Intracranial dermoid cysts are rare, benign, congenital, slow-growing cystic lesions. They are composed of mature squamous epithelium and can contain apocrine, eccrine, and sebaceous glands as well as other exodermal structures. Rupture of intracranial dermoid cysts is a relatively uncommon phenomenon but can cause more serious complications such as chemical meningitis, vasospasm, and cerebral infarction. Understanding of the appearance of both unruptured and ruptured dermoid cysts on computed tomography and MRI, especially awareness of existing low signal “blooming artefacts” on certain sequences, aids diagnosis and referral to the proper specialty for appropriate treatment.
Introduction: The aim of the study was to evaluate the impact of multiple risk factors (age, diabetes, hypertension, hyperlipidemia, BMI, smoking, alcohol) on the gray and white matter volumes as well as on the burden of white matter hyperintensities (WMH).Material and Methods: The study group consisted of 554 subjects (age range: 50–69 yrs, F/M: 367/187) recruited from the larger cohort of the Polish fraction of the Prospective Urban Rural Epidemiological (PURE) study. The participants answered questionnaires about their lifestyle, underwent physical and psychological examination (MoCA test), laboratory blood tests followed by brain MRI. Volumetric measurements of the total gray matter (GMvol), total white matter (WMvol) and WHM (WMHvol) normalized to the total intracranial volume were performed using the Computational Anatomy Toolbox 12 (CAT12) and Statistical Parametric Maps 12 (SPM12) based on 3D T1-weighted sequence. The influence of risk factors was assessed using multiple regression analysis before and after correction for multiple comparisons.Results: Older age was associated with lower GMvol and WMvol, and higher WMHvol (p < 0.001). Smaller GMvol volume was associated with higher WMHvol (p < 0.001). Higher WMHvol was associated with hypertension (p = 0.01) and less significantly with hyperlipidemia (only before correction p = 0.03). Diabetes, abnormal BMI, smoking and alcohol intake did not have any significant impact on GMvol, WMvol or WMHvol (p > 0.05). MoCA score was not influenced by any of the factors.Conclusions: Gray matter loss is strongly associated with the accumulation of WMH which seems to be potentially preventable by maintaining normal blood pressure and cholesterol levels.
The aim of this study was to assess the diagnostic value of non-contrast pituitary MRI in children with growth or puberty disorders (GPDs) and to determine the criteria indicating the necessity to perform post-contrast examination. A retrospective study included re-analysis of 567 contrast-enhanced pituitary MRIs of children treated in a tertiary reference center. Two sets of sequences were created from each MRI examination: Set 1, including common sequences without contrast administration, and Set 2, which included common pre- and post-contrast sequences (conventional MRI examination). The differences in the visibility of pituitary lesions between pairs of sets were statistically analyzed. The overall frequency of Rathke’s cleft cysts was 11.6%, ectopic posterior pituitary 3.5%, and microadenomas 0.9%. Lesions visible without contrast administration accounted for 85% of cases. Lesions not visible before and diagnosed only after contrast injection accounted for only 0.18% of all patients. Statistical analysis showed the advantage of the antero-posterior (AP) pituitary dimension over the other criteria in determining the appropriateness of using contrast in pituitary MRIs. The AP dimension was the most significant factor in logistic regression analysis: OR = 2.23, 95%CI, 1.35–3.71, p-value = 0.002, and in ROC analysis: AUC: 72.9% with a cut-off value of 7.5 mm, with sensitivity/specificity rates of 69.2%/73.5%. In most cases, the use of gadolinium-based contrast agent (GBCA) in pituitary MRI in children with GPD is unnecessary. The advantages of GBCA omission include shortening the time of MRI examination and of general anesthesia; saving time for other examinations, thus increasing the availability of MRI for waiting children; and acceleration in their further clinical management.
IntroductionAcute cerebral venous thrombosis (CVT) is a rare condition that can lead to a serious clinical state; thus, prompt diagnosis and treatment are mandatory. Head computed tomography (CT) plays a crucial role in the initial prompt diagnosis in the emergency setting. The aim of the study was to retrospectively analyse emergency head CT studies and the rate of incorrect diagnoses and main sources of pitfalls.Material and methodsRetrospective analysis of 31 emergency CT studies (22 without contrast, 19F/12M, age range: 4-94 years) of patients with confirmed acute CVT.ResultsThrombosed dural sinuses were found in 24/31 (77.4%) cases, thrombosed veins in 7/31 (22.6%) cases, no lesions within vessels in 2/31 (6.5%) cases. Haemorrhagic brain lesions were found in 9/31 (29%) cases, hypodense oedema in 6/31 (19.6%) cases, brain swelling in 1/31 (3.2%) cases, and no parenchymal lesions were revealed in 15/31 (48.4%) cases. Correct diagnosis of CVT was established in 15 cases (48.4%); however, it was incorrect in 16 cases (51.6%). Incorrect cases consist of 4 groups: 1 – with both vascular and parenchymal lesions that were overlooked (50%), 2 – with vascular lesions only, which were either overlooked, misinterpreted, or covered by artefacts (31.3%,), 3 – with parenchymal lesions only, which were misinterpreted (12.5%), and 4 – with no lesions present in the emergency head CT (6.2%).ConclusionsThe high rate of incorrect diagnoses of acute CVT based on emergency head CT requires constant training of radiologists and their close cooperation with clinicians because a delayed diagnosis may be lethal to the patient.
The early onset and rapid progression of cutaneous squamous cell carcinoma (cSCC) leads to high mortality rates in individuals with recessive dystrophic epidermolysis bullosa (RDEB). Currently, the molecular mechanisms underlying cSCC development in RDEB are not well understood and there are limited therapeutic options. RDEB-cSCC arises through the accumulation of genetic mutations; however, previous work analyzing gene expression profiles have not been able to explain its aggressive nature. Therefore, we generated a model to study RDEB-cSCC development using cellular reprograming and re-differentiation technology. We compared RDEB-cSCC to cSCC that were first reprogrammed into induced pluripotent stem cells (RDEB-cSCC-iPSC) and then differentiated back to keratinocytes (RDEB-cSCC-iKC). The RDEB-cSCC-iKC cell population had reduced proliferative capacities in vitro and in vivo, suggesting that reprogramming and re-differentiation leads to functional changes. Finally, we performed RNA-seq analysis for RDEB-cSCC, RDEB-cSCC-iPSC, and RDEB-cSCC-iKC and identified different gene expression signatures between these cell populations. Taken together, this cell culture model offers a valuable tool to study cSCC and provides a novel way to identify potential therapeutic targets for RDEB-cSCC.
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