Histopathological correlations of nuclear magnetic resonance imaging parameters in experimental cerebral ischemia

Helpern, J. A.; Dereski, Mary O.; Knight, Robert A.; Ordidge, Roger J.; Chopp, Michael; Qing, Z.X.

doi:10.1016/0730-725x(93)90028-c

Cited by 92 publications

(42 citation statements)

References 14 publications

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“…In shorter follow-up MR time series after MCAO (7 days), incomplete recovery of T 1 and T 2 values has been observed in some studies after transient (Neumann-Haefelin et al, 2000) and even permanent (Helpern et al, 1993;Knight et al, 1991) MCAO in rats. Knight et al (1994) described a heterogeneous response of MR relaxation times to MCAO, and noted large increases in T 2 times in the dorsolateral striatum with only moderate histological damage.…”

Section: Lesion Developmentmentioning

confidence: 98%

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Wegener

Weber

Ramos‐Cabrer

et al. 2005

J Cereb Blood Flow Metab

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Transient middle cerebral artery occlusion (MCAO) by an intraluminal thread leads to primarily subcortical infarctions with little sensorimotor impairment in the Wistar rat strain. We investigated the course of infarct development in this lesion type for 10 weeks using magnetic resonance imaging (MRI) along with histological characterization. MCAO was induced in male Wistar rats (260 to 300 g) for 60 mins. Animals received follow-up T 1 -and T 2 -weighted MRI from day 1 until week 10. Separate groups of animals were analyzed histologically after 2, 6, and 10 weeks. Histology included immunohistochemistry for neuronal and astrocytic markers as well as hematoxylin eosin and luxol fast blue-cresyl violet staining. In contrast to lesions involving the cortex, exclusively subcortical infarctions were characterized by a complete resolution of initially increased T 1 and T 2 relaxation times by 10 weeks. Between 2 and 10 weeks, neuronal death and gliosis as well as a dense inflammatory infiltrate were evident in these lesions, without damage to fiber tracts or development of cystic cavities. Exclusively subcortical lesions in Wistar rats are characterized by normalization of T 1 and T 2 relaxation times, which might, however, not be mistaken for tissue recovery. Despite this MRI normalization, selective neuronal death and gliosis develop. Although MRI at individual time points might therefore be ambiguous, the temporal profile of relaxation time changes over the chronic time period allows discrimination of the lesion development into selective neuronal death or pannecrosis.

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Section: Lesion Developmentmentioning

confidence: 98%

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Wegener

Weber

Ramos‐Cabrer

et al. 2005

J Cereb Blood Flow Metab

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“…28 However, ‰uid accumulation in the extracellular space was not apparent in the animal study 0.5-6 hours after ischemia. 10,28,29 On the contrary, the evolution of vacuoles, which corresponds to cytoplasmic swelling of oligodendroglia, astrocytes, and axons, was observed consistently in those studies. In addition, cell membrane disruption was not observed during that period.…”

mentioning

confidence: 90%

“…[25][26][27] In animal studies, the evolution of vacuoles, which corresponds to focal swelling of axons and glia, has been observed 0.5-6 hours following ischemia. 10,28,29 Therefore, as a simpliˆed model of nerve tissue including vacuoles and axons, we considered a 3-compartment model system composed of parallel, inˆnitely long cylinders (axons) and spheres (vacuoles) (Fig. 2).…”

Section: Nerve Tissue Modelmentioning

confidence: 99%

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How Does Water Diffusion in Human White Matter Change Following Ischemic Stroke?

Tamura¹,

Kurihara

Machida³

et al. 2009

magn reson med sci

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Purpose: Temporal evolution of the water apparent diŠusion coe‹cients (ADC) parallel (ADC¿) and perpendicular (ADC¥) to the human white matter tract following ischemia has not been investigated systematically. We attempted to quantify the evolution of ADC¿ and ADC¥ and examine whether it can be interpreted by a model of ischemic edema.Methods: We retrospectively selected 53 patients with ischemic lesions involving the posterior limb of the internal capsule (PLIC) and placed regions of interest in the right and left PLIC on ADC maps. We performed regression analysis of lesion-to-contralateral ratios of ADC¿ and ADC¥against the time (t＝1-1600 h) from onset. We thenˆtted the estimated time courses of ADC¿ and ADC¥obtained from the analysis to a model of nerve tissue composed of cylinders (axons) and spheres corresponding to isotropic structures, particularly focal cytoplasmic swellings of glial cells and axons seen in ischemic white matter.Results: The evolution of ADC¥ and ADC¿ diŠered. The estimated time course of ADC¿ in mm 2 ･ms -1 was 0.64＋0.88 exp (-0.24t) for 1ºtº54 h and 0.00059t＋0.61 for tAE54 h (contralateral normal value, 1.52). That of ADC¥ was 0.19-0.063 exp (-0.24t) for 1ºtº54 h and 0.00040t＋0.17 for tAE54 h (normal value 0.22). The modelˆtted to these values showed that the volume of the cylinders decreased, that of the spheres increased, and extracellular volume changed little from one hour to approximately one day after stroke onset.Conclusion: In the human PLIC, ADC¿ continued to decrease from one hour to a few days after stroke onset, and ADC¥tended to increase. The temporal evolution could be interpreted by progression of the focal cytoplasmic swelling of glial cells and axons previously observed in animal studies.Keywords: cytotoxic edema, glia, intracellular space, vasogenic edema Introduction DiŠusion-weighted (DW) magnetic resonance (MR) imaging enables noninvasive measurement of the diŠusivity of water molecules in the human brain. Prompt reduction of the apparent diŠusion coe‹cient (ADC) in ischemic tissue causes hyperintensity on DW images, which aids detection of early changes in the brain after onset of ischemic stroke. [1][2][3] ADC measurement may also be useful in characterizing ischemic damage and selecting therapeutic procedure. 4 Many studies have demonstrated temporal evolution of the mean diŠusivity (, trace/3 of the diŠusion tensor) in patients with stroke. 5-13Follow-122 122 H. Tamura et al. Magnetic Resonance in Medical Sciencesing acute reduction of after the onset of cerebral ischemia, decreases slightly over 24 hours in many cases, [5][6][7][8][9] reaches a minimum, gradually increases to a normal value (pseudonormalization) between several days and one month, and continues to increase. Although the decrease is generally attributed to cellular edema and the increase to vasogenic edema and degradation of membrane structure, 1,[10][11][12] the exact mechanisms of these changes in remain unclear.Human and animal studies show a decline in diŠusion anisot...

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“…This assumption also holds true early after onset of cerebral ischemia where vasogenic edema due to blood-brain barrier disruption is delayed. 76,77 In tumors or subacute stroke where extravasation is likely, it has been suggested to "preload" the patient with some gadolinium contrast to allow extravasation, thereby minimizing the concentration gradient when the true dynamic study is conducted.…”

Section: Measuring Perfusion With Mr: Basic Theorymentioning

confidence: 99%

Foundations of advanced magnetic resonance imaging

et al. 2005

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Summary:During the past decade, major breakthroughs in magnetic resonance imaging (MRI) quality were made by means of quantum leaps in scanner hardware and pulse sequences. Some advanced MRI techniques have truly revolutionized the detection of disease states and MRI can nowwithin a few minutes-acquire important quantitative information noninvasively from an individual in any plane or volume at comparatively high resolution. This article provides an overview of the most common advanced MRI methods including diffusion MRI, perfusion MRI, functional MRI, and the strengths and weaknesses of MRI at high magnetic field strengths.

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Histopathological correlations of nuclear magnetic resonance imaging parameters in experimental cerebral ischemia

Cited by 92 publications

References 14 publications

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

How Does Water Diffusion in Human White Matter Change Following Ischemic Stroke?

Foundations of advanced magnetic resonance imaging

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Histopathological correlations of nuclear magnetic resonance imaging parameters in experimental cerebral ischemia

Cited by 92 publications

References 14 publications

Temporal profile of T2-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Temporal profile of T2-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

How Does Water Diffusion in Human White Matter Change Following Ischemic Stroke?

Foundations of advanced magnetic resonance imaging

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Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat

Temporal profile of T₂-Weighted MRI Distinguishes between Pannecrosis and Selective Neuronal Death after Transient Focal Cerebral Ischemia in the Rat