Elevated blood pressure management in acute ischemic stroke remains controversial: could this issue be resolved?

A transient elevated arterial blood pressure is common in acute ischemic stroke and is often associated with a poor prognosis. The underlying mechanisms of blood pressure elevation are not well understood and its management is still unresolved. This article focuses on pathophysiology and management of elevated blood pressure in acute ischemic stroke. There is evidence that the main causes of a transient blood pressure elevation in acute ischemic stroke are the focal cerebral hypoperfusion and the stress responses with neuroendocrine systems activation. Clinical trials have reported that blood pressure lowering in acute ischemic stroke may have detrimental effect, probably because of impaired cerebral autoregulation. However, quantitative assessment of cerebral perfusion has not been performed during emergency blood pressure reduction in acute ischemic stroke. We suggest that ultrasound carotid artery disease evaluation and cerebral hemodynamics monitoring using bilateral transcranial ultrasonography, during blood pressure management in acute ischemic stroke might contribute to maintaining of an adequate penumbral perfusion and prevent infarct enlargement. Such an approach could individualize the antihypertensive treatment in acute ischemic stroke and improve functional outcome. Prospective studies are needed to confirm such a treatment strategy.

Antihypertensive treatment with cerebral hemodynamics monitoring by ultrasonography in elderly hypertensives without a history of stroke may prevent or slow down cognitive decline. A pending issue.

The role of the antihypertensive therapy in preventing cognitive disorders in elderly persons without a history of stroke is still a matter of debate. This article focuses on the pathogenesis of vascular cognitive disorders in hypertension and on the impact of antihypertensive treatment in their prevention. Cerebral white matter lesions, caused by small vessel disease and cerebral hypoperfusion, have been found in the majority of elderly hypertensives. They correlate with cognitive disorders, particularly impairments of attention and executive functions. Excessive blood pressure lowering in elderly patients with long-standing hypertension below a certain critical level, may increase the risk of further cerebral hypoperfusion because of disrupted cerebral blood flow autoregulation. As a result, worsening of the cognitive functions could occur, especially in cases with additional vascular risk factors. Five randomized, placebo-controlled trials have focused on the efficacy of antihypertensive treatments in preventing cognitive impairments in elderly patients without a prior cerebrovascular disease. Four of them have not found positive effects. We suggest that repeated neuropsychological assessments and ultrasonography for evaluation of carotid atherosclerosis, as well as cerebral hemodynamics monitoring could adjust the antihypertensive therapy with the aim to decrease the risk of cerebral hypoperfusion and prevent or slow down cognitive decline in elderly hypertensives. Prospective studies are needed to confirm such a treatment strategy.

Transient ischemic attack may present a target for normobaric hyperoxia treatment.

According to the new revised tissue-based definition, transient ischemic attack is a transient episode of neurological dysfunction caused by a focal brain, spinal cord, or retinal ischemia without acute infarction. This review addresses the pathophysiology of transient ischemic attack and the impact of normobaric hyperoxia on the penumbral tissue. Neuroimaging in transient ischemic attack patients and advances in penumbra imaging allow the transient ischemic attack, from pathophysiological viewpoint, to be defined as an ischemic penumbra of varied duration, which could proceed to a cerebral infarction or reduce to a benign oligemia. Persisting perfusion abnormalities are observed, despite resolution of the neurological symptoms. Preclinical and clinical studies have shown that the normobaric hyperoxia treatment is associated with improvement of hemodynamic and metabolic disturbances, particularly in the penumbral tissue. Transient ischemic attack, considered an ischemic penumbra, may present an ideal target for early normobaric hyperoxia therapy, administered as soon as possible after the onset of the neurological deficit. Follow-up perfusion imaging could guide and individualize the treatment.

A reappraisal of the definition and pathophysiology of the transient ischemic attack.

Recent data on the pathophysiology of brain ischemia obtained by neuroimaging methods and the new concept of transient ischemic attack (TIA) emergency have called for a redefinition of TIA. According to the new definition proposed by the TIA Working Group, TIA is a brief episode of neurological dysfunction caused by focal brain or retinal ischemia with clinical symptoms typically lasting less than one hour and without evidence of acute brain infarction. This new definition leads to a discussion on the duration of the neurological dysfunction and the availability of appropriate neuroimaging for all patients. It has been reported that the diffusion-weighted imaging abnormalities could be seen in TIA patients with durations of the neurological symptoms of less than 30 minutes, but they were not detected in 29% of patients with transient deficit lasting as much as 6 to 24 hours. Persisting perfusion abnormalities in TIA patients are also observed. Therefore, a cutoff period of any duration of TIA is inaccurate. From the pathophysiological viewpoint, TIA may be considered an ischemic penumbra of varied duration, which could proceed to cerebral infarction or reduce to benign oligemia. TIA, characterized as an ischemic penumbra, presents an ideal target for rapid reperfusion and neuroprotection. Follow-up perfusion imaging can guide and individualize its treatment.

Hypertension, vascular cognitive disorders and neuroprotection.

OBJECTIVE: 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.