Active upper aerodigestive tract hemorrhage in patients with head and neck cancers: the "dot-in-sludge" sign.

Active extravasation into the upper aerodigestive tract is a dramatic and potentially life-threatening complication in patients with head and neck cancers. It prompts presentation to the emergency room and subsequent urgent imaging to identify the source of hemorrhage. Imaging of these patients may be complicated by treatment-altered anatomy, posing a challenge to the emergency radiologist who needs to rapidly identify the presence of active hemorrhage and the potential source vessel. This retrospective review summarizes the clinical and imaging findings of 6 oropharyngeal and oral cavity squamous cell cancer (SCC) patients with active upper aerodigestive tract hemorrhage. Most patients had advanced stage disease and prior radiation therapy. All CECT or CTA exams on presentation demonstrated the "dot-in-sludge" sign of active extravasation, as demonstrated by a "dot" of avidly enhancing extravasated contrast material layered against a background "sludge" of non-enhancing debris in the lumen of the upper aerodigestive tract. Common sources of hemorrhage included the lingual, facial, and superior thyroidal arteries. Familiarity with these findings will help radiologists increase their accuracy and confidence in interpreting these urgent, complex examinations.

Brain on fire: an imaging-based review of autoimmune encephalitis.

Autoimmune encephalitis represents an increasingly recognized group of immune-mediated disorders the affect the central nervous system. The purpose of this article is to highlight the characteristic MR imaging findings associated with autoimmune encephalitis, describe the pathophysiology, review antibodies that have been identified and their patterns of CNS involvement, and discuss approaches to management. Familiarity with the imaging and clinical features of autoimmune encephalitis will prompt the radiologist to suggest the diagnosis which can facilitate appropriate management.

Regional White Matter Diffusion Changes Associated with the Cumulative Tensile Strain and Strain Rate in Nonconcussed Youth Football Players.

The purpose of this study is to assess the relationship between regional white matter diffusion imaging changes and finite element strain measures in nonconcussed youth football players. Pre- and post-season diffusion-weighted imaging was performed in 102 youth football subject-seasons, in which no concussions were diagnosed. The diffusion data were normalized to the IXI template. Percent change in fractional anisotropy (%ΔFA) images were generated. Using data from the head impact telemetry system, the cumulative maximum principal strain one times strain rate (CMPS1 × SR), a measure of the cumulative tensile brain strain and strain rate for one season, was calculated for each subject. Two linear regression analyses were performed to identify significant positive or inverse relationships between CMPS1 × SR and %ΔFA within the international consortium for brain mapping white matter mask. Age, body mass index, days between pre- and post-season imaging, previous brain injury, attention disorder diagnosis, and imaging protocol were included as covariates. False discovery rate correction was used with corrected alphas of 0.025 and voxel thresholds of zero. Controlling for all covariates, a significant, positive linear relationship between %ΔFA and CMPS1 × SR was identified in the bilateral cingulum, fornix, internal capsule, external capsule, corpus callosum, corona radiata, corticospinal tract, cerebral and middle cerebellar peduncle, superior longitudinal fasciculus, and right superior fronto-occipital fasciculus. Post hoc analyses further demonstrated significant %ΔFA differences between high-strain football subjects and noncollision control athletes, no significant %ΔFA differences between low-strain subjects and noncollision control athletes, and that CMPS1 × SR significantly explained more %ΔFA variance than number of head impacts alone.

Classification of brain tumor isocitrate dehydrogenase status using MRI and deep learning.

Isocitrate dehydrogenase (IDH) mutation status is an important marker in glioma diagnosis and therapy. We propose an automated pipeline for noninvasively predicting IDH status using deep learning and T2-weighted (T2w) magnetic resonance (MR) images with minimal preprocessing (N4 bias correction and normalization to zero mean and unit variance). T2w MR images and genomic data were obtained from The Cancer Imaging Archive dataset for 260 subjects (120 high-grade and 140 low-grade gliomas). A fully automated two-dimensional densely connected model was trained to classify IDH mutation status on 208 subjects and tested on another held-out set of 52 subjects using fivefold cross validation. Data leakage was avoided by ensuring subject separation during the slice-wise randomization. Mean classification accuracy of 90.5% was achieved for each axial slice in predicting the three classes of no tumor, IDH mutated, and IDH wild type. Test accuracy of 83.8% was achieved in predicting IDH mutation status for individual subjects on the test dataset of 52 subjects. We demonstrate a deep learning method to predict IDH mutation status using T2w MRI alone. Radiologic imaging studies using deep learning methods must address data leakage (subject duplication) in the randomization process to avoid upward bias in the reported classification accuracy.

Cortical Plasticity in the Setting of Brain Tumors.

Cortical reorganization of function due to the growth of an adjacent brain tumor has clearly been demonstrated in a number of surgically proven cases. Such cases demonstrate the unmistakable implications for the neurosurgical treatment of brain tumors, as the cortical function may not reside where one may initially suspect based solely on the anatomical magnetic resonance imaging (MRI). Consequently, preoperative localization of eloquent areas adjacent to a brain tumor is necessary, as this may demonstrate unexpected organization, which may affect the neurosurgical approach to the lesion. However, in interpreting functional MRI studies, the interpreting physician must be cognizant of artifacts, which may limit the accuracy of functional MRI in the setting of brain tumors.

Vascular Reactivity Maps in Patients with Gliomas Using Breath-Holding BOLD fMRI.

BACKGROUND AND PURPOSE: To evaluate whether breath-holding (BH) blood oxygenation level-dependent (BOLD) fMRI can quantify differences in vascular reactivity (VR), as there is a need for improved contrast mechanisms in gliomas. METHODS: 16 patients (gliomas, grade II = 5, III = 2, IV = 9) were evaluated using the BH paradigm: 4-second single deep breath followed by 16 seconds of BH and 40 seconds of regular breathing for five cycles. VR was defined as the difference in BOLD signal between the minimal signal seen at the end of the deep breath and maximal signal seen at the end of BH (peak-to-trough). VR was measured for every voxel and compared for gray versus white matter and tumor versus normal contralateral brain. VR maps were compared to the areas of enhancement and FLAIR/T2 abnormality. RESULTS: VR was significantly lower in normal white matter than gray matter (P < .05) and in tumors compared to the normal, contralateral brain (P < 0.002). The area of abnormal VR (1103 ± 659 mm²) was significantly greater (P = .019) than the enhancement (543 ± 530 mm²), but significantly smaller (P = .0011) than the FLAIR abnormality (2363 ± 1232 mm²). However, the variability in the areas of gadolinium contrast enhancement versus VR abnormality indicates that the contrast mechanism elicited by BH (caused by abnormal arteriolar smooth muscles) appears to be fundamentally different from the contrast mechanism of gadolinium enhancement (caused by the presence of "leaky" gap junctions). CONCLUSIONS: BH maps based on peak-to-trough can be used to characterize VR in brain tumors. VR maps in brain tumor patients appear to be caused by a different mechanism than gadolinium enhancement.

Millisecond flashes of light phase delay the human circadian clock during sleep.

The human circadian timing system is most sensitive to the phase-shifting effects of light during the biological nighttime, a time at which humans are most typically asleep. The overlap of sleep with peak sensitivity to the phase-shifting effects of light minimizes the effectiveness of using light as a countermeasure to circadian misalignment in humans. Most current light exposure treatments for such misalignment are mostly ineffective due to poor compliance and secondary changes that cause sleep deprivation. Using a 16-day, parallel group design, we examined whether a novel sequence of light flashes delivered during sleep could evoke phase changes in the circadian system without disrupting sleep. Healthy volunteers participated in a 2-week circadian stabilization protocol followed by a 2-night laboratory stay. During the laboratory session, they were exposed during sleep to either darkness (n = 7) or a sequence of 2-msec light flashes given every 30 sec (n = 6) from hours 2 to 3 after habitual bedtime. Changes in circadian timing (phase) and micro- and macroarchitecture of sleep were assessed. Subjects exposed to the flash sequence during sleep exhibited a delay in the timing of their circadian salivary melatonin rhythm compared with the control dark condition (p < 0.05). Confirmation that the flashes penetrated the eyelids is presented by the occurrence of an evoked response in the EEG. Despite the robust effect on circadian timing, there were no large changes in either the amount or spectral content of sleep (p values > 0.30) during the flash stimulus. Exposing sleeping individuals to 0.24 sec of light spread over an hour shifted the timing of the circadian clock and did so without major alterations to sleep itself. While a greater number of matched subjects and more research will be necessary to ascertain whether these light flashes affect sleep, our data suggest that this type of passive phototherapy might be developed as a useful treatment for circadian misalignment in humans.

Response of the human circadian system to millisecond flashes of light.

Ocular light sensitivity is the primary mechanism by which the central circadian clock, located in the suprachiasmatic nucleus (SCN), remains synchronized with the external geophysical day. This process is dependent on both the intensity and timing of the light exposure. Little is known about the impact of the duration of light exposure on the synchronization process in humans. In vitro and behavioral data, however, indicate the circadian clock in rodents can respond to sequences of millisecond light flashes. In a cross-over design, we tested the capacity of humans (n = 7) to respond to a sequence of 60 2-msec pulses of moderately bright light (473 lux) given over an hour during the night. Compared to a control dark exposure, after which there was a 3.5±7.3 min circadian phase delay, the millisecond light flashes delayed the circadian clock by 45±13 min (p<0.01). These light flashes also concomitantly increased subjective and objective alertness while suppressing delta and sigma activity (p<0.05) in the electroencephalogram (EEG). Our data indicate that phase shifting of the human circadian clock and immediate alerting effects can be observed in response to brief flashes of light. These data are consistent with the hypothesis that the circadian system can temporally integrate extraordinarily brief light exposures.

Faster REM sleep EEG and worse restedness in older insomniacs with HLA DQB1*0602.

HLA DQB1*0602 is found in most individuals with hypocretin-deficient narcolepsy, a disorder characterized by a severe disruption of sleep and wake. Population studies indicate that DQB1*0602 may also be associated with normal phenotypic variation of rapid eye movement (REM) sleep. Disruption of REM sleep has been linked to specific symptoms of insomnia. We here examine the relationship of sleep and DQB1*0602 in older individuals (n=46) with primary insomnia, using objective (polysomnography, wrist actigraphy) and subjective (logs, scales) measures. DQB1*0602 positivity was similarly distributed in the older individuals with insomnia (24%) as in the general population (25%). Most sleep variables were statistically indistinguishable between DQB1*0602 positive and negative subjects except that those with the allele reported that they were significantly less well rested than those without it. When sleep efficiencies were lower than 70%, DQB1*0602 positive subjects reported being less well rested at the same sleep efficiency than those without the allele. Examination of EEG during REM sleep also revealed that DQB1*0602 positive subjects had EEG shifted towards faster frequencies compared with negative subjects. Thus, DQB1*0602 positivity is associated with both a shift in EEG power spectrum to faster frequencies during REM sleep and a diminution of restedness given the same sleep quantity.