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The role of the antihypertensive therapy in preventing vascular cognitive disorders in elderly persons without a history of stroke is a matter of debate. This review focuses on cognitive disorders in elderly hypertensive patients.
Methods:
Relevant papers were identified by searches in PubMed from 1946 until February 2007 using the keywords ‘cerebral blood flow autoregulation’, ‘vascular cognitive disorders’, ‘neuroimaging in hypertension’, ‘antihypertensive treatment’ and ‘neuroprotection in cerebral ischemia’.
Results:
Excessive blood pressure lowering in patients with long-standing hypertension may increase the risk of cerebral hypoperfusion, white matter lesions and consequent cognitive decline. White matter lesions have been found in the majority of patients with long-standing hypertension. They correlate with vascular cognitive disorders, particularly impairments of attention and executive function, while memory is relatively preserved. Cerebral small vessel disease in elderly patients should be taken into account when antihypertensive treatment is considered. Renin–angiotensin blockade, some calcium channel blockers and statins are thought to possess neuroprotective action.
Conclusion:
For prevention of cerebral hypoperfusion in elderly hypertensives blood pressure lowering should be cautiously controlled. The increased risk of white matter lesions is an indication for early neuroprotection. The combination of renin–angiotensin blockade or calcium channel blockers with statins may become a promising preventive strategy against cognitive decline in elderly hypertensives. Cerebral white matter protection is a future challenge.
The injury spectrum in traumatic brain injury (TBI) encompasses not only the initial insult, but includes the cascade of systemic responses and pathophysiology that occur after the focal or diffuse brain injury. This chapter presents a case study of a 49-year-old male motorcyclist who was evaluated in the emergency room after a motor vehicle collision with an articulated truck. Around the time of computed tomography (CT) scanning, the patient's right pupil became dilated and unreactive. Hypoxic cerebral damage, a common postmortem finding in TBI, is associated with arterial hypoxemia, decreased mean arterial pressure, or cerebral hypoperfusion, occurring as a consequence of shock, intracranial hypertension, or cerebral vasospasm. Although a definitively effective neuroprotective therapy in central nervous system (CNS) trauma remains elusive, through the skilled interactions of prehospital, emergency department, anesthesiology, and surgical personnel, the lives of many critically injured individuals can be saved and their neurologic function preserved.
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