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What is an Aneurysm?
A cerebral or intracranial aneurysm is an abnormal focal dilation of an artery
in the brain that results from a weakening of the inner muscular layer (the intima) of a blood vessel wall.
The vessel develops a “blister-like” dilation that can become thin and rupture without warning.
The resultant bleeding into the space around the brain is called a subarachnoid hemorrhage (SAH).
This kind of hemorrhage can lead to a stroke, coma and/or death.
Aneurysms are usually found at the base of the brain just inside the skull,
in an area called the subarachnoid space. In fact, 90 percent of SAHs are attributed to
ruptured cerebral aneurysms and the two terms are often used synonymously.
Aneurysms range in size, from small – about 1/8 inch – to nearly one inch.
Aneurysms larger than one inch are called giant aneurysms, pose a particularly high risk and are difficult to treat.
The exact mechanisms by which cerebral aneurysms develop, grow and rupture are unknown.
However, a number of factors are believed to contribute to the formation of cerebral aneurysms, including:
- Hypertension (high blood pressure)
- Cigarette smoking
- Congenital (genetic) predisposition
- Injury or trauma to blood vessels
- Complication from some types of blood infections
Patients with intracranial aneurysms can present with SAH from aneurysmal rupture or with un-ruptured aneurysms, which may have been discovered incidentally or resulted in neurological symptoms. An aneurysm ruptures when a hole develops in the sac of the aneurysm.
The hole can be small, in which case only a small amount of blood leaks, or large, leading to a major hemorrhage. An un-ruptured aneurysm is the one whose sac has not previously leaked. Every year approximately 30,000 patients in the U.S. suffer from a ruptured cerebral aneurysm, and up to 6 percent of the population may have an un-ruptured cerebral aneurysm.
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Spontaneous Thrombosis of an Unruptured Anterior Communicating Artery Aneurysm
Location may also be important as a risk factor for TIAs or stroke from thrombosed saccular aneurysms. The most commonly reported sites are the ICA and middle cerebral artery. Thrombosis of fusiform aneurysms of the basilar, posterior cerebral, and cavernous carotid arteries has also been reported to cause TIAs or strokes. Similar events from an unruptured anterior communicating artery aneurysm, as in our patient, have not previously been reported.
Medical factors that may have contributed to aneurysm thrombosis in our patient include the presence of an occult malignancy and dehydration. These factors could have induced a setting of decreased blood flow and increased coagulability, which may have precipitated aneurysm thrombosis and extension of thrombus into adjacent vessels, resulting in ischemic stroke. Thrombosis of the aneurysm occurred despite an elevated partial thromboplastin time and international normalized ratio, which was thought to be related to alcoholic liver disease. At autopsy hepatic steatosis but no sclerosis was identified.
A series of 111 patients with un-ruptured aneurysms showed:
- 51 percent with asymptomatic aneurysms
- 17 percent with acute symptomatology — such as ischemia (37% of aneurysms)
- Headache (37 percent of aneurysms)
- Seizures (18 percent of aneurysms)
- Cranial neuropathies (12 percent of aneurysms)
- Chronic symptomatology (32 percent) which included headache (51%)
- Visual deficits (29 percent)
- Weakness (11 percent) and
- Facial pain (nine percent)
The management of both ruptured and un-ruptured cerebral aneurysms poses a significant challenge for patients and their treating physicians