Cerebral ischemia: evaluation with contrast-enhanced MR imaging

Eighty patients with a total of 82 ischemic lesions were examined with contrast-enhanced MR imaging 1 hr to 1 month after onset of symptoms. The studies were reviewed retrospectively to determine the presence of arterial enhancement and the patterns of parenchymal enhancement. Arterial enhancement was often detected on the initial MR examination (45%), was frequently demonstrated in cortical infarction (86%), in some cases preceded the development of signal changes on T2-weighted images, and resolved by 11 days. The presence of arterial enhancement appeared to be a better indicator of clinical severity than was the presence of proximal vessel occlusion on MR or angiographic studies. Two patterns of parenchymal enhancement were seen: progressive enhancement and early and/or intense enhancement. In patients with the progressive pattern, parenchymal enhancement on postcontrast T1-weighted images was rarely seen before 7 days, while signal abnormalities on T2-weighted images were intense during the first few days. The early and/or intense enhancement pattern was usually present within the first 3 days, approximated or exceeded the area and intensity of signal changes on T2-weighted images, and was usually associated with minimal or reversible neurologic sequelae (except when located in or near a watershed zone), suggesting a lesser degree of ischemic insult than was associated with the progressive pattern.(ABSTRACT TRUNCATED AT 250 WORDS)     

MR imaging enhancement patterns as predictors of hemorrhagic transformation in acute ischemic stroke

BACKGROUND AND PURPOSE: Early parenchymal gadolinium enhancement on T1-weighted MR images is predictive of hemorrhagic transformation (HT) in rodent focal ischemia models, but its value in humans is unknown. We sought to investigate gadolinium enhancement in acute ischemic stroke patients to determine their association with subsequent HT. METHODS: We retrospectively examined 22 patients with ischemic stroke who underwent MR imaging within 4.9 hours (+/-1.4) of symptom onset. Patients receiving intravenous tissue plasminogen activator (tPA) (n = 6) were included. Twenty-one patients underwent repeat MR studies at 48 hours, 13 underwent additional MR imaging at 1 week, and one underwent follow-up head CT at 24 hours. Initial images were analyzed for enhancement patterns (vascular, meningeal, parenchymal). Follow-up T2- and T2*-weighted images were evaluated for hemorrhage. RESULTS: In all patients, initial MR images showed vascular enhancement in the vascular territory of the stroke lesion: 19 with vascular enhancement alone and three with vascular and parenchymal enhancement. All three patients with both enhancement patterns had HT: two large and symptomatic, and one asymptomatic (petechial hemorrhage). They received tPA before MR imaging. None of the patients without early parenchymal enhancement developed symptomatic hemorrhage. Six (32%) patients with vascular enhancement alone had petechial hemorrhage at follow-up imaging. In this limited sample, initial mean volumes on diffusion-weighted images, National Institute of Health Stroke Scale scores, and intervals from stroke onset to imaging did not differ between patients with vascular and parenchymal enhancement versus those with vascular enhancement alone. CONCLUSION: Early parenchymal enhancement of stroke lesions may be a good predictor of subsequent symptomatic HT may help identify patients at risk, especially after thrombolytic therapy.     

Evolution of MR contrast enhancement patterns during the first week after acute ischemic stroke

BACKGROUND AND PURPOSE: Intravascular and parenchymal enhancement have been detected with contrast-enhanced T1-weighted MR imaging in patients with ischemic stroke. Diffusion-weighted MR imaging depicts infarct within minutes after the onset of symptoms. The aims of this study were to study the different MR enhancement findings during the first week after stroke and to ascertain whether the presence of intravascular enhancement over a larger area than the infarct on diffusion-weighted images on day 1 is able to predict substantial infarct growth during the first week. METHODS: Forty-eight patients were imaged on the first and second days and again 1 week after the onset of ischemic stroke. T1-weighted spin-echo imaging was performed before and after a 0.2 mmol/kg bolus of gadolinium chelate. Diffusion-weighted imaging was performed at the same slice positions. Enhancement findings were categorized as intravascular and parenchymal, with further categorization of parenchymal enhancement as cortical, subcortical, and deep; these findings were then compared with diffusion-weighted imaging findings. RESULTS: Intravascular enhancement in the infarcted area was detected on day 1 in 78% of the cases, on day 2 in 78% of the cases, and at 1 week in 30% of the cases. Parenchymal enhancement was detected in 26%, 56%, and 100% of the cases, respectively. Intravascular enhancement over a larger area than the infarct on diffusion-weighted images on day 1 was not associated with the extent of infarct growth. CONCLUSION: Detection of different patterns of contrast enhancement can help in determining the age of infarct. Parenchymal enhancement may be intense and can cause diagnostic uncertainty in cases in which the clinical history is obscure.     

Relationship between vascular enhancement, cerebral hemodynamics, and MR angiography in cases of acute stroke

BACKGROUND AND PURPOSE: The use of MR angiography and contrast-enhanced T1-weighted MR imaging in cases of acute cerebral ischemia may be helpful in the evaluation of middle cerebral artery (MCA) occlusion and leptomeningeal collaterals, respectively. The aim of our work was to investigate the relationship between MCA occlusion, T1-weighted vascular contrast enhancement, hemodynamic alterations, and tissue damage in cases of acute ischemic stroke. METHODS: We studied the MCA territory in 15 patients with acute ischemic stroke within 8 hr of symptom onset. The first MR imaging study (<8 hr after onset) comprised diffusion-weighted imaging, MR angiography, perfusion-weighted imaging, and contrast-enhanced T1-weighted MR imaging sequences. Follow-up MR imaging, performed 1 week later, consisted of MR angiography and T2-weighted fluid-attenuated inversion recovery MR imaging. RESULTS: Early MR angiography showed MCA stem occlusion in nine of 15 patients. Patients with MCA occlusion had significantly larger areas of abnormality on early diffusion-weighted images, significantly larger areas of altered hemodynamics, larger final lesion volumes, and poorer clinical outcome. Among the nine patients with MCA stem occlusion, vascular enhancement was marked in seven and absent in two who had complete MCA infarcts and poor clinical outcome. Among patients with MCA patency, vascular enhancement was marked in only one, mild in four, and absent in one. Patients with marked vascular enhancement had significantly larger regions of altered hemodynamics and significantly higher asymmetries in both regional cerebral blood volume and mean transit time because of increased values in the affected hemisphere. CONCLUSION: Among patients with stroke with MCA occlusion, marked vascular enhancement and increased blood volume indicate efficient leptomeningeal collaterals and compensatory hemodynamic mechanisms.     

Vascular occlusion sites determine differences in lesion growth from early apparent diffusion coefficient lesion to final infarct

BACKGROUND AND PURPOSE: Occlusion of major cerebral arteries is the primary source of tissue damage in ischemic stroke and the target of thrombolytic therapy. We hypothesized that large infarcts in more proximal vascular occlusions correspond with substantially increased ischemic lesions shown on initial apparent diffusion coefficient (ADC) maps. METHODS: Initial ADC lesions in 120 patients with acute ischemic stroke were analyzed within 6 hours of stroke onset. Patients were categorized on the basis of vascular occlusion, as shown on MR angiography. Lesion volumes were determined by using manual delineation (ADC(man)) and a threshold method for ADC values (<550 x 10(-9) mm(2)/s(-1), ADC(<550)). Infarct volumes were analyzed by using T2-weighted (n = 109) or CT (n = 11) images obtained on days 5-8. RESULTS: Median lesion volumes for ADC(<550), ADC(man), and infarcts, respectively, were as follows: proximal internal carotid artery (ICA)/middle cerebral artery (MCA) occlusions, 10, 23, and 32 cm(3); carotid-T occlusions, 11, 37, and 138 cm(3); MCA trunk occlusions, 11, 27, and 44 cm(3)); and MCA branch occlusions 8, 27, and 21 cm(3). Initial ADC lesion volumes were different only between the carotid T and the MCA branch (P < .05). On days 5-8, infarct volumes decreased from proximal to distal sites (P < .05), with the exception of MCA trunk versus proximal ICA/MCA occlusions. Recanalization rate in carotid-T occlusion was significantly lower than those of all other occlusion types. CONCLUSION: Initial ADC lesions can be small, even in patients with proximal vascular occlusions. These patients develop considerably large infarctions, suggesting a high potential for infarct growth. This growth might be averted with improved early recanalization of proximal vascular occlusions.     

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.     

Acute cerebral ischemia: evaluation with dynamic contrast-enhanced MR imaging and MR angiography.

Dynamic contrast-enhanced T2-weighted magnetic resonance (MR) imaging and MR angiography (MRA) were used to evaluate cerebral blood volume and the intracranial arterial system in 34 patients within 48 hours after the onset of cerebral ischemia. In 24 of the patients, an abnormality identified on T2-weighted images corresponded to the acute clinical deficit. Intracranial MRA demonstrated occlusions or severe stenoses of major vessels supplying the area of infarction in 16 of these patients, and decreased blood volume correlated well with MRA abnormalities. Infarcts less than 2 cm in diameter were not reliably shown with MRA or blood volume studies. Correlation between lesions seen with MRA and decreased blood volume in acute infarcts was good, and both techniques demonstrated lesions early in the clinical course. By providing information about hemodynamics not available with conventional T1- or T2-weighted images, MRA and dynamic MR imaging could prove helpful in describing the pathophysiologic characteristics of stroke and in guiding early therapeutic intervention.     

MR imaging of spinal cord and vertebral body infarction.

PURPOSE: To study the usefulness of MR in the evaluation of spinal cord infarctions and associated findings. MATERIALS AND METHODS: MR examinations of 12 patients (10 men and two women) were reviewed retrospectively. Onset of symptoms of spinal cord ischemia was abrupt in all patients; MR was performed 8 hr to 4 months after onset. Contrast-enhanced MR was performed in four of the patients. RESULTS: Abnormal MR findings of the spinal cord included abnormal cord signal (11 of 12), best demonstrated on T2-weighted images, and morphologic changes (cord enlargement during the acute phase in nine patients and cord atrophy during the chronic phase in two), best demonstrated on T1-weighted images. Vascular abnormalities (aortic) were detected by MR in four of the 12 patients. Three of these four patients also had abnormal bone marrow signal, predominantly in the anterior half (one) or in multiple areas near the endplate and/or deep medullary portion of the vertebral body involving several vertebrae (two). T1-weighted images were not sensitive in detecting signal changes in either the bone marrow (two of three) or spinal cord (nine of 12). Enhanced MR imaging was performed in four patients (two in the acute phase and two in the chronic phase) and showed diffuse enhancement of the spinal cord proximal to a relatively unenhancing distal conus in one of the two patients imaged during the acute phase. No abnormal enhancement was noted in the other three patients. CONCLUSION: MR is a useful means of detecting spinal cord infarction and associated vascular and bony changes. The patterns of bone marrow abnormalities reflect the underlying pathophysiology of the blood supply to the spinal cord and bone. The associated vascular and bone marrow abnormalities serve as additional information for the diagnosis of spinal cord infarction.     

MR and CT of lacunar infarcts

Twenty-two patients with clinical signs and symptoms compatible with lacunar transient ischemic attack or stroke of varying chronicity were evaluated with MR imaging. CT was also performed in 21 of these patients. MR revealed small, deep cerebral lesions in locations appropriate to the clinical symptoms in 19 patients. Lacunar infarcts were imaged by CT in 11 patients; however, no lesions were identified on CT that were not detected with MR. Presumed lacunar infarcts were identified on MR images in 17 additional patients. Lacunae generally appeared as focal areas of decreased signal intensity on T1-weighted images and as focal areas of increased signal intensity on T2-weighted images. T2-weighted MR images detected a greater number of lacunar infarcts than did mixed T1-/T2-weighted images, which in turn detected more lacunae than did T1-weighted images. In general, acute lacunar infarcts (within 1 week of onset or recurrence of clinical symptoms) were seen only on T2-weighted images, while chronic lesions (more than 1 week) were seen on both T1- and T2-weighted images. Our results indicate that MR is superior to CT for evaluating lacunar infarcts, and second, that T2-weighted images are more sensitive than T1- and mixed T1-/T2-weighted images for detecting lacunar infarcts.     

MR imaging of pontine infarction within 2 weeks after ictus

Magnetic resonance (MR) images of 10 patients with pontine infarction were reviewed. A total of 17 examinations were performed on a 1.5 Tesla high-field scanner (GE) within two weeks after ictus. The infarcted area was detected by MR as early as 20 hours after stroke in one case. However, MR images obtained in two cases three and nine hours after onset were unremarkable. It is therefore suggested that follow-up study should be performed when initial MR images within 20 hours postictus are normal. T1-weighted images at four, nine and twelve days after ictus were interpreted as normal. In two of these three examinations, the infarcted areas were clearly demonstrated as hyperintense lesions on T2-weighted images. In the other examination, however, an area of mildly increased signal intensity was seen on T2-weighted images. This case suggests that the fogging effect is also observed on MR imaging and that a small pontine infarction may be overlooked during the subacute stage. Basilar artery occlusion was detected as an absence-of-flow void in three of the ten patients. In conclusion, MR imaging proved to be a relatively useful diagnostic modality for evaluating acute and subacute pontine infarctions.     

Rapidly enhancing hepatic hemangiomas at MRI: Distinction from malignancies with T2-weighted images

The purpose of this study is to describe a subset of atypical hepatic hemangiomas that enhance rapidly and diffusely and to determine whether heavily T2-weighted images could distinguish between atypically enhancing liver hemangiomas and hypervascular malignancies. A retrospective search of MR records identified seven patients with liver hemangiomas that demonstrated diffuse early enhancement and 23 patients with biopsy-proven malignant liver lesions that were hypervascular on dynamic gadolinium-enhanced MR images. Quantitative analysis of signal intensity measurements was performed on the T2-weighted images, heavily T2-weighted (TE < 140), and dynamic gadolinium-enhanced images. Blinded reader comparison of the T2-weighted images and gadolinium-enhanced images was performed. Hypervascular hemangiomas enhanced to a greater degree than hypervascular malignant liver lesions on the early phase gadolinium-enhanced images. Perilesional parenchymal enhancement was demonstrated in five cases of rapidly enhancing hemangiomas. Signal intensity and contrast-to-noise ratios on the heavily T2-weighted images of the hemangiomas were significantly greater than that of the hypervascular malignant lesions (P < .05). Hemangiomas were differentiated from the hypervascular malignant liver lesions with high accuracy (97–100%) by three blinded readers based on the T2-weighted images. A subset of hemangiomas have atypical rapid diffuse enhancement on dynamic gadolinium-enhanced images. These atypical hemangiomas can be distinguished from hypervascular malignant liver lesions on T2-weighted MR images.     

Secondary parenchymal and vascular changes after middle cerebral artery stroke in children

Introduction

Ischemic brain lesions might present with unexpected increased signal intensity at MR angiography within the ischemic lesion and secondary parenchymal changes in regions distal to the ischemia itself. We retrospectively investigated the rate and time course of vascular and parenchymal changes in children with isolated middle cerebral artery (MCA) stroke.

Methods

Twelve children (mean age at stroke onset 4.8 years, range 0.8–15 years, six females, seven right MCA strokes) suffering from a first ever acute isolated MCA stroke had repeated MR scans (mean scan number, 3.5; range 2–6; mean follow-up, 11 months; range 0.5–24 months).

Results

Ipsilaterally to MCA stroke, we recorded increased vessel signal at MR angiography during first to fourth day in 4/7 children (all had MCA recanalization), corticospinal tract cytotoxic-like edema during second day to second month in 7/11 (three children with globus pallidum ischemia had concomitant substantia nigra changes during second to third week), corticospinal tract T2 abnormalities from fifth day onwards in 9/12, focal thalamic cytotoxic-like edema during fifth day to first month in 5/8, focal thalamic T2 hyperintensity during sixth day to third week in 2/4, and faint T2 hypointensity from second month in 7/10 children.

Conclusion

Vascular and secondary parenchymal changes, likely due to luxury perfusion, Wallerian, retrograde, or trans-synaptic degeneration, are common in pediatric MCA stroke population. They might mimic new ischemic lesions or suggest conditions different from stroke leading to diagnostic pitfalls and inappropriate treatment.     

Dynamic T1-weighted spin-echo MR imaging: the role of digital subtraction in the demonstration of enhancing brain lesions

We compared subtracted and non-subtracted images obtained from a contrast-enhanced dynamic T1-weighted spin echo (SE) magnetic resonance (MR) technique for the demonstration of enhancing brain lesions with and without associated hemorrhage. Thirty-four patients with enhancing brain lesions or subacute parenchymal hematomas were imaged using a contrast-enhanced dynamic T1-weighted SE MR technique modified by a keyhole scheme. On-line digital subtraction was performed. Non-subtracted and subtracted dynamic scans were compared for conspicuity and contrast-to-noise ratios (CNRs) of enhancing brain lesions. The presence and pattern of enhancement in the subacute parenchymal hematomas were evaluated on the subtracted images. In all, 47 enhancing brain lesions were detected on both the non-subtracted and the subtracted images. The enhancing brain lesions were more conspicuous on the subtracted images (P < 0.05). There was an increase in CNRs of the enhancing lesions on the subtracted images compared with the non-subtracted ones (P < 0.001). Seventeen subacute parenchymal hematomas were detected on the non-subtracted images. The subtracted images demonstrated enhancement in 15 hematomas (8 rim enhancement only/7 both nodular and rim enhancement). Digital subtraction in contrast-enhanced dynamic T1-weighted SE MR imaging is helpful in demonstrating enhancing brain lesions with and without associated hemorrhage.     

Biliary hamartomas: solitary and multiple lesions shown on current MR techniques including gadolinium enhancement.

The purpose of this study was to describe the magnetic resonance (MR) imaging features of biliary hamartomas on T1- and T2-weighted and gadolinium-enhanced sequences, and to correlate these findings with histopathology. MR imaging findings in four patients with pathologically proved biliary hamartomas are described. In all patients, MR imaging sequences, including T1- and T2-weighted and early and late gadolinium-enhanced images, were retrospectively evaluated for the size, morphology, signal intensity, and enhancement pattern of the lesions. Correlation was made between the MR imaging findings and histopathology. Biliary hamartomas ranged in diameter from 0.5 to 1.5 cm. Lesions were solitary in one patient and numerous in three patients. In all patients, the lesions were low signal on T1-weighted images and high signal and well-defined on T2-weighted images and demonstrated thin rim enhancement on early post-gadolinium images that persisted on late post-gadolinium images. No appreciable central enhancement of the lesions was observed. At histopathology, the lesions were composed of cystic spaces and fibrous stroma. Lesions showed compressed liver parenchyma surrounding the lesions (three cases) and inflammatory cell infiltrate (one case), which correlated with the rim enhancement on the gadolinium-enhanced MR images. Most of the biliary hamartomas in our small series were less than 1 cm in diameter and of high signal intensity on T2-weighted images, and had a thin rim of enhancement on early and late post-gadolinium images. The imaging features were explainable by the underlying histopathology. In patients with known malignancy, caution should be exercised not to misinterpret these lesions as metastases due to the presence of thin rim enhancement. J. Magn. Reson Imaging 1999;10:196-201, 1999.     

Wernicke encephalopathy: MR findings and clinical presentation

Wernicke encephalopathy (WE) is a severe neurological disorder caused by vitamin B1 deficiency. The aim of the study was to analyse MRI findings typical for this disease and to evaluate the significance of their correlations with clinical symptoms. Magnetic resonance images and clinical features of 12 patients with WE were analysed. The patients underwent MR imaging within 3–14 days after onset of clinical symptoms. In 7 of 12 patients MR imaging showed symmetrical diencephalic and midbrain lesions. Postcontrast T1-weighted images from 5 of 9 patients examined during the initial 6 days of acute WE showed a subtle enhancement of the mamillary bodies, the tectal plate, the periaqueductal area and the periventricular region of the third ventricle including the paramedian thalamic nuclei. In addition, T2-weighted and fluid-attenuated inversion recovery (FLAIR) images revealed hyperintense signals in these regions (except for 2 patients where the mamillary bodies were normal). Hyperintense lesions on T2-weighted images without any enhancement on postcontrast T1-weighted images were detected in 2 patients by MR imaging performed 11 or 14 days after onset of WE. Patients with hyperintensities on T2-weighted images of the periventricular region of the third ventricle and the paramedian thalamic nuclei had poor recovery from their mental dysfunction. The MR examination in case of WE shows a typical pattern of lesions in 58% of cases. Enhancement of the mamillary bodies, the periventricular region of the third ventricle including the paramedian thalamic nuclei, and the periaqueductal area on postcontrast T1-weighted images can be observed in the initial period after clinical onset of symptoms and are characteristic signs of the acute stage of WE. Hyperintense lesions in the periventricular region and the paramedian thalamic nuclei on T2-weighted and FLAIR images in the subacute stage of WE and enhancement on postcontrast T1-weighted images of the mamillary bodies and the paramedian thalamic nuclei are indicators of poor prognosis despite vitamin B1 substitution. Electronic Publication     

Various patterns of perfusion-weighted MR imaging and MR angiographic findings in hyperacute ischemic stroke.

BACKGROUND AND PURPOSE: Various clinical subtypes of patients presenting with sudden-onset ischemic stroke have been recognized, but classification of those types is not simple. We identified various patterns of perfusion-weighted MR imaging and MR angiographic findings in hyperacute ischemic stroke with relation to clinical outcomes. METHODS: Twelve patients with symptoms of acute ischemic stroke due to middle cerebral artery occlusion underwent perfusion-weighted MR imaging and MR angiography within 6 hours after the onset of symptoms. Perfusion-weighted imaging was performed with a conventional dynamic contrast-enhanced T2*-weighted sequence, and cerebral blood volume (CBV) maps were then created. CBV maps and MR angiographic findings were compared with 99mTc-HMPAO brain SPECT scans, short-term outcomes, and follow-up imaging findings. RESULTS: The combined CBV and MR angiographic findings were classified into three patterns: arterial occlusion and decreased CBV (n = 8), arterial occlusion and increased CBV (n = 2), and no arterial occlusion and normal CBV (n = 2). These three patterns were strongly related to SPECT findings, short-term outcomes, and follow-up imaging findings. Perfusion on SPECT decreased markedly in the affected regions in all patients with the first pattern, decreased slightly in the second pattern, and was normal in the third pattern. Symptoms were not significantly changed at 24 hours after onset in any of the patients with the first pattern, but resolved completely in all patients with the latter two patterns. Follow-up imaging showed large infarctions in all patients with the first pattern. Initially, no infarction was seen in the second pattern, but watershed infarction developed later in one of these patients. CONCLUSION: Hyperacute ischemic stroke may be differentiated into three imaging patterns with different clinical outcomes. The combined use of perfusion-weighted MR imaging and MR angiography may play a substantial role in guiding the choice of treatment of this disease.     

Diffusion-weighted imaging of patients with subacute cerebral ischemia: comparison with conventional and contrast-enhanced MR imaging

BACKGROUND AND PURPOSE: The importance of diffusion-weighted imaging (DWI) for delineating acute ischemic lesions has been investigated extensively; however, few studies have investigated the role of DWI in the subacute stage of stroke. Because these lesions tend to appear bright throughout the first days of ischemia, owing to restricted diffusion, we speculated that DWI could also improve the detection of subacute infarcts as compared with conventional and contrast-enhanced MR imaging. METHODS: Interleaved echo-planar DWI with phase navigation was performed on a 1.5-T MR unit in a consecutive series of 53 patients (mean age, 66 +/- 14 years) with suspected recent cerebral ischemia. The interval between onset of clinical symptoms and MR imaging ranged from 1 to 14 days (mean, 6 +/- 4 days). Contrast material was given to 28 patients in a dose of 0.1 mmol/kg. RESULTS: DWI clearly delineated recent ischemic damage in 39 patients (74%) as compared with 33 (62%) in whom lesions were identified or suspected on conventional T2-weighted images. DWI provided information not accessible with T2-weighted imaging in 17 patients when evidence of lesion multiplicity or detection of clinically unrelated recent lesions was included for comparison. Subacute ischemic lesions were also seen more frequently on DWI sequences than on contrast-enhanced images (20 versus 13 patients). DWI was more likely to make a diagnostic contribution in the first week of stroke and in patients with small lesions or preexisting ischemic cerebral damage than was conventional MR imaging. CONCLUSION: Recent ischemic damage is better shown on DWI sequences than on conventional and contrast-enhanced MR images throughout the first days after stroke and may provide further information about the origin of clinical symptoms. Adding DWI to imaging protocols for patients with subacute cerebral ischemia is recommended.     

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.     

Detection of acute avascular necrosis of the femoral head in dogs: dynamic contrast-enhanced MR imaging vs spin-echo and STIR sequences.

OBJECTIVE. Spin-echo MR imaging has been shown to be highly sensitive in the detection of avascular necrosis. Very early avascular necrosis can, however, appear normal on MR images. We compared dynamic contrast-enhanced MR imaging with conventional spin-echo and short Tl inversion-recovery (STIR) sequences for detecting acute osteonecrosis in an animal model. MATERIALS AND METHODS. Avascular necrosis was induced unilaterally in the femoral heads of five dogs that were imaged with a 1.5-T system within 3 hr of devascularization. After standard T1-weighted, T2-weighted, and STIR images, gradient-recalled echo images, 28/5 (TR/TE) with a 45 degrees flip angle, were obtained at 6-sec intervals for 90 sec synchronous with the IV administration of 0.2 mmol of gadoteridol per kilogram of body weight at a rate of 2 ml/sec via an automated injector. Two animals were reimaged after 7 days. RESULTS. Spin-echo and STIR images did not show any acute changes in the ischemic femoral heads. In contrast, significant differences were present in the enhancement profiles of the marrow spaces in the normal and ischemic femoral heads (p = .005). Normal marrow was characterized by rapid enhancement, with an average signal intensity increase of 83% peaking at 36 sec; no measurable enhancement was seen in the marrow of the ischemic femoral head. Spin-echo images, obtained 7 days after devascularization (n = 2), showed changes characteristic of avascular necrosis. Dynamic contrast-enhanced MR images showed persistent lack of enhancement in the avascular marrow of the ischemic femoral head. A junctional zone, characterized by rapid contrast enhancement in excess of 120% without early washout, was identified at the interface between normal and avascular marrow. CONCLUSION. In this experimental model, dynamic contrast-enhanced MR imaging proved significantly more sensitive than conventional spin-echo and STIR imaging in the detection of acute avascular necrosis.     

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.