bluuebunny/crossref_metadata_2025 huggingface dataset:
ISOLATION AND CHARACTERIZATION OF THE INFLAMMATORY INFILTRATE IN THE CENTRAL NERVOUS SYSTEM OF THE GUINEA‐PIG WITH EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
Authors: ALLSOPP GRETA , ROTERS SILENE , TURK J. L.
Published: May 2008

Allsopp G., Roters S. & Turk J.L. 1980 Neuropathology and Applied Neurobiology 6,109–118

Isolation and characterization of the inflammatory infiltrate in the central nervous system of the guinea‐pig with experimental allergic encephalomyelitis

The inflammatory infiltrate of the central nervous system in acute experimental allergic encephalomyelitis (EAE) in the guinea‐pig has been isolated and characterized. Inflammatory cells found over the surface of the brain and spinal cord and within the leptomeninges have been isolated by washing, and were subsequently identified by a number of methods. By light microscopy approximately 60% were lymphocytes, 30% were cells of the mononuclear phagocyte series, and 5% were neutrophils: the occasional plasma cell and eosinophil were also identified. E, EA and EAC rosetting tests were used to determine the proportions of T lymphocytes (both early and late), and cells with Fc and C3 receptors respectively. Particular attention was paid to cells of the mononuclear phagocyte series bearing Fc and C3 receptors to determine whether any change or loss of these receptors was apparent. The percentage of phagocytic cells from the brain and spinal cord washes was also determined. Transmission and scanning electron microscopy showed that a large proportion of the inflammatory infiltrate consisted of cells of the mononuclear phagocyte series. This study therefore confirms that the cells of the mononuclear phagocyte series play a predominant role in EAE.
MYELIN OEDEMA, OPTIC NEUROPATHY AND RETINOPATHY IN EXPERIMENTALSTYPANDRA IMBRICATA TOXICOSIS
Authors: HUXTABLE C. R. , DORLING P. R. , SLATTER D. H.
Published: May 2008

Huxtable C.R., Dorling P.R. & Slatter D.H. 1980 Neuropathology and Applied Neurobiology 6, 221–232

Myelin oedema, optic neuropathy and retinopathy in experimental Stypandra imbricata toxicosis

Rats experimentally poisoned with the toxic plant Stypandra imbricata developed acute oedema of central and peripheral myelin and extensive axonal degeneration in the optic nerves. The oedema developed with vacuolation and splitting of myelin lamellae at the intraperiod line. Following recovery from acute intoxication, myelin oedema resolved after 6 to 12 weeks, but severe retinal degeneration and optic nerve atrophy remained. Morphological abnormalties in glial cells and axons were only found in the optic nerves. It was concluded that there is probably also a direct toxic effect on the axons of the optic nerve and the photoreceptor cells of the retina. The chemical nature of the toxin remains to be defined but the marked similarity of its toxic effects to those of hexachlorophene are noted.
PROCEEDINGS OF THE FIFTY‐EIGHTH MEETING OF THE BRITISH NEUROPATHOLOGICAL SOCIETY HELD AT THE NATIONAL HOSPITAL AND THE INSTITUTE OF NEUROLOGY, LONDON, 18–19 JANUARY 1980
Authors: TOMLINSON B. E.
Published: May 2008

Allt G. & Ghabriel M.N. (introduced) (Middlesex Hospital Medical School, London WlP 6DB)

Clifford‐Jones R.E. (introduced), Landon D.N. & McDonald W.I. (Institute of Neurology, London WC1N 3BG)

Abrahams P.H. (introduced), Day A. (introduced) & Allt G. (The Middlesex Hospital Medical School, London W1P 6DP

Bruce M.E. & Dickinson A.G. (introduced) (ARC Animal Breeding Research Organisation, Edinburgh EH9 3JQ)

Fraser H. & Bruce M.E. (ARC Animal Breeding Research Organisation, Edinburgh EH9 3JQ)

Adams J.H., Graham D.I. (Department of Neuropathology, Institute of Neurological Sciences, Glasgow G51 4TF) & Gennarelli T.A. (introduced) (Department of Neurosurgery, University of Pennsylvania, Philadelphia 19104)

Hubbard B.M. & Anderson J.M. (Ninewells Hospital and Medical School, Dundee DD1 9SY)

Averback P. (introduced) (Department of Pathology, University of Cambridge Cambridge CB2 1QP)

Narang H.K. (Public Health Laboratory, Newcastle upon Tyne NE4 6BE)

Sturrock R.R. (introduced) (Department of Anatomy, University of Dundee, Scotland)

Jacobs J.M. & Duchen L.W. (Department of Neuropathology, Institute of Neurology London WC1N 3BG)

Gomez S. (introduced) & Queiroz L.S. (introduced) (Institute of Neurology, London WC1N 3BG)

Swash M., Schwartz M.S. (introduced) & Sar‐geant M.K. (introduced) (Department of Morbid Anatomy, The London Hospital, London El)

Deane B.R. (introduced) & Lantos P.L. (The Middlesex Hospital Medical School, London

Caine G. (introduced), Davis B.E. (introduced), Cox S. (introduced) & Weller R.O. (Department of Pathology (Neuropathology), University of Southampton S09 4XY)

McCormick D. & Wallace I. (introduced) (Pathology Department, Queen's University, Belfast BT12 6BA)

Scaravilli F., Teixeira F. (introduced) & Jacobs J.M. (Institute of Neurology, London, WC1N 3BG)

Griffiths I.R., Duncan I.D., McCulloch M. (introduced) & Carmichael S. (introduced) (Department of Veterinary Surgery, University of Glasgow, G61 1QH)

Blakemore W.F., Palmer A.C. & Patterson R.C. (introduced) (Department of Clinical Veterinary Medicine, Cambridge CB3 OES)

Lewis P.D. & Carr J. (introduced) (Royal Postgraduate Medical School, London W12 OHS)

Pratt O.E. (Institute of Psychiatry, London SE5 8AF)

Tomkins C. (introduced), King R.H.M. & Thomas P.K. (Department of Neurological Science, Royal Free Hospital, London NW3 2QG)

Woodhams P.L. (introduced) (MRC Developmental Neurobiology Unit, Institute of Neurology, London WC1N 2NS), Roberts G.W. (introduced) & Polak J.M. (Royal Postgraduate Medical School, London W12 OHS)

Reid H. (Department of Pathology, University of Manchester M13 9PL)
THE MITOCHONDRIAL CONTENT OF ENDOTHELIAL CELLS AND THE BASEMENT MEMBRANE THICKNESS OF RAT BRAIN CAPILLARIES AFTER PORTOCAVAL ANASTOMOSIS
Authors: LAURSEN H.
Published: May 2008

Laursen H. (1980) Neuropathology and Applied Neurobiology 6,375–386

The mitochondrial content of endothelial cells and the basement membrane thickness of rat brain capillaries after portocaval anastomosis

The volume of mitochondria in brain capillary endothelium and the harmonic mean basement membrane thickness were estimated in rats after portocaval anastomosis for 10 days, 30 days and 10 weeks. The mitochondrial volume was from 5–73% to 7–64% of the endothelial volume. There was no difference between the control and experimental animals. The harmonic mean thickness of the basement membrane was calculated from orthogonal intercepts measured on a reciprocal logarithmic scale. This method leads to an approximately normal distribution of the measurements. The harmonic mean thickness was 57–8 nm in controls, 54–6 nm after 10 days, 63–2 nm after 30 days and 600 nm after 10 weeks portocaval anastomosis. The increase after 30 days was significantly different from the first two measurements. It is concluded that only a small increase in harmonic mean thickness of the basement membrane, and thereby an increase in diffusion resistance, have occurred after 30 days portocaval anastomosis.
ULTRASTRUCTURE OF ALZHEIMER TYPE II GLIA IN HEPATOCEREBRAL DISEASE
Authors: HORITA N. , MATSUSHITA M. , ISHII T. , OYANAGI S. , SAKAMOTO K.
Published: May 2008

In a case of hepatocerebral disease of Inose type the astrocytes, corresponding to Alzheimer type II glia, had swollen cytoplasm containing glycogen granules and focal aggregates of lipofuscin granules. Their nuclei contained bodies of simple and of complex types as well as conglomerates of glycogen granules without any capsules. The nuclear bodies of simple type were also observed in the nuclei of endothelial cells. It is concluded that these changes in the appearance of Alzheimer type II glia suggest reactive and defensive changes in the brain against ammonium ions, rather than being merely degenerative in nature.
A HISTOQUANTITATIVE STUDY OF THE STRIATE CORTEX AND LATERAL GENICULATE BODY IN NORMAL, BLIND AND DEMENTED SUBJECTS
Authors: SCHOLTZ C. L. , SWETTENHAM K. , BROWN A. , MANN D. M. A.
Published: May 2008

The amount of myelin in the outer band of Baillarger in the human visual cortex stained by Luxol Fast Blue MBS, has been measured in normal individuals of wide age range, in a group of blind and severely visually impaired but otherwise normal individuals and in a series of demented patients of the Alzheimer and multi‐infarct type who were apparently visually normal. The amount of myelin is found to be significantly reduced in the blind and demented groups. Examination of the lateral geniculate body in the blind cases demonstrated slight reduction in neuron numbers and marked reduction in mean neuron diameter. Neuronal cytoplasmic ribonucleic acid, nucleolar volume and numbers of tetraploid glial nuclei in the blind or visually impaired cases were significantly reduced when compared with controls, indicating reduced function in these neurons. Similar results were obtained on examining this nucleus in Alzheimer and multi‐infarct cases, suggesting that the visual pathways may be involved in these conditions. It is concluded that loss of myelin from the outer band of Baillarger occurs in association with reduced function of neurons in the lateral geniculate body.
INTRACEREBRAL CALCIFICATION IN A CASE OF SYSTEMIC LUPUS ERYTHEMATOSUS WITH NEUROLOGICAL MANIFESTATIONS
Authors: ANDERSON JANICE R.
Published: May 2008

Intracerebral calcification was found in a young child with systemic lupus erythematosus. Vascular lesions characteristic of SLE were widespread and associated with systemic infarcts and multiple infarcts of the brain and spinal cord. The cerebral calcification was also related to blood vessels, but confined to certain regions of the brain.
THE PATHOLOGY OF MULTIPLE SCLEROSIS‐FACT, FICTION AND HYPOTHESIS
Authors: ALLEN INGRID V.
Published: May 2008

The present state of our pathological knowledge of multiple sclerosis is reviewed emphasizing the ‘hard facts’ while highlighting subjects of disputed interpretation and of ignorance.
THE TOXICITY TO RAT CEREBRAL CORTEX OF TOPICAL APPLICATIONS OF ACETALDEHYDE, AMMONIA OR BILIRUBIN
Authors: PHILLIPS S. C.
Published: May 2008

The relative toxicity of acetaldehyde, ammonia and bilirubin to cerebral cortex of rats has been tested by supervision of the intact dura for 1 h with each toxin separately. The cortex was examined histologically after 6 days survival using a silver stain which selectively impregnates degenerating axons and their synaptic terminals. A tissue concentration of 30 mM acetaldehyde was found to cause axonal and terminal degeneration, whereas 11 mM acetaldehyde was not toxic, and did not produce any structural changes detectable by electron microscopy. In terms of tissue concentrations, acetaldehyde was at least 27 times more toxic than ethanol on a molar basis. However, the acetaldehyde concentration necessary to produce neuronal degeneration in a 1 h exposure is many times greater than ever reported in CSF in human alcoholism. Both ammonia and bilirubin are capable of causing neuronal degeneration, but we have not measured the tissue concentrations that are toxic. Comparison of molar concentrations in the supervising fluids showed that ammonia is at least 39 times more toxic than acetaldehyde, and at least 1000 times more toxic than ethanol. Superfusion with an ethanolic solution of bilirubin (2–5 mM) was strongly toxic, but this solution diluted to 50% with saline was not toxic. The possibility exists that ammonia or bilirubin may reach concentrations toxic to neurons in alcoholism, especially in the presence of liver damage.
THE MODE OF DEVELOPMENT OF AN INHERITED FORM OF ANENCEPHALY IN THE HOUSE MOUSE
Authors: ANDERSON JANICE R.
Published: May 2008

Anencephaly in the xn strain of mouse is a condition determined by a single autosomal recessive gene. At birth, affected animals bear a cap of degenerate cerebral tissue devoid of bony covering. The early development of this malformation was studied in embryo mice from the stage of neural groove formation until after the neural tube has normally closed. The abnormal embryos could be recognized before the anterior neuropore had completely closed in normal litter mates. Detection of the cerebral malformation at this early stage of gestation suggests that the inherited murine anencephaly is due to primary failure of the neural tube to close.
A QUANTITATIVE ASSESSMENT OF DYSTROPHIC MOUSE (129 ReJ dy/dy) MYOGENESIS IN VITRO
Authors: SUMMERS P. J. , PARSONS R.
Published: May 2008

A quantitative assessment was made of the myogenic capability in vitro of muscle cells from dystrophic (129 Rej dy/dy) and normal mice from birth to 5 months old. Seeding efficiency was increased in dystrophic cells from neonatal and 1‐week‐old mice compared to age‐matched controls. The extent of myogenesis in cultures from neonatal and 1‐week‐old dystrophic mice did not differ from controls. Muscle colony formation in cultures established from 5‐month‐old dystrophic mice was reduced by 80% compared with normal cultures. Normal and dystrophic cultures established from 5‐month‐old mice contained equal numbers of fibroblast colonies. The results suggest that decreased myogenesis in cultures from 5‐month‐old dystrophic mice is due to a relative absence of myogenic cells rather than a numerical dilution of the cultures by fibroblasts. This may be due to population of nonviable satellite cells or to necrosis of dystrophic myotubes in vitro.
EFFECT OF ROUTE OF INFECTION ON THE FREQUENCY AND DISTRIBUTION OF CEREBRAL AMYLOID PLAQUES IN SCRAPIE MICE
Authors: BRUCE MOIRA E. , FRASER H.
Published: May 2008

Cerebral amyloid plaques are a conspicuous pathological feature in mice infected with certain strains of scrapie. The origin of the amyloid protein in these plaques, whether it is locally or systemically synthesized, and the mechanisms leading to its deposition are not known. The frequency of plaques and their distribution in the brain are greatly influenced by the route of injection of the scrapie inoculum. Intracerebral injection consistently results in greater numbers of plaques than are obtained if the same inoculum is introduced peripherally. Following intracerebral injection, plaques are commonly seen in areas close to the lateral ventricles, for example the corpus callosum and hippocampus, whereas they are absent from these areas with peripheral routes. Furthermore, when left‐ and right‐ sided intracerebral injections are compared, plaques are more frequent on the side of injection. These results suggest that the distribution of amyloid plaques is influenced either by the localization of some component of the inoculum or by traumatic damage at injection. The most plausible explanation is that amyloid deposition is associated with local concentrations of scrapie infectivity and that the amyloid protein originates in the brain.
THE DEVELOPMENT OF PERIVENTRICULAR LESIONS IN CHRONIC RELAPSING EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS IN GUINEA‐PIGS: A LIGHT AND SCANNING ELECTRON MICROSCOPIC STUDY
Authors: LASSMANN H. , KITZ K. , WISNIEWKSI H. M.
Published: May 2008

Lassmann H., Kitz K. & Wiśniewski H.M. (1981) Neuropathology and Applied Neurobiology 7,1–11

The development of periventricular lesions in chronic relapsing experimental allergic encephalomyelitis in guinea‐pigs: a light and scanning electron microscopic study

Periventricular lesions in the centrum semiovale are the most frequent changes in the brain in chronic relapsing experimental encephalomyelitis in guinea‐pigs. They are generally distributed symmetrically at the lateral angle of the ventricular wall. The number of lesions and their size increases in anterior‐posterior direction. Typically periventricular lesions in the later chronic stages are similar to those in multiple sclerosis. Earlier lesions generally originate in the depth of the white matter and secondarily, by extension, reach the ventricular surface. Lesions developing at later stages after sensitization may also originate from the ventricular wall and extent into the centrum semiovale. In these latter, severe structural changes in the ventricular ependyma may generally be found. Increased intracranial pressure in these animals may be one of the possible mechanisms leading to the peculiar topographical distribution of the periventricular lesions.
NEUROFIBRILLARY PATHOLOGY AND PROTEIN SYNTHETIC CAPABILITY IN NERVE CELLS IN ALZHEIMER'S DISEASE
Authors: MANN D. M. A. , NEARY D. , YATES P. O. , LINCOLN J. , SNOWDEN J. S. , STANWORTH P.
Published: May 2008

Mann D.M.A., Neary D., Yates, P.O., Lincoln J., Snowden J.S. & Stan‐worth P. (1981) Neuropathology and Applied Neurobiology 7, 37–47

Neurofibrillary pathology and protein synthetic capability in nerve cells in Alzheimer's disease Nucleolar volume was measured in nerve cells of the temporal cortex in cases of Alzheimer's disease, obtained at both biopsy and autopsy. Measurements were made on those nerve cells containing neurofibrillary tangles and also on ones free of such changes. Results showed that nucleolar volume is significantly reduced, by at least 40%, in both tangle and non‐tangle bearing cells, in both biopsy and autopsy cases, when compared with corresponding values from appropriate control cases. Furthermore, in the autopsy cases, nerve cell nucleolar volume was reduced by a further 30% in tangle bearing cells compared to non‐tangle bearing neighbours. No such difference was noted in these cells in the biopsy cases. These findings imply that alterations in protein synthetic capability occur in nerve cells early in the course of Alzheimer's disease, and that this change is not, at least in these initial stages, related to accumulation of neurofibrillary material within the cell body, although later on such accumulation may result in added disruption of cell metabolism.
A SURVEY OF ETHYLNITROSOUREA‐INDUCED RAT GLIOMAS FOR THE PRESENCE OF TUMOUR REJECTION ANTIGENS EXPRESSED IN VIVO
Authors: SPENCE ALEX M. , PRIESTLEY GREGORY
Published: May 2008

Spence A.M. & Priestley G. (1981) Neuropathology and Applied Neurobiology 7,63–75.

A survey of ethylnitrosourea‐induced rat gliomas for the presence of tumour rejection antigens expressed in vivo

Transplanted lines of seven F‐344 (Fischer) rat malignant gliomas induced transplacentally with ethylnitrosourea (ENU) were surveyed by in vivo im‐munoprotection assays for the presence of tumour rejection antigens. These gliomas were representative of commonplace histological types of human primary brain tumours and were analyzed in early transplantation passages. The classical tumour ligation method of immunizing animals was attempted with five glioma lines, but was found unusable in four of these because of a high incidence of local tumour recurrences and distant metastases. In most experiments the animals were immunized by repeated inoculations of heavily‐irradiated tumour cells. Two gliomas, a glioblastoma multiforme and a mixed astrocytoma‐ependymoma, demonstrated weak but statistically significant tumour rejection responses. Immunization with three other tumours, a mixed oligodendroglioma‐astrocytoma and two glioblastomas multiforme, led to enhanced outgrowth of the challenge cell inocula. Neither a rejection nor an enhancement response was observed in assays of the remaining two neoplasms, a glioblastoma multiforme and a mixed astrocytoma‐oligodendroglioma. Immunization with a 3‐methylcholanthrene‐induced urinary bladder carcinoma line, used as a control in assays of six gliomas, had no effect on the outgrowth of transplanted glioma cells. These results suggest that ENU‐induced malignant rat gliomas do not uniformly elicit strong tumour‐rejection responses in vivo.
THE DEVELOPMENT OF RAT DORSAL ROOT GANGLIA IN THREE EXPERIMENTAL MEDIA CONTAINING LANDRY‐GUILLAIN‐BARRÉ, ALCOHOLIC PERIPHERAL NEUROPATHY OR NORMAL ADULT SERA
Authors: ARMATI‐GULSON PATRICIA J.
Published: May 2008

Armati‐Gulson P.J. (1981) Neuropathology and Applied Neurobiology 7, 351–363

The development of rat dorsal root ganglia in three experimental media containing Landry‐Guillain‐Barré, alcoholic peripheral neuropathy or normal adult sera

Development of rat dorsal root ganglia in vitro mimics the development of rat dorsal root ganglia in vivo when grown in medium containing human cord serum. When serum from patients either in the acute phase of Landry‐Guillain‐Barré syndrome or with alcoholic peripheral neuropathy is substituted for human cord serum, maturation is inhibited. Development of fetal relationships occurs between the Schwann cells and axons and many axons become enclosed within the processes of a single Schwann cell. Formation of myelin does not occur. The substitution of normal adult blood for cord serum also inhibits maturation, but unlike development with neuropathic serum, the Schwann cells and axons do not become associated and myelination does not occur.
HEPATIC BETA GALACTOSIDASE AND FELINE GMI GANGLIOSIDOSIS
Authors: BARNES I. C. , KELLY D. F. , PENNOCK C. A. , RANDELL J. A. J.
Published: May 2008

Barnes I.C., Kelly D.F., Pennock C.A. & Randell J.A.J. (1981) Neuropathology and Applied Neurobiology 7, 463–476

Hepatic beta galactosidase and feline GMI gangliosidosis

This paper describes the clinical, morphological and biochemical features of three cats with a progressive neurological disorder. Clinical features were ataxia and progressive tremor. The morphological characteristics were those of a lysosomal storage disease affecting neurones of the central nervous system and autonomic ganglia; membranous cytoplasmic bodies were demonstrated by electron microscopy in cerebral neurones. Chemical analysis of brain from two of the cats revealed an increased content of total gangliosides, sialic acid and a specific increase in GMI ganglioside. Enzyme analysis of homogenates of leucocytes, spleen and brain showed less than 5% of normal 4‐methylumbelliferyl‐β galatosidase (4MU‐β gal) activity. In liver, activity was markedly reduced at pH values below 4.2, but there was considerable activity above this value. The properties of 4MU‐β gal in normal and diseased feline livers were investigated. Sephadex gel filtration of diseased liver homogenates showed an absence of two thermolabile ‘acid’ components, and reduced activity of a third thermostable ‘neutral’ component. The biochemical abnormalities found in the diseased cats are similar to those found in human juvenile GMI gangliosidosis (type 2).
ANNOTATION: THE CLASSIFICATION OF TUMOURS OF THE CENTRAL NERVOUS SYSTEM
Authors: BARNARD R. O.
Published: May 2008

Barnard R.O. (1981) Neuropathology and Applied Neurobiology 8, 1–10 Annotation. The classification of tumours of the central nervous system

Present day classification of CNS tumours is discussed in the light of the recent attempt by World Health Organization investigators to put forward a widely acceptable classification the use of which will facilitate communication between pathologists of different countries.
THE PATTERN OF RECOVERY OF AXONS IN THE NERVOUS SYSTEM OF RATS FOLLOWING 2,5‐HEXANEDIOL INTOXICATION: A QUESTION OF RHEOLOGY?
Authors: CAVANAGH J. B.
Published: May 2008

Cavanagh J.B. (1982) Neuropathology and Applied Neurobiology 8, 19–34

The pattern of recovery of axons in the nervous system of rats following 2,5‐hexanediol intoxication: a question of rheology?

Rats have been dosed with 2, 5‐hexanediol for 48 days and then allowed to recover. The changes in the accumulations of neurofilamentous masses in various pathways in CNS and PNS have been followed by light microscopy over the subsequent 9 weeks. It was found that many CNS pathways allow the argyrophilic masses to pass to their terminals from whence they subsequently disappear, usually over 5–6 weeks. Little or no axonal degeneration is seen where this happens. The same occurs in many peripheral nerves, particularly cranial nerves. However, in many tracts in the spinal cord and in many axons in the longer peripheral nerves, filamentous masses remain and becomes associated with axon degeneration, and, in tracts, gliosis. The importance of paranodal constrictions at nodes of Ranvier which tend to be greater in larger diameter axons is emphasized as a likely mechanism for the axon degeneration which largely took place during the recovery period.
DEMYELINATION INDUCED IN MICE BY AVIRULENT SEMLIKI FOREST VIRUS. I. VIROLOGY AND EFFECTS ON OPTIC NERVE
Authors: ILLAVIA SHIRIN J. , WEBB H. E. , PATHAK SNEHLATA
Published: May 2008

Illavia S.J., Webb H.E. & Pathak S. (1982) Neuropathology and Applied Neurobiology 8, 35–42

Demyelination induced in mice by avirulent Semliki Forest virus. I. Virology and effects on optic nerve

wiss A2G mice were infected intraperitoneally with an avirulent strain of Semliki Forest virus. The virus titres in the optic nerves, retina and brain were estimated on post‐inoculation days 3 to 8. High titres of virus were obtained in the optic nerve, retina and brain. The optic nerves, retina and brain were studied by light microscopy up to post‐inoculation day 67. Electron microscope studies were carried out on the optic nerve on post‐inoculation days 11 and 14. Inflammatory, microcystic changes and demyelination seen in the optic nerve were similar to those found in the central nervous system.
DEMYELINATION INDUCED IN MICE BY AVIRULENT SEMLIKI FOREST VIRUS. II. AN ULTRASTRUCTURAL STUDY OF FOCAL DEMYELINATION IN THE BRAIN
Authors: KELLY W. R. , BLAKEMORE W. F. , JAGELMAN S. , WEBB H. E.
Published: May 2008

Kelly W.R., Blakemore W.F., Jagelman S. & Webb H.E. (1982) Neuropathology and Applied Neurobiology 8, 43–53

Demyelination induced in mice by avirulent Semliki Forest virus. II. An ultrastructural study of the focal demyelination in the brain

Four‐week‐old mice were infected intraperitoneally with an avirulent strain A7(74) of Semliki Forest virus (SFV) and killed at 4, 10, 15, 21 and 29 days after inoculation. Focal demyelinating lesions were present by 10 days. These were usually accompanied by a mononuclear infiltrate which included lymphocytes possessing characteristic cytoplasmic projections. These latter extended deep into the cytoplasm of adjacent cells, which were usually astrocytes and macrophages. Other features of the focal lesions were expansion of the extracellular space and demyelination which appeared to be fragmentation or lysis rather than stripping of myelin by macrophages. Although healing occurred in some mice after 4 weeks, acute lesions were still found in others of the same age. It was concluded that the demyelination probably had an immunological basis, and interaction between elements of the immune system and glial cells was a factor which inhibited orderly remyelination of the relatively mild lesions resulting from this infection.
IMMUNOHISTOCHEMICAL STAINING OF SENILE PLAQUES
Authors: MANN D. M. A. , DAVIES J. S. , HAWKES J. , YATES P. O.
Published: May 2008

Mann D.M.A., Davies J.S., Hawkes J. & Yates P.O. (1982) Neuropathology and Applied Neurobiology 8, 55–61

Immunohistochemieal staining of senile plaques

Immunohistochemical staining of serum proteins, including immunoglobulins, was carried out on formalin‐fixed cerebral tissue from 24 autopsy cases (twenty dements, four controls) and fifteen biopsy cases (ten dements, five controls). Sixteen of the autopsy cases showed focal regions where there was staining of globulins and other serum proteins within senile plaque ‘cores’, nerve cell perikarya and astrocytes. This pattern of staining, generally, occurred either in relation to areas of cerebral infarction or in the neighbourhood of small arteries displaying arteriosclerotic changes. In tissue areas, distant from these vascular alterations, no staining occurred. Furthermore, none of the biopsy cases showed any such areas of staining. These findings indicate that the positive immunohistochemical reactions demonstrated within senile plaques (and other tissue components) are more likely to result from leakage of serum proteins, including immunoglobulins out of damaged vessels and into the brain parenchyma, rather than being indicative of the involvement of immunological mechanisms in the aetiology of plaques, as has been suggested by other workers.
HISTORICAL SURVEY THE CONCEPT OF A SENSORIMOTOR CORTEX: ITS LATER HISTORY DURING THE TWENTIETH CENTURY
Authors: MEYER ALFRED
Published: May 2008

Meyer A. (1982) Neuropathology and Applied Neurobiology 8, 81–93

Historical survey. The concept of a sensorimotor cortex: its later history during the twentieth century

This paper continues the historical review on the concept of a sensorimotor cortex into the twentieth century. Paul Flechsig was probably the first to accept this concept after the turn of the century. Like Munk, he believed in an almost reflex‐like unity between cortical sensory and motor function. With the help of his myelogenetic technique, Flechsig also demonstrated convincingly in the human brain that the two Rolandic convolutions receive a separate influx of thalamic afferents. Had this finding met with more attention, much experimental work by some of the distinguished later investigators might have proved to be unnecessary. Research has now reached a state when an early plausible explanation of the problem may be confidently expected.
CHANGES IN NERVOUS TISSUE IN BOVINE GENERALIZED GLYCOGENOSIS TYPE II
Authors: COOK R. D. , HOWELL J. McC. , DORLING P. R. , RICHARDS R. B.
Published: May 2008

Cook R.D., Howell J. McC, Dorling P.R. & Richards R.B. (1981) Neuropathology and Applied Neurobiology 8, 95–107

Changes in nervous tissue in bovine generalized glycogenosis type II

Generalized Glycogenosis type II has been diagnosed in seven calves from a herd of cattle maintained at the Murdoch University Veterinary School Farm. The syndromes seen are equivalent to the infantile and childhood forms of the disease in humans. In the brain and spinal cord of the calves acid a‐glucosidase activity was depressed and glycogen deposition was markedly increased. Swelling, vacuolation and glycogen deposition was present in neurones of the central and autonomic nervous systems and retina, in glia and in Schwann cells and fibroblasts within peripheral nerves. The distribution was similar to that seen in human cases. The glycogen was both membrane bound and free within the cytoplasm. Changes similar to those seen in axonal dystrophy were present and some nerve fibres showed Wallerian degeneration. Evidence of nerve cell destruction and nerve cell loss were not seen and the predominant clinical signs were related to muscle weakness.
NEURONAL AND LYMPHOCYTIC POPULATIONS IN HUMAN TRIGEMINAL GANGLIA: IMPLICATIONS FOR AGEING AND FOR LATENT VIRUS
Authors: BALL M. J. , NUTTALL K. , WARREN K. G.
Published: May 2008

Ball M. J., Nuttall K. & Warren K. G. (1982) Neuropathology and Applied Neurobiology 8, 177–187

Neuronal and lymphocytic populations in human trigeminal ganglia: implications for ageing and for latent virus

The number of neurones and of lymphocytes was determined morphometrically in serial sections of trigeminal ganglia harvested at autopsy from 64 human subjects dying at ages 2 months to 81 years. The nerve cell population varied from 20159 to 156 702 with a mean of 80 638 /ganglion and was unaffected by increasing age. The degree of lymphocytic infiltration, which was prominent and ubiquitous, also did not correlate with the subjects' age. There was no significant correlation between neuronal and lymphocyte counts. The inflammatory cells present throughout life apparently are unassociated with any detrimental effect upon the sensory neurones, and may represent a histopathological marker either of reactivating herpes virus or of virus maintained in a latent state within the Gasserian ganglia of man.
THE MITOCHONDRIAL DISORDERS: PATHOGENESIS AND AETIOLOGICAL CLASSIFICATION
Authors: TASSIN S. , BRUCHER J. M.
Published: May 2008

Tassin S. & Brucher J. M. 1982 Neuropathology and Applied Neurobiology 8, 251–263

Annotation. The mitochondrial disorders: pathogenesis and aetiological classification

Mitochondrial myopathies form a heterogeneous group of muscular diseases characterized by the presence of morphological mitochondrial abnormalities. These abnormalities are interpreted as the stereotyped morphological expression of a cellular energy deficiency. They represent a compensatory mechanism destined to increase ATP production. On this pathogenetic basis, an aetiological classification for the mitochondrial myopathies is proposed. The consequences of this hypothesis on the meaning of the morphological abnormalities, notably the changes in the amount of glycogen and lipids associated with mitochondrial alterations, are analysed.
RETARDED FETAL BRAIN DEVELOPMENT RESULTING FROM SEVERE DIETARY IODINE DEFICIENCY IN SHEEP
Authors: POTTER B. J. , MANO M. T. , BELLING G. B. , McINTOSH G. H. , HUA C. , CRAGG B. G. , MARSHALL J. , WELLBY M. L. , HETZEL B. S.
Published: May 2008

Potter B.J., Mano M.T., Belling G.B., Mcintosh G.H., Hua C, Cragg B.G., Marshall J., Wellby M.L. & Hetzel B.S. 1982 Neuropathology and Applied Neurobiology 8, 303–313

Retarded fetal brain development resulting from severe dietary iodine deficiency in sheep

Sheep have been used to study the effect of dietary iodine deficiency on the development of the fetal brain. Severe iodine deficiency caused reduction in fetal brain and body weights and in brain DNA and protein from 70 days gestation to parturition. The lowered brain weight and brain DNA at 70 days gestation indicates a reduced number of cells, probably due to slower neuroblast multiplication which normally occurs from 40–80 days in the sheep, and the reduction in DNA and protein after 80 days implies that the development of neuroglia could be slowed also in iodine deficiency. Morphological changes were observed in both the cerebral hemispheres and the cerebellum. In the cerebral hemispheres of the iodine‐deficient fetuses an increased density of neurons was apparent histologically in the motor cortex and visual cortex and in the CAI and CA4 areas of the hippocampus in comparison with controls. In the cerebellum there was delayed migration of cells from the external granular layer to the internal granular layer and increased density of Purkinje cells in the iodine‐deficient fetal brains. In addition, the molecular area was increased and the medullary area reduced in comparison with controls. These changes are indicative of delayed brain maturation. Evidence of fetal hypothyroidism was provided by low fetal thyroid iodine and plasma T4 values, thyroid hyperplasia from 70 days gestation, significant reduction in body weight at the same time as the brain retardation, and absence of wool growth and delayed skeletal maturation near parturition. It is apparent from the biochemical and histological changes observed during iodine deficiency that iodine is an essential element for normal fetal brain and physical development in the sheep.
VIRUS TITRES AND PERSISTENTLY RAISED WHITE CELL COUNTS IN CEREBROSPINAL FLUID IN MICE AFTER PERIPHERAL INFECTION WITH DEMYELINATING SEMLIKI FOREST VIRUS
Authors: PARSONS LINDA M. , WEBB H. E.
Published: May 2008

Parsons L.M. & Webb H.E.1982Neuropathology and Applied Neurobiology 8, 395–401

Virus titres and persistently raised white cell counts in cerebrospinal fluid in mice after peripheral infection with demyelinating Semliki Forest virus

Virus titres and cell counts in the cerebrospinal fluid of mice have been examined following intraperitoneal inoculation of demyelinating Semliki Forest virus (SFV). Virus titres in cerebrospinal fluid were highest 2–4 days after infection and fell again after day 4, 48 h before reduction in brain titres. White cell counts were very low in the first 48 h and showed a steep rise from 4 days after infection to a peak on day 6. After day 8, cell numbers fell to a plateau level which was sustained up to day 61. The significance of these findings in relation to the pathogenesis of virus‐induced disease of the central nervous system is discussed.
IN‐SITU CHARACTERIZATION OF MONONUCLEAR CELL INFILTRATES IN LESIONS OF MULTIPLE SCLEROSIS
Authors: NYLAND HARALD , MÖRK SVERRE , MATRE ROALD
Published: May 2008

Nyland H, Mork S & Matre R.1982Neuropathology and Applied Neurobiology 8, 403–411

In‐situ characterization of mononuclear cell infiltrates in lesions of multiple sclerosis

The mononuclear cell infiltrates in autopsy material from brains and spinal cords of six patients with multiple sclerosis (MS) were characterized in situ. Receptors for sheep erythrocytes and anti‐T lymphocyte serum were used to identify T lymphocytes. Receptors for the activated third components of complement and for the Fc‐portion of IgG (Fey receptors) were used as markers for macrophages and lymphocytes. In acute and recent MS lesions, perivascular infiltrates of mononuclear cells were commonly found. Most cells were T lymphocytes. Some B lymphocytes were also demonstrated. The demyelinating lesions contained large numbers of lipid macrophages expressing Fey receptors. The lipid macrophages are probably derived from microglial cells. The chronic, demyelinated lesions contain a few mononuclear cells, mainly B lymphocytes and plasma cells.
ELECTRON MICROSCOPIC STUDY OF INTRANUCLEAR SPHERES OF BOUTEILLE TYPE‐III IN ASTROCYTES WITH SPECIAL REFERENCE TO LIVER CARCINOMA
Authors: GIBSON PETER H.
Published: May 2008

Gibson P.H.1982
Neuropathology and Applied Neurobiology
8, 413 418

Electron microscopic study of intranuclear spheres of Bouteille type‐Ill in astrocytes with special reference to liver carcinoma

Astrocytic intranuclear spheres of Bouteille type‐Ill were studied with the electron microscope in the neocortex of 29 patients dying from various causes. The numbers of laminate whorls in these spheres in patients with carcinoma involving the liver were found statistically to be significantly more numerous than the whorls in the spheres of patients who did not have carcinoma of the liver. This second group included patients who were suffering from carcinoma of other organs or from cirrhosis of the liver. The frequency of cases with the spheres increased with age. The numbers of spheres found in people with liver carcinoma, carcinoma of other organs and cirrhosis were the same as the numbers found in people dying from other diseases. The possibility that the increase in numbers of whorls found in people with liver carcinoma was related to a raised metabolic activity of the astrocytes resulting from reduced catabolism of hormones or metabolites by the liver is briefly discussed.
THE DEVELOPMENT OF HUMAN FETAL DORSAL ROOT GANGLIA IN VITRO: THE FIRST 20 DAYS
Authors: CRAWFORD KATHRENE , ARMATI‐GULSON PATRICIA
Published: May 2008

Crawford K. & Armati‐Gulson P. 1982 Neuropathology and Applied Neurobiology 8, 477–488

The development of human fetal dorsal root ganglia in vitro: the first 20 days

Human fetal dorsal root ganglia aged from 8 to 12 weeks post‐menstrual were grown in vitro for up to 20 days. Outgrowth of Schwann cells, axons and fibroblasts occurred after 4 h. By the 7th day in vitro Schwann cells enclosed bundles of axons and after 10 days some Schwann cells were seen to enclose individual axons. By the 20th day in vitro there was still a predominance of Schwann cells enclosing axonal bundles, but there were more individual axons ensheathed by three or four turns of Schwann cells. This arrangement mimics the early development in vivo of human dorsal root ganglia and provides the potential for an experimental system utilizing human nervous tissue rather than non‐human animal models.
THE NUCLEUS BASALIS IN ALZHEIMER'S DISEASE: CELL COUNTS AND CORTICAL BIOCHEMISTRY
Authors: WILCOCK G. K. , ESIRI M. M. , BOWEN D. M. , SMITHS C. C. T.
Published: May 2008

The cell density in the Nucleus Basalis in six patients with clinical and histological evidence of Alzheimer's disease and reduced choline acetyltransferase activity in frontal and temporal cortex was found to be in approximately 50% of the cell count in five control subjects.
BASEMENT MEMBRANE SURFACES AND PERIVASCULAR COMPARTMENTS IN NORMAL HUMAN BRAIN AND GLIAL TUMOURS. A SCANNING ELECTRON MICROSCOPE STUDY
Authors: SAPSFORD I. , BUONTEMPO JEAN , WELLER R. O.
Published: May 2008

The relationships of perivascular tissues to arteries and veins in normal brain and glial tumours were investigated by light microscopy and by scanning and transmission electron microscopy. Vessels and perivascular tissues were separated through various planes by careful tearing of fixed tissue blocks of brain and tumour. Mirror surfaces of torn blocks were examined by scanning electron microscopy and the identity of the vessels and other structure confirmed by transmission electron microscopy. Perivascular glial basement membranes remained adherent to arterial adventitia in both normal brain and in tumour so that the torn surface around the vessel exposed perivascular glial processes attached to the vessel walls. A clear plane of separation of perivascular glial basement membrane from the adventitia of veins was achieved in glial tumours. Mirror surfaces showed the smooth undulating sheet of basement membrane separated from the fine fibrillary connective tissue of the vessel wall. Tears in the basement membrane revealed the perivascular glial processes. The structure of the perivascular basement membrane is discussed in relation to its role as an attachment site for perivascular glial and as an impedence to inflammatory cell migration into brain parenchyma.
BILIRUBIN ENCEPHALOPATHY
Authors: SHERWOOD ANTHEA J. , SMITH J. F.
Published: May 2008

In babies of low birth weight dying in the first week of life, bilirubin encephalopathy involving the thalamus only or the thalamus and one or two other areas occurred in nineteen of 376 cases examined over a 10 year period. Although coexistent germinal layer haemorrhage was present in sixteen, this was not thought to be an aetiological factor. Bile stained hyaline membranes in nine of the nineteen were considered to indicate the possibility of protein‐bound bilirubin traversing a vascular barrier in these cases. This pattern of predominant lateral thalamic involvement may indicate selective vulnerability of this area in this group. It contrasts sharply with the localization in classical kernicterus (three cases) and in a disparate group where yellow discolouration of future white matter areas was observed (thirteen cases).
FORM AND DISTRIBUTION OF SENILE PLAQUES SEEN IN SILVER IMPREGNATED SECTIONS IN THE BRAINS OF INTELLECTUALLY NORMAL ELDERLY PEOPLE AND PEOPLE WITH ALZHEIMER‐TYPE DEMENTIA
Authors: GIBSON P. H.
Published: May 2008

Brains came to autopsy from elderly cases that had been psychometrically tested and were shown to be either intellectually normal (n= 48) or suffering from dementia of the Alzheimer‐type (n= 56), as well as elderly cases that had not been tested (n= 32). Cortical senile plaques, impregnated by von Braunmuhl's silver method, were found to range in structure from amorphous (neuritic) through to discrete (amyloid). Large numbers of the amorphous plaques were most frequently found in the outer half of the cortex of the demented cases, aged 60–75, whereas small numbers of the discrete plaques were most frequently found in the inner half of the intellectually normal cases, aged 75 onwards. The distribution of the senile plaques per se was found for four different regions of the cortex as well as the correlation of their numbers with the ages of the cases. The pathogenesis of the plaques is discussed.
GLIAL BUNDLES IN SPINAL NERVE ROOTS: A FORM OF ISOMORPHIC GLIOSIS AT THE JUNCTION OF THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM
Authors: GHATAK N. R.
Published: May 2008

A morphologic study of the spinal nerve roots was undertaken in three cases of Werdnig‐Hoffmann disease to investigate the phenomenon of glial bundle formation. The glial elements extended along the ventral roots as discrete cylindrical bundles comprising a large number of parallel astrocytic processes and sparsely scattered cell bodies all enclosed by a basal lamina. The bundles tapered off at a variable distance from the root exit zones. The early stage of glial bundle formation was characterized by the protrusion of astrocytes into the neurilemmal tubes containing degenerated myelinated axons. It was concluded that axonal degeneration, evoking a glial reaction, was the initial event in this process. Subsequently, the reactive astrocytes from the vicinity of the root exit zones enter the neurilemmal tubes previously occupied by myelinated axons and migrated into the domain of the peripheral nervous system in an orderly fashion. Thus glial bundle formation might be considered a special form of isomorphic gliosis occurring in Werdnig‐Hoffmann disease and also in several other conditions all sharing a common feature, namely, degeneration of axons within the spinal nerve roots.
THE PERMEABILITY OF THE BASAL LAMINA AT THE NEUROMUSCULAR JUNCTION. AN ULTRASTRUCTURAL STUDY OF RAT SKELETAL MUSCLE USING PARTICULATE TRACERS
Authors: OLDFORS A. , FARDEAU M.
Published: May 2008

Various macromolecular substances, such as toxins and antibodies, may interfere with neuromuscular transmission. The neuromuscular junction is also known to be a site for the uptake of macromolecular substances into the axon for subsequent transport to the central nervous system. The synaptic cleft of the neuromuscular junction is separated from the rest of the extracellular compartment of muscle by the basal lamina, the permeability properties of which are not known. The penetration of macromolecular substances of varying size into the synaptic cleft of the neuromuscular junction has been studied in rats. Four different tracers: Imferon (an iron‐dextran measuring 11 times 7 × 7 nm), ferritin (a spherical iron‐protein 12 nm in diameter), Imposil (an iron‐dextran measuring 21 times 12 times 12 nm) and colloidal gold‐protein (20–25 nm in diameter) were injected into the palmaris longus muscle. Fifteen and 120 min after injection, the distribution of these particulate tracers was studied by electron microscopy. Imferon and ferritin penetrated rapidly through the basal lamina along the muscle fibres and also into the synaptic cleft of the neuromuscular junction. The larger Imposil and colloidal gold particles were restricted from penetrating the basal lamina even after 2 h, and these particles were traced only occasionally within the synaptic cleft. The results indicate that the basal lamina of muscle acts as a diffusion barrier to large macromolecules, preventing them from entering the synaptic cleft.
AGING OF DENDRITES IN THE CEREBRAL CORTEX OF THE MOUSE
Authors: LEUBA G.
Published: May 2008

Quantitative analysis of the dendritic branchings of pyramidal cells in layers V and III of the visual cortex was performed in aging mice (540 and 720 days) and compared to adult mice (180 days). The number of spines on apical dendrites of the same cells was also counted. Between 180 and 720 days of age, the decrease in dendritic branchings around the perikaryon was dramatic (30–40%) and that in dendritic spines was even more so (about 50%). However, most of the decrease in both dendritic branchings and spines has already occurred at 540 days, and the difference between 540 and 720 days was not statistically significant. This suggests a real loss in cortical connections with aging, taking place prior to the final months of the lifespan of the mouse.
ASPERGILLOSIS OF THE NERVOUS SYSTEM. REPORT OF TWO CASES
Authors: DIENGDOH J. V. , BARNARD R. O. , THOMAS D. G. T.
Published: May 2008

Two cases of Aspergillus infection of the nervous system are reported. In the first case it occurred in a healthy individual and presented as a space occupying lesion mimicking a tuberculous granuloma. In the second case it was an opportunistic infection in a patient with predisposing conditions and manifested as chronic meningitis with fatal arteritis.