Cerebral vasospasm

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Cerebral vasospasm

Narrowing of the brain base arteries after subarachnoid hemorrhage by rupture of saccular aneurysm (cerebral vasospasm) may cause secondary ischemia and cerebral infarction as a result of symptomatic cerebral vasospasm.

Symptomatic cerebral vasospasm - a major cause of subsequent morbidity and mortality in patients with rupture of the aneurysm. Symptomatic cerebral artery spasm (cerebral vasospasm) occurs in approximately 30 % of patients. After the rupture of an aneurysm in a patient is improving or temporary period of stabilization prior to the emergence of symptomatic vasospasm him. Neurological symptoms of spasm of cerebral arteries arise at the 4 day 14 after the first rupture of the aneurysm (usually 1 week after subarachnoid hemorrhage). Re-emergence of neurological symptoms in a patient can be distinguished only if you've previously identified a neurological deficit and were monitored for clinical signs of him. The resulting neurological symptoms of cerebral ischemia corresponds to the specific arterial basins. Severity of the brain arteries spasm (cerebral vasospasm) determines the likelihood of cerebral infarction.

Narrowing of the arteries of the brain (cerebral vasospasm) sharply worsens overall clinical condition of the patient.

Cerebral vasospasm - is a focal vascular phenomenon, caused by the presence of blood in the cerebrospinal fluid subarachnoid spaces. It is still not clear how and why patients with vasospasm occurs after brain haemorrhage. These laboratory studies suggest that chemicals such as serotonin, prostaglandins, and catecholamines, may lead to a narrowing of the arteries. However, all these substances quickly break down in vivo and in large quantities only provoke spasm vitro. Prolonged spasm of cerebral vessels (cerebral vasospasm) was obtained in experiments with whole blood and red blood cell degradation products.

Clinical data indicate that the magnitude and location of blood clots, detected by magnetic resonance (MRI) or computed tomography (CT) scan of the brain in the basal cisterns and sulci subarachnoid space can be used to predict the frequency, location and severity of cerebral spasm of the cerebral vessels brain (cerebral vasospasm) in patients after subarachnoid hemorrhage. The high frequency of symptomatic spasm of cerebral vessels (symptomatic cerebral vasospasm) was observed in those patients in whom an early magnetic resonance (MRI) or computed tomography (CT) scan of the brain were determined by ball-size blood clots larger than 5 mm 3 in the basal cisterns or layers of thick coagulated blood 1 mm or more in the fissures of the brain. If the clot burden was located in the subarachnoid space, it shows the localization of spasm in the artery, lying in the subarachnoid space.

Magnetic resonance (MRI) or computed tomography (CT) scan of the brain showed that their results can reliably predict the location and severity of vasospasm in the anterior and middle cerebral arteries. In the case of prediction with respect to vertebrates, the basic and below the posterior cerebral artery CT of the brain does not provide a clear visualization of a large clot in the posterior fossa. For an accurate predict brain computed tomography (CT) research should be done in the range of 24 to 96 hours after subarachnoid hemorrhage. Appears on computed tomography (CT) scan of the brain during the first hours after subarachnoid hemorrhage blood picture may disappear during the second study, after 24 h. This is probably due to the migration of a hematoma. Over time, indicators of X-ray attenuation on CT blood clots are reduced so that the entire volume and location can not be reliably characterized in 96 hours.

Due to the dependence of the localization of cerebral vessel spasm (cerebral vasospasm), and clotted blood surrounding it any hypothesis which considers the mechanism of vasospasm must take into account the long-term effect of hematoma formed. As one of them, a clot burden around the artery. Then a few days later the decay products of hemoglobin that can cause cramps, spasms of the arteries run in the brain. After arising spasm of the vessel, high-energy phosphate metabolism is disturbed in the vascular layer, as the vessel surrounding the clot prevents it from feeding through the cerebrospinal fluid (artery feeding the vascular layer (vasa vasorum) are absent in the vessels and the base of the cerebral cortex ). The isolation of peripheral arterial hematoma formed in the future may prevent relaxation of the wall, because it requires energy coming from the cerebrospinal fluid (CSF).

Cerebral vasospasm clinical symptoms

Cerebral vasospasm manifest symptoms related to a particular pool of blood supply of the brain specific artery. With the involvement of the trunk or main branches of the middle cerebral artery in a patient develops:

  • muscle weakness, half of the body opposite the side of intracerebral hemorrhage (contralateral hemiparesis)
  • speech disorder (dysphasia) in spasm arteries of the dominant hemisphere of the brain
  • disorder recognition (anosognosia, aproctognosia) in spasm arteries of the non-dominant hemisphere of the brain

Severe vasospasm in a patient may not manifest neurological symptoms of ischemia. This is the result of what the brain is formed by an adequate collateral blood flow through fusion (anastomosis) zones adjacent cerebral blood flow.

Narrowing of the arteries of the brain (cerebral vasospasm) often occurs in response to subarachnoid hemorrhage.

Ischemia in anterior cerebral artery bassin is manifested abulia:

  • the patient is awake
  • is open or closed eyes
  • responds to the instructions with delay
  • can not actively carry on a conversation, but the answers in short sentences, uttered in a whisper
  • long time to chew food, and often holds it between the cheek and gums

Severe spasm of the posterior cerebral artery may be associated with unilateral visual field defects. A strong core spasm or vertebral arteries can sometimes cause symptoms of focal ischemia of the brain stem.

All focal neurological symptoms as a result of spasm of the arteries in the brain (cerebral vasospasm) in patients developing over several days or may occur suddenly, reaching maximum intensity within minutes or hours.

If ischemia or infarction of the brain is exposed all the territory in the basin of the middle cerebral artery, it develops its swelling, which may lead to increased intracranial pressure with a fatal outcome. Early magnetic resonance (MRI) or computed tomography (CT) scan of the brain can predict such an outcome, if it is found a large clot burden in the lumen of the Sylvian fissure and / or the sylvian cistern and a second large clot in the basal frontal interhemispheric fissure. The simultaneous presence of coagulated blood in these areas, combined with severe symptomatic spasm of the middle and anterior cerebral arteries. In this situation, surface collaterals in the cerebral cortex of the anterior cerebral artery is not able to compensate for ischemia in the basin of the middle cerebral artery.


Cerebral vasospasm treatment

Drug prevention and treatment of symptomatic spasm of the arteries of the brain (cerebral vasospasm) in the presence of subarachnoid hemorrhage is ineffective. Futile purpose of reserpine and kanamycin with the whole lower serotonin levels in the blood serum, isoproterenol and aminophylline to increase cyclic AMP -mediated and nitroprusside for direct expansion of the arteries.

The next stage of selection of drugs in spasm arteries of the brain (cerebral vasospasm) was the search for preventive medicine that can prevent or greatly reduce the manifestations of spasm. It has been reported beneficial effect of nimodipine (Nimodipine) - Nimotop drug. Nimodipine (Nimotop) blokiruyuet calcium channels of the arteries of the brain. But symptomatic vasospasm develops in patients receiving this drug, and patients not receiving it.

At present, research is underway to confirm these data and work on the validation of other vasodilator drugs. Because patients with spasm of the arteries in the brain (cerebral vasospasm) there is an increase in blood volume and many of them - swelling of the parenchyma of the brain, even a slight increase in intracranial volume, which occurs under the influence of vasodilators may exacerbate neurological disorders. Therefore, if the patient has established a pronounced symptomatic cerebral vasospasm, vasodilator use is not recommended.

A common treatment option for symptomatic cerebral vasospasm is to increase cerebral perfusion pressure by increasing the mean arterial pressure. This is achieved by an increase in plasma volume and the appointment of vasopressor (fenilzfrin, dopamine). Dopamine is used in doses of 6.3 mg / kg in 1 minute. Therapy to increase perfusion pressure leads to improved picture of the neurological status in some patients, but high blood pressure is associated with the risk of re- bleeding from a ruptured aneurysm. In appointing this treatment requires data on cerebral perfusion pressure and cardiac output. It is also necessary to direct the study of central venous pressure (CVP). In severe cases the patient's intracranial pressure was measured and the pressure of pulmonary artery.

The development of massive edema of the brain parenchyma in patients with symptomatic cerebral vasospasm may lead to increased intracranial pressure. Perhaps a subsequent sharp decrease in cerebral blood circulation in the patient. Swelling of the brain requires increased serum osmolality of blood through the introduction of an osmotic diuretic mannitol, while maintaining adequate intravascular volume and mean arterial pressure. Calculation of the osmotic diuretic administration - 125 ml 20% solution of mannitol administered every 4 hours to as long as the plasma osmolality did not increase to 300-310 mOsm / liter. In extreme cases, to reduce intracranial pressure using barbiturate coma. Although some patients it reduces intracranial pressure, it is proved that this method has significant clinical benefit.

It must be remembered that there is no effective drug for the prevention and treatment of symptomatic cerebral vasospasm after subarachnoid hemorrhage. Further studies may show whether it is possible with MRI or CT of the brain to give a reliable prediction about the patients for whom there is a risk of development of cerebral vasospasm. If possible, it would require more careful study of previous operations to remove clots of coagulated blood, triggering a spasm of cerebral arteries, as well as prophylactic use of vasodilators and prostaglandin agonists.

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