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Cerebral infarction basically comprises two pathophysiologic processes one, a loss in the supply of oxygen and glucose secondary to vascular occlusion, and the other, an array of changes in cellular metabolism consequent to the collapse of energy-producing processes, ultimately with disintegration of cell membranes Of potential therapeutic importance are the observations that some of the cellular processes leading to neuronal death are not irrevocable and may be reversed by early intervention, either through restoration of blood ow, by prevention of the in ux of calcium into cells, or by interdicting intermediary processes involved in cell death Vascular Factors At the center of an ischemic stroke is a zone of infarction The necrotic tissue swells rapidly, mainly because of excessive intracellular and intercellular water content Since anoxia also causes necrosis and swelling of cerebral tissue (although in a different distribution), oxygen lack must be a factor common to both infarction and anoxic encephalopathy The effects of ischemia, whether functional and reversible or structural and irreversible, depend on its degree and duration The margins of the infarct are hyperemic, being nourished by meningeal collaterals, and here there is only minimal or no parenchymal damage If the brain is observed at the time of arterial occlusion, the venous blood is rst seen to darken, owing to an increase in reduced hemoglobin The viscosity of the blood and resistance to ow both increase, and there is sludging of formed elements within vessels The tissue becomes pale Arteries and arterioles become narrowed, especially in the pale areas Upon re-establishing ow in the occluded artery, the sequence is reversed and there may be a slight hyperemia If the ischemia is prolonged, sludging and endothelial damage prevent normal re ow (the no-re ow phenomenon described below) These ow factors have been studied in experimental animals by Heiss and by Siesjo and others and are reviewed in detail by Hossman These investigators have determined the critical threshold of cerebral blood ow (CBF), measured by xenon clearance, below which functional impairment occurs In several animal species, including macaque monkeys and gerbils, the critical level was 23 mL/100 g/min (normal is 55 mL); if, after short periods of time, CBF is restored to higher levels the impairment of function can be reversed Reduction of CBF below 10 to 12 mL/100 g/min causes infarction, almost regardless of its duration The critical level of hypoperfusion that abolishes function and leads to tissue damage is therefore a CBF between 12 and 23 mL/100 g/min At these levels of blood ow the EEG is slowed, and below this level it becomes isoelectric In the region of marginal perfusion ( ischemic penumbra ), the K level increases (ef ux from injured depolarized cells) and ATP and creatine phosphate are depleted These biochemical abnormalities are reversible if the circulation is restored to normal Disturbance of calcium ion homeostasis and accumulation of free fatty acids interfere with full recovery A CBF of 6 to 8 mL/100 g/min causes marked ATP depletion, increase in extracellular K, increase in intracellular Ca, and cellular acidosis,.

When a Windows 2000 or XP computer is started, the BIOS bootstrap phase is conducted, just as it is in Windows 9x Following this phase, the MBR locates the bootstrap loader, NTLDR NTLDR is responsible for initiating and organizing the boot process, much like IOSYS in Windows 9x First, it switches the processor into 32-bit protected mode, then it locates and reads the BOOTINI file BOOTINI is responsible for providing the boot menu in a Windows 2000 or XP dual-boot configuration Once Windows 2000 or XP has been selected, or if there are no other OSes in the computer, the message Starting Windows will appear on the screen At this time, NTLDR runs NTDETECTCOM, which detects existing hardware configurations This is known as the hardware detection phase The information gathered during this phase is placed in the Registry via NTLDR As this process is being conducted, an on-screen bar indicator is displayed to indicate its progress When the hardware detection phase is over, the kernel load phase begins This change is evident to the user because the display mode changes from text to graphics During this phase, NTLDR locates the Windows kernel (NTOSKRNLEXE) and loads it into memory NTLDR then locates the hardware device drivers referenced in the Registry These files are not yet initialized; rather, they are simply located and prepared for initialization by the kernel The last function of NTLDR is to initialize

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