PubMed · 10472969
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R N Bryan, A McLaughlin. 1999. MR perfusion imaging.. https://pubmed.ncbi.nlm.nih.gov/10472969/
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Intracranial hypertension develops from the initial cerebral effect of increased intracranial pressure and becomes symptomatical; then it acquires its individuality, surpassing the initial disease. The intracranial hypertension syndrome corresponds to the stage at which the increases in intracranial pressure (ICP) can be compensated and the ICH disease is in its acute form, equivalent to a decompensated ICH syndrome. Based on the etiopathogenesis of intracranial hypertension, a new classification is proposed: parenchymatous intracranial hypertension with an intrinsic cerebral cause; vascular intracranial hypertension, which has its etiology in disorders of the cerebral blood circulation; and essential or idiopathic intracranial hypertension, the former pseudotumor cerebri, an incomplete ICH syndrome. A synergetical pattern of the ICH is based on the relation between ICP and the period of high-pressure action: the critical pressure--time fluctuation causes the autoregulation of the cerebral blood flow to decrease or determines the brain herniation. The decompensation is a state of instability and appears when the intrinsic ratio of pressure--time fluctuation is changed: the high ICP lasts longer than the corresponding normal ICP, or the ICP is higher than the one that normally lasts the same period of time.
BACKGROUND AND PURPOSE: The authors investigate characteristics of ultrasound enhancement and diagnostic quality of a sulfurhexafluorides (SF6)-containing echocontrast agent (SonoVue) in cerebrovascular patients with insufficient temporal bone window by transcranial color-coded duplex (TCCD) sonography. METHODS: Thirty patients (mean age = 62.2 +/- 11.1 years) were enrolled. SF6 was administered intravenously in 4 different doses (0.3, 0.6, 1.2, and 2.4 mL). By videotape analysis, time to contrast appearance, duration of contrast enhancement, and duration of clinically useful signal enhancement were measured. Overall quality of ultrasound investigation was also assessed. RESULTS: Time to contrast appearance ranged from 11 to 74 seconds (mean = 26 seconds). For the 0.3, 0.6, 1.2, and 2.4 mL doses, average times to contrast appearance of 30 +/- 12 seconds, 28 +/- 10 seconds, 23 +/- 8 seconds, and 22 +/- 6 seconds were measured. Duration of TCCD signal enhancement was 438 +/- 169 seconds, 483 +/- 195 seconds, 713 +/- 299 seconds, and 788 +/- 344 seconds for the different doses. Clinically useful enhancement was 160 +/- 124 seconds, 200 +/- 157 seconds, 260 +/- 166 seconds, and 327 +/- 239 seconds. CONCLUSIONS: Administration of SonoVue led to a quality improvement in 21 patients. In TCCD, it optimizes visualization of the cerebral arteries in patients with inadequate bone window. A dose of at least 1.2 mL provides the best enhanced images.
The linearity of the cerebral perfusion response relative to stimulus duration is an important consideration in the characterization of the relationship between regional cerebral blood flow (CBF), cerebral metabolism, and the blood oxygenation level dependent (BOLD) signal. It is also a critical component in the design and analysis of functional neuroimaging studies. To study the linearity of the CBF response to different duration stimuli, the perfusion response in primary motor and visual cortices was measured during stimulation using an arterial spin labeling technique with magnetic resonance imaging (MRI) that allows simultaneous measurement of CBF and BOLD changes. In each study, the perfusion response was measured for stimuli lasting 2, 6, and 18 sec. The CBF response was found in general to be nonlinearly related to stimulus duration, although the strength of nonlinearity varied between the motor and visual cortices. In contrast, the BOLD response was found to be strongly nonlinear in both regions studied, in agreement with previous findings. The observed nonlinearities are consistent with a model with a nonlinear step from stimulus to neural activity, a linear step from neural activity to CBF change, and a nonlinear step from CBF change to BOLD signal change.