The presence of pachymeningeal hyperintensity on non-contrast flair imaging in patients with spontaneous intracranial hypotension.

PURPOSE: Traditionally, in the work-up of patients for spontaneous intracranial hypotension, T1 post-contrast imaging is performed in order to assess for pachymeningeal enhancement. The aim of this study is to assess whether pachymeningeal hyperintensity can be identified on a non-contrast FLAIR sequence in these patients as a surrogate sign for pachymeningeal enhancement. METHODS: The patient cohort was identified from a prospectively maintained database of patients with a clinical diagnosis of intracranial hypotension. Patients who had both a post-contrast T1 sequence brain as well as non-contrast FLAR sequence of the brain were reviewed. Imaging was retrospectively reviewed by three independent neuroradiologists. Each study was assessed for the presence or absence of pachymeningeal hyperintensity on the FLAIR sequence. RESULTS: From January 2010 to July 2022, 177 patients were diagnosed with spontaneous intracranial hypotension. In total, 121 were excluded as post-contrast imaging was not performed during their work-up. Twenty-four were excluded as the FLAIR sequence was performed after administration of contrast. Six were excluded as there was no pachymeningeal thickening present on T1 post-contrast imaging, although there were other signs of intracranial hypotension. The study group therefore consisted of 26 patients. Pachymeningeal thickening was correctly identified on the non-contrast FLAIR sequence in all patients (100%). CONCLUSION: Where present, diffuse pachymeningeal hyperintensity can be accurately identified on a non-contrast FLAIR sequence in patients with spontaneous intracranial hypotension. This potentially obviates the need for gadolinium base contrast agents in the work-up of these patients.

Molecular and Anatomical Imaging of Dementia With Lewy Bodies and Frontotemporal Lobar Degeneration.

Dementia with Lewy bodies (DLB) and frontotemporal lobar degeneration (FTLD) are common causes of dementia. Early diagnosis of both conditions is challenging due to clinical and radiological overlap with other forms of dementia, particularly Alzheimer's disease (AD). Structural and functional imaging combined can aid differential diagnosis and help to discriminate DLB or FTLD from other forms of dementia. Imaging of DLB involves the use of 123I-FP-CIT SPECT and 123I-metaiodobenzylguanidine (123I-MIBG), both of which have an established role distinguishing DLB from AD. AD is also characterised by more pronounced atrophy of the medial temporal lobe structures when compared to DLB and these can be assessed at MR using the Medial Temporal Atrophy Scale. 18F-FDG-PET is used as a supportive biomarker for the diagnoses of DLB and can distinguish DLB from AD with high accuracy. Polysomnography and electroencephalography also have established roles in the diagnoses of DLB. FTLD is a heterogenous group of neurodegenerative disorders characterised pathologically by abnormally aggregated proteins. Clinical subtypes include behavioral variant FTD (bvFTD), primary progressive aphasia (PPA), which can be subdivided into semantic variant PPA (svPPA) or nonfluent agrammatic PPA (nfaPPA) and FTD associated with motor neuron disease (FTD-MND). Structural imaging is often the first step in making an image supported diagnoses of FTLD. Regional patterns of atrophy can be assessed on MR and graded according to the global cortical atrophy scale. FTLD is typically associated with atrophy of the frontal and temporal lobes. The patterns of atrophy are associated with the specific clinical subtypes, underlying neuropathology and genetic mutations although there is significant overlap. 18F-FDG-PET is useful for distinguishing FTLD from other forms of dementia and focal areas of hypometabolism can often precede atrophy identified on structural MR imaging. There are currently no biomarkers with which to unambiguously diagnose DLB or FTLD and both conditions demonstrate a wide range of heterogeneity. A combined approach of structural and functional imaging improves diagnostic accuracy in both conditions.

Differentiating combined pulmonary fibrosis and emphysema from pure emphysema: utility of late gadolinium-enhanced MRI.

BACKGROUND: Differentiating combined pulmonary fibrosis with emphysema (CPFE) from pure emphysema can be challenging on high-resolution computed tomography (HRCT). This has antifibrotic therapy implications. METHODS: Twenty patients with suspected CPFE underwent late gadolinium-enhanced (LGE) thoracic magnetic resonance imaging (LGE-MRI) and HRCT. Data from twelve healthy control subjects from a previous study who underwent thoracic LGE-MRI were included for comparison. Quantitative LGE signal intensity (SI) was retrospectively compared in regions of fibrosis and emphysema in CPFE patients to similar lung regions in controls. Qualitative comparisons for the presence/extent of reticulation, honeycombing, and traction bronchiectasis between LGE-MRI and HRCT were assessed by two readers in consensus. RESULTS: There were significant quantitative differences in fibrosis SI compared to emphysema SI in CPFE patients (25.8, IQR 18.4-31.0 versus 5.3, IQR 5.0-8.1, p < 0.001). Significant differences were found between LGE-MRI and HRCT in the extent of reticulation (12.5, IQR 5.0-20.0 versus 25.0, IQR 15.0-26.3, p = 0.038) and honeycombing (5.0, IQR 0.0-10.0 versus 20.0, IQR 10.6-20.0, p = 0.001) but not traction bronchiectasis (10.0, IQR 5-15 versus 15.0, IQR 5-15, p = 0.878). Receiver operator curve analysis of fibrosis SI compared to similarly located regions in control subjects showed an area under the curve of 0.82 (p = 0.002). A SI cutoff of 19 yielded a sensitivity of 75% and specificity of 86% in differentiating fibrosis from similarly located regions in control subjects. CONCLUSION: LGE-MRI can differentiate CPFE from pure emphysema and may be a useful adjunct test to HRCT in patients with suspected CPFE.