Improved Visualization and Quantification of Net Water Uptake in Recent Small Subcortical Infarcts in the Thalamus Using Computed Tomography.

Diagnosing recent small subcortical infarcts (RSSIs) via early computed tomography (CT) remains challenging. This study aimed to assess CT attenuation values (Hounsfield Units (HU)) and net water uptake (NWU) in RSSI and explore a postprocessing algorithm's potential to enhance thalamic RSSI detection. We examined non-contrast CT (NCCT) data from patients with confirmed thalamic RSSI on diffusion-weighted magnetic resonance imaging (DW-MRI) between January 2010 and October 2017. Co-registered DW-MRI and NCCT images enabled HU and NWU quantification in the infarct area compared to unaffected contralateral tissue. Results were categorized based on symptom onset to NCCT timing. Postprocessing using window optimization and frequency-selective non-linear blending (FSNLB) was applied, with interpretations by three blinded Neuroradiologists. The study included 34 patients (median age 70 years [IQR 63-76], 14 women). RSSI exhibited significantly reduced mean CT attenuation compared to unaffected thalamus (29.6 HU (±3.1) vs. 33.3 HU (±2.6); p < 0.01). Mean NWU in the infarct area increased from 6.4% (±7.2) at 0-6 h to 16.6% (±8.7) at 24-36 h post-symptom onset. Postprocessed NCCT using these HU values improved sensitivity for RSSI detection from 32% in unprocessed CT to 41% in FSNLB-optimized CT, with specificities ranging from 86% to 95%. In conclusion, CT attenuation values and NWU are discernible in thalamic RSSI up to 36 h post-symptom onset. Postprocessing techniques, particularly window optimization and FSNLB, moderately enhance RSSI detection.

Comorbid cerebral amyloid angiopathy in dementia and prodromal stages-Prevalence and effects on cognition.

OBJECTIVES: To determine the contribution of cerebral amyloid angiopathy to cognitive impairment in MCI and dementia. METHODS: Patients with subjective memory impairment (SMI), amnestic and non-amnestic mild cognitive impairment ((n)aMCI), Alzheimer's disease (AD), mixed and vascular dementia (MD/VD) from our memory clinic were included in this retrospective analysis. Patients underwent neuropsychological testing and cranial magnetic resonance imaging (MRI). Magnetic resonance imaging data sets were analyzed regarding the presence of CAA-related MRI biomarkers to determine CAA prevalence. ANOVAs were used to investigate the contribution of CAA to cognitive impairment within diagnostic groups and to determine whether differences in cognitive test performance between the diagnostic groups are mediated by total CAA burden. RESULTS: 475 patients (222 male, 253 female) with SMI (n = 47), naMCI (n = 41), aMCI (n = 189), early AD (n = 9), AD (n = 114), MD (n = 71) and VD (n = 4) were included. Mean age was 73.2 (9.9) years. CAA prevalence was 14.9% in SMI, 14.6% in naMCI, 24.3% in aMCI, 22.2% in early onset AD, 18.4% in late onset AD, 46.5% in MD and 25% in VD. Patients with possible and probable CAA were older than patients without CAA. In particular, diagnosis of aMCI, early onset AD, MD and VD showed high CAA prevalence. In AD but not in aMCI, CAA diagnosis significantly influenced test performance in the CERAD word list recall (F (1,78) = 4505; p = 0.037; partial eta-square = 0.055). Differences in cognitive test performance between the diagnostic groups of naMCI, aMCI, AD and MD were mediated by total CAA burden within AAT simply nouns subtest (F (2,39) = 4059; p = 0.025; partial eta-square = 0.172) and in CERAD verbal fluency test (F (3,129) = 3533; p = 0.017; partial eta-square = 0.076). CONCLUSION: This retrospective analysis demonstrates high prevalence rates of CAA in cognitive diagnoses. Our data suggest that comorbid CAA independently impacts cognitive test performance in the course of AD with presumably stage-dependent effects. Especially in patients with AD comorbid CAA additionally impairs memory function. Total CAA small vessel disease burden further modulates psychometric differences in cognitive test performance between diagnostic groups regarding word finding and word fluency capabilities.

Increased relative biological effectiveness and periventricular radiosensitivity in proton therapy of glioma patients.

PURPOSE: Currently, there is an intense debate on variations in intra-cerebral radiosensitivity and relative biological effectiveness (RBE) in proton therapy of primary brain tumours. Here, both effects were retrospectively investigated using late radiation-induced brain injuries (RIBI) observed in follow-up after proton therapy of patients with diagnosed glioma. METHODS: In total, 42 WHO grade 2-3 glioma patients out of a consecutive patient cohort having received (adjuvant) proton radio(chemo)therapy between 2014 and 2017 were eligible for analysis. RIBI lesions (symptomatic or clinically asymptomatic) were diagnosed and delineated on contrast-enhanced T1-weighted magnetic resonance imaging scans obtained in the first two years of follow-up. Correlation of RIBI location and occurrence with dose (D), proton dose-averaged linear energy transfer (LET) and variable RBE dose parameters were tested in voxel- and in patient-wise logistic regression analyses. Additionally, anatomical and clinical parameters were considered. Model performance was estimated through cross-validated area-under-the-curve (AUC) values. RESULTS: In total, 64 RIBI lesions were diagnosed in 21 patients. The median time between start of proton radio(chemo)therapy and RIBI appearance was 10.2 months. Median distances of the RIBI volume centres to the cerebral ventricles and to the clinical target volume border were 2.1 mm and 1.3 mm, respectively. In voxel-wise regression, the multivariable model with D, D × LET and periventricular region (PVR) revealed the highest AUC of 0.90 (95 % confidence interval: 0.89-0.91) while the corresponding model without D × LET revealed a value of 0.84 (0.83-0.86). In patient-level analysis, the equivalent uniform dose (EUD11, a = 11) in the PVR using a variable RBE was the most prominent predictor for RIBI with an AUC of 0.63 (0.32-0.90). CONCLUSIONS: In this glioma cohort, an increased radiosensitivity within the PVR was observed as well as a spatial correlation of RIBI with an increased RBE. Both need to be considered when delivering radio(chemo)therapy using proton beams.

Rapidly Evolving Diffuse Omental Carcinomatosis of Prostate Cancer in 68Ga-PSMA PET/CT.

ABSTRACT: An 81-year-old man received androgen deprivation therapy for a locally advanced prostate cancer and, 6 months later, a curative radiation therapy. Half a year later, the patient presented with a steeply increased PSA value (32 ng/mL) and a suppressed testosterone level (0.48 nmol/L). The consecutively performed 68Ga-PSMA PET/CT revealed, besides local tumor remains and several PSMA-positive lymph node and soft tissue metastases, an extensive, diffuse PSMA ligand accumulation in the omentum, which was immunohistochemically proven to be a carcinomatosis of prostate cancer. None of the extraprostatic lesions were present in the pretherapeutic PSMA PET 1 year ago.

Disseminated inflammation of the central nervous system associated with acute hepatitis E: a case report.

BACKGROUND: Hepatitis E infection affects over 20 million people worldwide. Reports of neurological manifestations are largely limited to the peripheral nervous system. We report a middle-aged genotype 3c male patient with acute hepatitis E virus (HEV) infection and severe neurological deficits with evidence of multiple disseminated inflammatory lesions of the central nervous system. CASE PRESENTATION: A 42-year-old male patient presented to our emergency department with musculoskeletal weakness, bladder and bowel retention, blurred vision and ascending hypoesthesia up to the level of T8. Serology showed elevated liver enzymes and positive IgM-titers of hepatitis E. Analysis of cerebrospinal fluid (CSF) showed mild pleocytosis and normal levels of glucose, lactate and protein. HEV-RNA-copies were detected in the CSF and stool. Within 3 days after admission the patient became paraplegic, had complete visual loss and absent pupillary reflexes. MRI showed inflammatory demyelination of the optic nerve sheaths, multiple subcortical brain regions and the spinal cord. Electrophysiology revealed axonal damage of the peroneal nerve on both sides with absent F-waves. Treatment was performed with methylprednisolone, two cycles of plasma exchange (PLEX), one cycle of intravenous immunoglobulins (IVIG) and ribavirin which was used off-label. Liver enzymes normalized after 1 week and serology was negative for HEV-RNA after 3 weeks. Follow-up MRI showed progressive demyelination and new leptomeningeal enhancement at the thoracic spine and cauda equina 4 weeks after admission. Four months later, after rehabilitation was completed, repeated MRI showed gliotic transformation of the spinal cord without signs of an active inflammation. Treatment with rituximab was initiated. The patient remained paraplegic and hypoesthesia had ascended up to T5. Nevertheless, he regained full vision. CONCLUSIONS: Our case indicates a possible association of acute HEV infection with widespread disseminated central nervous system inflammation. Up to now, no specific drugs have been approved for the treatment of acute HEV infection. We treated our patient off-label with ribavirin and escalated immunomodulatory therapy considering clinical progression and the possibility of an autoimmune response targeting nerve cell structures. While response to treatment was rather limited in our case, detection of HEV in patients with acute neurological deficits might help optimize individual treatment strategies.