗
PubMed1977

The relation of axonal transport of mitochondria with microtubules and other axoplasmic organelles.

Axonal transport of mitochondria was studied in frog sciatic nerves incubated in agents selected for their known or alleged effect on microtubules or axonal flow. Quantitative data on mitochondria, microtubules, neurofilaments, endoplasmic reticulum, and cross-sectional area of the axon indicate that axonal transport of mitochondria is dependent on microtubules. When more than half of the microtubules are destroyed, the axonal transport of mitochondria is diminished in proportion to the destruction of microtubules. Axonal transport of mitochondria is not related to neurofilaments and endoplasmic reticulum. Changes in the cross-sectional area of axons, even upon reduction to half the normal size, do not noticeably affect mitochondrial transport. Cyanide which blocks oxidative metabolism also blocks axonal transport of mitochondria, but analysis of fine structure indicates that cyanide is destructive to microtubules as well.

Animals↗
PubMed1977

Supratentorial intracerebral epithelial (ependymal) cysts: review, case reports, and fine structure.

The paper concerns the rare supratentorial, intracerebral or convexity cysts in adults having a wall lined with an epithelium resembling ependyma. The clincopathological aspects of such cysts are reviewed from 15 published cases and two specimens of the authors which could be examined with the electronmicroscope. These cysts manifest at a median age of 46 years as progressive, space occupying lesions with a fairly rapid clinical course of about one to two years. Twelve of 17 cysts were located in the frontal lobes, most were unequivocally intracerebral and none communicated with the lateral ventricle. Microscopic examination of the cyst wall disclosed some variance in structure, the most common feature being a monolayer of ciliated cells sitting on a very thin collagen membrane. One of the present cases was unique in that the compression by the cyst had caused a shell of infarction in the encompassing tissue. The fine structure of the cysts is described and compared with that of potential host tissues from which such cysts may originate. It is concluded that the cysts arise from displaced segments of the wall of the neural tube which correspond to the sites from which the tela chorioidea forms.

Adult↗
PubMed1977

Osteolipomas of the tuber cinereum.

Osteolipomas of the tuber cinereum traditionally have been classified as meningeal lipomas that are located at the tuber cinereum. Examination of two cases and a review of 22 others found in the literature show that these lesions exhibit a remarkable consistency in their size and in their location between the corpora mamillaria and the pituitary stalk, and that approximately half of them contain a well-organized bone spherule with a central marrow space. These aspects differ from the features of meningeal lipomas in general; reasons are given for considering that the osteolipomas are displaced elements of the mesenchyme encompassing walls of the craniopharyngeal duct.

Adipose Tissue↗
PubMed1976

Chronic tonsillar herniation: an attempt at classifying chronic hernitations at the foramen magnum.

A system is presented for the classification of chronic herniations of the cerebellar tonsils in the absence of space-occupying intracranial lesions, based on a survey of the literature and 13 own cases. The Arnold-Chiari malformation in adults typically involves herniation of the cerebellar tonsils instead of herniation of the vermis as is typical when it occurs in infancy. Identification of chronic tonsillar herniation with the Arnold-Chiari malformation in adults was thought to require at least one other sign of the Arnold-Chiari complex, e.g. a medullary deformity. Cases for which chronic herniation and sclerosis of the cerebellar tonsils present as the only nervous lesion are classified as "chronic tonsillar herniation". Such cases may manifest with neurological symptoms during adult life, or they may be found incidentally at autopsy. Attention is drawn to the occurrence of chronic tonsillar herniation in 7 infants and children where it apparently represents a cause of sudden unexpected death. The overlap between chronic tonsillar herniation and the Arnold-Chiari malformation of adults is discussed in regard to the frequence of associated osseous anomalies, hydrocephalus and syringomyelia.

Adolescent↗
PubMed1975

Agenesis of arachnoid granulations and its relationship to communicating hydrocephalus.

The authors discuss reabsorption of cerebrospinal fluid in relation to the post-mortem findings in two children, one with total agenesis of the Pacchionian system accompanied by hydrocephalus, and the other with a subtotal agenesis and no hydrocephalus. Case 1 is the only known documented case of total agenesis of the Pacchionian system and gives credence to the idea that an impaired reabsorption of cerebrospinal fluid at the level of the Pacchionian system is a cause of hydrocephalus. The patient in Case 2 showed only two small areas of arachnoid granulations containing a few flattened, microscopic villi of normal cellularity.

Arachnoid↗