Intracerebral hemorrhage diagnosis

Intracerebral hemorrhage diagnosis

Computed tomography

Noncontrast computed tomography (NCCT) is the gold standard to detect intracerebral hemorrhage (ICH) in patients presenting with acute focal syndromes.

Although CT remains important in the acute setting, MR imaging has proved invaluable for diagnosis and characterization of intracranial hemorrhage.

Non-contrast head CT, given its availability and high sensitivity in detecting blood products, is frequently the first tool to readily detect ICH; however, different types of hemorrhages may share a common appearance on CT and the optimal therapeutic approach varies depending on etiology. An additional diagnostic work-up is frequently indicated to make the final diagnosis and to assist in urgent patient management. CT- and MR angiography, and digital angiography can diagnose vascular anomalies, CT venography can reveal cerebral vein thrombosis, diffusion-weighted MRI (DWI) may show hemorrhagic transformation of an infarct, and susceptibility-weighted MRI (SWI) may detect hypertensive and amyloid angiopathy-related microbleeds. MR also has a major role in revealing underlying etiologies such as cavernoma, primary brain tumor or metastases. These imaging tools assist in determining the cause of ICH, and also in assessing the risk of deterioration. Prognostic factors such as size, location, mass effect, and detection of the “spot sign” all play an important role in foreseeing possible deterioration, thus allowing prompt intervention 1).


Intracerebral hemorrhage volume is a powerful predictor of 30-day mortality after spontaneous intracerebral hemorrhage (ICH). Kothari et al., compared a bedside method of measuring CT ICH volume with measurements made by computer-assisted planimetric image analysis 2).

MRI

Diffusion weighted magnetic resonance imaging (DW-MRI) may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke.

DW-MRI at b1000 has a diagnostic yield similar to noncontrast computed tomography (NCCT) for detecting ICH and superior to NCCT for detecting ischemic stroke (IS). Therefore, DW-MRI may be considered as the initial screening tool for imaging patients presenting with focal neurologic symptoms suggestive of stroke 3).

Biomarkers

Results indicated that circulating miR-181b, miR-223, miR-155 and miR-145 in plasma samples could be served as a potential noninvasive tool in ICH detection 4).

References

1)

Eliahou R, Auriel E, Gomori M, Sosna J, Honig A. [SPONTANEOUS PARENCHYMAL INTRACRANIAL HEMORRHAGE – A DIAGNOSTIC CHALLENGE]. Harefuah. 2018 Mar;157(3):158-161. Hebrew. PubMed PMID: 29582945.
2)

((Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, Khoury J. The ABCs of measuring intracerebral hemorrhage volumes. Stroke. 1996 Aug;27(8):1304-5. PubMed PMID: 8711791.
3)

Keigler G, Goldberg I, Eichel R, Gomori JM, Cohen JE, Leker RR. Diffusion-weighted Imaging at b1000 for Identifying Intracerebral Hemorrhage: Preliminary Sensitivity, Specificity, and Inter-rater Variability. J Stroke Cerebrovasc Dis. 2014 May 1. pii: S1052-3057(14)00065-2. doi: 10.1016/j.jstrokecerebrovasdis.2014.02.005. [Epub ahead of print] PubMed PMID: 24795096.
4)

Gareev I, Yang G, Sun J, Beylerli O, Chen X, Zhang D, Zhao B, Zhang R, Sun Z, Yang Q, Li L, Pavlov V, Safin S, Zhao S. Circulating MicroRNAs as a Potential Non-invasive Biomarkers of Spontaneous Intracerebral Hemorrhage. World Neurosurg. 2019 Sep 13. pii: S1878-8750(19)32446-5. doi: 10.1016/j.wneu.2019.09.016. [Epub ahead of print] PubMed PMID: 31525485.

Intracranial aneurysm pathogenesis

Intracranial aneurysm pathogenesis

Until now, the exact etiology of intracranial aneurysms formation remains unclear.

Time-dependent and site-dependent morphological changes and the level of degradation molecules may be indicative of the vulnerability of aneurysm rupture 1).

Miyata et al. proposed the contribution of a structural change in an adventitia, i.e., vasa vasorum formation, to the rupture of IAs 2).

Although some previous reports have demonstrated an association between lipid accumulation and degenerative changes in aneurysm walls in humans, epidemiological studies have failed to identify dyslipidemia as a risk factor for intracranial aneurysm pathogenesis. Thus, Shimizu et al. examined whether an increase in serum cholesterol levels facilitates the progression of intracranial aneurysms in a rat model. Rats were given a high-fat diet (HFD) and subjected to an intracranial aneurysm model. The HFD elevated their serum cholesterol levels. The intracranial aneurysms induced at the anterior cerebral artery-olfactory artery bifurcation were significantly larger in the high-fat group than in the normal-chow group. Histological analysis demonstrated that the loss of medial smooth muscle layers was exacerbated in the high-fat group and indicated the presence of macrophage-derived foam cells in the lesions. In in vitro experiments, the expression levels of the pro-inflammatory genes induced by LPS in RAW264.7-derived foam cells were significantly higher than those in RAW264.7 cells. The combination of these results suggests that increased serum cholesterol levels facilitate degenerative changes in the media and the progression of intracranial aneurysms presumably through foam cell transformation 3).

Genetics

Pathophysiology

Hemodynamics

see Intracranial aneurysm hemodynamics.

In addition to ambiental factors (smoking, excessive alcohol consumption and hypertension), epidemiological studies have demonstrated a familiar influence contributing to the pathogenesis of intracranial aneurysms, with increased frequency in first- and second-degree relatives of people with subarachnoid hemorrhage.

Data suggest that macrophage-derived Matrix metalloproteinase 2 and Matrix metalloproteinase 9, may play an important role in the progression of intracranial aneurysms. The findings will shed a new light into the pathogenesis of cerebral aneurysms and highlight the importance of inflammatory response causing the degeneration of extracellular matrix in the process of this disease 4).

Investigations strongly suggest that the pathophysiology is closely associated with chronic inflammation in vascular walls. Nuclear factor kappaB (NF-kappaB) has a key role in the formation and progression.

Children with Sickle Cell Disease (SCD) are at risk for developing multiple intracranial aneurysms, and a high index of suspicion must be maintained during the interpretation of routine magnetic resonance imaging or angiography of the brain 5).

Dental bacterial DNA can be found using a quantitative polymerase chain reaction in both ruptured and unruptured aneurysm walls, suggesting that bacterial DNA plays a role in the pathogenesis of cerebral aneurysms in general, rather than only in ruptured aneurysms 6).

THSD1 in Intracranial aneurysm pathogenesis

Thrombospondin type-1 domain-containing protein 1 is a protein that in humans is encoded by the THSD1 gene.

The protein encoded by this gene contains a type 1 thrombospondin domain, which is found in thrombospondin, a number of proteins involved in the complement pathway, as well as extracellular matrix proteins. Alternatively spliced transcript variants encoding distinct isoforms have been observed.

As illustrated by THSD1 research, cell adhesion may play a significant role in IA 7).

A study discovered that harmful variants in THSD1 (Thrombospondin type-1 domain-containing protein 1) likely cause intracranial aneurysm and subarachnoid hemorrhage in a subset of both familial and sporadic patients with supporting evidence from two vertebrate models 8).

A report identified THSD1 mutations in familial and sporadic IA patients and shows that THSD1 loss results in cerebral bleeding in 2 animal models. This finding provides new insight into IA and subarachnoid hemorrhage pathogenesis and provides new understanding of THSD1 function, which includes endothelial cell to extracellular matrix adhesion 9).

References

1)

Yamaguchi T, Miyamoto T, Kitazato KT, Shikata E, Yamaguchi I, Korai M, Shimada K, Yagi K, Tada Y, Matsuzaki Y, Kanematsu Y, Takagi Y. Time-dependent and site-dependent morphological changes in rupture-prone arteries: ovariectomized rat intracranial aneurysm model. J Neurosurg. 2019 Sep 13:1-9. doi: 10.3171/2019.6.JNS19777. [Epub ahead of print] PubMed PMID: 31518986.
2)

Miyata H, Imai H, Koseki H, Shimizu K, Abekura Y, Oka M, Kawamata T, Matsuda T, Nozaki K, Narumiya S, Aoki T. Vasa vasorum formation is associated with rupture of intracranial aneurysms. J Neurosurg. 2019 Aug 16:1-11. doi: 10.3171/2019.5.JNS19405. [Epub ahead of print] PubMed PMID: 31419795.
3)

Shimizu K, Miyata H, Abekura Y, Oka M, Kushamae M, Kawamata T, Mizutani T, Kataoka H, Nozaki K, Miyamoto S, Aoki T. High-Fat Diet Intake Promotes the Enlargement and Degenerative Changes in the Media of Intracranial Aneurysms in Rats. J Neuropathol Exp Neurol. 2019 Jul 24. pii: nlz057. doi: 10.1093/jnen/nlz057. [Epub ahead of print] PubMed PMID: 31340038.
4)

Aoki T, Kataoka H, Morimoto M, Nozaki K, Hashimoto N. Macrophage-derived matrix metalloproteinase-2 and -9 promote the progression of cerebral aneurysms in rats. Stroke. 2007 Jan;38(1):162-9. Epub 2006 Nov 22. PubMed PMID: 17122420.
5)

Saini S, Speller-Brown B, Wyse E, Meier ER, Carpenter J, Fasano RM, Pearl MS. Unruptured Intracranial Aneurysms in Children With Sickle Cell Disease: Analysis of 18 Aneurysms in 5 Patients. Neurosurgery. 2015 Feb 12. [Epub ahead of print] PubMed PMID: 25710108.
6)

Pyysalo MJ, Pyysalo LM, Pessi T, Karhunen PJ, Lehtimäki T, Oksala N, Öhman JE. Bacterial DNA findings in ruptured and unruptured intracranial aneurysms. Acta Odontol Scand. 2016 May;74(4):315-20. doi: 10.3109/00016357.2015.1130854. Epub 2016 Jan 18. PubMed PMID: 26777430.
7)

Xu Z, Rui YN, Hagan JP, Kim DH. Intracranial Aneurysms: Pathology, Genetics, and Molecular Mechanisms. Neuromolecular Med. 2019 May 4. doi: 10.1007/s12017-019-08537-7. [Epub ahead of print] Review. PubMed PMID: 31055715.
8)

Rui YN, Xu Z, Fang X, Menezes MR, Balzeau J, Niu A, Hagan JP, Kim DH. The Intracranial Aneurysm Gene THSD1 Connects Endosome Dynamics to Nascent Focal Adhesion Assembly. Cell Physiol Biochem. 2017;43(6):2200-2211. doi: 10.1159/000484298. Epub 2017 Oct 25. PubMed PMID: 29069646.
9)

Santiago-Sim T, Fang X, Hennessy ML, Nalbach SV, DePalma SR, Lee MS, Greenway SC, McDonough B, Hergenroeder GW, Patek KJ, Colosimo SM, Qualmann KJ, Hagan JP, Milewicz DM, MacRae CA, Dymecki SM, Seidman CE, Seidman JG, Kim DH. THSD1 (Thrombospondin Type 1 Domain Containing Protein 1) Mutation in the Pathogenesis of Intracranial Aneurysm and Subarachnoid Hemorrhage. Stroke. 2016 Dec;47(12):3005-3013. Epub 2016 Nov 15. Erratum in: Stroke. 2017 Aug;48(8):e240. PubMed PMID: 27895300; PubMed Central PMCID: PMC5134902.

Imaging in Neurovascular Disease A Case-Based Approach

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About 600 high-quality noninvasive images, such as MR angiography/MR imaging, CT angiography/CT perfusion, with angiography where applicable, elucidate a spectrum of findings Analysis of the imaging appearance of a diverse array of common to rare neurovascular diseases provides diagnostic and treatment insights Each case concludes with the most important points clinicians need to know, high-yield facts about a specific cerebrovascular disease, and suggested readings for further exploration This unique case-based book is essential reading for radiology, neurology and neurosurgery residents. It will greatly benefit neurovascular disease specialists including radiologists, neurosurgeons and neurologists as well as interested in furthering their knowledge on the use of neuroimaging to guide neurointerventional and neurosurgical procedures to treat cerebrovascular disease.

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