|
|
Contents of This Section:
- What is a brain aneurysm?
- How common is a brain aneurysm? ("Prevalence" and "Incidence")
- What are the risk factors that lead to brain aneurysm formation?
- How does a brain aneurysm develop? ("Pathophysiology")
- What are the symptoms of a brain aneurysm? ("Clinical presentation"; "WFNS Grade")
- What are the complications of a brain aneurysm?
- How is a brain aneurysm detected? ("Investigation"; "Fisher Grade")
- Who should be screened for a brain aneurysm, and when?
- How is a brain aneurysm treated?
- To see radiological and operative images of brain aneurysm, click here!
- For information on the brain aneurysm ISAT study (including a very common misconception), click here!
- Persons seeking more detailed information on brain aneurysm investigation, treatment options and step-by-step procedure information, decision making issues, recovery, and so forth will be able to find such information in the book by Drs. Khurana & Spetzler.
1. What is a brain aneurysm?
Like a steel cylindrical
pipe, an artery is comprised of an inner space (the "lumen",
filled with blood) enclosed by a wall (
you can go to the section on Brain Artery
Structure by clicking here). The wall is made up of a
number of layers, two of which are muscle tissue and elastic
tissue. When a region of the blood vessel wall weakens, it
can balloon out to form a sac-like structure. This structure
is called an aneurysm (a word derived from the Greek, aneurysma
- a widening), and the major problem associated with aneurysms
is that they can rupture, an event which may be fatal.
At the outset, it should
be noted that there are different types of brain aneurysms.
They are usually classified as being either "true"
or "false" aneurysms.
A true brain
aneurysm is an expansion of a blood vessel wall involving
all layers of the wall. The two most recognized types of true
aneurysms are "saccular" and "fusiform",
although a third much rarer type called "mycotic"
is also recognized:
- The "saccular"
or "berry" aneurysm is the most common type
of aneurysm, and it's the one we refer to when we think
of "brain aneurysms" in general. Berry aneurysms
are ones that look like sacs or berries sticking out of
a side of a blood vessel wall (see Figure 2, below).
Most of these have a "neck" region (see Figure
6, below), although sometimes a neck cannot be readily
defined in this type of aneurysm, even at the time of
surgery. Berry aneurysms are associated with growth (see
Figures 3 - 7, below) and rupture (hemorrhage;
see Figure 8, below).
- The "fusiform"
aneurysm, less common than the berry aneurysm, is not
a saccular aneurysm. Unlike the saccular aneurysm, a fusiform
aneurysm looks like the blood vessel is expanded (i.e.,
"ectatic") in all directions. This type is typically
associated with fatty plaques or streaks in the artery
(i.e., atherosclerosis), or with cuts in the blood vessel
wall (i.e., arterial dissections). Fusiform aneurysms
don't have a "neck" region, and they seldom
rupture.
- The "mycotic"
(or "infectious") aneurysm, very rare,
is a saccular aneurysm that arises from an artery that
has had a certain part of the wall affected by a source
of infection usually originating from somewhere else in
the body (e.g., the heart) and spreading to the brain
blood vessel by the blood stream (i.e., "hematogenous
spread").
A false (or "pseudo-")
brain aneurysm is an expansion of a blood vessel wall that
does not involve all layers of the wall. Most commonly, it
involves the outermost layers of the brain artery only, and
usually follows injury or tearing of the vessel wall (referred
to as a "dissection" or "laceration").
Please note that
this section of the Website is concerned with the most common
type of brain aneurysm, namely, the "berry" or "saccular"
brain aneurysm.
Brain aneurysms can
also be classified according to their size. The most
common ones are "small" in that their diameter is
10 mm or less. "Giant" aneurysms are ones whose
diameter is 25 mm or greater. In-between, i.e., from 11 to
15 mm and from 20 to 24 mm in diameter are the "large"
and "near-giant" aneurysm sizes, respectively. There
is a gray area of classification for brain aneurysms between
16 to 19 mm. Of all aneurysms, 95% are less than 25 mm in
diameter; i.e., only 5% are "giant".
Interestingly, certain
differences exist between brain aneurysms of these different
sizes. For most purposes, small and large brain aneurysms
(i.e., together, 15 mm or less in diameter) behave in similar
ways in that they tend to grow and rupture. In fact, more
than 90% of these present following rupture (i.e., following
"subarachnoid hemorrhage"). On the other
hand, 75% of patients with near-giant and giant brain aneurysms
(together, 20 mm or larger in diameter) are admitted to hospital
with effects due to compression or irritation of brain structures
surrounding these aneurysms (i.e., with "mass effect",
seizures, etc.); the remaining 25% of patients with near-giant
and giant brain aneurysms are admitted following aneurysmal
rupture. The risks of death and disability associated with
bigger brain aneurysms, and particularly those in the back
portion of the brain arteries (i.e., in the "posterior
cerebral circulation"), are significantly higher than
smaller aneurysms in the front part of the brain arteries
("anterior cerebral circulation").
Brain Arteries and Brain Aneurysm:
Figure 1 shows
the under-surface of the brain. The major arteries in this
region are shown in red. Together, they form a ring-like structure
called the "Circle of Willis", a critical
point of communication between the main arteries supplying
the substance of the brain. The front part of this group of
arteries (in the top part the figure) is referred to as the
"anterior circulation", the back part (in
the bottom part of this figure) is referred to as the "posterior
circulation". All of these arteries lie in the "subarachnoid
space" (SAS), a space normally filled with circulating
cerebrospinal fluid.
The vast majority of
brain aneurysms arise from the parent arteries (or their main
branches) forming the circle of Willis, and more tend to occur
in the anterior (front) part of the brain circulation. Figure
2 shows a sac-like brain aneurysm (A) arising from the
wall of a brain artery (ba). It is well known that most brain
aneurysms form near regions where an artery branches out (i.e.,
at so-called "arterial bifurcations"). It is at
these regions where the turbulent forces exerted on the arterial
wall by the flowing blood may be the greatest. Of course,
we all have arterial bifurcations in the brain, but relatively
few of us will ever develop a brain aneurysm (see 3., below).
2. How common is a brain aneurysm? ("Prevalence" and "Incidence")
This really depends
on what you read! Some series have suggested that up to 5
to 10% of the general population may have one or more brain
aneurysms (i.e., a "prevalence" of 5 to 10%),
others have suggested this number may be less than half of
1%. In the U.S., with a population of approximately 275 million
people, these percentages mean that between approximately
1.5 million people (in the best-case scenario) and 27.5 million
(in the worst-case scenario) in this country may harbor a
brain aneurysm. Either way, that's a lot of people! Most reports
put them at a prevalence of somewhere between 1-5%.
Note that not all brain
aneurysms cause problems. On average, there are 10 cases of
brain aneurysmal rupture (i.e., bursting of the aneurysm sac,
or "subarachnoid hemorrhage") per 100,000 of the
general population per year (i.e., an "incidence"
of 10 per 100,000 per year). Note that this statistic has
often been misquoted. This does not mean that 10
out of 100,000 brain aneurysms rupture. Rather, it means that
every year, for every 100,000 persons in the community-at-large,
10 persons can be expected to be hospitalized for a newly
diagnosed "ruptured brain aneurysm." Therefore,
in the U.S., this amounts to about 30,000 persons diagnosed
with a ruptured brain aneurysm per year. Although it's not
the most common of illnesses, it still is a very serious one,
as brain aneurysmal rupture is associated with a high rate
of death ("mortality") and serious disability ("morbidity").
The "natural history"
of aneurysmal subarachnoid hemorrhage (i.e., the typical chain
of events following the sudden rupture of a brain aneurysm,
assuming no treatment is given) is often devastating for a
patient. In the absence of treatment, half-to-two-thirds of
all patients who suffer a brain hemorrhage from a ruptured
brain aneurysm will not survive 6-months - in fact, most of
the deaths occur between the time of rupture itself (approximate
10% instant mortality) and within a few weeks of the
initial rupture. Half of the remaining survivors will not
be able to return to work or maintain an independent life.
Of course, with better community awareness, earlier diagnosis
(including better imaging, and the prospect of a genetic
test for brain aneurysm rupture risk), and more and improved
treatment options (see below), the chances of a very good
outcome are much higher now than ever before.
3. What are the risk factors
that lead to brain aneurysm formation?
There are several risk
factors that increase the likelihood of a brain aneurysm forming.
It cannot be overstressed that smoking is an extremely
important risk factor for brain aneurysm formation. A history
of high blood pressure (hypertension), or a previous
aneurysm in the same person, or a family history
[i.e., one or more close (first-degree) relatives (i.e., a
parent or sibling) with a brain aneurysm] are also important
risk factors. In fact, 5-15% of persons diagnosed with a brain
aneurysm have a positive family history for brain aneurysm
(i.e., a close relative who also had a brain aneurysm). Age
is a risk factor, in that persons above the age of 40 tend
to present more commonly with brain aneurysms, and the majority
of patients diagnosed with brain aneurysms are females.
While the vast majority of brain aneurysms occur in adults,
they can also occur in children, and so the symptoms
and signs associated with a brain aneurysm (see below) should
not be ignored in kids. Note that a person suffering from
or having a first-degree relative with an inherited connective
tissue disorder such as polycystic kidney disease, alpha-1
anti-trypsin deficiency, Marfan's syndrome and Ehlers-Danlos
syndrome, or with Neurofibromatosis Type 1, is at a higher
risk of forming a brain aneurysm. It is also thought that
in persons born with abnormal blood vessel connections in
the brain (i.e., "congenitally abnormal cerebrovascular
anatomy"), or with a history of brain vessel injury (i.e.,
from head trauma), there may also be an increased risk of
brain aneurysm formation later in life.
The bottom line is that
each of the risk factors contributes to the weakening of a
region of the wall of a brain artery, and this in turn permits
a brain aneurysm to form.
Note that there are
no solid scientific trends regarding "race" or ethnicity
and brain aneurysm formation, with the exception of several
published reports citing higher incidence of brain aneurysm
rupture among Japanese persons. In other instances, racial
differences detected between study groups may be the result
of differences between the manner or pattern of referral to
institutions, geographically-dependent brain aneurysm reporting/detection
mechanisms, or to "confounding" factors such as
subpopulation-dependent smoking and hypertension rates, etc.
Main Risk Factors for
Brain Aneurysm Formation:
| Smoking |
| Hypertension |
| Previous
Aneurysm |
| Family
History of Brain Aneurysm |
| Older
Age |
| Female
Gender |
|
|
4. How does a brain aneurysm develop? ("Pathophysiology")
Like most diseases,
brain aneurysms develop for reasons that may be "congenital"
(i.e., the person was born with some defect in the brain artery
wall, or an abnormal communication in the brain circulation
or, e.g., a hereditary disease which lead to and worsened
a defect in a brain vessel wall) or "acquired"
(i.e., the person was not born with any such defect, but some
event or illness during life lead to the development of the
brain aneurysm). Although the congenital theory was thought
to be more important in the past (and it still is in cases
of persons with inherited connective tissue diseases which
weaken the artery wall from the beginning), it is now thought
that acquired reasons are the main ones underlying the development
of brain aneurysms. Perhaps the most significant of the acquired
reasons are smoking (which is associated with injury to the
blood vessel wall, particularly the endothelium;
take me to Brain Artery Structure now)
and high blood pressure (systemic hypertension; which causes
additional stress on the blood vessel wall).
How and why brain aneurysms
develop really relate to properties of the wall of the blood
vessel. As reviewed elsewhere (
take me to Brain Artery Structure now),
the artery wall is made up of a number of layers, each of
which plays an important role in the overall strength and
resilience (flexibility) of the vessel. In particular, there
is only one elastic layer in the brain artery
(there are two elastic layers in arteries elsewhere in the
body), which itself tends to have many normal openings (perforations),
and anything that damages this layer will predispose to a
brain aneurysm forming in this region of the artery. Also,
the smooth muscle layer of brain arteries has certain
naturally occurring defects (isolated regions where the layer
may be thinned out or absent), particularly where artery branch
points (arterial bifurcations) occur. This makes aneurysms
more likely to occur in such regions. In addition, at arterial
bifurcations, the forces exerted by the flow of blood (hemodynamic
forces) tend to be increased relative to other segments
along the artery, and any condition which increases blood
flow pressure and turbulence (such as high blood pressure
and high cholesterol) will aggravate the tendency for this
part of the artery to balloon out as a brain aneurysm.
The sequence of events
from early brain aneurysm formation, growth, and eventual
rupture is shown in Figures 3-8, below.
Sequence of Brain Aneurysm
Formation:
Figure 3 shows
a normal brain artery branch point with normal blood flow
(arrows) in the artery. No brain aneurysm is present. An aneurysm
then starts to develop from one side of the wall (Figure
4; green arrow), and with time it continues to expand
(Figure 5; green arrows).
As the brain aneurysm
gets larger, a "neck" may become apparent (Figure
6; green arrow heads), and the blood flow in the "body"
or sac of the brain aneurysm (Figure 6; curved arrows)
becomes more and more turbulent. This leads to progressive
weakening of the brain aneurysm wall, especially at the "dome"
of the brain aneurysm (Figure 7; arrows). Rupture eventually
occurs (Figure 8) and blood gushes out of artery (arrow)
and enters the space surrounding the vessel (the "subarachnoid
space") where it forms a clot (see Figure 9, below).
For this reason, this event is referred to "subarachnoid
hemorrhage".
5. What are the symptoms of a brain aneurysm? ("Clinical presentation")
Most brain aneurysms
are silent, the person totally unaware of a problem
till the time of rupture. This is the pattern of events in
approximately 90% of all brain aneurysm patients. At this
point, i.e., the time of rupture, the person experiences one
or more of the following: a sudden, extremely severe headache
[which may be described as "the worst headache
in (the person's) life", or as a "sledge-hammer
headache which struck like a bolt of lightening"],
vomiting, neck stiffness, collapse (loss of consciousness),
sudden loss of function in one or more parts of the body (like
a classic "stroke"), or a "fit"
(seizure). In the remainder of patients, the brain aneurysm
is either found by chance (i.e., incidentally; found
this way in 3% of all brain aneurysm patients) during investigation
for some other reason, or presents with symptoms due to its
relatively large size or "mass" (where it may compress
or irritates surrounding brain structures; seen in 7% of all
brain aneurysm patients). In these instances of so-called
"mass effect", the symptoms may be continuous
morning headaches, nausea, loss of function in one or more
of one of the nerve bundles in the brain or spinal cord (e.g.,
leading to facial muscle weakness, double vision, impaired
balance or hearing, tongue deviation, and weakness in the
limbs, etc.). Of course, these symptoms may also occur in
conditions not related to brain aneurysms (e.g., brain tumors),
so careful evaluation by a physician is required.
There are two other
aspects of brain aneurysm symptoms that are well worth mentioning.
First, many physicians recognize the occurrence of a "warning
leak" in brain aneurysms, where some don't frankly
rupture, but instead tear a little and release a small amount
of blood. A warning leak occurs in somewhere between 15 to
30% of truly "ruptured" brain aneurysm patients.
Leak frequently results in a severe headache and some degree
of neck stiffness and, as the term implies, the leak typically
occurs at some time (not precisely known) prior to the actual
"main bleed". Again, not all headache and neck stiffness
episodes are warning leaks from brain aneurysms. Second, the
American Heart Association and its Stroke Council coined the
catchy term "brain attack" (
take me to the Brain Attack section)
to describe the brain equivalent of the common "heart
attack". This term is an important one, aimed at increasing
community awareness of this important and potentially life-threatening
brain condition. The term encompasses the symptoms of a stroke
(many of which were mentioned above), although the stroke
itself may arise from blood vessel blockage (which is the
most common cause), or from the rupture of a brain aneurysm.
Based on the neurological presentation of the patient, the World Federation of Neurological Societies (WFNS) has designated a grading system for patients following aneurysmal SAH. This has implications for prognosis. The WFNS SAH grading system is as follows (Grade 1 is best, Grade 5 is worst; GCS = Glasgow Coma Score - made up of a combination of eye opening, vocalization, and peripheral motor response). Deficit is defined here as hemiparesis or aphasia. WFNS SAH:
- (Grade 1) GCS = 15, no focal deficit
- (Grade 2) GCS = 13-14, no focal deficit
- (Grade 3) GCS = 13-14, focal deficit present
- (Grade 4) GCS = 7-12, with or without deficit
- (Grade 5) GCS = < 7, with or without deficit
What are the complications of a brain aneurysm?
For any brain aneurysm,
the main problem or dangerous consequence (i.e., "complication")
is that it may grow and rupture. If a brain aneurysm
ruptures, the main complications are death and serious disability
from the initial rupture itself or due to events occurring
after the initial rupture. Of these events, the most important
two are "rebleeding" of the brain aneurysm
(i.e., it re-ruptures and bleeds again), and permanent brain
tissue injury (i.e., "infarction") from "cerebral
vasospasm" (i.e., where, following hemorrhage, brain
arteries go into severe spasm; i.e., they shut down, depriving
the nearby brain tissue of oxygen and other nutrients; see
Figure 9, below). These major complications are discussed
elsewhere (
take me to the section on Aneurysmal Rebleeding
or Cerebral Vasospasm now).
Spasm of Arteries Neighboring
Ruptured Brain Aneurysm:

Following rupture of
a brain aneurysm (see Figure 8, above), blood gushes
out of artery and enters the subarachnoid spacewhere it forms
a clot (Figure 9; green arrows). This clot releases
substances that can cause spasm (Figure 9; arrow heads)
of the neighboring brain arteries. This event is referred
as cerebral vasospasm, and causes death and serious disability
in about one in five patients with ruptured brain aneurysms
( take
me to the separate section on Cerebral Vasospasm
now).
In persons surviving
the above complications, other complications may arise. For
example, there may be some degree of obstruction (or blockage)
of normal cerebrospinal fluid (CSF) flow in the brain (i.e.,
resulting in high-pressure build up in the brain referred
to as "hydrocephalus"; see Figure 9B).
This is caused by the blood clot or blood products clogging
up the CSF drainage system following brain aneurysm rupture,
and it can lead to progressive, permanent brain injury. Also,
following brain aneurysm rupture, parts of the brain can become
electrically irritated, resulting in seizures. Finally,
it should be noted that the rupture of a brain aneurysm can,
in some patients, cause "cardiac stunning"
(a heart attack or arrhythmia that can even be fatal).
Hydrocephalus:
The
figure to the right depicts CSF flow and the development of
hydrocephalus. The brain contains fluid-filled spaces
called ventricles (drawn as light blue spaces in center
of brain, above). The fluid that fills these spaces is known
as cerebrospinal fluid (CSF). CSF, which is produced
by structures collectively referred to as the choroid plexus
(drawn as light red structures within brain, right), circulates
throughout the brain (blue arrows). It exits the brain near
the brainstem and makes its way either over the surface of
the brain (in the subarachnoid space; light blue spaces
around the brain, above), or into and around the spinal cord
(light blue space within and around spinal cord, above). Note
that in the lowest part of the spine, just above the level
of the tailbone, is a generous CSF-filled cavity known as
the lumbar cistern, which is the site from which CSF
is drawn during a “spinal tap” or lumbar puncture.
CSF is mostly absorbed at the very top surface of the brain
in structures called arachnoid granulations (drawn
as the three dark red stuctures on the top surface of the
brain, above).
When a brain aneurysm
ruptures, the blood, which should be on the inside of blood
vessels, now enters the subarachnoid space and eventually
makes its way to the arachnoid granulations. Cells and debris
in the blood can clog up and damage these granulations. This
leads to obstruction of CSF absorption. This damage may be
short term, or permanent. CSF now accumulates, like a dam
effect, and results in hydrocephalus (water in the
head), i.e., enlargement of the ventricles (green arrows,
above). This causes pressure to build up in the brain, and
it manifests in one or more of the following: headache, nausea,
vomiting, blurred or double vision, increasing drowsiness,
even coma and death. The way to treat this is to divert the
CSF, at first temporarily through a special drainage tube
placed either into the ventricles (an “external ventricular
drain”) or into the lumbar cistern (a “lumbar
drain”). CSF will intermittently be drained via
this tubing over several days and then an attempt made to
gradually clamp off (wean”) the drain in order to see
if the natural pathways for CSF absorption have recovered.
If so, good, the drain will be removed. If a drain can't be
weaned successfully (i.e., the patient gets symptomatic from
hydrocephalus each time the drain is clamped), then a “shunt”
usually needs to be placed by the neurosurgeon. Formal shunting
requires a separate operation and carries its own short and
long term risks. The literature reflects that one in three
ruptured brain aneurysm patients will develop hydrocephalus,
and many of these will require placement of a permanent shunt.
Therefore, from the get go, I prefer to be fairly aggressive
about CSF diversion techniques in patients with ruptured brain
aneurysms, with the aim to avoid the development of hydrocephalus
and therefore avoid the patient needing a shunt.
7. How is a brain aneurysm detected? ("Investigation")
Sadly, most brain aneurysms
are detected only after they have ruptured. As mentioned above,
in less than 10% of patients, the brain aneurysm is detected
by chance (3%) or, in the case of bigger brain aneurysms,
due to symptoms arising from compression of brain structures
(7%).
The gold-standard
for detection of a brain aneurysm is cerebral angiography.
Here, a contrast dye is first injected through a catheter
device inserted usually in a thigh (femoral) artery. From
here, the dye eventually enters one or more of the main brain
arteries, where it is X-ray imaged. It typically provides
a detailed roadmap of the brain circulation. An aneurysm appears
as an expansion of the vessel. If there is no clot (thrombus)
in the brain aneurysm, it will light up like a sac coming
off the parent artery. If the lumen (or inner space) of the
brain aneurysm is packed with clot (this is more common in
bigger brain aneurysms due to slowing of blood flow in the
lumen), then sometimes the real extent of the brain aneurysm
may not be seen by this method.
Other X-ray based
advanced imaging methods for detecting brain aneurysms
are magnetic resonance imaging (MRI) and its associated
method referred to as magnetic resonance angiography (MRA).
The advantages of these methods are that they are less invasive
than cerebral angiography, in that they do not involve femoral
(thigh) artery puncture and insertion and navigation of a
long catheter through the arteries. However, they may not
detect the smallest of brain aneurysms as well as cerebral
angiography can, and (due to problems with magnetic attraction
and interference; ferromagnetism) are not able to be used
in certain patients in whom metallic hardware has been placed.
Of course, some patients with certain metallic (nonferromagnetic,
e.g., titanium) hardware can still be safely and effectively
imaged by this method. Check with your physicians first.
Ordinary computer-assisted
tomographic (CAT or CT) scanning with a limited
injection of contrast dye is another way to detect brain aneurysms,
but not a very good way (note that without injection of contrast,
an ordinary CT scan is almost useless unless the brain aneurysm is very large, calcified or ruptured). Even when used as part of CT angiography (see below), this method is not as sensitive (i.e., can't quite pick up the smallest brain aneurysms or some aneurysms located around the brainstem) or as specific (i.e., can't really be sure it's a brain aneurysm that's been detected) compared with cerebral angiography. Note that if an aneurysm has ruptured, the amount of blood on the CAT scan can be prognostic in terms of the likelihood a patient will experience cerebral vasospasm ( take
me to the separate section on Cerebral Vasospasm now). The more the blood (i.e., the higher the "Fisher Grade"), the more likely it will be that a patient will experience cerebral vasospasm, but exceptions exist of course. Fisher SAH Grade 1 means no blood seen on the CT scan, while Fisher Grade 2 means very little blood seen on the CT scan. These first two grades are not associated with a high risk of cerebral vasospasm. Fisher grades 3 & 4 imply that a significant amount of blood is seen on the CT scan and, of these, Fisher Grade 3 seems to be the grade most strongly associated with vasospasm occurrence.
Ultrasound (e.g., Duplex-Doppler) plays no real role
in the detection of brain aneurysms in clinical practice,
although it is more useful for detecting spasm of arteries
following rupture of an aneurysm. Common X-rays are not used
for aneurysm detection, although highly calcified brain aneurysms
may show up as curvilinear lesions on a plain skull x-ray
(and in neurosurgery resident examinations!).
A combination of CT
scanning and angiography (referred to as CT-angiography,
CTA; where a larger amount of intravenous dye is introduced
into the patient at the time of CT scanning) is currently
gaining popularity as a very good means of detecting brain
aneurysms, and may one day replace conventional cerebral angiography
(with the obvious advantages that CT-angiography is so much
quicker, cheaper, and less invasive compared with conventional
angiography). The ability to create high-resolution and color
3-dimensional images with CTA is very useful
for surgeons planning to operate these lesions.
Lumbar puncture
is frequently used to determine whether or not a brain aneurysm
that may have been detected by one or more of the above methods
has ruptured. This involves the insertion of a spinal needle
into the lower part of the back, and examination of the cerebrospinal
fluid for blood pigments ("xanthochromia")
whose signature is first present from around 6 hours after
the hemorrhage and may linger for weeks).
At present there is
no single blood test that can reliably predict "sporadic"
brain aneurysm formation or rupture. However, researchers
have been working on developing such a test, although they
are still waiting for validation through a larger clinical
trial
(
take me to the section on Genetic Test
for Brain Aneurysm Rupture). It should be noted that certain
genetic (hereditary) diseases may have genetic fingerprints
that can be detected in the blood or after an appropriate
tissue biopsy which, if found, may indicate that a person
is at increased risk of developing a brain aneurysm.
8. Who should be screened for a brain aneurysm, and when?
Note that the possible
benefits of screening and any risks associated with screening
procedures should be discussed with your local physician or
attending neurologist or neurosurgeon.
Screening for
brain aneurysms refers to the attempt to detect a brain aneurysm
in a person who has had no symptoms related to, or previous
diagnosis of, brain aneurysmal disease. At present, there
are no hard and fast rules regarding brain aneurysm screening.
Some physicians recommend that if two or more first degree
relatives (i.e., close relatives such as a person's siblings
or parents) are known to have (or have had) brain aneurysms,
then the person in question should be a strong candidate for
screening. Some patients with certain inherited connective
tissue diseases are also considered by some physicians as
good candidates for brain aneurysm screening, particularly
if they have had problems in other parts of their body related
to their connective tissue disorder.
Screening is carried
out using an imaging device which scans the brain, such as
a magnetic resonance imaging (MRI) scanner, particularly in
its magnetic resonance angiography (MRA) mode. MRA
scanning is regarded as a safe and acceptable way of detecting
brain aneurysms, although some very small aneurysms may be
difficult to detect by this scanning technique. Ordinary CT
(or "CAT") scanning is not a good way to
detect unruptured brain aneurysms (because unless they are
large in size, ordinary CT scanning isn't sensitive enough
in detecting their presence). However, a newer mode of CT
scanning referred to as "CT-angiography" (CTA; described above) is showing promise as being a good alternative to MRA for brain aneurysm screening. Referring docs should ask for "high-resolution CTA with multiplanar views". CTA is quicker, less expensive, and is less claustrophobic than MRA, however, clinical studies are still required to conclusively compare the methods of MRA and CTA as effective screening tools for unruptured brain aneurysms.
Cerebral angiography
(see above) may be regarded by some as an alternative method
for screening. Although this procedure is the best (most accurate;
"gold standard") method known for detecting brain
aneurysms, it carries certain risks when compared with, say,
MRA or CTA. For example, angiography may cause local bleeding
at the femoral artery catheter entry site or in other more
distant arteries in the body during navigation of the catheter
itself. There is also a small (1%) risk of stroke during cerebral
angiography. Also, some patients may be allergic to the contrast
material, although more modern contrasts have been developed
to reduce this risk. Owing to its complexity and need for
an experienced interventional radiologist, cerebral angiography
is also a relatively costly form of imaging compared with
MRA and CTA.
In general, a screening
method should be least risky, relatively cost-effective, yet
should provide good and accurate information. In this context,
MRA may be the best method for brain aneurysm screening at
present, although CTA may be an upcoming acceptable method,
too. Again, the possible benefits of screening and any risks
associated with screening procedures should be discussed with
your local physician or attending neurologist or neurosurgeon.
Lastly, it should be
noted that one of the biggest questions that needs to be addressed
in screening for brain aneurysms is this: "What will
YOU do if you are found by screening to have a brain aneurysm,
yet had no symptoms related to it?" Will you be prepared
to undergo the necessary investigations and possible treatment?
This issue certainly makes the issue of screening more complex.
Certainly, some brain aneurysms that are discovered by screening
may be at a higher risk of rupture (particularly if they are
7-10 mm or greater in diameter, or found to be growing in
consecutive studies). However, smaller brain aneurysms (i.e.,
those less than 10 mm in diameter) may also rupture. So, if
an aneurysm that has been causing no symptoms has been found
"incidentally" by screening then,...should it be
treated? when? how? These are issues that require considerable
discussion between the patient and a team of physicians including
a neurosurgeon, neurologist, and neuroradiologist.
9. How is a brain aneurysm treated?
If a brain aneurysm
is detected, but hasn't ruptured, the choice of treatments
is very controversial at the moment. Some physicians have
found that a brain aneurysm diameter (size) of 10 mm may be
the critical number after which there is a significantly increased
risk of brain aneurysm rupture. Others, however, have found
that rupture occurs in even smaller brain aneurysms (e.g.,
3 to 6 mm in diameter), and therefore advocate that the 10
mm size "threshold" is not valid for determining
risks and deciding on close observation (which means
not actually treating the brain aneurysm, but rather following
the patient every so often with repeated scans to see if the
brain aneurysm is enlarging) versus actual treatment.
The bottom line is that each case of brain aneurysm should
be treated on an individualized basis, taking into
consideration the age of the patient, copresence of significant
medical conditions, the site and size and shape of the brain
aneurysm, whether there is a history of previous aneurysmal
hemorrhage in that patient, the experience of the treating
physician or surgeon, and the type and risk(s) of treatment
option most suitable for that brain aneurysm and person.
The picture is more clear if the brain aneurysm has ruptured. Here, the options are either surgery (which is generally recommended for as early as possible after the hemorrhage) or a nonsurgical (neuroradiological) intervention [i.e., involving insertion of a catheter (a long, thin, flexible, tube-like device) into an artery (usually the femoral artery in the thigh), and navigating the catheter through the artery up into the brain to the region of the brain aneurysm itself].
Immediate and early medical management of patients presenting following aneurysm rupture includes:
- Assessment of ABCD (airway, breathing, circulation, "deficit") -- some SAH patients present comatose, others may have significant cardiorespiratory issues secondary to the SAH ("cardiac stunning", "arrythmia", "myocardial ischaemia", and "neurogenic pulmonary oedema" can occur following SAH)
- Appropriate laboratory studies [complete blood count, electrolytes, creatinine, "coags"(APTT, PT/INR), electrocardiogram, chest x-ray, blood type & screen or "group and hold"]
- Keeping the patient in a relatively quite and (if photophobic) dim-lit environment
- Tight blood pressure control (aiming to keep systolic 120-140 mmHg max, and MAP around 85-90 mmHg max)
- Monitoring serum sodium and urine output ("cerebral salt wasting" is common in SAH patients) - usually seen in the 2-7 days after the ictus/SAH itself.
- Neurosurgical stat consultation
- Watch level of consciousness, if declines, need for intubation likely; inform intensive care and neurosurgical teams
- Postoperative management and management issues in comatose patients are complex and discussed elsewhere
- Medical management of patients experiencing cerebral vasospasm is discussed elsewhere
1. Surgical options for a brain aneurysm:
These include: (i) placing
a metallic clip across the neck of the brain aneurysm ("direct
clipping"; see Figure 10, below), regarded
as the best and most sure (definitive) method of treating
a brain aneurysm; (ii) placing a metallic clip across the
artery feeding the brain aneurysm ("proximal"
or "Hunterian" ligation) thereby allowing
the brain aneurysm to clot off and hopefully shrink; (iii)
placing a metallic clip across all arteries feeding and draining
the brain aneurysm ("trapping"; see Figure
11below); and (iv) "surgical reconstruction"
of the aneurysmal portion of the artery (where the brain aneurysm
is surgically cut out, and the vessel thereafter repaired
using an end-to-end resuturing technique or a natural or synthetic
vessel graft). These types of procedures are carried out according
to the individual patient's brain aneurysm and the experience
of the neurosurgeon. As with any neurosurgical procedure,
there are risks of injury to other vessels or brain
structures in the vicinity of the operation field (which can
result in a stroke-like picture), the possibility of bleeding
or rebleeding from the brain aneurysm, and brain tissue or
wound infection. There is also the risk that the brain aneurysm
can recur (or an entirely new brain aneurysm can develop)
despite surgery; this is very rare, however. Together, the
risk profile depends on the size and location of the brain
aneurysm, the age and general health of the patient, whether
the brain aneurysm is ruptured or unruptured, the time between
rupture and treatment, and the experience of the surgeon.
The risk of rupture from an untreated unruptured brain aneurysm,
or the risk of death or disability from the initial rupture
itself, or from rerupture or delayed vasospasm from a ruptured
brain aneurysm, may far outweigh the risks of surgery, but
again, these are factors determined on an individual basis.
It should be noted that in the most risky aneurysms, the surgeon
may (on rare occasions) elect or need to carry out part of
the procedure with the patient on heart (cardiopulmonary)
bypass, and cooled to relatively low temperatures (profound
hypothermia).
2. Neuroradiological options for a brain aneurysm:
The neuroradiological
(catheter-based or endovascular) nonsurgical procedures
include: (i) placement of metallic (e.g., titanium) microcoils
or a "glue" (or similar composite) in the
lumen of the brain aneurysm (in order to slow the flow of
blood in the lumen, encouraging the aneurysm to clot off (be
excluded) from the main artery and hopefully shrink; see Figure
12 below); (ii) placement of a balloon with or
without microcoils in the parent artery feeding the brain
aneurysm (again, with the intention of stopping the flow of
blood into the brain aneurysm lumen, encouraging it to clot
off and hopefully shrink); (iii) insertion of a synthetic
hollow bridge (a stent) across the aneurysmal part
of the artery to effectively cut off blood supply to the brain
aneurysm, or to allow coiling through openings in the stent,
without stopping blood flow across the open stent (see Figure
12 below); and (iv) a combination of the previous three
procedures. The advantages of a neuroradiological procedure
is that it doesn't require surgery, and yet may be as beneficial
(esp. for small brain aneurysms). In certain brain aneurysms
which are difficult to get to surgically, the interventional
procedures have the added advantage of access to the brain
aneurysm. However, there are complications associated
with the neuroradiological approaches; these include the possibility
of rupture of the brain aneurysm, stroke during the procedure,
injury to the parent or another artery during navigation of
the catheter, the possibility of incomplete stoppage of blood
flow to (or within) the brain aneurysm thereby allowing the
brain aneurysm to continue to grow and eventually rupture,
and the possibility that the hardware can accidentally migrate
away from the brain aneurysm, and cause a stroke by cutting
off brain blood supply from further along the artery. It should
be noted that a clotted brain aneurysm is not necessarily
a safe one.
In the ideal circumstance,
the decision as to how to best treat a brain aneurysm is made
in joint consultation between the patient, a neurosurgeon
and a neuroradiologist, taking into careful consideration
the specific circumstances of the patient and the brain aneurysm
itself.
Some Techniques for Treating a Brain Aneurysm:
Figure 10 shows
a directly clipped brain aneurysm, the clip being placed across
the brain aneurysm neck, thereby effectively removing (isolating)
the brain aneurysm from the circulation. Figure 11
shows trapping of a brain aneurysm, with surgical clips being
placed on the artery sections feeding and draining the brain
aneurysm. Figure 12 shows a hollow stent (S) placed
by a catheter across the region of the vessel that opens into
the lumen of the brain aneurysm, again, isolating the brain
aneurysm from the circulation (although this depends on the
type of stent). Metallic microcoils (C) can also be placed
in the lumen of the brain aneurysm to slow down and eventually
clot off its internal flow. See above text for details.
|