Hypertensive intracerebral hemorrhage

Hypertensive intracerebral hemorrhages causes

Hypertension brain hemorrhages typical localization:

  • hemorrhage in the putamen and adjacent internal capsule, with frequent spread to the central white matter of the brain (50%)
  • hemorrhage in the thalamus
  • bleeding in the pons
  • hemorrhage in the cerebellum

In the central white matter hemorrhages in hypertensive patients are rare. In hypertensive affected usually one of the penetrating arteries originating from the trunk of the middle cerebral artery, basilar artery, circle of Willis. These vessels are characterized by segmental filling of the lumen of an expanding connective tissue in their muscular wall and deposited on its inner wall of fat (lipohyalinosis), which is a consequence of hypertension.

MRI of the brain the patient with hemorrhage into the ventricles of the brain during Moyamoya disease. The cavity of the lateral ventricles filled with blood (indicated by arrows).

Initially, hemorrhage with hypertension in a patient is a small oval-shaped mass, then the hematoma extends from the bundle, increases in volume, pushing and squeezing its surrounding brain tissue. Hypertensive haemorrhage type almost always break or leak blood into the ventricular system, whereas the breakthrough of the white matter through the gray matter of the cortex is rarely observed. If the hemorrhage is insignificant in volume (1-2 cm3), it is localized only in the central gray and white matter of the brain. In this part izlivshayasya blood does not reach the cerebrospinal fluid (CSF, cerebrospinal fluid) through the ventricular system. Massive hemorrhage in hypertensive disease, the patient may cause compression of the ventricular system of the brain midline structures shift in the opposite direction and lead to stupor, coma and death of the patient.

Most of the hemorrhages in the brain in hypertension in a few minutes. Some hypertensive hemorrhage last for between half an hour, while others, especially given the patient's treatment with anticoagulants, continuing day or two. After his stop hemorrhage with hypertension usually do not start, what does not happen at break saccular aneurysm. In the constricted brain tissue around the center of hemorrhage (intracerebral hematoma) forms edema. Such an increase in edematous brain tissue leads to a significant mass effect. Increasing intracranial pressure after way heavier neurologic symptoms in a patient. Within 48 hours, the macrophages begin englobe izlivshuyusya blood from its outer surface. After 1-6 months of intracerebral hematoma usually forms a cavity, resembling the cut oranges, delimited by connective tissue (astrocytes, glial cells) with scar tissue and filled with hemosiderin and macrophages.

Hypertensive intracerebral hemorrhages clinical syndromes

Hypertensive intracerebral hemorrhage may occur in any patient with hypertension. But most often occur at a constant hemorrhage essential hypertension. Hypertensive intracerebral hemorrhage is almost always occur during waking, the patient's condition, but not always necessarily triggered by overexertion. In contrast to the abrupt onset of cerebral vascular emboli hemorrhagic stroke develops within a few minutes, but his symptoms were determined by the location and size of hemorrhage.


Putamen hypertensive intracerebral hemorrhages

Most often, patients with hypertension (hypertension) have to observe the clinical picture of bleeding in this area of the brain as a shell. Hemorrhage of this localization is also affected hematoma located near the internal capsule of brain.

Brain MRI with intracerebral hemorrhage in hypertensive disease. Revealed acute hematoma in the right external capsule and insular cortex (arrow).
On axial btrain CT shows hematoma in the left external capsule and the putamen (arrow).

With extensive hemorrhages patient immediately loses consciousness, sinking into a coma, he developed paralysis of half of the body (hemiplegia). But more often he can complain about the discomfort in the head. A few minutes appear skewed face, confusion, speech, or its complete absence (aphasia). The patient gradually increasing weakness in the limbs, a tendency to turn the eyes in the direction opposite to the side of paralysis. Typically, these events are developed for 5-30 min. These dynamics are likely symptoms indicate intracerebral hemorrhage.

Weakness of limbs growing to full paralysis of muscles (plegia). To pain stimuli patient does not respond, there is a pathological positive Babinski disappears speech (aphasia) in lesions of the dominant hemisphere hematoma. The consciousness of the patient drowsy replaced by a stupor. When particularly severe symptoms occur rapidly compression of the upper brain stem. Fault in a patient in for the next deep coma is accompanied by irregular or irregular breathing, with the expansion of the pupil (on the side of haemorrhage) and absence of its response to light, bilateral Babinski sign of decerebrate rigidity and muscle. The increase in neurological symptoms in the period from 12 to 72 hours after its occurrence is due to the development of edema in brain tissue around the hematoma (perifocal edema), rather than re-rupture of the vessel.


Thalamic hypertensive intracerebral hemorrhages

Thalamic hemorrhage of moderate size also makes the patient or partial paralysis and muscle weakness than half of the body (hemiplegia, hemiparesis) due to excessive pressure or hematoma bundle lying near the structures of the internal capsule. The patient will then be broken pain, temperature, proprioceptive and tactile sensitivity of the body. With lesions of the dominant hemisphere can be observed speech disorder (dysphasia), often with preservation of repeating aloud.

Brain MRI of a patient with intracerebral hemorrhage in the thalamus (arrows).

If the hemorrhage occurred in a patient with hypertension in the non-dominant hemisphere of the brain, it will mark a impairment of purposeful action and recognition (apraktoagnozia). Developing visual field defects gomonimnye patient is then usually disappear within a few days. Thalamic hemorrhage, extending in a direction inwards and downwards to the zone subtalamusa causes oculomotor disorders. They appear as:

  • in the form of vertical gaze palsy
  • enforced rotation of the eyeballs down
  • different diameter pupils (anisocoria) the lack of response to light
  • strabismus with a deviation of the eyeball, the opposite side with respect to hemorrhage, downward and medially
  • on the side of hemorrhage observed lowering of the upper eyelid (ptosis) and contraction of the pupil (miosis)
  • lack of convergence
  • eye movement disorders in the horizontal (paresis or psevdoparez VI nerve)
  • Retraction nystagmus
  • eyelid edema

There may be a shortening of the neck. Thalamic hemorrhage in the non-dominant hemisphere of the brain can sometimes cause the patient inability to speak (mutism).


Pontine hypertensive intracerebral hemorrhages

After hemorrhage in the pons, usually within a few minutes the patient falls into a deep coma. The clinical picture consists of paralysis of all limbs (quadriplegia), marked decerebrate rigidity, myosis (miosis) with up to 1 mm, and the lack of response to light. In a patient with hemorrhage into the pons will be broken reflex horizontal eye movements induced by rotations of the head (doll's eye sign), and irritation of the ears in cold water (caloric test). Often these patients have hyperventilation, high blood pressure and sweating (hyperhidrosis). As a rule, the death of a patient with hemorrhage into the pons comes in a few hours.

In rare cases consciousness remains intact and showed clinical signs of small lesions in the lid of the pons. It's such symptoms as disorders of movements of the eyeballs in a horizontal plane, coarse speech disorder (dysarthria), cross motor and sensory impairments, pupillary constriction (miosis), cranial nerve palsies, bilateral involvement of the pyramidal tract symptoms.


Cerebellar hypertensive intracerebral hemorrhages

Cerebellar hypertensive intracerebral hemorrhages usually develops within a few hours. At this location hemorrhage loss of consciousness in a patient initially rare. Characterized by repeated vomiting, the patient is unable to walk and stand. These clinical signs appear early and should cause a suspicion of this diagnosis, which allows the doctor a neurosurgeon in a timely manner to resolve the question of surgical intervention. Hemorrhage in the cerebellum, patients and headache in occipital area and dizziness. Neurological examination revealed the patient horizontal gaze palsy toward bleeding from the eyeballs turn violent in the opposite direction and paresis of the abducent (VI) nerve on the affected side.

Brain MRI of a patient with hemorrhage in the right hemisphere of the cerebellum (arrow).

In the acute phase of hemorrhage cerebellar signs of injury the patient may not be or they are weak. Only occasionally in patients with hemorrhage into the cerebellum detected on neurological examination, nystagmus or cerebellar ataxia in the limbs.

The eye hemorrhages in the cerebellum symptoms include muscle spasm eyelids (blepharospasm), involuntary closing of one eye and squint. Twitching of the eyeballs (ocular bobbing), usually regarded as a symptom of the damage of the pons may occur later in the oppression of consciousness to the level of the patient's coma. Eye movement are stored vertically, narrow pupils continue to react to light until very late stages of disease. On the affected side often report weak facial muscles and reduce corneal (corneal) reflex.

Paralysis of the limbs opposite half of the body (contralateral hemiplegia), and the weakness of facial muscles do not. Sometimes at the beginning of hemorrhage in the cerebellum have complete paralysis of the muscles of the arms and legs on both sides (tetraplegia) with preservation of consciousness. Sometimes the loss of voluntary movement in a patient is seen only in the form of spastic weakness of the muscles in the arms or legs (spastic paraparesis). Plantar responses (reflexes) are flexing first character in the future - extensor. Sometimes a few hours after hemorrhage in the cerebellum in a patient develops a sudden stupor and then coma as a result of compression of the brain stem, then therapeutic measures to reverse the development of the syndrome, and even surgical treatment is rarely effective.

Brain MRI of a patient with hemorrhage in the left hemisphere of the cerebellum (arrow).

Neurological symptoms of the eyes is important to establish the localization of bleeding into the brain:

  • haemorrhage in the shell of the eyeballs are deflected in the opposite side of the palsy;
  • hemorrhage in the thalamus eyeballs deflected down and lost pupillary reaction;
  • hemorrhage in the pons violated the reflex eye turns in the direction of the pupils, though, and react to light, but very weak;
  • hemorrhage in the cerebellum, the eyeballs are rotated in the opposite location of the lesion, in the absence of paralysis.

Headache is not considered mandatory symptom of intracerebral hemorrhage in hypertensive disease. Headache occurs in about 50% of patients, while vomiting - almost all. The patient does not necessarily develop depression of consciousness to coma. If the hematoma volume is small, the consciousness of the patient can be saved, even if the blood has penetrated into the ventricular system.

Epileptic seizures in patients with hemorrhage due to hypertension are rare - less than 10 % of cases. In most patients the correct diagnosis is based on a combination of objective and subjective symptoms.

However, if the patient's consciousness is stored, it is difficult to differentiate between cerebral infarction (ischemic stroke) and intracerebral hemorrhage. In such instances shown magnetic resonance (MRI) or computerized tomography (CT) scan of the brain. Timely application of magnetic resonance (MRI ) and computed tomography (CT) scan of the brain makes it possible to accurately differentiate the type of lesion and determine their location, especially during the most difficult to diagnose small hemorrhages in the brain against the background of hypertension in the patient.


Hypertensive intracerebral hemorrhages diagnosis (laboratory and imaging evaluation)

Computed tomography (CT) scan of the brain - this is a very reliable method for diagnosis of intracerebral hemorrhage. Using computerized tomography (CT) scan of the brain, can identify with high reliability, all hemorrhagic lesions in the cerebral hemispheres and cerebellar diameter not less than 1 cm, if the research carried out in the first 2 weeks after its occurrence. Since the value of x-ray attenuation by blood clots, through which it passes with time, decreased 2 weeks later, X-ray density of the hematoma and brain tissue is aligned, and the focus of hemorrhage may be omitted if it is not combined with perifocal edema and mass effect. In some cases, after 2-4 weeks there is a "rim" of contrast enhancement that lasts up to several months. It may be impossible to identify small hemorrhages in the brain of the pons because of the possible movements and bone artifacts.

Magnetic resonance imaging (MRI) of the brain compared with computed tomography (CT) is more reliable in the diagnosis of small hematomas, localized in the area of the pons and the medulla oblongata, and also hematoma, x-ray density of blood clots within which aligned with the density of brain tissue. However, in such cases to differentiate acute hematoma with prescription of at least 3 days of chronic hematoma, the patient appeared more than 3 days ago.

By further improving the methods of magnetic resonance (MRI) or computed tomography (CT) scan of the brain reduces the need for lumbar puncture, except in cases where we can not exclude small hemorrhages in the pons. In such hematomas (bleeding in the pons) may cause blood in the cerebrospinal fluid (CSF, CSF), but they are not visualized on computed tomography (CT) scan of the brain due to artifacts. Carrying out a lumbar puncture a patient with intracerebral hemorrhage is associated with significant risk, because it can cause break- temporal lobe hematoma, if large size and is located above the snaring of the cerebellum (supratentorial ). But when the performance of magnetic resonance (MRI) or computed tomography (CT) scan of the brain is not possible, the diagnosis requires a lumbar puncture (if you plan a destination therapy).

When intracerebral hematoma revealed by magnetic resonance (MRI) or computed tomography (CT) scan of the brain in the temporal lobe and near the Sylvian cisterns, that this patient likely break existing aneurysm at the bifurcation of the middle cerebral artery. In this regard, and also because of the existing edema in the temporal lobe hematoma around the possible risk of subsequent herniation of the temporal lobe, the cause and source of the hemorrhage is established by angiography. Then, if the temporal lobe edema threatens the emergence of herniation of the cerebellum into the opening gallop, you can remove the hematoma, given with or without aneurysm in this patient.

Angiography is also indicated in case of intracerebral hematoma is not localized in one of four areas, characteristic of hemorrhage with hypertension, including in shell, optic thalamus, and cerebellum of the pons. The source of hypertensive hemorrhage can be surgically accessible arteriovenous malformations (AVMs). According to the results of angiography can not completely exclude arteriovenous malformations (AVMs) as long as the total absorption does not occur (absorption) of a hematoma.

According to computed tomography (CT) scan of the brain performed without contrast enhancement and with that, we can assume that the AVM is a source of intracerebral hematoma, but the negative results of this study do not exclude such a possibility. With magnetic resonance imaging (MRI) of the brain can register arteriovenous malformation (AVM), immediately after hematoma resorption, because blood flow to part of the malformation does not affect the MRI signal. When scanning a large vascular channels arteriovenous malformation (AVM) are black structures.

X-ray chest and electrocardiogram often point to the secondary hypertrophy of the myocardium against prolonged hypertension and provide a key to elucidate the etiology of intracerebral hemorrhage.

The severity of the patient's condition and further prognosis of the disease the spontaneous subarachnoid hemorrhage is determined by Hunt and Hess scale, which was first described in 1968 by two american neurosurgeons (William Edward Hunt, Robert M Hess):

  1. Asymptomatic or slight headache with a slight tension of neck muscles – 70% survival
  2. Moderate or severe headache; neck muscles stiffness; muscle paresis, innervated by cranial nerves, lack of other focal neurological symptoms – 60% survival
  3. Pathological drowsiness, slight focal neurological deficit – 50% survival
  4. Stuporous; medium or severe expressed hemiparesis; possibly early decerebrate rigidity of muscles with vegetative disorders – 20% survival
  5. Deep coma; early decerebrate rigidity of muscles, moribund – 10% survival

The prognosis of hematomas, which are formed as a result of bleeding into the brain in patients with hypertension, largely depends on their size. When placed over the snaring of the cerebellum (supratentorial) hematomas with a diameter of 5 cm above the forecast cautious. With the localization of intracerebral hemorrhage in a patient below the gallop of the cerebellum (subtentorial) hematoma in the pons is larger than 3 cm almost always lead to his death. Often the prediction is complicated by cerebral edema, which developed within a week after intracerebral hemorrhage.

When intracerebral hemorrhages surrounding the hematoma, tissue is displaced and compressed, but not necessarily subjected to a heart attack. Consequently, after resorption of hematoma patient 's clinical condition can greatly improve, since brain tissue does not lose its function. Careful management of such patients during the critical phase of brain hematoma can result in a significant restoration of his lost neurological function.


Hypertensive intracerebral hemorrhages treatment

Surgical removal of clotted blood in the acute stage of intracerebral hemorrhage patients is shown only in rare cases. However, removing blood clots in hematoma, which lies above the snaring of the cerebellum (supratentorial), you can prevent break- temporal lobe of the brain in comatose patients with more preserved reflex eye movements. Surgical removal of the hematoma from the focus of acute hemorrhage in the cerebellum is usually the method of choice because it is often saves the life of the patient and provides an excellent prognosis in terms of recovery of disturbed functions.

If a patient has a clear conscience and no symptoms of focal lesions of the brain stem, in the presence of cerebellar hematoma in his small size neurosurgeon may waive immediate surgical intervention to remove it. However, we must bear in mind the probability of a rapid deterioration in clinical status in the localization of hematoma in the cerebellum. Therefore, such patients should always be possible to conduct an emergency operation in case of any clinical need.

To reduce brain edema around intracerebral hemorrhage appoint mannitol and other osmotic diuretics drugs. The activity of steroids in intracerebral hematoma is negligible. To evaluate the effectiveness of drug therapy, to avoid significant deviations in the direction of arterial hypo-and hypertension can help monitor the intracranial pressure. The sharp drop in blood pressure in order to "stop the bleeding" in intracerebral hemorrhage is inefficient because most stop bleeding occurred in intracranial hemorrhages occur spontaneously even before the examination of patients.

Conditions such as toxemia of pregnancy and malignant hypertension, are especially needed, early diagnosis and judicious treatment. This is necessary in order to avoid excessive or sudden drop in blood pressure in patients.

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