Regions Of High Signal Intensity Research Articles

Awake Surgery for Right Frontal Lobe Glioma: Preserving Emotional Recognition and Facilitating Early Return to Work.

Many glioma patients struggle to return to work after surgery because of higher brain dysfunction. Although the right frontal lobe has historically been considered functionally silent, reports of performing awake surgery to evaluate higher brain functions in patients with tumors in this area have increased. We present two cases of patients who underwent awake surgery for malignant glioma in the right frontal lobe to preserve emotional recognition and facilitate an early return to work. Case 1 was a 48-year-old right-handed woman employed as a nursery school teacher and case 2 was a 21-year-old right-handed man employed in sales. Both had contrast-enhancing right frontal lobe tumors exhibiting high signal intensity on fluid attenuated inversion recovery imaging and underwent awake surgery. During the operation, cortical mapping was performed using the Reading the Mind in the Eyes, calculation, and motor tasks. Resection of sites involved in motor and emotional recognition functions was avoided. In case 1, all regions of high signal intensity were completely resected; in case 2, all regions exhibiting enhancement were resected. Both patients were discharged home without neurological deficits and returned to work within 21 days after surgery. It may be important to focus not only on overall survival and progression-free survival in glioma patients, but also on factors associated with life satisfaction, such as time to return to work after surgery and time until work becomes difficult. Awake surgery aimed at preserving higher brain functions is useful and may also improve life satisfaction.

Phosphoglyceride crystal deposition with suspected malignant ovarian tumor: a case report and literature review.

Phosphoglyceride crystal deposition disease is a rare condition occurring in soft tissues, resulting in scarring and affecting the bones, making preoperative differentiation from malignant tumors challenging. Here, we describe a case of phosphoglyceride crystal deposition disease initially suspected to be a malignant ovarian tumor before surgery. A 50-year-old woman with a history of three cesarean sections presented with lower abdominal pain. Transvaginal ultrasonography revealed a 54 × 58mm tumor in the lower right abdomen. Pelvic contrast-enhanced magnetic resonance imaging showed a thickened cystic wall with diffusion restriction, a low signal intensity region on T1-weighted images, and a slightly high signal intensity region on T2-weighted images. The tumor markers, cancer antigen 125 and carbohydrate antigen 19-9 levels, were within normal ranges; however, positron emitting tomography-computed tomography revealed fluorodeoxyglucose accumulation (SUVmax 31.28) in the tumor wall. Suspecting a malignant ovarian tumor, a laparoscopy was performed to observe the abdominal cavity. A 10cm white solid tumor was identified in the midline of the lower abdominal wall, leading to an open surgery recommendation. The tumor, adhering to the pubic bone, was excised. The tumor measured 9 × 7cm, with the cut surface showing a yellow brownish solid periphery and central region with liquefied degeneration. Histologically, radial basophilic deposits, dense infiltration of macrophages, multinucleated giant cells, and foam-like tissue spheres were observed. The central region exhibited cholesterol clefts, fibrin exudation, and necrosis, leading to a diagnosis of phosphoglyceride crystal deposition disease. This disease is rare, occurring in patients with atypical fluorodeoxyglucose accumulation on positron emission tomography-computed tomography or with a history of tissue damage, such as abdominal surgery.

Quantitatively Measured Infrapatellar Fat Pad Signal Intensity Alteration is Associated with Joint Effusion-synovitis in Knee Osteoarthritis.

The objective of this study is to investigate whether quantitatively measured infrapatellar fat pad (IPFP) signal intensity alteration is associated with joint effusion-synovitis in people with knee osteoarthritis (OA) over two years. Among 255 knee OA patients, IPFP signal intensity alteration represented by four measurement parameters [standard deviation of IPFP signal intensity (IPFP sDev), upper quartile value of IPFP high signal intensity region (IPFP UQ (H)), ratio of IPFP high signal intensity region volume to whole IPFP volume (IPFP percentage (H)), and clustering factor of IPFP high signal intensity (IPFP clustering factor (H))] was measured quantitatively at baseline and two-year follow-up using magnetic resonance imaging (MRI). Effusion-synovitis of the suprapatellar pouch and other cavities were measured both quantitatively and semi-quantitatively as effusion-synovitis volume and effusion-synovitis score at baseline and two-year follow-up using MRI. Mixed effects models assessed the associations between IPFP signal intensity alteration and effusion-synovitis over two years. In multivariable analyses, all four parameters of IPFP signal intensity alteration were positively associated with total effusion-synovitis volume and effusion-synovitis volumes of the suprapatellar pouch and of other cavities over two years (all P＜0.05). They were also associated with the semi-quantitative measure of effusion-synovitis except for IPFP percentage (H) with effusion-synovitis in other cavities. Quantitatively measured IPFP signal intensity alteration is positively associated with joint effusion-synovitis in people with knee OA, suggesting that IPFP signal intensity alteration may contribute to effusion-synovitis and a coexistent pattern of these two imaging biomarkers could exist in knee OA patients.

Evaluation of in vivo MRI for detecting midodrine-induced arteritis in rats.

There are no specific and sensitive biomarkers for arteritis, and the occurrence of arteritis in nonclinical toxicological studies of a candidate drug makes development of the drug very difficult. However, we showed in a previous study that the high signal intensity region around the artery on magnetic resonance imaging (MRI) could be a candidate biomarker for detection of arteritis. The present study was conducted to clarify the details of midodrine hydrochloride (MH)-induced arteritis lesions and whether arteritis induced by a mechanism other than the vasodilatory effect, which was evaluated in a previous study, could be detected by MRI. MH is a selective peripherally acting alpha-1 adrenergic receptor agonist, known to induce arteritis due to its vasoconstrictor action, but there is not enough information about MH-induced arteritis. Based on the data obtained under multiple dosing conditions, MH was administered subcutaneously to each rat once daily for 2 days at a dose level of 40mg/kg/day for MRI assessment. The mesenteric arteries were examined using in vivo MRI at 1day or 7 days after administration of the final dose and examined histopathologically. On the day after the final dose, high signal intensity region around the artery was observed in animals with minimal perivascular lesions confirmed by histopathology and not observed in an animal without histological changes. On the 7th day after the final dose, no abnormality was observed in histopathological examinations and no high signal intensity regions were observed by MRI in any animal. In conclusion, although further investigation is needed to confirm that high signal intensity is a reliable biomarker for humans, it is suggested that high signal intensity around the artery could be a versatile candidate biomarker with high specificity and sensitivity.

No-reflow phenomenon and in vivo cholesterol crystals combined with lipid core in acute myocardial infarction

The release of lipid-laden plaque material subsequent to ST-segment elevation myocardial infarction (STEMI) may contribute to the no-reflow phenomenon. The aim of this study was to investigate the association between in vivo cholesterol crystals (CCs) detected by optical coherence tomography (OCT) and the no-reflow phenomenon after successful percutaneous coronary intervention (PCI) in patients with acute STEMI. We investigated 182 patients with STEMI. Based on the thrombolysis in myocardial infarction (TIMI) flow grade after PCI, patients were divided into a no-reflow group (n=31) and a reflow group (n=151). On OCT, CCs were defined as thin, high-signal intensity regions within a plaque. A multivariable logistic regression analysis was performed to determine predictors for the no-reflow phenomenon. The prevalence of CCs was higher in the no-reflow group than the reflow group (no-reflow group, 77% vs. reflow group, 53%; p=0.012). The multivariable logistic model showed that the CC number, lipid arc and ostial lesions were positive independent predictors of no-reflow. The combination of a lipid arc≥139°and CC number≥12 showed good predictive performance for the no-reflow phenomenon (sensitivity, 48%; specificity, 93%; and accuracy, 86%). In vivo CCs at the culprit plaque are associated with the no-reflow phenomenon after PCI in patients with STEMI. The combination of the number of CCs and lipid arc can predict the no-reflow phenomenon after PCI with a high accuracy of 86%.

Detection of fenoldopam-induced arteritis in rats using ex vivo / in vivo MRI

A method capable of identifying drug-induced arteritis is highly desirable because no specific and sensitive biomarkers have yet been defined. Although magnetic resonance imaging (MRI) may be used to find a biomarker candidate for drug-induced arteritis, there are no reports on the evaluation of drug-induced arteritis by MRI. The present study was conducted to clarify whether Fenoldopam mesylate (FM)-induced arteritis in rats can be detected by MRI. FM, a dopamine (D1 receptor) agonist, is known to induce arteritis in rats. FM was administered subcutaneously to each rat once daily for 2 days at a dose of 100 mg/kg/day. These arteries were examined with ex vivo high-resolution MRI or postmortem MRI after euthanasia. These arteries were also examined using in vivo MRI on the day after final dosing or 3 days after administration of the final dose. These arteries were examined histopathologically in all experiments. The ex vivo MRI showed low-intensity areas and a high signal intensity region around the artery, and these findings were considered to be erythrocytes infiltrating the arterial wall and perivascular edema, respectively. In the in vivo study, the MRI of the FM-administered group showed a high signal intensity region around the artery. The perivascular edema observed histopathologically was recognized as a high signal intensity region around the artery on the image of MRI. In conclusion, detection of the high signal intensity region around the artery by MRI is considered to be a useful method for identifying arteritis. Although further investigation is needed to be a reliable biomarker, it is suggested that it could be a biomarker candidate.

In vivo microstructural heterogeneity of white matter lesions in healthy elderly and Alzheimer's disease participants using tissue compositional analysis of diffusion MRI data

White matter hyperintensities (WMH) are regions of high signal intensity typically identified on fluid attenuated inversion recovery (FLAIR). Although commonly observed in elderly individuals, they are more prevalent in Alzheimer’s disease (AD) patients. Given that WMH appear relatively homogeneous on FLAIR, they are commonly partitioned into location- or distance-based classes when investigating their relevance to disease. Since pathology indicates that such lesions are often heterogeneous, probing their microstructure in vivo may provide greater insight than relying on such arbitrary classification schemes. In this study, we investigated WMH in vivo using an advanced diffusion MRI method known as single-shell 3-tissue constrained spherical deconvolution (SS3T-CSD), which models white matter microstructure while accounting for grey matter and CSF compartments. Diffusion MRI data and FLAIR images were obtained from AD (n = 48) and healthy elderly control (n = 94) subjects. WMH were automatically segmented, and classified: (1) as either periventricular or deep; or (2) into three distance-based contours from the ventricles. The 3-tissue profile of WMH enabled their characterisation in terms of white matter-, grey matter-, and fluid-like characteristics of the diffusion signal. Our SS3T-CSD findings revealed substantial heterogeneity in the 3-tissue profile of WMH, both within lesions and across the various classes. Moreover, this heterogeneity information indicated that the use of different commonly used WMH classification schemes can result in different disease-based conclusions. We conclude that future studies of WMH in AD would benefit from inclusion of microstructural information when characterising lesions, which we demonstrate can be performed in vivo using SS3T-CSD.

P3576Histopathological validation of optical coherence tomography assessment for cholesterol crystals

Abstract Background Cholesterol crystals (CCs) are well recognized as one of important components of advanced atherosclerotic plaques. Whilethe consensus document for intravascular optical coherence tomography (OCT) has proposed that CCs are appeared as thin, linear regions of high-signal intensity within a plaque, no study has validated CCs assessment by OCT in comparison with histopathology. Purpose Thepurpose of this study was to validate OCT assessments of CCs with histopathology. Methods A total of 27 diseased coronary artery samples (10–20 mm length) were resected from 7 randomly selected cadavers. OCT imaging was performed for the samples. Then, arterial samples were fixed in 10% formalin for ≥48 hours, decalcified and processed for standard paraffin embedding. Sections 5μm thick were sliced at the ink-marked imaging sites and stained with hematoxylin and eosin, and Masson's Trichrome. An independent pathologist blinded to the OCT results diagnosed all of the plaques. Subsequently, the OCT images were interpreted by an observer blinded to the histological results. In the OCT assessment, CCs were defined as thin, linear regions of high-signal intensity within a plaque. Results We obtained 27 pairs of OCT/ histopathology. CCs were diagnosed by histology in 10 (37%) of the 27 pairs. The sensitivity and specificity of OCT for detecting CCs were 60% and 94%, respectively. Conclusion OCT has a high specificity but modest sensitivity for detection of CCs in comparison with histopathology. CCs diagnosed with OCT would help the identification of advanced atherosclerotic plaques. Acknowledgement/Funding JSPS KAKENHI 17K09557

Olivary hypertrophy improved by steroid treatment: Two case reports with unique presentations

Olivary hypertrophy (OH) is the secondary degeneration of the inferior olivary nucleus (ION). It is observed one month after the onset of a primary lesion within the dento-rubro-olivary pathway and is usually associated with oculopalatal tremors. Here, we report two unique cases with rare autoimmune diseases leading to OH development with progressive cerebellar ataxia, both of which improved with steroid treatment. The first patient was a 59-year-old man with slowly progressive dysarthria and ataxic gait without palatal tremor. Anti-N-methyl-d-aspartate (NMDA) receptor antibody was positive in the CSF, supporting a diagnosis of anti-NMDA receptor encephalitis. The second patient was a 56-year-old man who developed dysarthria, ataxia, gait disturbance, and palatal tremor. He was diagnosed with chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS), based on presence of a punctate contrast-enhancing lesion in the middle cerebellar peduncle, pons, and cerebellum on magnetic resonance imaging (MRI). Brain MRI in both patients demonstrated high signal intensity regions in the bilateral IONs. Semi-quantitative volume analysis of MRI revealed significant reduction in ION volume after steroid treatment and accordingly cerebellar ataxia was improved in both cases. Clinical and radiological features of the two cases were unique, indicating potential novel etiologies in the pathophysiology of OH associated with cerebellar ataxia.

A novel method for assessing signal intensity within infrapatellar fat pad on MR images in patients with knee osteoarthritis

To assess reliability and validity of a semi-automated quantitative method to measure infrapatellar fat pad (IPFP) signal intensity in patients with knee osteoarthritis (OA). Hundred patients with knee OA were selected. Sagittal planes of fat-saturated T2-weighted images obtained on 1.5-T magnetic resonance imaging (MRI) were utilized to assess IPFP signal intensity using MATLAB. Knee structural abnormalities including cartilage defects, bone marrow lesions (BML) and radiographic OA (ROA) were evaluated. Clinical construct validity and concurrent validity were examined through describing associations of IPFP measurements with knee structural abnormalities and a semi-quantitative scoring method, respectively. The reliability was examined by calculating the intra- and inter-observer correlation coefficients. Significantly positive associations were found between standard deviation of IPFP signal intensity [sDev (IPFP)], clustering factor (H) and all knee structural abnormalities. The volume of high signal intensity regions [Volume (H)] and the ratio of Volume (H) to volume of whole IPFP [Percentage (H)] were positively associated with cartilage defects and ROA, but not with BMLs. The median value [Median (H)] and upper quartile value [UQ (H)] of high signal intensity were only significantly associated with quartiles of cartilage defect score. Significant correlations were found between all quantitative measurements and semi-quantitative scores (All P<0.001). Intraclass and interclass correlation coefficients for these quantitative measures were high (>0.90). A novel and efficient method to segment IPFP and calculate its signal intensity on T2-weighted MRI images is documented. This method is reproducible, and has concurrent and clinical construct validity, but its predictive validity needs to be examined by future longitudinal studies.

Correlation between neuromelanin-sensitive MR imaging and (123)I-FP-CIT SPECT in patients with parkinsonism.

Neuromelanin-sensitive MR imaging (MRI) can visualize neuromelanin-containing neurons in the substantia nigra pars compacta (SNc), and its utility has been reported in the evaluation of parkinsonism. Conversely, dopamine transporter imaging by (123)I-N-v-fluoropropyl-2b-carbomethoxy-3b-(4-iodophenyl)nortropane (FP-CIT) SPECT (DaTSCAN) is now an established method for evaluating parkinsonism, detecting presynaptic dopamine neuronal dysfunction. Both methods can assist differentiating neurodegenerative and other forms of parkinsonism. However, to our knowledge, there have been no studies concerning a correlation between the two methods. The aim of this study was to assess the utility of neuromelanin-sensitive MRI for diagnosing parkinsonism by examining a correlation with DaTSCAN. Twenty-three patients with parkinsonism who underwent both neuromelanin-sensitive MRI and DaTSCAN were included. We measured the neuromelanin-positive SNc region volume by manually contouring the high signal intensity region of the SNc on neuromelanin-sensitive MRI and measured the specific binding ratio (SBR) on DaTSCAN. The asymmetry index of neuromelanin-positive SNc volume and the asymmetry index of SBR were also calculated. The volume of the neuromelanin-positive SNc region showed significant correlation with specific binding ratio (SBR) (right P < .001, ρ = 0.78, left P < .001, ρ = 0.86). The asymmetry index of neuromelanin-positive SNc volume also showed significant correlations with the asymmetry index of SBR (P < .001, ρ = 0.73). Decrease of the high signal intensity region of the SNc on neuromelanin-sensitive MRI would indicate damage to the nigrostriatal dopaminergic function as well as loss of dopaminergic neurons. We conclude that neuromelanin-sensitive MRI is a useful diagnostic biomarker for parkinsonism.

Solid-state NMR structure determination from diagonal-compensated, sparsely nonuniform-sampled 4D proton-proton restraints.

We report acquisition of diagonal-compensated protein structural restraints from four-dimensional solid-state NMR spectra on extensively deuterated and 1H back-exchanged proteins. To achieve this, we use homonuclear 1H–1H correlations with diagonal suppression and nonuniform sampling (NUS). Suppression of the diagonal allows the accurate identification of cross-peaks which are otherwise obscured by the strong autocorrelation or whose intensity is biased due to partial overlap with the diagonal. The approach results in unambiguous spectral interpretation and relatively few but reliable restraints for structure calculation. In addition, the diagonal suppression produces a spectrum with low dynamic range for which ultrasparse NUS data sets can be readily reconstructed, allowing straightforward application of NUS with only 2% sampling density with the advantage of more heavily sampling time-domain regions of high signal intensity. The method is demonstrated here for two proteins, α-spectrin SH3 microcrystals and hydrophobin functional amyloids. For the case of SH3, suppression of the diagonal results in facilitated identification of unambiguous restraints and improvement of the quality of the calculated structural ensemble compared to nondiagonal-suppressed 4D spectra. For the only partly assigned hydrophobin rodlets, the structure is yet unknown. Applied to this protein of biological significance with large inhomogeneous broadening, the method allows identification of unambiguous crosspeaks that are otherwise obscured by the diagonal.

MR image mimicking the “eye of the tiger” sign in Wilson’s disease

Dear Sirs, The eye of the tiger sign (EOT), seen on T2 sequences of magnetic resonance imaging (MRI), is considered pathognomonic for neurodegeneration with brain iron accumulation type 1 (NBIA1, previously known as Hallervorden–Spatz syndrome) [1–3]. This sign is described as low signal intensity in both globi pallidi (due to iron accumulation) that surrounds a central region of high signal intensity (caused by gliosis, edema, and neuronal loss with subsequent secondary vacuolization and cavitation) [1–3]. It has been occasionally reported in neurodegenerative disorders other than NBIA1, including neuroferritinopathy, progressive supranuclear palsy, multisystem atrophy, pure akinesia, and corticobasal degeneration [1–3]. Here, we describe the first case of EOT-like MRI appearance in a 41-year-old man with Wilson’s disease. At the age of 24 years, the patient developed dysarthria, oromandibular dystonia, gait disturbances, and positional hand tremor. One year later he was diagnosed with Wilson’s disease, based on the presence of Kayser–Fleischer ring and abnormal copper metabolism [i.e. decreased serum ceruloplasmin (8.2 mg/dL, normal 25–45) and serum copper (30 μg/dL, normal 70–140 μg/dL) combined with increased copper urinary excretion (664 μg/24 h, normal 0–50)]. Genetic examination confirmed compound heterozygosity, with ATP7B mutations in exon 13 (G988R) and in exon 7 (IVS7 + 3A>G). After introduction of 1000 mg/day d-penicillamine, the patient gradually improved. In 2013 his remaining symptoms were only slight dysarthria and oromandibular dystonia (occasionally grimacing). The Kayser–Fleischer rings were no longer present. However, a routine control brain MRI revealed abnormalities very similar to EOT sign (Fig. 1). Fig. 1 The MR image mimicking the “eye of the tiger” sign in T2-weighted magnetic resonance sequences; bilateral hypointensity in both putaminal regions and lateral parts of globi pallidi, with a central hyperintensity (black arrows) The difference was that hypointensity tended to localize in the lateral part of the globus pallidus and putamen instead of the medial part of the globus pallidus. Subsequent MR spectroscopy showed that the mean N-acetyloaspartate/creatine ratio (TE-144mS) in the globus pallidus was 1.55, and the mean choline/creatine ratio (TE-144 mS) was 1.10 (Fig. 2a). In the normal appearing control region, the values were 2.37 and 1.08, respectively (Fig. 2b), which may reflect neuronal loss in the affected area. Noteworthy, the patient has no co-morbidities, does not drink alcohol and had no occupational risk factors for tissue metal accumulation. Normal levels of serum iron metabolism markers (ferritin, iron, total iron binding capacity) combined with the early age of the disease onset, lack of anemia and diabetes allowed to exclude aceruloplasminemia and neuroferritinopathy. The lack of acanthocytosis, pigmentary retinopathy, hypoprobetalipoproteinemia, and good response to d-penicillamine with no subsequent progression over 15 years allowed us to exclude NBIA1. The patient's brother was diagnosed with hepatic Wilson’s disease without any neurological signs at 28 years of age. Fig. 2 The magnetic brain spectroscopy from: a unaffected structures in the right temporal lobe; b central, hyperintensive part of “eye of the tiger” sign showing markedly decreased N-acetyloaspartate in the globus pallidus as a results of reactive ... Wilson’s disease is a treatable, inherited disorder leading to pathological copper accumulation that damages affected organs, especially the liver and brain. It has been suggested that disturbances of iron metabolism occur in the liver of Wilson’s disease patients, as copper-dependent enzymes are also involved in its metabolic pathways [4]. In a recent post-mortem study we demonstrated that iron accumulates also in the brain [5]. As the EOT sign suggests accumulation of iron [2, 3, 6, 7], its increased concentration in the basal ganglia of the reported patient appeared to be particularly pronounced. However, the exact role of iron-metabolism disturbances in Wilson’s disease is still unknown and further studies are needed. Considering that patients with EOT sign may occasionally have conditions other than NBIA1, it is advisable to carry out careful differential diagnosis in order not to miss a condition that can be effectively treated.

Automatically Quantified Diffuse Excessive High Signal Intensity on MRI Predicts Cognitive Development in Preterm Infants

BackgroundCognitive and language impairments constitute the majority of disabilities observed in preterm infants. It remains unclear if diffuse excessive high signal intensity on magnetic resonance imaging at term represents delayed white matter maturation or pathology. MethodsWe hypothesized that diffusion tensor imaging–based objectively quantified diffuse excessive high signal intensity measures at term will be strong predictors of cognitive and language development at 2 years in a cohort of 41 extremely low birth weight (≤1000 g) infants. Using an automated probabilistic atlas, mean diffusivity maps were used to objectively segment and quantify diffuse excessive high signal intensity volume and mean, axial, and radial diffusivity measures. Standardized neurodevelopment was assessed at 2 years of age using the Bayley Scales of Infant Development, third edition. ResultsThirty-six of the 41 infants (88%) had complete developmental data at follow-up. Objectively quantified diffuse excessive high signal intensity volume correlated significantly with cognitive and language scores at 2 years (P < 0.001 for both). The sum values of the three diffusivity measures in detected diffuse excessive high signal intensity regions also correlated significantly with the Bayley scores (r2 34.7%; P < 0.001 for each). Infants in the highest quartile for diffuse excessive high signal intensity volumes had scores between 19 and 24 points lower than infants in the lowest quartile (P < 0.01). When diagnosed subjectively by neuroradiologists however, Bayley scores were not significantly lower in infants with extensive diffuse excessive high signal intensity. ConclusionsThese findings lend further evidence that diffuse excessive high signal intensity is pathologic and that objectively quantified diffusion-based diffuse excessive high signal intensity volume at term is associated with cognitive and language impairments. Our approach could be used for risk stratification and early intervention for such high-risk extremely preterm infants.

Measuring strain using digital image correlation of second harmonic generation images

The micromechanical environment of bone is crucial to understanding both bone fracture and mechanobiological responses of osteocytes, yet few techniques exist that are capable of measuring strains on the micrometer scale. A method for measuring micrometer level strains has been developed based on digital image correlation (DIC) of second harmonic generation microscopy (SHGM) images. Bovine tibias milled into thin sections were imaged using SHGM under loads of 0 and 15MPa. Strains were measured using DIC and compared to applied strain values. First and second principal strains decreased in magnitude as the analysis region area increased from 1750µm2 to 60,920µm2, converging to 1.23±0.74 and −0.745±0.9816 times the applied strain respectively. A representative sample histogram revealed regions of pure tensile and compressive strain, and that strains were highly heterogeneous ranging from 8410 to −8840 microstrain for an applied 2870 microstrain. Comparison with applied strain measures suggested that analysis sizes of 1750µm2 and greater were measuring strains on the tissue scale, and higher resolution is required for collagen fibrillar strains. Regions of low SHGM intensity (“dark” regions) were seen which are believed to be lacunar and perilacunar regions of low collagen density. However, no significant differences in strain magnitude were present in dark regions versus regions of high signal intensity. The proposed technique is effective for strains on the size order of bone microarchitecture, and would be useful for studies into the mechanical microenvironment during loading. The technique also has potential for in vivo studies in small animal models.

Angle-sensitive MRI for quantitative analysis of fiber-network deformations in compressed cartilage

To demonstrate the feasibility of a novel experimental method to quantitatively analyze fiber-network deformation in compressed cartilage by angle-sensitive magnetic resonance imaging (MRI) of cartilage. Three knee cartilage samples of an adult sheep were imaged in a high-resolution MRI scanner at 7 T. Main fiber orientation and its "offset" from the direction perpendicular to the bone-cartilage boundary were derived from MR images taken at different orientations with respect to B0. Bending of the collagen fibers was determined from weight-bearing MRI with the load (up to 1.0 MPa) applied over the whole sample surface. A "fascicle" model of the cartilage ultrastructure was assumed to analyze characteristic intensity variations in T2-weighted images under load. T2-weighted MR images showed a strong variation of the signal intensities with sample orientation. In the T2-weighted weight-bearing series, regions of high signal intensity underwent shifts from the lateral to the central parts in all three cartilage samples. The bending of the collagen fibers was determined to be 27.2°, 35.4°, and 40.0° per MPa, respectively. Assuming a "fascicle" model, the presented MRI method provides quantitative measures of structural adjustments in compressed cartilage. Our preliminary analysis suggests that cartilage fiber deformation includes both bending and crimping.

Magnetic resonance imaging in pantothenate kinase-2-associated neurodegeneration

Pantothenate kinase-2-associated neurodegeneration (PKAN) is a rare autosomal recessive pediatric neurodegenerative disorder characterized by rigidity, dystonia, impaired postural reflexes, and progressive dementia. On T2-weighted magnetic resonance imaging images, marked low signal intensity is seen in the globus pallidus. This low signal intensity surrounds a central region of high signal intensity in the anteromedial globus pallidus, giving an eye-of-the-tiger appearance.

Imaging of Intracranial Plaques with Black-Blood Double Inversion Recovery MR Imaging and CT

We evaluated the feasibility of black-blood double inversion recovery magnetic resonance imaging (BBDIR) and CT imaging (CTI) for depiction of IAPs. We performed BBDIR on 20 control subjects and 13 patients with acute ischemic stroke. We measured the thickness of the normal vessel wall in control subjects and the maximal and minimal thickness of IAPs in patients on BBDIR. We evaluated signal intensity (SI) and the eccentricity of the IAP on BBDIR, and abnormal wall thickening and CT attenuation of IAPs on CTI. We correlated imaging features of BBDIR and CTI in the patients. The difference of wall thickness between control and patient group was statistically significant (control subjects; basilar artery 0.6 mm, MCA 0.51 mm, and patients; maximal 2.34 mm, minimal 1.3 mm, P value≤.001). The IAP showed eccentric remodeling and heterogeneous SI with the regions of high SI on BBDIR. CTI could not reveal abnormality in 10 patients. Suspicious intraplaque hemorrhage and calcification was demonstrated in 3 patients by CTI. BBDIR could reveal normal and abnormal wall of large intracranial arteries. CTI had limited role for detection of IAP, however, correlation of BBDIR and CTI could provide further characterization of the IAP's in terms of intraplaque calcification and hemorrhage.

An autopsied case of V180I Creutzfeldt‐Jakob disease presenting with panencephalopathic‐type pathology and a characteristic prion protein type

A 73-year-old Japanese woman showed slowly progressive aphasia, apraxia and dementia. She had no family history of prion disease or dementia. One year later she showed parkinsonism and corticobasal degeneration was initially suspected. On MRI, the left temporal neocortex seemed swollen on T2-weighted images in the initial stage, and a later high-signal intensity region was observed in the cerebral cortex in diffusion-weighted images. The patient developed myoclonus and an akinetic mutism state 15 months and 22 months after onset, respectively. Consecutive electroencephalography revealed no periodic sharp-wave complexes. Prion protein (PrP) gene analysis revealed a valine to isoleucine point mutation at codon 180, and methionine homozygosity at codon 129. This patient's clinical symptoms and disease course were atypical for Creutzfeldt-Jakob disease (CJD), and a stable state with nasal tube-feeding lasted several years. She died of respiratory failure at the age of 81, 102 months after the onset. Autopsy revealed widespread spongiform degeneration with weak synaptic-type PrP deposition, confirming the diagnosis of genetic CJD. Neurons in the cerebral cortex were relatively preserved in number and hypertrophic astrocytosis was generally moderate for such long-term disease, but cerebral white matter showed diffuse severe myelin pallor with tissue rarefaction suggestive of panencephalopatic-type pathology. The cerebellar cortex was relatively well preserved with observation of mild spongiform change in the molecular layer, moderate neuron loss in the Purkinje neuron layer, and scattered small plaque-like PrP deposition. Western blot analysis of protease-resistant PrP showed a characteristic pattern without a diglycoform band. V180I CJD is an interesting form of genetic CJD with regards to the clinicopathologic, molecular and genetic findings.

MRI Eye-of-the-Tiger Sign in Organophosphate Poisoning

We describe the eye-of-the-tiger sign on magnetic resonance imaging (MRI) of the brain in a 40-year-old man presenting with extra pyramidal symptoms like chorea, flexion neck dystonia, tongue tremors, dysarthria and postural instability as the sequelae of organophosphorus poisoning six months previously. This typical radiological sign has been described in extrapyramidal parkinsonian disorders including cortical-basal ganglionic degeneration, early onset levodopa-responsive parkinsonism and Steele-Richardson-Olszewski syndrome (progressive supranuclear palsy) but hitherto has not been reported in insecticide poisoning. T2-weighted scans showed low signal intensity surrounding a central region of high signal intensity in the anteromedial globus pallidus (gliosis), producing an eye-of-the-tiger appearance with the central hyperintense signal intensity better appreciated in T2W and fluid attenuated inversion recovery (FLAIR) sequences.