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Index Page » Health & Hygiene » Diseases & Ailments
 

Subarachnoid Hemorrhage: When a Brain Aneurysm Bleeds

 

Spontaneous subarachnoid (pronounced sub-uh-RACK-noid) hemorrhage is rightfully the most feared cause of sudden headache. Usually due to rupture of aneurysms (abnormal, balloon-like outpouchings of arteries) located near the base of the brain, subarachnoid hemorrhages involve bleeding into the space between the brain and its surrounding membrane, known as the meninges. A traumatic blow to the head can also cause subarachnoid hemorrhage, but this is a completely unrelated process and is not the subject of this essay.

About 10% of people with spontaneous subarachnoid hemorrhages die before they even get to a hospital and over a third die within the first four weeks following the bleed. Survivors can have significant impairments due to brain damage.

And while the effects of the initial bleed are bad enough, in the following few weeks individuals with subarachnoid hemorrhage can suffer additional, serious complications. One complication is that the aneurysm responsible for the initial hemorrhage can bleed a second time and cause even more damage. This occurs in 4% of cases within the first 24 hours and there is another 1.2% chance of re-bleeding each day thereafter for the first two weeks. Thus, without treatment 20% of cases have a second hemorrhage within the first two weeks.

The other serious complication is that the blood deposited in the subarachnoid space can cause otherwise healthy arteries passing through this space to go into spasm. The spasm decreases blood-flow to the parts of the brain ordinarily nourished by these arteries and thereby inflicts additional damage. Or, said another way, a blocked artery causes a new stroke, this time of the non-bleeding type. For reasons that are not entirely understood, these spasms of the arteries do not occur within the first few days after the initial hemorrhage. Instead, they typically develop after a delay of 4-9 days.

What can be done to reduce these complications? In the case of blood-vessel spasm, the best treatment is a preventive one. Administering a drug called nimodipine (prononounced nye-MO-dih-peen) intravenously makes spasming less likely to occur. But in order to prevent the other major complication, re-bleeding, the best treatments are those which physically stabilize the aneurysm. In one such procedure, a surgeon places a metal clip across the aneurysm where it joins the otherwise normal artery. An alternative surgery is to wrap the outside of the aneurysm with surgical gauze or plastic sheeting. A newer procedure involves filling the aneurysm with tiny metal coils inserted via a flexible catheter snaked through the arteries.

How can one tell if a particular headache is caused by a bleeding aneurysm? It can be a tough call, but certain features make a ruptured aneurysm more likely. First, a headache due to a ruptured aneurysm is typically of very abrupt onset (often described as a "thunderclap") and is classically the worst headache of one's life. In people who already have recurrent severe headaches from other causes, the headache due to a ruptured aneurysm might feel different from the more usual attacks.

Medical evaluation of patients with ruptured aneurysms can turn up additional clues, like a stiffened neck or changes in the backs of the eyes made visible through an ophthalmoscope. Of course, if the patient is drowsy or confused, this might suggest that something serious is going on, as would any new impairment in the ability to move the eyes, an arm or a leg. A computed tomographic (CT) scan of the head performed within the first 24 hours is very sensitive in detecting a hemorrhage, but if the scan is delayed it is less able to detect the bleed. A lumbar puncture (also known as a spinal tap) always detects subarachnoid hemorrhage even when it is a few days old, but if the needle causes bleeding by piercing a blood-vessel on its way to the subarachnoid space, the test might give the false impression that a subarachnoid hemorrhage occurred when it hadn't.

After discovery of subarachnoid hemorrhage, the next round of testing focuses on where exactly the bleeding occurred. While in over two-thirds of the cases it originates from ruptured aneurysms, other potential sources include tangles of abnormal blood-vessels known as arteriovenous malformations or from bleeds within the brain tissue that secondarily leak into the subarachnoid space. The managing physician can order any of three tests to image the blood vessels themselves and pinpoint the source of bleeding.

The oldest test--still considered the gold-standard--is known as an arteriogram or, alternatively, an angiogram. An arteriogram is considered an "invasive" test because the doctor must slide a long, flexible catheter through the arterial system (which is under much higher pressure than the veins) so that dye infused through the catheter will enter the arteries in question. Two newer tests are "non-invasive," though, in truth, they often involve an infusion into a vein. One is magnetic resonance arteriography (MRA) which is performed with the help of an MRI-scanner. The other is computed tomographic arteriography (CT-A) which is performed with the help of a CT-scanner. While the non-invasive tests are getting better all the time, they still occasionally miss aneurysms otherwise visible on arteriograms.

Apart from identifying the bleeding aneurysms, these tests can detect additional aneurysms, when present. About 20% of people experiencing a ruptured aneurysm have one or more co-existing, unruptured aneurysms.

Subarachnoid hemorrhages occur annually in about 10 people out of 100,000. This computes to a 0.01% rate of annual occurrence. Contrast this figure with the 12% of the adult population who have migraine (most of whom have at least one severe headache per year) and it is apparent that the vast majority of severe headaches are not due to ruptured aneurysms. But the concern about missing a ruptured aneurysm means that many people without subarachnoid hemorrhage must receive tests in order to diagnose the few who have it.

What causes aneurysms in the first place? More than one factor is involved. First, there can be an inborn weakening of the artery's wall. When the wall subsequently deteriorates in ways that can be accelerated by hypertension and smoking, an aneurysm can form.

Actually, aneurysms affecting the brain's arteries are fairly common. Autopsy and arteriogram studies indicate that about 1-4% of the general population have them. This is many more people than have subarachnoid hemorrhages, so a logical conclusion is that most people with aneurysms go through their entire lifetimes without having symptoms. Studies show that aneurysms less than 5 millimeters (0.2 inches) in diameter have a very low rate of rupture, while aneurysms greater than 10 millimeters (0.4 inches) in diameter have a significant risk of bleeding.

Do ruptured aneurysms run in families? A 2005 report from the Scottish Aneurysm Study Group showed a slight tendency for this trait to be shared by close relatives. The 10-year risk for subarachnoid hemorrhage in first-degree relatives (parents, siblings and children) was 1.2%. The risk was even lower in more distant relatives. In families with two affected first-degree relatives there was a trend toward higher risk. The authors felt that most relatives of patients suffering subarachnoid hemorrhages have low risk of future hemorrhages, and that routine screening of family members is inappropriate unless there are multiple affected individuals in the same family.

(C) 2005 by Gary Cordingley

Author: Gary Cordingley
 
Author Bio:

Gary Cordingley

Gary Cordingley graduated from Purdue University with a B.S. in chemistry and biology in 1971. He attended Duke University where he earned a Ph.D. in physiology and pharmacology in 1976, and an M.D. in 1977. He received internship training in internal medicine at the University of Michigan Hospitals 1977-1978, residency training in neurology at the Neurological Institute of Columbia-Presbyterian Medical Center in New York, 1978-1981, and fellowship training as a pharmacology research associate in the National Institute of General Medical Sciences in Bethesda, Maryland, 1981-1983.

He has practiced neurology in Athens, Ohio, since 1983. He is an associate professor of neurology at the Ohio University College of Osteopathic Medicine and a medical staff member of O'Bleness Memorial Hospital in Athens, Ohio.

Dr. Cordingley has been certified in neurology by the American Board of Psychiatry and Neurology. He is a fellow of the American Academy of Neurology and a member of the American Headache Society. He is also a member of the Ohio Academy of Medical History and was president of this organization 1994-1997. Dr. Cordingley's articles on neurology, neuroscience and medical history have appeared in numerous professional and general publications.

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