There are two main mechanisms causing change of the brain in a stroke: ischemic and haemorrhage. Ischemic strokes represent 85% of all strokes[Tow12] and associated with arterial occlusion of an intracranial vessel leading to hypoperfusion of the brain region it supplies preventing sufficient delivery of oxygen, glucose and others nutrients. The effects of ischemia are rapid because the brain has low respiratory reserves and depends on aerobic metabolism. If cerebral blood flow is not restored within a short period of time, ischemia leads to neuron death within the perfusion territory of the affected area. Ischemia leads to the development of ischemic core and ischemic penumbra. The core is the region of the brain parenchyma that suffers severe reduction of blood flow and irreversible damage. The ischemic pneumbra is tissue surrounding the core which may only be partly injured with further possibility to recover[Pra10]. Haemorrhagic stroke makes up the remaining 15% of all strokes[Tow12] and occurs due to the rupture of blood vessels in the brain. This form leads to irritation of brain parenchyma and vasculature due to released blood and increased intracranial pressure from bleeding. In this regards, haemorrhagic strokes are more dangerous and have a higher mortality rate compared to ischemic strokes. The two main types of hemorrhagic strokes are intracerebral and subarachnoid hemorrhage. The first occurs in small arteries and is commonly because of trauma, illicit drug use or hypertension. The second takes place as a result of rupture of aneurysms from base of the brain bleeding into subarachnoid space between the pial and arachnoid membranes[Bec14]. The main goal of acute stroke management is to stabilize the patient and provide rehabilitation avoiding recurrent stroke[Gov04]. It is vital to complete the initial evaluation so as to obtain a rapid diagnosis. The therapy in acute ischemic stroke aims to avoid development of brain infarction or prevent its further progression with help of proven pharmacological agents. The clinical guideline for stroke of the National Institute for Health and Care Excellence suggests that if a diagnosis of hemorrhage is considered unlikely, that the patient should receive intravenous thrombolytic treatment with alteplase within four hours after the onset of the stroke symptoms[NIC08]. Alteplase is tissue-type plasminogen activator which converts plasminogen to plasmin, degrading fibrin and so breaks up thrombi. This treatment has been shown to significantly improve clinical outcomes by reducing the rate of long term disabilities[Kla12]. Additionally in the management of ischemic stroke acetyl salicylic acid at a dose of 300 mg should be given to the patient as soon as possible from diagnosis[NIC08]. Antiplatelet drugs such as aspirin, clopidogrel and dipyridamole decrease platelet aggregation and inhibit thrombus formation so may be used to prevent thromboembolic events. In the case of aspirin it irreversibly inhibits the enzyme cyclooxygenase, a key enzyme in the production of thromboxane A2 which triggers the reactions of platelet activation and aggregation[Kla12]. Oxygenation is also recommended for hypoxic patients to prevent further brain damage after a stroke. It improves outcomes as hypoxia predisposes to raised intracranial pressure, cerebral oedema and may cause herniation. Additionally it is important to monitor blood glucose level as experimental models suggest that persistent hypoglycaemia worsen ischemic cerebral injury[NIC08]. It is important to note that the effect of raised blood pressure may differ between patients with haemorrhagic and those with ischaemic stroke. Even little changes in blood pressure can lead to alterations of cerebral perfusion pressure which affects the ability of neurones to survive[NIC08]. The treatment and management of patients with acute intracerebral haemorrhage aims to prevent further bleeding and de