Cerebrovascular accidents (CVA) or cerebrovascular attacks are the most important events that occur in the brain as a consequence of diseases of the blood vessels or embolizing cardiac dysfunctions. Vascular lesions generally occur in the vessels of the neck or in the intracranial arteries.
According to the World Health Organization, stroke is defined as "the acute or rapid onset of clinical signs that reflect a focal (and sometimes global) dysfunction of the brain, of vascular cause and that last longer than 24 hours". The term "global" refers to subarachnoid hemorrhage. The definition excludes transient ischemic attack (TIA), which is considered a threat or risk factor for stroke.
Sudden neurological deficit of vascular origin is now preferred to call a stroke, rather than stroke, to emphasize the severity of the disease and give it urgent diagnostic and treatment importance, similar to what occurs with myocardial infarction.
Cerebrovascular diseases are the third leading cause of death in the Western world after heart disease and cancer and the leading cause of severe disability in adults. Mortality from the disease is approximately 30% during the first year and 15% in subsequent years, and both figures increase with age.
Most of the neuronal damage occurs in the first hours of the episode, so it is essential to recognize it and treat it as quickly as possible (therapeutic window). Consequently, it is necessary to identify two critical characteristics: distribution or location of the pathology and nature of the underlying process.
The definition of stroke includes three categories of diseases: cerebral infarction, cerebral hemorrhage, and subarachnoid hemorrhage. The vascular lesions that cause them can be of two types: 1) the interruption or critical decrease in blood flow in an encephalic region or ischemia and 2) the rupture of the arterial wall with the consequent hemorrhage (Table 1)
|Table 1: Most important predisposing or causal factors in stroke
|Brain-vascular hemorrhagic accident
Of all strokes, ischemic cerebral infarction occurs in 84% of cases, 10% corresponds to cerebral hemorrhages and the rest to subarachnoid hemorrhages.
Cerebral Infartation (CI)
It is a localized area of ischemic necrosis that is produced by a critical reduction or interruption of the blood supply in an area of the brain that is supplied by specific arteries. It is necessary to point out some concepts to understand special aspects: a) a gradual vascular occlusion does not necessarily produce infarction (if the collateral system is sufficiently functional, it will take care of supplying the injured vessel) b) infarction can occur in certain circumstances in which the blood vessel has stenosis but not complete occlusion as can happen in cases of hemodynamic alterations In essence, the factors that determine the appearance of a cerebral infarction are: 1) the state of the cardiovascular system, 2) the anatomy of the vessels and collateral circulation,
Basic mechanisms of cerebral ischemia
There are essentially two: 1) vascular thrombosis that determines the stenosis of the vessel where it is located, with flow limitation and 2) fragmentation and detachment of a thrombus from the heart or blood vessels, resulting in occlusion by embolism of distal cerebral vessels.
It is very important to bear in mind that there is the so-called ischemic penumbra, which is an area that surrounds the infarction and where the viability of neurons is precariously maintained by collaterals with reduced flow. In this area, deleterious phenomena occur that, if they persist over time, will also lead to neuronal death. The early treatment of ischemic stroke should be directed quickly to regain that area of darkness before it progresses to cell death. This "therapeutic window" is between 3 and 6 hours after the acute episode occurred. Ultimately, the death of the patient or the degree of disability that results will depend on the magnitude of the infarction, the affected area and the effectiveness in the recovery of the penumbra area
There are a number of risk factors for developing vascular disease. Some are not modifiable, such as advanced age, or genetic predisposition, but many others are controllable with effective preventive measures. Modifiable risk factors: 1) arterial hypertension: it is the most important factor. Long-term high blood pressure produces alterations in the vascular wall and can both injure the large arteries, facilitating the abnormal deposit of cholesterol, calcium, inflammatory cells, etc., as well as giving rise to lipohyalinosis in the small penetrating arteries of the brain. In both cases, the end result will be stenosis of the affected vessel and the possibility, in large arteries such as carotid and vertebral, of thrombus formation and, from these, of embolisms that impact distally. 2) diabetes, which is generally associated with arterial hypertension, is another predisposing factor by producing changes in the arterial wall. 3) dyslipidemias are a very important risk factor for the arteries of the heart, but the role they may play in promoting atherosclerosis of the cerebral vessels has not yet been reliably clarified, even though in recent times, some experimental studies seem to indicate that there is a lower incidence of stroke if cholesterol is kept low. 4) Smoking carries a high risk for the coronary arteries and, although to a lesser extent, also for the arteries that supply the brain. 5) Oral contraceptives increase the possibility of ischemic accidents, particularly in women who smoke. 6) Atrial fibrillation is the most important cardiac origin factor and it grows with advancing age. It gives rise to emboli that can impact distally in any intracerebral vessel. 7) hyperhomocysteinemia and hyperfibrinogenemia are predisposing factors that have been added in recent times. Recently, new factors have emerged, some not yet sufficiently validated but which are in studies such as inflammation / infection in the genesis of atherosclerosis plaque and respiratory disturbances during sleep. 7) hyperhomocysteinemia and hyperfibrinogenemia are predisposing factors that have been added in recent times. Recently, new factors have emerged, some not yet sufficiently validated but which are in studies such as inflammation / infection in the genesis of atherosclerosis plaque and respiratory disturbances during sleep. 7) hyperhomocysteinemia and hyperfibrinogenemia are predisposing factors that have been added in recent times. Recently, new factors have emerged, some not yet sufficiently validated but which are in studies such as inflammation / infection in the genesis of atherosclerosis plaque and respiratory disturbances during sleep.
As already stated, the symptoms that occur as a result of a cerebral infarction will depend on the affected area and the extent of the infarction, which is directly related to the artery involved and can be separated into two groups: 1) attacks on the carotid territory and 2) those on the vertebrobasilar territory. In those of the carotid territory, the obstructive phenomena occur in the internal carotid, in the neck or inside the skull or in its branches within the same skull (mainly middle and anterior cerebral arteries) and the symptoms will be hemispherical, the most frequent being that the patient presents hemiparesis or hemiplegia with a sensitive hemisyndrome and that may be accompanied by alterations in the visual field (hemianopsias) all contralateral to the injury and / or language disorders (aphasias) if the one involved is the dominant hemisphere. When the territory supplied by the vertebro-basilar system is affected, symptoms will occur that are characterized by a deficit in one of the cranial nerves, which marks the level of the lesion (midbrain, protuberance, bulb) and the presence of a motor or sensory hemisyndrome on the other side of the affected cranial nerve (alternate syndrome). To this, an ipsilateral cerebellar hemisyndrome can be added. In general, these symptoms appear progressively in cases of thrombosis and abruptly in embolisms. It has already been mentioned that transient ischemic attacks (TIAs) do not constitute a stroke in themselves, but are brief episodes of neurological dysfunction that herald the true possibility of a future stroke. By definition, they last less than 24 hours, but generally their average duration is less than 20 minutes. They appear abruptly and disappear quickly and recur between one and several times before leading to a high percentage of cases, a stroke. They occur before complete occlusion and usually originate from an atheroma plaque that distally dislodges emboli. Other times they are produced by a momentary increase in atheromatous plaque or by transient hemodynamic changes such as in arterial hypotension. Among the most frequent symptoms are fugax amaurosis, paresis, unilateral queiro-oral paresthesias and dysphasias. It is very important to recognize these TIAs in order to act quickly and prevent a possible stroke. When this happens, it can happen that it does so in the form of an evolving stroke, which is when the symptoms gradually add up in a few hours or that it manifests as a constituted or complete stroke, which is when the total deficit appears initially.
Cerebral Hemorrhage (HC)
Brain hemorrhages are grouped according to whether or not the bleeding occupies the subarachnoid space, and in this way 2 categories emerge: hemorrhage within the parenchyma and subarachnoid hemorrhage.
Intraparenchymal hemorrhage: (HI) is produced by vascular rupture within the brain. The main cause for this to occur is arterial hypertension, but the hemorrhagic transformation of a cerebral infarction, vasculitis, some hemopathies, anticoagulant therapy, arteriovenous malformations and drug addiction should also be highlighted. In the most common case of arterial hypertension, vascular lesions, in the form of microaneurysms (Charcot's), settle preferentially in the penetrating arteries (lentulostriate and lentico-optic) originating in the middle brain. For this reason, the hemorrhage is usually located in the region of the central gray nuclei, affecting the putamen and can expand, sometimes dissecting the nerve fibers, to the internal capsule, thalamus, hypothalamus, midbrain and can reach the ventricles. This bleeding occurs in approximately 75% of cases. The other sites correspond to the pons and cerebellum. In any of these eventualities, it is a serious clinical picture that can lead to death in a short time. When the bleeding occurs in areas other than those indicated, such as the frontal or occipital poles, the cause is not usually hypertensive. In general, the symptoms appear abruptly, during daylight hours. It usually begins with a headache that is followed by hemiplegia. If the hemorrhage is significant, coma may occur immediately or it may occur more gradually as intracranial hypertension develops. If the bleeding makes its way to the ventricles, hypertension within the brain can be decompressed and have a more favorable outcome. When the bleeding is minor, the coma may be absent. If the blood reaches the subarachnoid space, in which case we speak of cerebromeningeal hemorrhage, the patient may also have a stiff neck. When the hemorrhage is in a lobe of the cerebellum, the symptoms consist of headaches, dizziness, ataxia and vomiting. In these cases, the evolution of the patient must be constantly monitored since, if a deterioration occurs, the evacuation of the hematoma in time can save the patient's life. the patient may also have a stiff neck. When the hemorrhage is in a lobe of the cerebellum, the symptoms consist of headaches, dizziness, ataxia and vomiting. In these cases, the evolution of the patient must be constantly monitored since, if a deterioration occurs, the evacuation of the hematoma in time can save the patient's life. the patient may also have a stiff neck. When the hemorrhage is in a lobe of the cerebellum, the symptoms consist of headaches, dizziness, ataxia and vomiting. In these cases, the evolution of the patient must be constantly monitored since, if a deterioration occurs, the evacuation of the hematoma in time can save the patient's life.
2- subarachnoid hemorrhage: (SAH) is the one that presents with bleeding directly into the leptomeningeal spaces and is called spontaneous when it occurs without previous trauma. This hemorrhage spreads rapidly to the entire subarachnoid space and is responsible for irritative alterations of the meninges and arteries (arterial spasms) present in these spaces. If it is very profuse, the bleeding can quickly lead to intracranial hypertension and if it is small (epistaxis or meningeal drooling) it can cause only a sudden-onset headache. Sometimes the impact of blood leaving the artery injures the underlying brain parenchyma (meningocerebral hemorrhage)
The rupture of sacciform arterial aneurysms, called congenital, is the main cause of nontraumatic subarachnoid hemorrhages. These aneurysms are located mainly in the arteries that make up the circle of Willis. Between the 10th and 15th day of bleeding, the bleeding can be repeated
Sometimes aneurysms do not rupture but can compress neighboring cranial nerves such as the III and IV.
The symptomatology of subarachnoid hemorrhage depends on the magnitude of the bleeding, but as it is usually important, it presents with a sudden headache with vomiting and photophobia many times, with signs of meningeal irritation - neck stiffness -
and usually no signs of focus. It can quickly lead to the death of the patient or recovery, which will still be at risk of rebleeding or a complication from arterial spasm (heart attack). Other causes of SAH include arteriovenous malformations (AVMs) and blood dyscrasias, but they will not be discussed here as they are beyond the scope of this chapter.
Since an acute stroke often carries the risk of death or significant disability, it is imperative to proceed promptly to determine the ischemic or hemorrhagic nature, its etiopathogenesis, and its magnitude. The reduced therapeutic window to establish thrombolytic treatment in cases of ischemia requires the same speed as for myocardial infarctions. The studies to be carried out must take into account the characteristics of the clinical picture and its usefulness for the case. The steps to follow will be:
1º: Computed Tomography: it is the first study to be carried out since it will allow to rule out bleeding and other non-vascular lesions that simulate a stroke. If it is a cerebral infarction of magnitude and not localized in the posterior fossa, it can also be revealed before 24 hours. 2nd. Magnetic Resonance: it will be carried out if the tomography does not show a hemorrhage and there is a strong suspicion of a heart attack, especially if it is presumed in the brain stem or cerebellum. With these two methods you should be able to make a diagnosis for the emergency. Magnetic resonance imaging can be more complete if it is performed with the effect of angiography, which allows visualization of the extra and intracerebral blood vessels, although it still has disadvantages to clearly distinguish an arterial occlusion from a severe stenosis. 3rd: Lumbar Puncture to analyze the CSF should only be performed if there is a suspicion of subarachnoid hemorrhage and the previously performed tomography will show negative results to show blood in the leptomeningeal space. With the availability of current imaging methods, the indications for lumbar puncture in stroke patients have decreased and if it is performed, it should always be with a previous tomography. Once the urgency of the first moments has passed, the study of the patient should be completed. 4th: Doppler ultrasound of the neck vessels: if the stroke were an infarct, it will allow visualizing the presence of stenosis or occlusions and their magnitude. 5th: complete cardiovascular evaluation to rule out embolinous heart disease. 6th: panarteriography when there is a subarachnoid hemorrhage to identify the presence of aneurysms or in the event of an ischemic event, if a vascular dissection is suspected. 7th: complete hematological studies especially in patients under 45 years of age, if an ischemic stroke has occurred and in order to discover prothrombotic states.
In the case of TIAs, the arterial tree should be evaluated with Doppler ultrasound of the neck vessels and the presence of embolic heart disease should be studied with the methods indicated by the specialist.