Cerebrovascular diseases are brain disorders caused by pathologic processes involving blood vessels. They are a major cause of death in the developed world and are the most prevalent cause of neurologic morbidity. The three main pathogenic mechanisms are (1) thrombotic occlusion, (2) embolic occlusion, and (3) vascular rupture. Stroke is the clinical designation applied to all of these conditions when symptoms begin acutely. Thrombosis and embolism have similar consequences for the brain: loss of oxygen and metabolic substrates, resulting in infarction or ischemic injury of regions supplied by the affected vessel. Similar injury occurs globally when there is complete loss of perfusion, severe hypoxemia (e.g., hypovolemic shock), or profound hypoglycemia. Hemorrhage accompanies rupture of vessels and leads to direct tissue damage as well as secondary ischemic injury. Traumatic vascular injury is discussed separately in the context of trauma.
Hypoxia,Ischemia,andInfarction
The brain is a highly oxygen-dependent tissue that requires a continual supply of glucose and oxygen from the blood. Although it constitutes no more than 2% of body weight, the brain receives 15% of the resting cardiac output and is responsible for 20% of total body oxygen consumption. Cerebral blood flow normally remains stable over a wide range of blood pressure and intracranial pressure because of autoregulation of vascular resistance. The brain may be deprived of oxygen by two general mechanisms:
Functional hypoxia, caused by a low partial pressure of oxygen (e.g., high altitude), impaired oxygen-carrying capacity (e.g., severe anemia, carbon monoxide poisoning), or toxins that interfere with oxygen use (e.g., cyanide poisoning)
Ischemia, either transient or permanent, due to tissue hypoperfusion, which can be caused by hypotension, vascular obstruction, or both
Widespread ischemic-hypoxic injury can occur in the setting of severe systemic hypotension, usually when systolic pressures fall below 50 mm Hg, as in cardiac arrest and shock. The clinical outcome varies with the severity and duration of the insult. When the insult is mild, there may be only a transient postischemic confusional state, with eventual complete recovery. Neurons are more susceptible to hypoxic injury than are glial cells, and the most susceptible neurons are the pyramidal cells of the hippo-campus and neocortex and Purkinje cells of the cerebellum. In some individuals, even mild or transient global ischemic insults may cause damage to these vulnerable areas. In severe global cerebral ischemia, widespread neuronal death occurs irrespective of regional vulnerability. Patients who survive often remain severely impaired neurologically and in a persistent vegetative state. Other patients meet the clinical criteria for so-called “brain death,” in which all voluntary and reflex brain and brain stem function is absent, including respiratory drive. When patients with this form of irreversible injury are maintained on mechanical ventilation, the brain gradually undergoes autolysis, resulting in the so-called “respirator brain.” http://ebooksmedicine.net
MORPHOLOGYInthesettingofglobalischemia,thebrainisswollen,withwidegyriandnarrowedsulci.Thecutsurfaceshowspoordemarcationbetweengraymatterandwhitematter.Thehistopathologicchangesthataccompanyirreversibleischemicinjury(infarction)aregroupedintothreecategories.Early changes, occurring12to24hoursaftertheinsult,includeacuteneuronalcellchange(redneurons)(see
Fig.23.1A )characterizedinitiallybymicrovacuolation,followedbycytoplasmiceosinophilia,andlaternuclearpyknosisandkaryorrhexis.Similarchangesoccursomewhatlaterinastrocytesandoligodendroglia.Afterthis,thereactiontotissuedamagebeginswithinfiltrationofneutrophils(