Amide proton transfer (APT) magnetic resonance imaging (MRI) is a pH-sensitive imaging technique that can potentially complement existing clinical imaging protocol for the assessment of ischemic stroke. This review aims to summarize the developments in the clinical research of APT imaging of ischemic stroke after 17 years of progress since its first preclinical study in 2003. Three electronic databases: PubMed, Scopus, and Cochrane Library were systematically searched for articles reporting clinical studies on APT imaging of ischemic stroke. Only articles in English published between 2003 to 2020 that involved patients presenting ischemic stroke-like symptoms that underwent APT MRI were included. Of 1,093 articles screened, 14 articles met the inclusion criteria with a total of 282 patients that had been scanned using APT imaging. Generally, the clinical studies agreed APT effect to be hypointense in ischemic tissue compared to healthy tissue, allowing for the detection of ischemic stroke. Other uses of APT imaging have also been investigated in the studies, including penumbra identification, predicting long term clinical outcome, and serving as a biomarker for supportive treatment monitoring. The published results demonstrated the potential of APT imaging in these applications, but further investigations and larger trials are needed for conclusive evidence. Future studies are recommended to report the result of asymmetry analysis at 3.5 ppm along with the findings of the study to reduce this contribution to the heterogeneity of experimental methods observed and to facilitate effective comparison of results between studies and centers. In addition, it is important to focus on the development of fast 3D imaging for full volumetric ischemic tissue assessment for clinical translation.
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BackgroundSpinocerebellar ataxia type 3 (SCA3) is a complex cerebrocerebellar disease primarily characterized by ataxia symptoms alongside motor and cognitive impairments. The heterogeneous clinical presentation of SCA3 necessitates correlations between magnetic resonance imaging (MRI) and clinical findings in reflecting progressive disease changes. At present, an attempt to systematically examine the brain-behavior relationship in SCA3, specifically, the correlation between MRI and clinical findings, is lacking.ObjectiveWe investigated the association strength between MRI abnormality and each clinical symptom to understand the brain-behavior relationship in SCA3.MethodsWe conducted a systematic review on Medline and Scopus to review studies evaluating the brain MRI profile of SCA3 using structural MRI (volumetric, voxel-based morphometry, surface analysis), magnetic resonance spectroscopy, and diffusion tensor imaging, including their correlations with clinical outcomes.ResultsOf 1,767 articles identified, 29 articles met the eligibility criteria. According to the National Institutes of Health quality assessment tool for case-control studies, all articles were of excellent quality. This systematic review found that SCA3 neuropathology contributes to widespread brain degeneration, affecting the cerebellum and brainstem. The disease gradually impedes the cerebral cortex and basal ganglia in the late stages of SCA3. Most findings reported moderate correlations (r = 0.30–0.49) between MRI features in several regions and clinical findings. Regardless of the MRI techniques, most studies focused on the brainstem and cerebellum.ConclusionsClinical findings suggest that rather than individual brain regions, the connectivity between different brain regions in distributed networks (i.e., cerebellar-cerebral network) may be responsible for motor and neurocognitive function in SCA3. This review highlights the importance of evaluating the progressive changes of the cerebellar-cerebral networks in SCA3 patients, specifically the functional connectivity. Given the relative lack of knowledge about functional connectivity on SCA3, future studies should investigate possible functional connectivity abnormalities in SCA3 using fMRI.
We report the case of a 25-year-old Malay woman, admitted for preterm delivery at 35 weeks' gestation. Vaginal swab did not isolate any organism. She delivered a baby girl who developed respiratory distress syndrome, requiring ventilation. Although chest radiograph showed hyaline membrane disease with pneumonia, septic workout was negative. The mother was discharged on the next day. Seven days postpartum, the mother presented with fever and fits and was diagnosed to have meningo-encephalitis. Lumbar puncture isolated group B Streptococcus (GBS) and MRI revealed a superior cerebellar abscess. She was treated and survived the episode. This case illustrates the uncommon situation where GBS infection was confirmed via maternal septic workout rather than neonatal, although both presented with severe disease.
To the Editor: Itraconazole, an azole with broad spectrum of fungal activity, has been used for the prevention and empirical therapy of invasive fungal infections (IFIs). Severe neurotoxicity following treatment with itraconazole and vincristine has been reported in 25 patients [1-5]. Here we presented two adult acute lymphoblastic leukemia (ALL) patients developed neurotoxicity after treated with itraconazole and another vinca alkaloids, vindesine. Case 1: A 20-year-old male was admitted to our hospital because of fever and night sweat in December 2004. He was diagnosed as having ALL according to the FAB criteria. He was treated with one courses of DVP regimen and achieved complete remission. This patient was readmitted to our hospital for consolidation on August 2005. He was treated with hyper-CVAD chemotherapy and vindesine was used in day 4 and day 11, respectively. Because he has a history of pulmonary IFI, antifungal prophylaxis with itraconazole solution was started on day 2. Nine days after itraconazole was started, some symptom of paralytic ileus including abdominal pain, abdominal bloating, cramps, inability to pass flatus, or stool were presented. An X-ray of the abdomen shows bulging loops of intestine and some fluid levels were present. He was diagnosed to have paralytic ileus secondary to neurotoxicity caused by itraconazole and vindesine. After the itraconazole was stopped, his paralytic ileus was improved rapidly. This patient received autologous peripheral blood stem cell transplantation in February 2006 and remains in remission at present. Case 2: A 37-year-old female was admitted to our hospital because of fever and petechia in April 2005. A diagnosis of B-cell/T-cell biphenotypic acute leukemia was established based on the results of morphological assay and flow cytometry analysis. She was commenced on induction chemotherapy as for ALL (dexamethasone, Idarubicin, and vindesine). Among them, vindesine was used in day 1, day 8, and day 15, respectively. She presented as pulmonary infection with fever, cough, and expectoration in day 9. Emperical antifungal treatment with itraconazole injection was initiated. Five days after itraconazole was started, some symptom of neurotoxicity including limbs anesthesia, abdominal pain, abdominal bloating, cramps, inability to pass flatus, or stool were presented. An X-ray of the abdomen shows that some fluid levels were present. After the itraconazole and vindesine were discontinued, these symptoms were resolved rapidly. Unfortunately, she died of intracranial hemorrhage on day 28 of induction chemotherapy. Since Böhme first described enhanced severe vincristine neurotoxicity associated with itraconazole in four adults with ALL in 1995 [1], there are 21 cases that have been reported in children [2-5]. The combined use of vinca alkaloids and itraconazole results in the enhanced neurotoxicity by the inhibition of cytochrome P450-mediated metabolism of vinca alkaloids and leading to increased plasma levels of the drug. The most frequent symptoms described were c...
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