Late evaluation of silent cerebral ischemia detected by diffusion-weighted MR imaging after filter-protected carotid artery stenting

BACKGROUND AND PURPOSE: Postoperative diffusion-weighted MR imaging (DWI) often discloses new lesions after carotid artery stent placement (CAS), most of them asymptomatic. Our aim was to investigate the fate of these silent ischemic lesions.MATERIALS AND METHODS: We prospectively studied 110 patients undergoing protected transfemoral CAS, 98 of whom underwent DWI before and after the intervention. Patients in whom DWI disclosed silent postoperative lesions also had delayed MR imaging. Preoperative, postoperative, and delayed scans were compared.RESULTS: Of the 92 patients without postoperative symptoms, DWI disclosed 33 new silent ischemic lesions in 14 patients (15.2%), 13 of whom (30 lesions) underwent delayed MR imaging after a mean follow-up of 6.2 months. In 8 of these 13 patients (61%), MR imaging disclosed 12 persistent lesions (12/30, 40%). The reversibility rate depended significantly on the location (cortical versus subcortical) and size (0–5 versus 5–10 mm) of the lesions (P < .05 by χ² test).CONCLUSIONS: Because many silent ischemic lesions seen on postoperative DWI after CAS reverse within months, the extent of permanent CAS-related cerebral damage may be overestimated.

Carotid artery stent placement (CAS) is today considered in many centers a valid alternative to carotid surgery for treating carotid artery stenosis because it achieves stroke and death rates matching those after surgery.^1,2Despite widespread use of cerebral protection systems in patients undergoing endovascular carotid interventions,^3,4 diffusion-weighted MR imaging (DWI) of the brain, currently the most effective tool for diagnosing acute cerebral ischemia,^5,6 detects a high incidence of asymptomatic ischemic lesions after CAS, ranging from 21% to 54% for unprotected procedures^7,8 and from 21% to 40% for protected procedures.^9–13 Few studies have described the late outcome of early postoperative DWI lesions.^14–16 Whether these silent ischemic lesions cause permanent brain damage with cognitive impairment or merely transient ischemia without sequelae remains unclear.In this prospective study, to investigate the extent of permanent cerebral ischemic damage in patients undergoing protected CAS, we used postoperative DWI and delayed MR imaging to assess the outcome (patient and lesion reversibility rates) of asymptomatic ischemic lesions after CAS and studied factors potentially influencing reversibility.     

Optimal diffusion-weighted imaging protocol for lesion detection in transient global amnesia

BACKGROUND AND PURPOSE: Diffusion-weighted imaging (DWI) can depict small punctate hyperintense lesions in the hippocampus in transient global amnesia (TGA). The purpose of this study was to find an optimal DWI protocol for lesion detection in TGA by investigating various imaging parameters and imaging timing after symptom onset.MATERIALS AND METHODS: Sixteen patients with TGA diagnosed during 14 months underwent DWI within 24 hours and again at follow-up 3 days after onset. Each DWI session included 4 different sequences using different b-values (seconds per square millimeter) and section thicknesses (millimeter): 1000/5, 1000/3, 2000/3, and 3000/3. The presence or absence of hyperintense lesions on the 8 DWIs was determined visually, and the number of lesions detected was compared.RESULTS: Thirteen of the 16 patients (81%) had either single or multiple punctate hyperintense lesions, totaling 24 lesions, and the remaining 3 patients had no lesions. All lesions detected were in the hippocampus except 1. The number of lesions detected on initial DWIs at a b-value/section thickness of 1000/5, 1000/3, 2000/3, and 3000/3 was 3, 9, 13, and 13, respectively, whereas that of follow-up DWIs was 17, 22, 24, and 24, respectively.CONCLUSION: On the basis of these preliminary results, the highest lesion detection was achieved for DWI with b = 2000/3 mm or b = 3000/3 mm at 3 days postonset. When no lesion is detected by DWI within 24 hours after onset, follow-up DWI is recommended several days later.

Transient global amnesia (TGA) is clinically defined as sudden onset anterograde amnesia with preserved alertness, attention, and personal identity, which occurs during a period of no more than 24 hours with no long-term sequelae.^1–3 The incidence of TGA has been reported to be 5–11 per 100,000 persons per annum.^2,4,5 The etiology and pathogenesis of TGA are uncertain, though several different causes are suggested, such as ischemia, migraine, epileptic seizure, venous congestion, and psychological disturbances.⁶Recent diffusion-weighted imaging (DWI) studies have indicated the presence of focal hyperintensities involving the hippocampus in TGA.^7–11 The lesions detected by DWI are small and punctate (1–3 mm) and located within the lateral portion of the hippocampus.^9,11,12 Since Strupp et al¹³ first detected hyperintense lesions in the hippocampus in TGA by using DWI, the frequency of lesions detected on DWI has been reported in a range of 0%–84%.^9,10,14,15 According to a recent study, this discrepancy in detection rates appears to be attributable to the different timing of imaging from the onset of symptoms.⁹ In this previous study, a detection rate of only 6% by DWI was achieved within several hours of symptom onset, but this increased up to 84% at 48 hours post-symptom onset.DWI parameters, such as b-value and section thickness, might also importantly influence the detection rate of the lesions. In particular, b-values higher than 1000 s/mm² might increase the ability of DWI to detect subtle diffusion restrictions caused by small lesions. Moreover, section thicknesses of <5 mm may also increase the detection rate of small punctate lesions by decreasing partial volume averaging effects. However, optimal DWI parameters for lesion detection have not been studied previously. The purpose of the present study was to find an optimal DWI protocol for lesion detection by investigating b-values, section thickness, and imaging timing after symptom onset.     

Predictors and timing of hypotension and bradycardia after carotid artery stenting

BACKGROUND AND PURPOSE: Hypotension and bradycardia are common in carotid artery stenting (CAS) and are particularly worrisome in the high risk patient who is typically referred for CAS. The purpose of this work was to assess the incidence and predictors of hypotension and bradycardia and the risk of their delayed occurrence after CAS.MATERIALS AND METHODS: A total of 53 men and 40 women (median age, 71 years) with symptomatic (57%) or asymptomatic (42%) carotid artery stenosis had CAS performed in our institution between December 2002 and January 2007. Patient vital sign records for the 12 hours post-CAS were analyzed. The relative decrease of blood pressure and pulse rate were used as primary end points, and the requirement of pressor or anticholinergic drugs was used as a surrogate end point. Significant predictors of hypotension and bradycardia were analyzed with a logistic regression model. Cumulative freedom from hypotension and bradycardia was calculated by using the Kaplan-Meier method. Negative predictive value (NPV) of screening for early hypotension and bradycardia was determined.RESULTS: The incidence of hypotension, bradycardia, and both was 14%, 23%, and 15%, respectively. Drug intervention was required in 45 patients (48%). Asymptomatic stenosis was an independent predictor of hypotension and bradycardia. Stenosis proximity to the bifurcation and dilation percentage were independent predictors of the drug intervention requirement. Seven patients (8%) had new onset of hypotension or bradycardia later than 6 hours post-CAS. The NPV of early hypotension and bradycardia was 97% and 93%, respectively.CONCLUSION: In this retrospective study, the risk of hypotension or bradycardia after CAS is significantly influenced by the degree of dilation performed, and the risk of their delayed occurrence may justify a minimum of 12 hours postprocedural vital sign monitoring.

Hypotension and bradycardia can occur during or after carotid artery stent placement (CAS) due to the stretching of the carotid sinus baroreceptors by the balloon and the stent. The role of this phenomenon as a predictor of adverse outcomes is still debated.^1-5 Because CAS represents a valuable alternative to carotid endarterectomy (CEA) among the high-risk patient population,⁶ patients with severe carotid artery stenosis also having cardiac or cerebrovascular comorbidities are increasingly referred for CAS. Those patients may be more vulnerable to hypotension or bradycardia. In fact, patients with coronary disease undergoing cardiac or noncardiac surgery are at higher risk of myocardial infarction (MI) if prolonged hypotension occurs during the procedure.^7-10 It has also been suggested that hypotension associated with CAS increases the risk of cerebrovascular events in impairing the distal washout of residual emboli not intercepted by the protection device.^2,11The concern about the potential harmfulness of hypotension and bradycardia during or after CAS has enhanced the scientific interest about its risk factors. So far, the reported predictors vary from one study to another.^1-3,12-18 The study end points, as well as the time point and the duration of the vital sign (VS) monitoring, are also highly variable. Absolute blood pressure (BP) and pulse rate (PR) values^{2,3,13,14,16-18} or absolute decrease in their initial values^1,3,16 are used in most reports, and a standardized follow-up time for VS monitoring is rarely defined.^3,14,18This study aimed to assess the predictors of hypotension and bradycardia occurring in the 12 hours after CAS by using the relative decrease of BP and PR as primary end points and the requirement of pressor or anticholinergic drugs as a surrogate end point. Because the current discussion about the safety of performing CAS in an outpatient setting has also increased the concern about the risk of hypotension and bradycardia after CAS, a secondary objective of the study was to evaluate the risk of their delayed appearance and the negative predictive value (NPV) of early (0–6 hours post-CAS) screening.     

Role of apparent diffusion coefficient values in differentiation between malignant and benign solitary thyroid nodules

BACKGROUND AND PURPOSE: Accurate imaging characterization of a solitary thyroid nodule has been clearly problematic. The purpose of this study was to evaluate the role of the apparent diffusion coefficient (ADC) values in the differentiation between malignant and benign solitary thyroid nodules.MATERIALS AND METHODS: A prospective study was conducted in 67 consecutive patients with solitary thyroid nodules who underwent diffusion MR imaging of the thyroid gland. Diffusion-weighted MR images were acquired with b factors of 0, 250, and 500 s/mm² by using single-shot echo-planar imaging. ADC maps were reconstructed. The ADC values of the solitary thyroid nodules were calculated and correlated with the results of histopathologic examination. Statistical analysis was performed.RESULTS: The mean ADC value of malignant solitary thyroid nodules was 0.73 ± 0.19 × 10⁻³ mm²/s and of benign nodules was 1.8 ± 0.27 × 10⁻³ mm²/s. The mean ADC values of malignant nodules were significantly lower than those of benign ones (P = .0001). There were no significant differences between the mean ADC values of various malignant thyroid nodules, but there were significant differences between the subtypes of benign thyroid nodules (P = .0001). An ADC value of 0.98 × 10⁻³ mm²/s was proved as a cutoff value differentiating between benign and malignant nodules, with 97.5%, 91.7%, and 98.9% sensitivity, specificity, and accuracy, respectively.CONCLUSION: The ADC value is a new promising noninvasive imaging approach used for differentiating malignant from benign solitary thyroid nodules.

Nodular thyroid is commonly detected on palpation in 4%–7% of the population,^1,2 on sonographic examination in 10%–40%, and by pathologic examination at autopsy in 50%.^3,4 In contrast, compared with the high prevalence of nodular thyroid disease, thyroid cancer is rare. The challenge of imaging thyroid nodules is to reassure most patients who have benign disease and to diagnose the minority of patients who will prove to have a malignancy.^5,6Ultrasonography has been used in the assessment of the thyroid nodules as a primary imaging technique.^2,7,8 Currently, there is no single sonographic criterion that can reliably distinguish benign from malignant thyroid nodules.^4,9 The results of predicting thyroid cancer with color Doppler sonography are controversial, with some reporting that Doppler sonography is helpful and others reporting that it did not improve diagnostic accuracy.^4,5,10,11 The hazards of radiation exposure are unavoidable in nuclear scintigraphy,² and not all functioning nodules on scintigraphy are benign.^6,9 The risk of cancer in a cold nodule is 4 times more common than in a hot nodule.^3,6 Fine-needle aspiration biopsy (FNAB) with cytologic evaluation is commonly used, but it is inconclusive in 15%–20% of patients, in addition to the possible, but less likely, associated hemorrhage.^2,4 The incidence of cancer in patients with thyroid nodules selected for FNAB is approximately 9.2%–13%.⁵ FNAB is considered an effective method for differentiating between benign and malignant thyroid nodules.^4,7,12–14Routine T1- and T2-weighted MR imaging has a limited role in the evaluation of thyroid nodules. It cannot distinguish benign from malignant nodules or assess the functional status of thyroid nodules.^12–15 Diffusion-weighted MR imaging has been used to characterize head and neck tumors, in which there are significant differences in the apparent diffusion coefficient (ADC) values of malignant tumors and benign lesions.^16–19 Tezuka et al,²⁰ in their study using diffusion-weighted MR imaging to assess the thyroid function, reported that the ADC values of patients with Grave''s disease exceeded those of patients with subacute thyroiditis, with a sensitivity and specificity of 75% and 80%, respectively, in differentiating between both disease entities. They concluded that diffusion-weighted MR imaging could be clinically important in evaluating the thyroid function. To our knowledge, there have been no articles about diffusion-weighted MR imaging evaluating thyroid nodules.The aim of our study was to evaluate the role of ADC values in differentiating between malignant and benign solitary thyroid nodules.     

Association between cerebral microbleeds on T2*-weighted MR images and recurrent hemorrhagic stroke in patients treated with warfarin following ischemic stroke

BACKGROUND AND PURPOSE: Although accumulating evidence suggests the presence of microbleeds as a risk factor for intracerebral hemorrhage (ICH), little is known about its significance in anticoagulated patients. The aim of this study was to determine whether the presence of microbleeds is associated with recurrent hemorrhagic stroke in patients who had received warfarin following atrial fibrillation–associated cardioembolic infarction.MATERIALS AND METHODS: A total of 87 consecutive patients with acute recurrent stroke, including 15 patients with ICH and 72 patients with cerebral infarction, were enrolled in this study. International normalized ratios (INRs), vascular risk factors, and imaging characteristics, including microbleeds on T2*-weighted MR images and white matter hyperintensity (WMH) on T2-weighted MR images, were compared in the 2 groups.RESULTS: Microbleeds were noted more frequently in patients with ICH than in patients with cerebral infarction (86.7% versus 38.9%, P = .0007). The number of microbleeds was larger in patients with ICH than in patients with cerebral infarction (mean, 8.4 versus 2.1; P = .0001). INR was higher in patients with ICH than in patients with cerebral infarction (mean, 2.2 versus 1.4; P < .0001). The frequency of hypertension was higher in patients with ICH than in patients with cerebral infarction (86.7% versus 45.8%, P = .0039). Multivariate analysis revealed that the presence of cerebral microbleeds (odds ratio, 7.383; 95% confidence interval, 1.052–51.830) was associated with ICH independent of increased INR and hypertension.CONCLUSION: The presence of cerebral microbleeds may be an independent risk factor for warfarin-related ICH, but more study is needed because of strong confounding associations with elevated INR and hypertension.

One of the major complications of warfarin treatment following atrial fibrillation–related cardioembolic infarction is the occurrence of intracerebral hemorrhage (ICH). With advancing age, the incidence of both atrial fibrillation–related cardioembolic infarction and warfarin-related ICH increases.Cerebral microbleeds detected by gradient-echo T2*-weighted MR imaging, which are shown as signal-intensity loss, represent hemosiderin deposit^1,2 and are associated with occurrence of ICH.^3–19 Although accumulating evidence suggests that the presence of microbleeds is a risk factor for ICH in patients treated by antiplatelet therapy^13,20 and hemorrhagic complications of anticoagulation in patients with prior ICH and atrial fibrillation have been reported,²¹ little is known about the significance of microbleeds in anticoagulated patients because, to our knowledge, no studies have focused on the association between cerebral microbleeds and anticoagulation therapy in a large number of patients. On the other hand, previous studies focusing on radiographic characteristics have shown that the presence of microangiopathy (leukoaraiosis) detected by CT is a risk factor for warfarin-related ICH.²² However, considering the close association between cerebral microbleeds and leukoaraiosis (white matter hyperintensity [WMH]),^{7,8,11,14–16,19,23,24} one could hypothesize that cerebral microbleeds, which represent bleeding from small vessels, may be more closely associated with ICH than WMH is. Therefore, the present study was performed to determine whether the presence of microbleeds is associated with recurrent hemorrhagic stroke in patients who have received warfarin treatment following atrial fibrillation–associated cardioembolic infarction.     

MR imaging of familial Creutzfeldt-Jakob disease: a blinded and controlled study

BACKGROUND AND PURPOSE: The E200K mutation of the PRNP (prion protein) gene is the most common cause of familial Creutzfeldt-Jakob disease (fCJD), which has imaging and clinical features that are similar to the sporadic form. The purpose of this study was to conduct a controlled and blinded evaluation of the sensitivity and specificity of MR imaging in this unique population.MATERIALS AND METHODS: We compared the MR imaging characteristics of 15 early stage familial CJD patients (age, 60 ± 7 years) with a group of 22 healthy subjects from the same families (age, 61 ± 8 years). MR imaging included diffusion-weighted imaging (DWI), T2-weighted fast spin-echo imaging, and a fluid-attenuated inversion recovery (FLAIR) sequence. The scans were rated for abnormalities by an experienced neuroradiologist blind to diagnosis, group assignment, age, and sex.RESULTS: Thirteen of 15 fCJD subjects had abnormal MR imaging. FLAIR signal intensity abnormality in the caudate or putamen nuclei demonstrated a sensitivity of 87% and specificity of 91%. DWI abnormality in the caudate nucleus showed a sensitivity of 73% and a specificity of 100%. Abnormalities in the thalamus (6 patients), cingulate gyrus (6 patients), frontal lobes (4 patients), and occipital lobes (3 patients) were best detected with DWI. No signal intensity abnormalities were demonstrated in the cerebellum. T2-weighted and T1-weighted sequences were uninformative.CONCLUSIONS: FLAIR and DWI abnormalities in the caudate nucleus and putamen offer the best sensitivity and specificity for diagnosing fCJD. Our findings support recent recommendations that MR imaging should be added to the diagnostic evaluation of CJD.

Creutzfeldt-Jakob disease (CJD) is the most common human prion disease. It is a rare neurodegenerative disorder that is progressive and invariably fatal, with nearly 90% of patients dying within 1 year of diagnosis.¹ CJD occurs in approximately 1 person per 1 million people per year worldwide.¹ The most common form is sporadic CJD (sCJD), which occurs randomly without a known risk factor and accounts for 85%-90% of cases. Familial or hereditary CJD (fCJD), seen in 5%-10% of cases, is caused by mutations in the gene that controls formation of the normal prion protein on chromosome 20.¹ The most common pathogenic mutation is the E200K mutation. The risk of fCJD is transmitted in an autosomal dominant inheritance pattern, with nearly 100% penetrance.²The imaging findings in sCJD typically consist of cortical atrophy and hyperintensities in the basal ganglia, thalamus, and cortex on fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted imaging (DWI).^3–13 fCJD has imaging findings and neuropathology that are, in general, similar to the most common forms of sCJD; however, most imaging studies on fCJD consist primarily of case reports or studies focused on sCJD that combine a few fCJD patients into a single CJD patient sample.^8,14–22 fCJD studies are limited not only by small sample sizes but also by nonstandardized imaging protocols and clinical and pathophysiologic heterogeneity. The complex interactions with disease duration and cognitive and neurologic severity have also made it difficult to interpret studies, especially because the sample sizes are small.²³To address the difficulties of clinical research in this area, we initiated a study of fCJD occurring among Libyan Jews living in Israel that is caused by familial transmission of the E200K mutation.^24–26 In a preliminary report, it was demonstrated that 4 patients with fCJD due to the E200K mutation had gray matter atrophy and decreased apparent diffusion coefficient (ADC) in the basal ganglia. Signal intensity hyperintensities were seen in the basal ganglia and thalamus with FLAIR and DWI.²⁷ The sample size in that study was insufficient to calculate sensitivity and specificity. Here we describe a rigorously blinded and controlled evaluation of MR imaging findings in a larger number of fCJD patients.     

In vivo differentiation of aerobic brain abscesses and necrotic glioblastomas multiforme using proton MR spectroscopic imaging

BACKGROUND AND PURPOSE: Abscesses caused by aerobic bacteria (aerobic abscesses) can simulate intracranial glioblastomas multiforme (GBMs) in MR imaging appearance and single voxel (SV) proton MR spectroscopy of the central cavity. The purpose of our study was to determine whether MR spectroscopic imaging (SI) can be used to differentiate aerobic abscesses from GBMs. Our hypothesis was that metabolite levels of choline (Cho) are decreased in the ring-enhancing portion of abscesses compared with GBMs.MATERIALS AND METHODS: Fifteen patients with aerobic abscesses were studied on a 1.5T MR scanner using an SV method and an SI method. Proton MR spectra of 15 GBMs with similar conventional MR imaging appearances were used for comparison. The resonance peaks in the cavity, including lactate, cytosolic amino acids, acetate, succinate, and lipids, were analyzed by both SV MR spectroscopy and MRSI. In the contrast-enhancing rim of each lesion, peak areas of N-acetylaspartate (NAA), choline (Cho), lipid and lactate (LL), and creatine (Cr) were measured by MRSI. The peak areas of NAA-n, Cho-n, and Cr-n in the corresponding contralateral normal-appearing (-n) brain were also measured. Maximum Cho/Cr, Cho/NAA, LL/Cr-n, and Cho/Cho-n and minimum Cr/Cr-n and NAA/NAA-n ratios in abscesses and GBMs were compared using the Wilcoxon rank sum test. After receiver operating characteristic curve analysis, diagnostic accuracy was compared.RESULTS: Cytosolic amino acid peaks were found in the cavity in 7 of 15 patients with aerobic abscesses. Means and SDs of maximum Cho/Cr, Cho/NAA, LL/Cr-n, and Cho/Cho-n and minimum Cr/Cr-n and NAA/NAA-n ratios were 3.38 ± 1.09, 3.88 ± 2.13, 2.72 ± 1.45, 1.98 ± 0.53, 0.53 ± 0.16, and 0.44 ± 0.09, respectively, in the GBMs, and 1.77 ± 0.49, 1.48 ± 0.51, 2.11 ± 0.67, 0.81 ± 0.21, 0.48 ± 0.2, and 0.5 ± 0.15, respectively, in the abscesses. Significant differences were found in the maximum Cho/Cr (P = .001), Cho/NAA (P = .006), and Cho/Cho-n ratios (P < .001) between abscesses and GBMs. Diagnostic accuracy was higher by Cho/Cho-n ratio than Cho/Cr and Cho/NAA ratios (93.3% versus 86.7% and 76.7%).CONCLUSION: Metabolite ratios and maximum Cho/Cho-n, Cho/Cr, and Cho/NAA ratios of the contrast-enhancing rim were significantly different and useful in differentiating aerobic abscesses from GBMs by MRSI.

Brain abscess can be a lethal condition if appropriate treatment is delayed. Thus, early diagnosis of brain abscess is desired and is a challenge for clinicians and radiologists. Radiologically, a brain abscess in the capsule stage appears in CT and in MR imaging as an expansile, rim-enhancing mass surrounded by edema, which is similar in appearance to necrotic malignant tumors, especially glioblastoma multiforme (GBM).^1,2 Clinically, both brain abscesses and GBMs may cause nonspecific headaches in the absence of fever, focal neurologic deficits, epileptic seizures, and disturbances in higher-level cortical function. In addition, laboratory examination often shows normal white blood cell count.^1,2 Further reduction of mortality from brain abscesses requires more rapid, accurate, and safe diagnostic techniques. Application of diffusion-weighted imaging (DWI) in distinguishing between pyogenic brain abscesses and cystic or necrotic brain tumors has been reported to be useful in many publications.^3–8 The cystic or necrotic portion of tumors almost always has a low signal intensity on DWI and a higher apparent diffusion coefficient (ADC) value; however, some exceptions have been reported for necrotic brain tumors.^7–12 Hyperintensity with restricted diffusion is diagnostic, but not pathognomonic, for pyogenic abscess on DWI. However, exceptions of DWI studies and substantial variability in the ADCs have been reported for pyogenic abscesses.^8,12–16Single-voxel proton MR spectroscopy of the central cystic portion has been reported to allow the broad group of pyogenic abscesses to be distinguished from malignant gliomas.^17–22 Acetate, succinate, and amino acids have been identified in cerebral abscesses in humans and were used as bacterial marker metabolites for noninvasive diagnosis by MR spectroscopy.^17–22 Abscesses caused by anaerobic bacteria have been distinguished from those caused by aerobic bacteria based on metabolites detectable with MR spectroscopy (acetate and succinate).^21–23 However, spectral patterns recorded for the cystic or necrotic components of GBMs and abscesses caused by aerobic bacteria (aerobic abscesses) were similar by single-voxel MR spectroscopy.^18,21,24 Diagnosis based on such subjectively selected metabolites or metabolite ratios was not possible.²⁴At pathologic examination, the enhancing rim of GBMs represents infiltrating tumor cells,^25,26 and an increased Cho/Cr ratio was observed. Pathologically, the enhancing rim of a pyogenic abscess represents an inflammatory infiltrate composed of neutrophils and, later, macrophages and lymphocytes. Granulation tissue surrounds the area of inflammation and eventually develops into a fibrous capsule. This capsule, in turn, is surrounded by gliotic, edematous brain tissue. In the experimental setting, brain abscesses have been shown to have relatively high amounts of mature collagen and decreased neovascularity.^27,28 The Cho/Cr ratio of rim-enhancing lesion of abscesses would be presumed to be less than that of GBMs.Recent developments in MR spectroscopy have made it possible to obtain spectroscopic MR imaging with high spatial resolution and multiple spectra simultaneously from contiguous voxels.^29,30 To date, proton MR spectroscopic imaging has not been used to differentiate aerobic abscesses from GBMs. We aimed to test the feasibility of MR spectroscopic imaging to distinguish between aerobic abscesses and GBMs by the evaluation of the contrast-enhancing rim of the lesions. Our hypothesis was that metabolite levels of Cho are decreased in the rim-enhancing portion of aerobic abscesses relative to the Cho seen in the rim-enhancing portion of necrotic GBMs.     

Nontraumatic skull base defects with spontaneous CSF rhinorrhea and arachnoid herniation: imaging findings and correlation with endoscopic sinus surgery in 27 patients

BACKGROUND AND PURPOSE: Defects at the skull base leading to spontaneous CSF rhinorrhea are rare lesions. The purpose of our study was to correlate CT and MR findings regarding the location and content of CSF leaks in 27 patients with endoscopic sinus surgery observations.MATERIALS AND METHODS: Imaging studies in 27 patients with intermittent CSF rhinorrhea (CT in every patient including 10 examinations with intrathecal contrast, plain CT in 2 patients, and MR in 15 patients) were analyzed and were retrospectively blinded to intraoperative findings.RESULTS: CT depicted a small endoscopy-confirmed osseous defect in 3 different locations: 1) within the ethmoid in 15 instances (53.6% of defects) most commonly at the level of the anterior ethmoid artery (8/15); 2) adjacent to the inferolateral recess of the sphenoid sinus in 7 patients including one patient with bilateral lesions (8/28 defects, 28.6%); 3) within the midline sphenoid sinus in 5 of 28 instances (17.9%). Lateral sphenoid defects (3.5 ± 0.80 mm) were larger than those in ethmoid (2.7 ± 0.77 mm, P ≤ 0.029) or midsphenoid location (2.4 ± 0.65 mm, P ≤ 0.026). With endoscopy proven arachnoid herniation in 24 instances as reference, MR was correct in 14 of 15 instances (93.3%), CT cisternography in 5 of 8 instances (62.5%). Plain CT in 1 patient was negative.CONCLUSION: In patients with a history of spontaneous CSF rhinorrhea, CT was required to detect osseous defects at specific sites of predilection. MR enabled differentiating the contents of herniated tissue and allowed identification of arachnoid tissue as a previously hardly recognized imaging finding.

The term “spontaneous” CSF rhinorrhea has been applied to describe nasal discharge of CSF unrelated to trauma, surgery, malformation, tumor, or previous radiation therapy.^1–4 Spontaneous CSF rhinorrhea is uncommon. Estimates of the spontaneous cause among all causes of CSF rhinorrhea are subject to variation ranging from only 6%,⁵ 11.4%,⁶ 14%,³ 21%,⁷ to 23%.⁸ Periodic release of CSF from the nose was first described by Galen in 200 B.C. and was considered a physiologic phenomenon until Thomson, in 1899, assembled 21 patients in a monograph reporting spontaneous CSF rhinorrhea as a pathologic clinical entity.^9,10Spontaneous CSF rhinorrhea has been recognized as a distinct entity with respect to clinical presentation,^2,11,12 treatment,^13–15 and propensity for recurrence.^8,16,17 As early as 1968, Ommaya et al⁹ postulated the existence of “high-pressure leaks” related to intracranial tumors and of “normal pressure leaks” occasionally associated with empty sella. The role of empty sella as an indicator of raised intracranial pressure as well was supported by the observation of elevated CSF pressure in individual patients¹¹ and in a series of 10 patients who underwent lumbar puncture after sealing of the defect.¹⁸ In addition to the presence of an empty sella as a radiologic sign,¹⁹ a common clinical constellation in patients with spontaneous CSF rhinorrhea is female sex, middle age, and obesity.^{8,14,15,18–22}Spontaneous CSF leaks have been postulated to represent a manifestation of benign intracranial hypertension²² or pseudotumor cerebri.²³ Pulsatile-increased hydrostatic pressure is capable of bone erosion during the course of many years.^2,24 To become effective as a CSF leak, bone erosion and creation of an osteodural defect is required to occur at pneumatized parts of the skull base leading to communication of the subarachnoid space with the sinonasal spaces or temporal bone cavity. Related to CSF rhinorrhea, a review of the literature up to 1972¹⁰ identified the cribriform plate, craniopharyngeal canal, sella, and spheno-occipital synchondrosis as possible sites of predilection. Arachnoid granulations in proximity to the ethmoid and sphenoid sinus have been implicated as precursors of osteodural leaks.² Accordingly, arachnoid granulations causing erosion of the temporal bone may present with CSF otorrhea.^2,25,26Among the imaging techniques used to localize the site of the fistula, radionuclide isotope cisternography and CT cisternography were of limited sensitivity in 66% of patients only.³ When active leaks were present, CT cisternography provided positive results in 85% of patients.²⁷ However, in cases of inactive fistulas, CT cisternography failed to recognize the site of leakage in 27.7%²⁸ and in 19% of patients.²⁹ Advances in CT and MR imaging techniques have improved sensitivity, which amounted to 88.25%³⁰ and 93%³¹ for high-resolution CT and for MR cisternography to 89%,^6,31 93.6%,²⁸ and 100%^32,33 even in patients with inactive leaks. Therefore, high-resolution CT, MR cisternography, or a combination of both techniques have replaced the previously used invasive procedures.A confounding nomenclature exists regarding the contents of osteodural defects such as meningocele,^10,14 meningoencephalocele,⁴ encephalocele,^11,34 meningeal or arachnoid hernia,^24,35 arachnoid diverticulum,³⁶ or arachnoid cyst.³⁷ These differing designations reflect variable contents of herniation and occasional inaccuracy because of the limited ability to visualize the lesions by imaging^24,29 and during transcranial surgery.^1,10 Knowledge of the contents of herniation may modify the grafting technique and therefore facilitates preoperative planning.¹⁶ The endoscopic skull base approach has rendered direct visualization of the defect and its contents feasible.^38–40 Therefore, endoscopy was chosen as a standard of reference in this study. CT and MR findings in this series of patients with spontaneous CSF rhinorrhea were particularly assessed regarding the contents of herniation and location and correlated with endoscopy. Predisposing factors (arachnoid granulation, empty sella) and the size of the osseous defect were assessed on CT images.     

Isolated cortical signal increase on MR imaging as a frequent lesion pattern in sporadic Creutzfeldt-Jakob disease

BACKGROUND AND PURPOSE: Hyperintense basal ganglia on MR imaging support the diagnosis of sporadic Creutzfeldt-Jakob disease (CJD). Our aim was to study the frequency of patients with sporadic CJD presenting with and without characteristic basal ganglia lesions on MR imaging and to examine the corresponding patient characteristics.MATERIALS AND METHODS: Fluid-attenuated inversion recovery (FLAIR) and diffusion-weighted images (DWI) of 55 patients with CJD were assessed for signal-intensity increase (FLAIR) or restricted diffusion (DWI) in 7 cortex regions and the basal ganglia, thalamus, and cerebellum. Patient characteristics as well as electroencephalography, CSF, and codon 129 genotype of the prion protein gene (PRNP) were correlated with the most frequent MR imaging lesion patterns.RESULTS: Two major lesion patterns were identified by DWI: cortex and basal ganglia involvement (two thirds) and isolated cortex involvement (one third). In the latter patient group, the cortex involvement was widespread (at least 3 regions affected in 89% on DWI) and usually included the frontal and parietal lobes (78%). The length of the disease course was significantly prolonged (median, 12 versus 5 months). No significant differences were observed concerning electroencephalography and CSF findings and codon 129 genotype distributions. Of 4 patients with normal MR imaging findings, the CSF was positive for the 14-3-3 protein in 3.CONCLUSION: A high number of patients with CJD present without basal ganglia lesions on MR imaging. Isolated cortex involvement on DWI and FLAIR should lead to suggestion of CJD, even if the disease course is only slowly progressive. Additional 14-3-3 protein analysis in the CSF may support the CJD diagnosis.

Sporadic Creutzfeldt-Jakob disease (CJD) is a rare and fatal disease caused by the accumulation of abnormal/pathologic prion protein (PrP^Sc; Sc indicates scrapie) in the human brain. The classic disease type is characterized by rapidly progressive dementia, ataxia, abnormal muscle tone, and myoclonus. It leads to a state of akinetic mutism and death after a median disease duration of 6 months.¹ The definite CJD diagnosis relies on the finding of PrP^Sc in the brain tissue, together with astrocytic gliosis, nerve cell loss, and spongiform degeneration as the typical neuropathologic changes.^2,3During one''s lifetime, MR imaging hyperintensity of the basal ganglia on T2-weighted (T2WI), fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) is increasingly used to support the CJD diagnosis, next to positive CSF (14-3-3 protein) and electroencephalography (EEG) findings of periodic sharp-wave complexes (PSWCs). Although the origin of the signal-intensity changes is still not fully understood, hyperintensity on T2WI and FLAIR has been thought to be caused by gliosis, whereas abnormalities on DWI are most likely derived from spongiform changes.^4–6 DWI was shown to be the most sensitive sequence in the detection of brain lesions, particularly in the neocortex.^7–10 Isolated cortex involvement was also found.^9,11Although abnormal MR imaging findings in CJD have been studied in detail with respect to their location, few attempts have been made to define the most frequently occurring patterns of hyperintensity in a spectrum of patients. Six disease phenotypes (MM1, MM2, MV1, MV2, VV1, and VV2) defined by the codon 129 genotype (MM, MV, VV) of the prion protein gene (PRNP) and pathologic isotype of the PrP^Sc type 1 or 2 have been recently described with distinctive neuropathologic features and various clinical and diagnostic findings.^1–3,12 On MR imaging, predominant cortical (VV1)¹³ or subcortical involvement (MV2 and VV2)^14,15 or no abnormalities (MM2)^16,17 were found in smaller case series.To date, to our knowledge, the overall distribution of MR imaging abnormalities has not been studied in a larger spectrum of patients with CJD, and it is unclear whether there are clinical correlates corresponding to specific MR imaging lesion patterns. The proportion of patients presenting without basal ganglia abnormalities is unknown.We defined the most frequent MR imaging lesion patterns and corresponding clinical characteristics in a CJD patient collective by using highly sensitive MR images, and we considered a possible influence of the codon 129 genotype of the PRNP. We particularly focused on patients lacking basal ganglia abnormalities on MR imaging and suggested criteria that might support the early CJD diagnosis in these patients.     

Sixty-four-section CT cerebral perfusion evaluation in patients with carotid artery stenosis before and after stenting with a cerebral protection device

BACKGROUND AND PURPOSE: Brain tissue viability depends on cerebral blood flow (CBF) that has to be kept within a narrow range to avoid the risk of developing ischemia. The aim of the study was to evaluate by 64-section CT (VCT) the cerebral perfusion modifications in patients with severe carotid stenosis before and after undergoing carotid artery stent placement (CAS) with a cerebral protection system.MATERIALS AND METHODS: Fifteen patients with unilateral internal carotid stenosis (≥70%) underwent brain perfusional VCT (PVCT) 5 days before and 1 week after the stent-placement procedure. CBF and mean transit time (MTT) values were measured.RESULTS: Decreased CBF and increased MTT values were observed in the cerebral areas supplied by the stenotic artery as compared with the areas supplied by the contralateral patent artery (P < .001). A significant normalization of the perfusion parameters was observed after the stent-placement procedure (mean pretreatment MTT value, 5.3 ± 0.2; mean posttreatment MTT value, 4.3 ± 0.18, P < .001; mean pretreatment CBF value, 41.2 mL/s ± 2.1; mean posttreatment CBF value, 47.9 mL/s ± 2.9, P < .001).CONCLUSIONS: PVCT is a useful technique for the assessment of the hemodynamic modifications in patients with severe carotid stenosis. The quantitative evaluation of cerebral perfusion makes it a reliable tool for the follow-up of patients who undergo CAS.

Carotid artery stenosis, with its thromboembolic complications causing cerebral ischemia,^1,2 can be successfully treated by carotid endarterectomy (CEA), which significantly reduces the risk of stroke in both symptomatic and asymptomatic patients, as compared with medical therapy alone.^3,4 Alternatively, carotid artery stent placement (CAS) is increasingly used thanks to the development of safe and effective protection systems that help reduce the periprocedural neurologic complications.^5,6 Two recent registry studies (ARCHeR, Caress) have demonstrated that CEA and CAS are comparable in terms of periprocedural complications in symptomatic or asymptomatic patients not presenting comorbidities.^7,8 The overlapping percentage of complications between these 2 techniques at 30 days is 2%.Cerebral perfusion changes, such as an asymmetry in the hemisphere corresponding to the affected carotid artery, have been observed in patients with unilateral severe carotid stenosis, however without a direct correlation to the degree of stenosis.^9,10 A measure of perfusion disturbance as provided by cerebral blood flow (CBF) and mean transit time (MTT) appears to be helpful in evaluating brain with a risk of developing a stroke and eventually in guiding the therapeutic decisions especially in acute ischemic events.¹¹Positron-emission tomography (PET), single-photon emission CT (SPECT), xenon-enhanced CT (Xe-CT), perfusion CT (PCT), and MR imaging have all been applied in the study of brain hemodynamics. However, the scarce availability of PET and SPECT in most radiology departments or the difficulty in obtaining a quantitative measurement by MR imaging has drawn attention for >20 years toward Xe-CT,¹² whose demonstrated accurate measurement of perfusion¹³ has permitted the differentiation of patients with normal CBF¹⁴ from those with reversible neurologic deficits (CBF, 10–20 mL/100 g per minute) or those with infarction (CBF < 10 mL/100 g per minute).¹³ PCT, validated by comparison with Xe-CT^13,14 and widely available in most radiology departments, can be easily performed at the end of a CT scanning and has, therefore, further simplified the approach to brain perfusion evaluation,^15,16 adding further information about hemodynamic parameters such as MTT and cerebral blood volume. More recently, the perfusion study by 64-section CT (VCT), allowing the assessment of a brain volume ≤4 cm, has offered an improved tool of investigation.The aim of our study was to measure by brain perfusional VCT (PVCT) the hemodynamic parameters in the cerebral hemisphere supplied by the severely stenotic internal carotid artery (ICA), in a group of patients undergoing an endovascular treatment with a protection device. The hypothesis is that CBF and MTT values in the hemisphere on the side of the carotid stenosis will be abnormal before the procedure and will approach the values on the contralateral side after the procedure.     

Comparison of echo-planar diffusion-weighted imaging and delayed postcontrast T1-weighted MR imaging for the detection of residual cholesteatoma

BACKGROUND AND PURPOSE: Echo-planar diffusion-weighted imaging (DWI) and delayed postcontrast T1-weighted MR imaging (DPI) have been proposed in previous studies to detect residual middle ear cholesteatomas, with varying results. We assessed and compared these 2 techniques in patients with canal wall-up tympanoplasty.MATERIALS AND METHODS: This was a prospective cohort study. Patients who underwent surgery for middle ear cholesteatoma had CT scanning 9 months after the surgery. If opacity was observed (64%) on CT scans, DWI and DPI were performed before second-look surgery. CT, MR imaging, and surgical data were available for 31 patients. Charts were reviewed independently by 3 blinded examiners. Interobserver agreement for MR imaging was calculated (Cohen κ). Sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) were calculated for these techniques: 1) alone or in association, and 2) according to the residual cholesteatoma size measured during surgery.RESULTS: Interobserver agreement was better for DWI (κ = 0.81) than for DPI (κ = 0.51). Sensitivity, specificity, PPV, and NPV values were 60%, 72.73%, 80%, and 50%, respectively, with DWI; and 90%, 54.55%, 78.26%, and 75%, respectively, with DPI. With cholesteatomas >5 mm, the sensitivity and specificity of DWI reached 100% and 88%, respectively, with values for DPI reaching 100% and 80%, respectively. The association of both techniques only allowed improvements in the specificity for lesions >5 mm.CONCLUSIONS: Both techniques gave acceptable results for residual cholesteatoma detection. DWI is more specific but less sensitive than DPI. Their concurrent use may benefit patients by avoiding undue surgery.

Unlike recurrent cholesteatoma, developing from recurring retraction pockets or defects in the tympanic membrane reconstruction, residual cholesteatoma cannot be detected by a simple clinical examination. Several methods, such as eustachian tube endoscopy,^1-3 have been proposed to detect residual cholesteatomas. However, these techniques are not routinely performed and canal wall-up (CWU) tympanoplasties for middle ear cholesteatoma usually require second-look surgery to rule out the presence of residual cholesteatoma, observed in 6%–57% of patients in large series.^4,5 Any reliable noninvasive method of detecting residual cholesteatomas could allow the avoidance of second-look surgery in patients with no hearing loss after the first surgery.Imaging may prove useful in this respect. High-resolution CT displays a high negative predictive value (NPV)⁶ because of the lack of opacity in the middle ear cleft or because the mastoid cavity correlates well with the absence of a residual lesion. Nevertheless, CT does not allow a distinction between residual cholesteatoma and granulation or postoperative inflammatory or scar tissue.^3,7 However, MR imaging has been proposed to discriminate these tissues. T1- and T2-weighted sequences associated with diffusion-weighted imaging (DWI) or delayed postcontrast T1 sequences (DPI), though not early postcontrast T1 sequences, seem able to detect residual cholesteatoma among other types of tissue.^8-10 Results of sensitivity, specificity, positive predictive value (PPV), and NPV vary among previous studies.^8,11-15 One explanation for this discrepancy may be the different sizes of residual cholesteatomas studied in these series.In the present study, we aimed to compare echo-planar imaging (EPI) DWI and DPI for the detection of residual cholesteatoma after CWU surgery. Here we describe the results obtained by using both types of sequences in each patient, along with the size of the residual cholesteatoma as surgically verified in all patients.     

Primary cerebral lymphoma and glioblastoma multiforme: differences in diffusion characteristics evaluated with diffusion tensor imaging

BACKGROUND AND PURPOSE: Differentiating between primary cerebral lymphoma and glioblastoma multiforme (GBM) based on conventional MR imaging sequences may be impossible. Our hypothesis was that there are significant differences in fractional anisotropy (FA) and apparent diffusion coefficient (ADC) between lymphoma and GBM, which will allow for differentiation between them.MATERIALS AND METHODS: Preoperative diffusion tensor imaging (DTI) was performed in 10 patients with lymphoma and 10 patients with GBM. Regions of interest were placed in only solid-enhancing tumor areas and the contralateral normal-appearing white matter (NAWM) to measure the FA and ADC values. The differences in FA and ADC between lymphoma and GBM, as well as between solid-enhancing areas of each tumor type and contralateral NAWM, were analyzed statistically. Cutoff values of FA, FA ratio, ADC, and ADC ratio for distinguishing lymphomas from GBMs were determined by receiver operating characteristic curve analysis.RESULTS: FA and ADC values of lymphoma were significantly decreased compared with NAWM. Mean FA, FA ratio, ADC (×10⁻³ mm²/s), and ADC ratios were 0.140 ± 0.024, 0.25 ± 0.04, 0.630 ± 0.155, and 0.83 ± 0.14 for lymphoma, respectively, and 0.229 ± 0.069, 0.40 ± 0.12, 0.963 ± 0.119, and 1.26 ± 0.13 for GBM, respectively. All of the values were significantly different between lymphomas and GBM. Cutoff values to differentiate lymphomas from GBM were 0.192 for FA, 0.33 for FA ratio, 0.818 for ADC, and 1.06 for ADC ratio.CONCLUSIONS: The FA and ADC of primary cerebral lymphoma were significantly lower than those of GBM. DTI is able to differentiate lymphomas from GBM.

Primary cerebral lymphoma represents 4%–7% of primary brain tumors, and its incidence has increased in the last 3 decades.¹ Despite some characteristic conventional MR imaging findings, it may be difficult or even impossible to distinguish cerebral lymphomas from glioblastoma multiforme (GBM).² Accurate preoperative differentiation between these 2 tumors is important for the determination of appropriate treatment strategies.Lymphomas are relatively hyperintense to gray matter on trace diffusion-weighted images (DWIs) and isointense to hypointense on apparent diffusion coefficient (ADC) maps, findings consistent with restricted water diffusion.^3–5 In contrast, high-grade gliomas are relatively hyperintense to gray matter on both trace DWIs and ADC maps, findings consistent with elevated diffusivity.^3,6,7 Prior studies have shown statistically significant differences in ADC between the cerebral lymphoma and GBM.^4,5 However, the GBM with restricted water diffusion, that is, hyperintense on trace images and hypointense on ADC maps, has also been reported.^8–12 Therefore, discrimination of lymphoma from some GBMs may be difficult.Diffusion tensor imaging (DTI) provides a sensitive means to detect alterations in the integrity of white matter structures.^13,14 Fractional anisotropy (FA) is a quantitative index for diffusion anisotropy that correlates with microstructural integrity of myelinated fiber tracts.^15,16 FA decreases in a wide variety of intracranial pathologies including brain tumors.^17–20 Previous studies found significant FA differences in tumors with different histologic grades or cellularity.^20–23 FA was also reported to have a strong correlation with cellularity.²⁰ Because the cellularity of lymphoma is higher than that of GBM, we hypothesized that the diffusion characteristics of lymphoma and GBM are different on DTI and will allow us to differentiate between the two.     

Diagnostic accuracy of CT angiography with matched mask bone elimination for detection of intracranial aneurysms: comparison with digital subtraction angiography and 3D rotational angiography

BACKGROUND AND PURPOSE: Our aim was to determine the diagnostic accuracy of multisection CT angiography combined with matched mask bone elimination (CTA-MMBE) for detection of intracranial aneurysms compared with digital subtraction angiography (DSA) and 3D rotational angiography (3DRA).MATERIALS AND METHODS: Between January 2004 and February 2006, 108 patients who presented with clinically suspected subarachnoid hemorrhage underwent both CTA-MMBE and DSA for diagnosis of an intracranial aneurysm. Two neuroradiologists, independently, evaluated 27 predefined vessel locations in the CTA-MMBE images for the presence of an aneurysm. After consensus, diagnostic accuracy of CTA was calculated per predefined location and per patient. Interobserver agreement was calculated with κ statistics.RESULTS: In 88 patients (81%), 117 aneurysms (82 ruptured, 35 unruptured) were present on DSA. CTA-MMBE detected all ruptured aneurysms except 1. Overall specificity, sensitivity, positive predictive value, and negative predictive value of CTA-MMBE were 0.99, 0.90, 0.98, and 0.95 per patient and 0.91, 1.00, 0.97, and 0.99 per location, respectively. Sensitivity was 0.99 for aneurysms ≥3 mm and 0.38 for aneurysms <3 mm. Interobserver agreement for aneurysm detection was excellent (κ value of 0.92 per location and 0.80 per patient).CONCLUSION: CTA-MMBE is accurate in detecting intracranial aneurysms in any projection without overprojecting bone. CTA-MMBE has limited sensitivity in detecting very small aneurysms. Our data suggest that DSA and 3DRA can be limited to the vessel harboring the ruptured aneurysm before endovascular treatment, after detection of a ruptured aneurysm with CTA.

In current clinical practice, CT angiography (CTA) is the most frequently used noninvasive diagnostic tool for detection of intracranial aneurysms in the acute setting.^1–8 However, detection of intracranial aneurysms by CTA is limited because axial source section evaluation is tedious and 3D visualization is hampered by overprojecting bone, especially in the region of the skull base.^2,9–13 Several methods to remove bone, such as subtraction and manual or automated bone editing, have been developed.^7,8,14–19 Drawbacks of these methods are the complexity of use, dependence on the user, or high dose of radiation.Matched mask bone elimination (MMBE) is a relatively new technique to remove bone from CTA source images (CTA-MMBE) in an automatic and user-independent way with little additional radiation dose.^20–22 In CTA-MMBE, a second nonenhanced low-dose scan (about a quarter of the radiation dose of a regular CTA) is used to identify bony structures that can subsequently be masked in the CTA scan.Digital subtraction angiography (DSA) is the gold standard for detection of intracranial aneurysms. Extension of DSA with 3D rotational angiography (3DRA) can further improve detection of intracranial aneurysms that may be obscured by overprojecting vessels.^23–25 The advantages of DSA over CTA are superior spatial and contrast resolution, no interference of bony structures, and the possibility to perform direct endovascular interventions.^26,27 However, DSA is an invasive technique with a small but significant risk of neurologic complications, estimated to occur in 0.3%–1.8% of patients.^28,29The purpose of this study was to determine the diagnostic accuracy of CTA-MMBE for detection of intracranial aneurysms in a large patient population with clinically suspected subarachnoid hemorrhage (SAH) with DSA and 3DRA as reference standards.     

Assessment of craniospinal arteriovenous malformations at 3T with highly temporally and highly spatially resolved contrast-enhanced MR angiography

BACKGROUND AND PURPOSE: Patients with arteriovenous malformation (AVM) are known to have an elevated risk of complications with conventional catheter angiography (CCA) but nonetheless require monitoring of hemodynamics. Thus, we aimed to evaluate both anatomy and hemodynamics in patients with AVM noninvasively by using contrast-enhanced MR angiography (CE-MRA) at 3T and to compare the results with CCA.MATERIALS AND METHODS: Institutional review board approval and informed consent were obtained for this Health Insurance Portability and Accountability Act–compliant study. Twenty control subjects without vascular malformation (6 men, 18–70 years of age) and 10 patients with AVMs (6 men, 20–74 years of age) underwent supra-aortic time-resolved and high-spatial-resolution CE-MRA at 3T. Large-field-of-view coronal acquisitions extending from the root of the aorta to the cranial vertex were obtained for both MRA techniques. Image quality was assessed by 2 specialized radiologists by using a 4-point scale. AVM characteristics and nidus size were evaluated by using both CE-MRA and CCA in all patients.RESULTS: In patients, 96.6% (319/330) of arterial segments on high-spatial-resolution MRA and 87.7% (272/310) of arterial segments on time-resolved MRA were graded excellent/good. MRA showed 100% specificity for detecting feeding arteries and venous drainage (n = 8) and complete obliteration of the AVM in 2 cases (concordance with CCA). Nidus diameters measured by both MRA and CCA resulted in a very strong correlation (r = 0.99) with a mild overestimation by MRA (0.10 cm by using the Bland-Altman plot).CONCLUSION: By combining highly temporally resolved and highly spatially resolved MRA at 3T as complementary studies, one can assess vascular anatomy and hemodynamics noninvasively in patients with AVM.

Craniospinal arteriovenous malformation (AVM) typically presents in a young adult with intracranial hemorrhage (30%–82%), headache, seizures, or focal neurologic deficits that are either related to mass effect or to vascular steal phenomena.¹ Hemorrhage occurs with an annual incidence of 2%–4%^2,3 and remains the prime vector for mortality and morbidity (10% and 16%–50%, respectively).^4–6 Several investigators have identified features predictive of hemorrhage, including small nidus size, deep nidus location, single deep venous drainage, associated arterial aneurysm, impaired venous drainage, and high intranidal pressure.^7–10 Safe and accurate diagnostic work-up is essential to provide an architectural map and to define hemodynamic indices and risk predictors. Moreover, follow-up studies may be required for monitoring posttherapy. The current gold standard for assessment of AVM is conventional catheter angiography (CCA), which is associated with ≤1.3% of major complications and death (<0.1%).^11–13 In this context, multiple catheter examinations in patients with AVM are expected to elevate the risk of complications and hemorrhage.Recent advances in the performance of contrast-enhanced MR angiography (CE-MRA) at 3T have underscored its growing potential for detailed evaluation of the supra-aortic arteries and veins.^14–16 Techniques have been established for both highly temporally resolved and highly spatially resolved CE-MRA, by using only modest contrast doses.^17,18 Whereas high-spatial-resolution MRA can quickly provide detailed images of intracranial and extracranial vessels, time-resolved MRA adds hemodynamic information and can capture transient processes, such as early venous filling, which is the hallmark of an arteriovenous fistula (AVF).^17,19 Moreover, cortical venous reflux has a high yearly risk of hemorrhage^20–24 and influences treatment.^24–28 Micro-AVMs as a potential source of fatal intracranial hematoma represent approximately 8%–10% of surgically treated brain AVMs.^29,30 Time-resolved MRA may potentially identify an early filling vein in a micro-AVF because the anatomy of a very small nidus may not be assessable. Furthermore, an early filling vein may be the only evidence of a residual shunt after radiosurgery or endovascular therapy.These 2 approaches can, therefore, provide complementary diagnostic information to each other for evaluation of high-flow AVMs. The purpose of our study was to evaluate the potential of these complementary modes in defining the relevant vascular anatomy and hemodynamics noninvasively in patients with AVM and to compare the findings with those on digital subtraction angiography (DSA).     

New ischemic brain lesions on diffusion-weighted MRI after carotid artery stenting with filter protection: frequency and relationship with plaque morphology

BACKGROUND AND PURPOSE:CAS carries an inherent risk of distal cerebral embolization, precipitating new brain ischemic lesions and neurologic symptoms. Our purpose was to evaluate the frequency of new ischemic lesions found on DWI after protected CAS placement and to determine its association with plaque morphology.MATERIALS AND METHODS:Fifty patients (mean age 65.13 ± 7.08 years) with moderate and severe internal carotid artery stenosis underwent CAS with distal filter protection. Fibrolipid and fibrocalcified plaque morphology was determined by sonography according to the relative contribution of echogenic and echolucent material, and by multisection CT using plaque attenuation. There were 46.81% of patients with fibrolipid and 53.19% with fibrocalcified plaques. DWI was performed before and 24 hours after CAS.RESULTS:Seven (14.89%) patients showed new lesions. Four (8.51%) had 6 new lesions inside the treated vascular territory. Three had a single lesion and 1 patient had 3 lesions (mean: 1.5 ± 1). Most lesions (66.66%) were subcortical, with a mean diameter of 9 mm (range 5–15 mm). All lesions occurred in the area supplied by the middle cerebral artery and were clinically silent. A significant relationship was found between plaque morphology and the appearance of new lesions. Patients with fibrolipid plaques had a significantly higher number of new lesions compared with patients with fibrocalcified plaques (P = .041). The absolute risk of new lesions in the fibrolipid group was 18.18%.CONCLUSIONS:New ischemic lesions were observed in the treated vascular territory in 8.51% of patients. The appearance of new ischemic lesions was significantly related to the plaque morphology. Fibrolipid plaques were associated with higher numbers of new lesions.

CAS carries an inherent risk of distal cerebral embolization, precipitating new brain ischemic lesions and neurologic symptoms.^1–4 This has led to the development and widespread application of cerebral protection devices.^5,6 The most widely used devices are those based on distal filter placement that capture emboli dislodged from plaque; however, their application may result in additional complications.^7–12Several reviews have reported contradictory data concerning the rate of stroke and ischemia after protected versus unprotected stent placement.^3,13–15 The frequency of new ischemic lesions after CAS may be associated with numerous factors, such as clinical status, vascular anatomy, plaque morphology, and complexity. Therefore, the need to identify patients at risk for embolic events has become increasingly important. The morphologic characteristics of atherosclerotic carotid plaques may be useful in heralding embolic potential in the carotid arteries. Several authors have reported that plaques in the carotid arteries that are associated with large lipid pools or soft extracellular lipid are more prone to rupture and production of emboli.¹⁶ DWI is the most sensitive tool for the detection of neurologically silent or asymptomatic infarcts at a very early stage.^17–19The aim of this study was to determine the frequency of new ischemic DWI lesions in patients with moderate and severe ICA stenosis after protected CAS using a filter device, and to determine its potential association with plaque morphology.     

Transcranial color-coded duplex sonography for detection of distal internal carotid artery stenosis

BACKGROUND AND PURPOSE: Gradation of high-grade intracranial internal carotid artery (ICA) stenosis poses a challenge to noninvasive neurovascular imaging, which seems critical for angioplasty in the ICA segments C1 and C5. We investigated cutoff values of intracranial ICA stenosis for transcranial color-coded sonography (TCCS) and compared this method with the “gold standard,” digital subtraction angiography (DSA).Materials and METHODS: Forty patients (mean age, 58.9 ± 13.8 years) with intracranial ICA lesions were prospectively examined by using TCCS and DSA. Two standard TCCS coronal imaging planes were used to evaluate the intracranial ICA. In addition, a control group of 128 volunteers without cerebrovascular disease (mean age, 48.8 ± 15.9 years) was investigated to establish standard velocity values.RESULTS: DSA confirmed 96 stenoses and 8 occlusions of the intracranial ICA in the study population. In 9% and 7% of cases, stenosis confined to the C1 or C5 segment was >50% and 70%, respectively. Receiver-operating curves demonstrated cutoff values for >70% stenosis in C1 when the peak systolic velocity (PSV) was >200 cm/s (specificity, 100%; sensitivity, 71%) or the C1/submandibular ICA index was >3 (specificity, 93%; sensitivity, 86%).CONCLUSIONS: TCCS is a reliable adjunctive method to detect and quantify significant stenosis of the intracranial ICA. The assessment of the C1/ICA index and peak systolic velocities maximizes the diagnostic accuracy of C1 stenosis to >70% when extracranial ICA stenosis coexists. Further studies need to be performed to compare the diagnostic accuracies of MR angiography and TCCS with that of DSA.

Detection of atherosclerotic narrowing of intracranial cerebral arteries is important in stroke management and aids in the identification of patients with high risk for vascular events.^1–3 Ischemic stroke due to atherosclerosis of intracranial large arteries has been reported in approximately 8%–29% of adults in general, with a higher prevalence in African and Asian populations.^4–6 The intracranial internal carotid artery (ICA) is the most common location for intracranial stenosis of >50%; such cases compose up to 49% of all intracranial artery stenoses.^1,7 Patients with severe (≥70%) intracranial stenosis have a higher risk of stroke than patients with moderate (50%–69%) intracranial stenosis.⁸ Treatment of significant stenosis relies on antiplatelet and antithrombotic agents as well as on aggressive lipid-lowering therapies.^9,10 Endovascular treatments involving angioplasty for 50%–99% ICA stenosis have also been applied but are considered experimental approaches in need of validation by controlled studies.^11–13Because the course of intracranial ICA is complicated due to its tortuosity and variability, classification of this portion of the vessel may differ between authors,^14–16 in turn complicating interpretation of the data. The “gold standard” used to assess the intracranial ICA remains digital subtraction angiography (DSA). DSA is usually performed only after noninvasive imaging procedures, such as MR angiography (MRA) and, to a lesser degree, conventional transcranial Doppler (TCD) sonography, have suggested intracranial stenosis. With TCD sonography, intracranial ICA stenosis is considered when flow velocities exceed normal values and/or exhibit abnormal flow patterns. Unlike cases of extracranial ICA disease, stenosis gradation of the intracranial ICA has not been calculated.^17,18 With MRA, intracranial ICA stenosis in the C5 as well as the C3 and C1 segments is frequently indicated by flow-void artifacts, especially when using time-of-flight sequences, because of the inherent signal-intensity loss of parallel imaging, which can only be compensated in part by the use of MR imaging contrast agents.¹⁹ Due to these MRA artifacts, calculation of ICA stenosis gradation is difficult, and semiquantitative scales, rather than percentages of stenosis, are frequently used to describe the lesion.²⁰Although the criteria for detecting significant (>50%) stenosis of basal cerebral arteries has been defined for transcranial color-coded sonography (TCCS),^21–24 little data can be found on grading intracranial ICA stenosis. The aim of this study was to elaborate the TCCS criteria for detection and quantification of significant intracranial ICA stenosis and to correlate them with conventional DSA criteria as the standard of reference.     

Carotid artery stenting for calcified lesions

BACKGROUND AND PURPOSE: Our aim was to assess the feasibility of carotid artery stent placement (CAS) for calcified lesions.MATERIALS AND METHODS: Using embolic protection devices (EPDs), we performed 51 CAS procedures in 43 patients with severe carotid artery stenosis accompanied by plaque calcification. Before intervention, all lesions were subjected to multidetector-row CT. The arc of the circumferential plaque calcification was measured on axial source images at the site of maximal luminal stenosis, and the total volume of the plaque calcification was determined. The angiographic outcome immediately after CAS, and intra- and postoperative complications were recorded.RESULTS: The mean arc of calcification was 201.1 ± 72.3° (range, 76–352°), and the mean of the total calcification volume was 154.9 ± 35.4 mm³ (range, 92–2680 mm³). Balloon rupture occurred in 1 procedure (2.0%) at predilation angioplasty; all 51 CAS procedures were successful without clinical adverse effects. Although there was a correlation between the arc of plaque calcification and residual stenosis (r = 0.6, P < .001), excellent dilation with residual stenosis ≤30% was achieved in all lesions. There was no correlation between the total volume of calcification and residual stenosis. None of the patients developed stroke or death within 30 days of the CAS procedure.CONCLUSION: CAS by using EPDs to treat lesions with plaque calcification is feasible even in patients with near-total circumferential plaque calcification.

Carotid artery stent placement (CAS) is being evaluated as an alternative to carotid endarterectomy. CAS procedures are currently performed in high-risk patients, and favorable outcomes have been reported.¹ The characteristics of the lesion are important factors influencing technical results and outcomes. Heavily calcified stenoses have been classified as complex lesions because their treatment success rate is lower and the incidence of acute dissection of the coronary artery and other vessels in the peripheral vascular territory is higher.^2,3 Severe lesion calcification has been considered a relative contraindication for CAS because it prevents adequate stent expansion.^4,5 However, the lesion calcifications had been evaluated only angiographically. A correlation between severe lesion calcification and stroke after CAS was reported⁶; most of the affected patients were treated without the use of embolic protection devices (EPDs). Therefore, the outcomes of CAS by using EPDs to address calcified lesions have not been well established.We performed morphologic and quantitative evaluation of plaque calcification by multidetector-row CT (MDCT) before CAS. Here we report the characteristics of plaque calcifications and the short-term angiographic and clinical outcomes after CAS with EPDs.