Longitudinal thalamic diffusion changes after middle cerebral artery infarcts (509 views)
J Neurol Neurosurg Psychiatry (ISSN: 0022-3050), 2005 Feb; 76(2): 200-205.
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Paper type: Journal Article,
Impact factor: 3.122, 5-year impact factor: 5.345
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-12444269130&partnerID=40&md5=bc293c2e1e1363510f6dce3e07ec1906
Keywords: Adult, Aged, Article, Brain Dysfunction, Brain Infarction Size, Brain Injury, Brain Metabolism, Brain Nerve Cell, Brain Region, Cell Activation, Cell Loss, Cell Swelling, Cerebral Artery Disease, Clinical Article, Controlled Study, Diffusion Tensor Imaging, Female, Fractional Anisotropy, Glia Cell, Human, Image Analysis, In Vivo Study, Mean Diffusivity, Neuroimaging, Nuclear Magnetic Resonance Imaging, Parameter, Priority Journal, Quantitative Analysis, Stroke, Thalamus, Tissue Structure, Diffusion Magnetic Resonance Imaging, Disease Progression, Middle Cerebral Artery, Longitudinal Studies, Middle Aged, Neuroglia,
Affiliations:
*** IBB - CNR ***
Service de Neurologie, Hôpital Lariboisière, 3 rue Ambroise Paré, 75010 Paris, France
Department of Neurology, CHU Lariboisière, Paris, France
INSERM U562, SHFJ-CEA, Orsay, France
UNAF-IFR 49, SHFJ-CEA, Orsay, France
The Department of Neurology, CHU Lariboisiere, Paris, France.
References:
Not available.
J Neurol Neurosurg Psychiatry (ISSN: 0022-3050), 2005 Feb; 76(2): 200-205.
Export to BibTeX Export to EndNote
Paper type: Journal Article,
Impact factor: 3.122, 5-year impact factor: 5.345
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-12444269130&partnerID=40&md5=bc293c2e1e1363510f6dce3e07ec1906
Keywords: Adult, Aged, Article, Brain Dysfunction, Brain Infarction Size, Brain Injury, Brain Metabolism, Brain Nerve Cell, Brain Region, Cell Activation, Cell Loss, Cell Swelling, Cerebral Artery Disease, Clinical Article, Controlled Study, Diffusion Tensor Imaging, Female, Fractional Anisotropy, Glia Cell, Human, Image Analysis, In Vivo Study, Mean Diffusivity, Neuroimaging, Nuclear Magnetic Resonance Imaging, Parameter, Priority Journal, Quantitative Analysis, Stroke, Thalamus, Tissue Structure, Diffusion Magnetic Resonance Imaging, Disease Progression, Middle Cerebral Artery, Longitudinal Studies, Middle Aged, Neuroglia,
Affiliations:
*** IBB - CNR ***
Service de Neurologie, Hôpital Lariboisière, 3 rue Ambroise Paré, 75010 Paris, France
Department of Neurology, CHU Lariboisière, Paris, France
INSERM U562, SHFJ-CEA, Orsay, France
UNAF-IFR 49, SHFJ-CEA, Orsay, France
The Department of Neurology, CHU Lariboisiere, Paris, France.
References:
Not available.
Longitudinal thalamic diffusion changes after middle cerebral artery infarcts
Background: Cerebral infarcts are responsible for functional alterations and microscopic tissue damage at distance from the ischaemic area. Such remote effects have been involved in stroke recovery. Thalamic hypometabolism is related to motor recovery in middle cerebral artery (MCA) infarcts but little is known concerning the tissue changes underlying these metabolic changes. Diffusion tensor imaging (DTI) is highly sensitive to microstructural tissue alterations and can be used to quantify in vivo the longitudinal microscopic tissue changes occurring in the thalamus after MCA infarcts in humans. Methods: Nine patients underwent DTI after an isolated MCA infarct. Mean diffusivity (MD), fractional anisotropy (FA), and thalamic region volume were measured from the first week to the sixth month after stroke onset in these patients and in 10 age matched controls. Results: MD significantly increased in the ipsilateral thalamus between the first and the sixth month (0.766×10-3 mm2/s first month; 0.792×10-3 mm2/s third month; 0.806×10-3 mm2/s sixth month). No significant modification of FA was detected. In six patients, the ipsilateral/contralateral index of MD was higher than the upper limit of the 95% CI calculated in 10 age matched controls. An early decrease of MD preceded the increase of ipsilateral thalamic diffusion in one patient at the first week and in two other patients at the first month. Conclusion: After MCA infarcts, an increase in diffusion is observed with DTI in the ipsilateral thalamus later than 1 month after the stroke onset. This is presumably because of the progressive loss of neurons and/or glial cells. In some patients, this increase is preceded by a transient decrease in diffusion possibly related to an early swelling of these cells or to microglial activation. Further studies in larger series are needed to assess the clinical correlates of these findings.
Background: Cerebral infarcts are responsible for functional alterations and microscopic tissue damage at distance from the ischaemic area. Such remote effects have been involved in stroke recovery. Thalamic hypometabolism is related to motor recovery in middle cerebral artery (MCA) infarcts but little is known concerning the tissue changes underlying these metabolic changes. Diffusion tensor imaging (DTI) is highly sensitive to microstructural tissue alterations and can be used to quantify in vivo the longitudinal microscopic tissue changes occurring in the thalamus after MCA infarcts in humans. Methods: Nine patients underwent DTI after an isolated MCA infarct. Mean diffusivity (MD), fractional anisotropy (FA), and thalamic region volume were measured from the first week to the sixth month after stroke onset in these patients and in 10 age matched controls. Results: MD significantly increased in the ipsilateral thalamus between the first and the sixth month (0.766×10-3 mm2/s first month; 0.792×10-3 mm2/s third month; 0.806×10-3 mm2/s sixth month). No significant modification of FA was detected. In six patients, the ipsilateral/contralateral index of MD was higher than the upper limit of the 95% CI calculated in 10 age matched controls. An early decrease of MD preceded the increase of ipsilateral thalamic diffusion in one patient at the first week and in two other patients at the first month. Conclusion: After MCA infarcts, an increase in diffusion is observed with DTI in the ipsilateral thalamus later than 1 month after the stroke onset. This is presumably because of the progressive loss of neurons and/or glial cells. In some patients, this increase is preceded by a transient decrease in diffusion possibly related to an early swelling of these cells or to microglial activation. Further studies in larger series are needed to assess the clinical correlates of these findings.
Longitudinal thalamic diffusion changes after middle cerebral artery infarcts
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Longitudinal thalamic diffusion changes after middle cerebral artery infarcts
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Neurology (ISSN: 0028-3878, 1526-632x, 1526-632xelectronic), 2005 Jul 26; 65(2): 280-285.
Impact Factor: 5.065
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Molko N, Pappata S, Mangin JF, Poupon F, Lebihan D, Bousser MG, Chabriat H
* Monitoring disease progression in CADASIL with diffusion magnetic resonance imaging: A study with whole brain histogram analysis (842 views)
Stroke (ISSN: 0039-2499), 2002 Dec; 33(12): 2902-2908.
Impact Factor: 5.176
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Dringenberg HC, Kornelsen RA, Pacelli R, Petersen K, Vanderwolf CH
Effects of amygdaloid lesions, hippocampal lesions, and buspirone on black-white exploration and food carrying in rats (446 views)
Behav Brain Res (ISSN: 0166-4328), 1998 Nov; 96(1-2): 161-172.
Impact Factor: 2.796
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Brunetti A, Tedeschi G, Di Costanzo A, Covelli EM, Aloj L, Bonavita S, Ciarmiello A, Alfano B, Salvatore M
White matter lesion detection in multiple sclerosis: Improved interobserver concordance with multispectral MRI display (484 views) (PDF 321 views)
J Neurol (ISSN: 0340-5354, 1432-1459, 1432-1459electronic), 1997 Sep; 244(9): 586-590.
Impact Factor: 1.976
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24 Records (24 excluding Abstracts).
Total impact factor: 102.706 (102.706 excluding Abstracts).
Total 5 year impact factor: 101.804 (101.804 excluding Abstracts).
Total impact factor: 102.706 (102.706 excluding Abstracts).
Total 5 year impact factor: 101.804 (101.804 excluding Abstracts).
509 views. Last view on Friday 06 December 2024, 7:51:05
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