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Striatal Infarction Elicits Secondary Extrafocal MRI Changes in Ipsilateral Substantia Nigra.

Winter B, Brunecker P, Fiebach JB, Jungehulsing GJ, Kronenberg G, Endres M - PLoS ONE (2015)

Bottom Line: Apparent diffusion coefficient (ADC) values in the secondary lesions showed a delayed sharp decline through day 10.Normalization of ADC values was observed at late measurements.Taken together, our study demonstrates that striatal infarction elicits delayed degenerative changes in ipsilateral substantia nigra pars compacta.

View Article: PubMed Central - PubMed

Affiliation: Center for Stroke Research Berlin (CSB), Charité-Universitätsmedizin Berlin, Berlin, Charitéplatz 1,10117, Berlin, Germany; Department of Neurology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.

ABSTRACT
Focal ischemia may induce pathological alterations in brain areas distant from the primary lesion. In animal models, exofocal neuron death in the ipsilateral midbrain has been described after occlusion of the middle cerebral artery (MCA). Using sequential magnetic resonance imaging (T2- and diffusion-weighted) at 3 Tesla, we investigated acute ischemic stroke patients on days 1, 2, 6, 8, and 10 after stroke onset. Sixteen consecutive patients who had suffered a stroke involving the caudate nucleus and/or putamen of either hemisphere were recruited into the study. Four additional patients with strokes sparing the caudate nucleus and putamen but encompassing at least one-third of the MCA territory served as controls. Ischemic lesions involving striatal structures resulted in hyperintense lesions in ipsilateral midbrain that emerged between days 6 and 10 after stroke and were not present on the initial scans. In contrast, none of the control stroke patients developed secondary midbrain lesions. Hyperintense lesions in the pyramidal tract or the brain stem caused by degeneration of the corticospinal tract could be clearly distinguished from these secondary midbrain gray matter lesions and were detectable from day 2 after ischemia. Co-registration of high-resolution images with a digitized anatomic atlas revealed localization of secondary lesions primarily in the substantia nigra pars compacta. Apparent diffusion coefficient (ADC) values in the secondary lesions showed a delayed sharp decline through day 10. Normalization of ADC values was observed at late measurements. Taken together, our study demonstrates that striatal infarction elicits delayed degenerative changes in ipsilateral substantia nigra pars compacta.

No MeSH data available.


Related in: MedlinePlus

Subacute hyperintensity in ipsilateral midbrain at a delayed time point after striatal stroke.(A, B) MRI scans of two exemplary patients showing primary ischemic lesion confined to striatum (A) or involving striatum (B) in axial diffusion-weighted (DWI, left) and coronal T2-weighted (T2) imaging (white arrows; 2nd from left). On the right side, coronal views through the midbrain display the development of an ipsilateral hyperintense lesion occuring between days 6 to 10 after stroke (red arrows). Note that corticospinal degeneration (blue arrows in B) associated with cortical involvement is detectable before the emergence of these secondary exofocal changes in midbrain. (C) Frequency of the anatomic distributions of the primary ischemic lesions (12 striatal stroke and 4 control stroke patients). Lesions are overlayed on the ICBM human brain template. Infarcts associated with secondary midbrain changes are coded in red, infarcts not associated with midbrain changes are coded in blue. Only frequencies of at least 25% are displayed. (D) Localization of secondary exofocal midbrain changes (n = 12 striatal stroke patients). For the purpose of this illustration, secondary lesions (day 10 or latest available scan before day 10) were adjusted to and superimposed on coronal and transverse T1-weighted images of a single patient.
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pone.0136483.g001: Subacute hyperintensity in ipsilateral midbrain at a delayed time point after striatal stroke.(A, B) MRI scans of two exemplary patients showing primary ischemic lesion confined to striatum (A) or involving striatum (B) in axial diffusion-weighted (DWI, left) and coronal T2-weighted (T2) imaging (white arrows; 2nd from left). On the right side, coronal views through the midbrain display the development of an ipsilateral hyperintense lesion occuring between days 6 to 10 after stroke (red arrows). Note that corticospinal degeneration (blue arrows in B) associated with cortical involvement is detectable before the emergence of these secondary exofocal changes in midbrain. (C) Frequency of the anatomic distributions of the primary ischemic lesions (12 striatal stroke and 4 control stroke patients). Lesions are overlayed on the ICBM human brain template. Infarcts associated with secondary midbrain changes are coded in red, infarcts not associated with midbrain changes are coded in blue. Only frequencies of at least 25% are displayed. (D) Localization of secondary exofocal midbrain changes (n = 12 striatal stroke patients). For the purpose of this illustration, secondary lesions (day 10 or latest available scan before day 10) were adjusted to and superimposed on coronal and transverse T1-weighted images of a single patient.

Mentions: Fig 1 illustrates the emergence of secondary exofocal midbrain changes. Primary ischemic infarcts (Fig 1A and 1B) involving striatal structures resulted in hyperintense ipsilateral midbrain lesions that emerged between days 6 and 10 after stroke (red arrows in Fig 1A and 1B). None of the 4 patients with MCA infarctions sparing striatal structures showed any evidence of such secondary changes through day 10 (Table 1; patients 17–20). Note that exofocal midbrain changes in gray matter have to be distinguished from hyperintense lesions in the pyramidal tract within the brain stem white matter. The latter result from Wallerian degeneration of the corticospinal tract (blue arrows in Fig 1B) and become clearly detectable from day 2 of stroke onwards.


Striatal Infarction Elicits Secondary Extrafocal MRI Changes in Ipsilateral Substantia Nigra.

Winter B, Brunecker P, Fiebach JB, Jungehulsing GJ, Kronenberg G, Endres M - PLoS ONE (2015)

Subacute hyperintensity in ipsilateral midbrain at a delayed time point after striatal stroke.(A, B) MRI scans of two exemplary patients showing primary ischemic lesion confined to striatum (A) or involving striatum (B) in axial diffusion-weighted (DWI, left) and coronal T2-weighted (T2) imaging (white arrows; 2nd from left). On the right side, coronal views through the midbrain display the development of an ipsilateral hyperintense lesion occuring between days 6 to 10 after stroke (red arrows). Note that corticospinal degeneration (blue arrows in B) associated with cortical involvement is detectable before the emergence of these secondary exofocal changes in midbrain. (C) Frequency of the anatomic distributions of the primary ischemic lesions (12 striatal stroke and 4 control stroke patients). Lesions are overlayed on the ICBM human brain template. Infarcts associated with secondary midbrain changes are coded in red, infarcts not associated with midbrain changes are coded in blue. Only frequencies of at least 25% are displayed. (D) Localization of secondary exofocal midbrain changes (n = 12 striatal stroke patients). For the purpose of this illustration, secondary lesions (day 10 or latest available scan before day 10) were adjusted to and superimposed on coronal and transverse T1-weighted images of a single patient.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4556671&req=5

pone.0136483.g001: Subacute hyperintensity in ipsilateral midbrain at a delayed time point after striatal stroke.(A, B) MRI scans of two exemplary patients showing primary ischemic lesion confined to striatum (A) or involving striatum (B) in axial diffusion-weighted (DWI, left) and coronal T2-weighted (T2) imaging (white arrows; 2nd from left). On the right side, coronal views through the midbrain display the development of an ipsilateral hyperintense lesion occuring between days 6 to 10 after stroke (red arrows). Note that corticospinal degeneration (blue arrows in B) associated with cortical involvement is detectable before the emergence of these secondary exofocal changes in midbrain. (C) Frequency of the anatomic distributions of the primary ischemic lesions (12 striatal stroke and 4 control stroke patients). Lesions are overlayed on the ICBM human brain template. Infarcts associated with secondary midbrain changes are coded in red, infarcts not associated with midbrain changes are coded in blue. Only frequencies of at least 25% are displayed. (D) Localization of secondary exofocal midbrain changes (n = 12 striatal stroke patients). For the purpose of this illustration, secondary lesions (day 10 or latest available scan before day 10) were adjusted to and superimposed on coronal and transverse T1-weighted images of a single patient.
Mentions: Fig 1 illustrates the emergence of secondary exofocal midbrain changes. Primary ischemic infarcts (Fig 1A and 1B) involving striatal structures resulted in hyperintense ipsilateral midbrain lesions that emerged between days 6 and 10 after stroke (red arrows in Fig 1A and 1B). None of the 4 patients with MCA infarctions sparing striatal structures showed any evidence of such secondary changes through day 10 (Table 1; patients 17–20). Note that exofocal midbrain changes in gray matter have to be distinguished from hyperintense lesions in the pyramidal tract within the brain stem white matter. The latter result from Wallerian degeneration of the corticospinal tract (blue arrows in Fig 1B) and become clearly detectable from day 2 of stroke onwards.

Bottom Line: Apparent diffusion coefficient (ADC) values in the secondary lesions showed a delayed sharp decline through day 10.Normalization of ADC values was observed at late measurements.Taken together, our study demonstrates that striatal infarction elicits delayed degenerative changes in ipsilateral substantia nigra pars compacta.

View Article: PubMed Central - PubMed

Affiliation: Center for Stroke Research Berlin (CSB), Charité-Universitätsmedizin Berlin, Berlin, Charitéplatz 1,10117, Berlin, Germany; Department of Neurology, Charité-Universitätsmedizin Berlin, Charitéplatz 1, 10117, Berlin, Germany.

ABSTRACT
Focal ischemia may induce pathological alterations in brain areas distant from the primary lesion. In animal models, exofocal neuron death in the ipsilateral midbrain has been described after occlusion of the middle cerebral artery (MCA). Using sequential magnetic resonance imaging (T2- and diffusion-weighted) at 3 Tesla, we investigated acute ischemic stroke patients on days 1, 2, 6, 8, and 10 after stroke onset. Sixteen consecutive patients who had suffered a stroke involving the caudate nucleus and/or putamen of either hemisphere were recruited into the study. Four additional patients with strokes sparing the caudate nucleus and putamen but encompassing at least one-third of the MCA territory served as controls. Ischemic lesions involving striatal structures resulted in hyperintense lesions in ipsilateral midbrain that emerged between days 6 and 10 after stroke and were not present on the initial scans. In contrast, none of the control stroke patients developed secondary midbrain lesions. Hyperintense lesions in the pyramidal tract or the brain stem caused by degeneration of the corticospinal tract could be clearly distinguished from these secondary midbrain gray matter lesions and were detectable from day 2 after ischemia. Co-registration of high-resolution images with a digitized anatomic atlas revealed localization of secondary lesions primarily in the substantia nigra pars compacta. Apparent diffusion coefficient (ADC) values in the secondary lesions showed a delayed sharp decline through day 10. Normalization of ADC values was observed at late measurements. Taken together, our study demonstrates that striatal infarction elicits delayed degenerative changes in ipsilateral substantia nigra pars compacta.

No MeSH data available.


Related in: MedlinePlus