**Author details**

Kristiina Rannikmäe1 and Cathie Sudlow1,2

\*Address all correspondence to: cathie.sudlow@ed.ac.uk

1 Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK

2 Institute for Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK

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**Chapter 6**

**Src Family Kinases in Intracerebral Hemorrhage**

Intracerebral hemorrhage (ICH), which accounts for 2 million (10–15%) of about 15 million strokes worldwide each year [1], has very high mortality rates of 31% at 7 days, 59% at 1 year, 82% at 10 years, and greater than 90% at 16 years [2,3]. ICH is associated with increased intracranial pressure, hematoma, blood brain barrier (BBB) disruption, brain edema, neuron loss, motor deficits, cognitive impairment and high mortality in humans. The major challenges immediately after ICH are re-bleed, hematoma induced brain injury, brain edema and neurological deficits [4]. Potential treatments of ICH include slowing the initial bleeding during the first hours after onset; removing blood from the parenchyma or ventricles to eliminate both mechanical and chemical factors that cause brain injury; management of complications of blood in the brain; and supportive medical care and surgery for certain patients [5]. Since these treatments have great variability, there is currently no FDA approved

The time course after ICH can be divided into two stages (acute/injury and chronic/recovery) (Fig. 1). At the acute stage, glutamine, thrombin, TNF-α, VEGF and other endogenous molecules are rapidly released following ICH. These molecules team up leading to brain cell death and severe brain injury via multiple neurotoxicity pathways, including (1) Excitatory amino acid (AA) and NMDA receptor-mediated excitatory toxicity; (2) Thrombin and other mitogen-mediated mitogenic stress; (3) Vascular endothelial growth factor (VEGF) and matrix metalloproteinases (MMPs)-mediated changes of vascular permeability; (4) Cytokines-

As time course transits into chronic/recovery stage post-ICH, the elevated molecules resolve gradually and in turn participate in neurogenesis via populating neural progenitor cells (NPCs) to fix the damaged brain tissue. The possible mechanisms include (1) Excitatory amino acid (AA) and NMDA receptor-mediated excitatory genesis; (2) Thrombin and other mitogen-

> © 2014 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Additional information is available at the end of the chapter

mediated inflammatory responses; and others (Fig. 1).

DaZhi Liu

**1. Introduction**

treatment for ICH.

http://dx.doi.org/10.5772/58488
