The cardiovascular and central nervous systems (CNS) are closely related. Coronary artery disease and ischemic stroke share similar risk factors, including age, gender, hypertension, diabetes, hyperlipidemia, and cigarette smoking (1,2). In addition, structural heart disease, such as atrial fibrillation, decreased left ventricular function, patent foramen ovale, and atrial septal aneurysm, are independent risk factors for stroke (3–6). The cardiovascular system in turn is closely regulated by the nervous system, which helps modulate cardiovascular changes to demand during various physiological and pathologic states (7,8) (see also Chapter 10). Afferent fibers from the heart and arterial baroreceptors are carried to the nucleus tractus solitarius (NTS) and dorsal vagal nucleus (DVN), located in the brainstem via the glossopharyngeal and vagus nerves. The efferent parasympathetic fibers arise in the DVN, and the efferent sympathetic fibers arise in the intermediolateral column (IML) of the spinal cord. These nuclei are extensively connected to each other and in turn receive input from the hypothalamus and the cerebral cortex (9–13). The CNS acts primarily by modulating the autonomic nervous system by excitatory or inhibitory impulses. The resultant changes in efferent sympathetic and parasympathetic activity allow for rapid changes in heart rate, blood pressure, vasomotor tone, cardiac metabolism and cardiac output (14,15). Therefore lesions affecting the CNS can be caused by a primary cardiac problem or may cause cardiovascular dysfunction in a previously normal heart or may precipitate underlying cardiac disease. Cardiovascular diseases can be grouped under three clinical entities: arrhythmias, myocardial contractile dysfunction, and hemodynamic changes.