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Biomedical subjects

G Gerard

Publications and source records attributed to G Gerard.

41 records · Page 3Linked to original sources
PubMedDate not supplied

Tuberous sclerosis: CT findings and differential diagnosis.

The CT findings in a patient with tuberous sclerosis are described with special emphasis upon the differential diagnosis. The presence of multiple bilateral subependymal nodular nonenhancing hyperdense calcified lesions is relatively characteristic of tuberous sclerosis when combined with the appropriate clinical findings. In some cases, cerebral cortical heterotopias are visualized as hypodense nonenhancing subependymal lesions. The finding of a subependymal giant cell astrocytoma is sometimes seen in patients with tuberous sclerosis, and the finding of a subependymal hyperdense enhancing lesion is consistent with this diagnosis.

Calcinosis↗
PubMedDate not supplied

Computerized tomographic findings and differential diagnostic considerations in subcortical arteriosclerotic encephalopathy (Binswanger's disease).

This paper discusses the conditions which may be associated with diffuse periventricular hypodensity on CT. Of these conditions, subacute arteriosclerotic encephalopathy (Binswanger's disease) is a common differential diagnostic consideration. This condition results from ischemic demyelination with loss of axons and astrogliosis. CT usually shows diffuse bilateral confluent hypodensities in the cerebral white matter. This is most prominent and seen earliest in the periventricular region and may extend more diffusely into the centrum semiovale. It is important to differentiate this condition from normal pressure hydrocephalus and primary nonischemic demyelinating disease (multiple sclerosis).

Aged↗
PubMedDate not supplied

Effect of biofeedback-assisted relaxation on migraine headache and changes in cerebral blood flow velocity in the middle cerebral artery.

Twenty-three patients with diagnosed migraine headaches were randomly assigned to a biofeedback-assisted relaxation therapy group or to a group who relaxed on their own. The biofeedback trained group decreased pain and medication more than the self relax group. Cerebral blood flow velocity was measured in the middle cerebral artery with transcranial doppler (TCD). The trained group significantly reduced systolic and mean cerebral blood flow velocity on the side with the highest velocity.

Adult↗
PubMedDate not supplied

Relationship between natriuresis and changes in plasma atrial natriuretic factor, renin activity and aldosterone levels in fasting obese subjects.

This study was conducted to assess whether changes in atrial natriuretic factor (ANF) secretion could account for the natriuresis of the early phase of fasting. To this end, 8 AM (supine) and 10 AM (standing) plasma ANF concentrations were determined daily and compared with plasma renin activity and aldosterone levels in 8 obese subjects submitted to a 7-day total fast. Depiste constant daily sodium intake (51 mmol), urinary sodium excretion increased from 35 +/- 7 to 109 +/- 8 mmol/day after 4 days of fast (p less than 0.001) and declined thereafter. Urinary ketone excretion progressively increased over the whole period of fasting (p less than 0.001). Interestingly, fasting induced a decrease in plasma ANF concentrations (p less than 0.05). A contrast analysis revealed no significant change in ANF during the initial natriuretic phase of fasting but a decrease at the end of fasting averaging 36% (p less than 0.05) and 18% (p less than 0.05) at 8 and 10 AM respectively. In contrast, plasma aldosterone rose during fasting (p less than 0.05), the difference being significant at the end of fasting (p less than 0.01). Plasma renin activity and cortisol did not change significantly over the fasting period. Postural and/or diurnal changes of ANF, aldosterone, renin and cortisol were preserved during fasting (p less than 0.01). Postural changes of ANF were, however, attenuated at the end of fasting (p less than 0.05). These data indicate that the fasting natriuresis cannot be explained by changes in ANF levels but that the loss of sodium may contribute to a decline of basal ANF levels, with an attenuation of their physiological postural changes, and to a stimulation of the aldosterone secretion.

Aldosterone↗