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Biomedical subjects

R A Rodda

Publications and source records attributed to R A Rodda.

12 recordsLinked to original sources
PubMed1984

Intracranial meningeal chondrosarcoma--probable mesenchymal type.

A 12 year old girl with episodes of left hemiparesis for 9 months was found to have a large, partly calcified brain tumour which at craniotomy presented on the parasagittal and medial surfaces of the right frontal lobe. No dural or falx attachment could be found and naked eye removal of the tumour was achieved. At a second craniotomy 10 weeks later there was recurrent tumour attached to the falx and involving the sagittal sinus. She died 5 months later. Pathologically, almost all this malignant intracranial neoplasm comprised differentiated cartilaginous tumour. Although only a very small amount of undifferentiated mesenchymal tissue was found in the surgical material available for histological study, it is suggested the tumour can be regarded as a predominantly mature mesenchymal chondrosarcoma of the meninges.

Brain Neoplasms↗
PubMed1983

Parenchymal brain lesions in spontaneously hypertensive stroke-prone rats.

The gross and histological features of 189 parenchymal brain lesions in 57 spontaneously hypertensive stroke prone rats are described. There were 127 lesions many of them cystic, showing evidence of old haemorrhage. Of these, 71 also showed recent haemorrhage and there were 26 lesions showing recent haemorrhage only. There were 21 small focal lesions with necrosis and scarring but without any old or recent haemorrhage and 15 other lesions showing focal oedema with microcysts. Undoubted histological evidence of recent ischaemic necrosis was not seen. In this animal model which spontaneously develops severe hypertension, the brain lesions are predominantly the result of leakage of blood components from small vessels.

Animals↗
PubMed1981

Cerebellar atrophy in Huntington's disease.

The clinical features are outlined and the neuropathological changes described in 3 cases (2 adults and 1 child) of Huntington's disease with severe atrophy of the cerebellum. Onset occurred at the ages of 56, 55 and 3 and death at 70, 62 and 6 years, respectively. All cases presented with cerebellar ataxia and this is also recorded in one relative of each adult case. The family history of Huntington's disease was not ascertained until the later stages of each patient's illness. At necropsy, the 3 cases showed the characteristic striatal and cerebral cortex atrophy and the shrunken cerebellum showed diffuse thinning of the molecular and granular layers with almost complete loss of Purkynĕ cells.

Atrophy↗
PubMed1978

Elastofibroma dorsi.

A case of bilateral subscapular elastfibroma dorsi in a 60-year-old woman is described. The striking clinical and pathological features of this rare benign tumour-like lesion are described and illustrated.

Female↗
PubMed1977

A case of Creutzfeldt-Jakob disease.

The case is reported of a 64-year-old woman with ataxia and dementia progressing to a state of extrapyramidal rigidity and death in 10 months. The neuropathological changes characterised by severe nerve cell degeneration and loss, a hypertrophic astrocytic gliosis and a status spongiosus were widespread in the cerebral cortex, corpus striatum and cerebellum and confirmed the clinical diagnosis of Creutzfeldt-Jakob disease.

Brain↗
PubMed1975

Some effects of methyl mercury salts on the rabbit nervous system.

Young adult rabbits have been given methyl mercury salts by subcutaneous injections or by gastric intubation. After 3 daily doses of 7.5 mg/kg by the 8th day moderate to severe ataxia developed, and after 4 doses, severe ataxia. Some of these latter animals might die. This species, therefore, seems to be about twice as sensitive to the neurotoxic properties of methyl mercury salts as the laboratory rat. With the light microscope extensive degenerative changes were seen in primary sensory ganglion cells, in both Purkinje and granule cells of the cerebellum, and in certain cells in several regions of the forebrain. The earliest changes became visible microscopically about the fourth day after commencing dosing, and reached a maximum of severity from the 7th to 10th day. The pattern of neuronal damage more closely resembled that found in the cat and in man than that seen in the rat. No evidence of changes vascular permeability was detected.

Animals↗
PubMed1975

Bone growth changes in pyridoxine-deficient rats.

Male and female rats were fed a commercial diet lacking pyridoxine. Using radiological and histological methods the growth of the long bones in the pyridoxine-deficient rats from 2 wk to 6 mth of age was compared with that in paired-fed and in paired-weight-gain control rats of the same age and sex given the same diet supplemented by daily injections of pyridoxine hydrochloride. Measurements of tibial bone length were significantly reduced in the deficient male rats but not females, possibly due to the reduced requirements for growth in the female. Thin epiphyseal plates were a feature of the limb radiographs in all the pyridoxine-deficient rats. Histologically the growing long-bone ends showed a diminished activity of endochondral ossification with thin epiphyseal cartilage and fewer shorter, broad and irregular bone trabeculae in the metaphyses of the deficient rats. These metaphyseal changes resemble those described in starvation.

Animals↗
PubMedDate not supplied

The arterial patterns associated with internal carotid disease and cerebral infarcts.

In 20 necropsies with 15 stenosed and 17 thrombotic occluded internal carotid arteries there were 46 cerebral infarcts larger than 1 cm diameter. Using portmortem arteriographic and pathological techniques the patterns of the neck and brain artery systems were correlated with the situation and extent of the brain infarcts. Massive infarcts involving two major cerebral artery territories were associated with distal internal carotid artery occlusion and grossly ineffective cervical and circle of Willis anastomoses. Isolated middle cerebral artery territory infarcts were associated with internal carotid occlusion or stenosis and impairment of the circle of Willis anastomoses, perhaps with middle cerebral artery stenosis. The pattern of adequate size arteries determined if these infarcts were total, deep central, anterior, medium or posterior partial territory infarcts. Boundary zone infarcts were associated with internal carotid artery disease and limitation of anterior or posterior circle of Willis anastomoses. These limitations determined which boundary zones were affected. Isolated anterior cerebral artery territory infarcts were associated with bilateral internal carotid disease and an anterior cerebral artery stenosis or small caliber anterior communicating artery. Isolated posterior cerebral artery territory infarcts were associated with internal carotid disease and a direct impairment of the ipsilateral posterior cerebral artery capability.

Adult↗
PubMedDate not supplied

Fatal non-missile head injury: a cohort study of patients with and without an intracranial hematoma.

Brain damage in fatal non-missile head injury is outlined in 100 cases with and in 100 cases without an intracranial hematoma. The patients with intracranial hematomas were significantly older, and had a higher incidence of lucid interval and of unilateral diffuse brain swelling but a lower incidence of ischemic lesions in the cerebral cortex and of bilateral diffuse brain swelling than the patients with no hematoma. Cases with unilateral hematomas and cases with unilateral diffuse brain swelling had significantly more severe ipsilateral cerebral contusions.

Adolescent↗