Review articleDiagnostic imaging for intracerebral hemorrhage
Section snippets
Biochemical evolution of intracerebral hemorrhage
Hemoglobin is a tetramer of polypeptide chains, with each polypeptide chain having a prosthetic heme group bound within a hydrophobic cleft [11]. Each heme group contains an iron atom in a ferrous (Fe2+) state. The heme iron molecule has six bonds. In the oxyhemoglobin state, which is the predominant state as blood leaves the lungs, there is an oxygen molecule attached to the sixth bond. The interaction of the six bonds with the metal core causes six outer electrons in the five d orbitals to
MRI of intracerebral hemorrhage
The MRI appearance of ICH is an evolving pattern of variable signal intensities that depends on the various oxygenation states of hemoglobin and hemoglobin byproducts present. This evolution is rather predictable, although variations exist. Several other factors, including location of the hematoma, operating field strength, mode of image acquisition, status of the RBCs, presence of underlying brain lesion, and coagulopathy influence the MRI appearance. Basic understanding of the biochemical
Temporal evolution of intraparenchymal hemorrhage defined by MRI
Most parenchymal hematomas evolve in a predictable fashion, although variations exist (Table 1). The exact time course of biochemical changes may vary depending on the precipitating pathophysiologic state. The MRI appearance is influenced by the acquisition mode and field strength [13]. Five stages of hemorrhage can be identified by MRI. Although it is practical to describe the evolution of a hematoma in these well-defined stages, they frequently coexist. By convention, the stage of the
CT of intracerebral hemorrhage
Acute hemorrhage is seen as increased attenuation on CT. This increased attenuation is related to the high electron density of the protein (globin) component of the hemoglobin molecule [32]. The CT attenuation value of whole nonclotted blood with a hematocrit of 45% is 56 Hounsfield units (HU), and that of the cerebral cortex is 37 to 40 HU [32], [33]. A few hours after acute hemorrhage, the hematocrit is measured at 90% as a result of clot retraction, which continues to occur in the first
Hypertensive intracerebral hemorrhage
Seventy percent to 90% of the patients who present with acute ICH have elevated blood pressure [1], [38], [39]. Increased blood pressure, however, may be secondary to increased intracranial pressure and the resulting Cushing's reflex. In one study, only 45% of the patients with acute ICH had a history of hypertension [40]. In another study, 48% of the thalamic, putaminal, or posterior fossa hematomas and 65% of the lobar hematomas were associated with an underlying structural lesion in patients
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