Background and Clinical Significance: Intracranial dermoid cysts (IDCs) are rare benign congenital intracranial lesions. In the case of IDC rupture, these lesions may manifest clinically. Cysts may be visualized on non-enhanced computed tomography (NECT) and magnetic resonance imaging (MRI), facilitating discussions between clinicians and radiologists to determine cyst content and potential dissemination in cases of rupture. This case report describes an IDC rupture presenting as fat-containing lesions in the subarachnoid space and ventricular system, resembling a subarachnoid hemorrhage on MRI. Case Presentation: A thirty-two-year-old Caucasian male patient was admitted to the hospital due to recurrent headaches and visual impairment that began at the age of thirty-one. MRI revealed a lesion radiologically consistent with a ruptured dermoid or epidermoid cyst in the anterior fossa with a mass effect on the optic nerve intracranial segments, the chiasma opticum, and proximal optic tracts. The patient underwent a successful neurosurgical resection of the lesion, and histopathological analysis confirmed the diagnosis of a dermoid cyst. The postoperative period was uneventful. MRI follow-up revealed residual tissue of the IDC without any volume increase. Multiple punctate fat-containing lesions were noted, similar to previous MRIs. The patient reported no complaints at discharge. Follow-up MRI imaging demonstrated no recurrence or progression of the dermoid cyst at 4 months, 1 year, and 2 years. Conclusions: IDC rupture is a rare event that may present clinically and appear as a blooming artifact on MRI, mimicking subarachnoid hemorrhage. Fat-containing lesions in the subarachnoid space and ventricular system can demonstrate findings indicative of an IDC rupture. MRI diffusion-weighted imaging (DWI) and decreased apparent diffusion coefficient (ADC) values may mimic an epidermoid cyst, a phenomenon rarely described in the literature, further complicating the diagnostic process.
Background and objectives: Recurrence of venous thromboembolism (VTE) after a primary event is common; however, no sufficient risk scores have been widely introduced in clinical practice. The aim of this study was to assess the risk factors for VTE recurrences, as well as the effect of treatment strategies on the recurrence rate in a single-center patient cohort. Materials and Methods: The prospective cohort study included consecutive patients in a single center from June 2014 till June 2018 presenting with acute VTE confirmed by imaging tests. All patients were followed up for at least one year or till death. Statistical analyses were conducted using IBM SPSS Statistics 23 and Stata 13. Competing risk of death was considered. Results: A total of 219 eligible patients were identified during the study period. Pulmonary embolism with or without deep vein thrombosis (DVT) was present in 95.9% (n = 210), isolated DVT was present in 4.1% (n = 9) of patients. The total number of documented recurrences was 13 (5.9%). Incidence rate was 5.6 per 100 person-years. Recurrent VTE predicted significantly higher mortality rate (hazard ratio (HR) 6.64 [95% CI 2.61–16.93]). In univariate analysis, active cancer was associated with higher recurrence rate (p = 0.036). In competing-risks regression model (with death as the competing risk), active cancer (subdistribution hazard ratio (SHR) 2.11 (95% CI 0.58–7.76)) did not retain statistical significance for VTE recurrence. Discontinuation and duration of anticoagulant treatment (≤6 or >6 months), and drug class in acute or long-term therapy (parenteral, vitamin K antagonist (VKA), direct oral anticoagulant (DOAC)) were not associated with recurrences (p > 0.05). Conclusions: Patients who experienced recurrent VTE had 6.6-fold higher mortality rate than patients with no recurrences. The presence of active cancer was not a statistically significant risk factor for recurrence when taking into account the competing risk of death. Duration and drug class of anticoagulation did not seem to impact recurrence rate.
Background and Objectives: COVID-19 disease, caused by the SARS-CoV-2 virus, has presented significant challenges to global health, with acute and chronic implications for various aspects of well-being, including sleep and quality of life. This study aimed to investigate the impact of SARS-CoV-2 infection on sleep quality, daytime sleepiness, and quality of life in hospitalised and home-treated patients after three and six months. Materials and Methods: A longitudinal cohort study was conducted, enrolling hospitalised patients from a single clinical university hospital and home-treated participants through a survey spread through social networks. Individuals who had tested positive for the SARS-CoV-2 virus in the past three months and had a symptomatic course of the disease were included in the study. Participants with previously diagnosed sleep disorders were excluded from the study. Participants were evaluated using internationally validated self-evaluation scales, including the Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Patient Health Questionnaire-9 (PHQ-9) and Fatigue Severity Scale (FSS). Data were collected three and six months after laboratory-confirmed SARS-CoV-2 infection, with informed consent obtained from all participants. Statistical analysis was performed using the Wilcoxon signed rank test, Fisher–Freeman–Halton exact, Pearson Chi tests and Spearman correlation. Results were considered statistically significant with p value < 0.05. Results: In total, 66 participants with a mean age of 44.05 ± 21.61 years were enrolled in the study. Most patients (n = 36) were treated at home and 30 at hospital. Six months after SARS-CoV-2 infection, home-treated patients reported a higher prevalence of poor sleep quality (52.8%, n = 19, p = 0.015, PSQI) and hospitalised patients showed a lower prevalence of depressive symptoms (p < 0.001, PHQ-9) as 90% (n = 27) had minimal or no symptoms compared to 30.6% (n = 11) in a home-treated group. Conclusions: These findings mark the importance of the COVID-19 patients’ management settings as people treated at home had worse sleep quality and more depressive symptoms six months after infection indicating worse life quality.
Background. Intracranial dermoid cysts (IDC) are rare benign congenital intracranial lesions. In the case of IDC rupture, these lesions may manifest clinically. Cysts may be visualized on non-enhanced computed tomography (NECT) and magnetic resonance imaging (MRI), facilitating discussions between clinicians and radiologists to determine cyst content and potential dissemination in cases of rupture. This case report describes an IDC rupture presenting as fat-containing lesions in the subarachnoid space and ventricular system, resembling a subarachnoid hemorrhage on MRI. Case report. A thirty-two-year-old Caucasian male patient was admitted to the hospital due to recurrent headache and visual impairment that began at the age of thirty-one. MRI revealed a lesion radiologically consistent with a ruptured dermoid or epidermoid cyst in the anterior fossa with a mass effect on the optic nerve intracranial segments, the chiasma opticum, and proximal optic tracts. The patient underwent a successful neurosurgical resection of the lesion, and histopathological analysis confirmed the diagnosis of a dermoid cyst. The postoperative period was uneventful. MRI follow-up revealed residual tissue of the IDC without any volume increase. Multiple punctate fat-containing lesions were noted, similar to previous MRI. The patient reported no complaints at discharge. Follow-up MRI imaging demonstrated no recurrence or progression of the dermoid cyst at 4 months, 1 year, and 2 years. Conclusion. IDC rupture is a rare event that may present clinically and appear as a blooming artifact on MRI, mimicking subarachnoid hemorrhage. Fat-containing lesions in the subarachnoid space and ventricular system can demonstrate findings indicative of an IDC rupture. MRI diffusion-weighted imaging (DWI) and decreased apparent diffusion coefficient (ADC) values may mimic an epidermoid cyst, a phenomenon rarely described in the literature, further complicating the diagnostic process.
Background: Unilateral basal ganglia calcinosis (BGC) is a rare radiological finding that can be diagnosed on computed tomography (CT) and magnetic resonance imaging (MRI) but often presents challenges for clinicians and radiologists in determining its underlying cause. So far, only a few potential causes that could explain unilateral BGC have been described in the literature. Case Report: A 54-year-old Caucasian male was admitted to a tertiary university hospital due to the sudden onset of speech impairment and right-sided weakness. The patient had no significant medical history prior to this event. Non-enhanced computed tomography (NECT) of the brain revealed no evidence of acute ischemia; CT angiography (CTA) showed acute left middle cerebral artery (MCA) M2 segment occlusion. CT perfusion (CTP) maps revealed an extensive penumbra-like lesion, which is potentially reversible upon achieving successful recanalization. However, a primary neoplastic tumor with calcifications in the basal ganglia was initially interpreted as the potential cause; therefore, acute stroke treatment with intravenous thrombolysis was contraindicated. A follow-up CT examination at 24 h revealed an ischemic lesion localized to the left insula, predominantly involving the left parietal lobe and the superior gyrus of the left temporal lobe. Subsequent gadolinium-enhanced brain MRI revealed small blood vessels draining into the subependymal periventricular veins on the left basal ganglia. Digital subtraction angiography was conducted, confirming the diagnosis of venous angioma. Conclusions: Unilateral BGC caused by venous angioma is a rare entity with unclear pathophysiological mechanisms and heterogeneous clinical presentation. It may mimic conditions such as intracerebral hemorrhage or hemorrhagic brain tumors, complicating acute stroke management, as demonstrated in this case. Surrounding tissue calcification may provide a valuable radiological clue in diagnosing venous angiomas DVAs and vascular malformations.