Intracranial Calcification Research Articles

Progressive neurological decline associated with intracranial calcification in Down syndrome; Fahr disease mimic?

Progressive neurological decline associated with intracranial calcification in Down syndrome; Fahr disease mimic?

Intracranial Carotid Artery Calcification Subtype in Patients with Anterior Circulation Acute Ischemic Stroke Undergoing Intravenous Thrombolysis.

The aim of this study was to investigate the potential value of intracranial carotid artery calcification (ICAC) in therapeutic efficacy and functional outcomes in patients with anterior circulation acute ischemic stroke (AIS) undergoing intravenous thrombolysis. A total of 207 patients with anterior circulation AIS who underwent intravenous thrombolysis were enrolled in this retrospective study. We divided them into three groups according to thin-slice head noncontrast computed tomography as follows: no ICAC, medial ICAC, and intimal ICAC. The differences in risk factors of different ICAC subtypes were compared, and the effect of ICAC subtype on hemorrhage transformation (HT) after intravenous thrombolysis was also evaluated. Functional outcomes were assessed at 90 days using the modified Rankin Scale. Compared to the no and intimal ICAC, patients with the medial ICAC were older and more likely to have diabetes mellitus, hyperlipidemia, previous stroke, and atrial fibrillation. Moreover, the medial ICAC group had a high baseline National Institute of Health Stroke Scale (NIHSS) score and a high incidence of HT. Multivariate logistic regression analysis showed that baseline NIHSS score (odds ratio [OR]: 1.121, 95% confidence interval [CI]: 1.027-1.224) was independently associated with HT. Medial ICAC (OR: 7.418, 95% CI: 1.190-46.231) and baseline NIHSS score (OR: 1.141, 95% CI: 1.042-1.250) were independent risk factors of poor functional outcome at 90 days. Medial ICAC could be a new imaging biomarker for predicting functional outcomes in patients with anterior circulation AIS undergoing intravenous thrombolysis. Medial ICAC and baseline NIHSS score were independently associated with poor prognosis at 90 days.

Differential diagnosis of acute intracranial hemorrhage and calcification by cranial dual-energy computed tomography.

To evaluate the application value of dual-energy computed tomography (DECT) in the differential diagnosis of acute intracranial hemorrhage and calcification. This retrospective study involved patients who underwent non-contrast-enhanced cranial DECT in Anhui Wannan Rehabilitation Hospital from January 2015 to November 2022. The processed mixed images obtained after DECT were used as the conventional CT images. Each hyperdense lesion was analyzed based on virtual non-calcium and calcium overlay and classified as calcification or hemorrhage. The sensitivity, specificity, and accuracy of conventional CT and DECT were calculated by the chi-square test according to the unified reference standard. Sixty-six hyperdense intracranial lesions of 60 patients were analyzed; of these lesions, 41 (62.12%) were calcifications and 25 (37.88%) were hemorrhages. The sensitivity, specificity, and accuracy of DECT in identifying hemorrhage were 96.00%, 100%, and 98.48%, respectively, while those of conventional CT were 72.00%, 97.56%, and 87.88%, respectively. Of the 66 lesions, 4 (6.06%) could not be qualitatively identified and 3 (4.55%) were misdiagnosed by conventional CT but correctly identified by DECT. DECT can accurately distinguish acute intracranial hemorrhage from calcification, especially in cases that are difficult to diagnose by conventional CT.

Bilateral ovarian fibromas as the sole manifestation of Gorlin syndrome in a 22-year-old woman: a case report and literature review

BackgroundNevoid basal cell carcinoma syndrome (NBCCS, Gorlin syndrome) is a rare autosomal dominantly inherited disorder that is characterized by multisystem disorder such as basal cell carcinomas, keratocystic odontogenic tumors and skeletal abnormalities. Bilateral and/or unilateral ovarian fibromas have been reported in individuals diagnosed with NBCCS.Case presentationA 22-year-old female, presented with low back pain, and was found to have bilateral giant adnexal masses on pelvic ultrasonography, which had been suspected to be malignant ovarian tumors. Positron emission tomography/computed tomography showed multiple intracranial calcification and skeletal abnormalities. The left adnexa and right ovarian tumor were resected with laparotomy, and pathology revealed bilateral ovarian fibromas with marked calcification. We recommended the patient to receive genetic testing and dermatological examination. No skin lesion was detected. Germline testing identified pathogenic heterozygous mutation in PTCH1 (Patched1).ConclusionsThe possibility of NBCCS needs to be considered in patients with ovarian fibromas diagnosed in an early age. Skin lesions are not necessary for the diagnosis of NBCCS. Ovarian fibromas are managed with surgical excision with an attempt at preserving ovarian function. Follow-up regime and counseling on options for future fertility should be offered to patients.

Evaluation of intracranial physiological calcifications in Computed Tomography

Introduction: Intracranial physiological calcifications are not related to any pathological conditions, rather they are due to the normal deposition of calcium or iron in the different parts of the brain. Computed Tomography (CT) scan is superior to all other modalities in terms of sensitivity in the detection of intracranial physiological calcifications. The objective of the study was to evaluate the frequency and location of intracranial physiological calcifications and also study them according to age and gender.
 Methods: A prospective cross-sectional study with a purposive sampling technique was conducted from November 2020 to February 2021 at the Department of Radiology and Imaging. CT scan images of every age group were reviewed from the base of the skull to the vertex excluding images with intracranial pathologies, injuries, artifacts, contrast enhancement and the patients with follow-up scans. Data were analyzed using SPSS version 25. Descriptive analysis was primarily preferred accompanied by inferential statistics.
 Results: Out of 412 patients, 60.7% were male and the mean age was 41.16 ±19.915 years. The total number of calcifications was 795. 92.8% of patients showed calcifications. Males had a higher number of calcifications. The highest number of calcifications was seen in the age group 20-30. The highest calcification was seen in the pineal gland (76%) followed by the choroid plexus (70.4%) and the lowest in the caudate nucleus (0.38%). The earliest age of calcification was 8 years. There was a significant relationship between the increase in age and the increase in calcification (p<0.05). There was also a significant difference between male and female calcifications (p<0.05).
 Conclusion: This study can be useful for clinicians to differentiate normal physiological intracranial calcifications from pathological calcification which will reduce misinterpretation of the calcifications.

Skin Cancer

ABSTRACT Basal cell nevus syndrome is a genetically linked multisystem disorder with a hallmark tendency for development of multiple basal cell carcinomas at a young age. It is associated with a multitude of other anomalies including keratocytes of the jaw, palmar or plantar pits, and ectopic intracranial calcifications. This disease is most commonly caused by loss of function in tumor suppressor gene PTCH1 resulting in overactivation of the Hedgehog pathway and basal cell carcinoma formation. Diagnosis is largely clinical; patients must meet criteria of both major and minor categories. Genetic testing is warranted in specific situations where clinical diagnosis is unclear or for genetic counseling purposes. Given that basal cell carcinoma is a very common dermatologic disorder, it is important to recognize when it arises in the setting of genetically associated diseases. Early detection allows for proper management and surveillance of not only basal cell carcinomas but also the other multisystem effects of basal cell nevus syndrome. This review gives an in-depth overview of the etiology, pathogenesis, diagnosis, and management of basal cell nevus syndrome.

Risk factors associated with hemorrhagic cerebrovascular accident: A cross-sectional study in patients from a hospital in Peru.

In Peru, cardiovascular accidents (CVA) cause around 15% of premature death, with an increase in CVA due to the prevalence of risk factors for CVA in the Peruvian population. Hemorrhagic CVA presents higher mortality compared to ischemic. This research aimed to identify the risk factors associated with hemorrhagic CVA. We carried out a retrospective cross-sectional study using the medical records of patients with a diagnosis of CVA treated at the Regional Hospital of Ica during the years 2018 and 2019. Independent variables included age, sex, type 2 diabetes, dyslipidemia, hypertension, smoking, obesity, and intracranial carotid artery calcification. To identify factors associated with an increased probability for hemorrhagic CVA compared to ischemic CVA, a generalized linear model with logit link and binomial family, obtaining the odds ratio (OR) and its 95% confidence interval (CI). we evaluated the data from 132 patients. Of them, 46 (34.85%) had hemorrhagic CVA. Only systolic blood pressure (OR: 1.04; 95% CI: 1.02-1.06) and hypertension (OR: 0.29; 95% CI: 0.10-0.89) were significantly associated with hemorrhagic CVA compared to ischemic CVA. Hypertension is associated with hemorrhagic CVA compared to ischemic CVA. These results are consistent with the literature.

Tocilizumab reduces the unmanageable inflammatory reaction of a patient with Aicardi-Goutières syndrome type 7 during treatment with ruxolitinib

BackgroundAicardi-Goutières syndrome (AGS) is a rare hereditary early-onset encephalopathy characterized by upregulation of the type I interferon pathway, poorly responsive to conventional immunosuppression.Case presentationWe describe a 7-year-old Chinese boy who developed symptoms at the age of 6 months. He presented with a chilblain-like rash, leukopenia, neutropenia, elevated liver enzymesgrowth retardation, microcephaly, elevated acute phase reactants, intracranial calcification and leukodystrophy. At the age of 3 years old, whole-exome sequencing confirmed a de novo heterozygous gain-of-function mutation, c.1016 C > A (p.Ala339Asp), in the IFIH1 gene, and he was diagnosed with AGS7. He was treated with ruxolitinib accompanied by steroids and thalidomide for about four years. The rash, hematological manifestations, and the liver function were all improved, but the erythrocyte sedimentation rate remained consistently elevated until the addition of tocilizumab, a monoclonal antibody against interleukin 6.ConclusionsRuxolitinib was not successful in suppressing the inflammatory process, and tocilizumab produced highly encouraging results in reducing the inflammatory reaction of AGS. The study makes a significant contribution to the literature because we may found a potential alternative therapeutic option for AGS.

Intracranial arteriosclerosis and the risk of dementia: A population-based cohort study.

The impact of intracranial arteriosclerosis on dementia remains largely unclear. In 2339 stroke-free and dementia-free participants (52.2% women, mean age 69.5 years) from the general population, we assessed intracranial carotid artery calcification (ICAC) and vertebrobasilar artery calcification (VBAC) as proxy for arteriosclerosis. Associations with dementia were assessed using Cox models. In addition, indirect effects through cerebral small vessel disease (cSVD) and subcortical brain structure volumes were assessed using causal mediation analyses. During a median of 13.4 years (25th-75th percentiles 9.9-14.5) of follow-up, 282 participants developed dementia. Both ICAC presence (hazard ratio [HR]: 1.53, 95% confidence interval [CI]: 1.00-2.32]) and volume (HR per standard deviation: 1.19, 95% CI: 1.01-1.40) increased dementia risk. For VBAC, severe calcifications increased dementia risk (HR for third vs first volume tertile: 1.89, 95% CI: 1.00-3.59). These effects were mediated partly through increased cSVD (percentage mediated for ICAC: 13% and VBAC: 24%). Intracranial arteriosclerosis increases the risk of dementia.

Intra-Cranial Arterial Calcifications in Hemodialysis Patients.

Background and objectives: Vascular calcification is an integral part of atherosclerosis and has been reported to be an independent risk factor for cardiovascular diSsease. Intra Cranial Arterial Calcifications (ICAC) in maintenance hemodialysis (MHD) is highly prevalent. Materials and Methods: The aim of this retrospective study was to assess the predictors and outcomes of ICAC in MHD patients compared to a control group without kidney disease. A blinded neuroradiologist graded ICAC in brain imaging (computerized tomography) of MHD patients. Age- and sex-matched patients with normal kidney function served as the control group. Results: A total of 280 patients were included in the cohort; 140 of them were MHD patients with a mean ICAC score of 2.3 ± 0.2 versus a mean ICAC score of 1.4 ± 0.2 in the control group (p < 0.01). More than 90% of hemodialysis patients in our study had some degree of ICAC. Lower albumin and higher phosphorus and CRP levels were associated with increased ICACs. The multivariate analysis model for predictors of 1-year mortality demonstrated an increased odds ratio for mortality as the ICAC score increased. Conclusions: ICAC is very prevalent among MHD patients and results not simply from passive deposition of calcium and phosphate but rather from complex and active processes involving inflammation and structural changes in blood vessels. ICAC independently predicted all-cause mortality and may help with risk stratification of this high-risk population.

Association between Obstructive Sleep Apnea and Intracranial Artery Calcification Stratified by Gender and Body Mass Index: A Hospital-Based Observational Study

Background and Objectives: Obstructive sleep apnea (OSA) is an independent risk factor for stroke. Furthermore, intracranial arterial calcification (IAC) has been validated as a marker for subclinical cerebrovascular disease. However, the relationship between OSA with IAC was less studied compared with its established association with coronary artery calcification. In this study, we aimed to investigate the association between the severity of OSA and the degree of IAC in hospitalized patients without preexisting cardiovascular disease. Methods: This hospital-based observational study was conducted from June 1, 2017, to May 1, 2019. In total, 901 consecutive patients who underwent head computed tomography scans and portable sleep monitoring were included. On the basis of the apnea-hypopnea index (AHI), patients were divided into four OSA severity groups (normal: AHI <5/h; mild: 5≤ AHI <15/h; moderate: 15≤ AHI <30/h; severe: AHI ≥30/h). Associations of OSA with IAC scores were assessed by using multivariate logistic regression analysis. Results: Of the 901 patients, 484 (53.7%) were men; the mean (SD) age was 66.1 (10.0) years. The non-OSA group included 207 (23.0%) patients; mild OSA, 209 (23.2%); moderate OSA, 235 (26.1%); and severe OSA, 169 (18.8%). Mean IAC scores were higher in the severe OSA group compared with non-, mild, and moderate OSA groups (4.79 vs. 2.58; 4.79 vs. 2.94; 4.79 vs. 3.39; p < 0.001). Multivariate analysis adjusted for confounding factors revealed that only severe OSA was associated with a higher IAC score (odds ratio [OR]: 1.65; 95% confidence interval [CI]: 1.43–1.91; p < 0.001). In stratified analyses by BMI, among participants with a BMI <25 kg/m², the positive association between AHI values and IAC scores was found in the moderate OSA group (OR: 1.23; 95% CI: 1.05, 1.43; p = 0.01) and the severe OSA group (OR: 1.96; 95% CI: 1.55, 2.48; p < 0.001). When stratified by gender, in women, the positive association was found in the moderate OSA group (adjusted OR: 1.21; 95% CI: 1.02–1.51; p = 0.016) and the severe OSA group (adjusted OR: 1.76; 95% CI: 1.36–2.25; p < 0.001). For the men group, a positive association between IAC scores and AHI was only observed in the severe OSA group. Discussion: These findings suggest that OSA, in particular severe OSA (AHI ≥30), is independently associated with higher IAC scores. Women and no-obesity individuals appeared more susceptible to adverse OSA-related subclinical cerebrovascular disease as measured by IAC scores.

P24 Recurrent skin ulcerations as an isolated manifestation of ISG15 deficiency

Abstract Type I interferonopathies are characterized by a very broad phenotypic spectrum; however, some overlapping clinical features are seen across the type I interferonopathies, most particularly brain and skin involvement. We report a female patient presenting at 7 months of age with ulcerations in her groin and axilla. The lesions in her axilla healed; however, she continued having recurrent ulcerations in both sides of her groin and she developed lipoatrophy of the lower abdomen. Skin biopsy revealed deep-seated inflammation with abnormal adipose tissue; no bacteria were isolated. Extensive immunology blood work-up did not reveal any abnormalities, and the inflammatory markers were normal. Because of the extent of the clinical findings and pending results of genetic screening with targeted next-generation sequencing, we commenced methotrexate at 1 year of age (15 mg m–2). Following the initiation of methotrexate, there was marked improvement in the clinical features, with resolution of active skin ulceration. Genetic screening revealed a homozygous stop mutation in ISG15 p.Q16X. A CT scan of her head did not show any calcifications. Methotrexate was stopped at age 3 years. She remains well with no further skin ulcerations, and her development continues to be age appropriate. ISG15 deficiency is a type I interferonopathy, previously described in association with intracranial calcifications and increased susceptibility to mycobacteria infections. However, more recent reports have described skin ulcerations as a main finding in addition to neurological and immunological manifestations. Our patient is not showing any signs of neurological or other immunological manifestations but remains under careful monitoring.

The correlation between medial pattern of intracranial arterial calcification and white matter hyperintensities

Background and aimsDespite reported correlations between intracranial arterial calcification (IAC) and white matter hyperintensities (WMH), little is known about the relationship between IAC pattern and WMH. By differentiating intimal and medial IAC, we aimed to investigate the relationship between IAC pattern and WMH. MethodsConsecutive acute stroke patients were included. IAC pattern was categorized as intimal or medial on plain brain CT. The number of cerebral arteries involved by IAC for each patient was recorded. IAC severity was defined as focal or diffuse. On brain MRI, the burden of WMH was visually graded and classified as absent mild, moderate and severe. Multiple logistic regression was performed to examine the relationship between IAC and WMH. ResultsAmong 265 patients, intimal IAC was detected in 54.7% patients and medial IAC in 48.5% patients. Diffuse IAC was present in 27.9% patients, all of which were medial. WMH was found in 75.5% patients, including 39.6% patients with mild WMH, 26.0% with moderate WMH, and 9.8% with severe WMH. The severity of medial IAC was correlated with WMH occurrence (p < 0.001). Chi-square linear trend suggested the number of arteries involved by medial IAC (p < 0.001) and the severity of medial IAC (p < 0.001) were correlated with WMH burden. Multiple ordinal logistic regression demonstrated a positive correlation of WMH burden with the number of arteries involved by medial IAC (p < 0.001) and the severity of medial IAC (p < 0.001). ConclusionsMedial IAC was correlated with WMH. The dose-effect relationship between medial IAC and WMH suggests underlying shared mechanisms of intracranial large artery disease and small vessel disease.

Aortic Stiffness Is Independently Associated with Intracranial Carotid Artery Calcification in Patients with Ischemic Stroke.

Intracranial carotid artery calcification (ICAC), as a strong contributor to the occurrence of ischemic stroke, might be present in the medial or intimal arterial layer. Traditional cardiovascular risk factors (CVRFs) are associated with ICAC; however, its association with new markers of vascular function is less understood. The paper aimed to evaluate the relationship between carotid-femoral pulse wave velocity (CF-PWV) and ICAC subtypes. We enrolled 65 patients with ischemic stroke. CF-PWV, systolic, diastolic, mean blood pressure, and pulse pressure were measured within 6 ± 2 days after stroke onset, and CT was performed within 24 h. ICAC on the stroke site was classified by two methods: volume and score based. Tertiles of ICAC volume were determined, and low-grade ICAC (T1) was regarded as a reference. According to the score-based method, (dominant) medial and (dominant) intimal ICAC subtypes were determined. Data were analyzed with multivariate logistic regression. Medial and intimal ICAC subtypes were found in 34 (52%) and 24 (37%) patients, respectively. In 11% of patients, no ICAC calcifications were found. CF-PWV was higher in patients with high-grade ICAC (OR = 1.56, 95% CI = 1.03-2.35, p = 0.035). CF-PWV was higher in patients with the medial ICAC subtype (OR = 1.60, 95% CI = 1.00-2.55, p = 0.049) after adjustment for traditional CVRFs. Our study demonstrates that among patients with ischemic stroke, aortic stiffness is independently associated with ICAC and that medial ICAC, compared with intimal ICAC, is accompanied by more advanced aortic stiffness.

Could Toxomplasma gondii infection be dangerous? - Systematic review

Introduction: Toxoplasma gondii is an intracellular protozoan commonly found in humans in the form of three main forms: tachyzoite, tissue cyst and oocyst. The definitive host is the Felidae family, and one of the intermediate hosts is humans. The most common routes of infection are ingestion of raw or undercooked meat, water and food contaminated with oocysts. Among the forms of infection, we distinguish between the acquired form and the much more dangerous congenital form. Aim of the study: The objective of the study was to rewiev the literature describing the dangerous impact of Toxoplasma gondii infection on human.Methods and materials: : We reviewed the literature available in the PubMed database, using the key words: "toxoplasma gondii"; "congenital toxoplasmosis"; "pregnacy".Results: T. gondii infection is particularly dangerous in pregnant women, due to the high risk of vertical transmission of the infection to the developing fetus. The clinical presentation of congenital toxoplasmosis depends on the gestational age at which the infection occurred. Pathognomonic signs of congenital toxoplasmosis include Sabin-Pinkerton Triad, which includes inflammation of the retina and choroid of the eye, dilatation of the brain's ventricular system and intracranial calcifications. Available pharmacotherapy works on tachyzoites present in the initial phase of acquired infection, congenital infection and reactivated infection in immunodeficient patients, available drugs do not work on tissue cysts.Conclusion: The consequences of Toxoplasma gondii infection are particularly dangerous for the fetus, so pregnant women should pay special attention to hand hygiene and thorough washing of the food they eat. For this reason, it is extremely important to educate pregnant women about health issues and draw attention to the possible consequences of T.gondii infection.

Brachial-ankle pulse wave velocity is associated with intracranial artery calcification in acute stroke patients

BackgroundIntracranial artery calcification (IAC) is closely associated with cerebrovascular disease. Brachial-ankle pulse wave velocity (baPWV) is a noninvasive method for estimating arterial stiffness, which reflects the stiffness of peripheral arteries. This study aimed to examine the association of baPWV with the presence and degree of IAC in patients with acute ischemic stroke. MethodsA total of 143 ischemic stroke subjects were recruited. A head computed tomography (CT) scan was used to assess the presence and severity of IAC. The oscillometric method was used to simultaneously measure bilateral brachial and posterior tibial arterial pulse waveforms and arterial BP. Multiple logistic regression analysis was used to identify the independent relationship between baPWV and IAC. Results143 subjects were included in this study. The demographic and clinical characteristics of the study population were classified according to the baPWV quartile. A higher prevalence of IAC was noted across increasing baPWV quartiles (Q1: 53 %, Q2: 69 %, Q3: 86 %, Q4: 94 %, P < 0.001). IAC scores were also increased with elevated ccPWV values (1.60 ± 1.71; 2.56 ± 1.99; 3.44 ± 1.91; 4.64 ± 1.58. P < 0.001). After an additional adjustment for age and hypertension, the odds ratio (95 % confidence interval) for the IAC scores was 1.61 (1.06–2.45; P = 0.025) in the top quartile of baPWV compared with those in the lowest quartile. ConclusionsArterial stiffness as defined by baPWV was positively associated with the degree of IAC in patients with acute ischemic stroke, suggesting the severity of IAC may also be a marker of peripheral or systemic arterial stiffness.

Cathepsin-C mutation in an individual with phenotypic features of Haim-Munk syndrome: A case report.

Haim-Munk syndrome and Papillon-Lefèvre syndrome are rare genodermatoses caused by mutations in the cathepsin C (CTSC) gene. They both cause palmoplantar keratoderma and are associated with periodontitis. Existing literature reports additional Haim-Munk syndrome characteristics including pes planus, radiographic deformity of the fingers and arachnodactyly, whilst Papillon-Lefèvre syndrome is associated with intracranial calcification and susceptibility to infection. We report a variant in CTSC which has previously been described in Papillon-Lefèvre syndrome but has not previously been reported in Haim-Munk syndrome. Our patient's presentation supports the suggestion that Papillon-Lefèvre syndrome and Haim-Munk syndrome are a spectrum of diseases which are caused by CTSC mutations, with significant overlap in their phenotypic features. This genetic report adds to the literature to improve our understanding of these rare, clinically related syndromes.

Symptomatic Intracranial Hemorrhage after Ischemic Stroke Treated with Bridging Revascularization Therapy.

(1) Background: bridging revascularization therapy is now the standard of care in patients with ischemic stroke due to large vessel occlusion. This study aimed to determine the frequency of symptomatic intracranial hemorrhage (sICH) related to this treatment, and to assess contributing factors and patients' outcomes. (2) Methods: consecutive ischemic stroke patients treated with bridging therapy were prospectively enrolled. sICH (intracranial hemorrhage with an increase in NIHSS score of ≥4 points) was assessed on imaging at 24 h. The functional status of patients was measured at 6 months using the mRS score; (3) Results: 176 patients were included (mean age 68.7 ± 1.2 years, 52.3% women), among whom 15 (8.5%) had sICH. Patients with sICH had more frequent alcohol abuse (30.1% versus 9.7%, p = 0.023), prestroke use of dual antiplatelet therapy (14.3% versus 1.3%, p = 0.002), higher NIHSS scores at admission (median score 20.5 versus 15, p = 0.01), greater systolic blood pressure upon admission, more frequent vascular intracranial calcifications (p = 0.004), leukoaraiosis (p = 0.001), and intracranial atheroma (p = 0.02), and higher neutrophil-to-lymphocyte ratios (p = 0.02) and neutrophil-to-platelet ratios (p = 0.04). At 6-month follow-up, 9 (60%) patients with sICH died, versus 18% of patients without sICH (p < 0.001). Only 1 (7%) patient with sICH had a good functional outcome, defined as an mRS score of 0 to 2, versus 51% of patients without sICH. (4) Conclusions: one in twelve ischemic stroke patients treated with bridging therapy suffered sICH. Given the observed poor outcomes after sICH, further studies are required to better identify patients at risk to help clinicians in guiding therapeutic strategies.

Association between intracranial vessel calcifications, structural brain damage, and cognitive impairment after minor strokes: a prospective study.

Vascular calcifications are a hallmark of atherosclerosis, and in the coronary arteries are routinely used as a prognostic marker. Calcifications of intracranial vessels (ICC) are frequently observed on non-contrast CT (NCCT) and their effect on post-stroke cognitive impairment (PSCI) remains unclear. Our aim was to explore the association of ICC with prospective long-term cognitive function and advanced MRI-measures in a large prospective cohort of cognitively intact mild stroke survivors. Data from the Tel-Aviv brain acute stroke cohort (TABASCO) study [ClinicalTrials.gov #NCT01926691] were analyzed. This prospective cohort study (n = 575) aimed to identify predictors of PSCI, in cognitively intact mild stroke survivors. A quantitative assessment of the intracranial calcium content - The ICC score (ICCS) was calculated semi-automatically on NCCT using a validated calcium quantification application. Participants underwent a 3 T-MRI and prospective comprehensive cognitive clinical and laboratory assessments at enrollment, 6, 12, and 24-months. Data were available for 531 participants (67.4 years, 59.5% males). The incidence of PSCI at two-years doubled in the high ICCS group (26% vs. 13.7%, p < 0.001). The high ICCS group had significantly greater small-vessel-disease (SVD) tissue changes and reduced microstructural-integrity assessed by Diffusion-Tensor-Imaging (DTI) maps (p < 0.05 for all). In multivariate analysis, a higher ICCS was independently associated with brain atrophy manifested by lower normalized white and gray matter, hippocampal and thalamic volumes (β = -0.178, β = -0.2, β = -0.137, β = -0.157; p < 0.05) and independently predicted PSCI (OR 1.83, 95%CI 1.01-3.35). Our findings suggest that the ICCS, which is a simple and readily available imaging marker on NCCT, is associated with brain atrophy, microstructural damage, the extent of SVD, and may predict PSCI. This finding has implications for identifying individuals at risk for PSCI and implementing targeted interventions to mitigate this risk.

Hypocalcemia in thalassemia major patients requires an extra-careful approach

Thalassemia is a hematological disorder caused by a gene mutation that leads to defective synthesis of hemoglobin complex. One of the complications of thalassemia is hypocalcemia which is presented with paresthesia, muscle spasm, low-serum calcium, and intracranial calcification. Hypocalcemia can affect thalassemic patients via various mechanisms. Blood transfusion-related and transfusion-independent iron overload, drug side effects, vitamin D3 deficiency, and genetic disorders and polymorphisms are among the etiologies of hypocalcemia in major thalassemia. A careful approach to the differential etiology of this phenomenon is crucial for a resultful treatment.