Interrelation between Spectral Online Monitoring and Postoperative T1-Weighted MRI in Interstitial Photodynamic Therapy of Malignant Gliomas

In a former study, interstitial photodynamic therapy (iPDT) was performed on patients suffering from newly diagnosed glioblastoma (n = 11; 8/3 male/female; median age: 68, range: 40–76). The procedure includes the application of 5-ALA to selectively metabolize protoporphyrin IX (PpIX) in tumor cells and illumination utilizing interstitially positioned optical cylindrical diffuser fibers (CDF) (2–10 CDFs, 2–3 cm diffusor length, 200 mW/cm, 635 nm, 60 min irradiation). Intraoperative spectral online monitoring (SOM) was employed to monitor treatment light transmission and PpIX fluorescence during iPDT. MRI was used for treatment planning and outcome assessment. Case-dependent observations included intraoperative reduction of treatment light transmission and local intrinsic T1 hyperintensity in non-contrast-enhanced T1-weighted MRI acquired within one day after iPDT. Intrinsic T1 hyperintensity was observed and found to be associated with the treatment volume, which indicates the presence of methemoglobin, possibly induced by iPDT. Based on SOM data, the optical absorption coefficient and its change during iPDT were estimated for the target tissue volumes interjacent between evaluable CDF-pairs at the treatment wavelength of 635 nm. By spatial comparison and statistical analysis, it was found that observed increases of the absorption coefficient during iPDT were larger in or near regions of intrinsic T1 hyperintensity (p = 0.003). In cases where PpIX-fluorescence was undetectable before iPDT, the increase in optical absorption and intrinsic T1 hyperintensity tended to be less. The observations are consistent with in vitro experiments and indicate PDT-induced deoxygenation of hemoglobin and methemoglobin formation. Further investigations are needed to provide more data on the time course of the observed changes, thus paving the way for optimized iPDT irradiation protocols.

A Case Report on Tuberculous Meningitis

Introduction: The most common cause of tuberculous meningitis is a hematogenous spread of mycobacteria from the lungs. tuberculous meningitis is a fatal disease. Symptoms typically worsen over time, and there are three clinical stages to the disease (prodromal phase, phase of neurological symptoms and phase of paresis) Case Presentation: The chief complaint of a one-year-old boy was fever, irritability, vomiting, and Generalized Tonic-Clonic Seizure convulsions. The patient's pupils were found to be unequal on physical examination, prompting a repeat neuroimaging. It was done on MRI (magnetic resonance imaging) with T1 hyperintensity on T2 and restricted diffusion on DWI (diffusion-weighted imaging) he has not improved after taking treatment and the patient is on a ventilator as well, we nasogastric tube also. I was receiving treatment and will continue to do so until the end of my care. Conclusion: In our environment, tuberculous meningitis that presents late is not uncommon. It arrived late at our medical facility. After a full recovery, the patient's comprehensive health care team collaborates to help him regain his previous level of independence and satisfaction. This report is intended to raise clinician awareness of tuberculous meningitis' unusual clinical presentation. Tuberculous meningitis is treated holistically with a focus on medical and nursing management.

Don’t Forget That Chorea!

Background: Hemichorea-hemiballismus is a spectrum of involuntary, continuous non-patterned movement involving one side of the body. Possible causes of hemichorea-hemiballismus include haemorrhagic or ischemic stroke, neoplasm, systemic lupus erythematosus, NHH (non-ketotic hyperglycaemic hemichorea), Wilson’s disease, and thyrotoxicosis. Amongst the metabolic causes, chorea associated with NHH is noteworthy and is mainly reported in elderly Asian women. The pathophysiology of this syndrome remains controversial. It is likely that a combination of hyperglycaemia induced basal ganglia metabolic derangement and failure of cerebral blood flow autoregulation contribute to the syndrome.Case presentation: A 45-year-old Malay gentleman presented to our Emergency Department with right upper and lower limb weakness associated with hemichorea for 3-4 days. His initial blood glucose level was 22 mg/dl with normal serum ketone and bicarbonate levels. CT brain showed a hyperdensity in the left caudate nucleus and globus pallidus region. Subsequent brain MRI revealed an asymmetric T1 hyperintensity of the left putamen. This specific finding was compatible with hyperglycaemia-induced hemichorea-hemiballismus syndrome. The hemiballismus/hemichorea improved rapidly within the next day. Conclusions: This unusual clinical presentation is often accompanied by severe hyperglycaemia. Appropriate blood glycaemic control is important because it is reversible with correction of hyperglycaemia. Thus, prompt recognition and treatment is essential to avoid adverse outcomes.

Detecting neonatal acute bilirubin encephalopathy based on T1-weighted MRI images and learning-based approaches

Background Neonatal hyperbilirubinemia is a common clinical condition that requires medical attention in newborns, which may develop into acute bilirubin encephalopathy with a significant risk of long-term neurological deficits. The current clinical challenge lies in the separation of acute bilirubin encephalopathy and non-acute bilirubin encephalopathy neonates both with hyperbilirubinemia condition since both of them demonstrated similar T1 hyperintensity and lead to difficulties in clinical diagnosis based on the conventional radiological reading. This study aims to investigate the utility of T1-weighted MRI images for differentiating acute bilirubin encephalopathy and non-acute bilirubin encephalopathy neonates with hyperbilirubinemia. Methods 3 diagnostic approaches, including a visual inspection, a semi-quantitative method based on normalized the T1-weighted intensities of the globus pallidus and subthalamic nuclei, and a deep learning method with ResNet18 framework were applied to classify 47 acute bilirubin encephalopathy neonates and 32 non-acute bilirubin encephalopathy neonates with hyperbilirubinemia based on T1-weighted images. Chi-squared test and t-test were used to test the significant difference of clinical features between the 2 groups. Results The visual inspection got a poor diagnostic accuracy of 53.58 ± 5.71% indicating the difficulty of the challenge in real clinical practice. However, the semi-quantitative approach and ResNet18 achieved a classification accuracy of 62.11 ± 8.03% and 72.15%, respectively, which outperformed visual inspection significantly. Conclusion Our study indicates that it is not sufficient to only use T1-weighted MRI images to detect neonates with acute bilirubin encephalopathy. Other more MRI multimodal images combined with T1-weighted MRI images are expected to use to improve the accuracy in future work. However, this study demonstrates that the semi-quantitative measurement based on T1-weighted MRI images is a simple and compromised way to discriminate acute bilirubin encephalopathy and non-acute bilirubin encephalopathy neonates with hyperbilirubinemia, which may be helpful in improving the current manual diagnosis.

Imaging findings of trichilemmal cyst and proliferating trichilemmal tumour

Purpose The purpose of this study was to evaluate computed tomography and magnetic resonance imaging of benign trichilemmal cysts and proliferating trichilemmal tumours. Methods Nineteen histologically confirmed cutaneous lesions with trichilemmal keratinisation (12 trichilemmal cysts and seven proliferating trichilemmal tumours) were enrolled. Among them, 10 lesions (six trichilemmal cysts and four proliferating trichilemmal tumours) were examined by computed tomography, while 13 lesions (eight trichilemmal cysts and five proliferating trichilemmal tumours) were examined by magnetic resonance imaging. Computed tomography and magnetic resonance imaging characteristics were retrospectively reviewed. RESULTS Sixteen lesions (84%, 10 trichilemmal cysts and six proliferating trichilemmal tumours) occurred on the scalp. Lobulated margins were observed in five lesions (26%, three trichilemmal cysts and two proliferating trichilemmal tumours). With respect to computed tomography attenuation, calcification (>200 Hounsfield units) was observed in seven lesions (70%, five trichilemmal cysts and two proliferating trichilemmal tumours), hyperdense areas (≥80 and ≤200 Hounsfield units) in six (60%, three trichilemmal cysts and three proliferating trichilemmal tumours), and soft tissue density areas (<80 Hounsfield units) in nine (90%, five trichilemmal cysts and four proliferating trichilemmal tumours). On T1-weighted images, intratumoral hyperintensity was only observed in eight trichilemmal cysts but no proliferating trichilemmal tumours (100% vs. 0%, P<0.01). On T2-weighted images, hypointense rim and intratumoral hypointensity was observed in all 13 lesions (100%, eight trichilemmal cysts and five proliferating trichilemmal tumours), and linear or reticular hypointensity was observed in 10 (77%, six trichilemmal cysts and four proliferating trichilemmal tumours). Conclusion Trichilemmal cysts and proliferating trichilemmal tumours predominantly occurred on the scalp with calcification, and usually exhibited linear or reticular T2 hypointensity. Intratumoral T1 hyperintensity may be a useful imaging feature for differentiating trichilemmal cysts from proliferating trichilemmal tumours.

Abstract 35: Vessel Wall Magnetic Resonance Imaging Biomarkers of Symptomatic Intracranial Atherosclerosis: A Meta-Analysis

Background: Intracranial vessel wall MR imaging (VWI) may be able to identify imaging biomarkers of symptomatic plaque. A meta-analysis was performed to evaluate the strength of association of imaging features of symptomatic plaque on VWI and downstream ischemia. Methods: PubMed, Scopus, Web of Science, EMBASE and Cochrane databases were searched up to October 2019. Studies evaluating acute/subacute cerebrovascular ischemia using VWI on 1.5 or 3 Tesla MR were included. Studies with insufficient exclusion of other stroke etiologies, insufficient or duplicated data and conference abstracts were excluded. Two independent reviewers extracted data on study design, VWI techniques, imaging endpoints, and conducted a study design risk bias assessment using the QUADAS-2 tool. Per-lesion odds ratios (OR) were calculated and pooled using a bivariate random-effects model. Subgroup analyses and evaluation of publication bias were performed. Results: Twenty-one articles met inclusion criteria (1,750 lesions; 1,542 subjects). Plaque enhancement (OR 7.4, 95% CI 3.4-16.4; Figure), positive remodeling (OR 5.6, 95% CI 2.2-14.0), surface irregularity (OR 4.5, 95% CI 1.4-8.6), and T1 hyperintensity (OR 2.1, 95% CI 1.3-3.3) were significantly associated with downstream ischemia. T2 signal intensity was not significant (p=0.59). Plaque enhancement showed stronger associations when measured in retrospectively designed studies (OR 35.3, 95% CI 7.4-141, p=0.02), by a radiologist as a rater (OR 12.6, 95% CI 5.3-29.7, p<0.001), and on VWI pulse sequences with lower spatial resolution (OR 30.4, 95% CI 7.0-132.4, p=0.02). There was no publication bias (Egger’s test p=0.48). Conclusions: Plaque enhancement, positive remodeling, T1 hyperintensity and surface irregularity emerged as imaging biomarkers of symptomatic plaque. Plaque enhancement had the strongest association and remained significant accounting for sources of bias and variability in both study design and instrument.