Biomedical subjects
Publications and source records attributed to C Vidyasagar.
Tuberculosis is still a major cause of spinal compression in the developing countries. In this study 200 patients presenting with neurological lesions secondary to tuberculosis of the spine have been classified according to the Frankel classification and the results evaluated. A combination of surgical decompression and chemotherapy is advocated. The dangers of non-operative treatment are discussed.
Arterialized venous channels in the arteriovenous malformations of the brain represent persistent embryonic veins. The configuration of these veins resembles embryonic venous channels. Their microscopic features also resembles those of the foetal cerebral veins. The intimal liming of the persisting embryonic veins suggests the approximate age of the foetus at which the arteriovenous fistual is likely to have occurred.
The diencephalic arteriovenous malformation is produced by the posterior cerebral, posterior choroidal, and anterior choroidal arteries. The abnormal arterialised vessels seen in these malformation represent dorsal and ventral diencephalic veins. The drainage of the shunted blood is primarily into the transverse sinus. This is later diverted medially into the great cerebral vein, with the formation of the basal vein. The medial drainage, in keeping with the normal developmental pattern, is seen frequently. The presence and locations of angiomas are very variable and do not follow any predictable pattern.
In the arteriovenous malformations of the posterior fossa the arterial feeders and the dural venous sinuses can be identified in anatomical terminology. The arterialised veins which do not conform to adult anatomical descriptions represent the persistent embryonic veins of the metencephalic and myelencephalic segments of the developing brain. These can be identified and described when related to the embryo.
The arterial components of the telencephalic arteriovenous malformations arise from the anterior cerebral and middle cerebral arteries. The complexity of the development process in this region obscures the fundamental segmental pattern. There are three regions where the primitive pial vessels cross at right angles. They are: a) over the convexity of the cerebral hemispheres, b) in the Sylvian territory, c) in the region of the basal ganglia. The malformations over the surface drain into the superior sagittal sinus. The Sylvian and deep telencephalic malformations drain primarily into the tentorial sinus, and this is often replaced by a medial drainage into the internal cerebral vein through the tributaries of the basal vein.
The basic anatomy of the arteriovenous malformations of the dura is similar to that of the internal carotid (pial) malformations, as the arterial feeders in both these lesions arise from the internal carotid artery in the embryo. The venous drainage occurs through definite channels into the major venous sinuses. Therefore, the dural and the pial malformations should be classified together. The scalp malformations have no features similar to these groups. The prominent occipital artery is not necessarily the primary feeder. Whenever a prominent occipital artery is seen, special efforts must be made to locate the primary dural feeders arising from the internal carotid artery.
A young man developed a paraplegia of relatively sudden onset. A myelogram revealed an obstruction at the T8 level. Laminectomy at T7-9 disclosed a remarkably thick dura mater compressing the spinal cord. Microscopic examination of the dura mater was suggestive of syphilitic granulation tissue. Serum and CSF samples examined for evidence of syphilis were strongly reactive.
The course and direction of persistent foetal venous channels are easily defined in the relatively simple segmental portions of the nervous system, such as the spinal cord, the myelencephalon, the metencephalon, and the mesencephalon. In sites were embryonic development is more complicated, like the diencephalon and the telencephalon, rapid growth and folding of the cortex complicate the patterns of the foetal blood vessels. Arteriovenous malformations in such sites are correspondingly more complex.
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Two hundred patients suffering from tuberculosis (TB) of the spine with neurological complications were the subjects of this review. They were graded according to the Frankel system into--A: complete neurological deficit; B: sparing of some sensation; C: sparing of sensation but no useful motor function; D: sparing of sensation and useful motor function; and E: no deficits. Investigations carried out included detailed neurological assessment, radiography, contrast myelography and, in the later stages of the study, spinal computerized tomography (CT) scan. The authors believe that contrast myelography provides the best indication of spinal compression in TB spine. Treatment was by surgical decompression followed by chemotherapy. The surgical approach for thoracic spine disease was by the anterior transthoracic route. Cervical lesions were also approached by the anterior route, lateral to the carotid vessels. Unexpected findings during operation included lymphoma, plasmacytoma, non-tuberculous granulation tissue, salmonella osteomyelitis and tumour metastasis. Ten patients died during the postoperative period, all of whom had extensive systemic TB. When indicated, antituberculous drugs were administered postoperatively for two years and immobilization was done in a plaster cast for 3 months. Only 30 patients showed partial recovery. Improvement was found to be related to the grade of deficit; thoracic lesions with severe neurological deficits showed the least improvement while lumbar disease had the best outcome. The study recommended a combination of surgery and chemotherapy for all cases of TB spine with neurological deficits after a short delay during which respiratory function should be improved. The surgery should aim at decompression of the cord by removal of pus, granulation tissue and sequestra, with internal splintage with bone grafts to reduce the hospital stay. Conservative treatment is unwise because it is not always possible to distinguish between TB and neoplastic lesions.