Madhavan, Ajay

Cerebrospinal fluid (CSF)–venous fistulas are an increasingly recognized source of spontaneous intracranial hypotension, for which endovascular embolization has emerged as an effective treatment option.1–3 Advances in diagnostic imaging have improved detection of CSF–venous fistulas throughout the cervical, thoracic, and lumbar spine; however, identification of lesions at the cranial and caudal extremes of the spine remains challenging.4 In video 1, we present the novel case of an anterior condylar confluence CSF–venous fistula arising from a hypoglossal canal nerve root sleeve diverticulum. We demonstrate the diagnostic evaluation, preprocedural planning, and transvenous embolization of the fistula using the pressure cooker technique, highlighting key technical considerations for navigating this uncommon venous anatomy. Finally, we review the patient’s postprocedural course and imaging findings demonstrating radiographic resolution of spontaneous intracranial hypotension. Video 1 Endovascular embolization of a cerebrospinal fluid–venous fistula arising from a hypoglossal canal nerve root sleeve diverticulum using a transvenous pressure cooker technique.

A 49-year-old woman presented with a dorsal column-predominant sensory myelopathy secondary to superficial siderosis. She had Marfan syndrome and was found to have dural ectasia. Superficial siderosis results from subpial haemosiderin deposition due to chronic subarachnoid space bleeding, often from a dural pathology, such as a tear. Dural ectasia is common in Marfan syndrome, but superficial siderosis is not. Gait ataxia, often with hearing impairment, is a common clinical presentation of superficial siderosis. Patients may develop myelopathy, here being a pure sensory myelopathy with predominant dorsal column deficit. Meningeal diverticulae and superficial siderosis are both associated with cerebrospinal fluid (CSF) leaks. This patient had dural ectasia and meningeal diverticulae, but the CT myelogram found no CSF leak. Superficial siderosis should be considered in patients with sensory myelopathy. Lumbosacral dural ectasia, or less likely CSF leak, can cause superficial siderosis in people with Marfan syndrome.

Photon-counting computed tomography (PCCT) is a new imaging technology that has advanced diagnostic imaging by offering improved spatial and contrast resolution as well as novel spectral imaging capabilities. Unlike conventional CT, which uses energy-integrating detectors, PCCT employs photon-counting detectors that directly measure individual photon energies, enabling applications such as virtual monochromatic imaging (VMI) and material decomposition. These innovations allow for artifact reduction, better visualization of fine anatomic structures, and improved diagnostic accuracy, all while reducing radiation dose. This review explores select applications of PCCT in neuroimaging, focusing on the brain, temporal bone, and spine. In the brain, we discuss how PCCT demonstrates superior performance for evaluating aneurysms, metallic prostheses, and vessel stenosis, offering enhanced visualization of vascular structures and minimizing artifacts. For temporal bone imaging, we review assessment of both complex anatomy and potentially subtle pathologies such as otosclerosis, as well as visualization of implants like cochlear devices and their intricate components. In spinal imaging, we explore how PCCT improves precise detection of causes of cerebrospinal fluid leaks, improves localization of tiny vessels such as the artery of Adamkiewicz and spinal dural arteriovenous fistulas, and reduces metal artifacts associated with postoperative hardware. PCCT addresses limitations of conventional CT while unlocking new diagnostic possibilities across neuroimaging applications. As clinical adoption of PCCT grows, ongoing research and development will refine imaging protocols and expand its utility. The accumulating evidence underscores PCCT’s transformative potential to improve diagnostic confidence in neuroimaging and beyond.

Background Cerebrospinal fluid-venous fistulas (CSFVF) are a common cause of spontaneous intracranial hypotension (SIH). Transvenous embolization has emerged as a reliable treatment option. We review the clinical presentation, imaging, and clinical outcomes of 100 consecutive CSFVF patients who underwent embolization over 2 years. Methods Baseline clinical characteristics, imaging findings (including Bern SIH score), technical outcomes, and long-term imaging and clinical outcomes were collected. All patients had at least 3 months of clinical follow-up and had baseline MRI. 99/100 patients underwent follow-up imaging at ≥3 months post-treatment. Results 100 patients were included. Mean imaging and clinical follow-up duration was 8.3±7.7 months and 15.0±6.8 months, respectively. The mean duration of symptoms before embolization was 40.9±52 months. Mean baseline Bern SIH score was 5.9±3.3. The most common baseline symptoms were headache (96 patients), tinnitus (55 patients), and cognitive dysfunction (44 patients). Technical success rate was 100%. Mean post-treatment Bern SIH score was 0.9±1.6 (P<0.0001). Following treatment, 95% of patients reported significant improvement or resolution in symptoms (58 patients reporting resolution and 37 reporting improvement). 5 patients reported no improvement. There were no major procedural or periprocedural complications. 10 patients had minor procedural complications that did not result in any change in management (Onyx emboli, venous perforation). 19 patients had rebound intracranial hypertension requiring acetazolamide therapy. 7 patients had recurrent fistula at the initially treated level. Conclusions Transvenous embolization of CSFVF in SIH patients is safe and effective with a 95% treatment response, significant improvement in imaging outcomes, and a very low rate of complications.

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.