Jacob Abraham

Cerebral angiographic features in tuberculous meningitis

SUMMARYCerebral angiographic findings of 10 cases of tuberculous meningitis are presented. Narrowing and occlusion of intracranial arteries were the major findings, the most common sites of abnormalities being the supraclinoid portion of the carotid artery and proximal portion of the anterior and middle cerebral arteries. The branches of the intracranial arteries were also involved. The extracranial portion of the internal carotid was found to be uniformly narrow in few cases. Three types of collaterals were seen—the net-like cluster of thin vessels in the region of basal ganglia and base of the brain, transdural external-internal carotid anastomosis, and increased cortical anastomosis with altered architecture of the arrangement. “Early veins” were also seen. Hydrocephalic pattern and delayed circulation were the other features. The resemblance of the net-like cluster of the vessels at the region of the basal ganglia to those described in moyamoya disease is pointed out. It is suggested that these peculiar collaterals are confined to intracranial arterial occlusions related to some inflammatory process in young people.

Intradural hydatid cysts of the spinal cord

Abstract A patient with primary intradural spinal hydatid disease presenting with complete paraplegia is described. The diagnosis was made at operation. The patient did not have any clinical evidence of visceral or extradural hydatid lesions. This, we believe, is the first case of primary spinal intradural hydatid disease reported from India.

Avoiding empiric therapy for brain masses in Indian patients using CT-guided stereotaxy

Empiric therapy, especially antituberculous therapy, is frequently given to Indian patients with brain masses. This report documents our experience in avoiding such therapy using CT-guided stereotaxy. Out of 101 procedures done on 99 patients with brain masses, 80 were done to obtain a histological diagnosis and 21 for therapeutic purposes. There was no mortality and 2% morbidity. A positive diagnosis was obtained in 94% (75/80) of patients undergoing a biopsy. Diagnosis of tuberculous lesions was based mainly on the presence of acid-fast bacilli in the biopsy specimen or pus. In six patients the radiological diagnosis was wrong and in one the diagnosis was not certain. Inappropriate therapy was given to three patients, on the basis of a CT or MRI scan, before a biopsy was done. It is essential that a histological diagnosis be obtained in all patients with brain masses and there is no role for empirical therapy except in isolated cases.

Free Fatty Acids, Lipid Peroxidation, and Lysosomal Enzymes in Experimental Focal Cerebral Ischemia in Primates: Loss of Lysosomal Latency by Lipid Peroxidation

Experimental focal cerebral ischemia was produced in monkeys (Macaca radiata) by occlusion of the right middle cerebral artery (MCA). The release of the lysosomal glycosidases, β-d-hexosaminidase, α-l-fucosidase and α-d-mannosidase into the soluble fraction in the right basal ganglia of the experimental animals was measured at different periods from 30 min to 12 hr after occlusion and compared with the corresponding sham operated control animals. There was a significant increase in the released lysosomal enzymes in the MCA occluded animals at all periods and particularly at 4 hr after occlusion. The CSF from the experimental animals also showed elevated levels of hexosaminidase and fucosidase. The free fatty acids (FFA) measured in the basal ganglia at 30 min and 2 hr after occlusion showed a 100 fold increase in the experimental animals. The predominant fatty acid released was linoleic acid (18:2) followed by arachidonic acid (20:4). Lipid peroxidation in the basal ganglia measured by the thiobarbituric acid (TBA) reaction in the presence or absence of ascorbic acid also showed a significant increase in the experimental animals at all periods with a maximum at 30 min to 2 hr after occlusion. In order to assess whether lipid peroxidation causes damage to the lysosomes and release of the enzymes, a lysosome enriched P2 fraction from the normal monkey basal ganglia was prepared and the effect of peroxidation studied. Maximum peroxidation in the P2 fraction was observed in the presence of arachidonic acid, ascorbic acid and Fe2+. There was a good correlation between the extent of lipid peroxidation and the in vitro release of lysosomal hexosaminidase from the P2 fraction. Anti-oxidants which strongly inhibited lipid peroxidation in the P2 fraction prevented the release of hexosaminidase. The results suggested that in ischemia produced by MCA occlusion lipid peroxidation which damages the lysosomal membrane causes the release of lysosomal hydrolytic enzymes.

Non-traumatic cerebrospinal fluid rhinorrhea: The “Normal pressure leaks”

SummaryNon-traumatic cerebrospinal fluid (CSF) rhinorrhea is an uncommon condition. 15 patients with non-traumatic CSF rhinorrhea having “normal pressure leaks” are presented. Metrizamide CT cisternography failed to reveal the site of the fistula in 3 patients. 11 of the 15 patients underwent surgery for closure of the fistulous communication. In 8 of them the fistula was in the anterior fossa, in one it was in the sellar floor and in two the fistula site was not seen either radiologically or at surgery. In all except the one patient with sellar floor defect an intracranial approach was used. 12 patients have been followed up for 6 months to 9 years and 10 (83%) have been cured of their rhinorrhea. The intracranial approach is preferred to an extracranial approach in the repair of anterior fossa fistulae. Conservative treatment may be effective in selected patients.

Late complications of hemispherectomy: report of a case relieved by surgery

A case of Sturge-Weber disease treated with left hemispherectomy presented, 11 years later, with complications related to delayed intracranial haemorrhage. A loculation syndrome of the right lateral ventricle was detected and it was corrected by a ventriculoatrial shunt operation. The side of the hemispherectomy was evacuated of all the chronic products of haemorrhage, including the subdural membrane. The patient was relieved of her symptoms. It is considered that complications related to delayed haemorrhage after hemispherectomy are remediable.

The paradox of increased microvascular visualization with decreased perfusion in cerebral focal ischaemia in a primate model

Microvasculature of the right caudate nucleus and insular cortex of monkeys with their right middle cerebral artery occluded was morphometrically measured with an image analysis system at 1/2, 4, 12, 24, and 48 hr and 2 weeks. A biphasic change in the microvasculature was observed. In the first phase up to 12 hr an increase in the number and length of the total microvasculature, visualized by alkaline phosphatase staining, along with a reduction in the number and length of the perfused part of the microvasculature, visualized by India ink perfusion, was observed. In the second phase after 48 hr, the number and length of the total microvascular bed as well as the perfused functional bed were significantly reduced.

TEMPORAL PROFILE OF TISSUE LEVELS OF DOPAMINE AND ITS METABOLITES, HVA AND DOPAC FOLLOWING FOCAL CEREBRAL ISCHAEMIA IN ANAESTHETIZED PRIMATES

1. Occlusion of the middle cerebral artery produced ischaemia and consequent changes in basal ganglia in the primate model of stroke within 0.5 h.

CHANGES IN THE CONTENT OF DOPAMINE AND ITS METABOLITES IN THE BASAL GANGLIA FOLLOWING RIGHT MIDDLE CEREBRAL ARTERY OCCLUSION AND REFLOW IN MONKEYS

1. Focal ischaemia was produced experimentally in Macaca radiata monkeys by occlusion of middle cerebral artery (MCA). There was a lowering of the dopamine (DA) content of basal ganglia after 4 and 12 h of occlusion.

Pathology of Ischaemic Brain Damage — Implications for Therapy

An ischaemic infarct was produced in primates by applying a clip to the right middle cerebral artery. Enzyme histochemical data are presented, documenting the development of a focal ischaemic brain lesion. The relatively slow demarcation of the ischaemic brain infarct appears to be correlated with the efficiency of the collateral blood supply. The extent of the collateral blood supply is documented by morphometric data on the brain capillaries. It was evident that effective intervention in the infarction process with a view to limiting the extent of an ischaemic brain lesion is possible only at an early stage. A reduction of blood viscosity by bloodletting and haemodilution is the most important measure to be taken in the first few hours after a stroke. The second important step in the treatment of acute stroke is inhibition of blood platelet aggregation to arrest the thrombotic process and avoid complete occlusion of the artery, or in the case of an embolism to limit the extent of the infarct.