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Biomedical subjects

R O Barnard

Publications and source records attributed to R O Barnard.

At least 19 recordsLinked to original sources
PubMed1994

A comparison of the pathology of primary and secondary progressive multiple sclerosis.

The dynamics of primary progressive multiple sclerosis differ from those of the more common secondary progressive form. The observation by MRI that the frequency of enhancement with gadolinium-DTPA, a marker for blood-brain barrier dysfunction, is significantly less in the primary progressive form, has led to the hypothesis that inflammation is less intense in this group. To test this, we have studied postmortem material from nine cases judged from a retrospective analysis of case notes to show clear clinical evidence of either primary progressive or secondary progressive disease. Five hundred and seventy-eight lesions were analysed. There was significantly more inflammation in secondary progressive multiple sclerosis (as judged by the frequency of perivascular cuffing and cellularity of the parenchyma) than in primary progressive disease. These observations have implications for therapeutic strategies in progressive multiple sclerosis.

Adult↗
PubMed1993

Multiple sclerosis: remyelination of nascent lesions.

The relationship between plaque pathology and disease duration was examined in 15 patients with multiple sclerosis who died early in the course of their illness. Myelin-stained sections revealed that most plaques examined in patients who died during the first month of their illness showed evidence of ongoing myelin destruction accompanied by a loss of oligodendrocytes. Plaques containing large numbers of oligodendrocytes were not observed in these patients, but were relatively common in patients who died more than 1 month after clinical onset. Remyelination affecting more than 10% of the plaque area was observed in 3 of 82 plaques in 5 patients who died within 10 weeks of clinical onset, in 38 of 105 plaques in 5 patients who died 3 to 10 months after clinical onset, and in 19 of 92 plaques in 5 patients who died 18 months or longer after clinical onset. The study provides new evidence that both oligodendrocytes and myelin are destroyed in new lesions, that this activity ceases completely in many lesions within a few weeks, and that remyelination frequently ensues following repopulation of the plaque by oligodendrocytes. The findings suggest that new lesions normally remyelinate unless interrupted by recurrent activity and that remyelinated shadow plaques are the outcome of a single previous episode of focal demyelination.

Adolescent↗
PubMed1993

Multiple sclerosis. Pathology of recurrent lesions.

Recent autopsy studies suggest that remyelinated shadow plaques located in otherwise intact white matter are the outcome of a previous single episode of acute demyelination. In the present study, of 98 remyelinated plaques examined in 15 patients with multiple sclerosis who died between 27 days and 5 years after clinical onset, 15 showed evidence of a superimposed new demyelinating lesion. Inspection of old shadow plaques in a separate series of patients with subacute and long-standing multiple sclerosis revealed that such lesions sometimes exhibit punched-out areas of demyelination and gliosis similar in size and shape to fresh lesions located within or overlapping remyelinated shadow plaques. The findings support magnetic resonance imaging evidence that local recurrence may be as important or more important than progressive edge activity in determining plaque growth and the conversion of nascent lesions into classical demyelinated plaques. The findings also support experimental evidence that recurrent demyelination of the same area of white matter may be one of the factors underlying failed remyelination in multiple sclerosis.

Adult↗
PubMed1992

Cerebellar syndrome in myxoedema revisited: a published case with carcinomatosis and multiple system atrophy at necropsy.

One of six patients in a 1960 paper on "Cerebellar syndrome in myxoedema" was subsequently found to have adenocarcinoma. General post-mortem revealed carcinomatosis and basal pneumonia. Neuropathological examination revealed the changes of multiple system atrophy. The relationship between hypothyroidism, carcinoma, and cerebellar, pontine and striatonigral degeneration is discussed.

Adenocarcinoma↗
PubMed1991

Destructive lesions in demyelinating disease.

Three cases are presented in which clinical and radiological features suggested the diagnosis of glioma but surgical biopsy revealed a demyelinating process, with tissue destruction and cyst formation in two. One patient had clinically definite multiple sclerosis. Two had probable acute disseminated encephalomyelitis. Treatment with high dose steroids is appropriate when there is clinical or investigative evidence to suggest the presence of demyelinating disease, before deciding on biopsy.

Adolescent↗
PubMed1990

Familial cerebral amyloid angiopathy with nonneuritic amyloid plaque formation.

Two families have been described previously with the features of an autosomal dominant familial cerebral amyloid angiopathy with nonneuritic plaque formation. The clinical features of the cases were dementia, spastic paralysis and ataxia. It has now been established that both families were descended from a common ancestor and the case histories of 26 affected individuals in 5 generations of this pedigree are reported. An autopsy study has been performed on a recent case. The findings are described and compared with the four previously published autopsy studies in this family, which is then discussed in the context of recent advances in the nosology of familial disorders in which cerebral amyloid angiopathy and other forms of cerebral amyloid deposition occur.

Amyloidosis↗
PubMed1989

Tropical spastic paraparesis and human T cell lymphotropic virus type 1 in the United Kingdom.

Twenty-one patients with tropical spastic paraparesis (TSP), all of whom were born in the Caribbean and who had migrated to the United Kingdom, are described. All had a progressive spastic paraparesis developing many years after immigration and all 19 tested had antibodies to the human T cell lymphotropic retrovirus type 1 (HTLV1). The clinical and laboratory features and visual, auditory and somatosensory evoked potentials are described. Details of magnetic resonance scanning of the brain and, in a few cases, the spinal cord are compared with those found in multiple sclerosis. The antibody titres to HTLV1 assessed by particle agglutination, Western blot, antibody-directed cell mediated cytotoxicity and pseudotype neutralization were higher than in asymptomatic infected relatives and in patients with adult T cell leukaemia. Some, but not all, of the IgG oligoclonal bands in the CSF were directed against HTLV1. IgM oligoclonal bands directed against HTLV1 were found in 2 patients. Sixty of the 64 first degree relatives of 11 Jamaican patients with TSP were traced in the UK and the Caribbean; 20-30% of those born in the Caribbean had antibodies to HTLV1, irrespective of their present place of residence, whilst none of those born in the UK, who were the children of the patients, had antibodies. The original pathological material obtained from the Caribbean by Montgomery et al. (1964) is reviewed. These results are discussed in relation to animal retroviral neurological diseases, particularly visna in sheep which has clinical and pathological features closely similar to TSP. It is proposed that TSP is due to a HTLV1 infected lymphocyte/macrophage immune-mediated inflammatory response in the spinal cord.

Adult↗
PubMed1989

Pathological findings correlated with magnetic resonance imaging in subcortical arteriosclerotic encephalopathy (Binswanger's disease).

Formalin-fixed brain slices from four cases of subcortical arteriosclerotic encephalopathy in which a firm diagnosis could be made both clinically and pathologically have been studied by magnetic resonance imaging (MRI). The slices were subsequently embedded in paraffin-wax or celloidin and sections were cut in the same plane as the MRI slices. There was a good correlation between the extent and severity of the abnormal MRI signal and the pathological changes. Areas of diffuse MRI abnormality corresponded with areas of axonal and myelin loss with gliosis, and small "lacune"-like lesions corresponded with lacunar infarcts histologically. Sparing of the subcortical U-fibres was seen histologically and on MRI. The abnormal signal probably originates from increased tissue water attributable to gliosis and an expanded extracellular space.

Adult↗
PubMed1989

Cerebellar desmoplastic medulloblastomas. A further immunohistochemical characterization of the reticulin-free pale islands.

We studied by immunohistochemistry the features of differentiation in 24 desmoplastic and 16 classic medulloblastomas (median patient ages, 18 and 6.5 years, respectively) with the use of a panel of cytoskeletal and synaptosomal markers. A distinctive pattern of immunoreactivity with a series of monoclonal antibodies (Mabs) was documented in the polar tumor cells forming the reticulin-free pale islands of the desmoplastic variant, denoting overt neuritogenesis. These comprised the following: (1) Mab Tp-NFP1A3 recognizing an epitope in the high-molecular-weight (Mr) isoform of neurofilament protein; (2) Mab AP18 to the high-Mr microtubule-associated protein 2; (3) Mab TUJ1 recognizing the class III beta-tubulin isotype (human h beta 4); and (4) Mab SY38 to synaptophysin. Immunoblot analysis confirmed the expression of h beta 4 in three medulloblastomas, yielding strong single bands in two desmoplastic medulloblastomas and a considerably weaker band in one classic medulloblastoma. Glial fibrillary acidic protein-positive tumor cells frequently formed an integral component of the pale islands. Oligodendrogliallike areas in one classic and in three desmoplastic medulloblastomas were immunopositive for the Mabs to synaptophysin, microtubule-associated protein 2, and h beta 4, indicating a neuroblastic nature. We propose that the reticulin-free structures of desmoplastic medulloblastomas constitute neoplastic foci with features of predominantly neuronal and, to a lesser degree, astroglial differentiation.

Adolescent↗
PubMed1988

A case of progressive subcortical gliosis presenting clinically as Steele-Richardson-Olszewski syndrome.

A patient presenting with the characteristic clinical features of Steele-Richardson-Olszewski syndrome is described, in whom neuropathological examination revealed atypical features, including extensive cortical and subcortical gliosis. The clinical and pathological features are discussed with particular reference to Creutzfeldt-Jacob disease and it is proposed that the case should be classified as progressive subcortical gliosis.

Astrocytes↗
PubMed1987

The incidence of multifocal cerebral gliomas. A histologic study of large hemisphere sections.

A series of 241 gliomas (astrocytomas, oligodendrogliomas, glioblastomas, and subependymal giant-cell astrocytomas) was studied. This represents all the gliomas examined post mortem over 25 years at one hospital. Two hundred and one cases (85%) were apparently solitary tumors; of the 40 cases with multiple tumor foci, 23 (9.5%) were true multicentric gliomas. After excluding cases in which there was concomitant disease (neurofibromatosis, tuberose sclerosis, or multiple sclerosis), 18 cases of multicentric tumor (7.5%) remained. Multicentric tumors with different histologic appearances accounted for 2.9% of the series. Celloidin-embedded whole brain sections proved invaluable for the detection of microscopic neoplastic foci and unsuspected diffuse spread. The estimated incidence of multiplicity in gliomas is higher than in most series, but the findings suggest that detection of multifocal neoplastic change in these tumors is directly related to the extent to which the brain is sampled, and that figures obtained in this study may well underestimate the true incidence.

Adolescent↗
PubMed1986

Gliomyosarcoma. Report of a case of rhabdomyosarcoma arising in a malignant glioma.

The development of sarcoma within a glioblastoma is a well recognised complication: in the majority of cases it is a fibro-sarcoma originating in the tissues of the proliferating hyperplastic blood vessels. In the case described here the tumour is a rhabdomyosarcoma, apparently derived from abnormal prolific vascular mesenchyme. Only one comparable example has been recorded previously.

Brain Neoplasms↗