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The persisting burden of intracerebral haemorrhage: can effective treatments be found?

Josephson CB, Frantzias J, Samarasekera N, Al-Shahi Salman R - PLoS Med. (2010)

View Article: PubMed Central - PubMed

Affiliation: Division of Clinical Neurosciences, Centre for Clinical Brain Sciences, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.

ABSTRACT

Intracerebral haemorrhage (ICH) accounts for ∼10% and ∼20% of strokes in high and low-middle income countries, respectively, but ICH incidence and case fatality do not appear to be declining. Evidence supports organised stroke unit care and secondary prevention with blood pressure lowering after ICH. Ongoing randomised controlled trials of treatments that are either intended to limit early ICH growth, reduce perihaematomal oedema, or modify other key pathophysiological mechanisms underlying deterioration after acute ICH, offer hope for future improvements in outcome.

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Selected pathophysiological mechanisms that have been identified in humans after acute, spontaneous intracerebral haemorrhage.Shapes are approximate illustrations of when pathophysiological mechanisms are at their peak and their known durations. Uncertainties about the duration and intensity of mechanisms are indicated by dashed lines.
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pmed-1000353-g001: Selected pathophysiological mechanisms that have been identified in humans after acute, spontaneous intracerebral haemorrhage.Shapes are approximate illustrations of when pathophysiological mechanisms are at their peak and their known durations. Uncertainties about the duration and intensity of mechanisms are indicated by dashed lines.

Mentions: In humans, known pathophysiological mechanisms underlying further clinical deterioration soon after ICH include hydrocephalus, intraventricular extension of ICH, and recurrent ICH [10]; pathological and radiological studies have illuminated additional mechanisms (Figure 1). Human studies performing brain computed tomography within two time windows after ICH onset have documented haematoma expansion (Figure 2)—either due to growth of the original haemorrhage or re-bleeding [11]–[21]—that is associated with poor outcome [12],[16],[18],[22]. Imaging studies have demonstrated peri-haematomal hypoperfusion within the first week of ICH onset [23],[24], but not an “ischaemic penumbra” [25],[26]. However, there is evidence of a compensatory reduction in the metabolic rate, or a “metabolic penumbra”, around ICH [25],, as well as peri-haematomal hyperglycolysis (possibly due to inflammation, excitotoxicity, spreading depression, or seizures) [27]. Perihaematomal oedema appears to be vasogenic (plasma-derived) [28], its volume may increase within 24 hours of ICH onset and peak within 14 days [29]–[31], and it may be caused or exacerbated by thrombin and activated platelets [32],[33].


The persisting burden of intracerebral haemorrhage: can effective treatments be found?

Josephson CB, Frantzias J, Samarasekera N, Al-Shahi Salman R - PLoS Med. (2010)

Selected pathophysiological mechanisms that have been identified in humans after acute, spontaneous intracerebral haemorrhage.Shapes are approximate illustrations of when pathophysiological mechanisms are at their peak and their known durations. Uncertainties about the duration and intensity of mechanisms are indicated by dashed lines.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2957399&req=5

pmed-1000353-g001: Selected pathophysiological mechanisms that have been identified in humans after acute, spontaneous intracerebral haemorrhage.Shapes are approximate illustrations of when pathophysiological mechanisms are at their peak and their known durations. Uncertainties about the duration and intensity of mechanisms are indicated by dashed lines.
Mentions: In humans, known pathophysiological mechanisms underlying further clinical deterioration soon after ICH include hydrocephalus, intraventricular extension of ICH, and recurrent ICH [10]; pathological and radiological studies have illuminated additional mechanisms (Figure 1). Human studies performing brain computed tomography within two time windows after ICH onset have documented haematoma expansion (Figure 2)—either due to growth of the original haemorrhage or re-bleeding [11]–[21]—that is associated with poor outcome [12],[16],[18],[22]. Imaging studies have demonstrated peri-haematomal hypoperfusion within the first week of ICH onset [23],[24], but not an “ischaemic penumbra” [25],[26]. However, there is evidence of a compensatory reduction in the metabolic rate, or a “metabolic penumbra”, around ICH [25],, as well as peri-haematomal hyperglycolysis (possibly due to inflammation, excitotoxicity, spreading depression, or seizures) [27]. Perihaematomal oedema appears to be vasogenic (plasma-derived) [28], its volume may increase within 24 hours of ICH onset and peak within 14 days [29]–[31], and it may be caused or exacerbated by thrombin and activated platelets [32],[33].

View Article: PubMed Central - PubMed

Affiliation: Division of Clinical Neurosciences, Centre for Clinical Brain Sciences, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.

ABSTRACT

Intracerebral haemorrhage (ICH) accounts for ∼10% and ∼20% of strokes in high and low-middle income countries, respectively, but ICH incidence and case fatality do not appear to be declining. Evidence supports organised stroke unit care and secondary prevention with blood pressure lowering after ICH. Ongoing randomised controlled trials of treatments that are either intended to limit early ICH growth, reduce perihaematomal oedema, or modify other key pathophysiological mechanisms underlying deterioration after acute ICH, offer hope for future improvements in outcome.

Show MeSH