Trainee radiologist reports as a source of confirmation bias in radiology.

AIM: To assess and quantify the relationship between trainee reporting and radiology errors. MATERIALS AND METHODS: A retrospective analysis of the 100 most recent cases reviewed by a discrepancy forum in a tertiary neuroradiology service was performed. Data on the time of the scan and the presence of a trainee report were collected, with comparison being made between the cohort of erroneous reports and the overall service. RESULTS: Although out-of-hours imaging only constituted 18% of the overall service, 36% of erroneous reports originated from scans performed out-of-hours. Eighteen percent of scans were first reported by a trainee and then checked by a consultant, with the remaining 82% being solely reported by the consultant. Despite this, 52% of errors were from consultant-checked trainee reports. CONCLUSION: Although out-of-hours imaging has long been associated with error, this study identifies consultant checking of trainee reports as another error-associated reporting context. This is likely to relate to confirmation bias, in which the pre-existing trainee report may result in inattentional blindness on the part of the checking consultant. Awareness of this phenomenon is important for the reduction of error in this specific and widely underestimated reporting context.

THE MAYAK WORKER DOSIMETRY SYTEM (MWDS-2013): DETERMINATION OF THE INDIVIDUAL SCENARIO OF INHALED PLUTONIUM INTAKE IN THE MAYAK WORKERS.

In order to estimate doses of workers exposed to plutonium, it is necessary to make assumptions about both the route and the time course of intake. The objective of this study was to determine a time course for the inhalation rate for plutonium (intake regime) useful for biokinetic modeling. Records from workplace air sampling, personnel biophysical examinations and autopsy data from former Mayak Production Association (MPA) workers were used. Plutonium accumulation strongly correlated with the volumetric activity of plutonium in workplace air. Using data from activity in air at MPA workplaces over time, a three-step function of intake was adopted. The adequacy of this three-step function was tested by comparing predicted doses using more complicated intake regimes. Uncertainties on the three-step function were also characterized based on air sampling data. The three-step function was assumed to be common to all workers, but an individual intake regime for each worker was calculated by convoluting it with the worker's actual employment history.

Novel HSPB1 mutation causes both motor neuronopathy and distal myopathy.

OBJECTIVE: To identify the cause of isolated distal weakness in a family with both neuropathic and myopathic features on EMG and muscle histology. METHODS: Case study with exome sequencing in 2 affected individuals, bioinformatic prioritization of genetic variants, and segregation analysis of the likely causal mutation. Functional studies included Western blot analysis of the candidate protein before and after heat shock treatment of primary skin fibroblasts. RESULTS: A novel HSPB1 variant (c.387C>G, p.Asp129Glu) segregated with the phenotype and was predicted to alter the conserved α-crystallin domain common to small heat shock proteins. At baseline, there was no difference in HSPB1 protein levels nor its binding partner αB-crystallin. Heat shock treatment increased HSPB1 protein levels in both patient-derived and control fibroblasts, but the associated increase in αB-crystallin expression was greater in patient-derived than control fibroblasts. CONCLUSIONS: The HSPB1 variant (c.387C>G, p.Asp129Glu) is the likely cause of distal neuromyopathy in this pedigree with pathogenic effects mediated through binding to its partner heat shock protein αB-crystallin. Mutations in HSBP1 classically cause a motor axonopathy, but this family shows that the distal weakness can be both myopathic and neuropathic. The traditional clinical classification of distal weakness into "myopathic" or "neuropathic" forms may be misleading in some instances, and future treatments need to address the pathology in both tissues.

Radiological appearances in olfactory dysfunction: pictorial review.

BACKGROUND: Olfactory dysfunction is a common condition that may in some cases require imaging to investigate a potential underlying cause. OBJECTIVES: This review describes the anatomy of normal olfaction and illustrates the pathological substrates of olfactory dysfunction amenable to imaging.

Spatial ability in radiologists: a necessary prerequisite?

Visuospatial ability is fundamental to the cognitive understanding of the three-dimensional environment and is widely recognized as an important skill in the performance of challenging visuospatial tasks. Its contribution to attainment and performance in a variety of professional disciplines is recognized, but there is relatively little known in relation to its relevance in radiological practice. On the basis of a review of the existing cognitive psychological literature and on the basis of the author's own observations, and on the assumption that spatial ability is of increasing and fundamental importance to high-level performance as a radiologist, it is proposed that consideration should be given to the testing of visuospatial ability as part of the selection process for prospective applicants to radiology training programmes.

Increased expression of fatty acid binding protein 4 and leptin in resident macrophages characterises atherosclerotic plaque rupture.

OBJECTIVE: Resident macrophages play an important role in atheromatous plaque rupture. The macrophage gene expression signature associated with plaque rupture is incompletely defined due to the complex cellular heterogeneity in the plaque. We aimed to characterise differential gene expression in resident plaque macrophages from ruptured and stable human atheromatous lesions. METHODS AND RESULTS: We performed genome-wide expression analyses of isolated macrophage-rich regions of stable and ruptured human atherosclerotic plaques. Plaques present in carotid endarterectomy specimens were designated as stable or ruptured using clinical, radiological and histopathological criteria. Macrophage-rich regions were excised from 5 ruptured and 6 stable plaques by laser micro-dissection. Transcriptional profiling was performed using Affymetrix microarrays. The profiles were characteristic of activated macrophages. At a false discovery rate of 10%, 914 genes were differentially expressed between stable and ruptured plaques. The findings were confirmed in fourteen further stable and ruptured samples for a subset of eleven genes with the highest expression differences (p < 0.05). Pathway analysis revealed that components of the PPAR/Adipocytokine signaling pathway were the most significantly upregulated in ruptured compared to stable plaques (p = 5.4 × 10(-7)). Two key components of the pathway, fatty-acid binding-protein 4 (FABP4) and leptin, showed nine-fold (p = 0.0086) and five-fold (p = 0.0012) greater expression respectively in macrophages from ruptured plaques. CONCLUSIONS: We found differences in gene expression signatures between macrophages isolated from stable and ruptured human atheromatous plaques. Our findings indicate the involvement of FABP4 and leptin in the progression of atherosclerosis and plaque rupture, and suggest that down-regulation of PPAR/adipocytokine signaling within plaques may have therapeutic potential.

Use of high-resolution MRI of the optic nerve in Graves' ophthalmopathy.

The aim of this study was to test the hypothesis that optic neuropathy in Graves' disease is associated with measurable optic nerve compression. Magnetic resonance appearances of 32 normal subjects and 27 patients with Graves' disease were evaluated using T(1) weighted volume imaging with multiplanar reformats along the course of the optic nerve. The optic nerve diameter was measured at seven positions along its course. Patients with thyroid orbitopathy were evaluated clinically and categorised into those with (n = 6) and without (n = 48) optic neuropathy. The mean diameter of the optic nerve in normal subjects ranged from 2.2-5.2 mm. The average orbital nerve diameter decreased the further the distance from the globe within the orbit; however, it increased within the optic canal and in the pre-chiasmal region. Optic nerve diameter in patients with Graves' disease without neuritis was not significantly different from that of subjects with normal optic nerves. In patients with optic neuritis, the optic nerve was narrower throughout the length of the nerve but narrowing was most marked in the apex of the orbit (p<0.05) and in the pre-chiasmal intracranial optic nerve (p<0.05). The normal optic nerve has a variable but predictable diameter throughout its course. In Graves' optic neuropathy the diameter of the nerve is significantly reduced in the orbital apex and in the pre-chiasmal portion. The study supports the hypothesis and provides further evidence that the likely mechanism of Graves' ophthalmopathy is compression of the optic nerve at the apex.

Analysis of haemodynamic factors involved in carotid atherosclerosis using computational fluid dynamics.

Atherosclerosis presents a massive healthcare burden in both the developing and developed world. There is mounting evidence relating to the involvement of haemodynamic factors in the pathogenesis of this process. This article aims to review the current understandings that have developed in this area, and to present a demonstrative case study obtained using state of the art computational fluid dynamics (CFD) methodology to model and analyse haemodynamic factors within the atheromatous carotid artery bifurcation.

The disengage deficit in hemispatial neglect is restricted to between-object shifts and is abolished by prism adaptation.

We sought to determine the effects of prism adaptation on peripherally cued visual attention shifting in patients with spatial neglect, using a task devised by Egly et al. (J Exp Psychol Gen 123:161-177, 1994) based on the classic Posner paradigm. This task allowed a comparison of "within-object" versus "between-object" attention shifts. A display was presented containing two parallel outline rectangles, and subjects were asked to make rapid responses to a target, which would appear at one end of one of the rectangles. The target location was pre-cued with 75% validity: on invalid trials attention was directed either to the other end of the same rectangle, or to the other rectangle. Healthy subjects and right-hemisphere patients without neglect showed a left-right symmetrical pattern, with a larger validity effect when required to shift attention between rectangles, thus indicating a greater difficulty of attention-shifting between than within the respective shapes. The neglect patients showed the typical leftward "disengage deficit" previously observed in neglect, but only for attention shifts between objects, indicating that the effect is object-based rather than purely spatial. A comparison of vertical and horizontal shift costs showed that this attention-shifting deficit for left-hemifield target stimuli was directional rather than hemifield-based: it was absent for vertical shifts of attention within the left hemifield. Finally, we found that prism adaptation abolished the disengage deficit. We found no effects of prism adaptation in the control subjects. We argue that prism adaptation has a powerful effect on one of the fundamental manifestations of the neglect syndrome.

T2* and FSE MRI distinguishes four subtypes of neurodegeneration with brain iron accumulation.

BACKGROUND: Neurodegeneration with brain iron accumulation (NBIA) defines a group of genetic disorders characterized by brain iron deposition and associated with neuronal death. The known causes of NBIA include pantothenate kinase-associated neurodegeneration (PKAN), neuroferritinopathy, infantile neuroaxonal dystrophy (INAD), and aceruloplasminemia. OBJECTIVE: To define the radiologic features of each NBIA subtype. METHODS: Brain MRIs from patients with molecularly confirmed PKAN (26 cases), neuroferritinopathy (21 cases), INAD (four cases), and aceruloplasminemia (10 cases) were analyzed blindly to delineate patterns of iron deposition and neurodegeneration. RESULTS: In most cases of PKAN, abnormalities were restricted to globus pallidus and substantia nigra, with 100% having an eye of the tiger sign. In a minority of PKAN cases there was hypointensity of the dentate nuclei (1/5 on T2* sequences, 2/26 on fast spin echo [FSE]). In INAD, globus pallidus and substantia nigra were involved on T2* and FSE scans, with dentate involvement only seen on T2*. By contrast, neuroferritinopathy had consistent involvement of the dentate nuclei, globus pallidus, and putamen, with confluent areas of hyperintensity due to probable cavitation, involving the pallida and putamen in 52%, and a subset having lesions in caudate nuclei and thalami. More uniform involvement of all basal ganglia and the thalami was typical in aceruloplasminemia, but without cavitation. CONCLUSIONS: In the majority of cases, different subtypes of neurodegeneration associated with brain iron accumulation can be reliably distinguished with T2* and T2 fast spin echo brain MRI, leading to accurate clinical and subsequent molecular diagnosis.

Single-center experience of cerecyte coils in the treatment of intracranial aneurysms: initial experience and early follow-up results.

BACKGROUND AND PURPOSE: Endovascular treatment of intracranial aneurysms using platinum coils is effective, but uncommonly aneurysms recur. New-generation coils, such as Cerecyte, aim to address this problem. This study examines the safety and efficacy of these coils in the treatment of a cohort of ruptured and unruptured aneurysms MATERIALS AND METHODS: Sixty-seven patients with 68 aneurysms were included in the study. Of these, 51 were treated exclusively with the new polyglycolic acid (PGA)-containing coils, and 17 were treated with a combination of new PGA-containing and other coils. Initial and follow-up angiograms were graded according to the 3-point scale of occlusion. Follow-up angiography was available in 46 cases at 6 months. Based on occlusion grading at initial and follow-up angiography, aneurysms were classified into stable, improved, and worsened (recanalized) groups. RESULTS: Of the exclusive new-coil cohort, 36 cases (70.6%) were initially completely occluded (grade 1), 12 (23.5%) showed filling at the neck (grade 2), and 3 (5.9%) showed contrast within the neck and sac (grade 3). Analysis of the follow-up angiograms showed 24 (70.6%) had stable occlusion, 3 (8.8%) had improved occlusion, and 7 (20.6%) had worsening occlusion. Data for cases treated with new PGA-containing coils together with bare platinum coils were also analyzed separately. Intraprocedural adverse events were noted in 4 cases (7.8%), but there were no clinical sequelae. There were no rebleeds in the follow-up period. CONCLUSION: New PGA-containing coils show no excess in procedural and periprocedural complications over bare platinum coils, and the recanalization rate is comparable with bare platinum coils in the short term.

MRI for the demonstration of subclinical muscle involvement in muscular dystrophy.

AIM: To compare magnetic resonance imaging (MRI) with clinical examination for the detection of muscle abnormality in patients with muscular dystrophy. METHODS: Muscle power in 20 patients with a variety of forms of muscular dystrophy was examined clinically using the Medical Research Council (MRC) grading scale, and patients were subsequently imaged with MRI. MRI and clinical examination for the detection of muscle normality and abnormality were compared using a McNemar chi-squared test to examine differences between the two methods. RESULTS: MRI demonstrated radiological evidence of muscle abnormality more often than clinical examination; 50% of movements assessed as normal on clinical examination were associated with muscle abnormalities on MRI, including a significant proportion where there was severe radiological abnormality, indicating that focally advanced disease may be undetectable clinically. CONCLUSION: The combination of clinical examination and MRI could improve the accuracy of phenotypic characterization of patients with muscular dystrophy, and this in turn could allow a more focussed molecular analysis through muscle biopsy or genetic investigation. This may also be very helpful in the assessment of the degree of muscle compromise not only in the early phases of the disease but especially during follow-up and can be used in therapeutic trials.

A case of syringomyelia associated with cervical spondylosis.

Cervical spondylosis is an extremely common condition causing spinal cord compression, and yet it very rarely causes secondary syrinx formation. We report a case of cervical spondylosis with associated syringomyelia and review the possible pathogenesis of this condition.

Proton magnetic resonance spectroscopy in frontotemporal dementia.

This study of frontotemporal dementia (FTD) was carried out to determine whether MR spectroscopy can provide an in vivo marker for the neuronal loss and gliosis that occur in this condition. We compared spectra in frontal and temporal regions known to be affected early in the course of the disease with spectra in the parietal lobe that is spared until late stages of FTD. We were interested in the relative concentrations of two compounds, NAA (a marker of neuronal integrity) and mI (a marker of gliosis), expressed as ratios to creatine (a relatively stable brain constituent). MR spectroscopy was performed on the temporal, parietal, and anterior cingulate cortices of five patients with the established semantic dementia form of FTD, two patients with the frontal form of FTD and 13 age matched controls. Structural MRI and neuropsychometry were also performed. Patients with FTD had reduced NAA/Cr in frontal and temporal, but not parietal lobes. The two patients with the frontal form of FTD had increased mI/Cr in their cingulate cortices. These data show for the first time that MR spectroscopy can reveal regionally selective abnormalities in patients with FTD. This opens up the possibility of using MR spectroscopy as a clinical tool to identify earlier presentations of the condition.