A case of chronic subdural hematoma demonstrating the epileptic focus at the area with sulcal hyperintensity on fluid-attenuated inversion recovery image

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

Although the sulcal hyperintensity on fluid-attenuated inversion recovery (FLAIR) images is detected in some chronic subdural hematoma (CSDH) cases, its clinical significance remains determined. A 77-year-old man with symptomatic CSDH presented with generalized tonic-clonic seizures at 9 days after surgery. ¹²³I-iomazenil -single photon emission computed tomography revealed transient reduction in cortical benzodiazepine receptors binding potential at the region corresponding to that of the sulcal hyperintensity on FLAIR images. Findings of sulcal hyperintensity on FLAIR imaging under the CSDH may have a relation with the cause of epileptic seizure.

Related collections

Most cited references 12

Record: found
Abstract: found
Article: not found

Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma.

H Mizukoshi, T Komai, H Ito … (1976)

The authors describe studies performed on material aspirated from chronic subdural hematomas. Patients were given 51Cr-labeled red cells prior to aspiration, and it was possible to demonstrate that the mean daily hemorrhage into the hematoma space amounted to 10.2% of its volume. Immunoelectrophoresis of the aspirated hematoma fluid by monospecific anti-human fibrinogen revealed the presence of fibrin and fibrinogen degradation products that, measured by hemagglutination-inhibition immunoassay techniques, varied between 5.0 and 10,500 mug/ml with an average of 2604 mug/ml in 18 cases. The tissue activator was demonstrated by Todd's histological localization in the outer membrane of the chronic subdural hematoma in 11 cases, but not in the inner membrane. These results indicate that if a clot in the subdural space causes the formation of neomembrane, and excessive fibrinolysis occurs, the subdural clot would not only liquefy, but also enlarge by continuous hemorrhage from the neomembrane. Therefore, local hyperfibrinolysis and continuous bleeding are important in the etiology of the chronic subdural hematoma.

0 comments Cited 27 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

The origin ofsubdural neomembranes. II. Fine structural of neomembranes.

R L Friede, W Schachenmayr (1978)

A comparison of the fine structure of subdural neomembranes with the fine structural organization of the normal human dura-arachnoid interface discloses that neomembranes are not de novo proliferations of tissue from a smooth inner dural surface. Rather, a neomembrane is the result of proliferation and excessive thickening of the normal layer of dural border cells. On proliferation, the dural border cells form multilayered tiers and clusters of cells, transfixed by capillaries, with collagen fibrils and elastic fibers between them. Capillaries and collagen fibrils are absent from the normal interface layer. Pathogenetic concepts of chronic subdural hematoma need to be revised. Any pathologic condition inducing cleavage of tissue within the dural border layer at dura-arachnoid interface will be followed by proliferation of fural border cells with production of a neomembrane. There is no compelling reason to postulate that proliferation of the border cell layer is always secondary to traumatic hemorrhage.

0 comments Cited 25 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: not found

Selective neuronal loss in rescued penumbra relates to initial hypoperfusion.

STANI DAY, J Guadagno, Joshua Smith … (2008)

Selective neuronal loss (SNL) in the rescued penumbra could account for suboptimal clinical recovery despite effective early reperfusion. Previous studies of SNL used single-photon emission tomography (SPECT), did not account for potential volume loss secondary to collapse of the infarct cavity, and failed to show a relationship with initial hypoperfusion. Here, we obtained acute-stage computerized tomography (CT) perfusion and follow-up quantitative (11)C-flumazenil (FMZ)-PET to map SNL in the non-infarcted tissue and assess its relationship with acute-stage hypoperfusion. We prospectively recruited seven patients with evidence of (i) acute ( or =6 at 24 h), good clinical outcome (NIHSS < or =5) and small final infarct (6/7 subcortical) on late-stage MRI. Ten age-matched controls were also studied. FMZ image analysis took into account potential post-stroke volume loss. Across patients, clusters of significantly reduced FMZ binding were more prevalent and extensive in the non-infarcted middle cerebral artery cortical areas than in the non-affected hemisphere (P = 0.028, Wilcoxon sign rank test). Voxel-based between-group comparisons revealed several large clusters of significantly reduced FMZ binding in the affected peri-insular, superior temporal and prefrontal cortices (FDR P < 0.05), as compared with no cluster on the unaffected side. Finally, comparing CTp and PET data revealed a significant negative correlation between FMZ binding and initial hypoperfusion. Applying correction for volume loss did not substantially alter the significance of these results. Although based on a small patient sample sometimes studied late after the index stroke, and as such preliminary, our results establish the presence and distribution of FMZ binding loss in ultimately non-infarcted brain areas after stroke. In addition, the data suggest that this binding loss is proportional to initial hypoperfusion, in keeping with the hypothesis that the rescued penumbra is affected by SNL. Although its clinical counterparts remain uncertain, it is tempting to speculate that peri-infarct SNL could represent a new therapeutic target.

0 comments Cited 23 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Contributors

Hiroshi Kashimura

Journal

Journal ID (nlm-ta): Radiol Case Rep

Journal ID (iso-abbrev): Radiol Case Rep

Title: Radiology Case Reports

Publisher: Elsevier

ISSN (Electronic): 1930-0433

Publication date PMC-release: 13 July 2019

Publication date Collection: September 2019

Publication date (Electronic): 13 July 2019

Volume: 14

Issue: 9

Pages: 1109-1112

Affiliations

[a ]Department of Neurosurgery, Iwate Prefectural Chubu Hospital, 17-10 Murasakino, Kitakami, Iwate 024-8507, Kitakami, Iwate, Japan

[b ]Department of Neurosurgery, Iwate Medical University School of Medicine, Morioka, Iwate, Japan

Author notes

[* ]Corresponding author. hkashimura@ 123456icloud.com

Article

Publisher ID: S1930-0433(19)30237-7

DOI: 10.1016/j.radcr.2019.06.021

PMC ID: 6629924

PubMed ID: 31338136

SO-VID: d0379bde-8c8f-4100-9f69-d0a84b387022

License:

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

History

Date received : 7 May 2019

Date revision received : 13 May 2019

Date accepted : 27 June 2019

Comments

Comment on this article

scite_

Cited by 2

See all cited by

Most referenced authors 90

See all reference authors

- Version 1

A case of chronic subdural hematoma demonstrating the epileptic focus at the area with sulcal hyperintensity on fluid-attenuated inversion recovery image

Read this article at

Abstract

Related collections

Orthopedics

Most cited references 12

Role of local hyperfibrinolysis in the etiology of chronic subdural hematoma.

The origin ofsubdural neomembranes. II. Fine structural of neomembranes.

Selective neuronal loss in rescued penumbra relates to initial hypoperfusion.

Author and article information

Contributors

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 443

Cited by 2

Most referenced authors 90