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Neurology India | October-December 2008 | Vol 56 | Issue 4 with Cushing’s disease is approximately 80% whereas in children and adolescents it is approximately 47%.[1] The causes of hypertension in patients with Cushing’s disease are multifactorial. These include intrinsic glucocorticoid activity, activation of the renin-angiotensin system, and suppression of the vasodilatory systems.[1] Hypertension has been regarded as the most prevalent and powerful of the risk factors for intracerebral hemorrhage. The mechanism is thought to involve a hypertension-induced degeneration of the walls of small arteries (lipohyalinosis) that leaves them prone to rupture. Accelerated atherosclerosis after prolonged corticosteroid administration has been shown in both animals[2,3] and humans.[4] Faggiano, et al. found a higher prevalence of atherosclerotic damage in patients with Cushing’s disease.[5] Also, patients with Cushing’s disease have elevated plasma endothelin levels. There are reasons to assume that elevated endothelin levels mediate the accelerated early atherosclerosis and hypertension typical of this disorder.[6] Hence, theoretically patients with Cushing’s disease are at an increased risk of developing intracerebral bleeds both due to hypertension and the accelerated atherosclerosis. Despite this, the incidence of reported hypertensive intracerebral bleeding in a case with Cushing’s disease is extremely rare. Our patient also had radiological features that suggested pituitary apoplexy. Apoplexy is most often obvious and discrete but may have a more subtle onset, or even be clinically silent.[7] Hypertension is also known to precipitate pituitary apoplexy.

Duplication of the common carotid artery and the ipsilateral vertebral artery with a fenestration of the contralateral common carotid artery