Impedance Rhythms in Human Limbic System.

The impedance is a fundamental electrical property of brain tissue, playing a crucial role in shaping the characteristics of local field potentials, the extent of ephaptic coupling, and the volume of tissue activated by externally applied electrical brain stimulation. We tracked brain impedance, sleep-wake behavioral state, and epileptiform activity in five people with epilepsy living in their natural environment using an investigational device. The study identified impedance oscillations that span hours to weeks in the amygdala, hippocampus, and anterior nucleus thalamus. The impedance in these limbic brain regions exhibit multiscale cycles with ultradian (∼1.5-1.7 h), circadian (∼21.6-26.4 h), and infradian (∼20-33 d) periods. The ultradian and circadian period cycles are driven by sleep-wake state transitions between wakefulness, nonrapid eye movement (NREM) sleep, and rapid eye movement (REM) sleep. Limbic brain tissue impedance reaches a minimum value in NREM sleep, intermediate values in REM sleep, and rises through the day during wakefulness, reaching a maximum in the early evening before sleep onset. Infradian (∼20-33 d) impedance cycles were not associated with a distinct behavioral correlate. Brain tissue impedance is known to strongly depend on the extracellular space (ECS) volume, and the findings reported here are consistent with sleep-wake-dependent ECS volume changes recently observed in the rodent cortex related to the brain glymphatic system. We hypothesize that human limbic brain ECS changes during sleep-wake state transitions underlie the observed multiscale impedance cycles. Impedance is a simple electrophysiological biomarker that could prove useful for tracking ECS dynamics in human health, disease, and therapy.SIGNIFICANCE STATEMENT The electrical impedance in limbic brain structures (amygdala, hippocampus, anterior nucleus thalamus) is shown to exhibit oscillations over multiple timescales. We observe that impedance oscillations with ultradian and circadian periodicities are associated with transitions between wakefulness, NREM, and REM sleep states. There are also impedance oscillations spanning multiple weeks that do not have a clear behavioral correlate and whose origin remains unclear. These multiscale impedance oscillations will have an impact on extracellular ionic currents that give rise to local field potentials, ephaptic coupling, and the tissue activated by electrical brain stimulation. The approach for measuring tissue impedance using perturbational electrical currents is an established engineering technique that may be useful for tracking ECS volume.

Progressive motor impairment from "critical" demyelinating lesions of the cervicomedullary junction.

BACKGROUND: Progressive motor impairment anatomically associated with a "critical" lesion has been described in primary demyelinating disease. Most "critical" lesions occur within the spinal cord. OBJECTIVE: To describe the clinical and radiological features of "critical" lesions of the cervicomedullary junction (CMJ). METHODS: Observational study on people presenting with a CMJ lesion associated with primary demyelinating disease-related progressive motor impairment. Clinical data were extracted by chart review. Brain and spinal cord magnetic resonance images were reviewed to characterize the CMJ lesion and determine additional demyelination burden. RESULTS: Forty-one people were included: 29 (71%) had progression from onset and 12 (29%) had a relapse onset (secondary progressive) course. Most had progressive hemiparesis (21 (51%)) or progressive quadriparesis (15 (37%)) with a median Expanded Disability Status Scale (EDSS) of 5.5 (2.0-8.5) at last follow-up. No "critical" CMJ lesion enhanced; most were bilateral (25 (61%)). Brain magnetic resonance images were otherwise normal in 16 (39%) or with a restricted demyelination burden in 15 (37%). Cervical and thoracic cord MRIs were without additional lesions in 25 (61%) and 22/37 (59%), respectively. CONCLUSION: CMJ "critical" lesions can correlate with progressive motor impairment even with few or no additional magnetic resonance imaging (MRI) lesions. Lesion location is an important determinant of progressive motor impairment in demyelinating disease.

Inflammatory activity following motor progression due to critical CNS demyelinating lesions.

BACKGROUND: New inflammatory activity is of unclear frequency and clinical significance in progressive multiple sclerosis (MS); it is uncertain in patient cohorts with motor progression due to critical demyelinating lesions. OBJECTIVES: The aim of this study is to determine the likelihood of central nervous system (CNS) inflammatory activity, assessed by new clinical relapses or active magnetic resonance imaging (MRI) lesions, following onset of motor progression due to critical demyelinating lesions. METHODS: Patients with progressive upper motor neuron impairment for ⩾1 year attributable to critical demyelinating lesions with single CNS lesion (progressive solitary sclerosis (PSS)), 2 to 5 total CNS demyelinating lesions (progressive "pauci-sclerosis" (PPS)), or >5 CNS demyelinating lesions and progressive exclusively unilateral monoparesis or hemiparesis (PUHMS) were identified. Clinical data were reviewed for acute MS relapses, and subsequent MRI was reviewed for active T1-gadolinium-enhancing or T2-demyelinating lesions. RESULTS: None of the 91 patients (22 PSS, 40 PPS, 29 PUHMS) identified experienced clinical relapses over a median clinical follow-up of 93 months (range: 12-518 months). Nine patients (10%) developed active lesions over median 84 months radiologic follow-up (range: 12-518 months). Active lesions occurred in 24% PUHMS, 5% PSS, and 3% PPS cohorts. CONCLUSION: New inflammatory activity, defined by active lesions and clinical relapses following motor progression in patients with critical demyelinating lesions, is low. Disease-modifying therapies that reduce demyelinating relapses and active MRI lesions are of uncertain benefit in these cohorts.

Critical spinal cord lesions associate with secondary progressive motor impairment in long-standing MS: A population-based case-control study.

BACKGROUND: Progressive motor impairment anatomically attributable to prominent, focally atrophic lateral column spinal cord lesions ("critical lesions") can be seen in multiple sclerosis (MS), for example, progressive hemiparetic MS. OBJECTIVE: The aim of this study was to investigate whether similar spinal cord lesions are more frequent in long-standing MS patients with secondary progressive motor impairment (secondary progressive MS (SPMS)) versus those maintaining a relapsing-remitting course (relapsing-remitting MS (RRMS)). METHODS: We retrospectively identified Olmsted County (MN, USA) residents on 31 December 2011 with (1) RRMS or SPMS for ⩾25 years, and (2) available brain and spine magnetic resonance imaging (MRI). A blinded neuroradiologist determined demyelinating lesion burden and presence of potential critical lesions (prominent focally atrophic spinal cord lateral column lesions). RESULTS: In total, 32 patients were included: RRMS, 18; SPMS, 14. Median (range) disease duration (34 (27-53) vs. 39 (29-47) years) and relapse number (4 (1-10) vs. 3 (1-15)) were similar. In comparison to RRMS, SPMS patients more commonly showed potential critical spinal cord lesions (8/18 (44%) vs. 14/14 (100%)), higher spinal cord (median (range) 4 (1-7) vs. 7.5 (3-12)), and brain infratentorial (median (range) 1 (0-12) vs. 2.5 (1-13)) lesion number; p < 0.05. By multivariate analysis, only the presence of potential critical lesions independently associated with motor progression (p = 0.02). CONCLUSION: Critical spinal cord lesions may be important contributors to motor progression in MS.

Anterior nucleus of the thalamus seizure detection in ambulatory humans.

There is a paucity of data to guide anterior nucleus of the thalamus (ANT) deep brain stimulation (DBS) with brain sensing. The clinical Medtronic Percept DBS device provides constrained brain sensing power within a frequency band (power-in-band [PIB]), recorded in 10-min averaged increments. Here, four patients with temporal lobe epilepsy were implanted with an investigational device providing full bandwidth chronic intracranial electroencephalogram (cEEG) from bilateral ANT and hippocampus (Hc). ANT PIB-based seizure detection was assessed. Detection parameters were cEEG PIB center frequency, bandwidth, and epoch duration. Performance was evaluated against epileptologist-confirmed Hc seizures, and assessed by area under the precision-recall curve (PR-AUC). Data included 99 days of cEEG, and 20, 278, 3, and 18 Hc seizures for Subjects 1-4. The best detector had 7-Hz center frequency, 5-Hz band width, and 10-s epoch duration (group PR-AUC = .90), with 75% sensitivity and .38 false alarms per day for Subject 1, and 100% and .0 for Subjects 3 and 4. Hc seizures in Subject 2 did not propagate to ANT. The relative change of ANT PIB was maximal ipsilateral to seizure onset for all detected seizures. Chronic ANT and Hc recordings provide direct guidance for ANT DBS with brain sensing.

Brainstem and cerebellar involvement in MOG-IgG-associated disorder versus aquaporin-4-IgG and MS.

OBJECTIVE: To determine the frequency and characteristics of brainstem or cerebellar involvement in myelin-oligodendrocyte-glycoprotein-antibody-associated-disorder (MOGAD) versus aquaporin-4-IgG-seropositive-neuromyelitis optica spectrum disorder (AQP4-IgG-NMOSD) and multiple sclerosis (MS). METHODS: In this observational study, we retrospectively identified 185 Mayo Clinic MOGAD patients with: (1) characteristic MOGAD phenotype, (2) MOG-IgG seropositivity by live cell-based assay and (3) MRI lesion(s) of brainstem, cerebellum or both. We compared the symptomatic attacks to AQP4-IgG-NMOSD (n=30) and MS (n=30). RESULTS: Brainstem or cerebellar involvement occurred in 62/185 (34%) MOGAD patients of which 39/62 (63%) were symptomatic. Ataxia (45%) and diplopia (26%) were common manifestations. The median age in years (range) in MOGAD of 24 (2-65) was younger than MS at 36 (16-65; p=0.046) and AQP4-IgG-NMOSD at 45 (6-72; p=0.006). Isolated attacks involving the brainstem, cerebellum or both were less frequent in MOGAD (9/39 (23%)) than MS (22/30 (73%); p<0.001) but not significantly different from AQP4-IgG-NMOSD (14/30 (47%); p=0.07). Diffuse middle cerebellar peduncle MRI-lesions favoured MOGAD (17/37 (46%)) over MS (3/30 (10%); p=0.001) and AQP4-IgG-NMOSD (3/30 (10%); p=0.001). Diffuse medulla, pons or midbrain MRI lesions occasionally occurred in MOGAD and AQP4-IgG-NMOSD but never in MS. Cerebrospinal fluid (CSF) oligoclonal bands were rare in MOGAD (5/30 (17%)) and AQP4-IgG-NMOSD (2/22 (9%); p=0.68) but common in MS (18/22 (82%); p<0.001). Disability at nadir or recovery did not differ between the groups. CONCLUSION: Involvement of the brainstem, cerebellum or both is common in MOGAD but usually occurs as a component of a multifocal central nervous system attack rather than in isolation. We identified clinical, CSF and MRI attributes that can help discriminate MOGAD from AQP4-IgG-NMOSD and MS.

Altered integrity of corpus callosum in generalized epilepsy in relation to seizure lateralization after corpus callosotomy.

OBJECTIVE: Generalized-onset seizures are usually conceptualized as engaging bilaterally distributed networks with no clear focus. However, the authors previously reported a case series demonstrating that in some patients with generalized-onset seizures, focal seizure onset could be discovered after corpus callosotomy. The corpus callosum is considered to be a major pathway for seizure generalization in this group of patients. The authors hypothesized that, in patients with generalized-onset seizures, the structure of the corpus callosum could be different between patients who have lateralized seizures and those who have nonlateralized seizures after corpus callosotomy. The authors aimed to evaluate the structural difference through statistical analysis of diffusion tensor imaging (DTI) scalars between these two groups of patients. METHODS: Thirty-two patients diagnosed with generalized-onset motor seizures and without an MRI lesion were included in this study. Among them, 16 patients developed lateralized epileptic activities after corpus callosotomy, and the remaining 16 patients continued to have nonlateralized seizures after corpus callosotomy. Presurgical DTI studies were acquired to quantify the structural integrity of the corpus callosum. RESULTS: The DTI analysis showed significant reduction of fractional anisotropy (FA) and increase in radial diffusivity (RD) in the body of the corpus callosum in the lateralized group compared with the nonlateralized group. CONCLUSIONS: The authors' findings indicate the existence of different configurations of bilateral epileptic networks in generalized epilepsy. Generalized seizures with focal onset relying on rapid spread through the corpus callosum might cause more structural damage related to demyelination in the corpus callosum, showing reduced FA and increased RD. This study suggests that presurgical DTI analysis of the corpus callosum might predict the seizure lateralization after corpus callosotomy.

Progressive multifocal leukoencephalopathy after allogeneic stem cell transplantation: Case report and review of the literature.

Progressive multifocal leukoencephalopathy (PML) is a rare, yet typically fatal complication of allogeneic stem cell transplantation. It is caused by reactivation of the John Cunningham (JC) virus in an immunocompromised host. This report describes an unfortunate case of PML in a recipient of an allogeneic stem cell transplant for acute myelogenous leukemia. The JC virus was undetectable in the patient's cerebrospinal fluid by polymerase chain reaction (PCR); however, a positive diagnosis was made after a brain biopsy. This and other published cases demonstrate that recipients of allogeneic stem cells can develop PML. Moreover, early diagnosis of the disease is often difficult and, as demonstrated in this case, screening with PCR does not appear to have strong diagnostic significance. With no effective treatment presently available, restoration of immune function is the only intervention that can affect prognosis. Further prospective studies are needed to understand the pathophysiology and treatment of this disease.

Recognizing intraventricular silicone.

Retinal detachment with subsequent silicone oil retinopexy is not uncommon. A known complication of silicone retinopexy is intraventricular migration of the intraocular silicone oil. While the oil itself does not result in direct pathology, misdiagnosis may lead to an unnecessary diagnostic workup and possibly predispose the patient to surgery intervention. Silicone oil typically appears hyperdense on computer tomography (CT) and hyperintense on T1-weighted magnetic resonance (MR). These imaging findings may mimic a mass or blood products. However, MR imaging of silicone results in chemical shift artifact which should help narrow the imaging differential. We present a patient with incidental CT and MRI findings which resulted in a prolonged hospital course following misidentification of intraventricular silicone oil. Although the imaging differential for an intraventricular lesion may include metastasis, lymphoma, hemorrhage, choroid plexus papilloma/carcinoma, meningioma, subependymoma, and ependymoma, secondary imaging findings should be noted to ensure an accurate diagnosis. In patients with evidence of prior silicone retinopexy, visualization of an intraventricular lesion with associated chemical shift artifact should raise the possibility of intraventricular silicone oil migration.

Direct pseudomeningocele contrast injection for spinal CSF leak localization.

CT myelography has been traditionally used to evaluate post-operative paraspinal fluid collections to discern CSF leaking into a pseudomeningocele versus a contained seroma. Rather than performing a lumbar puncture and injecting intrathecal contrast for myelography, we present the first report of direct contrast injection into a post-operative paraspinal pseudomeningocele for CSF leak confirmation and localization. This is a simple procedure that has several advantages over a conventional CT myelogram for the evaluation of post-operative paraspinal fluid collections.

Magnetic Resonance Imaging Artifact Associated With Transcutaneous Bone Conduction Implants: Cholesteatoma and Vestibular Schwannoma Surveillance.

OBJECTIVE: To evaluate the magnetic resonance (MR) image artifact and image distortion associated with the two transcutaneous bone conduction implants currently available in the United States. STUDY DESIGN: Cadaveric study. METHODS: Two cadaveric head specimens (1 male, 1 female) were unilaterally implanted according to manufacturer guidelines and underwent MR imaging (General Electric and Siemens 1.5 T scanners) under the following device conditions: (1) no device, (2) Cochlear Osia with magnet and headwrap, (3) Cochlear Osia without magnet, and (4) MED-EL Bonebridge with magnet. Maximum metal mitigation techniques were employed in all conditions, and identical sequences were obtained. Blinded image scoring (diagnostic vs nondiagnostic image) was performed by experienced neuroradiologists according to anatomical subsites. RESULTS: All device conditions produced artifact and image distortion. The Osia with magnet produced diagnostic T1- and T2-weighted images of the ipsilateral temporal bone, however, non-echo planar imaging diffusion-weighted imaging (DWI) was nondiagnostic. The Osia without magnet scanned on the Siemens MR imaging demonstrated the least amount of artifact and was the only condition that allowed for diagnostic imaging of the ipsilateral temporal bone on DWI. The Bonebridge produced a large area of artifact and distortion with the involvement of the ipsilateral and contralateral temporal bones. CONCLUSION: In summary, of the three device conditions (Osia with magnet, Osia without magnet, and Bonebridge), Osia without magnet offered the least amount of artifact and distortion and was the only condition in which diagnostic DWI was available for the middle ear and mastoid regions on the Siemens MR imaging scanner.

7T MRI for Cushing Disease: A Single-Institution Experience and Literature Review.

BACKGROUND AND PURPOSE: Cushing disease is typically caused by a pituitary adenoma that frequently is small and challenging to detect on conventional MR imaging. High-field-strength 7T MR imaging can leverage increased SNR and contrast-to-noise ratios compared with lower-field-strength MR imaging to help identify small pituitary lesions. We aimed to describe our institutional experience with 7T MR imaging in patients with Cushing disease and perform a review of the literature. MATERIALS AND METHODS: We performed a retrospective analysis of 7T MR imaging findings in patients with pathology-proved Cushing disease from a single institution, followed by a review of the literature on 7T MR imaging for Cushing disease. RESULTS: Our institutional experience identified Cushing adenomas in 10/13 (76.9%) patients on 7T; however, only 5/13 (38.5%) lesions were discrete. Overall, the imaging protocols used were heterogeneous in terms of contrast dose as well as type of postcontrast T1-weighted sequences (dynamic, 2D versus 3D, and type of 3D sequence). From our institutional data, specific postgadolinium T1-weighted sequences were helpful in identifying a surgical lesion as follows: dynamic contrast-enhanced, 2/7 (28.6%); 2D FSE, 4/8 (50%); 3D sampling perfection with application-optimized contrasts by using different flip angle evolution (SPACE), 5/6 (83.3%); and 3D MPRAGE, 8/11 (72.7%). The literature review identified Cushing adenomas in 31/33 (93.9%) patients on 7T. CONCLUSIONS: 7T MR imaging for pituitary lesion localization in Cushing disease is a new technique with imaging protocols that vary widely. Further comparative research is needed to identify the optimal imaging technique as well as assess the benefit of 7T over lower-field-strength MR imaging.

High-Grade Astrocytoma with Piloid Features: A Dual Institutional Review of Imaging Findings of a Novel Entity.

High-grade astrocytoma with piloid features (HGAP) is a recently identified brain tumor characterized by a distinct DNA methylation profile. Predominantly located in the posterior fossa of adults, HGAP is notably prevalent in individuals with neurofibromatosis type 1. We present an image-centric review of HGAP and explore the association between HGAP and neurofibromatosis type 1. Data were collected from 8 HGAP patients treated at two tertiary care institutions between January 2020 and October 2023. Demographic details, clinical records, management, and tumor molecular profiles were analyzed. Tumor characteristics, including location and imaging features on MR imaging, were reviewed. Clinical or imaging features suggestive of neurofibromatosis 1 or the presence of NF1 gene alteration were documented. The mean age at presentation was 45.5 years (male/female = 5:3). Tumors were midline, localized in the posterior fossa (n = 4), diencephalic/thalamic (n = 2), and spinal cord (n = 2). HGAP lesions were T1 hypointense, T2-hyperintense, mostly without diffusion restriction, predominantly peripheral irregular enhancement with central necrosis (n = 3) followed by mixed heterogeneous enhancement (n = 2). Two NF1 mutation carriers showed signs of neurofibromatosis type 1 before HGAP diagnosis, with one diagnosed during HGAP evaluation, strengthening the HGAP-NF1 link, particularly in patients with posterior fossa masses. All tumors were IDH1 wild-type, often with ATRX, CDKN2A/B, and NF1 gene alteration. Six patients underwent surgical resection followed by adjuvant chemoradiation. Six patients were alive, and two died during the last follow-up. Histone H3 mutations were not detected in our cohort, such as the common H3K27M typically seen in diffuse midline gliomas, linked to aggressive clinical behavior and poor prognosis. HGAP lesions may involve the brain or spine and tend to be midline or paramedian in location. Underlying neurofibromatosis type 1 diagnosis or imaging findings are important diagnostic cues.

Radiologic Classification of Hippocampal Sclerosis in Epilepsy.

Temporal lobe epilepsy is a common form of epilepsy that is often associated with hippocampal sclerosis (HS). Although HS is commonly considered a binary assessment in radiologic evaluation, it is known that histopathologic changes occur in distinct clusters. Some subtypes of HS only affect certain subfields, resulting in minimal changes to the overall volume of the hippocampus. This is likely a major reason why whole hippocampal volumetrics have underperformed versus expert readers in the diagnosis of HS. With recent advancements in MRI technology, it is now possible to characterize the substructure of the hippocampus more accurately. However, this is not consistently addressed in radiographic evaluations. The histologic subtype of HS is critical for prognosis and treatment decision-making, necessitating improved radiologic classification of HS. The International League Against Epilepsy (ILAE) has issued a consensus classification scheme for subtyping HS histopathologic changes. This review aims to explore how the ILAE subtypes of HS correlate with radiographic findings, introduce a grading system that integrates radiologic and pathologic reporting in HS, and outline an approach to detecting HS subtypes by using MRI. This framework will not only benefit current clinical evaluations, but also enhance future studies involving high-resolution MRI in temporal lobe epilepsy.

Imaging Findings in Giant Cell Arteritis: Don't Turn a Blind Eye to the Obvious!

Giant cell arteritis (GCA) is the most common primary large vessel systemic vasculitis in the Western World. Even though the involvement of scalp and intracranial vessels has received much attention in the neuroradiology literature, GCA, being a systemic vasculitis, can involve multiple other larger vessels including the aorta and its major head and neck branches. Herein, the authors present a pictorial review of the various cranial, extracranial, and orbital manifestations of GCA. An increased awareness of this entity may help with timely and accurate diagnosis, helping expedite therapy and preventing serious complications.

Additional Diagnostic Value of Cone Beam CT Myelography Performed After Digital Subtraction Myelography for Detecting CSF-venous Fistulas.

BACKGROUND AND PURPOSE: CSF-venous fistulas are a common cause of spontaneous intracranial hypotension. The diagnosis and precise localization of these fistulas hinges on specialized myelographic techniques, which mainly include decubitus digital subtraction myelography and decubitus CT myelography (using either energy integrating or photon counting detector CT). A previous case series showed that cone beam CT myelography, performed as an adjunctive tool with digital subtraction myelography, increased the detection of CSF-venous fistulas. Here, we sought to determine the additive yield of cone beam CT myelography for CSF-venous fistula detection in a consecutive series of patients with spontaneous intracranial hypotension who underwent concurrent decubitus digital subtraction myelography and cone beam CT myelography. MATERIALS AND METHODS: We retrospectively searched our institutional database for all consecutive patients who underwent decubitus digital subtraction myelography with adjunctive cone beam CT myelography between 8/5/2021 and 8/5/2024. We excluded any patients harboring extradural CSF on spine imaging, not meeting International Classification of Headache Disorders (3rd edition) criteria for spontaneous intracranial hypotension, or not having undergone technically successful cone beam CT myelography in combination with digital subtraction myelography. All myelographic images were independently reviewed by two neuroradiologists. We calculated the diagnostic yield of both myelographic tests for localizing a CSF-venous fistula. RESULTS: We identified 100 patients who underwent decubitus digital subtraction myelography with adjunctive cone beam CT. We excluded 15 patients based on above criteria. 59/85 patients had a single definitive CSF-venous fistula. Among positive cases, the fistula was visible on digital subtraction myelography in 38/59 patients and visible on cone beam CT myelography in 59/59 patients. In 26/85 patients, no definitive fistula was identified on either modality. CONCLUSIONS: Cone beam CT myelography increased the diagnostic yield for CSF-venous fistula detection and may be a useful addition to digital subtraction myelography. ABBREVIATIONS: CB-CTM = cone beam CT myelography; CVF = CSF-venous fistula; DSM = digital subtraction myelography; EID-CTM = energy integrating detector CT myelography; PCD CTM = photon counting detector CT myelography; SIH = spontaneous intracranial hypotension.

MR Imaging Features of Critical Spinal Demyelinating Lesions Associated with Progressive Motor Impairment.

BACKGROUND AND PURPOSE: Progressive MS is typically heralded by a myelopathic pattern of asymmetric progressive motor weakness. Focal individual "critical" demyelinating spinal cord lesions anatomically associated with progressive motor impairment may be a compelling explanation for this clinical presentation as described in progressive solitary sclerosis (single CNS demyelinating lesion), progressive demyelination with highly restricted MR imaging lesion burden (2-5 total CNS demyelinating lesions; progressive paucisclerotic MS), and progressive, exclusively unilateral hemi- or monoparetic MS (>5 CNS demyelinating progressive unilateral hemi- or monoparetic MS [PUHMS] lesions). Critical demyelinating lesions appear strikingly similar across these cohorts, and we describe their specific spinal cord MR imaging characteristics. MATERIALS AND METHODS: We performed a retrospective, observational MR imaging study comparing spinal cord critical demyelinating lesions anatomically associated with progressive motor impairment with any additional "noncritical" (not anatomically associated with progressive motor impairment) spinal cord demyelinating lesions. All spinal cord MR images (302 cervical and 91 thoracic) were reviewed by an experienced neuroradiologist with final radiologic assessment on the most recent MR imaging. Anatomic association with clinical progressive motor impairment was confirmed independently by MS subspecialists. RESULTS: Ninety-one individuals (PUHMS, 37 [41%], progressive paucisclerosis 35 [38%], progressive solitary sclerosis 19 [21%]) with 91 critical and 98 noncritical spinal cord MR imaging demyelinating lesions were evaluated. MR imaging characteristics that favored critical spinal cord demyelinating lesions over noncritical lesions included moderate-to-severe, focal, lesion-associated spinal cord atrophy: 41/91 (45%) versus 0/98 (0%) (OR, 161.91; 9.43 to >999.9); lateral column axial location (OR, 10.43; 3.88-28.07); central region (OR, 3.23; 1.78-5.88); ventral column (OR, 2.98; 1.55-5.72); and larger lesion size of the axial width (OR, 2.01;1.49-2.72), transverse axial size (OR, 1.66; 1.36-2.01), or lesion area (OR, 1.14; 1.08-1.2). Multiple regression analysis revealed focal atrophy and lateral axial location as having the strongest association with critical demyelinating lesions. CONCLUSIONS: Focal, lesion-associated atrophy, lateral column axial location, and larger lesion size are spinal cord MR imaging characteristics of critical demyelinating lesions. The presence of critical demyelinating lesions should be sought as these features may be associated with the development of progressive motor impairment in MS.

Deep Learning-Based Reconstruction of 3D T1 SPACE Vessel Wall Imaging Provides Improved Image Quality with Reduced Scan Times: A Preliminary Study.

BACKGROUND AND PURPOSE: Intracranial vessel wall imaging is technically challenging to implement, given the simultaneous requirements of high spatial resolution, excellent blood and CSF signal suppression, and clinically acceptable gradient times. Herein, we present our preliminary findings on the evaluation of a deep learning-optimized sequence using T1-weighted imaging. MATERIALS AND METHODS: Clinical and optimized deep learning-based image reconstruction T1 3D Sampling Perfection with Application optimized Contrast using different flip angle Evolution (SPACE) were evaluated, comparing noncontrast sequences in 10 healthy controls and postcontrast sequences in 5 consecutive patients. Images were reviewed on a Likert-like scale by 4 fellowship-trained neuroradiologists. Scores (range, 1-4) were separately assigned for 11 vessel segments in terms of vessel wall and lumen delineation. Additionally, images were evaluated in terms of overall background noise, image sharpness, and homogeneous CSF signal. Segment-wise scores were compared using paired samples t tests. RESULTS: The scan time for the clinical and deep learning-based image reconstruction sequences were 7:26 minutes and 5:23 minutes respectively. Deep learning-based image reconstruction images showed consistently higher wall signal and lumen visualization scores, with the differences being statistically significant in most vessel segments on both pre- and postcontrast images. Deep learning-based image reconstruction had lower background noise, higher image sharpness, and uniform CSF signal. Depiction of intracranial pathologies was better or similar on the deep learning-based image reconstruction. CONCLUSIONS: Our preliminary findings suggest that deep learning-based image reconstruction-optimized intracranial vessel wall imaging sequences may be helpful in achieving shorter gradient times with improved vessel wall visualization and overall image quality. These improvements may help with wider adoption of intracranial vessel wall imaging in clinical practice and should be further validated on a larger cohort.