Cerebral aneurysm

A cerebral aneurysm or brain aneurysm is a cerebrovascular disorder in which weakness in the wall of a cerebral artery or vein causes a localized dilation or ballooning of the blood vessel.

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Locations

A common location of cerebral aneurysms is on the arteries at the base of the brain, known as the Circle of Willis. Approximately 85% of cerebral aneurysms develop in the anterior part of the Circle of Willis, and involve the internal carotid arteries and their major branches that supply the anterior and middle sections of the brain. The most common sites include the anterior communicating artery (30-35%), the bifurcation of the internal carotid and posterior communicating artery (30-35%), the bifurcation of the middle cerebral artery (20%), the bifurcation of the basilar artery, and the remaining posterior circulation arteries (5%).

Causes

Aneurysms may result from congenital defects, preexisting conditions such as high blood pressure and atherosclerosis (the buildup of fatty deposits in the arteries), or head trauma. Cerebral aneurysms occur more commonly in adults than in children but they may occur at any age. They are slightly more common in women than in men.

The pursuit to identify Genetics of Intracranial Aneurysms has identified a number of locations, most recently 1p34-36, 2p14-15, 7q11, 11q25, and 19q13.1-13.3.

Classification

Cerebral aneurysms are classified both by size and shape. Small aneurysms have a diameter of less than 15mm. Larger aneurysms include those classified as large (15 to 25mm), giant (25 to 50mm), and super giant (over 50mm). Saccular aneurysms are those with a saccular outpouching and are the most common form of cerebral aneurysm. Berry aneurysms are saccular aneurysms with necks or stems resembling a berry. Fusiform aneurysms are aneurysms without stems.

Symptoms

A small, unchanging aneurysm will produce no symptoms. Before a larger aneurysm ruptures, the individual may experience such symptoms as a sudden and unusually severe headache, nausea, vision impairment, vomiting, and loss of consciousness, or the individual may be asymptomatic, experiencing no symptoms at all. Onset is usually sudden and without warning. Rupture of a cerebral aneurysm is dangerous and usually results in bleeding into the meninges or the brain itself, leading to a subarachnoid hemorrhage (SAH) or intracranial hematoma (ICH), either of which constitutes a stroke. Rebleeding, hydrocephalus (the excessive accumulation of cerebrospinal fluid), vasospasm (spasm, or narrowing, of the blood vessels), or multiple aneurysms may also occur. The risk of rupture from an unruptured cerebral aneurysm varies according to the size of an aneurysm, with the risk rising as the aneurysm size increases. The overall rate of aneurysm rupture is estimated at 1.3% per year. The risk of short term re-rupture increases dramatically after an aneurysm has bled, though after approximately 6 weeks the risk returns to baseline.

Classification of ruptured aneurysm severity

In outlining symptoms of ruptured cerebral aneurysm, it is useful to make use of the Hunt and Hess scale of subarachnoid hemorrhage severity:

• Grade 1: Asymptomatic; or minimal headache and slight nuchal rigidity. Approximate survival rate 70%.
• Grade 2: Moderate to severe headache; nuchal rigidity; no neurologic deficit except cranial nerve palsy. 60%.
• Grade 3: Drowsy; minimal neurologic deficit. 50%.
• Grade 4: Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances. 20%.
• Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.

The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan:

• Grade 1: No hemorrhage evident.
• Grade 2: Subarachnoid hemorrhage less than 1mm thick.
• Grade 3: Subarachnoid hemorrhage more than 1mm thick.
• Grade 4: Subarachnoid hemorrhage of any thickness with intra-ventricular hemorrhage (IVH) or parenchymal extension.

The Fisher Grade is most useful in communicating the description of SAH. It is less useful prognostically than the Hunt-Hess scale.

Vasospasm

One complication of aneurysmal subarachnoid hemorrhage is the development of vasospasm. Approximately 1 to 2 weeks following the initial hemorrhage, patients may experience 'spasm' of the cerebral arteries, which can result in stroke. The etiology of vasospasm is thought to be secondary to an inflammatory process that occurs as the blood in the subarachnoid space is resorbed. It appears that macrophages and neutrophils that enter the subarachnoid space to phagocytose senescent erythrocytes and clear extracorpuscular hemoglobin, remain trapped in the subarachnoid space, die and degranulate 3-4 days after their arrival, and release massive quantities of endothelins and free radicals that in turn induce vasospasm. ^[1]. Vascular narrowing, however, is only one component of the transient inflammatory injury, which is extensive.

Vasospasm is monitored in a variety of ways. Non-invasive methods include transcranial Doppler, which is a method of measuring the velocity of blood in the cerebral arteries using ultrasound. As the vessels narrow due to vasospasm, the velocity of blood increases. The amount of blood reaching the brain can also be measured by CT or MRI or nuclear perfusion scanning.

The definitive, but invasive method of detecting vasospasm is cerebral angiography. It is generally agreed that in order to prevent or reduce the risk of permanent neurological deficits, or even death, vasospasm should be treated aggressively. This is usually performed by early delivery of drug and fluid therapy, or 'Triple H' (hypertensive-hypervolemic-hemodilution therapy) (which elevates blood pressure, increases blood volume, and thins the blood) to drive blood flow through and around blocked arteries. For patients who are refractive (resistant) to Triple H therapy, narrowed arteries in the brain can be treated with medication delivered into the arteries that are in spasm and with balloon angioplasty to widen the arteries and increase blood flow to the brain. Although the effectiveness of these treatments is well established, angioplasty and other treatments delivered by interventional radiologists have been in evolution over the past several years. It is generally recommended that aneurysms be evaluated at specialty centers which provide both neurosurgical and interventional radiology treatment and which also permit angioplasty, if needed, without transfer.

Treatment

Emergency treatment for individuals with a ruptured cerebral aneurysm generally includes restoring deteriorating respiration and reducing intracranial pressure. Currently there are two treatment options for brain aneurysms: surgical clipping or endovascular coiling. Surgical clipping was introduced by Walter Dandy of the Johns Hopkins Hospital in 1937. It consists of performing a craniotomy, exposing the aneurysm, and closing the base of the aneurysm with a clip. The surgical technique has been modified and improved over the years. Surgical clipping has a lower rate of aneurysm recurrence after treatment. Endovascular coiling was introduced by Guido Guglielmi at UCLA in 1991. It consists of passing a catheter into the femoral artery in the groin, through the aorta, into the brain arteries, and finally into the aneurysm itself. Once the catheter is in the aneurysm, platinum coils are pushed into the aneurysm and released. These coils initiate a clotting or thrombotic reaction within the aneurysm that, if successful, will eliminate the aneurysm. In the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted coiling").Either surgical clipping or endovascular coiling is usually performed within the first three days to occlude the ruptured aneurysm and reduce the risk of rebleeding.

At this point it appears that the risks associated with surgical clipping and endovascular coiling, in terms of stroke or death from the procedure, are the same. The major problem associated with endovascular coiling, however, is a higher aneurysm recurrence rate. For instance, the most recent study by Jacques Moret and colleagues from Paris, France, (a group with one of the largest experiences in endovascular coiling) indicates that 28.6% of aneurysms recurred within one year of coiling, and that the recurrence rate increased with time. ^[2] These results are similar to those previously reported by other endovascular groups. For instance Jean Raymond and colleagues from Montreal, Canada, (another group with a large experience in endovascular coiling) reported that 33.6% of aneurysms recurred within one year of coiling. ^[3] The long-term coiling results of one of the two prospective, randomized studies comparing surgical clipping versus endovascular coiling, namely the International Subarachnoid Aneurysm Trial (ISAT) are turning out to be similarly worrisome. In ISAT, the need for late retreatment of aneurysms was 6.9 times more likely for endovascular coiling as compared to surgical clipping. ^[4]

Therefore it appears that although endovascular coiling is associated with a shorter recovery period as compared to surgical clipping, it is also associated with a significantly higher recurrence rate after treatment. It is unclear, however, whether the higher recurrence rate translates into a higher rebleeding rate, as the data thus far do not show a difference in the rate of recurrent hemorrhage in patients who had aneurysms clipped vs. coiled after rupture. ^[4] The long-term data for unruptured aneurysms are still being gathered.

Patients who undergo endovascular coiling need to have annual studies (such as MRI/MRA, CTA, or angiography) indefinitely to detect early recurrences. If a recurrence is identified, the aneurysm needs to be retreated with either surgery or further coiling. The risks associated with surgical clipping of previously-coiled aneurysms are very high. Ultimately, the decision to treat with surgical clipping versus endovascular coiling should be made by a cerebrovascular team with extensive experience in both modalities.

Prognosis

The prognosis for a patient with a ruptured cerebral aneurysm depends on the extent and location of the aneurysm, the person's age, general health, and neurological condition. Some individuals with a ruptured cerebral aneurysm die from the initial bleeding. Other individuals with cerebral aneurysm recover with little or no neurological deficit. The most significant factors in determining outcome are grade (see Hunt and Hess grade above) and age. Generally patients with Hunt and Hess grade I and II hemorrhage on admission to the emergency room and patients who are younger within the typical age range of vulnerability can anticipate a good outcome, without death or permanent disability. Older patients and those with poorer Hunt and Hess grades on admission have a poor prognosis. Generally, about two thirds of patients have a poor outcome, death, or permanent disability ^{[5] [6]}

References

See also

• Charcot-Bouchard aneurysm
• Intracranial berry aneurysm
• Stroke
• International Subarachnoid Aneurysm Trial
• Neil Young, a famous recipient of a coil embolization for a brain aneurysm. Dennis Danell, Laura Branigan, Bill Berry and Quincy Jones are among the notable musicians who have suffered ruptured brain aneurysms; Branigan's was fatal, as was Danell's.