**2. Acute stroke**

#### **2.1 Definition and epidemiology**

Abrupt disturbance of cerebral circulation due to thrombosis or embolism which results in focal neurologic deficit that persist for at least 24 hours is termed as stroke. Cerebral ischemia due to arterial occlusion results in an irreversibly damaged core area with a surrounding reversibly dysfunctional area, which is called penumbra. Cerebral ischemia owing to occluded arterial supply produces focal symptoms and signs that correlate with the influenced cerebral territory. Diagnosis is made by history and detailed neurological examination and confirmed by imaging studies (computerized tomography and magnetic resonance imaging). Further investigations are carried out in order to determine a specific cause responsible for the cerebral ischemia [1]. Yearly more than 13.7 million people have stroke, and 5.8 million people die as a result of stroke in the world [2]. Ischemic stroke comprises about 70% of stroke cases, and this proportion is estimated at about 85–87% in USA [3]. Stroke is the second most common cause of death and adult disability and it affects about 1.1 million people every year in European Union (EU) countries. According to EU cardiovascular disease statistics, treatment and care costs and costs due to labor loss because of stroke were estimated about €45 billion in year 2017 [4, 5].

#### **2.2 Pathology, etiology, and pathophysiology**

Oxygen and glucose insufficiency due to ischemia result in depletion of energy stores of neural cells to maintain membrane potentials and transmembrane ion gradients. Leak of potassium and increased calcium entry due to depolarization initiate series of events resulting in activation of calcium-dependent enzymes. This enhanced enzymatic activity of catabolic enzymes and their metabolic products with the oxygen-free radicals result in cell death. Prolonged ischemia leads to irreversible injury results with infarctions and persistent neurologic sequella [1, 6]. Pathological examinations defines two types of cerebral infarctions: First, the infarctions in a major cerebral artery distribution; both the gray and white matter are influenced and acute ischemic changes in neurons, destruction of glial cells, disruption of axons and myelins, and interstitial edema are visible changes in pathology. The second is the lacunar infarctions that are usually seen in chronic hypertensive people; small infarction cavities in size from 0.5 to 1.5 diameter due to occlusion of small cerebral arterioles are the characteristic of pathological finding [1].

The thrombosis comprises about two thirds of ischemic stroke cases. Thrombotic strokes are produced by occlusion of large cerebral arteries. Embolic strokes are produced from thrombi from heart, aortic arch, and large cerebral arteries. The distinction between them is very difficult and the establishment of the source necessitates detailed clinical examination [1].

Vascular disorders as a result of atherosclerosis of the large extracranial arteries in the neck and at the base of the brain are responsible for the cerebral ischemia in the great majority of cases. Atherosclerosis affects large and medium-sized elastic

#### *The Probable Role of* Chlamydia pneumoniae *Infection in Acute Stroke DOI: http://dx.doi.org/10.5772/intechopen.109582*

and muscular arteries of cerebral circulation. This complex chronic inflammation initiates in endothelial injury, and followed by the migration of monocytes with T-lymphocytes, transforming of these monocytes into lipid-laden macrophages and in continuation with the vascular smooth muscle cell proliferation; finally, the lesion proceeds into atheroma. The process of atherosclerosis is prevalent in patients with hypertension, diabetes mellitus, hypercholesterolemia/ hypertriglyceridemia, homocystinuria, and cigarette smokers. The enlargement and/or ulcerations of the atheroma would result in cerebral circulation disturbances. The severity of the circulatory problem and the localization of the threatened cerebral territory present with various clinical/neurologic scenarios. The detailed explanation of the arise and evolution of the atherosclerotic lesions and the probable role of Chlamydia pneumonia (CP) will be discussed in detail in this chapter [1, 7].

Inflammatory disorders other than atherosclerosis with arterial involvement can also result in cerebral ischemic syndromes: Giant cell arteritis, systemic lupus erythematous, polyarteritis nodosa, granulomatous angiitis, syphilitic arteritis are some examples of these diseases with central nervous system involvement due to vasculitis of arteries/arterioles. Fibromuscular dysplasia, carotid or vertebral artery dissection, lacunar infarctions in hypertensive individuals, vasculitis and vasopasms in drug abusers (cocaine, amphetamines, etc.), and multiple progressive intracranial arterial occlusions (Moyamoya disease) are other vascular causes of cerebral strokes [8–10].

Cardiac diseases comprises about one quarter of ischemic strokes [11]. Mural thrombus formation especially after first weeks of myocardial infarction is a welldocumented source of cardiac embolism. Atrial fibrillation is a very common and preventable cause of cardiac embolism especially in patients with risk factors for hypercoagulable state. Infective and marantic endocarditis, atrial myxoma, and paradoxical embolus from venous system through a patent foramen ovale (PFO) are other rare causes of cardiac embolism [12].

Chronic myeloproliferative disorders such as thrombocytosis and polycythemia vera, sickle cell anemia, hypercoagulable states due to paraproteinemias, hereditary thrombophilia syndromes are the mostly recognized hematological disorders that cause cerebral strokes chiefly due to increased blood viscosity and thrombophilia [1].
