MR detection of secondary changes remote from ischemia: preliminary observations after occlusion of the middle cerebral artery in rats.

PURPOSETo determine whether secondary MR changes occur in the thalamus or the substantia nigra after middle cerebral artery (MCA) occlusion in rats.METHODSSprague-Dawley rats were subjected to MCA occlusion. At varying intervals, proton density-, T1-, and T2-weighted images were obtained with a 4.7-T superconductive MR unit.RESULTST2-weighted images revealed an area of high signal intensity in the ipsilateral substantia nigra 4 days after occlusion. A lesion of low signal intensity appeared in the ipsilateral thalamus 7 days after surgery on proton density- and/or T2-weighted images.CONCLUSIONMR showed secondary changes in the thalamus and the substantia nigra after MCA occlusion in rats. MR imaging should provide more information on the neuropathology of the delayed neuronal degeneration after cerebral ischemia.     

Topographical alterations of the midbrain and the substantia nigra following unilateral posteroventral pallidotomy in patients with Parkinson's disease using routine and multishot diffusion-weighted magnetic resonance imaging

To determine whether posteroventral pallidotomy (PVP) induces topographical changes of the ipsilateral midbrain and degeneration of the substantia nigra in Parkinson's disease patients, we obtained magnetic resonance (MR) images of 18 patients who had undergone PVP and measured the width of the cerebral peduncle at the mid-point of the inner margin. Then, we assessed MR signal changes in the substantia nigra on T2-weighted images in all patients and on multishot diffusion-weighted images in seven patients. In MR images taken within 1 year of PVP, a comparison between the ratio of the ipsilateral side/contralateral side of the cerebral peduncle of patients after PVP and that of the unaffected side/affected side in the preoperative images revealed no significant difference ( P>0.05). In MR images 1 to 2 years after PVP, there was a significant difference in the ratio of the cerebral peduncle ( P<0.01). A significant difference was still evident in MR images more than 2 years after PVP ( P<0.001). On T2-weighted images obtained within 1 year of PVP, an area of patchy high signal appeared in the posterolateral region of the ipsilateral substantia nigra in six of 13 patients. However, there was no signal change in the substantia nigra in any T2-weighted images more than 1 year after PVP. Multishot diffusion-weighted images obtained from all six patients more than 1 year after PVP revealed an abnormal area of high signal in the posterolateral region of the ipsilateral substantia nigra, however, within 1 year of PVP such a signal change was not seen. PVP would induce degeneration of the ipsilateral substantia nigra and atrophy of the ipsilateral midbrain.     

Secondary degeneration of the substantia nigra and corticospinal tract after hemorrhagic middle cerebral artery infarction: diffusion-weighted MR findings.

Middle cerebral artery (MCA) infarction involving the striatum can cause secondary degeneration of the substantia nigra and corticospinal tract. We present a patient with subacute hemorrhagic MCA infarction in whom diffusion-weighted MR images showed high signal intensity in the ipsilateral substantia nigra and corticospinal tract. A corresponding apparent diffusion coefficient map revealed a uniformly decreased signal in the same area. This represents secondary degeneration and should not be mistaken for other pathological conditions, such as a new infarction.     

Evaluation of the substantia nigra in patients with Parkinsonian syndrome accomplished using multishot diffusion-weighted MR imaging.

BACKGROUND AND PURPOSE: Although it is important to evaluate the substantia nigra in patients with parkinsonian syndrome, it is difficult to depict its anatomy, even by MR imaging. Using anatomic studies of the direction of nerve fibers around the substantia nigra, we attempted to depict this entity with multishot diffusion-weighted MR imaging to evaluate its topographic changes in patients with Parkinson's disease and secondary parkinsonism. METHODS: We measured the substantia nigra on 72 diffusion-weighted axial MR images obtained in 36 healthy control subjects, on 47 images obtained in 25 patients with Parkinson's disease, and on 10 images obtained in five patients with secondary parkinsonism. We considered the width of the minor axis of the substantia nigra as its "thickness," which appeared as a crescent-shaped region in the midbrain. RESULTS: Diffusion-weighted imaging portrayed the substantia nigra distinctly better than did T2-weighted imaging, because the surrounding white matter appeared as an area of high signal intensity. The mean (+/- SD) thickness values of the substantia nigra were 5.1+/-0.89 mm in control subjects, 4.8+/-0.75 mm in patients with Parkinson's disease, and 3.4+/-0.53 mm in patients with secondary parkinsonism. CONCLUSION: Multishot diffusion-weighted imaging is a better imaging technique than T2-weighted imaging for demonstrating a change in size of the substantia nigra in vivo. The substantia nigra is not reduced in size in patients with Parkinson's disease, but it is reduced in patients with secondary parkinsonism.     

Diffusion-weighted MR imaging of acute stroke: correlation with T2-weighted and magnetic susceptibility-enhanced MR imaging in cats

We evaluated the temporal and anatomic relationships between changes in diffusion-weighted MR image signal intensity, induced by unilateral occlusion of the middle cerebral artery in cats, and tissue perfusion deficits observed in the same animals on T2-weighted MR images after administration of a nonionic intravascular T2 shortening agent. Diffusion-weighted images obtained with strong diffusion-sensitizing gradient strengths (5.6 gauss/cm, corresponding to gradient attenuation factor, b, values of 1413 sec/mm2) displayed increased signal intensity in the ischemic middle cerebral artery territory less than 1 hr after occlusion, whereas T2-weighted images without contrast usually failed to detect injury for 2-3 hr after stroke. After contrast administration (0.5-1.0 mmol/kg by Dy-DTPA-BMA, IV), however, T2-weighted images revealed perfusion deficits (relative hyperintensity) within 1 hr after middle cerebral artery occlusion that corresponded closely to the anatomic regions of ischemic injury shown on diffusion-weighted MR images. Close correlations were also found between early increases in diffusion-weighted MR image signal intensity and disrupted phosphorus-31 and proton metabolite levels evaluated with surface coil MR spectroscopy, as well as with postmortem histopathology. These data indicate that diffusion-weighted MR images more accurately reflect early-onset pathophysiologic changes induced by acute cerebral ischemia than do T2-weighted spin-echo images.     

Transient MR signal changes in patients with generalized tonicoclonic seizure or status epilepticus: periictal diffusion-weighted imaging.

BACKGROUND AND PURPOSE: Our purpose was to investigate transient MR signal changes on periictal MR images of patients with generalized tonicoclonic seizure or status epilepticus and to evaluate the clinical significance of these findings for differential diagnosis and understanding of the pathophysiology of seizure-induced brain changes. METHODS: Eight patients with MR images that were obtained within 3 days after the onset of generalized tonicoclonic seizure or status epilepticus and that showed seizure-related MR signal changes had their records retrospectively reviewed. T1- and T2-weighted images were obtained of all eight patients. Additional diffusion-weighted images were obtained of five patients during initial examination. After adequate control of the seizure was achieved, follow-up MR imaging was performed. We evaluated the signal changes, location of the lesions, and degree of contrast enhancement on T1- and T2-weighted images and the signal change and apparent diffusion coefficient (ADC) on diffusion-weighted images. We also compared the signal changes of the initial MR images to those of the follow-up MR images. RESULTS: The initial MR images revealed focally increased T2 signal intensity, swelling, and increased volume of the involved cortical gyrus in all eight patients. The lesions were located in the cortical gray matter or subcortical white matter in seven patients and at the right hippocampus in one. T1-weighted images showed decreased signal intensity at exactly the same location (n = 6) and gyral contrast enhancement (n = 4). Diffusion-weighted images revealed increased signal intensity at the same location and focally reduced ADC. The ADC values were reduced by 6% to 28% compared with either the normal structure opposite the lesion or normal control. Follow-up MR imaging revealed the complete resolution of the abnormal T2 signal change and swelling in five patients, whereas resolution of the swelling with residual increased T2 signal intensity at the ipsilateral hippocampus was observed in the other two patients. For one of the two patients, hippocampal sclerosis was diagnosed. For the remaining one patient, newly developed increased T2 signal intensity was shown. CONCLUSION: The MR signal changes that occur after generalized tonicoclonic seizure or status epilepticus are transient increase of signal intensity and swelling at the cortical gray matter, subcortical white matter, or hippocampus on periictal T2-weighted and diffusion-weighted images. These findings reflect transient cytotoxic and vasogenic edema induced by seizure. The reversibility and typical location of lesions can help exclude the epileptogenic structural lesions.     

Magnetic resonance imaging and histologic findings of experimental cerebral fat embolism

RATIONALE AND OBJECTIVES: The purpose of this study was to determine whether cerebral fat embolism demonstrated reversible or irreversible findings in magnetic resonance (MR) imaging over time and to compare the features in MR images with histologic findings in a cat model. MATERIALS AND METHODS: MR images were obtained serially at 2 hours, 1 and 4 days, and 1, 2, and 3 weeks after embolization with 0.05 mL of triolein into the internal carotid artery in 19 cats. Any abnormal signal intensity and change in the signal intensity were evaluated on T2-weighted images, T1-weighted images, diffusion-weighted images (DWIs; including apparent diffusion coefficient [ADC] maps), and gadolinium-enhanced T1-weighted images (Gd-T1WI) over time. After MR imaging at 3 weeks, brain tissue was obtained and evaluated for light microscopic (LM) examination using hematoxylin-eosin and Luxol fast blue staining. For electron microscopic examination, the specimens were obtained at the cortex. The histologic and MR findings were compared. RESULTS: The embolization lesions showed hyperintensity on T2-weighted images, hyperintensity, or isointensity on DWIs, hypointensity, or isointensity on ADC maps and contrast enhancement on Gd-T1WIs at 2 hours. The T2-weighted hyperintensity extended to the white matter at day 1 and decreased thereafter. Contrast enhancement decreased continuously from day 1, and hyperintensity on DWI decreased after day 4. Hypointensity on ADC maps became less prominent after day 4. By week 3, most lesions had reverted to a normal appearance on MR images and were correlated with LM findings. However, small focal lesions remained in the gray matter of 8 cats and in the white matter of 3 cats on MR images, and this correlated with the cystic changes on LM findings. Electron microscopic examination of the cortical lesions that reverted to normal at week 3 in MR images showed that most of these lesions appeared normal but showed sporadic intracapillary fat vacuoles and disruption of the endothelial walls. CONCLUSIONS: The embolized lesions of the hyperacute stage were of 2 types: type 1 lesions, showing hyperintensity on DWIs and hypointensity on ADC maps, have irreversible sequelae, such as cystic changes; whereas type 2 lesions, showing isointensity or mild hyperintensity on DWIs and ADC maps, reverted to a normal appearance in the subacute stage.     

Diffusion-weighted MR imaging in patients with phenylketonuria: relationship between serum phenylalanine levels and ADC values in cerebral white matter

PURPOSE: To prospectively determine the relationship between serum phenylalanine levels and apparent diffusion coefficient (ADC) values in the cerebral white matter of patients with phenylketonuria (PKU). MATERIALS AND METHODS: Institutional review board approval was obtained, and participants provided informed consent. Magnetic resonance (MR) imaging, which included T1- and T2-weighted, fluid-attenuated inversion-recovery (FLAIR), and diffusion-weighted examinations, was performed in 21 patients with PKU (nine male and 12 female patients; age range, 3-44 years; mean age, 19.4 years). ADC values in deep cerebral white matter were calculated for each patient. Serum phenylalanine levels were obtained in all patients within 12 days after MR imaging. Serum phenylalanine levels were measured in 16 patients 1 year before MR imaging. ADC values in cerebral white matter and serum phenylalanine levels were compared. A total of 21 control subjects (12 male and nine female patients; age range, 3-33 years; mean age, 20.6 years) underwent MR imaging. ADC values in cerebral white matter were compared with serum phenylalanine levels by using the Pearson correlation. RESULTS: Abnormal high signal intensity in white matter on T2-weighted and FLAIR MR images was noted in patients with PKU who had serum phenylalanine levels of more than 8.5 mg/dL (514.2 micromol/L). Diffusion in posterior deep cerebral white matter tended to be restricted in patients when increased serum phenylalanine levels were measured after MR imaging (r = -0.62). There was a correlation between ADC values in posterior cerebral white matter and serum phenylalanine levels measured 1 year before MR imaging (r = -0.77). ADCs of control subjects were significantly higher than ADCs of patients with PKU (P < .005). CONCLUSION: Posterior deep white matter in patients with PKU and a serum phenylalanine level of more than 8.5 mg/dL showed high signal intensity in white matter on T2-weighted and FLAIR MR images and revealed decreased ADC. We suggest that to avoid brain-restricted diffusion due to hyperphenylalanemia, patients with PKU should maintain serum phenylalanine levels of less than 8.5 mg/dL (514.2 micromol/L).     

Value of diffusion-weighted imaging and apparent diffusion coefficient in recent cerebral infarctions: a correlative study with contrast-enhanced T1-weighted imaging

BACKGROUND AND PURPOSE: The clinical usefulness and the time course of diffusion-weighted imaging and apparent diffusion coefficient (ADC) in acute and subacute cerebral infarction have not yet been established, although it is known that contrast-enhanced T1-weighted spin-echo imaging can detect a subacute infarct. Our aim was to study which imaging technique is useful in detecting recent infarcts, and whether an increase in ADC or a decrease in signal intensity on diffusion-weighted images is correlated with enhancement on T1-weighted spin-echo images. METHODS: Forty-one infarctions with a duration of 9 hours to 27 days were studied in 29 patients. The ADC and signal intensity on diffusion-weighted images were compared with the contrast-enhancement ratio (CER) on T1-weighted spin-echo images (CER = signal intensity after contrast injection/signal intensity before contrast injection). RESULTS: ADC was linearly correlated with CER, and signal intensity on diffusion-weighted images was inversely correlated with CER. The correlation between ADC and age of the infarct in the subacute phase was weak. CONCLUSION: Diffusion-weighted and contrast-enhanced T1-weighted spin-echo images complement each other in detecting subacute infarcts. Neovascularization and disruption of the blood-brain barrier in infarcts can be important in increasing ADC in subacute infarcts.     

MR imaging of Parkinson disease with spin-echo and gradient-echo sequences

High-field MR with both spin-echo and gradient-echo sequences was performed in 21 patients with (idiopathic, drug-responsive) Parkinson disease. The use of gradient echoes allowed more sensitive detection than did spin echoes of susceptibility changes in the putamina and substantia nigra. No statistically significant difference in putaminal hypointensity on long TR/long TE spin-echo sequences or on T2*-weighted images using gradient-echo sequences was observed between Parkinson patients and controls. There was also no statistically significant difference in the frequency of restoration of the signal intensity of the substantia nigra between the two groups of patients. The width of the pars compacta of the substantia nigra in patients with Parkinson disease was 2.12 + 0.82 mm (mean +/- SD). This value in age- and gender-matched controls was 2.67 +/- 0.5. Comparing these two groups with an unpaired t test resulted in a p value less than or equal to .005. Our MR study with spin-echo and gradient-echo images in Parkinson and control patients was able to substantiate and elaborate on previously described MR features of Parkinson disease.     

Brain MRI in neurodegeneration with brain iron accumulation with and without PANK2 mutations

BACKGROUND AND OBJECTIVE: Patients with a clinical diagnosis of neurodegeneration with brain iron accumulation (NBIA, formerly called Hallervorden-Spatz syndrome) often have mutations in PANK2, the gene encoding pantothenate kinase 2. We investigated correlations between brain MR imaging changes, mutation status, and clinical disease features. METHODS: Brain MRIs from patients with NBIA were reviewed by 2 neuroradiologists for technical factors, including signal intensity abnormalities in specific brain regions, presence and location of atrophy, presence of white matter abnormality, contrast enhancement, and other comments. PANK2 genotyping was performed by polymerase chain reaction amplification of patient genomic DNA followed by automated nucleotide sequencing. RESULTS: Sixty-six MR imaging examinations from 49 NBIA patients were analyzed, including those from 29 patients with mutations in PANK2. All patients with mutations had the specific pattern of globus pallidus central hyperintensity with surrounding hypointensity on T2-weighted images, known as the eye-of-the-tiger sign. This sign was not seen in any studies from patients without mutations. Even before the globus pallidus hypointensity developed, patients with mutations could be distinguished by the presence of isolated globus pallidus hyperintensity on T2-weighted images. Radiographic evidence for iron deposition in the substantia nigra was absent early in disease associated with PANK2 mutations. MR imaging abnormalities outside the globus pallidus, including cerebral or cerebellar atrophy, were more common and more severe in mutation-negative patients. No specific MR imaging changes could be distinguished among the mutation-negative patients. CONCLUSION: MR imaging signal intensity abnormalities in the globus pallidus can distinguish patients with mutations in PANK2 from those lacking a mutation, even in the early stages of disease.     

星形细胞肿瘤ADC与细胞密度导航导引下的对照研究

目的:分析脑肿瘤的ADC及细胞密度,评价肿瘤组织ADC值与细胞密度的相关性及ADC值在评价肿瘤良恶性中的价值.材料和方法:10例脑肿瘤病例术前行DWI及导航序列扫描,在导航手术中切除肿瘤时,同时在导航仪图像上标记相应肿瘤组织的部位,标本送病理检查.采用NIH Image软件分析肿瘤组织细胞密度.在导航标记图的指导下测量相应部位的ADC值及T2信号强度,比较ADC值,T2信号强度与细胞密度的相关性及其在评价肿瘤良、恶性中的作用.结果:10例脑肿瘤中毛细胞型星形细胞瘤1例,星形细胞瘤3例,间变性星形细胞瘤1例,胶质母细胞瘤5例.ADC值与肿瘤细胞密度呈明显负相关,r=0.74,P＜0.001,T2信号强度与细胞密度仅有轻度相关,r=0.33,P＜0.05.WHO1～2级肿瘤的ADC值1.30±0.16×10-3mm2/s,T2信号强度1374±336;3～4级肿瘤ADC值0.90±0.16×10-3mm2/s,T2信号强度1110±171,良、恶性肿瘤各种参数之间两组比较均有显著性差异(P＜0.01).结论:ADC是评价星形细胞肿瘤细胞密度的一个有效手段.ADC值低的部位可能是肿瘤细胞密度高的部位,也就可能是恶性程度最高的部位,对于立体定向选择活检部位非常有效.良、恶性星形细胞肿瘤ADC值有明显差异,结合常规MRI,ADC值可用于推测脑肿瘤的良、恶性.     

Cerebrotendinous xanthomatosis: the spectrum of imaging findings and the correlation with neuropathologic findings

PURPOSE: To describe imaging findings and their neuropathologic correlate in patients with cerebrotendinous xanthomatosis (CTX). MATERIALS AND METHODS: Computed tomographic (CT) and magnetic resonance (MR) images in 24 patients with symptoms (mean age at time of imaging, 37 years; mean disease duration, 18 years) were reviewed for site and frequency of brain, spinal cord, and Achilles tendon involvement. Two patients died, and imaging findings were compared with postmortem neuropathologic findings. RESULTS: Apart from nonspecific supratentorial atrophy and deep white matter changes, more typical hyperintense lesions were seen on T2-weighted images in the dentate nucleus (in 79% of patients), globus pallidus, substantia nigra, and inferior olive and extended into adjacent white matter as disease progressed. In these locations, lipid crystal clefts and perivascular macrophages, neuronal loss, demyelination, fibrosis, and reactive astrocytosis were found at microscopic examination. Hypointensity was sometimes found on T2-weighted images in the dentate nucleus and was related to deposition of hemosiderin and calcifications. CT depicted fewer lesions; all had low attenuation, except for the calcifications. Spinal cord MR imaging revealed increased signal intensity in the lateral and dorsal columns on T2-weighted images. Achilles tendon xanthomas displayed intermediate signal intensity on T1- and T2-weighted images. CONCLUSION: The typical pattern of MR imaging findings reflects the classic histopathologic findings and should prompt the diagnosis of CTX.     

Wallerian degeneration after cerebral infarction: evaluation with sequential MR imaging

The dynamic signal intensity changes at magnetic resonance (MR) imaging in active and chronic wallerian degeneration in the corticospinal tract were evaluated. Forty-three patients with wallerian degeneration seen on MR images after cerebral infarction were studied. When possible, patients with acute stroke were examined with MR imaging prospectively at the onset of symptoms and then at weekly intervals for several months. Focal infarction without distal axonal degeneration is demonstrated for the 1st month following onset of clinical symptoms. At 4 weeks, a well-defined band of hypointense signal appears on T2-weighted images in the topographic distribution of the corticospinal tract. After 10-14 weeks, the signal becomes permanently hyperintense. Over several years, accompanying ipsilateral brain stem shrinkage occurs. The dark signal intensity observed on T2-weighted images between 4 and 14 weeks is believed to result primarily from transitory increased lipid-protein ratio.     

Comparison of diffusion- and T2-weighted MRI for the early detection of cerebral ischemia and reperfusion in rats

The sensitivity of diffusion-weighted MRI was compared to that of T2-weighted MRI following temporary middle cerebral artery occlusion (MCA-O) for 33 min followed by 4 h of reperfusion in rats. Diffusion-weighted spin-echo images using strong gradients (b value of 1413 s/mm2) demonstrated a significant increase in signal intensity in ischemic regions as early as 14 min after onset of ischemia in comparison to the normal, contralateral hemisphere (p less than 0.05). This hyperintensity returned to baseline levels during reperfusion. T2-weighted images showed no evidence of brain injury during the temporary occlusion. In three rats subjected to permanent MCA-O, diffusion-weighted MRI demonstrated an increased signal intensity on the first image following occlusion and continued to increase during the 4-h observation period. T2-weighted images failed to demonstrate significant injury until approximately 2 h after MCA-O. Signal intensity ratios of ischemic to normal tissues were greater in the diffusion-weighted images than in the T2-weighted MR images at all time points (p less than 0.05). Close anatomical correlation was found between the early and sustained increase in diffusion-weighted MRI signal intensity and localization of infarcts seen on post-mortem histopathology.     

Experimental cerebral fat embolism: embolic effects of triolein and oleic acid depicted by MR imaging and electron microscopy

BACKGROUND AND PURPOSE: In fat embolism, free fatty acid is more toxic than neutral fat in terms of tissue damage. We evaluated the hyperacute embolic effects of triolein and oleic acid in cat brains by using MR imaging and electron microscopy. METHODS: T2-weighted imaging, diffusion-weighted imaging, and contrast-enhanced T1-weighted imaging were performed in cat brains after the injection of triolein (group 1, n = 8) or oleic acid (group 2, n = 10) into the internal carotid artery. MR images were quantitatively assessed by comparing the signal intensity ratios of the lesions with their counterparts on T2-weighted images, apparent diffusion coefficient (ADC) maps, and contrast-enhanced T1-weighted images. Electron microscopic findings in group 1 were compared with those in group 2. RESULTS: Qualitatively, MR images revealed two types of lesions. Type 1 lesions were hyperintense on diffusion-weighted images and hypointense on ADC maps. Type 2 lesions were isointense or mildly hyperintense on diffusion-weighted images and isointense on ADC maps. Quantitatively, the signal intensity ratios of type 1 lesions in group 2 specimens were significantly higher on T2-weighted images (P =.013)/(P =.027) and lower on ADC maps compared with those of group 1. Electron microscopy of type 1 lesions in both groups revealed more prominent widening of the perivascular space and swelling of the neural cells in group 2, in contrast to notable endothelial defects in group 1. CONCLUSION: MR and electron microscopic data on cerebral fat embolism induced by either triolein or oleic acid revealed characteristics suggestive of both vasogenic and cytotoxic edema in the hyperacute stage. Tissue damage appeared more severe in the oleic acid group than in the triolein group.     

Apparent diffusion coefficient measurements in progressive supranuclear palsy

We measured the apparent diffusion coefficient (ADC), using diffusion-weighted imaging (DWI) and signal intensity on T2-weighted MRI in the cerebral white matter of patients with progressive supranuclear palsy (PSP) and age-matched normal subjects. In PSP, ADC in the prefrontal and precentral white matter was significantly higher than in controls. There was no significant difference in signal intensity on T2-weighted images. The ADC did correlate with signal intensity. The distribution of the elevation of ADC may be the consequence of underlying pathological changes, such as neurofibrillary tangles or glial fibrillary tangles in the cortex. Our findings suggest that ADC measurement might be useful for demonstrating subtle neuropathological changes. Received: 27 September 1999/Accepted: 7 January 2000     

Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia.

BACKGROUND AND PURPOSE: Early detection of arterial occlusion and perfusion abnormality is necessary for effective therapy of hyperacute cerebral ischemia. We attempted to assess the utility of the fast fluid-attenuated inversion recovery (fast-FLAIR) sequence in detecting occluded arteries as high signal (referred to as intraarterial signal) and to establish the role of fast-FLAIR in detecting ischemic penumbra of hyperacute stroke within 24 hours after ictus. METHODS: We studied 60 patients with hyperacute cerebral ischemia caused by occlusion of intracranial major arteries. We compared intraarterial signal on FLAIR images with time of flight (TOF) on MR angiograms, flow voids on T2-weighted images, hyperintense lesions on diffusion-weighted images, and results of follow-up CT or MR scans. RESULTS: In 58 (96.7%) patients, FLAIR detected intraarterial signals as early as 35 minutes after stroke onset. In 48 (80.0%) patients, intraarterial signal on FLAIR images coincided with lack of TOF on MR angiograms. In 41 (74.5%) of 55 patients, the intraarterial signals of fast T2-weighted imaging depicted occlusion better than did deficient flow void on T2-weighted images. In 25 (41.7%) of 60 patients, the area of intraarterial signal distribution was larger than the hyperintense lesion measured on diffusion-weighted images. Areas of final infarction had sizes between those of intraarterial signal distribution on FLAIR images and lesions measured on diffusion-weighted images. In 35 (87.5%) of 40 patients, areas of intraarterial signal distribution were equal to regions of abnormal perfusion. CONCLUSION: Intraarterial signal on FLAIR images is an early sign of occlusion of major arteries. FLAIR combined with diffusion-weighted imaging can be helpful to predict an area at risk for infarction (ischemic penumbra). FLAIR plays an important role for determining whether a patient should undergo perfusion study.     

Asymmetrical FDG-PET and MRI findings of striatonigral system in multiple system atrophy with hemiparkinsonism.

The asymmetry of the local cerebral metabolic rate for glucose (lCMRglc) and magnetic resonance (MR) imaging was studied in five patients with multiple system atrophy (MSA) presenting hemiparkinsonism. lCMRglc was measured with 18F-2-fluoro-2-deoxy-D-glucose and positron emission tomography (PET) in these patients and five normal control subjects. MR images were obtained in five patients and 11 control subjects. In all patients, T2-weighted MR images showed hypointense areas in the posterior lateral putamen. They were bigger or lower in intensity on the contralateral side than on the ipsilateral side. Significant glucose hypometabolism was found in the posterior putamen on the contralateral side to hemiparkinsonism. A significant decrease in size was found in the contralateral putamen, caudate nucleus, and pars compacta of the substantia nigra. However, no significant correlation was seen between PET and MRI data. In the control subjects, no apparent asymmetry was observed. PET and MR imaging demonstrated the characteristic asymmetry corresponding to the pathological findings reported in MSA.     

Spontaneous intracerebral hematoma on diffusion-weighted images: influence of T2-shine-through and T2-blackout effects

BACKGROUND AND PURPOSE: On diffusion-weighted (DW) images, primary hematomas are initially mainly hyperintense, and then hypointense during the first few days after stroke onset. As in other brain disorders, variations in the T2 relaxation time of the hematoma influence the DW imaging signal intensity. Our aim was to evaluate the contribution of the T2 signal intensity and apparent diffusion coefficient (ADC) changes to signal intensity displayed by DW imaging through the course of hematoma. METHODS: The MR images of 33 patients with primary intracranial hemorrhage were retrospectively reviewed. Variations in T2-weighted echo planar images, DW imaging signal intensity, and apparent diffusion coefficient (ADC) ratios (core of hematoma/contralateral hemisphere) were analyzed according to the putative stages of hematoma, as seen on T1- and T2-weighted images. RESULTS: On both T2-weighted echo planar and DW images, the core of the hematomas was hyperintense at the hyperacute (oxyhemoglobin, n = 11) and late subacute stages (extracellular methemoglobin, n = 4), while being hypointense at the acute (deoxyhemoglobin, n = 11) and early subacute stages (extracellular methemoglobin, n = 7). There was a positive correlation between the signal intensity ratio on T2-weighted echo planar and DW images (r = 0.93, P < .05). ADC ratios were significantly decreased in the whole population and in each of the first three stages of hematoma, without any correlation between DW imaging findings and ADC changes (r = 0.09, P = .6). CONCLUSION: Our results confirm that the core of hematomas is hyperintense on DW images with decreased ADC values at the earliest time point, and may thus mimic arterial stroke on DW images. T2 shine-through and T2 blackout effects contribute to the DW imaging findings of hyperintense and hypointense hematomas, respectively, while ADC values are moderately but consistently decreased during the first three stages of hematoma.