1.What is hypertensive cerebral hemorrhage?
Hypertensive cerebral hemorrhage refers to the cerebral hemorrhage caused by the rupture of cerebral blood vessels when the blood pressure rises sharply due to hypertension with small arterial lesions in the brain. The severity of the condition varies greatly depending on the site of bleeding, the extent of bleeding, the body’s reaction and the general condition, and serious cases may die on the spot.
2.What are the common sites of hypertensive cerebral hemorrhage?
The common sites of hypertensive cerebral hemorrhage are basal ganglia hemorrhage (also called internal capsule hemorrhage), pontocerebral hemorrhage, cerebellar hemorrhage, ventricular hemorrhage and so on. Depending on the site of hemorrhage, the clinical manifestations are also different. The characteristics are described as follows.
(1) Internal capsule hemorrhage: It is the most common site of hemorrhage in hypertensive cerebral hemorrhage, and its most typical manifestation is “three deviations”, namely, hemiparesis, hemianesthesia and hemianopsia. Specifically, hemiplegia means paralysis of the contralateral limb of the hemorrhagic lesion; hemianesthesia means the contralateral hemianesthesia of the hemorrhagic lesion; hemianopsia means the contralateral visual field loss of the hemorrhagic lesion.
(2) Lobar hemorrhage: It is manifested as hemorrhage in each lobe of the brain. There are different clinical manifestations depending on the site of hemorrhage. Generally, in addition to sudden onset, headache and coma, there are often symptoms of the corresponding brain lobe. For example, frontal lobe and temporal lobe hemorrhage often show mental symptoms; frontal parietal lobe hemorrhage often shows symptoms such as hemiplegia and aphasia; occipital lobe hemorrhage often shows symptoms such as hemianopia.
(3) Pontocerebral hemorrhage: It often starts suddenly with headache, vomiting, and goes into coma within minutes. The hemorrhage often starts on one side and soon affects the opposite side, resulting in facial and limb paralysis on both sides and extremely narrow pupils with pinpoint pupils, which are the characteristic symptoms. In addition, pontocerebral hemorrhage often blocks the normal regulation of body temperature by the lower thalamus and causes a rise in body temperature, resulting in a state of continuous hyperthermia. The condition of bilateral pontocerebral hemorrhage is often extremely critical, and due to the influence of the respiratory center of the brainstem, respiratory distress and irregular breathing often appear early, and some patients can die quickly. However, small amount of hemorrhage on one side of the pontocerebrum may be milder and the prognosis is better.
(4) Cerebellar hemorrhage: Most cerebellar hemorrhages occur in one cerebellar hemisphere, which can lead to acute intracranial pressure increase, brainstem compression, and even brain herniation. Any hypertensive patient with sudden onset of severe pain on one side of the posterior occipital region, frequent vomiting, severe vertigo, pupil narrowing, progressive worsening of consciousness and no obvious paralysis must be alert to the possibility of cerebellar hemorrhage.
(5) Ventricular hemorrhage: Most ventricular hemorrhages are caused by hemorrhage at the basal ganglia of the brain that breaks into the lateral ventricles, resulting in blood filling the entire ventricular system and subarachnoid space. Primary ventricular hemorrhage is rare. In addition, cerebellar hemorrhage and pontocerebral hemorrhage can also break into the IV ventricle, which is an extremely serious condition. Consciousness often falls into a deep coma within 1 – 2 hours after the onset of the disease, with tetanic seizures or tetraplegia, and the disease is critical if blood pressure drops and body temperature rises.
3, what is the cause of hypertensive cerebral hemorrhage?
Many people who have brain hemorrhage and fear of brain hemorrhage are concerned about this issue. Generally speaking, the causes of cerebral hemorrhage are many, such as hypertension, cerebral arteriosclerosis, cerebrovascular sakiasis, congenital cerebral hemangioma, inflammation of cerebral vessels and so on. In addition, diabetes, obesity and smoking are all related to cerebral hemorrhage. However, in terms of hypertensive cerebral hemorrhage, hypertension and atherosclerosis are the basis of its development. The sudden increase of blood pressure is the direct cause of hypertensive cerebral hemorrhage.
Why are patients with hypertension prone to cerebral hemorrhage? Simply put, because people who suffer from hypertension for a long time have increased vascular tone and excessive stretching of the intima, which easily causes damage to the intima, becomes unsmooth, loses elasticity, and even forms microaneurysms in the small cerebral arteries, and then if the blood pressure suddenly rises, the arterial wall cannot tolerate it, and it will easily rupture and bleed. In addition, the spasm of small cerebral arteries caused by hypertension may cause hypoxia and necrosis in its distal brain tissue, and punctate hemorrhage and cerebral edema may occur. If this process is prolonged and severe, the necrotic and hemorrhagic areas will fuse and expand into a large hemorrhage.
Patients with hypertension are prone to cerebral hemorrhage if they are untreated or undergo irregular treatment intermittently. Second, another major cause of hypertensive cerebral hemorrhage is atherosclerosis. Atherosclerosis is the formation of hardened plaques due to the deposition of fatty substances and the proliferation of fibrous tissue in the intima of arteries. When necrosis, softening and collapse occur in the central part of the sclerotic plaque due to malnutrition, the appearance is “celiac disease”, so it is also called atherosclerosis. The necrotic tissue within the plaque often calcifies, gradually making the arterial wall harden and become brittle and lose its elasticity and contractility.
In the early stage, the plaques are mainly in the deep part of the arterial intima, and then involve other parts. When the cholesterol deposition extends to the surface of the intima, the sclerotic plaque can protrude into the lumen, thus making the lumen narrow and curved; when the lesion extends to the middle layer of the wall, it can destroy the muscle fibers and elastic fibers and replace them with connective tissue proliferation, thus making the arterial wall thicken, harden, and even lose elasticity. As the elastic and muscular layers of the arterial wall are damaged, the wall becomes brittle, and when combined with hypertension, it is easy to rupture the blood vessel and produce cerebral hemorrhage.
4.What are the main clinical manifestations of cerebral hemorrhage?
Generally speaking, the onset of hypertensive cerebral hemorrhage is very rapid, and it usually occurs during the daytime when there are physical or mental stress activities such as emotional excitement, overexcitement, straining to defecate, and overexertion. There is often no premonition before the onset, and the symptoms appear suddenly, often developing to a peak within a few minutes to a few hours. The clinical manifestations depend on various factors such as the site of bleeding, the extent of bleeding, the body’s reaction, and the general condition. The onset of the disease is usually characterized by a sudden severe headache, hemiplegia, followed by frequent vomiting, and in severe cases, a maroon color of vomitus due to the combination of gastrointestinal bleeding. Then, the consciousness gradually blurs, and often turns into coma within minutes or tens of minutes. The main symptoms at the onset of the disease are described as follows.
(1) Headache: Headache is one of the common symptoms in cerebral hemorrhage. It can be used as an early manifestation of brain hemorrhage or as a warning sign of brain hemorrhage. Patients suffering from hypertension and arteriosclerosis, if they suddenly develop severe headache, it suggests the possibility of brain hemorrhage.
As already mentioned, the basis of cerebral hemorrhage is hypertensive cerebral atherosclerosis, and the majority of hypertensive patients have headaches of varying degrees from early on. The degree of headache is generally related to the level of blood pressure, especially when the blood pressure suddenly rises and the headache is intense. This is because the sudden increase in intra-arterial pressure causes strong stimulation of the nociceptive receptors in the wall of the artery. Usually a significant increase in blood pressure (especially diastolic pressure) is even accompanied by nausea and vomiting. If the headache changes from intermittent to persistent, or if the headache suddenly worsens to an “explosion-like” headache and is accompanied by a sudden increase in blood pressure, it is important to be aware of the possibility of cerebral hemorrhage.
The incidence of headache in cerebral hemorrhage is about 80% – 90%. The headache is caused by the stimulation of the meninges by blood, followed by the formation of cerebral edema or hematoma, resulting in increased intracranial pressure, which causes compression or traction of large blood vessels and nerves in the skull, and is mostly accompanied by frequent vomiting. In cerebral hemorrhage, the headache is usually less severe than in subarachnoid hemorrhage. The incidence and severity of headaches are often less than they actually are because the patient is mostly comatose. The headache tends to persist throughout the course of the attack if the patient is conscious. In the case of brain hemorrhage, headache can be used as an indicator to observe the change of the condition. When the condition improves or stabilizes, the headache decreases, and when the condition worsens, the headache increases; while the original headache has already decreased or disappeared, if it suddenly appears or worsens sharply again, the possibility of rebleeding should be considered and should be given high attention.
It is worth noting that some elderly people do not have obvious headaches when they have brain hemorrhage, which may be related to the smaller amount of bleeding, slower bleeding rate (bleeding), less irritation, and slower reaction of the elderly. In addition, elderly people have mental disorders due to cerebral arteriosclerosis, thus masking the headache.
(2) Hemiplegia Hemiplegia, also called hemiplegia: i.e., paralysis of one side of the face and upper and lower extremities, is a very common symptom of cerebral hemorrhage and is caused by damage to the motor nerves in the brain parenchyma. Usually, right-sided hemiparesis occurs when the left hemisphere is diseased, while left-sided hemiparesis occurs when the right hemisphere is diseased. This is because the innervation of the brain is crossed. This is mainly due to two reasons: First, because the heart is biased to the left, the left common carotid artery emanates directly from the left side of the aortic arch at a right angle, and continues down to the internal carotid artery and the middle cerebral artery, which have a large difference in caliber, so the blood flow impact and mechanical pressure are greater, and atherosclerotic plaques are easily formed locally. Second, because the functions of the left hemisphere are generally more complex than those of the right hemisphere, they are also more likely to be damaged. Because the left hemisphere is easily damaged, right hemiplegia is more common. As for the so-called male left and female right, some people say that there is no scientific basis for the view that men are left hemiplegic and women are right hemiplegic when they have a stroke.
There are light and heavy hemiplegia, the light ones are just weak in the upper and lower limbs and have no movement; the heavy ones are completely paralyzed and are not at all at their disposal. How to determine the degree of paralysis? The main thing to look at is muscle strength. Muscle strength refers to the strength of the muscles. In paralysis, the motor neurons are damaged, resulting in loss of active movement or reduced muscle strength. It is usually classified according to the degree of paralysis as
Complete paralysis (also called total paralysis): complete loss of muscle strength and inability to do any active movement of the limb.
Incomplete paralysis (also called mild paralysis): some degree of muscle strength is reduced and the limb is more or less able to do some active movements.
Generally speaking, patients with mild paralysis have every hope of resuming walking after active exercise.
(3) Language impairment: Usually, when brain hemorrhage occurs, the patient enters a coma quickly, so the language impairment is not very prominent, and only when the hemorrhage is small and the condition is relatively mild, the language impairment can be manifested.
The human language function is very complex. It mainly consists of two parts: one is the motor part of language, that is, the expression part, to express thoughts and emotions through speech; the second is the sensory part of language, that is, the feeling part, to comprehend the meaning of other people’s speech.
The occurrence of a speech disorder is medically called aphasia, which means the loss of the function of speech. There is a specialized body in the cerebral cortex that is responsible for language functions, called the language center. The most common cause of speech disorders is when a brain hemorrhage occurs and the hematoma compresses the speech center. In general, people with right-handedness, i.e., those who are used to writing, holding chopsticks and working with their right hand, have their language center in the left cerebral cortex, so when lesions occur in the left cerebral hemisphere, aphasia is often produced.
Due to the different sites and manifestations of lesions, aphasia can be divided into the following categories.
The most common one is motor aphasia. In normal people, there is a body in charge of language expression in the posterior part of the frontal inferior gyrus of the left cerebral cortex, called the “motor language center”, if this part is damaged, it can produce motor aphasia, mainly appearing in the language expression disorder, the patient can not speak at all, or can only say some simple words, sentences, sometimes can not say, they also sound awkward The patient can understand the meaning of other people’s speech.
The second is sensory aphasia. In normal people, there is a body in charge of language perception in the posterior part of the superior temporal gyrus of the left cerebral cortex, called the “sensory language center”, when this part is damaged, it can produce sensory aphasia, mainly appearing language perception disorder, lack of understanding of language, the patient can hear the sound of other people’s speech, but can not comprehend its meaning. Because of this, the patient speaks, but often does not answer the question, and the language is confusing, upside-down and difficult to understand.
When both the motor and sensory language centers are damaged, a mixed aphasia occurs in which the patient has both motor and sensory aphasia. The patient can neither speak nor understand what is being said. Another type of aphasia is named aphasia. The center is in the left posterior temporal lobe and the lower parietal lobe, and when this area is damaged, naming aphasia is produced. This is characterized by the patient being able to speak, but not being able to name objects, but he will use many adjectives to describe the nature and use of the object. For example, pointing to a cup and asking the patient, “What is this?” He will answer, “It’s for drinking water”; if he shows a pen and asks the patient, he will say, “It’s for writing”. This condition is called naming aphasia.
Generally, motor aphasia recovers faster than sensory aphasia or mixed aphasia because the recovery of language function mainly depends on exercise, while the latter two types of patients have difficulty in exercising their subjective initiative because they cannot understand the meaning of other people’s speech, and it is also more difficult to exercise.
(4) Coma
Coma is delirium, which is caused by brain hemorrhage when the brain suffers. It is caused by severe and extensive damage to the brain, and is one of the main signs of the severity of the disease. Due to the different degrees of coma, the performance is also different. Some patients sleep in a daze all day long and can still cause some pain or motor responses to strong external stimuli, such as painful expressions when needling the face, or swallowing and coughing reflexes when feeding water to the pharynx, which is considered shallow coma. In more severe cases, the patient is completely unconscious and does not respond to external stimuli, which is considered deep coma. In deep coma, the limbs are often flaccid and incontinent.
There is another kind of coma called “open-eye coma”, which is a coma patient with eyes open, eyes drifting, as if looking around the scene, thus also known as “waking coma”. This is because both hemispheres of the brain are extensively damaged, while the function of the brainstem is still preserved.
Usually, the earlier the coma appears, the deeper and longer it is, the more serious the patient’s condition is.