T2 weighted imaging

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Title:T2 * -weighted sequences in acute stroke diagnosis in the mouse model: improvement of MRI imaging in early cerebral ischemiaLanguage:GermanAuthor:Gersing, Alexandra SophiaTags:MRI; Cerebral ischemia; T2 *; neuroradiology; MRI; stroke; T2 *GND keywords:Neuroradiology; Stroke; NMR tomographyPublication date:2013Day of the oral exam:2013-08-12Summary:
Clinical studies show that local changes in the T2 * -weighted sequence are more specific predictors of infarct growth than the TTP> ADC mismatch concept. This gave rise to the assumption that the informative value of the T2 * WI sequences can be of great clinical value in the choice of the optimal therapeutic method. The aim of this study was to analyze and compare the dynamics of the signal intensities as well as the infarct growth of the sequences T2 * and DWI. For this purpose, an onion skin-like extension of the infarct area with the lowest T2 * values ​​was hypothesized. Under experimental conditions, 30 mice were i. p. anesthetized. After the baseline measurement of T2 *, qT2 and DWI in the 3T MRI, MCAO was carried out in 12 mice over 40 minutes and in 6 mice over 60 minutes using a suture closure model. Serial T2 * WI images as well as qT2 and DWI were acquired four minutes after MCAO. Decreased signal intensities marked oligemic tissue. T2 * WI signal intensities and infarct volumes were calculated. The final infarct volume was quantified histologically post mortem using TTC staining. As early as 4 minutes after MCAO, a drop in T2 * signal intensity of 7.0% (SD: 2.8%) was recorded in the affected hemisphere. There was no further significant reduction in signal intensity in the center of the T2 * WI lesion over the duration of the MCAO. A continuous increase in the volume of the T2 * WI lesion volume was observed over the duration of the MCAO. The volume growth took place mainly in the regions with a lower signal intensity drop. The volume of the regions with a serious decrease in signal intensity remained stable over the measured time periods, both before and after recanalization. The T2 * lesion volume was greater than the ADC lesion volume in the majority of the mice. The results show a volume growth in the area surrounding the infarct nucleus in the first 50 minutes after MCAO and volume reduction after vascular recanalization. The T2 * -weighted sequence and the sequences based on it offer the possibility to differentiate non-invasively between different pathophysiological tissue stages and thus to make a statement about the status of the cerebral perfusion.

We aimed to analyze the growth dynamic of T2 * -WI signal intensities under experimental conditions. Lesion expansion was hypothesized, the lesion center exhibiting greatest T2 * signal decreases. 30 mice were i.p. anaesthetized and temporal occlusion of middle cerebral artery (MCAO) was induced with occlusion time varying between 40 and 60 minutes. Subsequently, early dynamic T2 * signal changes were examined chronologically utilizing a 3T vertical magnet with a scan every 2 minutes until 60 minutes after recanalization. Baseline imaging of T2 *, qT2 and DWI was acquired. Recanalization was conducted by retracting the occluding filament. Infarct volume were evaluated histopathologically with triphenyltetrazolium chloride (TTC) staining. Continuous volume growth of the outer layer has been observed during MCAO, while the center layer volume was constant within 4 or 60 minutes after ischemia. Reperfusion lead to further gradual signal increase with initial signal abnormality in the affected hemisphere compared to the vital hemisphere. Degree of signal increase was associated with occlusion time. Continuous reduction of outer layer volume was found after reperfusion after 60 minutes. TTC staining of final penumbra location correlated with T2 * signal loss. Histologically, the total T2 * lesion was larger than infarct core in 16/18 mice (46.9%). As acute decrease in T2 * -signal is attributed to increased local deoxyhemoglobin concentration and is hypothesized to reflect the penumbra on a metabolic level. In the original penumbra concept, the penumbra shrinks from the center by infarct growth while its outer extent is constant. Instead, we observed an increase of the T2 * lesion volume after MCAO and a decrease after reperfusion. The T2 * reading was larger than the infarct core. It is likely that T2 * -WI reflects differences in pathophysiological states of tissue during ischemia.
Url:https://ediss.sub.uni-hamburg.de/handle/ediss/5195URN:urn: nbn: de: gbv: 18-64982Document type:dissertationSupervisor:Fiehler, Jens (Prof. Dr.)Included in the collections:Electronic dissertations and habilitations