"Clinical syndrome of rapid onset of cerebral deficit (usually focal), lasting more than 24 hours or leading to death, with no apparent cause other than a vascular one." (Kumar and Clark, 2008)
As above for Stroke but additionally "Patients recover without significant deficit, usually within a week." (Kumar and Clark,2008)
Transient Ischaemic Attack (TIA):
"A focal deficit, such as weak limb, aphasia, loss of vision lasting from a few seconds to 24 hours, there is COMPLETE recovery." (Kumar and Clark, 2008)
A stroke is caused either by ischaemia and infarction of the brain or an intracranial haemorrhage, both resulting in damage to the brain tissue, causing altered functioning. The clinical presentation therefore is very variable, as it depends on the site affected and to what extent.
Intracranial haemorrhage, is a bleed within the cranial cavity, and can be subdivided into:
1. Intracerebral Haemorrhage
Haemorrhage within the cerebral hemispheres accounts for around 10% of strokes. The underlying cause of the haemorrhage is mainly due to rupture of micro aneurysms, and degeneration of small penetrating arteries. Usually these haemorrhages are massive and often fatal. These strokes tend to be more dramatic in presentation and with an associated severe headache, than those of ischaemic origin.
2. Cerebellar Haemorrhage
Haemorrhages within the cerebellum usually have the same underlying cause as intracerebral haemorrhages. Patients can present with headache, and can have rapid detoriation in their GCS. Due to the close proximity with the brainstem, they can also present with brainstem signs such as nystagmus and ocular palsies, and their gaze may deviate TOWARDS the haemorrhage.
3. Subarachnoid Haemorrhage
Subarachnoid haemorrhages (SAH), account for 5% of strokes, with an annual incidence of 6 per 100 000. SAH is when spontaneous arterial bleeding occurs in the subarachnoid space. Usually it has a dramatic onset, with a sudden very severe (thunderclap) headache, usually in the occipital region, followed by vomiting and often by coma.
The most common underlying cause of SAH include Saccular (Berry) aneurysms (accounting for around 70% of SAH), and Ateriovenous malformations (accounting for around 10% of SAH). Rarer causes include bleeding disorders, acute bacterial meningitis, brain tumours, arteritis and polycystic kidneys. However, it is unusual to find any contributing disease.
4. Subdural Haemorrhage
Subdural haemorrhage occurs when there is an accumulation of blood within the subdural space following rupture of a vein. Often it follows a head injury, which maybe trivial, and presentation may not be for days, weeks or even months after the injury. The elderly and alcoholics are more likely to present with chronic, unsuspected or spontaneous haemorrhages.
Clinical presentation is headache, drowsiness and confusion, symptoms of which often fluctuate. Additionally focal deficits such as hemiparesis or sensory loss may develop. Chronic subdural haemorrhage should always be considered in an elderly patient with new or worsening confusion.
5. Extradural Haemorrhage
Extradural haemorrhage is when a branch of the middle meningeal artery tears. This occurs through a linear skull fracture and leads to the accumulation of blood in the extradural space. Often a patient will suffer a head trauma, followed by a brief period of unconsciousness followed by a luccid interval of recovery. Next the patient can go on to develop progressive hemiparesis and stupor. Additionally transtentorial coning may occur, leading causing an ipsilateral dilated pupil, which may progress to bilateral fixed dilated pupils, tetraplegia and respiratory arrest.
Ischaemia and Infarction
Brain infarcts, in both cerebral hemispheres and brainstem, are caused by local interruption of blood flow to the brain and are the commonest cause of strokes, accounting for 70% of all strokes. Cerebral atherosclerosis is the most common cause of brain infarcts, with the most severe atherosclerotic lesions typically encountered within the larger vessels such as the internal carotid arteries, proximal middle cerebral arteries and basilar arteries. Additionally patients with atherosclerosis can have an occlusion due to a thrombosis of an atherosclerotic arterial segment, occuring most commonly near the carotid bifrucation or basilar artery.
Finally other causes of occulsion include emboli, mainly originating from the heart (as in chronic AF) or from atherosclerotic plaques. Vasculitis and trauma are less common causes of occlusion. Assessment of individuals presenting with embolic stroke should involve searching for their source (ECG, echo, carotid dopplers)
Clinical presentation will vary depending on site and extent of infarction, but generally present as:
1. Cerebral Infarction (50% of Infarcts - most common)
2. Brainstem Infarction (25% of Infarcts)
Causes complex signs depending on the relationship of the infarct to the cranial nerve nuclei, long tracts and brainstem connections.
3. Lacunar Infarction (25% of Infarcts)
Small infarcts around basal ganglia, internal capsule, thalamus and pons.
The Bamford classification system, is a simple bedside method of classifying acute ischaemic strokes. It uses the patients' symptoms to classify which region of the brain has been affected, and once classified it allows for prediction of a patient's prognosis.
Total Anterior Circulation Stroke (TACS)
Higher Cerebral Dysfunction & Homonymous Visual Field Defect & Ipsilateral Motor +/- Sensory Deficit
Mortality: 39% at 1 month, 60% at 1 year, Recurrence: Low Risk
Partial Anterior circulation stroke (PACS)
2 out of 3 of TACS Symptoms OR Higher Cerebral Dysfunction Alone OR Monoparesis
Mortality: 4% at 1 month, 16% at 1 year, Recurrence: Very High Risk
Lacunar stroke (LACS)
Motor Stroke OR Sensory Stroke OR Sensori-motor Stroke OR Ataxic Hemiparesis
Mortality: 2% at 1 month, 11% at 1 year, Reccurrence: Low Risk
Posterior circulation stroke (POCS)
Ipsilateral Cranial Nerve Palsy with Contralateral Motor Deficit OR Bilateral Deficit OR Disorder of Conjugate Eye Movement OR Cerebellar Dysfunction OR Isolated Homonymous Hemianopia
Mortality: 7% at 1 month, 19% at 1 year, Recurrence: High Risk
The purpose of investigations is to confirm the clinical diagnosis and to distinguish between strokes caused by infarction or haemorrage. Additionally, it is important to identify if there is an underlying cause of the stroke and to use the investigations to assist in directing the managment of the patient.
As previously discussed, when an ischaemic stroke occurs there is an interuption of the blood supply to part of the brain, this has affects in two ways.
Firstly to the brain tissue in the immediate area of the ischaemia, otherwise known as the 'Umbra'. The lack of oxygen causes the brain tissue to cease functioning. If this is prolonged and hasn't been restored after approximately 3 hours, the tissue will suffer irreversible injury, possibly leading to death of the tissue.
Secondly, the tissue area surrounding the ischaemic event can also be affected, it is tissue which is potentially destined for infarction but not yet irreversibly injured, this is known as the 'Penumbra'. Since the blood supply to the adajacent brain tisue is now restricted, the lack of oxygen delivery into metabolic pathways is affected. So, to improve this situation, the brain resorts to using anaerobic respiration in these areas. This form of respiration produces the by product lactic acid, which is an irritant and alters the acid-base balance of the brain.
Additionally, as oxygen and glucose depletion in these areas continue, the production of ATP fails. The knock on effect is failure of energy-dependent processes (i.e. ion pumps) necessary for tissue survival, setting off a cascade of events resulting in cellular injury and death. This cascade is known as the 'Ischaemic Cascade' and occurs in other tissues, but the brain differs to other tissue by having little respiratory reserve and being far more dependent on aerobic respiration.
So, to protect the 'Penumbra' region of the brain, it is vital to restore blood flow as quickly as possible. This is where thrombolysis can play a key role.
Thrombolysis, is the break down of a thrombus by pharmacological means. The pharmacological agent most commonly used today is 'Alteplase'. The pathway is described in the diagram below.
(Provided by Kumar and Clarke, 2002 - Pg 1214)
1. Kumar P, Clark M. Clinical Medicine , 6th Edition. Elsevier Saunders, 2008. Pg 1209 - 1219.
2. Kumar V, Cotran RS, Robbins SL. Robbins Basic Pathology, 7th Edition. Elsevier, India, 2004. Pg 814 - 815.
3. Longmore M, Wilkinson I, Turmezei T, Cheung CK. Oxford Handbook of Clinical Medicine, 7th Edition. Oxford University Press, Oxford, 2008. Pg 462.
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