Background: Chronic subdural hematomas (cSDH) are increasingly prevalent worldwide with the increased aging population and anticoagulant use. Different surgical, medical, and endovascular treatments have had varying success rates. Primary neurosurgical interventions include burr hole drainage of the cSDH and mini-craniotomies/craniotomies with or without fenestration of the inner membrane. A key assessment of the success or failure of cSDH treatments has been symptomatic recurrence rates which have historically ranged from 5 to 30%. Pre-operative prediction of the inner subdural membrane by CT scan was used to guide our decision to perform mini-craniotomies. Release of the inner membrane facilitates the expansion of the brain and likely improves glymphatic flow.Methods: Consecutive mini-craniotomies (N = 34) for cSDH evacuation performed by a single neurosurgeon at a quaternary academic medical center/Level I trauma center from July 2018-September 2020 were retrospectively reviewed. Patient characteristics [age, gender, presenting GCS, GOS, initial CTs noting the inner subdural membrane, midline shift (MLS), cSDH width, inner membrane fenestration, cSDH recurrence, post-operative seizures, infections, length of stay] were extracted from the EMR.Results: Twenty nine patients had mini-craniotomies as primary treatment of the cSDH. Mean age = 68.9 ± 19.7 years (range 22–102), mean pre-operative GCS = 14.5 ± 1.1, mean MLS = 6.75 ± 4.2 mm, and mean maximum thickness of cSDH = 17.7 ± 6.0 mm. Twenty four were unilateral, five bilateral, 34 total craniotomies were performed. Thirty three had inner membrane signs on pre-operative head CTs and an inner subdural membrane was fenestrated in all cases except for the one craniotomy that didn't show these characteristic CT findings. Mean operating time = 79.5 ± 26.0 min. Radiographic and clinical improvement occurred in all patients. Mean improvement in MLS = 3.85 ± 2.69. There were no symptomatic recurrences, re-operations, surgical site infections, or deaths during the 6 months of follow-up. One patient was treated for post-operative seizures with AEDs for 6 months.Conclusion: Pre-operative CT scans demonstrating inner subdural membranes may guide one to target the treatment to allow release of this tension band. Mini-craniotomy with careful fenestration of the inner membrane is very effective for this. Brain re-expansion and re-establishment of normal brain interstitial flow may be important in long term outcomes with cSDH and may be related to the recent interests in brain glymphatics and dural lymphatics.
Background: Ependymomas are rare tumors originating from neuroepithelial cells lining the wall of the ventricles or central canal of the spinal cord. While these tumors mainly occur within the central nervous system (CNS), there are occasional reports in children and young adult patients with a primary tumor occurrence outside of the CNS. Ependymomas of the sacrococcygeal region have been infrequently described in the literature with no standard of care established. We present a case report and review of the literature regarding this rare entity. Case Description: A 24-year-old woman presented with right gluteal pain worsened by sitting and a palpable soft tissue mass of the sacrococcygeal region. Magnetic resonance imaging revealed a 3.7 cm cystic mass centered in the right gluteal region. She underwent a biopsy at an outside institution, with histology revealing myxopapillary ependymoma. The patient was referred to our hospital and underwent an interdisciplinary neurosurgical and orthopedic oncology en bloc resection of the ependymoma, which intraoperatively appeared to originate from the coccygeal nerve. Conclusion: In the present report, the authors demonstrate that a myxopapillary ependymoma may present as an isolated gluteal mass attached to the coccygeal nerve, without frank CNS involvement. Furthermore, an interdisciplinary approach to surgical resection of this lesion appears to represent an effective treatment modality.
Brain atrophy is associated with degenerative neuropathologies as well as clinical status of dementia. Whether dementia is associated with atrophy independent of neuropathologies is not known. In this study, we examined the pattern of atrophy associated with dementia while accounting for the most common dementia-related neuropathologies. We used data from National Alzheimer’s Coordinating Center (NACC, n = 129) and Alzheimer’s Disease Neuroimaging Initiative (ADNI, n = 47) participants with suitable in-vivo 3D-T1w MRI and autopsy data. We determined dementia status at visit closest to MRI. We examined the following dichotomized neuropathological variables: Alzheimer’s disease neuropathology, hippocampal sclerosis, Lewy Bodies, cerebral amyloid angiopathy, atherosclerosis. Voxel-based morphometry identified areas associated with dementia after accounting for neuropathologies. Identified regions of interest were further analyzed. We used multiple linear regression models adjusted for neuropathologies and demographic variables. We also examined models with dementia and Clinical Dementia Rating sum of the boxes (CDR-SB) as the outcome and explored the potential mediating effect of medial temporal lobe structure volumes on the relationship between pathology and cognition. We found strong associations for dementia with volumes of the hippocampus, amygdala, and parahippocampus (semi-partial correlations ≥ 0.28, P < 0.0001 for all regions in NACC; semi-partial correlations ≥ 0.35, P ≤ 0.01 for hippocampus and parahippocampus in ADNI). Dementia status accounted for more unique variance in atrophy in these structures (∼8%) compared with neuropathological variables; the only exception was hippocampal sclerosis which accounted for more variance in hippocampal atrophy (10%). We also found that the volumes of the medial temporal lobe structures contributed towards explaining the variance in CDR-SB (ranging from 5% to 9%) independent of neuropathologies and partially mediated the association between Alzheimer’s disease neuropathology and cognition. Even after accounting for the most common neuropathologies, dementia still had among the strongest associations with atrophy of medial temporal lobe structures. This suggests that atrophy of the medial temporal lobe is most related to clinical status of dementia rather than Alzheimer's disease or other neuropathologies, with the potential exception of hippocampal sclerosis.
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