Geriatrics - Stroke Flashcards
What are the three main mechanisms of cerebrovascular disease?
Cerebrovascular diseases are subdivided into 3 major categories that include:
1) Thrombosis
2) Infarction
3) Haemorrhage
Pathophysiologic process that produces CVDs includes:
- reduced blood supply and oxygenation of tissue due to hypoxia, ischaemia and infarction (complication of ischaemia)
- CNS haemorrhage (parenchyma, subarachnoid) from rupture of cerebral vessels
What two mechanisms can derive the brain of oxygen?
The brain is a highly oxygen dependent tissue, and receives 15% of cardiac output. Cerebral blood flow is usually stable over a range of intracranial pressures due to autoregulation of vascular resistance. The brain may be deprived of oxygen in 2 circumstances:
1) FUNCTIONAL hypoxia = caused by low arterial pressure of oxygen (e.g. high altitude), impaired oxygen carrying capacity (e.g. severe anaemia, carbon monoxide poisoning) or inhibition of oxygen use by tissues (e.g. cyanide poisoning)
2) ISCHAEMIA (i.e. stroke) = either transient or permanent due to tissue hypoperfusion, which can be caused by hypotension, vascular occlusion or both
What can cause global ischaemia?
Widespread ischaemic-hypoxic can occur in the setting of severe systemic hypotension, usually when the systolic pressure falls below 50 mmHg, as in cardiac arrest, shock and severe hypotension. The clinical outcome varies with the duration and severity of the insult.
Which neurones are more susceptible to global ischaemic injury?
Neurons are more susceptible to ischaemic injury than are glial cells, and the most susceptible neurones are the pyramidal cells of the hippocampus and neocortex, and Purkinje cells of the cerebellum. In some individuals, even mild or transient global ischaemia insults may cause damage to these vulnerable areas.
In severe global ischaemia, widespread neuronal death occurs irrespective of regional vulnerability. Patients who survive often remain severely neurologically impaired and in a persistent vegetative state. Other patients meet the criteria for brainstem death, including evidence of diffuse cortical injury (isoelectric or “flat” EEG) and brain stem damage, including absent reflexes or respiratory drive. When these patients are sustained on a ventilator the brain gradually undergoes autolysis, leading to “respirator brain”.
What are the important morphological features of global ischaemia?
The brain is swollen with wide gyri and narrow sulci.
Features of irreversible ischaemic injury (infarction) are grouped as follows:
- EARLY CHANGES: occurring 12-24 hrs after, include acute neuronal cell change (red neurones). Individual cell bodies are shrunken, along with nuclei. After this, the reaction to tissue damage begins with infiltration of neutrophils
- SUBACUTE CHANGES: occurring at 24 hrs to 2 weeks. Includes necrosis of tissue, influx of macrophages, vascular proliferation and reactive gliosis
- REPAIR: seen after 2 weeks, is characterised by removal of necrotic tissue, loss of organised CNS structure and gliosis. The distribution of neuronal loss in the neocortex is typically uneven, with preservation of some layers and loss of others - termed pseudolaminar necrosis
What are watershed infarcts?
These are wedge shaped areas of infarction that occur in regions of the brain and spinal cord that lie at the most distal portions of arterial territories. They are usually seen after hypotensive episodes. In the cerebral hemispheres, the border zone between the anterior and middle cerebral arteries is at greatest risk. Damage to this region produces a band of necrosis over the cerebral convexivity a few centimetres lateral to the interhemispheric fissure.
What causes focal ischaemia? What is the role of collateral blood flow?
Cerebral arterial occlusion leads first to focal ischaemia then to infarction in the distribution of the affected vessel. The size, location and shape of the infarct and the extent of tissue damage that results can be modified by the presence of tissue collaterals. Specifically, collateral blood flow through the circle of Willis or cortico-leptomeningeal anastamoses can limit damage in some regions. By contrast, there is little collateral flow to structures such as the thalamus, basal ganglia and deep white matter which are supplied by deep penetrating vessels.
What is more common, embolic or thrombotic ischaemia?
Embolic infarctions are more common than infarctions due to thrombosis. Cardiac mural thrombi are a frequent cause of emboli; myocardial dysfunction, valvular disease and atrial fibrillation are important predisposing factors. Thromboemboli also arise in arteries, most often from atheromatous plaques within the carotid arteries or the aortic arch. Other emboli of venous origin cross over to the arterial circulation through cardiac defects and lodge in the brain (paradoxical emboli). These include thromboemboli from deep vein thrombosis and fat emboli (usually following long bone injury). The territory of the middle cerebral artery, a direct extension of the internal carotid artery) is most frequently affected by embolic infarction. Emboli tend to lodge where vessels branch or in areas of stenosis, usually caused by atherosclerosis.
Where do thrombotic occlusions usually occur?
Thrombotic occlusions causing cerebral infarctions usually are superimposed on atherosclerotic plaques. Common sites are around the carotid bifurcation, the origin of the middle cerebral artery, and at either end of the basilar artery. These occlusions may be accompanied by anterograde extension, as well as thrombus fragmentation and distal embolisation.
What are the two types of infarcts?
Infarcts can be divided into two types based on their macroscopic and microscopic appearance. Nonhaemorrhagic infarcts result from acute vascular occlusions (usually caused by atherosclerosis) and can be treated with thrombolytic therapy. This approach is contraindicated in haemorrhagic infarcts, which result from reperfusion of ischaemic tissue either through collaterals or after dissolution of emboli and often produce multiple, sometimes confluent petechial haemorrhages.
Emboli tend to produce haemorrhagic infarcts. Vessel reperfusion after lysis of embolic material causes haemorrhage.
What are common causes of haemorrhagic stroke?
Haemorrhage within the brain is associated with (1) hypertension and other diseases leading to vascular wall injury, (2) structural lesions such as AVMs and cavernous malformations and (3) tumours. Subarachnoid haemorrhage most commonly are caused by a ruptured berry aneurysm but can also occur in other vascular malformations. Subdural or epidural haemorrhages are usually associated with trauma.
What types of patients are most affected by primary brain parenchymal haemorrhage?
Spontaneous intraparenchymal haemorrhages are most common in mid to late adult life, with a peak incidence at about 60 years of age. Most are due to rupture of small intraparenchymal vessels. Hypertension is the leading cause, and brain haemorrhage accounts for roughly 50% of deaths amongst patients with hypertension.
In hypertension, branches of the lenticulostriate vessels develop Charcot-Bouchard microaneurysms. Rupture of these aneurysms produces intracerebral haemorrahage (haematoma). This pushes the brain parenchyma aside.
Which areas of the brain are most vulnerable to intracerebral haemorrhage?
Intracerebral haemorrhage can be devastating when it affects large portions of the brain or extends into the ventricular system. Hypertensive intraparenchymal haemorrhages typically occur in the basal ganglia, thalamus, pons and cerebellum. If the person survives the event, gradual resolution of the haematoma ensues sometimes with considerable clinical improvement.
What is the morphology of intracerebral haemorrhage?
Acute haemorrhages are characterised by extravasated blood, which compresses the adjacent parenchyma. With time, haemorrhages are converted to a cavity with a brown discoloured rim. On microscopic examination, early lesions consist of clotted blood surrounded by brain tissue showing anoxic neuronal and glial changes as well as oedema. Eventually, the oedema resolves and pigment and lipid laden macrophages appear.
What is cerebral amyloid angiopathy?
CAA is a disease in which amyloid peptides, typically the same as those found in Alzheimer’s disease, deposit in the walls of medium sized and small caliber meningeal and cortical vessels. The amyloid causes a rigid, pipe-like appearance and stains with Congo red. Amyloid deposition weakens the vessel walls and increases the risk of haemorrhages which differ in the distribution compare to those caused by hypertension. Specifically, CAA associated haemorrhages often occur in the lobes of the cerebral hemispheres (lobar haemorrhages).
What is the most common cause of a subarachnoid haemorrhage?
The most frequent cause of a clinically significant, non traumatic subarachnoid haemorrhage is rupture of a saccular (berry) aneurysm. Haemorrhage into the subarachnoid space also may result from vascular malformation, trauma, rupture of an intracerebral haemorrhage into the ventricular system, haematologic disturbances and tumours.
What precipitates subarachnoid haemorrhage?
Rupture of the saccular aneurysm can occur at any point, but about one third of cases are associated with an increase in intracranial pressure, such as with straining or sexual activity. Blood under arterial pressure is forced into the subarachnoid space, and the patient is stricken with a sudden, excruciating headache and rapidly looses consciousness. Between 25% and 50% die from the initial bleed.
Where is the most common location for aneurysms to develop leading to sub arachnoid haemorrhage?
About 90% of aneurysms occur in the anterior circulation near major arterial branch points. Multiple aneurysms exist in 20-30% of cases. Although they are sometimes referred to as “congenital” they are not present at birth but develop over time due to underlying defects in the vascular media. There is an increased risk of aneurysms in patients with autosomal dominant polycystic kidney disease, as well as those with disorders of extracellular matrix proteins.
The most common site is the anterior communicating artery (40%).
How is aneurysm size related to bleeding risk?
Overally, roughly 1.3% of aneurysms bleed per year with the probability of rupture increasing nonlinearly with size. For example, aneurysms larger than 1cm in diameter have a roughly 50% chance of bleeding each year. In the early period of SAH, there is an additional risk of ischaemic injury from vasospasm of other vessels. Healing and meningeal fibrosis and scarring sometimes obstruct CSF outflow or disrupt absorption leading to hydrocephalus.
What is the morphology of an aneurysm?
An unruptured aneurysm is a thin walled out-pouching of an artery. Beyond the neck of the aneurysm, the muscular wall and intimal elastic lamina are absent, such that the aneurysm sac is lined only by thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery.
What other types of aneurysms can be present other than saccular?
Atherosclerotic, mycotic, traumatic and dissecting aneurysms can also occur intracranially. The last three types (like saccular aneurysms) are most often found in the anterior circulation, whereas atherosclerotic aneurysms frequently involve the basilar artery. Non saccular aneurysms usually caused cerebral infarction due to vascular occlusion rather than haemorrhage.
Name the four different types of vascular malformation
Arteriovenous malformation (AVMs)
Cavernous malformations
Capillary telangiectasia
Venous angiomas
AVMs are the most common of these.
What patients are at risk of AVMs?
AVMs affect males twice as frequently as females and most commonly present during ages 10 to 30 years, with seizures, intracranial haemorrhage or SAH. Large AVMs occurring in the newborn can cause high output heart failure because of blood shunting from arteries to veins. The risk of bleeding makes AVMs the most dangerous type of vascular malformation.
Multiple AVMs can be seen in hereditary haemorrhagic telangiectasia, an autosomal dominant condition often associated with mutations affecting the TGF beta pathway.
