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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

Ischemic lesions of striatum elicit secondary changes in ipsilateral substantia nigra.(A) Color coding of the relative frequency of “ischemic” voxels in the primary ischemic lesion of striatal stroke patients (n = 12) who subsequently developed secondary midbrain changes. Cd: Caudate nucleus (nmax = 11); Pu: putamen (nmax = 10). (B) Color coding of the relative frequency of voxels showing secondary changes in midbrain in these patients. SNC: substantia nigra, pars compacta (nmax = 9). SNR: substantia nigra, pars reticulata. Numbers ranging from -12.5 to +21.2 denote Talairach y-coordinates.
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pone.0136483.g002: Ischemic lesions of striatum elicit secondary changes in ipsilateral substantia nigra.(A) Color coding of the relative frequency of “ischemic” voxels in the primary ischemic lesion of striatal stroke patients (n = 12) who subsequently developed secondary midbrain changes. Cd: Caudate nucleus (nmax = 11); Pu: putamen (nmax = 10). (B) Color coding of the relative frequency of voxels showing secondary changes in midbrain in these patients. SNC: substantia nigra, pars compacta (nmax = 9). SNR: substantia nigra, pars reticulata. Numbers ranging from -12.5 to +21.2 denote Talairach y-coordinates.

Mentions: Next, we studied the anatomic distributions and relative frequencies of the primary ischemic lesions in relation to the emergence of secondary midbrain changes (Table 1; Figs 1C and 2A). Infarcts associated with delayed exofocal midbrain changes (red color-coded in Fig 1C) consistently involved striatal structures (caudate nucleus, putamen; Fig 2A). Similarly, we studied the frequencies of the precise anatomic localizations of secondary exofocal lesions (Figs 1D and 2B). Co-registration with a digitized anatomic atlas [22, 23] showed that the core area of the secondary exofocal midbrain lesions was consistently located in the pars compacta of the substantia nigra.


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)

Ischemic lesions of striatum elicit secondary changes in ipsilateral substantia nigra.(A) Color coding of the relative frequency of “ischemic” voxels in the primary ischemic lesion of striatal stroke patients (n = 12) who subsequently developed secondary midbrain changes. Cd: Caudate nucleus (nmax = 11); Pu: putamen (nmax = 10). (B) Color coding of the relative frequency of voxels showing secondary changes in midbrain in these patients. SNC: substantia nigra, pars compacta (nmax = 9). SNR: substantia nigra, pars reticulata. Numbers ranging from -12.5 to +21.2 denote Talairach y-coordinates.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4556671&req=5

pone.0136483.g002: Ischemic lesions of striatum elicit secondary changes in ipsilateral substantia nigra.(A) Color coding of the relative frequency of “ischemic” voxels in the primary ischemic lesion of striatal stroke patients (n = 12) who subsequently developed secondary midbrain changes. Cd: Caudate nucleus (nmax = 11); Pu: putamen (nmax = 10). (B) Color coding of the relative frequency of voxels showing secondary changes in midbrain in these patients. SNC: substantia nigra, pars compacta (nmax = 9). SNR: substantia nigra, pars reticulata. Numbers ranging from -12.5 to +21.2 denote Talairach y-coordinates.
Mentions: Next, we studied the anatomic distributions and relative frequencies of the primary ischemic lesions in relation to the emergence of secondary midbrain changes (Table 1; Figs 1C and 2A). Infarcts associated with delayed exofocal midbrain changes (red color-coded in Fig 1C) consistently involved striatal structures (caudate nucleus, putamen; Fig 2A). Similarly, we studied the frequencies of the precise anatomic localizations of secondary exofocal lesions (Figs 1D and 2B). Co-registration with a digitized anatomic atlas [22, 23] showed that the core area of the secondary exofocal midbrain lesions was consistently located in the pars compacta of the substantia nigra.

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