Stroke; a journal of cerebral circulation
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A classification of brain edema is provided as well as an extensive review of the animal models from which we have derived most of the basic information we have about the formation and resolution of edema. The clinical aspects of cerebral edema in stroke are discussed and also modern methods for identifying cerebral edema in the human. Attention is given to computed tomography and enhanced CT and advances in their application to this condition. Treatment of cerebral edema in the stroke patient using glycerol, dextran 40, mannitol, steroids, and other drugs is discussed and the need pointed out for controlled clinical trials of the therapeutic effectiveness of these agents.
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Regional cerebral blood flow (rCBF) was measured in normotensive rate (NTR) and spontaneously hypertensive rats (SHR), in a lightly anesthetized state and with control of PaCO2 by artificial ventilation. Without carotid artery ligation, NTR and SHR showed almost identical rCBF values and distribution, despite significantly elevated levels of blood pressure in SHR. ⋯ The reduction of rCBF in SHR was rather homogenous and symmetrical. Mechanisms causing the differences between NTR and SHR are discussed.
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Respiratory rates and patterns were studied in 23 patients with acute brain stem infarction using impedance pneumography. Autopsy was obtained in six of eight fatal cases. Pontine lesions were present in all patients, with coexistent infarction of midbrain in four and of medulla in nine. ⋯ In ten patients (one fatal, nine nonfatal), normal respiratory rate and pattern predominated with only rare or occasional apperance of Cheyne-Stokes respiration or Cheyne-Stokes variant pattern, especially during sleep. The types of respiratory rate and pattern abnormalities in acute brain stem infarction were not specifically related to the level of lesions, but rather to the size and bilaterality of the lesions. Respiratory alkalosis was present in varying degrees in most patients with either tachypnea or prominent CSR.
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In this cooperative study among 13 institutions, 502 patients were treated with antifibrinolytic medication (epsilon-aminocaproic acid or tranexamic acid) within a 14-day period following rupture of an intracranial aneurysm. Mortality at the end of 14 days was 11.6%; proved rebleed rate was 12.7%. Patients with an internal carotid or anterior cerebral aneurysm had the highest mortality and rebleed rate. ⋯ Significantly higher mortality was reported among patients with cerebral vasospasm, yet rebleed rate was no different among those patients with or without vasospasm. The same pattern was observed among patients with a mean blood pressure value above and below 110 mm Hg. We conclude that antifibrinolytic therapy provides beneficial treatment to patients with recent onset subarachnoid hemorrhage (SAH) following rupture of an intracranial aneurysm.