Disease relevance of Cerebral Hemorrhage

• BACKGROUND: Recurrent lobar intracerebral hemorrhage is the hallmark of cerebral amyloid angiopathy [1].
• Abnormal metabolism or reduced transport of CSF gamma-trace microprotein in hereditary cerebral hemorrhage with amyloidosis [2].
• An amyloid protein that precipitates in the cerebral vessel walls of Dutch patients with hereditary cerebral hemorrhage with amyloidosis is similar to the amyloid protein in vessel walls and senile plaques in brains of patients with Alzheimer's disease, Down syndrome, and sporadic cerebral amyloid angiopathy [3].
• These findings indicate that PN2/AbetaPP plays a significant role in regulating cerebral thrombosis and that modest increases in this protein can profoundly enhance cerebral hemorrhage [4].
• Thus, by introducing VEGF-overexpressing glioblastoma cells into the brain, we have established a reproducible and predictable in vivo model of tumor-associated intracerebral hemorrhage caused by the enhanced expression of single molecular species [5].

Psychiatry related information on Cerebral Hemorrhage

• In 31 symptomatic and 5 asymptomatic carriers of the amyloid precursor protein (APP) gene codon 693 mutation, 10 family members without mutation, and 5 carriers of the APP gene codon 692 mutation (3 with early-onset Alzheimer dementia, 2 with cerebral hemorrhage), a high frequency of the apolipoprotein E epsilon 4 allele was found [6].
• Four young individuals with histories of heavy cocaine abuse occurring several hours to days before the development of acute symptoms of severe headaches, disorientation, and subsequent stupor were shown to harbor subcortical cerebral hemorrhages [7].
• Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings [8].
• Correction by propranolol of the abnormal adrenaline discharge induced by emotional stress in cerebral hemorrhage patients [9].
• Anorexia nervosa with recurrent hypoglycemic coma and cerebral hemorrhage [10].

High impact information on Cerebral Hemorrhage

• The only cerebral hemorrhage occurred in a 73-year-old patient in the warfarin group [11].
• After the subjects were stratified according to their level of consciousness (Glasgow Coma Scale), those with objectively documented primary supratentorial intracerebral hemorrhage were randomly assigned to either dexamethasone or placebo [12].
• In experimental embolic stroke models, MMP inhibitors decreased cerebral hemorrhage and injury after treatment with tPA [13].
• Amyloid beta protein precursor gene and hereditary cerebral hemorrhage with amyloidosis (Dutch) [14].
• Abeta is targeted to the vasculature in a mouse model of hereditary cerebral hemorrhage with amyloidosis [15].

Chemical compound and disease context of Cerebral Hemorrhage

• Serum cholesterol was inversely associated with cerebral hemorrhage in the early cohort but not in the later.(ABSTRACT TRUNCATED AT 400 WORDS)[16]
• These findings suggest that endogenous tPA, through the enhancement of MMP 9 expression and proteolytic activation, plays an essential role in the pathogenesis of heparin-produced cerebral hemorrhage [17].
• When hydroxyurea dosage was increased, pancytopenia developed and was not resolved until 2 months after hydroxyurea was discontinued; Patient B developed a cerebral hemorrhage on hydroxyurea; he died shortly thereafter [18].
• These results suggest that pharmacological strategies targeting A2A receptors may provide effective inhibition of acute neurotoxic proinflammatory events that occur following intracerebral hemorrhage [19].
• Multiple intracerebral hemorrhages after smoking "crack" cocaine [20].

Biological context of Cerebral Hemorrhage

• GPI 562 caused a dose-dependent increase in tail vein bleeding time, but intracerebral hemorrhage (ICH) was not significantly increased at therapeutic doses; however, there was an increase in ICH at the highest doses tested [21].
• We also tested for the APP codon 693 mutation associated with hereditary cerebral hemorrhage with amyloidosis-Dutch type, for PRIP gene missense mutations at codons 102, 117, and 200, and for the PRIP insertion mutations which are associated with Creutzfeld-Jakob disease and Gerstmann-Straussler Scheinker syndrome [22].
• Adenosine A2A receptor activation reduces proinflammatory events and decreases cell death following intracerebral hemorrhage [19].
• Apo E4 phenotype, present in 111 (27%) of the 409 patients, was not related to a favorable 3 month outcome, response to t-PA, 3 month mortality, or risk of intracerebral hemorrhage [23].
• Public health implications would differ in different countries depending on the relative frequency of intracerebral hemorrhage and on the distribution of serum cholesterol levels in the population [24].

Anatomical context of Cerebral Hemorrhage

• Mutations in Krev1 interaction trapped gene 1 (KRIT1) cause cerebral cavernous malformation, an autosomal dominant disease featuring malformation of cerebral capillaries resulting in cerebral hemorrhage, strokes, and seizures [25].
• Alzheimer's disease and hereditary cerebral hemorrhage with amyloidosis-Dutch type share a decrease in cerebrospinal fluid levels of amyloid beta-protein precursor [26].
• Conditional deletion of alphav integrin in both central nervous system glia and neurons also leads to cerebral hemorrhage, but additionally to severe neurological defects [27].
• CGS 21680 administration directly into the striatum immediately prior to the induction of intracerebral hemorrhage inhibited TNF-alpha mRNA and, 24 hours following induction, reduced parenchymal neutrophil infiltration (p < 0.001) and TUNEL-positive cells (p < 0.002) within and bordering the hematoma [19].
• In hereditary cerebral hemorrhage with amyloidosis, Dutch type (HCHWA-D), a genetic variant (E22Q) of amyloid beta (Abeta) accumulates predominantly in the small vessels of leptomeninges and cerebral cortex, leading to fatal strokes in the fifth or sixth decade of life [28].

Gene context of Cerebral Hemorrhage

• Twenty-eight patients (8.2%) had asymptomatic intracerebral hemorrhage within 3 days of treatment with tPA [29].
• In contrast to Alzheimer disease (AD), the brains of those affected by hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) show few parenchymal amyloid plaques [15].
• However, Psen1 expression in neural progenitors rescued the cortical lamination defects, as well as the cerebral hemorrhages, and restored a normal vascular pattern in Psen1(-/-) embryos [30].
• In this study, we investigated the effect of EPO in experimental intracerebral hemorrhage (ICH) [31].
• Erythropoietin reduces perihematomal inflammation and cell death with eNOS and STAT3 activations in experimental intracerebral hemorrhage [31].

Analytical, diagnostic and therapeutic context of Cerebral Hemorrhage

• We studied the incidence of cerebral hemorrhage in an animal model of embolic stroke to determine the safety of aspirin, heparin, and tissue plasminogen activator therapies [32].
• CONCLUSIONS: In the absence of any clinically or statistically significant difference in outcome between the treated and control groups, this trial provides no justification for glycerol therapy following acute cerebral hemorrhage [33].
• These results justify clinical trials with levemopamil in cerebral disorders such as stroke, brain trauma, and peritumoral brain edema, which may be accompanied by intracerebral hemorrhage from the beginning or where transition to intracerebral hemorrhage may occur [34].
• We also analyzed samples from patients with meningitis or cerebral hemorrhage, or who were receiving total parenteral nutrition [35].
• Recent studies on transgenic APP23 mice suggest a relationship between passive immunization and amyloid angiopathy-associated cerebral hemorrhage, although the mechanism of hemorrhage was unclear from the data presented [36].

References