Computed tomography of intracerebral hematomas. II. Radionuclide and transmission CT studies of the perihematoma region

Dolinskas, CA; Bilaniuk, L T; Ra, Zimmerman; Kuhl, D.E.; Alavi, Abass

doi:10.2214/ajr.129.4.689

Cited by 36 publications

(9 citation statements)

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“…Radionuclide and CT studies showing pertechnetate uptake and contrast enhancement, respectively, 1 to 14 weeks after ICH indicate blood-brain barrier (BBB) breakdown to macromolecules. 19,34,35 This corresponds to the development of new vessels around the hematoma, which lack a fully developed BBB. 36 Thus, late edema progression after ICH might represent vasogenic edema associated with angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Progression of Mass Effect After Intracerebral Hemorrhage

Zazulia

Diringer

Derdeyn

et al. 1999

Stroke

363

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Background and Purpose-While the evolution of mass effect after cerebral infarction is well characterized, similar data regarding intracerebral hemorrhage (ICH) are scant. Our goal was to determine the time course and cause for progression of mass effect after ICH. Methods-Patients with spontaneous supratentorial ICH who underwent Ն2 CT scans were identified in our prospectively collected database. CT lesion size and midline shift of the pineal and septum pellucidum were retrospectively measured and correlated with clinical and CT characteristics. Causes for increased midline shift were determined by 2 independent observers. Results-Seventy-six patients underwent 235 scans (3.1Ϯ1.3 per patient). Initial CT was obtained within 24 hours of ICH in 66. Twenty-five scans were repeated on day 1, 80 on days 2 through 7, 31 on days 8 through 14, and 24 Ͼ14 days after ICH. Midline shift was present on 88% of the initial scans. There were 17 instances of midline shift progression: 10 occurred early (0.2 to 1.7 days) and were associated with hematoma enlargement, and 7 occurred late (9 to 21 days) and were associated with edema progression. Progression of mass effect due to edema occurred with larger hemorrhages (PϽ0.05). Of 65 scans repeated for clinical deterioration, only 10 were associated with increased mass effect. Conclusions-Progression of mass effect after ICH occurred at 2 distinct time points: within 2 days, associated with hematoma enlargement, and in the second and third weeks, associated with increase in edema. The clinical significance of later-developing edema is unclear.

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Section: Discussionmentioning

confidence: 99%

Progression of Mass Effect After Intracerebral Hemorrhage

Zazulia

Diringer

Derdeyn

et al. 1999

Stroke

363

241

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“…A larger region might have included both abnormal and normal periclot tissue, reducing sensitivity to detect an area of increased OEF. Another approach would have been to analyze a region encompassing the periclot lucency as seen on CT scan, because this lucency is sometimes interpreted to represent a zone of ischemia (Dolinskas et al, 1977;Kendall and Radue, 1978;Liliequist, 1983). Upon attempting to outline such a region, however, it became readily apparent that in the majority of subjects in whom the periclot area extended into white matter, a distinction between periclot lucency and white matter would be highly subjective.…”

Section: No Ischemia Around Intracerebral Hemorrhage 807mentioning

confidence: 99%

Hypoperfusion without Ischemia Surrounding Acute Intracerebral Hemorrhage

Zazulia

Diringer

Videen

et al. 2001

J Cereb Blood Flow Metab

340

200

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A zone of hypoperfusion surrounding acute intracerebral hemorrhage (ICH) has been interpreted as regional ischemia. To determine if ischemia is present in the periclot area, the authors measured cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) with positron emission tomography (PET) in 19 patients 5 to 22 hours after hemorrhage onset. Periclot CBF, CMRO2, and OEF were determined in a 1-cm-wide area around the clot. In the 16 patients without midline shift, periclot data were compared with mirror contralateral regions. All PET images were masked to exclude noncerebral structures, and all PET measurements were corrected for partial volume effect due to clot and ventricles. Both periclot CBF and CMRO2 were significantly reduced compared with contralateral values (CBF: 20.9 +/- 7.6 vs. 37.0 +/- 13.9 mL 100 g(-1) min(-1), P = 0.0004; CMRO2: 1.4 +/- 0.5 vs. 2.9 +/- 0.9 mL 100 g(-1) min(-1), P = 0.00001). Periclot OEF was less than both hemispheric OEF (0.42 +/- 0.15 vs. 0.47 +/- 0.13, P = 0.05; n = 19) and contralateral regional OEF (0.44 +/- 0.16 vs. 0.51 +/- 0.13, P = 0.05; n = 16). In conclusion, CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia. Thus, the authors found no evidence for ischemia in the periclot zone of hypoperfusion in acute ICH patients studied 5 to 22 hours after hemorrhage onset.

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“…In other words, attenuation of the X-ray beam is determined by the density of the electron clouds in the tissues it traverses [5]. The attenuation properties of intracranial blood are determined by the aggregation of globin molecules in the hematoma [6]. There is a linear relationship between CT attenuation, protein content (mainly hemoglobin), and hematocrit [7]; however, artifacts located close to the skull base can easily mimic hemorrhage on spiral-CT scans [8].…”

Section: Computed Tomographymentioning

confidence: 99%

Intracranial hemorrhage: principles of CT and MRI interpretation

et al. 2001

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Accurate diagnosis of intracranial hemorrhage represents a frequent challenge for the practicing radiologist. The purpose of this article is to provide the reader with a synoptic overview of the imaging characteristics of intracranial hemorrhage, using text, tables, and figures to illustrate time-dependent changes. We examine the underlying physical, biological, and biochemical factors of evolving hematoma and correlate them with the aspect on cross-sectional imaging techniques. On CT scanning, the appearance of intracranial blood is determined by density changes which occur over time, reflecting clot formation, clot retraction, clot lysis and, eventually, tissue loss. However, MRI has become the technique of choice for assessing the age of an intracranial hemorrhage. On MRI the signal intensity of intracranial hemorrhage is much more complex and is influenced by multiple variables including: (a) age, location, and size of the lesion; (b) technical factors (e.g., sequence type and parameters, field strength); and (c) biological factors (e.g., pO2, arterial vs. venous origin, tissue pH, protein concentration, presence of a blood-brain barrier, condition of the patient). We discuss the intrinsic magnetic properties of sequential hemoglobin degradation products. The differences in evolution between extra- and intracerebral hemorrhages are addressed and illustrated.

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Computed tomography of intracerebral hematomas. II. Radionuclide and transmission CT studies of the perihematoma region

Cited by 36 publications

References 0 publications

Progression of Mass Effect After Intracerebral Hemorrhage

Progression of Mass Effect After Intracerebral Hemorrhage

Hypoperfusion without Ischemia Surrounding Acute Intracerebral Hemorrhage

Intracranial hemorrhage: principles of CT and MRI interpretation

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