METHODS: Patients with IIM, excluding inclusion body myositis, were recruited along with age- and sex-matched healthy controls (HC). All participants underwent muscle ultrasound and clinical assessments. Six limb muscles were unilaterally scanned using a standardized protocol, measuring muscle thickness (MT) and echo intensity (EI). Results were compared with HC, and correlations were made with outcome measures.
RESULTS: Twenty IIM patients and 24 HC were recruited. The subtypes of IIM were dermatomyositis (6), necrotizing myositis (6), polymyositis (3), antisynthetase syndrome (3), and nonspecific myositis (2). Mean disease duration was 8.7 ± 6.9 years. There were no significant differences in demographics and anthropometrics between patients and controls. MT of rectus femoris in IIM patients was significantly lower than HC. Muscle EI of biceps brachii and vastus medialis in IIM patients were higher than HC. There were moderate correlations between MT of rectus femoris and modified Rankin Scale, Physician Global Activity Assessment, and Health Assessment Questionnaire, as well as between EI of biceps brachii and Manual Muscle Testing-8.
DISCUSSION: Muscle ultrasound can detect proximal muscle atrophy and hyperechogenicity in patients with IIM. The findings correlate with clinical outcome measures, making it a potential tool for evaluating disease activity of patients with IIM in the late phase of the disease.
MATERIALS AND METHODS: 18F-FDG PET/CT images of 14 healthy control (HC) subjects (MoCA score > 26 (mean+SD~ 26.93+0.92) with no clinical evidence of cognitive deficits or neurological disease) and 16 AD patients (MoCA ≤22 (mean+SD~18.6+9.28)) were pre-processed in SPM12 while using our developed Malaysian healthy control brain template. The AD patients were assessed for disease severity using ADAS-Cog neuropsychological test. KNE96 template was used for registration-induced deformation in comparison with the ICBM templates. All deformation fields were corrected using the Malaysian healthy control template. The images were then nonlinearly modified by DARTEL to segment grey matter (GM), white matter (WM) and cerebrospinal fluid (CSF) to produce group-specific templates. Age, intracranial volume, MoCA score, and ADASCog score were used as variables in two sample t test between groups. The inference of our brain analysis was based on a corrected threshold of p<0.001 using Z-score threshold of 2.0, with a positive value above it as hypometabolic. The relationship between regional atrophy in GM and WM atrophy were analysed by comparing the means of cortical thinning between normal control and three AD stages in 15 clusters of ROI based on Z-score less than 2.0 as atrophied.
RESULTS: One-way ANOVA indicated that the means were equal for TIV, F(2,11) = 1.310, p=0.309, GMV, F(2,11) = 0.923, p=0.426, WMV, F(2,11) = 0.158, p=0.856 and CSF, F(2,11) = 1.495 p=0.266. Pearson correlations of GM, WM and CSF volume between HC and AD groups indicated the presence of brain atrophy in GM (p=-0.610, p<0.0001), WM (p=-0.178, p=0.034) and TIV (p=-0.374, p=0.042) but showed increased CSF volume (p=0.602, p<0.0001). Voxels analysis of the 18FFDG PET template revealed that GM atrophy differs significantly between healthy control and AD (p<0.0001). Zscore comparisons in the region of GM & WM were shown to distinguish AD patients from healthy controls at the prefrontal cortex and parahippocampal gyrus. The atrophy rate within each ROI is significantly different between groups (c2=35.9021, df=3, p<0.0001), Wilcoxon method test showed statistically significant differences were observed between Moderate vs. Mild AD (p<0.0001), Moderate AD vs. healthy control (p=0.0005), Mild AD vs. HC (p=0.0372) and Severe AD vs. Moderate AD (p<0.0001). The highest atrophy rate within each ROI between the median values ranked as follows severe AD vs. HC (p<0.0001) > mild AD vs. HC (p=0.0091) > severe AD vs. moderate AD (p=0.0143).
CONCLUSION: We recommend a reliable method in measuring the brain atrophy and locating the patterns of hypometabolism using a group-specific template registered to a quantitatively validated KNE96 group-specific template. The studied regions together with neuropsychological test approach is an effective method for the determination of AD severity in a Malaysian population.
METHODS: Patients with CBHA in 176 families were genetically examined using exome sequencing. Patients with disease-causing variants were clinically evaluated.
RESULTS: Disease-causing variants were identified in 96 of the 176 families (54.5%). After excluding 6 families, 48 patients from 42 families were categorized as having syndromic associations with CBHA, whereas the remaining 51 patients from 48 families had isolated CBHA. In 51 patients, 26 aberrant genes were identified, of which, 20 (76.9%) caused disease in 1 family each. The most prevalent genes were CACNA1A, ITPR1, and KIF1A. Of the 26 aberrant genes, 21 and 1 were functionally annotated to atrophy and hypoplasia, respectively. CBHA+S was more clinically severe than CBHA-S. Notably, ARG1 and FOLR1 variants were identified in 2 families, leading to medical treatments.
CONCLUSION: A wide genetic and clinical diversity of CBHA was revealed through exome sequencing in this cohort, which highlights the importance of comprehensive genetic analyses. Furthermore, molecular-based treatment was available for 2 families.
METHODS: Data from 133 participants from the Rapid Intervention with Glyceryl Trinitrate in Hypertensive Stroke-2 Trial trial were analysed. Measures included ICHV (using ABC/2) and ICV (XYZ/2) (by independent observers); ICHV, ICV and CPV (semiautomated segmentation, SAS); atrophy (intercaudate distance, ICD, Sylvian fissure ratio, SFR); midline shift; leukoaraiosis and cistern effacement (visual assessment). The effects of these measures on death at day 4 and poor functional outcome at day 90 (modified Rankin scale, mRS of >3) was assessed.
RESULTS: ICV was significantly different between XYZ and SAS: mean (SD) of 1357 (219) vs 1420 (196), mean difference (MD) 62 mL (p<0.001). There was no significant difference in ICHV between ABC/2 and SAS. There was very good agreement for ICV measured by SAS, CPV, ICD, SFR, leukoaraiosis and cistern score (all interclass correlations, n=10: interobserver 0.72-0.99, intraobserver 0.73-1.00). ICHV/ICV and ICHV/CPV were significantly associated with mRS at day 90, death at day 4 and acute neurological deterioration (all p<0.05), similar to ICHV. Midline shift and cistern effacement at baseline were associated with poor functional outcome but old infarcts, leukoaraiosis and brain atrophy were not.
CONCLUSIONS: Intracranial compartment measures and visual estimates are reproducible. ICHV adjusted for ICH and CPV could be useful to prognosticate in acute stroke. The presence of midline shift and cistern effacement may predict outcome but the mechanisms need validation in larger studies.
METHODS: Twenty-nine asymptomatic subjects were enrolled prospectively (age: mean 34.31, range 23-50; 14 men, 15 women) from August 2016 to April 2017. Qualitative analysis of muscles was done using Goutallier's system on CT and MRI. Quantitative analysis entailed cross sectional area (CSA) on CT and MRI, Hounsfield unit (HU) on CT, fat fraction using two-point Dixon technique on MRI. Three readers independently analyzed the images; intra- and inter-observer agreements were measured. Linear regression and Spearman's analyses were used for correlation with demographic data.
RESULTS: CSA values were significantly higher in men (p
METHODS: 50 POAG patients and 50 normal subjects were recruited and an MRI brain with T1-magnetization-prepared rapid gradient-echo was performed. Medial temporal lobe and parietal lobe atrophy were by MTA and PCA/Koedam scoring. The score of the PCA and MTA were compared between the POAG group and the controls.
RESULTS: There was a significant statistical difference between PCA score in POAG and the healthy control group (p-value = 0.026). There is no statistical difference between MTA score in POAG compared to the healthy control group (p-value = 0.58).
CONCLUSION: This study suggests a correlation between POAG and PCA score. Potential application of this scoring method in clinical diagnosis and monitoring of POAG patients.
ADVANCES IN KNOWLEDGE: The scoring method used in AD may also be applied in the diagnosis and monitoring of POAGMRI brain, specifically rapid volumetric T1 spoiled gradient echo sequence, may be applied in POAG assessment.
MATERIALS AND METHODS: This study was conducted at Department of Anatomy, Faculty of Medicine, Public Health, and Nursing, Universitas Gadjah Mada starting on July 20th, 2020. A total of 24 male Wistar rats were randomly divided into six groups (four rats per group), i.e., control, DM 1.5 months (DM1.5), and DM 2 months (DM2); and DM groups treated with CGA in three different doses, namely CGA1 (12.5 mg/kg BW), CGA2 (25 mg/kg BW), and CGA3 (50 mg/kg BW). Control group was only injected with normal saline, while diabetic model was induced by intraperitoneal injection of streptozotocin. Blood glucose levels were measured twice (one week after diabetic induction and before termination). The soleus muscle tissue was harvested to analyse the mRNA expressions of SOD-1, SOD- 2, CN and PGC-1α using RT-PCR. In addition, the tissue samples were stained with immunohistochemistry for CN and haematoxylin-eosin (HE) for morphologic analysis under light microscopy.
RESULTS: The mRNA expressions of SOD-1 and SOD-2 in the CGA1 group were relatively higher compared to the DM2 groups. The mRNA expression of CN in the CGA1 group was significantly higher compared to the DM2 group (p = 0.008). The mRNA expression of PGC-1α in the CGA1 group was significantly higher compared to the DM2 group (p = 0.025). Immunohistochemical staining showed that CNimmunopositive expression in the CGA1 group was more evident compared to the other groups. Haematoxylin-eosin staining showed that muscle tissue morphology in the CGA1 group was similar to that in the control group.
CONCLUSION: Chlorogenic acid at a dose of 12.5 mg/kg BW shows lower blood glucose level, good skeletal muscle tissue morphology and higher mRNA expressions of SOD-1, SOD-2, CN and PGC-1α compared to the DM groups.
Material and Methods: Fifty-eight patients with a full-thickness SSP tendon tear who fulfilled the inclusion criteria were enrolled in the study. They were evaluated for tear retraction, fatty degeneration, and other rotator cuff tendon pathologies. Supraspinatus muscle was assessed using the Goutallier classification, and its average area was also measured. Accompanying lesions of the subscapularis and infraspinatus tendons and degree of supraspinatus muscle atrophy were evaluated using magnetic resonance imaging.
Results: Our results showed that supraspinatus tendon tears ranged between 3mm and 41mm, and the estimated average cross-sectional area of the SSP muscle was 247.6mm2. Any degree of infraspinatus tendon pathology, ranging from tendinosis to full-thickness tears, was significantly correlated with the SSP muscle area (P < 0.05). The subscapularis tendon pathologies did not show a similar correlation. The interobserver and intraobserver reliabilities of the measurements were graded as excellent.
Conclusion: Impairment of any of the rotator cuff muscles may affect the other muscles inversely. Our study showed that all infraspinatus tendon pathologies and partial subscapularis tears affect and alter the SSP muscle belly. We suggest early intervention for supraspinatus tears to avoid further fatty degeneration, as muscle atrophy and fatty degeneration progress in combination with the accompanying lesions.