Leukoaraiosis (LA) appears as white matter hyperintensities on T2-weighted brain magnetic resonance imaging scans. Age and hypertension are considered the primary risk factors for LA, but its pathogenesis remains uncertain. This study aims to investigate the correlation between the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism and LA. A total of 140 patients with LA and 136 neuroimaging alteration-free controls were recruited in a case-control study. ACE I/D polymorphism was determined using the polymerase chain reaction method. The allele and genotype distributions of the ACE I/D polymorphism were significantly different between subjects with and without LA. Significant difference was observed in the genotypic distribution between LA patients and controls for recessive and additive models. A statistically significant association remained apparent after adjusting for potential risk factors (D/D vs. I/D + I/I: adjusted OR 3.251, 95% CI 1.185-8.918; D/D vs. I/I: adjusted OR 3.277, 95% CI 1.187-9.047). Our results indicate that the D/D genotype and D allele are important risk factors for LA. Future studies with larger populations are needed to validate our results.

UNASSIGNED: Emerging evidence suggests that white matter (WM) disruption is associated with the incidence of subcortical vascular cognitive impairment (SVCI). However, our knowledge regarding this relationship in the early stage of SVCI is limited. We aimed to investigate the associations between WM disruptions and cognitive declines at the early stage of SVCI.
UNASSIGNED: We performed a case-control study, involving 22 cases and 19 controls. The cases were patients at the early stage of SVCI, which was defined as subcortical ischemic vascular disease with normal global cognitive measures (pre-SVCI). The controls were healthy people matched by age, sex, and education years. We assessed the differences in a battery of neuropsychological tests between the two groups, investigated the diffusion changes in 40 WM tracts among the participants via an atlas-based segmentation strategy, and compared the differences between the cases and controls by multiple linear regression analysis. We then evaluated the relationships between diffusion indices and cognitive assessment scores by Pearson\'s correlation.
UNASSIGNED: The pre-SVCI group exhibited significant differences in the Montreal cognitive assessment (MoCA), Rey-Osterrieth Complex Figure (R-O)-copy, and Trail Making Test (TMT)-B test compared with the controls. Compared with the controls, some long associative and projective bundles, such as the right anterior corona radiata (ACR), the right inferior fronto-occipital fasciculus (IFOF), and the left external capsule (EC), were extensively damaged in cases after Bonferroni correction (p < 0.05/40). Damages to specific fibers, such as the right ACR, IFOF, and posterior thalamic radiation (PTR), exhibited significant correlations with declines in MoCA, R-O delay, and the Mini-Mental State Examination (MMSE), respectively, after Bonferroni correction (p < 0.05/14).
UNASSIGNED: Long WM tracts, especially those in the right hemisphere, were extensively damaged in the pre-SVCI patients and correlated with declines in executive functions and spatial processing. Patients of pre-SVCI are likely at an ultra-early stage of SVCI, and there is a very high risk of this condition becoming SVCI.

Posterior reversible encephalopathy syndrome (PRES) can develop in patients following exposure to multiple triggers, including blood pressure fluctuations, kidney diseases, immunosuppressive agents, chemotherapy, or autoimmune disorders. However, to the best of our knowledge, the development of PRES secondary to food poisoning has not been previously reported, especially in a pediatric patient. Here, we report a 13-year-old boy who presented with PRES following the consumption of palmatum (a chicken feet dish). The patient presented with headache, vomiting, and altered consciousness. Neuroimaging findings revealed white matter hyperintensities in a bilateral, symmetrical, and parieto-occipital pattern. The patient was diagnosed with PRES and was managed with fluid expansion and a short-term mannitol regimen (1 g/kg every 12 hours for 3 days). Neuroimaging findings returned to normal at 8 days after admission. Food poisoning may therefore be a new possible trigger for PRES. A timely PRES diagnosis is recommended to prevent possible central nervous system complications.

In a woman with Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) followed for 15 years, we observed magnetic resonance imaging white matter hyperintensities that vanished in the anterior temporal poles while the brain volume decreased unexpectedly. These imaging changes were transient and detected when the patient was being treated by valproic acid for stabilizing mood disturbances. This intriguing case supports that mechanisms underlying white matter hyperintensities can vary from one brain area to another and that important modifications of water influx into the brain tissue might be involved in some imaging features of CADASIL.

Leukoaraiosis, or white matter rarefaction, is a common imaging finding in aging and is presumed to reflect vascular disease. When severe in presentation, potential congenital or acquired etiologies are investigated, prompting referral for neuropsychological evaluation in addition to neuroimaging. T2-weighted imaging is the most common magnetic resonance imaging (MRI) approach to identifying white matter disease. However, more advanced diffusion MRI techniques may provide additional insight into mechanisms that influence the abnormal T2 signal, especially when clinical presentations are discrepant with imaging findings.
We present a case of a 74-year-old woman with severe leukoaraoisis. She was examined by a neurologist, neuropsychologist, and rheumatologist, and completed conventional (T1, T2-FLAIR) MRI, diffusion tensor imaging (DTI), and advanced single-shell, high b-value diffusion MRI (i.e., fiber ball imaging [FBI]).
The patient was found to have few neurological signs, no significant cognitive impairment, a negative workup for leukoencephalopathy, and a positive antibody for Sjogren\'s disease for which her degree of leukoaraiosis would be highly atypical. Tractography results indicate intact axonal architecture that was better resolved using FBI rather than DTI.
This case illustrates exceptional cognitive resilience in the face of severe leukoaraiosis and the potential for advanced diffusion MRI to identify brain reserve.

Microcephaly is a fairly common feature observed in children with delayed development, defined as head circumference less than 2 standard deviations below the mean for age and gender. It may be the result of an acquired insult to the brain, such prenatal or perinatal brain injury (congenital infection or hypoxic ischemic encephalopathy), or be a part of a genetic syndrome. There are over 1000 conditions listed in OMIM (Online Mendelian Inheritance in Man) where microcephaly is a key finding; many of these are associated with specific somatic features and non-CNS anomalies. The term primary microcephaly is used when microcephaly and delayed development are the primary features, and they are not part of another recognized syndrome. In this case report, we present the clinical features of siblings (brother and sister) with primary microcephaly and delayed development, and subtle dysmorphic features. Both children had brain MRI studies that showed periventricular and subcortical T2/FLAIR hyperintensities, without signs of white matter volume loss, and no parenchymal calcifications by CT scan. The family was enrolled in a research study for whole exome sequencing of probands and parents. Analysis of variants determined that the children were compound heterozygotes for nonsense mutations, c.277C>T (p.Arg93*) and c.397C>T (p.Arg133*), in the TRMT10A gene. Mutations in this gene have only recently been reported in children with microcephaly and early onset diabetes mellitus. Our report adds to current knowledge of TRMT10A related neurodevelopmental disorders and demonstrates imaging findings suggestive of delayed or abnormal myelination of the white matter in this disorder. Accurate diagnosis through genomic testing, as in the children described here, allows for early detection and management of medical complications, such as diabetes mellitus.

Objective. There exists uncertainty regarding the role of magnetic resonance imaging in the evaluation of intensive care unit delirious patients. This case series describes preliminary magnetic resonance imaging findings obtained because of delirium, subsequent in-hospital clinical decisions, and post-discharge neurocognitive outcomes in intensive care unit survivors.Design. Case series.Setting. Intensive care unit.Participants. Eight patients who underwent magnetic resonance imaging for delirium in the absence of focal neurological findings as part of their intensive care unit clinical care.Measurements. Magnetic resonance imaging findings, clinical decisions following magnetic resonance imaging, and three-month neuropsychological outcomes were obtained.Results. Of the eight patients, six (75%) demonstrated white matter hyperintensities, one (12%) had mild atrophy, and no patient had ischemic/hemorrhagic lesions. Magnetic resonance imaging did not lead to new diagnoses or immediate changes in therapy. All six patients who underwent neuropsychological testing had severe impairments in memory, executive function, and attention at three months, despite the absence of baseline cognitive impairment.Conclusion. Magnetic resonance imaging findings in these delirious intensive care unit patients did not alter the immediate treatment course and these patients had neuropsychological impairments at three months. Future research is warranted to define the role of current and newer magnetic resonance imaging techniques in assessing and managing delirious intensive care unit patients, and to examine relationships between in-hospital magnetic resonance imaging findings (i.e. white matter hyperintensities) and short- and long-term neurological outcomes.