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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Localized magnetic resonance spectroscopy (MRS) yields sensitive metabolic markers to provide insight into the pathophysiology of mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) in vivo. Findings in full MELAS syndrome at 1H MRS of the brain typically include severely elevated lactate and reduced N-acetylaspartate, glutamate, myo-inositol, and total creatine concentrations in stroke-like lesions. Similar but less extreme alterations are also common in gray matter (GM) regions that appear normal at magnetic resonance imaging. Phosphorus spectroscopy of peripheral muscle permits investigation of the bioenergetic status. A decline of the phosphorylation potential indicates a low energy reserve at rest. Phosphocreatine resynthesis during post-exercise recovery is delayed pointing to reduced mitochondrial capacity. As MRS is inherently non-invasive, follow-up studies can be performed to assess treatment response quantitatively.
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PMID:Magnetic resonance spectroscopy in patients with MELAS. 1576 Jun 31

Cerebral small vessel disease results in lacunar infarcts and cognitive impairment. Diffusion tensor imaging (DTI) demonstrates a reduction in fractional anisotropy and increase in mean diffusivity, which correlates more strongly with cognition than conventional MRI. The underlying pathological basis for these DTI changes is not known. In this study magnetic resonance spectroscopy was used to determine the biochemical basis of these DTI alterations. Twenty-five patients with lacunar stroke and radiological leukoaraiosis were recruited. Chemical shift imaging (CSI) and DTI were performed on a 1.5 T MRI scanner. A region of interest was positioned in the white matter of the centrum semiovale. Multivoxel CSI data were processed and the metabolite ratios estimated. DTI parameters corresponding to the exact region of tissue excited by CSI were obtained. Mean spectroscopy data and DTI values for each subject were correlated. Univariate analysis revealed a positive correlation between N-acetyl aspartate-creatine (NAA/Cr) and fractional anisotropy (r = 0.52, p = 0.008), and a negative correlation with mean diffusivity (r = -0.51, p = 0.009). Results remained little changed after controlling for mean percentage lesion and mean percentage white matter per voxel (with fractional anisotropy r = 0.54, p = 0.008, and with mean diffusivity r = -0.52, p = 0.01). These findings are consistent with axonal loss or dysfunction, or both, accounting for at least part of the DTI abnormalities found in patients with small vessel disease. It provides evidence that DTI identifies axonal disruption in white matter tracts.
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PMID:Correlations between MRS and DTI in cerebral small vessel disease. 1681 Jun 32

We report the case of a patient with bilateral and symmetrical T2 hyperintensities of the middle cerebellar peduncles. She had a history of left pontine infarction 8 months before. This was attributed to bilateral Wallerian degeneration. MR Spectroscopy showed decreased N-acetyl aspartate/Creatine (NAA/Cr) ratio in the cerebellar peduncles as well as in the whole cerebellum. We hypothesize that this could reflect neuronal degeneration following a stroke.
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PMID:Bilateral wallerian degeneration of the middle cerebellar peduncles due to unilateral pontine infarction. 1704 32

Mood disorders are associated with structural, metabolic and spectroscopic changes in prefrontal regions. In the case of depression associated with stroke, there is little information about the biochemical profile of these regions, as assessed by proton magnetic resonance spectroscopy ((1)H-MRS). In a group of first-ever stroke patients, we studied the association between post-stroke depression and (1)H-MRS measurements in unaffected frontal lobes. Twenty-six patients with a first ischemic stroke located outside the frontal lobes were included in the study. Single voxel proton magnetic resonance spectroscopy ((1)H-MRS) was performed to assess N-acetylaspartate/creatine (NAA)/Cr, glutamate+glutamine (Glx)/Cr, choline (Cho)/Cr and myo-inositol (mI)/Cr ratios. Patients were assessed within the first 10 days after stroke and again four months later. The diagnosis of depression was made on the basis of clinical observation, interview and Hamilton Depression Rating Scale scores. In a group of 26 patients, eight (31%) met criteria for depression at the first assessment, and nine (35%) met criteria for depression at follow-up. Patients with depression in the immediate post-stroke phase had significantly higher Glx/Cr ratios in the contralesional hemisphere than non-depressive patients. No biochemical differences were found between the groups at 4-month follow-up. These findings suggest that post-stroke depression is accompanied by changes in frontal lobe glutamate/glutamine levels, perhaps reflecting abnormalities in glutamatergic transmission in the immediate post-stroke period.
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PMID:Single voxel proton magnetic resonance spectroscopy in post-stroke depression. 1708 51

Structural MRI measures have been used to predict cognitive decline in elderly subjects, but few studies have used proton magnetic resonance spectroscopy ((1)H-MRS) for this purpose, particularly after stroke. We studied the potential of (1)H-MRS to predict cognitive decline in patients with stroke or TIA and healthy ageing controls over 12 months and 3 years. Structural MRI and single-voxel (1)H-MRS in the frontal white matter and the occipito-parietal gray matter were performed at the index assessment (3-6 months post-stroke) in 49 stroke/TIA patients and 60 controls. Neuropsychological testing was performed at the index assessment and repeated at 12 months in 30 stroke/TIA patients and 49 controls, and at 3 years in 25 patients and 48 controls. In stroke/TIA patients, frontal NAA/Cr predicted cognitive decline over 12 months and 3 years, and in elderly control subjects frontal NAA predicted cognitive decline over 12 months only. In stroke/TIA patients, the (1)H-MRS measures were better predictors of cognitive decline than structural measures. (1)H-MRS may be useful in assessing early cognitive impairment after stroke/TIA and in normal ageing.
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PMID:Prediction of cognitive decline after stroke using proton magnetic resonance spectroscopy. 1709 17

Conventional ways of monitoring reperfusion in acute ischemic stroke have several limitations. In searching for an alternative, we evaluated biochemical serum markers of stroke change in relation to reperfusion. N-acetylaspartate (NAA) is a small amino acid synthesized by neuronal mitochondria, which can be released in the extracellular space after reperfusion in animal models of brain ischemia. S100B is a well-known peripheral marker of brain damage in various neurologic diseases, including stroke. Serum samples were analyzed from 13 patients with ischemic stroke who were either treated conservatively or with recombinant tissue plasminogen activator. Blood was drawn at baseline; after 30 minutes; after 1, 2, 4, and 8 hours; and between 12 to 24 hours. Serum concentrations of NAA were analyzed using a gas chromatography-mass spectrometry method. S100B was analyzed using an automated immunoluminometric assay. Reperfusion was assessed using transcranial Doppler and clinical criteria. Reperfusion (n = 4) was associated with a transient rapid increase in serum NAA levels. Such an early rapid increase of NAA was not observed for patients with persistent occlusion at 12 to 24 hours (n = 4) and patients with no occlusion on baseline transcranial Doppler (n = 5). NAA peak levels and area under the curve values were significantly higher after reperfusion in comparison with normal transcranial Doppler findings or persistent occlusion (P = .003 and P = .05, respectively). No differences were found between these groups for S100B levels. In patients with acute ischemic stroke, serum NAA levels transiently raise after reperfusion.
J Stroke Cerebrovasc Dis
PMID:N-acetylaspartate: serum marker of reperfusion in ischemic stroke. 1790 83

We report 2 patients of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) and consider the pathophysiology of stroke-like lesions, using magnetic resonance imaging (MRI), diffusion-weighted imaging (DWI) on MRI, perfusion imaging on MRI, and 1H magnetic resonance spectroscopy (1H-MRS). In Patient 1, T2-weighted imaging (T2-WI) on MRI at onset and even at 44 days after onset of the stroke-like episode showed high intensity in left parietal, temporal, and occipital lobe lesions. In the temporal lobe lesion, the apparent diffusion coefficient (ADC) at 44 days after onset was higher (average: 1.219x10(-3)mm2/s) than that in a normal region (average: 0.796x10(-3)mm2/s). (1)H-MRS of the left parietal lobe lesion at the same day showed a decrease in N-acetylaspartate/(creatine+phosphocreatine) (NAA/Cr) (0.43) and a peak in lactate. 1H-MRS of the contralateral side at the same day showed NAA/Cr (1.57) and no peak in lactate. Thereafter, ADC gradually decreased and NAA/Cr gradually increased, and the peak in lactate disappeared in the lesion. In Patient 2, T2-WI at onset showed high intensity in bilateral occipital lobe lesions. In the left occipital lobe lesion, ADC at the same day was higher (1.082x10(-3)mm2/s) than that in a normal region (average: 0.841x10(-3)mm2/s). (1)H-MRS of the left occipital lobe lesion at the same day showed a decrease of NAA (3.0mM) and a peak in lactate (13.1mM) (measured by LCModel). In 1H-MRS of the normal left parietooccipital lobe at 4 months before onset, NAA was 7.6mM and there was no peak in lactate (0mM). Perfusion imaging at onset showed high intensity in bilateral occipital lobes, which indicated hyperperfusion in stroke-like lesions. Thereafter, ADC gradually decreased and the peak in lactate partially decreased, and the low concentration of NAA persisted (regardless of the partial recovery) in the lesion. These results suggest that the stroke-like episodes is related to vasogenic edema, hyperperfusion, and neuronal damage. Acute oxidative phosphorylation defect may have a crucial role in the pathophysiology of stroke-like episodes.
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PMID:Serial brain imaging analysis of stroke-like episodes in MELAS. 1828 16

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an important genetic cause of stroke, but pathogenic mechanisms and functional alterations remain poorly characterized. The purpose of this study was to investigate adaptive metabolic and functional changes in white matter hyperintensities and normal-appearing white matter in CADASIL patients using (1)H-magnetic resonance spectroscopic imaging (MRSI). Eight CADASIL patients and eight matched healthy controls were studied. (1)H-MRSI data were acquired on a 3T scanner using high-resolution multi-spin echo spectroscopic imaging (T (E) = 288 ms) and non-accelerated medium-resolution MRSI (T (E) = 35 ms). MRI of all CADASIL patients demonstrated characteristic white matter hyper-intensities (WMH) in the subcortical periventricular white matter. Cre/Cho, Glx/Cho and Glx/Cre ratios were significantly decreased in WMH compared to normal-appearing white matter (NAWM) in patients, while Glx/Cre and mI/Cho ratios in NAWM showed a significant increase compared to healthy controls. In severely affected patients derived spectra reflected a decrease of NAA concentrations inside WMH when compared to healthy white matter. Metabolic abnormalities in WMH of CADASIL patients are compatible with axonal loss due to chronic micro-infarctions. Increased Glx/Cre and mI/Cho ratios in NAWM indicate an augmented glial cell density and decreased neuronal cell density. This altered tissue composition might be interpreted as adaptation to hypoperfusion and impaired vasoreactivity in NAWM of CADASIL patients. Our data might contribute to the general understanding of adaptive processes induced by hypoperfusion and chronic ischemia.
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PMID:Adaptive metabolic changes in CADASIL white matter. 1969 Sep 6

Previous studies in patients with a major depressive disorder show functional abnormalities in the medial frontal cortex. Functional and structural abnormalities in patients with post-stroke depression (PSD) are not well studied. The major goals of this study were to determine the biochemical abnormalities that occur in PSD and to assess the effect of antidepressants in patients with PSD at the biochemical level. We used magnetic resonance imaging to detect structural or functional abnormalities in PSD patients. In a prospective study, we included 30 patients with PSD and 20 age-matched subjects as controls. Magnetic resonance spectroscopy (MRS) of the brain was conducted in all subjects at the beginning of the study. Patients with PSD were treated with the antidepressant paroxetine (20-40mg/days) for 6 months. After the 6-month period, all PSD subjects underwent MRS again. PSD patients were evaluated with the Hamilton Depression Scale (HAMD) both before and after treatment with the antidepressant. The mean age of the PSD patients was 70.0+/-4.2 years and that of the controls was 67.2+/-5.4 years. Before treatment, N-acetyl aspartate/creatine (NAA/Cr) ratios in the bilateral hippocampus and thalami were significantly lower in PSD patients than in controls. Choline/creatine (Cho/Cr) ratios were significantly higher in the bilateral hippocampus and left thalamus in PSD patients than in controls. The Cho/Cr ratios were significantly higher in the left thalamus than in the right in PSD patients. The HAMD scores were significantly correlated with the Cho/Cr ratios in the left and right hippocampus. Compared with PSD patients before antidepressant treatment, the PSD subjects after treatment had significantly higher NAA/Cr ratios in the left hippocampus and bilateral thalami. They had significantly lower Cho/Cr ratios in bilateral hippocampus and left thalamus. Our study suggests that metabolic abnormalities in the hippocampus and thalamus are implicated in PSD. Antidepressants may alter the local metabolic abnormalities in these areas.
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PMID:Effects of antidepressant treatment on N-acetyl aspartate and choline levels in the hippocampus and thalami of post-stroke depression patients: a study using (1)H magnetic resonance spectroscopy. 2022 56

Mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS) shows sudden neurological deficits that are called 'stroke-like episodes'. With regard to the pathophysiology of stroke-like episodes, so-called mitochondrial angiopathy and cytopathy theories have been proposed, but the subject is still controversial. To clarify this matter and to contribute to the development of a treatment for MELAS, we review here current neuroimaging research and consider the pathophysiology of stroke-like lesions. With regard to diffusion-weighted imaging findings, early reports often showed an elevated apparent diffusion coefficient (ADC) in stroke-like lesions; this was considered to be mainly vasogenic edema in the acute phase and is a different pattern than that in stroke. However, there has recently been an increase in the number of reports of a decrease in ADC; these cases are considered to be cytotoxic edema in the acute phase, which is compatible with stroke. With regard to (1)H-magnetic resonance spectroscopy findings in stroke-like lesions, a decrease in N-acetylaspartate and an increase in lactate have been reported. With regard to single photon emission computed tomography findings for stroke-like lesions in MELAS, an overall trend is hyperperfusion in the acute stage (within 1 month) of stroke-like episodes and hypoperfusion in the chronic stage (several months later). With regard to positron emission tomography, nearly all of these reports are consistent with the mitochondrial cytopathy theory. With regard to neuropathology in MELAS, the most common findings during the chronic stage of stroke-like episodes include foci of necrosis and peculiar vascular changes (abnormalities of mitochondria in small arteries). Concerning the pathology of the acute stage of stroke-like episodes, extensive petechial hemorrhage along the gyri of the cortex corresponding to acute stroke-like lesions has been reported. To clarify the true pathophysiology of stroke-like episodes, we offer three suggestions. First, we must define the precise onset of stroke-like episodes. Second, current studies are limited by the difficulty of imaging just before and just after (within a few minutes) the onset of stroke-like episodes. Third, we hope to establish an experimental animal model. We should conduct a simultaneous multimodal imaging and histological study just before and just after (within a few minutes) the onset of stroke-like episodes in an experimental animal model.
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PMID:Neuroimaging of stroke-like episodes in MELAS. 2060 41


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