Pathophysiology of vasospasm following pituitary apoplexy remains unknown. Trans-diaphragmatic rupture of the sellar tumour into the subarachnoid space is the most probable cause behind vasospasm. Documented cases of cerebral infarction in consequence to pituitary apoplexy are a few (Mohindra et al. 2010).

As discussed earlier, mechanical obstruction has been cited by many authors as an important cause behind development of ischaemic neurological deficits. As intra-tumoural pressures in comparison to arterial pressures have not been documented, this theory is far from facts and remains a mere presumption.

Totally occluded great vessels as visualized on angiograms have been attributed to mechanical obstruction by the authors. Nevertheless, such an angiogram may be seen on account of severe vasospasm also, and hence, both theories go hand in hand in explaining ischaemic neurological deficits.

Closed loop of circle of Willis is bonded by internal carotid artery (ICA) and anterior cerebral artery (ACA) and should bear the brunt of mechanical occlusion in cases of pituitary apoplexy and raised intra-tumoral pressures. Middle cerebral artery (MCA), being not a part of closed loop, escapes mechanical brunt. However, partial occlusion of ICA may cause MCA territory ischaemia, especially when MCA being an end artery while ACA has dual supply.

Vasospasm as the pathophysiology behind cerebral ischaemia, in cases of pituitary apoplexy, assumes importance owing to significant number of patients demonstrating subarachnoid bleed on CT scans (Mohindra et al. 2010). Literature has described ten such cases and subarachnoid haemorrhage (SAH) on CT scans was evident in four cases (Mohindra et al. 2010).

Pituitary apoplexy usually does not present with focal neurological deficits or side preponderance. Henceforth, new-onset focal neurological deficits or side preponderance in association with clinical features of pituitary apoplexy indicates cerebral ischaemia superimposed upon apoplexy. Focal neurological deficits like hemiparesis, dysphasia or frontal lobe syndrome have been described as the presenting features (Mohindra et al. 2010).

Whenever ischaemic insult is suspected, urgent CT scan of brain may be performed (Figs. 9.2 and 9.3). CT scan may demonstrate florid subarachnoid bleed in association with haemorrhagic mass in sellar-suprasellar region. As clear diagnostic criteria are not available, digital subtraction angiogram may be performed to delineate the exact site of occlusion. None of the reported cases have performed computerized tomographic angiogram (CTA), but CTA may be considered in the present era owing to its non-invasive nature. Varying sites of cerebral infarction have been described. These include ACA territory, MCA territory, areas of deep nuclei and even multiple cortical regions.