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Intracerebral hemorrhage

also known as Cerebral hemorrhage.

Its a subtype of intracranial hemorrhage that occurs within the brain tissue itself, also called intraaxial hemorrhage.

Intraparenchymal hemorrhage (IPH) is one extension of intracerebral hemorrhage (the other is intraventricular hemorrhage (IVH)) with bleeding within brain parenchyma).


Intracerebral hemorrhage causes 15% of strokes annually in the United States, and there is currently no effective therapy.

A systematic review of epidemiological studies reported intracerebral hemorrhage (ICH) incidence and mortality as unchanged over time; however, comparisons between studies conducted in different health services obscure assessment of trends.

Overall and fatal ICH rates have fallen in a large Australian population. Improvements in cardiovascular prevention and acute care may explain declining rates. There was no evidence of an increase in devastated survivors because the longer term mortality of 30-day survivors has not increased over time 1).




MicroRNAs (miRNAs) are important regulators of translation and have been reported to be associated with the pathogenesis of numerous cerebrovascular diseases, including ICH.

A study explored the role of miRNA (miR)‑126 in ICH. Adult male Wistar rats were randomly assigned to ICH model and sham groups. ICH was induced by intracerebral injection of collagenase. The mRNA expression levels of miR‑126 in the two groups were determined. The miR‑126 lentivirus expression vector pWPXL‑miR‑126 or negative control vector was then constructed and delivered via intraparenchymal injection. Following transduction, behavioral testing (rotarod and limb placement tests), relative hemorrhagic lesion size, apoptotic cells and protein levels of vascular endothelial growth factor (VEGF)‑A and caspase‑3 were determined. The relative expression levels of miR‑126 were significantly decreased in the ICH group compared to the sham group (P=0.026). Overexpression of miR‑126 significantly improved the relative duration of stay on the rotarod at day 2 (P=0.029) and 3 (P=0.033), and statistically reduced the deficit score (P=0.036), the relative size of hemorrhagic lesion (P=0.019) and the number of apoptotic cortical neurons (P=0.024) compared with the sham group. Additionally, the protein levels of VEGF‑A were significantly elevated, however levels of caspase‑3 were downregulated by overexpression of miR‑126 compared with the negative control group. MiR‑126 therefore exhibits a protective role in ICH. Overexpression of miR‑126 protects against ICH, and may be involved in the process of angiogenesis and exhibit an anti-apoptotic effect 2).

Calcium is a key cofactor of the coagulation cascade and may play a role in the pathophysiology of intracerebral hemorrhage (ICH).

Hypocalcemia correlates with the extent of bleeding in patients with ICH. A low calcium level may be associated with a subtle coagulopathy predisposing to increased bleeding and might therefore be a promising therapeutic target for acute ICH treatment trials 3).

A recent increase in interest in the pathophysiology of ICH, has led to elucidation of the pathways underlying ICH-induced brain injury, pathways where intercellular and hematoma to cell signaling play important roles 4).





As with other types of hemorrhages within the skull, intraparenchymal bleeds are a serious medical emergency because they can produce intracranial hypertension, which if left untreated can lead to coma and death.

Intracerebral hemorrhage (ICH) is a cerebrovascular disease with high mortality and morbidity, and the effective treatment is still lacking.

It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause intracranial hypertension and potentially fatal brain herniation syndromes.

They have high rates of morbidity and rates of mortality of up to 50%. Initial hematoma size and subsequent hematoma expansion are among the most important predictors of poor outcome.

Efforts to improve clinical outcome through mitigation of hematoma expansion have so far been unsuccessful.

Data suggest that outcomes can be improved with standardized medical care.

A strong association exists between the amount of intraventricular hemorrhage (IVH) and poor outcome in intracerebral hemorrhage. An IVH volume of 5 to 10 mL emerges as a significant threshold for decision making on prognosis in these patients 5).

The ICH score is a simple and reliable clinical grading scale that is used for predicting the early mortality of patients with ICHs.

Neurological deterioration (ND) occurs frequently and predicts poor outcomes. Hematoma expansion and intraventricular hemorrhage in early ND, and cerebral edema, fever, and medical complications in later ND 6).

Hematoma expansion is a potentially modifiable predictor of poor outcome following an acute intracerebral hemorrhage (ICH). The ability to identify patients with ICH who are likeliest to experience hematoma expansion and therefore likeliest to benefit from expansion-targeted treatments remains an unmet need. Hypodensities within an ICH detected by noncontrast computed tomography (NCCT) have been suggested as a predictor of hematoma expansion.


Brain abscess after intracerebral hemorrhage.

Intracerebral hemorrhage recurrence.

Inflammatory response mediates secondary brain injury during intracerebral hemorrhage (ICH).

Hematoma expansion is associated with poor outcome in intracerebral hemorrhage (ICH) patients. The spot sign and the blend sign are reliable tools for predicting hematoma expansion in ICH patients.

Stress ulcer.

Case series

Gattellari M, Goumas C, Worthington J. Declining rates of fatal and nonfatal intracerebral hemorrhage: epidemiological trends in Australia. J Am Heart Assoc. 2014 Dec 8;3(6):e001161. doi: 10.1161/JAHA.114.001161. PubMed PMID: 25488294.
Kong F, Zhou J, Zhou W, Guo Y, Li G, Yang L. Protective role of microRNA-126 in intracerebral hemorrhage. Mol Med Rep. 2017 Jan 19. doi: 10.3892/mmr.2017.6134. [Epub ahead of print] PubMed PMID: 28112373.
Morotti A, Charidimou A, Phuah CL, Jessel MJ, Schwab K, Ayres AM, Romero JM, Viswanathan A, Gurol ME, Greenberg SM, Anderson CD, Rosand J, Goldstein JN. Association Between Serum Calcium Level and Extent of Bleeding in Patients With Intracerebral Hemorrhage. JAMA Neurol. 2016 Nov 1;73(11):1285-1290. doi: 10.1001/jamaneurol.2016.2252. PubMed PMID: 27598746.
Egashira Y, Hua Y, Keep RF, Xi G. Intercellular cross-talk in intracerebral hemorrhage. Brain Res. 2015 Apr 8. pii: S0006-8993(15)00291-7. doi: 10.1016/j.brainres.2015.04.003. [Epub ahead of print] Review. PubMed PMID: 25863131.
Chan E, Anderson CS, Wang X, Arima H, Saxena A, Moullaali TJ, Heeley E, Delcourt C, Wu G, Wang J, Chen G, Lavados PM, Stapf C, Robinson T, Chalmers J, Huang Y; INTERACT2 Investigators. Significance of intraventricular hemorrhage in acute intracerebral hemorrhage: intensive blood pressure reduction in acute cerebral hemorrhage trial results. Stroke. 2015 Mar;46(3):653-8. doi: 10.1161/STROKEAHA.114.008470. Epub 2015 Feb 12. PubMed PMID: 25677598.
Lord AS, Gilmore E, Choi HA, Mayer SA; VISTA-ICH Collaboration. Time course and predictors of neurological deterioration after intracerebral hemorrhage. Stroke. 2015 Mar;46(3):647-52. doi: 10.1161/STROKEAHA.114.007704. Epub 2015 Feb 5. PubMed PMID: 25657190.
intracerebral_hemorrhage.txt · Last modified: 2019/11/04 09:57 by administrador