Acute Focal Ischemia - Oren Zarif - Cerebral Ischemia

A global ischemic insult can disrupt blood flow to the brain. Causes of global cerebral ischemia include cardiac arrest, carotid occlusion, hypotension, asphyxia, and anemia. Focal cerebral ischemia is associated with cerebral vascular disease. High calcium levels in the brain trigger cell death. This deterioration can be accompanied by a proliferation of proteases, which attack DNA and structural proteins.

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While cerebral vasospasm may be a cause of acute ischemic stroke, a delayed form is often a result of DCI. New insights in recent years have shifted our understanding of DCI pathogenesis. Large-vessel cerebral vasospasm has been challenged as the sole causal mechanism. Instead, new hypotheses emphasize early brain injury, impaired autoregulation, and microcirculation dysfunction. In the absence of any known causative agent, prevention of DCI relies on nimodipine administration, optimization of blood volume, and cardiac performance. In addition, neurological monitoring is necessary to identify early DCI.

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Severe infections and trauma can decrease blood pressure in the brain. Often, low blood pressure reduces the flow of blood to a specific region of the brain. This is known as focal cerebral ischemia. It can be caused by a blood clot or by a piece of clot called an embolism. The brain tissue affected by focal cerebral ischemia is more susceptible to the effects of the condition.

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Rapid assessment is essential for patients with acute focal neurologic deficits. In addition to CT scans, magnetic resonance imaging (MRI) may be used instead. DWI is useful for identifying areas of dense ischemia. T2 sequences and gradient-echo sequences can rule out old infarcts. If an acute cerebral ischemia is diagnosed, it may be possible to treat the patient immediately. A faster diagnosis and treatment can lead to better outcomes.

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The initial workup for cerebral ischemia includes basic labs, such as a complete blood count, coagulation factors, EKG, and cardiac enzymes. Usually, a stat non-contrast head CT will help rule out other conditions, such as hemorrhage or a mass lesion. Vascular imaging is also valuable for determining the underlying cause of the ischemia. Sometimes, acute large vessel occlusion can be obvious on MRI, and the vascular distribution may be inflamed.

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Delayed cerebral ischemia is a major cause of death among subarachnoid hemorrhage patients. It affects up to 30% of patients and leaves the majority of survivors with impaired motor function and cognitive abilities. A delayed cerebral ischemia after a subarachnoid hemorrhage is also associated with lower quality of life. It is important to recognize that the symptoms of cerebral ischemia may vary from one patient to another.

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The mortality rate following global ischemia is highest at days 3 to 5 after the insult. The first three days of life after SAH after an experimental ischemia are critical for survival. These early events are not associated with focal cerebral ischemia, blood-brain barrier, or microcirculatory failure. In experimental studies, global ischemia is only one component of the pathophysiology of SAH. The remaining factors may contribute to the delayed sequelae of the disease.

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Increasing our knowledge about autophagy and ER stress can lead to therapeutic strategies for stroke. Further research will help determine whether autophagy is beneficial or detrimental for the brain. In vitro and in vivo studies suggest that the activation of autophagy can promote neuronal survival. The induction of autophagy, which is essential for cell survival, protects the brain from cerebral ischemia. However, the effects of autophagy are contradictory.