Sir Astley Paston Cooper stated in 1804 that a sound knowledge of proper anatomy of hernia is vital. But even in the succeeding two centuries, the confusion has only multiplied by varied and overly enthusiastic descriptions, some speculative and others real, by different workers. An attempt has been made to highlight the size of the controversies surrounding the anatomical structures forming the inguinal canal and groin. The inguinal and femoral hernias should be viewed collectively as one entity and together be called groin hernias. Therefore, the passage for their superficial emergence through the anterior abdominal wall is redefined and is called pubomyoaponeurotic foramen. It is uniformly accepted that the strong posterior wall of the groin area is the only preventive factor towards the emergence of hernia; it has been renamed as posterior groin plait. Therefore, proper understanding of its structure towards effective repair and reinforcement is the only safe method, whether the procedure is carried out by anterior or posterior route or laparoscopically. Hence, an attempt has been made to elucidate its true structure. In spite of so many descriptions, the exact anatomy of hernia is yet to be resolved.

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The concept of temporal and spatial relationship between neuronal and vascular changes in the central nervous system following different kinds of anoxia still remains debatable, in that it is uncertain if anoxia-ischaemia primarily produces vascular changes in the brain or it initially damages the cerebral neurons. The present investigation has been undertaken to denote the sequential relationship between neuronal and vascular changes following experimental cerebral ischaemic anoxia. Adult healthy albino rats were subjected to ischaemic anoxia by bilateral clamping of their common carotid arteries for varying intervals of 5, 10 and 15 min. The animals of each group were subsequently sacrificed on days 1, 3, 5, 7 and 10 after the clamping procedure, for light-microscopic study of their brains. Our findings are characterized by initial vascular changes, which appear to have resulted in ‘no-reflow’ leading subsequently to neuronal damage. The latter, in turn, secondarily caused damage to the microvasculature.

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