Abstract Background The heme oxygenase‐1 (HO‐1) is known as up‐regulator in AD. The peptidylprolyl isomerase A (PPIA) (also known as cyclophilin A, CyPA) provides protection of neurons against copper‐mediated oxidative stress. The inositol‐requiring enzyme 1 (IRE1) is a major stress transducer in endoplasmic reticulum (ER) stress and abnormal protein aggregation. There is no study to evaluate the relationship between gray matter volume (GMV) loss and the three blood‐based biomarkers. Therefore, in this study, we evaluated the relationship between imaging biomarker by GMV changes and blood biomarkers by plasma levels of HO‐1, PPIA, and IRE1 in the groups of cognitively normal (CN), amnestic mild cognitive impairment (MCI), and AD participants. Method We obtained MRI and plasma levels of the three blood biomarkers from 45 CN, 34 amnestic MCI, and 39 AD. To assess the relationship between GMV or WMV loss and the three blood biomarkers, the voxel‐based multiple regression analysis was performed for using all participant data. In addition, region‐of‐interest (ROI)‐based analysis was performed to determine correlations between ROI‐based brain tissue volumes and plasma biomarkers. To investigate the relationship between GMV or WMV at each ROI and the plasma levels of HO‐1, PPIA, and IRE1, we performed the Pearson correlation analyses. Result The CypA value was significantly positively correlated with MMSE scores. The HO‐1 value was significantly negatively correlated with age, but was positively correlated with the K‐MMSE score. The IRE1 value was significantly positively correlated with age, but was negatively correlated with K‐MMSE scores. GMV was positively correlated with CypA and HO‐1, but negatively correlated with IRE1. Conclusion Our study demonstrates that subjects with AD have lower circulating levels of HO‐1 than subjects with MCI and the plasma HO‐1 levels were positively associated with the global GMV. This also shows that subjects with AD have lower circulating levels of CyPA than cognitively normal control and the plasma CyPA levels were positively associated with the GMV whereas subjects with AD have higher circulating levels of IRE1 than subjects with MCI and normal control.
Nonseptic inflammation of the olecranon bursa is frequent because of its superficial location.1 This olecranon bursitis can be due to variable causes such as trauma, overuse, inflammatory arthropathy, chronic degenerative osteoarthritis, rheumatoid arthritis (RA), and gout.2–4 A cyst (or geode) is a subarticular cystic lesion, and this is often seen in osteoarthritis and RA.5 Other forms of arthritis, such as hemophilia, calcium pyrophosphate deposition disease, and gout, can show cysts.5–7 These cysts are usually small but can enlarge and reach 5 or 6 cm in diameter.8 Although cysts are common in RA, cysts occurring in the olecranon have been rarely reported,9–12 and most of them were related to spontaneous fractures through olecranon cysts.9–11 To our knowledge, a report of communication between olecranon bursitis and an olecranon cyst has not been reported in the English literature. We present a case of olecranon bursitis in a 23-year-old rheumatoid patient in which communication with an olecranon cyst was confirmed on sonography and at surgery. On color scale sonography, compression with the ultrasound transducer on the bursa was useful for confirming the communication between the olecranon bursa and the cyst by observation of the color flow signal. A 23-year-old woman had pain, swelling, and a soft, palpable, masslike lesion in the left elbow. She had known RA with polyarthralgia, especially in both wrists and the left elbow, for 3 years. Radiographs of the left elbow joint (Figure 1) showed a large cystic lesion in the olecranon of the ulna and elbow changes consistent with RA. In the olecranon, a relatively well-defined osteolytic lesion with a narrow transitional zone, a thin sclerotic rim, and inner bony ridges or septations was shown. There was no matrix calcification or periosteal reaction. In addition, anterior joint capsular distension and posterior soft tissue bulging were noted. The changes suggested an olecranon cyst as the underlying abnormality, but a differential diagnosis such as a giant cell tumor or other bone tumor had to be included. Radiograph (lateral view) of the left elbow shows a relatively well-defined osteolytic lesion in the olecranon. Soft tissue swelling (white arrows) is shown in the posterior aspect of elbow, and anterior joint capsular bulging (black arrows) is suggested. On sonography (Figure 2), olecranon bursitis was noted, with inner marked synovial hypertrophies, an echogenic fluid collection, and septations. In addition, a communication between the olecranon bursitis and the intramedullary portion of the olecranon was shown through a posterior cortical defect of the olecranon. To-and-fro flow movements were noted through this cortical defect on compression with the ultrasound transducer, and this finding was noted as movement of echogenic material on gray scale sonography and a color flow signal on color scale sonography. In addition, irregular cortical margins, subchondral erosions, a hypertrophied, echogenic synovium with hypervascularity, and joint effusion were shown in the elbow joint. These findings suggested prominent and chronic synovitis such as RA. Magnetic resonance imaging (MRI) was then performed. A, Transverse sonogram shows the olecranon bursa (B) with inner echogenic material. A posterior cortical defect (arrow) of the olecranon (O) is also shown. B, Longitudinal sonogram shows echogenic material and posterior enhancement (arrows) from the bursa (B) in the intraosseous portion of the olecranon (O). C, Transverse color scale sonogram shows a color flow signal (F) from to-and-fro movements of inner fluid and debris through the cortical defect (communication between the bursa and geode) on compression with the transducer. On MRI (Figure 3), it was possible to easily see that the osteolytic lesion in the olecranon was a cyst. Magnetic resonance imaging also showed the presence of communications between the bursitis and the cyst and between the cyst and the articular joint space of the elbow. The patient underwent open synovectomy, removal of the bursa, and careful curettage of the cyst with autogenous iliac bone grafts to relieve the elbow arthritis with bursitis and to prevent a pathologic fracture. During surgery, marked synovial hypertrophy and rice bodies were visible all over the elbow joint. The bursa was distended with inner fluid and inflammatory granulelike tissue, and the cyst was filled with an extensive granulationlike appearance of the tissue. In addition, there were communications between the olecranon bursitis and the olecranon cyst and between the olecranon cyst and the articular elbow joint space. Histologic examination of the tissue in the bursa and cyst revealed nonspecific chronic inflammation similar to a pannus, with lymphoplasmacytic infiltration and eosinophilic nodular proliferation. There was no bacterial growth on a culture of aspirated fluid. The postoperative course of the patient was uneventful, and she was asymptomatic with no radiologic findings of recurrence at the 5-month follow-up. The olecranon bursa is a subcutaneous space lined with a synovial membrane that secretes fluid to provide smooth and almost frictionless motion between the skin, the subcutaneous tissues, and the olecranon. Nonseptic olecranon bursitis can be due to overuse, repetitive trauma, inflammatory arthropathy, or obesity.1 In addition, diseases that lead to a complicated aspect of affected and noninfected bursae include chronic degenerative arthritis, repetitive trauma, acute trauma, RA, and gout.1 Bursitis can be diagnosed by sonography, computed tomography, and MRI. On these imaging modalities, a fluid collection with lobulation, septation, complexity, wall thickening, adjacent joint effusion, soft tissue edema, and wall enhancement posterior to the olecranon can indicate a diagnosis of olecranon bursitis.1 A. Sagittal proton-weighted fat-suppressed MRI (repetition time, 2200 milliseconds; echo time, 20 milliseconds) shows a large cyst (C) in the olecranon. A communication (arrow) between the cyst and the articular joint space is clearly shown. There are synovial changes and subchondral changes in the elbow joint with joint capsular bulging. B, Enhanced axial T1-weighted fat-suppressed MRI (repetition time, 600 milliseconds; echo time, 20 milliseconds) shows a communication between the olecranon bursa (B) and the olecranon cyst (C) through a posterior cortical defect. Thick peripheral enhancements are shown in the walls of the cyst and bursa. Thick and irregular synovial enhancements (arrows) are visible in the elbow joint space. The term “geode” was originally a geologic term meaning a rounded pocket of gas in a mineral specimen.5,13 Geode (or cyst) is used interchangeably with subchondral cyst and can be subarticular, subchondral, or synovial.7 Cyst formation is most commonly associated with osteoarthritis but is also associated with other forms of arthritis such as RA, hemophilia, calcium pyrophosphate deposition disease, and gout.7 In RA, the commonly affected sites by cysts are the tibial plateau and the femoral neck.13,14 Large cysts may be confused with other destructive lesions that develop close to joints. These include osteomyelitis, septic arthritis, pigmented villonodular hyperplasia, hemophilia, and tumors such as giant cell tumors and metastases.7 Although the mechanism of cyst formation has not been made clear, 2 theories have been suggested.7,13 One is that the pannus, arising from the synovial membrane under inflammatory conditions, causes destruction of articular cartilage and extends to the subchondral bone. At this time, the pannus becomes a cyst, with increased pressure from the joint cavity being transmitted to subchondral space.15 In this theory, communication between the articular cavity and the cyst may be essential. Actually, there were communications between cysts and joint cavities in surgically proven and image-based reports by Maher et al,5 Torikai et al,12 and Lohse et al.16 Another theory involves the development of true intraosseous rheumatoid nodules in the subchondral regions.13,17 In our case, a cortical defect between the nonarticular cortex of the olecranon and the olecranon bursa was present. In addition, there were several cortical defects in the articular side of the olecranon, showing communications with the articular cavity and the cyst. Therefore, we think that first the cyst formation was made from invagination of the intra-articular synovium into the olecranon; the second inflammatory synovium in the cyst eroded the posterior olecranon cortex; and then a communication between the olecranon cyst and the olecranon bursa was formed, rather than secondary cyst formation after direct erosion of the posterior olecranon cortex by the inflammatory olecranon bursa. We think that detection of communications between an olecranon cyst and a bursa/articular joint is important because communications through the cortex are weak areas, and these can be beginnings of cortical fractures. In addition, more careful procedures are needed to prevent intraoperative fractures and recurrence of intraosseous cysts and superficial bursitis in these areas during the curettage and bone grafting. In conclusion, we report unusual findings of communication between the olecranon bursa and an olecranon cyst confirmed by sonography before MRI and surgery. On color scale sonography, compression with the ultrasound transducer on the bursa was useful for confirming the communication between the olecranon bursa and the cyst by observation of the color flow signal.
High-resolution MR imaging can depict intracranial arterial atherosclerotic plaques. Our aim was to evaluate the relationship between the degree of enhancement of MCA plaques on contrast-enhanced high-resolution MR imaging and ischemic stroke and stenosis severity.
MATERIALS AND METHODS:
This study enrolled 36 patients diagnosed with moderate-to-severe atherosclerotic MCA stenosis. A contrast-enhanced T1-weighted volume isotropic turbo spin-echo acquisition sequence was acquired for assessing plaque enhancement. Plaque-to-CSF contrast ratio was calculated after the signal intensity of plaques at the stenotic segment was measured. Univariate comparison and multivariate logistic regression analyses were performed for symptomatic and asymptomatic groups to assess the relationship between symptomatic stenosis and independent variables, including plaque-to-CSF contrast ratio, degree of stenosis, and clinical risk factors. Plaque-to-CSF contrast ratio was compared between the moderate and severe stenosis groups.
RESULTS:
Twenty-one patients had symptomatic MCA stenosis, and 15 had asymptomatic stenosis. The plaque-to-CSF contrast ratio was significantly higher in the symptomatic group than in the asymptomatic group (63.6 ± 10.6% versus 54.1 ± 13.5%, respectively; P < .05). The degree of stenosis also differed significantly between the 2 groups (P < .05). Multivariate analysis revealed that the degree of stenosis was the only independent predictor of ischemic stroke symptoms. The plaque-to-CSF contrast ratio of severe stenosis was significantly higher than that of moderate stenosis (66.8 ± 8.7% versus 55.9 ± 12.8%, respectively; P < .05).
CONCLUSIONS:
Plaque enhancement was significantly higher in patients with symptomatic plaques and may have been affected by the degree of stenosis. A difference in plaque enhancement according to the degree of stenosis has implications for understanding the development of intracranial atherosclerotic plaques.
Abstract Purpose To evaluate the effectiveness of Kami Guibi‐tang (KGT) in the treatment of mild cognitive impairment (MCI) using magnetic resonance imaging (MRI) on brain metabolites, neurotransmitter, and cerebral blood flow (CBF). Methods We randomly allocated a total of 30 MCI patients to a KGT (N = 16) or a placebo (N = 14) group and performed MRI scans before and after 24 weeks of treatment. The participants underwent brain magnetic resonance spectroscopy and MRI scans to obtain brain metabolites using Point‐RESolved Spectroscopy (PRESS) single‐voxel spectroscopy, gamma‐aminobutyric acid (GABA) neurotransmitter using Mescher–Garwood PRESS, and CBF using pseudocontinuous arterial spin labeling sequences using a 3.0 Tesla MRI system. We analyzed metabolite and neurotransmitter levels and CBF using repeated‐measure analysis of variance to evaluate between‐subject group effect, within‐subject treatment condition effect, and interaction of group by condition (group x condition). Results The GABA+/creatine (Cr) ratio values were not significantly different between the before and after treatment conditions. The glutamate complex/Cr ratio difference before and after treatment was lower in the KGT group than in the placebo group, but was not statistically significant ( p = 0.077). The result of region of interest–based CBF measurement showed that CBF values were significantly lower after treatment at Cluster 2 for the KGT group ( p = 0.003) and the placebo group ( p = 0.011), at hippocampus for the KGT group ( p = 0.004) and the placebo group ( p = 0.008), and at the fusiform gyrus for the KGT group ( p = 0.002). Furthermore, the absolute CBF difference before and after treatment in the fusiform gyrus was significantly lower in the KGT group than in the placebo group ( p = 0.024). Conclusions Although a KGT treatment of 24 weeks showed some significant impact on the level of CBF, the Korean version of the mini‐mental state examination score was not significantly different between before and after treatment conditions, indicating that there was no memory function improvement after treatment in amnestic MCI patients. Therefore, further studies should be performed with a relatively larger population and extending the duration of the KGT treatment.
To assess the cerebral microvascular alteration in the demented patients relative to a non-demented population using in vivo microvascular index maps by using Gd-based contrast agent at a 3T MRI system, we included 11 non-demented participants and 11 AD patients. Compared with the non-demented group, BVf and MvWI were significantly increased in the demented group. Both mVD and VSI were only significantly decreased in the demented group at the white matter hyperintensity (WMHI) area. BVf and MvWI were significantly positively correlated with age and VSI was significantly positively correlated with MMSE.
The Alberta Stroke Program Early CT Score (ASPECTS) was devised to quantify the extent of early ischemic changes in the middle cerebral artery territory on brain CT. We performed a systematic review and meta-analysis of studies that presented clinical outcomes and baseline ASPECTS in ischemic stroke patients managed with endovascular methods to validate the use of ASPECTS for risk prognostication.We searched the MEDLINE, EMBASE, and Cochran databases for observational or interventional studies that reported clinical outcomes and baseline ASPECTS in ischemic stroke patients treated with endovascular methods. Data were pooled to perform a meta-analysis for comparisons of clinical outcomes between high and low ASPECTS patients.A meta-analysis of 13 studies (six observational and seven interventional) revealed favorable outcomes (mRS sore 0-2 at 90 days) for high baseline ASPECTS (odds ratio=2.22; 95% CI: 1.74-2.86).High ASPECTS is a predictor of favorable outcome after endovascular therapy for ischemic stroke.
A 24-year-old patient with left eye proptosis and intermittent pain for 5 months was admitted to our hospital. Physical examination revealed neither extra ocular muscle limitations nor visual field defects. Magnetic resonance imaging (MRI) revealed a multicystic mass in the left extraconal space compressing the superior oblique muscle and adjacent frontal lobe. Layered hemorrhage was observed within the lesion in the 1-month follow-up MRI. Dynamic contrast enhanced imaging showed mild increased perfusion of the surrounding peripheral portion. Magnetic resonance spectroscopy showed an increased lactate/lipid peak of 1.3 ppm. Combined open and endonasal surgery was performed, and the final diagnosis was psammomatoid ossifying fibroma. The tumor was positive for vimentin, and negative for smooth muscle actin, S100 and epithelial membrane antigen. Despite its rarity, psammomatoid ossifying fibroma should be considered when multicystic lesions with peripheral enhancement near the orbit exhibit progressive inner hemorrhage.
In June, I heard on the news about the world's first stem cell medication. The news said that a cardiac stem cell therapy was expected to be approved for use at hospitals. The approval will be the first of its kind in the world to allow the use of this form of treatment. The nation's drug safety agency said that a stem cell medication for treating heart attack victims, passed all the required safety and quality tests. The vendor said that the cardiac stem cell therapy could improve ventricular contraction in patients with refractory post-infarct heart failure. They also said that the phase III study is underway on the stem cell therapy for recovery of brain [1].
Before Dr. Woo-Suk Hwang made ethical problems in his research, the stem cell therapy had had a high public attention 5 years ago. The hard controversy about ethical problems about embryonic stem cell and the intangible achievement led to draw public attention away from stem cell therapy. However, many efforts have been made to use the stem cells driven from umbilical cord blood or bone marrow instead of embryonic stem cell. Somatic cells, such as fibroblasts extracted from the patient's own body, can be reprogrammed to pluripotent stem cells by the introduction of transcription factors. These induced pluripotent stem cells are then differentiated to specific neuron types for transplantation with this technology. Patient-specific cells can be produced without the need for immunosuppressive treatment after transplantation. Then, the ethical issue with the use of human embryonic stem cells can be avoided [2]. Results of many basic researches bring us much closer to the day when clinical grade stem cells might be available. Stem cell therapy offers a remarkable potential for the recovery of brain function after stroke, and treatment of stroke using stem cell is a challenge that is worthy of high expectations. Nowadays, we can easily find out a lot of researches about stem cell for stroke recovery from Google or Pubmed search engine.
The delivery of stem cell to targeting an area is the cause that neurointerventionists should be concerned about the stem cell therapy in stroke. There are multimodal delivery methods from stereotactic injection to intra-arterial routes. In view of the results so far achieved, intra-arterial delivery of stem cells is performed via the catheter that is traced though the feeding artery to the target area. This method will have a chance to take up as a commercialize method, and can have benefits than other delivery methods. Stereotactic injection is more invasive than intra-arterial delivery. In addition, targeted intra-arterial transplantation of stem cells to the injured brain is more effective than intravenous administration [3]. Intra-arterial delivery can be disseminated into specific affected areas of the brain through the arterial system. Delivered stem cells differentiate into neurons, and migrate toward the ischemic lesion in brain [4]. There is growing evidence that stem cells can induce functional improvement by mechanisms other than neuronal replacement. Products from transplanted stem cells can induce modulation of inflammation, promotion of angiogenesis, and neuroprotection [5]. The catheterization safely in intracranial arteries is the unique business of neurointerventionists. Therefore, I think that neurointerventionists are most suitable to perform the intra-arterial injection of stem cell to a lesion in brain.
However, stem cell therapy is not always wonderful, and is just beginning to be translated into the clinical realm. In order to apply into clinical fields, several items have to be investigated. Most importantly, the safety and efficacy should be confirmed. It should be proved whether intra-arterial injection of neural stem cells using a catheter technique causes microembolic strokes or not. The risk for tumor formation also should be eliminated. To bring the stem cells therapy much closer to clinical applications, several clinical studies using intra-arterial infusion of non-NSCs or MSCs in patients with stroke are ongoing or planned (www.clinicaltrials.gov).
It is certain that the stem cell therapy for brain recovery is just beginning to be translated into the clinical realm and we are entering a new era in which neurointerventionist can work. In order to play a leading role in stem cell therapy, we should be concerned about this item and actively participate in the stage of basic and clinical research.
'%3e%3cg id='b'%3e%3cpath id='a' stroke='%23000' stroke-width='2' d='M-6-25H6m-12 3H6m-12 3H6'/%3e%3cuse xlink:href='%23a' y='44'/%3e%3c/g%3e%3cpath stroke='%23fff' d='M0 17v10'/%3e%3ccircle r='12' fill='%23cd2e3a'/%3e%3cpath fill='%230047a0' d='M0-12A6 6 0 0 0 0 0a6 6 0 0 1 0 12 12 12 0 0 1 0-24z'/%3e%3c/g%3e%3cg transform='rotate(-123.69)'%3e%3cuse xlink:href='%23b'/%3e%3cpath stroke='%23fff' d='M0-23.5v3M0 17v3.5m0 3v3'/%3e%3c/g%3e%3c/svg%3e)