The term “cerebrovascular disorders” refers to a constellation of thromboembolic and hemorrhagic diseases of the arteries and veins that contribute to perfusion of the central nervous system (CNS). Cardioembolic processes involve intracradiac thrombi embolizing to and occluding CNS vessels, and are due to such processes as atrial fibrillation, coronary artery disease with myocardial hypokinesis, or valvular problems. Thromboembolic disease involves atherosclerosis of the large vessels which arise from the heart (aorta) and travel to the neck (carotid or vertebral arteries), which may culminate in the development of thrombosis with embolization to cerebral vessels. Atherothrombotic disease involves a similar process within the large cerebral intracranial vessels, and lipohyalinosis pertains to chronic hypertrophic stenotic changes within the small penetrating cerebral arterioles that may result in lacunar infarction. Thromboembolic and atherothrombotic processes are collectively referred to as large vessel or macrovascular disease, whereas lipohyalinotic processes are considered small vessel or microvascular. Hemorrhagic cerebrovascular disease relates to rupture of small cerebral vessels causing intracerebral hemorrhage, or of larger cerebral vessel aneurysms that results in subarachnoid hemorrhage (hemorrhage into fluid surrounding the CNS). Venous sinus thrombosis and cerebral venous thrombosis relate to thrombotic events in the large cerebral venous sinuses and smaller cerebral veins respectively.
Cerebrovascular disease is currently the leading cause of disability in modernized societies such as the United States and the European Union, and is the 4th leading cause of mortality after heart disease, cancer and lung disease. Major risk factors for cerebrovascular disease include hypertension, diabetes, hyperlipidemia, atrial fibrillation, coronary artery disease, tobacco use, excessive alcohol use, inactivity, obesity, male gender and older age. Since most of the risk factors are modifiable and can be ameliorated by lifestyle changes or by medications, the risk for a cerebrovascular event can be substantially decreased and prevented if action is taken in a timely fashion. Male gender and older age represent the only nonmodifiable risk factors that cannot be changed. Reducing tobacco use, which is markedly prevalent in some Mediterranean countries and cultures, may represent a particularly important target in reducing the incidence of cerebrovascular disease.
Cerebrovascular events typically present with acute symptoms which are typically focal or lateralized, and which localize to the damaged area of the CNS – aphasia (expressive and/or receptive language dysfunction), spatial deficits (neglect and extinction), facial asymmetry, dysarthria, dysphonia, dysphagia, visual loss, hypsesthesia, and paresis. The development of any of these symptoms warrants emergent evaluation including cerebral imaging with CT or MR imaging. Radiologic imaging will demonstrate whether the process is ischemic due to vessel occlusion or hemorrhagic due to vessel rupture, and will thus dictate the most appropriate therapeutic course of action. Whereas management of intracerebral hemorrhage is limited to acute treatment of hypertension, management of subarachnoid hemorrhage involves endovascular coiling or surgical clipping of the ruptured aneurysm, and potentially the need for additional ancillary treatments for the many potential complications that may follow SAH. Cardioembolic, macrovascular thromboembolic & atherothrombotic, and microvascular processes compromise perfusion and result in cerebral (or spinal) ischemia that may progress to permanent damage, or infarction. Treatment for such ischemic processes involves the emergent administration of thrombolytic therapy in the form of intravenous tissue plasminogen activator (tPA), and sometimes the endovascular removal of occlusive thrombi (thrombectomy). Generally, tPA may be given within the first 4 ½ hours following an acute ischemic event, and thrombectomy may be performed within 6-8 hours after the onset of symptoms, depending on the amount of viable tissue as determined by special CT or MR perfusion scans in conjunction with CTA or MRA vessel imaging scans to identify the involved vessel.
About the author:
Doctor Moussouttas completed residency training at Mount Sinai Medical Center in New York City, subspecialty training in Cerebrovascular Diseases at Yale New Haven Hospital in New Haven CT, and additional subspecialty training in Neurocritical Care at Columbia University Medical Center in New York City. Doctor Moussouttas is board certified in Neurology by the American Academy of Neurology, Cerebrovascular Diseases also by the American Academy of Neurology, Neurocritical Care by the United Council for Neurologic Subspecialties, and in Neurosonology by the American Society for Neuroimaging.
Doctor Moussouttas has participated as an investigator in numerous multicenter clinical trials, has initiated several investigator initiated research projects, and has published numerous articles on cerebrovascular and neurocritical care research in several peer reviewed journals. Doctor Moussouttas’ interests include subarachnoid hemorrhage, intracerebral hemorrhage, and cerebral ischemia.
Doctor Moussouttas is currently a neurointensivist in the Capital Institute for Neurosciences at Capital Regional Medical Center in Trenton NJ.