BACKGROUND: Acute ischemic stroke causes irreversible damage to the brain parenchyma surrounded by salvageable tissue known as the ischemic penumbra. Magnetic resonance imaging (MRI), particularly the mismatch between abnormal diffusion-weighted imaging (DWI) signals and normal fluid-attenuated inversion recovery (FLAIR) signals, plays a critical role in detecting ischemic penumbra. It also allows for the identification of patients who may benefit from reperfusion therapy. Hence, this prospective cohort study aimed to explore the correlation between DWI-FLAIR mismatch and clinical outcomes in acute ischemic stroke patients, specifically those with delayed or uncertain symptom onset, offering potential insights into reperfusion therapy.
METHODS: A total of 38 thrombotic stroke patients aged above 18 were included in this prospective cohort study. Baseline data, including demographics, lifestyle factors, and medical history, were recorded. DWI-FLAIR mismatch was evaluated through brain MRI within 4.5 hours to 12 hours of symptom onset.
RESULTS:  Of the cohort, 63.2% were males, predominantly in the 61-70 age group. Smoking and alcohol consumption were reported by 15.79% each. DWI-FLAIR mismatch was present in 20 out of 38 subjects. No statistically significant differences were noted in the mean National Institutes of Health Stroke Scale (NIHSS) and Modified Rankin Scale (MRS) scores between subjects with and without DWI-FLAIR mismatch. Thrombolysis in wake-up stroke subjects demonstrated a substantial reduction in mean MRS at discharge (1.29±0.95) and at six to eight weeks (1.71±1.11), suggesting potential benefits on functional outcomes.
CONCLUSIONS:  The prevalence of DWI-FLAIR mismatch was seen in the majority of patients beyond their window period and also showed beneficiary outcomes with a mean reduction in NHISS and MRS scores following thrombolysis.

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OBJECTIVE: This study aimed to determine the risk factors and stroke subtypes for young ischemic stroke patients and their outcomes at the time of discharge.
METHODS: This is a retrospective cross-sectional study of ischemic stroke patients (n = 264) between the age groups of 18 and 45. The study population was divided into two broad age groups: 18 to 35 years and 36 to 45 years; and compared based on demographics, risk factors, the Trial of Org 10172 in Acute Stroke Treatment (TOAST) classification, and outcomes. The outcomes were compared based on the National Institutes of Health Stroke Scale (NIHSS) and Modified Rankin Scale (MRS) systems at the time of admission and discharge.
RESULTS: The mean age of patients was 37.84±6.19 years. The male-to-female ratio was 2.5:1. The most common vascular risk factors identified were diabetes (29.16%), hypertension (49.62%), dyslipidaemia (DLP, 44.4%), and smoking (10.9%). The most common TOAST subtype was large vessel disease (38.63%), followed by the undetermined category (35.6%). The elderly group showed a high proportion of strokes secondary to small vessel disease (14.13%; p = 0.03), while cardioembolic strokes were common in the female subgroup (p = 0.05). The majority of strokes were in the anterior circulation (66.6%) as compared to the posterior (25.75%), and nearly 50% of the patients had intracranial disease. Overall, there was a favourable MRS outcome at discharge.
CONCLUSIONS: Conventional vascular risk factors are equally prevalent, even among young stroke patients. The benchmark for young stroke age is showing a downward shift as more stroke patients above the age of 35 are showing similar risk factor trends as those of their older counterparts. The majority of stroke burden still falls under the undermined category, which requires aggressive risk factor identification and management.

We aim to assess a straightforward technique to enhance spectral quality in the brain, particularly in the cerebellum, during 7 T MRI scans. This is achieved through a wireless RF array insert designed to mitigate signal dropouts caused by the limited transmit field efficiency in the inferior part of the brain. We recently developed a wireless RF array to improve MRI and 1H-MRS at 7 T by augmenting signal via inductive coupling between the wireless RF array and the MRI coil. In vivo experiments on a Siemens 7 T whole-body human scanner with a Nova 1Tx/32Rx head coil quantified the impact of the dorsal cervical array in improving signal in the posterior fossa, including the cerebellum, where the transmit efficiency of the coil is inherently low. The 1H-MRS experimental protocol consisted of paired acquisition of data sets, both with and without the RF array, using the semi-LASER and SASSI sequences. The overall results indicate that the localized 1H-MRS is improved significantly in the presence of the array. Comparison of in vivo 1H-MRS plots in the presence versus absence of the array demonstrated an average SNR enhancement of a factor of 2.2. LCModel analysis reported reduced Cramér-Rao lower bounds, indicating more confident fits. This wireless RF array can significantly increase detection sensitivity. It may reduce the RF transmission power and data acquisition time for 1H-MRS and MRI applications, specifically at 7 T, where 1H-MRS requires a high-power RF pulse. The array could provide a cost-effective and efficient solution to improve detection sensitivity for human 1H-MRS and MRI in the regions with lower transmit efficiency.

UNASSIGNED: Evidence from animal and human studies suggests glutamatergic dysfunction in posttraumatic stress disorder (PTSD). The purpose of this study was to investigate glutamate abnormalities in the dorsolateral prefrontal cortex (DLFPC) of individuals with PTSD using 7T MRS, which has better spectral resolution and signal-to-noise ratio than lower field strengths, thus allowing for better spectral quality and higher sensitivity. We hypothesized that individuals with PTSD would have lower glutamate levels compared to trauma-exposed individuals without PTSD and individuals without trauma exposure. Additionally, we explored potential alterations in other neurometabolites and the relationship between glutamate and psychiatric symptoms.
UNASSIGNED: Individuals with PTSD (n=27), trauma-exposed individuals without PTSD (n=27), and individuals without trauma exposure (n=26) underwent 7T MRS to measure glutamate and other neurometabolites in the left DLPFC. The severities of PTSD, depression, anxiety, and dissociation symptoms were assessed.
UNASSIGNED: We found that glutamate was lower in the PTSD and trauma-exposed groups compared to the group without trauma exposure. Furthermore, N-acetylaspartate (NAA) was lower and lactate was higher in the PTSD group compared to the group without trauma exposure. Glutamate was negatively correlated with depression symptom severity in the PTSD group. Glutamate was not correlated with PTSD symptom severity.
UNASSIGNED: In this first 7T MRS study of PTSD, we observed altered concentrations of glutamate, NAA, and lactate. Our findings provide evidence for multiple possible pathological processes in individuals with PTSD. High-field MRS offers insight into the neurometabolic alterations associated with PTSD and is a powerful tool to probe trauma- and stress-related neurotransmission and metabolism in vivo.

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Proton MRS is used clinically to collect localized, quantitative metabolic data from living tissues. However, the presence of baselines in the spectra complicates accurate MRS data quantification. The occurrence of baselines is not specific to short-echo-time MRS data. In short-echo-time MRS, the baseline consists typically of a dominating macromolecular (MM) part, and can, depending on B0 shimming, poor voxel placement, and/or localization sequences, also contain broad water and lipid resonance components, indicated by broad components (BCs). In long-echo-time MRS, the MM part is usually much smaller, but BCs may still be present. The sum of MM and BCs is denoted by the baseline. Many algorithms have been proposed over the years to tackle these artefacts. A first approach is to identify the baseline itself in a preprocessing step, and a second approach is to model the baseline in the quantification of the MRS data themselves. This paper gives an overview of baseline handling algorithms and also proposes a new algorithm for baseline correction. A subset of suitable baseline removal algorithms were tested on in vivo MRSI data (semi-LASER at TE = 40 ms) and compared with the new algorithm. The baselines in all datasets were removed using the different methods and subsequently fitted using spectrIm-QMRS with a TDFDFit fitting model that contained only a metabolite basis set and lacked a baseline model. The same spectra were also fitted using a spectrIm-QMRS model that explicitly models the metabolites and the baseline of the spectrum. The quantification results of the latter quantification were regarded as ground truth. The fit quality number (FQN) was used to assess baseline removal effectiveness, and correlations between metabolite peak areas and ground truth models were also examined. The results show a competitive performance of our new proposed algorithm, underscoring its automatic approach and efficiency. Nevertheless, none of the tested baseline correction methods achieved FQNs as good as the ground truth model. All separately applied baseline correction methods introduce a bias in the observed metabolite peak areas. We conclude that all baseline correction methods tested, when applied as a separate preprocessing step, yield poorer FQNs and biased quantification results. While they may enhance visual display, they are not advisable for use before spectral fitting.

Ischemic stroke is a significant public health concern, with its incidence expected to double over the next 40 years, particularly among individuals over 75 years old. Previous studies, such as the DAWN trial, have highlighted the importance of correlating clinical severity with ischemic stroke volume to optimize patient management. Our study aimed to correlate the clinical severity of ischemic stroke, as assessed by the NIHSS score, with ischemic stroke volume measured using DWI, and short-term prognosis quantified by the mRS score at discharge. Conducted at the largest hospital in Gorj County from January 2023 to December 2023, this study enrolled 43 consecutive patients with acute ischemic stroke. In our patient cohort, we observed a strong positive correlation between NIHSS score and ischemic stroke volume (Spearman correlation coefficient = 0.982, p < 0.01), and a strong negative correlation between ASPECTS-DWI score and mRS score (Spearman correlation coefficient = -0.952, p < 0.01). Multiple linear regression analysis revealed a significant collective relationship between ASPECTS score, ischemic stroke volume, and NIHSS score (F(1, 41) = 600.28, p < 0.001, R2 = 0.94, R2adj = 0.93). These findings underscore the importance of DWI in assessing ischemic stroke severity and prognosis, warranting further investigation for its integration into clinical practice.

UNASSIGNED: Melkersson-Rosenthal syndrome can cause recurring bilateral facial paralysis. When steroids fail, surgical decompression of facial nerve is recommended, with endoscopic trans-canal decompression as a safe, minimally invasive, and effective option.
UNASSIGNED: Melkersson-Rosenthal syndrome (MRS) is a rare neuro-mucocutaneous disorder, clinically diagnosed by a triad of orofacial swelling, recurrent facial palsy, and fissured tongue. Due to the lack of a comprehensive understanding of MRS, there is no accepted standard of care. In this study we report a 30-year-old female patient, who was referred to the otolaryngology clinic of Rasool Akram Hospital, with classical triad of MRS that was managed by endoscopic trans-canal facial nerve decompression. Bilateral endoscopic trans-canal facial nerve decompression was done when we did not find any improvement with systemic steroids. Endoscopic trans-canal facial nerve decompression could be a safe, reliable minimal invasive treatment of facial paralysis in MRS patients. It needs no external incision or temporal bone drilling which makes this method more convenient for patients with shorter recovery time.

Clozapine is the only antipsychotic approved for treating treatment-resistant schizophrenia (TRS), characterized by persistent positive symptoms despite adequate antipsychotic treatment. Unfortunately, clozapine demonstrates clinical efficacy in only ~30-60 % of patients with TRS (clozapine-responders; ClzR+), while the remaining ~40-70 % are left with no pharmacological recourse for improvement (clozapine-resistant; ClzR-). Mechanism(s) underlying clozapine\'s superior efficacy remain unclear. However, in vitro evidence suggests clozapine may mitigate glutamatergic dysregulations observed in TRS, by modulating astrocyte activity in ClzR+, but not ClzR-. A factor that if proven correct, may help the assessment of treatment response and development of more effective antipsychotics. To explore the presence of clozapine-astrocyte interaction and clinical improvement, we used 3 T proton-magnetic resonance spectroscopy to quantify levels of myo-Inositol, surrogate biomarker of astrocyte activity, in regions related to schizophrenia neurobiology: Dorsal-anterior-cingulate-cortex (dACC), left-dorsolateral-prefrontal-cortex (left-DLPFC), and left-striatum (left-striatum) of 157 participants (ClzR- = 30; ClzR+ = 37; responders = 38; controls = 52). Clozapine treatment was assessed using clozapine to norclozapine plasma levels, 11-12 h after last clozapine dose. Measures for symptom severity (i.e., Positive and Negative Symptoms Scale) and cognition (i.e., Mini-Mental State Examination) were also recorded. Higher levels of myo-Inositol were observed in TRS groups versus responders and controls (dACC (p < 0.001); left-striatum (p = 0.036); left-DLPFC (p = 0.023)). In ClzR+, but not ClzR-, clozapine to norclozapine ratios were positively associated with myo-Inositol levels (dACC (p = 0.004); left-DLPFC (p < 0.001)), and lower positive symptom severity (p < 0.001). Our results support growing in vitro evidence of clozapine-astrocyte interaction in clozapine-responders. Further research may determine the viability of clozapine-astrocyte interactions as an early marker of clozapine response.