The vascular system that carries blood to the brain includes the heart, aorta and great vessels, carotid and vertebro-basilar arteries, as well as intracranial branches and the cerebral capillary network. There is an important need to evaluate cardiac pathology underlying or associated with ischemic stroke, as well as abnormality in the intracranial arteries, including arteriosclerosis, the most common disorder affecting cerebral circulation.
The carotid system has two segments, one extracranial and one intracranial, with their respective branches. In the extracranial system there are certain branches: occipital, superficial temporal and maxillary arteries, from which the middle meningeal artery originates. The intracranial system has other branches: posterior communicating artery, which connects with the posterior cerebral artery.
The characteristics of the brain mean that it basically depends on glucose to function normally, consuming 75mg per minute (18% of the glucose used in the body). Hence, the cerebral circulation has a self-regulating mechanism, involving biogenic, biochemical and neurogenic factors that ensure a constant flow, as long as the mean arterial pressure is between 50 and 160 mm of mercury. Maintained arterial hypertension, for example, prevents the arterioles from functioning correctly, as their diameter does not change with changes in pressure.
Cerebral infarction or stroke: when does it occur, incidence and risk factors?
Arterial obstruction may or may not lead to cerebral infarction, depending on: the speed of onset, the time of obstruction and adequate collateral circulation. Neurons do not function when cerebral flow is less than 23ml/100g/mn. When this occurs, there is an electrical failure that can be “solved” if the flow is restored in less than 3 hours. This phenomenon is called ischemic penumbra and produces infarction regardless of its duration. Regarding its incidence by sex, it affects slightly more men, with an overall incidence of 160 cases per 100,000 inhabitants.
There are also certain important risk factors for cerebral vascular disease:
- Arterial hypertension
- Diabetes mellitus
- Hyperlipidemia
- Smoking (increases the risk threefold)
- Alcohol consumption
- Heart disease, the most important being atrial fibrillation, mitral stenosis and dilated cardiomyopathy.
- Stress
- Obesity
- Sedentary lifestyle
- Increased blood viscosity
Symptoms perceived by the patient during cerebral infarction or stroke
It is difficult to explain the different clinical pictures of cerebral infarcts, depending on the artery and the infarcted territory. Roughly speaking, it could be said that the middle cerebral artery infarction depends on the internal carotid artery, so it shows symptoms of left brachio-crural hemiparesis (decreased motor strength or paralysis) if the infarction is right and right hemiparesis if the infarction is left. In the case of left infarction it also entails aphasia or language disorder, which we call Broca’s aphasia. Sensory symptomatology of the left or right limbs is also associated when the infarcted territory includes the parietal lobe or the thalamus.
If the infarct comes from the territory supplying the basilar artery and posterior cerebral artery, ocular manifestations such as diplopia and conjugated gaze palsy occur. Also an alteration of the cortico-spinal motor pathway, producing Heli or tetraparesis, dysarthria, dysphagia, emotional lability, paralysis of the VII pair, deterioration of the level of consciousness, which is produced by lesion of the reticular substance of the brain stem.
Posterior cerebral artery infarction results in choreoathetosis, tremor, contralateral hemiparesis or thalamic syndrome. Also vertical gaze palsy, hemianopsia alexia, hallucinations and visual illusions, cortical blindness if occipital infarction is bilateral.
Transient ischemic stroke or ictus
Transient ischemic attacks (TIA) are sudden deficit disorders, secondary to reversible ischemia of an encephalic vessel, whose duration does not exceed 24 hours. Magnetic resonance imaging has shown tissue damage in patients with TIA.
TIA can be caused by fibrinoplatelet emboli from large arteries or by emboli of cardiac origin. Hemoconcentration, hypotension, severe carotid stenosis are contributing factors.
The cynecology depends on the territory affected. TIAs can be of carotid or vertebral origin. Thus, territories affecting the ophthalmic artery result in transient monocular blindness. If it affects the middle cerebral artery, it leads to motor or sensory impairment of the contralateral hemibody, and if it affects the left, to language impairment. In the vertebro-basilar territory it gives rise to ataxia, diplopia, vertigo, dysarthria, hemiparesis, or drop attacks with sudden loss of strength of the lower extremities due to ischemia of the bulbar pyramids.
Treatment of stroke
The treatment of stroke depends on the mechanism of production. Thus, if it is a cardioembolic stroke, the neurologist will provide anticoagulation; if it is an artery-artery embolism, the treatment will be antiplatelet therapy. In addition, it is necessary to explore the supra-aortic trunks by Doppler ultrasound or angioresonance, in case it is susceptible to surgery if there is carotid stenosis greater than 70%. Doppler ultrasound of the supra-aortic and transcranial trunks, angioresonance, general laboratory tests and, in specific cases, arteriography via the femoral artery will be very important for the diagnosis.
The aim of treatment is to reduce the area of necrosis at the acute stage, in addition to treatment and prevention of complications, rehabilitation and secondary prevention.
On the other hand, the efficacy of fibrionolytics in the first three hours after stroke, intravenous tPA and intra-arterial prourokinase after activation of the stroke code, has been tested in hospital stroke units.
In addition, cardiac monitoring, hypoglycemia control, blood pressure monitoring, urinary control, PCO2 and PO2 control, coagulation tests and radiological tests such as brain CT and MRI are required during treatment. Likewise, it is also necessary to add the assessment of the level of consciousness, the existence of coma crises, fever and a correct position at 30º in supine decubitus (stretched face up), maintaining the electrolyte balance, airway, possible cerebral edema or infections and with prevention of pulmonary thrombo embolism.
During rehabilitation, secondary prevention should be carried out by controlling risk factors with ASA antiplatelet therapy, clopidogrel or derivatives. Surgical treatment is endarterectomy or carotid endovascular angioplasty.
In cardioembolic infarctions, anticoagulation with sodium heparin is recommended for 48 hours after the infarction. The prognosis of atherothrombotic infarction is 20% mortality, while more than 70% of the affected population can lead a normal and autonomous life after six months, combining the appropriate medication prescribed by the neurologist.