of the cerebrospinal fluid and autopsy results indicated cerebral vasospasm. Treatment The occurrence of vasospasm can be reduced by preventing the occurrence of atherosclerosis. This can be done in several ways, the most important being lifestyle modifications—decreasing low-density lipoprotein (LDL), quitting smoking, physical activity, and control for other risk factors including diabetes, obesity, and hypertension. Pharmacological therapies include hypolipidemic agents, thrombolytics and anticoagulants. Pharmacological options for reducing the severity and occurrence of ischemic episodes include the organic nitrates, which are rapidly metabolized to release nitric oxide in many tissues, and are classified as having either long-acting (i.e. isosorbide dinitrate) or short-acting (i.e. nitroglycerin) durations of action. These drugs work by increasing nitric oxide levels in the blood and inducing coronary vasodilation which will allow for more coronary blood flow due to a decreased coronary resistance, allowing for increased oxygen supply to the vital organs (myocardium). The nitric oxide increase in the blood resulting from these drugs also causes dilation of systemic veins which in turn causes a reduction in venous return, ventricular work load and ventricular radius. All of these reductions contribute to the decrease in ventricular wall stress which is significant because this causes the demand of oxygen to decrease. In general organic nitrates decrease oxygen demand and increase oxygen supply. It is this favourable change to the body that can decrease the severity of ischemic symptoms, particularly angina. Other medications used to reduce the occurrence and severity of vasospasm and ultimately ischemia include L-type calcium channel blockers (notably nimodipine, as well as verapamil, diltiazem, nifedipine) and beta-receptor antagonists (more commonly known as beta blockers or β-blockers) such as propranolol. L-type calcium channel blockers can induce dilation of the coronary arteries while also decreasing the heart's demand for oxygen by reducing contractility, heart rate, and wall stress. The reduction of these latter three factors decreases the contractile force that the myocardium must exert in order to achieve the same level of cardiac output. Beta-receptor antagonists do not cause vasodilation, but like L-type calcium channel blockers, they do reduce the heart's demand for oxygen. This reduction similarly results from a decrease in heart rate, afterload, and wall stress. Adverse effects Like most pharmacological therapeutic options, there are risks that should be considered. For these drugs in particular, vasodilation can be associated with some adverse effects which might include orthostatic hypotension, reflex tachycardia, headaches and palpitations. Tolerance may also develop over