Secondary thalamic degeneration after cerebral infarction in the middle cerebral artery distribution: evaluation with MR imaging.

Ogawa, Toshihide; Yoshida, Yuki; Okudera, Toshio; Noguchi, Kei; Kado, Hirotsugu; Uemura, K

doi:10.1148/radiology.204.1.9205256

Cited by 88 publications

(72 citation statements)

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“…The significant increase in diffusion detected in the thalamus ipsilateral to the infarction is in favor of a loss of microscopic thalamic components because of the interruption of some thalamo-cortical fibers by retrograde degeneration as already observed in post-mortem studies after MCA occlusion (Ogawa et al, 1997b). This was recently reported by Hervé et al (54th Meeting of the American Academy of Neurology, Denver, 2002) who performed a study focusing on this aspect based on regions of interest delineated after anatomical segmentation of the thalamus in the same sample of subjects.…”

Section: Discussionsupporting

confidence: 56%

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Buffon

Molko

Hervé

et al. 2005

J Cereb Blood Flow Metab

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Diffusion tensor imaging can be used in vivo to assess the longitudinal and regional microstructural changes occurring after middle cerebral artery (MCA) infarcts in humans. Nine patients were investigated 1 week (D7), 1 (M1), 3 (M3), and 6 months (M6) after the occurrence of an isolated MCA infarction. First, an overall analysis was performed using histograms of mean diffusivity (MD) and fractional anisotropy (FA) in each hemisphere. Thereafter, the regional pattern of diffusion changes was investigated voxel by voxel with statistical parametric mapping 99. In the hemisphere ipsilateral to the infarction, histogram analysis revealed a significant decrease in FA between D7 and M6 associated with a progressive increase in MD from D7 to M3. Remote from the MCA territory, the voxel by voxel analyses detected a significant increase in MD within the thalamus at M3 and M6 and a reduction in FA along the pyramidal tract at M6. In the contralateral hemisphere, between D7 and M6, a significant hemispheric atrophy was observed in association with a global reduction in anisotropy, in the absence of distinctive regional diffusion changes. These results suggest that micro-and macrostructural tissue modifications can be detected with diffusion tensor imaging in regions remote from the ischemic area in both hemispheres.

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Section: Discussionsupporting

confidence: 56%

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Buffon

Molko

Hervé

et al. 2005

J Cereb Blood Flow Metab

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“…35,36 Therefore, damage to these cortical areas and thalamic radiations may cause secondary degeneration in the corresponding thalamic nuclei. 16,17 In this study, reduced diffusion in the thalamus occurred when a sufficient amount of central tissue containing thalamic radiation was damaged. Particularly, damage to the posterior thalamic radiations and the PFC resulted in degeneration of the pulvinar and dorsomedial nucleus, respectively.…”

Section: Discussionmentioning

confidence: 76%

“…19 The strength of our study is the more precise anatomic correlation between damaged cortical areas and distribution of striatal signal abnormalities based on the assessment of a larger number of cases. In addition, previous reports of secondary thalamic degeneration in humans focused on T2WI, 16,17 not on DWI, though reduced diffusion in the early phase of secondary thalamic degeneration has been reported in rat models of MCA infarction. 11 In our cases of postoperative secondary degeneration, reduced diffusion was not observed on days 0 -6 but appeared later on days 7-46.…”

Section: Discussionmentioning

confidence: 98%

“…[5][6][7][8][9][10][11][12][13][14][15] Diffusion abnormality due to Wallerian degeneration is known to develop within as little as 2 days after injury 12 and to last for at least 2 weeks. 13 Although it has been well-documented that secondary degeneration occurs in the thalamus following ischemic infarction in the MCA territory, [16][17][18] reports on MR imaging findings of secondary degeneration in the striatum have been very sparse. 19 In addition, there have been no reports on the depiction of the early phase of postoperative secondary degeneration by using DWI.…”

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confidence: 99%

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Postoperative Transient Reduced Diffusion in the Ipsilateral Striatum and Thalamus

Kamiya

Sato²,

Nakata³

et al. 2012

AJNR Am J Neuroradiol

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“…An area of slightly higher signal was observed in the dorsomedial nucleus of the thalamus on T2-weighted images about 6 wk after the onset. Similarly, hypointense areas in the ipsilateral thalamus were observed on T2-weighted spin-echo images in 47% of the patients at 1-12 mo after the stroke onset (27). In parallel, hypoperfusion of the ipsilateral thalamus was observed in 21 of 23 patients who underwent additional SPECT studies.…”

Section: Imaging Thalamic Degeneration With Mri and Petmentioning

confidence: 73%

Detection of Secondary Thalamic Degeneration After Cortical Infarction Using cis-4-18F-Fluoro- D-Proline

Langen¹,

Salber²,

Hamacher³

et al. 2007

Journal of Nuclear Medicine

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The amino acid cis-4-18 F-fluoro-D-proline (D-cis-18 F-FPro) exhibits preferential uptake in the brain compared with its L-isomer, but the clinical potential of the tracer is as yet unkown. In this study we explored the cerebral uptake of D-cis-18 F-FPro in rats with focal cortical infarctions. Methods: Focal cortical infarctions were induced in different areas of the cortex of 20 Fisher CDF rats by photothrombosis (PT). At variable time points after PT (1 d to 4 wk), the rats were injected intravenously with D-cis-18 F-FPro. For comparison, 12 rats were injected simultaneously with 3 H-deoxyglucose ( 3 H-DG), 3 rats were injected with 3 H-methyl-L-methionine ( 3 H-MET), and 2 rats were injected with 3 H-PK11195. Within 2 h after injection of the tracers, coronal cryosections of the brains were produced and evaluated by dualtracer autoradiography. Lesion-to-brain ratios (L/B ratios) were calculated by dividing the maximal uptake in areas with increased tracer uptake by the mean uptake in normal brain tissue. Histologic slices were stained by toluidine blue and by immunostainings for glial fibrillary acidic protein (GFAP), CD68 for macrophages, and CD11b for microglia. Results: Prominent uptake of D-cis-18 F-FPro was found in ipsilateral thalamic nuclei (TN) and partially in the corpus striatum starting at 3 d after infarction with increasing L/B ratios up to 4 wk (mean L/B ratio 6 SD, 6.7 6 3.5). The involved TN varied with the site of the cortical lesion corresponding to their thalamocortical projections connecting them with their specific target region in the cerebral cortex. The TN were positive for CD11b and GFAP from day 7 onward, whereas uptake of 3 H-DG, 3 H-MET, and 3 H-PK11195 and immunostaining for CD68 were similar to that of normal brain. Furthermore, increased uptake of D-cis-18 F-FPro was found in the area of the cortical infarctions (mean L/B ratio 6 SD, 12.1 6 8.1). From day 5 onward, the pattern of uptake was congruent with that of immunostaining for CD11b and CD68 but was different from that of GFAP. Conclusion: D-cis-18 F-FPro appears to be a sensitive PET tracer for detection of secondary degeneration of TN after cortical injury. The uptake mechanisms of D-cis-18 F-FPro remain to be elucidated, but the relationship to microglial activation suggests a diagnostic potential in various brain diseases.

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Secondary thalamic degeneration after cerebral infarction in the middle cerebral artery distribution: evaluation with MR imaging.

Abstract: MR imaging is useful in evaluating secondary thalamic degeneration after cerebral infarction. In clinical practice, this secondary degeneration should not be mistaken for other lesions such as further cerebral infarction.

Cited by 88 publications

References 0 publications

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Longitudinal Diffusion Changes in Cerebral Hemispheres after MCA Infarcts

Postoperative Transient Reduced Diffusion in the Ipsilateral Striatum and Thalamus

Detection of Secondary Thalamic Degeneration After Cortical Infarction Using cis-4-18F-Fluoro- D-Proline

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