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Spontaneous intracranial hypotension (SIH) is caused by spinal cerebrospinal fluid (CSF) leaks, which result in continued loss of CSF volume and multiple debilitating clinical manifestations. The estimated annual incidence of SIH is 5/100,000. Diagnostic methods have evolved in recent years due to improved understanding of pathophysiology and implementation of advanced myelographic techniques. Here, we synthesize recent updates and contextualize them in an algorithm for diagnosis and treatment of SIH, highlighting basic principles and points of practice variability or continued debate. This discussion includes finer points of SIH diagnosis, CSF leak classification systems, less common types and variants of CSF leaks, brain MRI Bern scoring, potential SIH complications, key technical considerations, and positioning strategies for different types of dynamic myelography. The roles of conservative measures, non-targeted or targeted blood patches, surgery, and recently developed endovascular techniques are presented. [ABSTRACT FROM AUTHOR]

Purpose: Dural tears are a common cause of spontaneous spinal CSF leaks. The majority of such leaks occur ventrally along the thecal sac, typically due to ventral osseous spicules that cause a rent in the dura. A minority of dural leaks are posterolateral in location. These leaks usually do not have an identifiable anatomic cause. We have anecdotally observed cases of posterolateral leaks caused by osseous spicules and sought to describe this phenomenon. Methods: We retrospectively reviewed our imaging database, searching for cases of posterolateral CSF leaks caused by osseous spicules. We identified and included three such patients and reviewed imaging and clinical information from each patient. Results: All three patients had been diagnosed using hyperdynamic CT myelography or conventional CT myelography. Their imaging showed dorsal epidural fluid collections that were related to posterolateral leaks adjacent to dorsal osseous spicules. Conclusion: Dorsal osseous spicules have the potential to cause posterolateral CSF leaks. [ABSTRACT FROM AUTHOR]

Background: Different clinical syndromes can arise from Alzheimer's disease (AD) neuropathology, including dementia of the Alzheimer's type (DAT), logopenic primary progressive aphasia (lvPPA), and posterior cortical atrophy (PCA).Objective: To assess similarities and differences in patterns of white matter tract degeneration across these syndromic variants of AD.Methods: Sixty-four subjects (22 DAT, 24 lvPPA, and 18 PCA) that had diffusion tensor imaging and showed amyloid-β deposition on PET were assessed in this case-control study. A whole-brain voxel-based analysis was performed to assess differences in fractional anisotropy, mean diffusivity, axial diffusivity, and radial diffusivity across groups.Results: All three groups showed overlapping diffusion abnormalities in a network of tracts, including fornix, corpus callosum, posterior thalamic radiations, superior longitudinal fasciculus, inferior longitudinal fasciculus, inferior fronto-occipital fasciculus, and uncinate fasciculus. Subtle regional differences were also observed across groups, with DAT particularly associated with degeneration of fornix and cingulum, lvPPA with left inferior fronto-occipital fasciculus and uncinate fasciculus, and PCA with posterior thalamic radiations, superior longitudinal fasciculus, posterior cingulate, and splenium of the corpus callosum.Conclusion: These findings show that while each AD phenotype is associated with degeneration of a specific structural network of white matter tracts, striking spatial overlap exists among the three network patterns that may be related to AD pathology. [ABSTRACT FROM AUTHOR]