Quantitative analysis of injured, necrotic, and apoptotic cells in a new experimental model of intracerebral hemorrhage

Qureshi, Adnan I.; Ling, Geoffrey; Khan, Jehanzeb; Suri, M. Fareed K.; Miskolczi, Laszlo; Guterman, Lee R.; Hopkins, L. Nelson

doi:10.1097/00003246-200101000-00030

Cited by 97 publications

(61 citation statements)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…There is general agreement that the acute formation of an intraparenchymal mass lesion (the hematoma itself) produces tissue disruption and displacement. 1 A number of secondary pathophysiological processes have been implicated as causes of ongoing injury including ischemia surrounding the hematoma, 2-4 the development of cerebral edema, [5][6][7] activation of apoptotic processes 8 and toxic effects of components of the hematoma. 9,10 The role of ischemia as a cause of secondary injury has recently been investigated with positron-emission tomography.…”

mentioning

confidence: 99%

Perihematomal Mitochondrial Dysfunction After Intracerebral Hemorrhage

Kim-Han

Kopp

Dugan

et al. 2006

Stroke

125

View full text Add to dashboard Cite

Background and Purpose-Recent measurements in intracerebral hemorrhage (ICH) patients suggest a primary reduction in brain metabolism is responsible for reduced cerebral blood flow and low oxygen extraction surrounding the hematoma. We sought to determine whether reduced mitochondrial respiratory function could account for reduced metabolic demand in ICH patients. Methods-Brain-tissue samples from 6 patients with acute spontaneous ICH and 6 control patients undergoing brain resection for management of seizure were evaluated. Only tissue removed from the brain adjacent to the hematoma was studied. Specimens were collected in the operating room; mitochondrial studies were begun within 1-hour. Mitochondrial oxygen consumption was measured after the addition of pyruvate, malate, and ADP, followed by oligomycin and carbonylcyanide. Results-The ICH patients ranged in age from 40 to 54 years; 2 were female and half black. Hemorrhages were located in the temporal lobe (3), cerebellum (2) and parietal lobe (1).

show abstract

mentioning

confidence: 99%

Perihematomal Mitochondrial Dysfunction After Intracerebral Hemorrhage

Kim-Han

Kopp

Dugan

et al. 2006

Stroke

125

View full text Add to dashboard Cite

show abstract

“…Previous reports demonstrated induction of apoptosis, inflammation, and excitotoxic cascades after ICH, 14 and statins may provide multi-faceted protective effects that could reduce such damage. 2,3,5 However, findings regarding the effects of statins in humans with ICH have been limited and inconclusive, with one study reporting protective effects 12 and another failing to find such effects.…”

Section: Discussionmentioning

confidence: 91%

Prior Use of Statins Improves Outcome in Patients With Intracerebral Hemorrhage

Leker

Khoury

Rafaeli

et al. 2009

Stroke

View full text Add to dashboard Cite

“…1 ICH is considered primary in 78% to 88% of cases often attributed to hypertensive vasculopathy and cerebral amyloid angiopathy (CAA). 2 CAA accounts for the majority of primary lobar ICH in the elderly.…”

mentioning

confidence: 99%

The Spot Sign Is More Common in the Absence of Multiple Prior Microbleeds

Evans

Demchuk

Symons

et al. 2010

Stroke

View full text Add to dashboard Cite

Background and Purpose-Mural thickening and permeability changes in patients with amyloid angiopathy (CAA) and chronic hypertension are implicated in the pathophysiology of multiple, chronic subclinical microbleeds. The Spot sign, contrast extravasation on CT angiography, predicts hematoma expansion and is presumed to represent acute vessel damage. We hypothesize that the Spot sign is more common in patients without multiple prior chronic microbleeds. Methods-A retrospective study was conducted of 59 patients presenting within 6 hours of primary intracranial hemorrhage onset undergoing CT angiography and MRI. CT angiography spot sign presence was documented blinded to MRI. Hematoma expansion was defined as Ͼ6 mL or 30% enlargement. The Boston criteria were applied to microbleed interpretation dichotomizing subjects into probable and negative CAA. Basal ganglia, thalamic, and brain stem microbleed location were interpreted as chronic hypertensive pattern. Univariate logistic regression and ordinal logistic regression analysis identified significant predictive factors between spot-positive and -negative patients or microbleed pattern. Results-The incidence of spot positivity was 42%, 22%, and 0% for CAA-negative, chronic hypertensive, and CAA-positive patients, respectively (Pϭ0.01). CAA-negative patients had higher baseline National Institutes of Health Stroke Scale (Pϭ0.039), larger follow-up hematoma volume (Pϭ0.02), and poorer Rankin score (Pϭ0.049) than chronic hypertensive or CAA-positive patients. After age adjustment, spot-positive (Pϭ0.023), age-related white matter change (Pϭ0.041), number of microbleeds (PϽ0.0001), and modified Rankin score (Pϭ0.027) remained significantly different between groups. Conclusion-Boston criteria-defined CAA-negative status demonstrates the highest risk of spot positivity compared with patients with probable CAA and chronic hypertension. (Stroke. 2010;41:2210-2217.)

show abstract

Quantitative analysis of injured, necrotic, and apoptotic cells in a new experimental model of intracerebral hemorrhage

Abstract: A reproducible model of ICH in rabbits is described. At 24 hrs, the perihematoma region contains relatively large proportions of morphologically intact or reversibly injured (swollen) cells, suggesting the possibility of an extended window for therapeutic intervention.

Cited by 97 publications

References 35 publications

Perihematomal Mitochondrial Dysfunction After Intracerebral Hemorrhage

Perihematomal Mitochondrial Dysfunction After Intracerebral Hemorrhage

Prior Use of Statins Improves Outcome in Patients With Intracerebral Hemorrhage

The Spot Sign Is More Common in the Absence of Multiple Prior Microbleeds

Contact Info

Product

Resources

About