You are on page 1of 23

A subarachnoid hemorrhage (SAH, pronounced /ˌsʌbəˈræknɔɪd ˈhɛm(ə)rɪdʒ/, or subarachnoid haemorrhage in British

English) is bleeding into the subarachnoid space—the area between the arachnoid membrane and the pia mater
surrounding the brain. This may occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head
Symptoms of SAH include a severe headache with a rapid onset ("thunderclap headache"), vomiting, confusion or a lowered
level of consciousness, and sometimes seizures.[1] The diagnosis is generally confirmed with a CT scan of the head, or
occasionally by lumbar puncture. Treatment is by prompt neurosurgery or radiologically guided interventions with
medications and other treatments to help prevent recurrence of the bleeding and complications. Surgery for aneurysms was introduced
in the 1930s, but since the 1990s many aneurysms are treated by a less invasive procedure called " coiling", which is carried out by
instrumentation through large blood vessels.[1]
SAH is a form of stroke and comprises 1–7% of all strokes.[2] It is a medical emergency and can lead to death or severe
disability—even when recognized and treated at an early stage. Up to half of all cases of SAH are fatal and 10–15% die before
reaching a hospital,[1] and those who survive often have neurological or cognitive impairment.[3]
Signs and symptoms
The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the
head",[4] or the "worst ever", developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the
head).[5] About one-third of sufferers have no symptoms apart from the characteristic headache, and about one in ten people who seek
medical care with this symptom are later diagnosed with a subarachnoid hemorrhage.[1] Vomiting may be present, and 1 in 14
have seizures.[1] Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of
meningism.[1] Neck stiffness usually presents six hours after initial onset of SAH.[6] Isolated dilation of a pupil and loss of the
pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull).[1]
Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure: subhyaloid hemorrhage (bleeding
under the hyaloid membrane, which envelops the vitreous body of the eye) and vitreous hemorrhage may be visible on
fundoscopy. This is known as Terson syndrome (occurring in 3–13% of cases) and is more common in more severe SAH.[7]
Oculomotor nerve abnormalities (affected eye looking downward and outward and inability to lift the eyelid on the same
side) or palsy (loss of feeling) may indicate bleeding from the posterior communicating artery.[1][5] Seizures are more
common if the hemorrhage is from an aneurysm; it is otherwise difficult to predict the site and origin of the hemorrhage from the
symptoms.[1] SAH in a person known to have fits is often diagnostic of an arteriovenous malformation.[5]
As a result of the bleeding, the body releases large amounts of adrenaline and similar hormones. This leads to a sharp increase in
the blood pressure; the heart comes under substantial strain, and neurogenic pulmonary edema (accumulation of fluid in the
lungs), cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (in 27% of cases)[8]
and cardiac arrest (in 3% of cases) may occur rapidly after the onset of hemorrhage.[1][9]
Subarachnoid hemorrhage may also occur in people who have suffered a head injury. Symptoms may include headache, decreased
level of consciousness and hemiparesis (weakness of one side of the body). SAH is a frequent occurrence in traumatic brain injury,
and carries a poor prognosis if it is associated with deterioration in the level of consciousness. [10]
Arteriogram showing a partially coiled aneurysm (indicated by yellow arrows) of the posterior cerebral artery with a residual
aneurysmal sac. The patient was a 34-year-old woman initially treated for a subarachnoid hemorrhage.

A lumbar puncture in progress. A large area on the back has been washed with an iodine based disinfectant leaving brown
The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a medical history and performing
a physical examination; these are aimed at determining whether the symptoms are due to SAH or to another cause. The diagnosis
cannot, however, be made on clinical grounds alone; therefore medical imaging is generally required to confirm or exclude
bleeding. The modality of choice is computed tomography (CT scan) of the brain. This has a high sensitivity and will correctly
identify over 95% of cases—especially on the first day after the onset of bleeding. Magnetic resonance imaging (MRI) may be
more sensitive than CT after several days.[1]
Lumbar puncture, in which cerebrospinal fluid (CSF) is removed with a needle from the lumbar sac, will show evidence of
hemorrhage in 3% of people in whom CT was found normal; lumbar puncture is therefore regarded as mandatory in people with
suspected SAH if imaging is negative.[1] At least three tubes of CSF are collected.[6] If an elevated number of red blood cells is
present equally in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that
it is due to damage to a small blood vessel during the procedure (known as a "traumatic tap"). [3] The CSF sample is also examined for
xanthochromia—the yellow appearance of centrifugated fluid. More sensitive is spectrophotometry (measuring the absorption
of particular wavelengths of light) for detection of bilirubin, a breakdown product of hemoglobin from red blood cells.[1][11]
Xanthochromia and spectrophotometry remain reliable ways to detect SAH several days after the onset of headache. [11] An interval
of at least 12 hours between the onset of the headache and lumbar puncture is required, as it takes several hours for the hemoglobin
from the red blood cells to be metabolized into bilirubin.[1][11]
As only 10% of people admitted to the emergency department with a thunderclap headache are suffering from an SAH, other possible
causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis.[4]
Intracerebral hemorrhage, in which bleeding occurs within the brain itself, is twice as common as SAH and is often misdiagnosed
as the latter.[12] It is not unusual for SAH to be initially misdiagnosed as a migraine or tension headache, which can lead to a delay
in obtaining a CT scan. In a 2004 study, this occurred in 12% of all cases and was more likely in people who had smaller hemorrhages
and no impairment in their mental status. The delay in diagnosis led to a worse outcome. [13] In some people, the headache resolves by
itself, and no other symptoms are present. This type of headache is referred to as "sentinel headache", because it is presumed to result
from a small leak (a "warning leak") from an aneurysm. A sentinel headache still warrants investigations with CT scan and lumbar
puncture, as further bleeding may occur in the subsequent three weeks.[3]
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an
aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through
a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify
aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below). [1][3]
In 85% of cases of spontaneous SAH, the cause is rupture of a cerebral aneurysm—a weakness in the wall of one of the arteries in the
brain that becomes enlarged. They tend to be located in the circle of Willis and its branches. While most cases of SAH are due to
bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture. [1]
In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first angiogram.[14] About half of these are attributed to
non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e.
mesencephalon). In these, the origin of the blood is uncertain.[1] The remainder are due to other disorders affecting the blood vessels
(such as arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumors.[1]
Cocaine abuse and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy, problems with blood
clotting and pituitary apoplexy can also result in SAH.[6][14]
Subarachnoid blood can be detected on CT scanning in as many as 60% of people with traumatic brain injury.[15] Traumatic
SAH (tSAH) usually occurs near the site of a skull fracture or intracerebral contusion.[14] It usually happens in the setting of
other forms of traumatic brain injury and has been linked with a poorer prognosis. It is unclear, however, if this is a direct result of the
SAH or whether the presence of subarachnoid blood is simply an indicator of severity of the head injury and the prognosis is
determined by other associated mechanisms.[15]

There are several grading scales available for SAH. The Glasgow Coma Scale is ubiquitously used for assessing consciousness.
Three specialized scores are used to evaluate SAH; in each, a higher number is associated with a worse outcome. [16] These scales
have been derived by retrospectively matching characteristics of patients with their outcomes.
The first scale of severity was described by Hunt and Hess in 1968:[17]
Grade Signs and symptoms Survival
1 Asymptomatic or minimal headache and slight neck stiffness 70%
2 Moderate to severe headache; neck stiffness; no neurologic deficit except cranial nerve palsy 60%
3 Drowsy; minimal neurologic deficit 50%
4 Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances 20%
5 Deep coma; decerebrate rigidity; moribund 10%
The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan. [18] This scale has been modified by Claassen
and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage.[19]
Grade Appearance of hemorrhage
1 None evident
2 Less than 1 mm thick
3 More than 1 mm thick
4 Any thickness with intraventricular hemorrhage or parenchymal extension
The World Federation of Neurosurgeons (WFNS) classification uses Glasgow coma score (GCS) and focal neurological deficit to
gauge severity of symptoms.[20]
Grade GCS Focal neurological deficit
1 15 Absent
2 13–14 Absent
3 13–14 Present
4 7–12 Present or absent
5 <7 Present or absent
A comprehensive classification scheme has been suggested by Ogilvy and Carter to predict outcome and gauge therapy.[21] The
system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; Hunt and
Hess grade 4 or 5; Fisher scale 3 or 4; aneurysm size greater than 10 mm; and posterior circulation aneurysm 25 mm or more.[21]

[ edit] Treatment
Management involves general measures to stabilize the patient while also using specific investigations and treatments. These include
the prevention of rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention
and treatment of complications.[1]

[edit] General measures

Stabilizing the patient is the first priority. Those with a depressed level of consciousness may need to be intubated and
mechanically ventilated. Blood pressure, pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the
diagnosis is confirmed, admission to an intensive care unit may be preferable, especially since 15% may have further bleeding soon
after admission. Nutrition is an early priority, with oral or nasogastric tube feeding being preferable over parenteral routes.
Analgesia (pain control) is generally restricted to less sedating agents such as codeine, as sedation may impact on the mental
status and thus interfere with the ability to monitor the level of consciousness. Deep vein thrombosis is prevented with
compression stockings, intermittent pneumatic compression of the calves or both.[1] A bladder catheter is usually inserted
to monitor fluid balance. Benzodiazepines may be administered to help relieve distress.[6] Antiemetic drugs should be given to
awake persons.[5]

The arteries of the brain, viewed from underneath. Image originally from Gray's Anatomy, 1918.
People whose CT scan shows a large hematoma, depressed level of consciousness or focal neurologic symptoms may benefit
from urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo
an transfemoral angiogram or CT angiogram later. It is hard to predict who will suffer a rebleed, yet it may happen at any time and
carries a dismal prognosis. After the first 24 hours have passed, rebleeding risk remains around 40% over the subsequent four weeks,
suggesting that interventions should be aimed at reducing this risk as soon as possible. [1]
If a cerebral aneurysm is identified on angiography, two measures are available to reduce the risk of further bleeding from the same
aneurysm: clipping[22] and coiling.[23] Clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed
by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels (endovascularly): a
catheter is inserted into the femoral artery in the groin and advanced through the aorta to the arteries (both carotid arteries and
both vertebral arteries) that supply the brain. When the aneurysm has been located, platinum coils are deployed that cause a
blood clot to form in the aneurysm, obliterating it. The decision as to which treatment is undertaken is typically made by a
multidisciplinary team consisting of a neurosurgeon, neuroradiologist and often other health professionals.[1]
Generally, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of
the patient. Aneurysms of the middle cerebral artery and its related vessels are hard to reach with angiography and tend to be
amenable to clipping. Those of the basilar artery and posterior cerebral artery are hard to reach surgically and are more accessible for
endovascular management.[24] These approaches are based on general experience, and the only randomized controlled trial
directly comparing the different modalities was performed in relatively well patients with small (less than 10 mm) aneurysms of the
anterior cerebral artery and anterior communicating artery (together the "anterior circulation"), who constitute about 20% of
all patients with aneurysmal SAH.[24][25] This trial, the International Subarachnoid Aneurysm Trial (ISAT), showed that in this
group the likelihood of death or being dependent on others for activities of daily living was reduced (7.4% absolute risk
reduction, 23.5% relative risk reduction) if endovascular coiling was used as opposed to surgery.[24] The main drawback of
coiling is the possibility that the aneurysm will recur; this risk is extremely small in the surgical approach. In ISAT, 8.3% needed
further treatment in the longer term. Hence, people who have undergone coiling are typically followed up for many years afterwards
with angiography or other measures to ensure recurrence of aneurysms is identified early.[26] Other trials have also found a higher
rate of recurrence necessitating further treatments.[27][28]

[edit] Vasospasm

Vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of SAH. It can cause
ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the
brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms, and can be confirmed by
transcranial doppler or cerebral angiography. About one third of all people admitted with subarachnoid hemorrhage will have
delayed ischemia, and half of those suffer permanent damage as a result.[29] It is possible to screen for the development of vasospasm
with transcranial doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of
The use of calcium channel blockers, thought to be able to prevent the spasm of blood vessels by preventing calcium from
entering smooth muscle cells, has been proposed for the prevention of vasospasm.[15] The oral calcium channel blocker nimodipine
improves outcome if administered between the fourth and twenty-first day after the hemorrhage, even if it does not significantly reduce
the amount of vasospasm detected on angiography.[30] In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term
outcome, and is not recommended.[31] Other calcium channel blockers and magnesium sulfate have been studied, but are not
presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously. [29]
A protocol referred to as "triple H" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of
intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation) and
hemodilution (mild dilution of the blood).[32] Evidence for this approach is inconclusive; no randomized controlled trials have been
undertaken to demonstrate its benefits.[33]
If the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of
vasospasms and administer vasodilator medication (drugs that relax the blood vessel wall) directly into the artery. Angioplasty
(opening the constricted area with a balloon) may also be performed.[3]

[edit] Other complications

Hydrocephalus (obstruction of the flow of cerebrospinal fluid) may complicate SAH in both the short- and long term. It is detected
on CT scanning, on which there is enlargement of the lateral ventricles. If the level of consciousness is decreased, drainage of the
excess fluid is performed by therapeutic lumbar puncture, extraventricular drain (a temporary device inserted into the one of the
ventricles) or occasionally a permanent shunt.[1][3] Relief of hydrocephalus can lead to an enormous improvement in a person's
condition.[5] Fluctuations in blood pressure and electrolyte disturbances, as well as pneumonia and cardiac
decompensation occur in about half the hospitalized persons with SAH and may worsen prognosis.[1] Seizures occur during the
hospital stay in about a third of cases.[3] Many believe that patients might benefit from prevention with antiepileptic drugs.[3]
Although this is widely practiced,[34] it is controversial and not based on good evidence.[35][36] In some studies, use of these
drugs was associated with a worse prognosis; this might be because they actually cause harm, or because they are used more often in
persons with a poorer prognosis.[37][38] There is a possibility of a gastric hemorrhage due to stress ulcers. [39]

[edit] Early morbidity and mortality

SAH is often associated with a poor outcome.[2] The death rate (mortality) for SAH is between 40 and 50%,[12] but trends for
survival are improving.[1] Of those who survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and
less than a fifth have no residual symptoms whatsoever.[24] Delay in diagnosis of minor SAH (mistaking the sudden headache for
migraine) contributes to poor outcome.[13] Factors found on admission that are associated with poorer outcome include poorer
neurological grade; systolic hypertension; a previous diagnosis of heart attack or SAH; liver disease; more blood and larger
aneurysm on the initial CT scan; location of an aneurysm in the posterior circulation; and higher age.[37] Factors that carry a
worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of
intracerebral hematoma or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the
eighth day of admission.[37]
So-called "angiogram-negative subarachnoid hemorrhage", SAH that does not show an aneurysm with four-vessel angiography, carries
a better prognosis than SAH with aneurysm; however, it is still associated with a risk of ischemia, rebleeding and hydrocephalus.
[14] Perimesencephalic SAH (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or
delayed ischemia, and the prognosis of this subtype is excellent. [40]
The prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. [15] It is
difficult to isolate the effects of SAH from those of other aspects of traumatic brain injury; it is unknown whether the presence of
subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. [15] People
with moderate and severe traumatic brain injury who have SAH when admitted to a hospital have as much as twice the risk of dying as
those who do not.[15] They also have a higher risk of severe disability and persistent vegetative state, and traumatic SAH has
been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the
intensive care unit.[15] However, more than 90% of people with traumatic subarachnoid bleeding and a Glasgow Coma Score over 12
have a good outcome.[15]
There is also modest evidence that genetic factors influence the prognosis in SAH. For example, having two copies of ApoE4 (a variant
of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seems to increase risk for delayed ischemia
and a worse outcome.[41] The occurrence of hyperglycemia (high blood sugars) after an episode of SAH confers a higher risk of
poor outcome.[42]

[edit] Long-term outcomes

Neurocognitive symptoms, such as fatigue, mood disturbances, and other related symptoms are common sequelae. Even in those
who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder and cognitive impairment are
common; 46% of people who have suffered a subarachnoid hemorrhage have cognitive impairment that affects their quality of life. [3]
Over 60% report frequent headaches.[43] Aneurysmal subarachnoid hemorrhage may lead to damage of the hypothalamus and the
pituitary gland, two areas of the brain that play a central role in hormonal regulation and production. More than a quarter of people
with a previous SAH may develop hypopituitarism (deficiencies in one or more of the hypothalamic-pituitary hormones such as
growth hormone, luteinizing hormone or follicle-stimulating hormone).[44]
Average number of people with SAH per 100,000 person-years, broken down by age.[45]
According to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000
annually. Studies from Japan and Finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not
entirely understood. South and Central America, in contrast, have a rate of 4.2 per 100,000 on average.[45]
Although the group of people at risk for SAH is younger than the population usually affected by stroke,[2] the risk still increases with
age. Young people are much much less likely than middle-aged people (risk ratio 0.1, or 10%) to suffer a subarachnoid hemorrhage.
[45] The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.[45] Risk of
SAH is about 25% higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from
the menopause, such as a decrease in estrogen levels.[45]
Genetics may play a role in a person's disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people who
have suffered a subarachnoid hemorrhage.[4] However, lifestyle factors are more important in determining overall risk.[2] These risk
factors are smoking, hypertension (high blood pressure) and excessive alcohol intake.[12] Having smoked in the past confers a
doubled risk of SAH compared to those who have never smoked.[2] Some protection of uncertain significance is conferred by
Caucasian ethnicity, hormone replacement therapy, diabetes mellitus and higher than normal levels of cholesterol.[2]
Approximately 4% of aneurysmal bleeds occur after sexual intercourse and 10% of people with SAH are bending over or lifting
heavy objects at the onset of their symptoms.[5]
Overall, about 1% of all people have one or more cerebral aneurysms. Most of these, however, are small and unlikely to rupture. [46]

[ edit] Screening and prevention

Screening for aneurysms is not performed on a population level; because they are relatively rare, it would not be cost-effective. If
someone has two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage, screening may be
Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with
cerebral aneurysms in 8% of cases, but most such aneurysms are small and therefore unlikely to rupture. As a result, screening is only
recommended in families with ADPKD where one family member has suffered a ruptured aneurysm.[48]
An aneurysm may be detected incidentally on brain imaging; this presents a conundrum, as all treatments for cerebral aneurysms are
associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic
data both in people who had previously suffered a subarachnoid hemorrhage and people who had aneurysms detected by other means.
Those who had previously suffered SAH were more likely to bleed from other aneurysms. In contrast, those who had never bled and
had small aneurysms (smaller than 10 mm) were very unlikely to suffer SAH and were likely to sustain harm from attempts to repair
these aneurysms.[46] On the basis of the ISUIA and other studies, it is now recommended that people are only considered for
preventative treatment if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture.[47]

[ edit] History
While the clinical picture of subarachnoid hemorrhage may have been recognized by Hippocrates, the existence of cerebral
aneurysms and the fact that they could rupture was not established until the 18th century.[49] The associated symptoms were
described in more detail in 1886 by Edinburgh physician Dr Byrom Bramwell.[50] In 1924, London neurologist Sir Dr Charles
P. Symonds (1890–1978) gave a complete account of all major symptoms of subarachnoid hemorrhage, and he coined the term
"spontaneous subarachnoid hemorrhage".[49][51][52] Symonds also described the use of lumbar puncture and xanthochromia in
The first surgical intervention was performed by Mr Norman Dott, who was a pupil of Dr Harvey Cushing then working in
Edinburgh. He introduced the wrapping of aneurysms in the 1930s, and was an early pioneer in the use of angiograms.[52] American
neurosurgeon Dr Walter Dandy, working in Baltimore, was the first to introduce clips in 1938.[22] Microsurgery was
applied to aneurysm treatment in 1972 in order to further improve outcomes. [54] The 1980s saw the introduction of triple H
therapy[32] as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine [30][55] in an attempt to prevent this
complication. In 1983, the Russian neurosurgeon Zubkov and colleagues reported the first use of transluminal balloon angioplasty for
vasospasm after aneurysmal SAH.[56][57] The Italian neurosurgeon Dr Guido Guiglielmi introduced his endovascular coil treatment
in 1991.[23][58]

A stroke (sometimes called a cerebrovascular accident (CVA)) is the rapidly developing loss of brain function(s) due to
disturbance in the blood supply to the brain, caused by a blocked or burst blood vessel. This can be due to ischemia (lack of
blood flow) caused by thrombosis or arterial embolism or due to a hemorrhage.[1] As a result, the affected area of the brain is
unable to function, leading to inability to move one or more limbs on one side of the body, inability to understand or formulate
speech, or inability to see one side of the visual field.[2]
A stroke is a medical emergency and can cause permanent neurological damage, complications, and death. It is the leading cause
of adult disability in the United States and Europe. It is the number two cause of death worldwide and may soon become the leading
cause of death worldwide.[3] Risk factors for stroke include advanced age, hypertension (high blood pressure), previous stroke
or transient ischemic attack (TIA), diabetes, high cholesterol, cigarette smoking and atrial fibrillation.[4] High blood
pressure is the most important modifiable risk factor of stroke.[2]
A stroke is occasionally treated with thrombolysis ("clot buster"), but usually with supportive care (speech and language
therapy, physiotherapy and occupational therapy) in a "stroke unit" and secondary prevention with antiplatelet drugs
(aspirin and often dipyridamole), blood pressure control, statins, and in selected patients with carotid endarterectomy and

The traditional definition of stroke, devised by the World Health Organization in the 1970s,[5] is a "neurological deficit of
cerebrovascular cause that persists beyond 24 hours or is interrupted by death within 24 hours". This definition was supposed to reflect
the reversibility of tissue damage and was devised for the purpose, with the time frame of 24 hours being chosen arbitrarily. The 24-
hour limit divides stroke from transient ischemic attack, which is a related syndrome of stroke symptoms that resolve completely
within 24 hours.[2] With the availability of treatments that, when given early, can reduce stroke severity, many now prefer alternative
concepts, such as brain attack and acute ischemic cerebrovascular syndrome (modeled after heart attack and acute coronary
syndrome respectively), that reflect the urgency of stroke symptoms and the need to act swiftly. [6]
A slice of brain from the autopsy of a person who suffered an acute middle cerebral artery (MCA) stroke
Strokes can be classified into two major categories: ischemic and hemorrhagic.[7] Ischemic strokes are those that are due to
interruption of the blood supply, while hemorrhagic strokes are the ones which are due to rupture of a blood vessel or an abnormal
vascular structure. 87% of strokes are due to ischemia; the remainder are due to hemorrhage. Some hemorrhages develop inside areas
of ischemia ("hemorrhagic transformation"). It is unknown how many hemorrhages actually start off as ischemic stroke. [2]

[edit] Ischemic stroke

Main articles: Cerebral infarction and Brain ischemia

In an ischemic stroke, blood supply to part of the brain is decreased, leading to dysfunction of the brain tissue in that area. There are
four reasons why this might happen:
1. Thrombosis (obstruction of a blood vessel by a blood clot forming locally)
2. Embolism (obstruction due to an embolus from elsewhere in the body, see below),[2]
3. Systemic hypoperfusion (general decrease in blood supply, e.g. in shock)[8]
4. Venous thrombosis.[9]
Stroke without an obvious explanation is termed "cryptogenic" (of unknown origin); this constitutes 30-40% of all ischemic strokes.
There are various classification systems for acute ischemic stroke. The Oxford Community Stroke Project classification (OCSP, also
known as the Bamford or Oxford classification) relies primarily on the initial symptoms; based on the extent of the symptoms, the
stroke episode is classified as total anterior circulation infarct (TACI), partial anterior circulation infarct (PACI), lacunar
infarct (LACI) or posterior circulation infarct (POCI). These four entities predict the extent of the stroke, the area of the brain
affected, the underlying cause, and the prognosis.[11][12] The TOAST (Trial of Org 10172 in Acute Stroke Treatment)
classification is based on clinical symptoms as well as results of further investigations; on this basis, a stroke is classified as being due
to (1) thrombosis or embolism due to atherosclerosis of a large artery, (2) embolism of cardiac origin, (3) occlusion of a small
blood vessel, (4) other determined cause, (5) undetermined cause (two possible causes, no cause identified, or incomplete

[edit] Hemorrhagic stroke

Main articles: Intracranial hemorrhage and intracerebral hemorrhage

CT scan showing an intracerebral hemorrhage with associated intraventricular hemorrhage.
Intracranial hemorrhage is the accumulation of blood anywhere within the skull vault. A distinction is made between intra-axial
hemorrhage (blood inside the brain) and extra-axial hemorrhage (blood inside the skull but outside the brain). Intra-axial
hemorrhage is due to intraparenchymal hemorrhage or intraventricular hemorrhage (blood in the ventricular system). The
main types of extra-axial hemorrhage are epidural hematoma (bleeding between the dura mater and the skull), subdural
hematoma (in the subdural space) and subarachnoid hemorrhage (between the arachnoid mater and pia mater). Most of
the hemorrhagic stroke syndromes have specific symptoms (e.g. headache, previous head injury).

[ edit] Signs and symptoms

Stroke symptoms typically start suddenly, over seconds to minutes, and in most cases do not progress further. The symptoms depend on
the area of the brain affected. The more extensive the area of brain affected, the more functions that are likely to be lost. Some forms of
stroke can cause additional symptoms: in intracranial hemorrhage, the affected area may compress other structures. Most forms of
stroke are not associated with headache, apart from subarachnoid hemorrhage and cerebral venous thrombosis and occasionally
intracerebral hemorrhage.

[edit] Early recognition

Various systems have been proposed to increase recognition of stroke by patients, relatives and emergency first responders. A
systematic review, updating a previous systematic review from 1994, looked at a number of trials to evaluate how well different
physical examination findings are able to predict the presence or absence of stroke. It was found that sudden-onset face weakness,
arm drift (e.g. if a person, when asked to raise both arms, involuntarily lets one arm drift downward) and abnormal speech are the
findings most likely to lead to the correct identification of a case of stroke (+ likelihood ratio of 5.5 when at least one of these is
present). Similarly, when all three of these are absent, the likelihood of stroke is significantly decreased (– likelihood ratio of 0.39).
[14] While these findings are not perfect for diagnosing stroke, the fact that they can be evaluated relatively rapidly and easily make
them very valuable in the acute setting.
Proposed systems include FAST (face, arm, speech, and time),[15] as advocated by the Department of Health (United
Kingdom) and The Stroke Association, the Los Angeles Prehospital Stroke Screen (LAPSS)[16] and the Cincinnati
Prehospital Stroke Scale (CPSS).[17] Use of these scales is recommended by professional guidelines.[18]
For people referred to the emergency room, early recognition of stroke is deemed important as this can expedite diagnostic tests and
treatments. A scoring system called ROSIER (recognition of stroke in the emergency room) is recommended for this purpose; it is
based on features from the medical history and physical examination.[18][19]

[edit] Subtypes

If the area of the brain affected contains one of the three prominent Central nervous system pathways—the spinothalamic
tract, corticospinal tract, and dorsal column (medial lemniscus), symptoms may include:
• hemiplegia and muscle weakness of the face
• numbness
• reduction in sensory or vibratory sensation

In most cases, the symptoms affect only one side of the body (unilateral). The defect in the brain is usually on the opposite side of the
body (depending on which part of the brain is affected). However, the presence of any one of these symptoms does not necessarily
suggest a stroke, since these pathways also travel in the spinal cord and any lesion there can also produce these symptoms.
In addition to the above CNS pathways, the brainstem also consists of the 12 cranial nerves. A stroke affecting the brain stem
therefore can produce symptoms relating to deficits in these cranial nerves:
• altered smell, taste, hearing, or vision (total or partial)
• drooping of eyelid (ptosis) and weakness of ocular muscles
• decreased reflexes: gag, swallow, pupil reactivity to light
• decreased sensation and muscle weakness of the face
• balance problems and nystagmus
• altered breathing and heart rate
• weakness in sternocleidomastoid muscle with inability to turn head to one side
• weakness in tongue (inability to protrude and/or move from side to side)
If the cerebral cortex is involved, the CNS pathways can again be affected, but also can produce the following symptoms:
• aphasia (inability to speak or understand language from involvement of Broca's or Wernicke's area)
• apraxia (altered voluntary movements)
• visual field defect
• memory deficits (involvement of temporal lobe)
• hemineglect (involvement of parietal lobe)
• disorganized thinking, confusion, hypersexual gestures (with involvement of frontal lobe)
• anosognosia (persistent denial of the existence of a, usually stroke-related, deficit)
If the cerebellum is involved, the patient may have the following:
• trouble walking
• altered movement coordination
• vertigo and or disequilibrium

[edit] Associated symptoms

Loss of consciousness, headache, and vomiting usually occurs more often in hemorrhagic stroke than in thrombosis because of the
increased intracranial pressure from the leaking blood compressing on the brain.
If symptoms are maximal at onset, the cause is more likely to be a subarachnoid hemorrhage or an embolic stroke.

[ edit] Causes
This section needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged and
removed. (September 2008)
Thrombotic stroke

In thrombotic stroke a thrombus (blood clot) usually forms around atherosclerotic plaques. Since blockage of the artery is gradual,
onset of symptomatic thrombotic strokes is slower. A thrombus itself (even if non-occluding) can lead to an embolic stroke (see below)
if the thrombus breaks off, at which point it is called an "embolus." Two types of thrombosis can cause stroke:
• Large vessel disease involves the common and internal carotids, vertebral, and the Circle of Willis. Diseases that may
form thrombi in the large vessels include (in descending incidence): atherosclerosis, vasoconstriction (tightening of the
artery), aortic, carotid or vertebral artery dissection, various inflammatory diseases of the blood vessel wall
(Takayasu arteritis, giant cell arteritis, vasculitis), noninflammatory vasculopathy, Moyamoya disease and
fibromuscular dysplasia.
• Small vessel disease involves the smaller arteries inside the brain: branches of the circle of Willis, middle cerebral artery,
stem, and arteries arising from the distal vertebral and basilar artery. Diseases that may form thrombi in the small vessels
include (in descending incidence): lipohyalinosis (build-up of fatty hyaline matter in the blood vessel as a result of high
blood pressure and aging) and fibrinoid degeneration (stroke involving these vessels are known as lacunar infarcts) and
microatheroma (small atherosclerotic plaques).
Sickle cell anemia, which can cause blood cells to clump up and block blood vessels, can also lead to stroke. A stroke is the
second leading killer of people under 20 who suffer from sickle-cell anemia. [20]
Embolic stroke

An embolic stroke refers to the blockage of an artery by an arterial embolus, a travelling particle or debris in the arterial
bloodstream originating from elsewhere. An embolus is most frequently a thrombus, but it can also be a number of other substances
including fat (e.g. from bone marrow in a broken bone), air, cancer cells or clumps of bacteria (usually from infectious
Because an embolus arises from elsewhere, local therapy only solves the problem temporarily. Thus, the source of the embolus must be
identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient
as the embolus is partially resorbed and moves to a different location or dissipates altogether.
Emboli most commonly arise from the heart (especially in atrial fibrillation) but may originate from elsewhere in the arterial tree.
In paradoxical embolism, a deep vein thrombosis embolises through an atrial or ventricular septal defect in the heart into
the brain.
Cardiac causes can be distinguished between high and low-risk:[21]
• High risk: atrial fibrillation and paroxysmal atrial fibrillation, rheumatic disease of the mitral or aortic valve
disease, artificial heart valves, known cardiac thrombus of the atrium or vertricle, sick sinus syndrome, sustained
atrial flutter, recent myocardial infarction, chronic myocardial infarction together with ejection fraction <28 percent,
symptomatic congestive heart failure with ejection fraction <30 percent, dilated cardiomyopathy, Libman-Sacks
endocarditis, Marantic endocarditis, infective endocarditis, papillary fibroelastoma, left atrial myxoma and
coronary artery bypass graft (CABG) surgery
• Low risk/potential: calcification of the annulus (ring) of the mitral valve, patent foramen ovale (PFO), atrial septal aneurysm,
atrial septal aneurysm with patent foramen ovale, left ventricular aneurysm without thrombus, isolated left atrial "smoke" on
echocardiography (no mitral stenosis or atrial fibrillation), complex atheroma in the ascending aorta or proximal arch
Systemic hypoperfusion

Systemic hypoperfusion is the reduction of blood flow to all parts of the body. It is most commonly due to cardiac pump failure from
cardiac arrest or arrhythmias, or from reduced cardiac output as a result of myocardial infarction, pulmonary embolism,
pericardial effusion, or bleeding. Hypoxemia (low blood oxygen content) may precipitate the hypoperfusion. Because the
reduction in blood flow is global, all parts of the brain may be affected, especially "watershed" areas - border zone regions supplied by
the major cerebral arteries. A watershed stroke refers to the condition when blood supply to these areas is compromised. Blood flow
to these areas does not necessarily stop, but instead it may lessen to the point where brain damage can occur. This phenomenon is also
referred to as "last meadow" to point to the fact that in irrigation the last meadow receives the least amount of water.
Venous thrombosis

Cerebral venous sinus thrombosis leads to stroke due to locally increased venous pressure, which exceeds the pressure generated
by the arteries. Infarcts are more likely to undergo hemorrhagic transformation (leaking of blood into the damaged area) than other
types of ischemic stroke.[9]
Intracerebral hemorrhage

It generally occurs in small arteries or arterioles and is commonly due to hypertension, intracranial vascular malformations (including
cavernous angiomas or arteriovenous malformations), cerebral amyloid angiopathy, or infarcts into which secondary
haemorrhage has occurred.[2] Other potential causes are trauma, bleeding disorders, amyloid angiopathy, illicit drug use
(e.g. amphetamines or cocaine). The hematoma enlarges until pressure from surrounding tissue limits its growth, or until it
decompresses by emptying into the ventricular system, CSF or the pial surface. A third of intracerebral bleed is into the brain's
ventricles. ICH has a mortality rate of 44 percent after 30 days, higher than ischemic stroke or even the very deadly subarachnoid
hemorrhage (which, however, also may be classified as a type of stroke[2]).

[ edit] Pathophysiology
[edit] Ischemic

This section needs additional citations for verification.

Please help improve this article by adding reliable references. Unsourced material may be challenged and
removed. (September 2008)
Ischemic stroke occurs due to a loss of blood supply to part of the brain, initiating the ischemic cascade.[22] Brain tissue ceases to
function if deprived of oxygen for more than 60 to 90 seconds and after approximately three hours, will suffer irreversible injury
possibly leading to death of the tissue, i.e., infarction. (This is why TPA's (e.g. Streptokinase, Altapase) are given only until three
hours since the onset of the stroke.) Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessels leading to a
reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of small emboli through
the disintegration of atherosclerotic plaques. Embolic infarction occurs when emboli formed elsewhere in the circulatory system,
typically in the heart as a consequence of atrial fibrillation, or in the carotid arteries, break off, enter the cerebral circulation, then lodge
in and occlude brain blood vessels. Since blood vessels in the brain are now occluded, the brain becomes low in energy, and thus it
resorts into using anaerobic respiration within the region of brain tissue affected by ischemia. Unfortunately, this kind of
respiration produces less ATP but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy
cells since it is an acid and disrupts the normal acid-bace balance in the brain. The ischemia area is referred to as the "ischemic
Then, as oxygen or glucose becomes depleted in ischemic brain tissue, the production of high energy phosphate compounds such
as adenosine triphosphate (ATP) fails, leading to failure of energy-dependent processes (such as ion pumping) necessary for tissue cell
survival. This sets off a series of interrelated events that result in cellular injury and death. A major cause of neuronal injury is release
of the excitatory neurotransmitter glutamate. The concentration of glutamate outside the cells of the nervous system is normally kept
low by so-called uptake carriers, which are powered by the concentration gradients of ions (mainly Na+) across the cell membrane.
However, stroke cuts off the supply of oxygen and glucose which powers the ion pumps maintaining these gradients. As a result the
transmembrane ion gradients run down, and glutamate transporters reverse their direction, releasing glutamate into the extracellular
space. Glutamate acts on receptors in nerve cells (especially NMDA receptors), producing an influx of calcium which activates
enzymes that digest the cells' proteins, lipids and nuclear material. Calcium influx can also lead to the failure of mitochondria, which
can lead further toward energy depletion and may trigger cell death due to apoptosis.
Ischemia also induces production of oxygen free radicals and other reactive oxygen species. These react with and damage a
number of cellular and extracellular elements. Damage to the blood vessel lining or endothelium is particularly important. In fact,
many antioxidant neuroprotectants such as uric acid and NXY-059 work at the level of the endothelium and not in the brain per se.
Free radicals also directly initiate elements of the apoptosis cascade by means of redox signaling.[20]
These processes are the same for any type of ischemic tissue and are referred to collectively as the ischemic cascade. However, brain
tissue is especially vulnerable to ischemia since it has little respiratory reserve and is completely dependent on aerobic metabolism,
unlike most other organs.
Brain tissue survival can be improved to some extent if one or more of these processes is inhibited. Drugs that scavenge reactive
oxygen species, inhibit apoptosis, or inhibit excitotoxic neurotransmitters, for example, have been shown experimentally to reduce
tissue injury due to ischemia. Agents that work in this way are referred to as being neuroprotective. Until recently, human clinical
trials with neuroprotective agents have failed, with the probable exception of deep barbiturate coma. However, more recently
NXY-059, the disulfonyl derivative of the radical-scavenging spintrap phenylbutylnitrone, is reported to be neuroprotective in stroke.
[24] This agent appears to work at the level of the blood vessel lining or endothelium. Unfortunately, after producing favorable results
in one large-scale clinical trial, a second trial failed to show favorable results. [20]
In addition to injurious effects on brain cells, ischemia and infarction can result in loss of structural integrity of brain tissue and blood
vessels, partly through the release of matrix metalloproteases, which are zinc- and calcium-dependent enzymes that break down
collagen, hyaluronic acid, and other elements of connective tissue. Other proteases also contribute to this process. The loss of
vascular structural integrity results in a breakdown of the protective blood brain barrier that contributes to cerebral edema, which
can cause secondary progression of the brain injury.
As is the case with any type of brain injury, the immune system is activated by cerebral infarction and may under some
circumstances exacerbate the injury caused by the infarction. Inhibition of the inflammatory response has been shown
experimentally to reduce tissue injury due to cerebral infarction, but this has not proved out in clinical studies.

Head CT showing deep intracerebral hemorrhage due to bleeding within the cerebellum, approximately 30 hours old.
Hemorrhagic strokes result in tissue injury by causing compression of tissue from an expanding hematoma or hematomas. This can
distort and injure tissue. In addition, the pressure may lead to a loss of blood supply to affected tissue with resulting infarction, and the
blood released by brain hemorrhage appears to have direct toxic effects on brain tissue and vasculature.[20]

[ edit] Diagnosis
Stroke is diagnosed through several techniques: a neurological examination (such as the Nihss), CT scans (most often without contrast
enhancements) or MRI scans, Doppler ultrasound, and arteriography. The diagnosis of stroke itself is clinical, with assistance
from the imaging techniques. Imaging techniques also assist in determining the subtypes and cause of stroke. There is yet no
commonly used blood test for the stroke diagnosis itself, though blood tests may be of help in finding out the likely cause of stroke.

[edit] Imaging

For diagnosing ischemic stroke in the emergency setting:[26]

• CT scans (without contrast enhancements)

sensitivity= 16%
specificity= 96%

• MRI scan
sensitivity= 83%
specificity= 98%

For diagnosing hemorrhagic stroke in the emergency setting:

• CT scans (without contrast enhancements)
sensitivity= 89%
specificity= 100%

• MRI scan
sensitivity= 81%
specificity= 100%

For detecting chronic hemorrhages, MRI scan is more sensitive.[27]

For the assessment of stable stroke, nuclear medicine scans SPECT and PET/CT may be helpful. SPECT documents cerebral blood
flow and PET with FDG isotope the metabolic activity of the neurons.

[edit] Underlying etiology

When a stroke has been diagnosed, various other studies may be performed to determine the underlying etiology. With the current
treatment and diagnosis options available, it is of particular importance to determine whether there is a peripheral source of emboli.
Test selection may vary, since the cause of stroke varies with age, comorbidity and the clinical presentation. Commonly used
techniques include:
• an ultrasound/doppler study of the carotid arteries (to detect carotid stenosis) or dissection of the precerebral
• an electrocardiogram (ECG) and echocardiogram (to identify arrhythmias and resultant clots in the heart which may
spread to the brain vessels through the bloodstream)
• a Holter monitor study to identify intermittent arrhythmias
• an angiogram of the cerebral vasculature (if a bleed is thought to have originated from an aneurysm or arteriovenous
• blood tests to determine hypercholesterolemia, bleeding diathesis and some rarer causes such as homocysteinuria

[ edit] Prevention
Given the disease burden of stroke, prevention is an important public health concern.[28] Primary prevention is less effective
than secondary prevention (as judged by the number needed to treat to prevent one stroke per year).[28] Recent guidelines detail
the evidence for primary prevention in stroke.[29] Because stroke may indicate underlying atherosclerosis, it is important to determine
the patient's risk for other cardiovascular diseases such as coronary heart disease. Conversely, aspirin prevents against first stroke
in patients who have suffered a myocardial infarction or patients with a high cardiovascular risk. [30][31]
[edit] Risk factors
The most important modifiable risk factors for stroke are high blood pressure and atrial fibrillation (although magnitude of this effect is
small: the evidence from the Medical Research Council trials is that 833 patients have to be treated for 1 year to prevent one
stroke[32][33]). Other modifiable risk factors include high blood cholesterol levels, diabetes, cigarette smoking [34][35] (active and
passive), heavy alcohol consumption[36] and drug use,[37] lack of physical activity, obesity and unhealthy diet.[38]
Alcohol use could predispose to ischemic stroke, and intracerebral and subarachnoid hemorrhage via multiple mechanisms (for
example via hypertension, atrial fibrillation, rebound thrombocytosis and platelet aggregation and clotting disturbances).[39]
The drugs most commonly associated with stroke are cocaine, amphetamines causing hemorrhagic stroke, but also over-the-
counter cough and cold drugs containing sympathomimetics.[40][41]
No high quality studies have shown the effectiveness of interventions aimed at weight reduction, promotion of regular exercise,
reducing alcohol consumption or smoking cessation.[42] Nonetheless, given the large body of circumstantial evidence, best
medical management for stroke includes advice on diet, exercise, smoking and alcohol use.[43] Medication or drug therapy is the
most common method of stroke prevention; carotid endarterectomy can be a useful surgical method of preventing stroke.

[edit] Blood pressure

Hypertension accounts for 35-50% of stroke risk.[44] Epidemiological studies suggest that even a small blood pressure
reduction (5 to 6 mmHg systolic, 2 to 3 mmHg diastolic) would result in 40% fewer strokes.[45] Lowering blood pressure has been
conclusively shown to prevent both ischemic and hemorrhagic strokes.[46][47] It is equally important in secondary prevention.[48]
Even patients older than 80 years and those with isolated systolic hypertension benefit from antihypertensive therapy.[49][50]
[51] Studies show that intensive antihypertensive therapy results in a greater risk reduction.[52] The available evidence does not
show large differences in stroke prevention between antihypertensive drugs —therefore, other factors such as protection against other
forms of cardiovascular disease should be considered and cost.[52][53]

[edit] Atrial fibrillation

Patients with atrial fibrillation have a risk of 5% each year to develop stroke, and this risk is even higher in those with valvular atrial
fibrillation.[54] Depending on the stroke risk, anticoagulation with medications such as coumarins or aspirin is warranted for stroke

[edit] Blood lipids

High cholesterol levels have been inconsistently associated with (ischemic) stroke. [47][56] Statins have been shown to reduce the
risk of stroke by about 15%.[57] Since earlier meta-analyses of other lipid-lowering drugs did not show a decreased risk,[58]
statins might exert their effect through mechanisms other than their lipid-lowering effects. [57]

[edit] Diabetes mellitus

Patients with diabetes mellitus are 2 to 3 times more likely to develop stroke, and they commonly have hypertension and
hyperlipidemia. Intensive disease control has been shown to reduce microvascular complications such as nephropathy and
retinopathy but not macrovascular complications such as stroke.[59][60]

[edit] Anticoagulation drugs

Oral anticoagulants such as warfarin have been the mainstay of stroke prevention for over 50 years. However, several studies have
shown that aspirin and antiplatelet drugs are highly effective in secondary prevention after a stroke or transient ischemic
attack[30]. Low doses of aspirin (for example 75–150 mg) are as effective as high doses but have fewer side-effects; the lowest
effective dose remains unknown.[61] Thienopyridines (clopidogrel, ticlopidine) are modestly more effective than aspirin and
have a decreased risk of gastrointestinal bleeding, but they are more expensive.[62] Their exact role remains controversial.
Ticlopidine has more skin rash, diarrhea, neutropenia and thrombotic thrombocytopenic purpura.[62] Dipyridamole
can be added to aspirin therapy to provide a small additional benefit, even though headache is a common side-effect. [63] Low-dose
aspirin is also effective for stroke prevention after sustaining a myocardial infarction. [31] > Oral anticoagulants are not advised for
stroke prevention —any benefit is offset by bleeding risk.[64]
In primary prevention however, antiplatelet drugs did not reduce the risk of ischemic stroke while increasing the risk of major bleeding.
[65][66] Further studies are needed to investigate a possible protective effect of aspirin against ischemic stroke in women. [67][68]

[edit] Surgery
Surgical procedures such as carotid endarterectomy or carotid angioplasty can be used to remove significant atherosclerotic
narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this
procedure in selected cases.[43] Endarterectomy for a significant stenosis has been shown to be useful in the secondary prevention
after a previous symptomatic stroke.[69] Carotid artery stenting has not been shown to be equally useful.[70][71] Patients are
selected for surgery based on age, gender, degree of stenosis, time since symptoms and patients' preferences. [43] Surgery is most
efficient when not delayed too long —the risk of recurrent stroke in a patient who has a 50% or greater stenosis is up to 20% after 5
years, but endarterectomy reduces this risk to around 5%. The number of procedures needed to cure one patient was 5 for early surgery
(within two weeks after the initial stroke), but 125 if delayed longer than 12 weeks.[72][73]
Screening for carotid artery narrowing has not been shown to be a useful screening test in the general population.[74] Studies of
surgical intervention for carotid artery stenosis without symptoms have shown only a small decrease in the risk of stroke. [75][76] To
be beneficial, the complication rate of the surgery should be kept below 4%. Even then, for 100 surgeries, 5 patients will benefit by
avoiding stroke, 3 will develop stroke despite surgery, 3 will develop stroke or die due to the surgery itself, and 89 will remain stroke-
free but would also have done so without intervention.[43]

[edit] Nutritional and metabolic interventions

Nutrition, specifically the Mediterranean-style diet, has the potential of more than halving stroke risk. [77]
With regards to lowering homocysteine, a meta-analysis of previous trials has concluded that lowering homocysteine with folic
acid and other supplements may reduce stroke risk.[78] However, the two largest randomized controlled trials included in the
meta-analysis had conflicting results. One reported positve results;[79] whereas the other was negative.[80]
The European Society of Cardiology and the European Association for Cardiovascular Prevention and Rehabilitation have developed
an interactive tool for prediction and managing the risk of heart attack and stroke in Europe. HeartScore is aimed at supporting
clinicians in optimising individual cardiovascular risk reduction. The Heartscore Programme is available in 12 languages and offers
web based or PC version [81].

[ edit] Treatment
[edit] Stroke unit
Ideally, people who have had a stroke are admitted to a "stroke unit", a ward or dedicated area in hospital staffed by nurses and
therapists with experience in stroke treatment. It has been shown that people admitted to a stroke unit have a higher chance of
surviving than those admitted elsewhere in hospital, even if they are being cared for by doctors without experience in stroke. [2]
When an acute stroke is suspected by history and physical examination, the goal of early assessment is to determine the cause.
Treatment varies according to the underlying cause of the stroke, thromboembolic (ischemic) or hemorrhagic. A non-contrast head CT
scan can rapidly identify a hemorrhagic stroke by imaging bleeding in or around the brain. If no bleeding is seen, a presumptive
diagnosis of ischemic stroke is made.

[edit] Treatment of ischemic stroke

Ischemic stroke is caused by a thrombus (blood clot) occluding blood flow to an artery supplying the brain. Definitive therapy is
aimed at removing the blockage by breaking the clot down (thrombolysis), or by removing it mechanically (thrombectomy). The
more rapidly blood flow is restored to the brain, the fewer brain cells die.[82]
Other medical therapies are aimed at minimizing clot enlargement or preventing new clots from forming. To this end, treatment with
medications such as aspirin, clopidogrel and dipyridamole may be given to prevent platelets from aggregating[30].
In addition to definitive therapies, management of acute stroke includes control of blood sugars, ensuring the patient has adequate
oxygenation and adequate intravenous fluids. Patients may be positioned with their heads flat on the stretcher, rather than sitting up, to
increase blood flow to the brain. It is common for the blood pressure to be elevated immediately following a stroke. Although high
blood pressure may cause some strokes, hypertension during acute stroke is desirable to allow adequate blood flow to the brain.

[edit] Thrombolysis
In increasing numbers of primary stroke centers, pharmacologic thrombolysis ("clot busting") with the drug tissue plasminogen
activator (tPA), is used to dissolve the clot and unblock the artery. However, the use of tPA in acute stroke is controversial. On one
hand, it is endorsed by the American Heart Association and the American Academy of Neurology as the recommended treatment
for acute stroke within three hours of onset of symptoms as long as there are not other contraindications (such as abnormal lab values,
high blood pressure, or recent surgery). This position for tPA is based upon the findings of two studies by one group of
investigators[83] which showed that tPA improves the chances for a good neurological outcome. When administered within the first
three hours, 39% of all patients who were treated with tPA had a good outcome at three months, only 26% of placebo controlled
patients had a good functional outcome. A recent study using alteplase for thrombolysis in ischemic stroke suggests clinical benefit
with administration 3 to 4.5 hours after stroke onset.[84] However, in the NINDS trial 6.4% of patients with large strokes developed
substantial brain hemorrhage as a complication from being given tPA. tPA is often misconstrued as a "magic bullet" and it is important
for patients to be aware that despite the study that supports its use, some of the data is flawed and the safety and efficacy of tPA is
controversial. A recent study found the mortality to be higher among patients receiving tPA versus those who did not. [85] Additionally,
it is the position of the American Academy of Emergency Medicine that objective evidence regarding the efficacy, safety, and
applicability of tPA for acute ischemic stroke is insufficient to warrant its classification as standard of care.[86].

Another intervention for acute ischemic stroke is removal of the offending thrombus directly. This is accomplished by inserting a
catheter into the femoral artery, directing it into the cerebral circulation, and deploying a corkscrew-like device to ensnare the
clot, which is then withdrawn from the body. Mechanical embolectomy devices have been demonstrated effective at restoring blood
flow in patients who were unable to receive thrombolytic drugs or for whom the drugs were ineffective,[87][88][89][90] though
no differences have been found between newer and older versions of the devices.[91] The devices have only been tested on patients
treated with mechanical clot embolectomy within eight hours of the onset of symptoms.

[edit] Angioplasty and stenting

Angioplasty and stenting have begun to be looked at as possible viable options in treatment of acute ischemic stroke. In a
systematic review of six uncontrolled, single-center trials, involving a total of 300 patients, of intra-cranial stenting in symptomatic
intracranial arterial stenosis, the rate of technical success (reduction to stenosis of <50%) ranged from 90-98%, and the rate of major
peri-procedural complications ranged from 4-10%. The rates of restenosis and/or stroke following the treatment were also favorable.
[92] This data suggests that a large, randomized controlled trial is needed to more completely evaluate the possible therapeutic
advantage of this treatment.

[edit] Therapeutic hypothermia

Main article: therapeutic hypothermia
Most of the data concerning therapeutic hypothermia’s effectiveness in treating ischemic stroke is limited to animal studies. These
studies have focused primarily on ischemic as opposed to hemorrhagic stroke, as hypothermia has been associated with a lower clotting
threshold. In these animal studies investigating the effect of temperature decline following ischemic stroke, hypothermia has been
shown to be an effective all-purpose neuroprotectant.[93] This promising data has led to the initiation of a variety of human studies. At
the time of this article’s publishing, this research has yet to return results. However, in terms of feasibility, the use of hypothermia to
control intracranial pressure (ICP) after an ischemic stroke was found to be both safe and practical. The device used in this study
was called the Arctic Sun.[94]

[edit] Secondary prevention of ischemic stroke

Anticoagulation can prevent recurrent stroke. Among patients with nonvalvular atrial fibrillation, anticoagulation can reduce stroke by
60% while antiplatelet agents can reduce stroke by 20%.[95]. However, a recent meta-analysis suggests harm from anti-coagulation
started early after an embolic stroke.[96] Stroke prevention treatment for atrial fibrillation is determined according to the
CHADS/CHADS2 system.
If studies show carotid stenosis, and the patient has residual function in the affected side, carotid endarterectomy (surgical removal of
the stenosis) may decrease the risk of recurrence if performed rapidly after stroke.

[edit] Treatment of hemorrhagic stroke

Patients with intracerebral hemorrhage require neurosurgical evaluation to detect and treat the cause of the bleeding, although
many may not need surgery. Anticoagulants and antithrombotics, key in treating ischemic stroke, can make bleeding worse and cannot
be used in intracerebral hemorrhage. Patients are monitored and their blood pressure, blood sugar, and oxygenation are kept at
optimum levels.

[edit] Care and rehabilitation

Stroke rehabilitation is the process by which patients with disabling strokes undergo treatment to help them return to normal life as
much as possible by regaining and relearning the skills of everyday living. It also aims to help the survivor understand and adapt to
difficulties, prevent secondary complications and educate family members to play a supporting role.
A rehabilitation team is usually multidisciplinary as it involves staff with different skills working together to help the patient. These
include nursing staff, physiotherapy, occupational therapy, speech and language therapy, and usually a physician trained in
rehabilitation medicine. Some teams may also include psychologists, social workers, and pharmacists since at least one
third of the patients manifest post stroke depression. Validated instruments such as the Barthel scale may be used to assess the
likelihood of a stroke patient being able to manage at home with or without support subsequent to discharge from hospital.
Good nursing care is fundamental in maintaining skin care, feeding, hydration, positioning, and monitoring vital signs such as
temperature, pulse, and blood pressure. Stroke rehabilitation begins almost immediately.
For most stroke patients, physical therapy (PT) and occupational therapy (OT) are the cornerstones of the rehabilitation process, but
in many countries Neurocognitive Rehabilitation is used, too. Often, assistive technology such as a wheelchair, walkers,
canes, and orthosis may be beneficial. PT and OT have overlapping areas of working but their main attention fields are; PT involves
re-learning functions as transferring, walking and other gross motor functions. OT focusses on exercises and training to help relearn
everyday activities known as the Activities of daily living (ADLs) such as eating, drinking, dressing, bathing, cooking, reading
and writing, and toileting. Speech and language therapy is appropriate for patients with problems understanding speech or written
words, problems forming speech and problems with swallowing.
Patients may have particular problems, such as complete or partial inability to swallow, which can cause swallowed material to pass
into the lungs and cause aspiration pneumonia. The condition may improve with time, but in the interim, a nasogastric tube may
be inserted, enabling liquid food to be given directly into the stomach. If swallowing is still unsafe after a week, then a percutaneous
endoscopic gastrostomy (PEG) tube is passed and this can remain indefinitely.
Stroke rehabilitation should be started as immediately as possible and can last anywhere from a few days to over a year. Most return of
function is seen in the first few days and weeks, and then improvement falls off with the "window" considered officially by U.S. state
rehabilitation units and others to be closed after six months, with little chance of further improvement. However, patients have been
known to continue to improve for years, regaining and strengthening abilities like writing, walking, running, and talking. Daily
rehabilitation exercises should continue to be part of the stroke patient's routine. Complete recovery is unusual but not impossible and
most patients will improve to some extent : a correct diet and exercise are known to help the brain to self-recover.

[ edit] Prognosis
This section needs additional citations for verification.
Please help improve this article by adding reliable references. Unsourced material may be challenged
and removed. (September 2008)
Disability affects 75% of stroke survivors enough to decrease their employability.[97] Stroke can affect patients physically, mentally,
emotionally, or a combination of the three. The results of stroke vary widely depending on size and location of the lesion. [98]
Dysfunctions correspond to areas in the brain that have been damaged.
Some of the physical disabilities that can result from stroke include paralysis, numbness, pressure sores, pneumonia,
incontinence, apraxia (inability to perform learned movements), difficulties carrying out daily activities, appetite loss, speech loss,
vision loss, and pain. If the stroke is severe enough, or in a certain location such as parts of the brainstem, coma or death can result.
Emotional problems resulting from stroke can result from direct damage to emotional centers in the brain or from frustration and
difficulty adapting to new limitations. Post-stroke emotional difficulties include anxiety, panic attacks, flat affect (failure to
express emotions), mania, apathy, and psychosis.
30 to 50% of stroke survivors suffer post stroke depression, which is characterized by lethargy, irritability, sleep disturbances,
lowered self esteem, and withdrawal.[99] Depression can reduce motivation and worsen outcome, but can be treated with
Emotional lability, another consequence of stroke, causes the patient to switch quickly between emotional highs and lows and to
express emotions inappropriately, for instance with an excess of laughing or crying with little or no provocation. While these
expressions of emotion usually correspond to the patient's actual emotions, a more severe form of emotional lability causes patients to
laugh and cry pathologically, without regard to context or emotion.[97] Some patients show the opposite of what they feel, for
example crying when they are happy.[100] Emotional lability occurs in about 20% of stroke patients.
Cognitive deficits resulting from stroke include perceptual disorders, speech problems, dementia, and problems with attention and
memory. A stroke sufferer may be unaware of his or her own disabilities, a condition called anosognosia. In a condition called
hemispatial neglect, a patient is unable to attend to anything on the side of space opposite to the damaged hemisphere.
Up to 10% of all stroke patients develop seizures, most commonly in the week subsequent to the event; the severity of the stroke
increases the likelihood of a seizure.[101][102]

[ edit] Epidemiology
Stroke could soon be the most common cause of death worldwide.[103] Stroke is currently the second leading cause of death in the
Western world, ranking after heart disease and before cancer,[2] and causes 10% of deaths worldwide.[104] Geographic disparities
in stroke incidence have been observed, including the existence of a "stroke belt" in the southeastern United States, but causes
of these disparities have not been explained.
The incidence of stroke increases exponentially from 30 years of age, and etiology varies by age.[105] Advanced age is one of
the most significant stroke risk factors. 95% of strokes occur in people age 45 and older, and two-thirds of strokes occur in those over
the age of 65.[99][20] A person's risk of dying if he or she does have a stroke also increases with age. However, stroke can occur at
any age, including in fetuses.
Family members may have a genetic tendency for stroke or share a lifestyle that contributes to stroke. Higher levels of Von
Willebrand factor are more common amongst people who have had ischemic stroke for the first time.[106] The results of this
study found that the only significant genetic factor was the person's blood type. Having had a stroke in the past greatly increases
one's risk of future strokes.
Men are 25% more likely to suffer strokes than women,[20] yet 60% of deaths from stroke occur in women.[100] Since women live
longer, they are older on average when they have their strokes and thus more often killed (NIMH 2002).[20] Some risk factors for
stroke apply only to women. Primary among these are pregnancy, childbirth, menopause and the treatment thereof (HRT).

Hippocrates first described the sudden paralysis that is often associated with stroke.
Hippocrates (460 to 370 BC) was first to describe the phenomenon of sudden paralysis that is often associated with ischemia.
Apoplexy, from the Greek word meaning "struck down with violence,” first appeared in Hippocratic writings to describe this
The word stroke was used as a synonym for apoplectic seizure as early as 1599,[109] and is a fairly literal translation of the Greek
In 1658, in his Apoplexia, Johann Jacob Wepfer (1620–1695) identified the cause of hemorrhagic stroke when he suggested that
people who had died of apoplexy had bleeding in their brains.[107][20] Wepfer also identified the main arteries supplying the
brain, the vertebral and carotid arteries, and identified the cause of ischemic stroke [also known as cerebral infarction] when
he suggested that apoplexy might be caused by a blockage to those vessels.[20]
Rudolf Virchow first described the mechanism of thromboembolism as a major factor.[110]

Cerebral Shunts
Cerebral shunts are commonly used to treat hydrocephalus, the swelling of the brain due to excess buildup of cerebrospinal
fluid (CSF). If left unchecked, the cerebral spinal fluid can build up leading to an increase in intracranial pressure (ICP) which
can lead to intracranial hematoma, cerebral edema, crushed brain tissue or herniation.[1] The cerebral shunt can be used to
alleviate or prevent these problems in patients who suffer from hydrocephalus or other related diseases. Shunts can come in a variety of
forms but all of them consist of a pump or drain connected to a long catheter, the end of which is usually placed in the stomach. The
main differences between shunts are usually in the materials used to construct them, the types of pumps used, and whether the pump is
programmable or not.[2]

[ edit] Types of Valves

Valve Type Description
Delta Designed to prevent overdrainage. Remains closed until ICP reaches a predetermined level. Leaves shunted
ventricle larger than the non-shunted ventricles. [3][4]
Medium Pressure
Can lead to uneven drainage of ventricles.[3]
Contains two ball-valve units connected with a spring. Does not have an adjustable pressure setting. First mass
Nulsen and Spitz
produced valve used to treat hydrocephalus in 1956.[5]
Prevents over drainage by preventing the siphon effect. The device closes when the pressure within the valve
Anti-Siphon becomes negative relative to the ambient pressure. Prevents overdrainage that might occur when a patient sits,
stands or rapidly changes posture.[6]
The Sigma valve operates on a flow-control mechanism as opposed to the pressure-control system of other valves.
Sigma The device can regulate CSF flow changes without being programmed or surgically changed. The first iteration
was introduced in 1987. Valve operated in three stages to prevent over and under drainage. [7]

[ edit] Shunt Location

The location of the shunt is determined by the neurosurgeon based on the type and location of the blockage causing hydrocephalus. All
brain ventricles are candidates for shunting. The catheter is most commonly placed in the abdomen but other locations include the heart
and lungs.[8] Shunts can often be named after the route used by the neurosurgeon. The distal end of the catheter can be located in just
about any tissue with enough epithelial cells to absorb the incoming CSF. Below are some common routing plans for cerebral shunts.

[edit] Shunt Routing

Route Location of Fluid Drain
Ventriculo-peritoneal shunt (VP shunt) Peritoneal Cavity
Ventriculo-atrial shunt (VA shunt) Right atrium of the heart
Ventriculo-pleural shunt (VPL shunt) Pleural Cavity
In addition to these three common locations for shunt drainage, the gallbladder and ureter can be suitable locations as well.

[ edit] Complications
There are a number of complications associated with shunt placement. Many of these complications occur during childhood and cease
once the patient has reached adulthood. Many of the complications seen in patients require immediate shunt revision(the replacement
or reprogramming of the already existing shunt). The common symptoms often resemble the new onset of hydrocephalus such as
headaches, nausea, vomiting, double-vision, and an alteration of consciousness. [8] Furthermore the shunt failure rate 2 years after
implantation has been estimated to be as high as 50%.[9]

[edit] Infection
Infection is a common complication that normally affects pediatric patients because they have not yet built up immunities to a number
of different diseases. Normally the incidence of infection decreases as the patient grow older, and the body gains immunity to various
infectious agents.[8] Shunt infection is a common problem and can occur in up to 27% of patients with a shunt. Infection can lead to
long term cognitive defects, neurological problems and in some cases death. Common microbial agents for shunt infection include
Staphylococcus epidermidis, Staphylococcus aureus, and Candida albicans. Further factors leading to shunt infection include shunt
insertion at a young age (<6 months old) and the type of hydrocephalus being treated. There is no strong correlation between infection
and shunt type.[10] The symptoms of a shunt infection are very similar to the symptoms seen in hydrocephalus but can also include
fever and elevated white blood cell counts.[11]

[edit] Obstruction
Another leading cause of shunt failure is the blockage of the shunt at either the proximal or distal end. At the proximal end the shunt
valve can become blocked due to the buildup of excess protein in the CSF. The extra protein will collect at the point of drainage and
slowly clog the valve. The shunt can also become blocked at the distal end if the shunt is pulled out of the abdominal cavity (in the case
of VP shunts), or from similar protein buildup. Other causes of blockage are overdrainage and slit ventricle syndrome. [8]

[edit] Over Drainage

Over drainage occurs when a shunt has not been adequately designed for the particular patient. Overdrainage can lead to a number of
different complications some of which are highlighted below. Usually one of two types of overdrainage can occur. First when the CSF
drains too rapidly, a condition known as extra-axial fluid collection can occur. In this condition the brain collapses on itself resulting in
the collection of CSF or blood around the brain. This can cause severe brain damage by compressing the brain. Furthermore a
subdural hematoma may develop. Extra-axial fluid collection can be treated in three different ways depending on the severity of the
condition. Usually the shunt will be replaced or reprogrammed to release less CSF and the fluid collected around the brain will be
drained. The second condition known as slit ventricle syndrome occurs when CSF slowly overdrains, over several years. More
information on slit ventricle syndrome appears below.[8][12]
[edit] Chiari I Malformation
Recent studies have shown that over drainage of CSF due to shunting can lead to acquired Chiari I Malformation.[13] It was
previously thought that Chiari I Malformation was a result of a congenital defect but new studies have shown that overdrainage of
Cysto-peritoneal shunts used to treat arachnoid cysts can lead to the development of posterior fossa overcrowding and tonsillar
herniation, the latter of which is the classic definition of Chiari Malformation I. Common symptoms include major headaches,
hearing loss, fatigue, muscle weakness and loss of cerebellum function.

[edit] Slit Ventricle Syndrome

Slit Ventricle Syndrome is an uncommon disorder associated with shunted patients, but results in a large number of shunt
revisions. The condition usually occurs several years after shunt implantation. The most common symptoms are similar to normal shunt
malfunction, but there are several key differences. First the symptoms are often cyclical and will appear and then subside several times
over a lifetime. Second, the symptoms can be alleviated by lying prone. In the case of shunt malfunction neither time nor postural
position will affect the symptoms. The condition is often thought to occur during a period where overdrainage and brain growth occur
simultaneously. In this case the brain fills the intraventricular space leaving the ventricles collapsed. Furthermore, the compliance of
the brain will decrease which prevents the ventricles from enlarging thus reducing the chance for curing the syndrome. The collapsed
ventricles can also block the shunt valve leading to obstruction. Since the effects of slit ventricle syndrome are irreversible, constant
care in managing the condition is needed.[12][13]

[edit] Intraventricular Hemorrhage

An intraventricular hemorrhage can occur at any time during or after a shunt insertion or revision. The hemorrhage can cause an
impairment in shunt function which can lead to severe neurological deficiencies.[14] Studies have shown that intraventricular
hemorrhage can occur in nearly 31% of shunt revisions. [15]

[ edit] Conditions Requiring Shunting

Below is a short list of known complications that can lead to hydrocephalus requiring shunting.
Diagnoses Description Incidence
Congenital 0.04-
A wide range of genetic abnormailities that could lead to hydrocephalus at birth.
Hydrocephalus 0.08%[16]
A number of different tumors can lead to CSF blockage if they are located in certain areas.
Tumor Some of these areas include the lateral ventricles, the posterior fossa, and intraspinal tumors. Unknown
The tumors may be malignant or benign.[17]
Specifically Spina Bifida Myelomeningocele can cause the development of hydrocephalus
Spina Bifida because the cerebellum will block the flow of CSF in a development of Chiari Malformation .125%[18]
Congenital Aqueductal A genetic disorder which can cause deformations of the nervous system. The defect is
Stenosis commonly associated with mental retardation, abducted thumbs and spastic paraplegia.[16]
Craniosynostosis occurs when the sutures of the skull close too early. The result of multiple
Craniosynostosis sutures fusing before the brain stops growing is an increase in ICP leading to hydrocephalus. 0.05%[19]
Patients usually present with a cystic deformity of the fourth ventricle, hypoplasia of the
Syndrome cerebellar vermis, and an enlarged posterior fossa. The condition is a genetically heritable 0.003%[21]
arachnoid mater]. The resulting cyst can then block the normal flow of CSF from the brain
resulting in hydrocephalus as well as other defects. The most common locations for an
arachnoid cyst are the middle fossa and the posterior fossa. The most common symptoms 0.05%[23]
Arachnoid Cyst
are nausea and vertigo.[22]

[ edit] Removing Shunts

Though there have been many cases of patients reaching "shunt independence", there is no common accord in which doctors can agree
in which a patient might survive without a shunt. Another problem with shunt removal is that it is very difficult to discern when a
patient might be shunt independent without very specific conditions. Overall shunt removal is a rare but not unheard of procedure. [24]
A craniotomy is a surgical operation in which a bone flap is removed from the skull, to access the brain. Craniotomies are often a
critical operation performed on patients suffering from brain lesions or traumatic brain injury (TBI), and can also allow doctors to
surgically implant deep brain stimulators for the treatment of Parkinson's disease, epilepsy and cerebellar tremor. The
procedure is also widely used in neuroscience for extracellular recording, brain imaging, and for neurological manipulations such as
electrical stimulation and chemical titration.
Human craniotomy is usually performed under general anesthesia but can be also done with the patient awake using a local anaesthetic;
the procedure generally does not involve significant discomfort for the patient. In general, a craniotomy will be preceded by an MRI
scan which provides a picture of the brain that the surgeon uses to plan the precise location for bone removal and the appropriate
angle of access to the relevant brain areas. The amount of skull that needs to be removed depends to a large extent on the type of
surgery being performed. The bone flap is then replaced using titanium plates and screws or another form of fixation (wire, suture,
Craniotomy is distinguished from craniectomy, in which the skull flap is not replaced to allow the brain to swell reducing
intracranial pressure, and from trepanation, which is performed voluntarily without medical necessity.
Bacterial meningitis occurs in approximately 0.8 to 1.5% of individuals undergoing craniotomy.[1]

[ edit] References
A cerebral 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. 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 cerebral
artery and anterior communicating artery (30-35%), the bifurcation, division of two branches, 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%).

[ edit] 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 more common in women than in men, by a ratio of 2 to 1.[1]
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.

[ edit] Classification
Cerebral aneurysms are classified both by size and shape. Small aneurysms have a diameter of less than 15 mm. Larger aneurysms
include those classified as large (15 to 25 mm), giant (25 to 50 mm), and super giant (over 50 mm). 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.

[ edit] Symptoms
A small, unchanging aneurysm will produce little, if any, 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, resulting in approximately
27,000 new cases of SAH in the United States per year.[1] Screening for aneurysms with annual imaging is possible, but not viewed as
cost effective.[2] The risk of short term re-rupture decreases dramatically after an aneurysm has bled in about 3 days (R. Torrejon
M.D), though after approximately 6 weeks the risk returns to baseline.

[edit] Classification of ruptured aneurysm severity

This section does not cite any references or sources.

Please help improve this article by adding citations to reliable sources. Unsourced material may be challenged and
removed. (January 2009)
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.
• Grade 5: Deep coma; decerebrate rigidity; moribund. 10%.
• Grade 6: Death. By definition, someone who presents brain dead following SAH is grade 6.

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

• Grade 1: No hemorrhage evident.
• Grade 2: Subarachnoid hemorrhage less than 1 mm thick.
• Grade 3: Subarachnoid hemorrhage more than 1 mm 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.

[edit] 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. [3]. 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

A selection of aneurysm clips ready for implantation.

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. If possible, either surgical clipping or endovascular coiling is usually performed within the first 24 hours after bleeding to
occlude the ruptured aneurysm and reduce the risk of rebleeding.

[edit] Surgical clipping

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 chosen specifically for the site. The surgical
technique has been modified and improved over the years. Surgical clipping has a lower rate of aneurysm recurrence after treatment.
In January 2009, a team of doctors at UNC Hospital in Chapel Hill, North Carolina pioneered a new approach for aneurysm treatment -
clipping aneurysms through an endoscopic endonasal approach. The team was lead by UNC neurosurgeon, Dr. Anand Germanwala.
This procedure may be groundbreaking for patients with aneurysms near the skull base, as an approach through the nose is less
invasive than traditional approaches. Two videos related to this procedure can be seen on the UNC Neurosurgery website:
and [4]

[edit] Endovascular coiling

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. These procedures require a small incision, through which a catheter is inserted. In the
case of broad-based aneurysms, a stent may be passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted
coiling"), although the long-term studies of patients with intracranial stents have not yet been done.
A resected MCA aneurysm with multiple coils.
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 [5]. The ISAT trials have shown, however, that patients who have experienced aneurysmal rupture have a 7%
lower mortality rate when treated by coiling than patients treated by clipping, when all other factors are equal. Coiled aneurysms,
however, do have a higher recurrence rate as demonstrated by angiography. For instance, the 2007 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. [6] (Read up on endovacular coiling. The
recovery rate of this is 22.6% HIGHER than surgical clipping. endovascular coiling)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. [7] The most recent data
from Moret's group reveals even higher aneurysm recurrence rates, namely a 36.5% recurrence rate at 9 months (which breaks down as
31.1% for small aneurysms less than 10 mm, and 56.0% for aneurysms 10 mm or larger). [8] However, no studies to date have shown
that the higher angiographic recurrence rate equals a higher rate of rebleeding. Thus far, the ISAT trials listed above show no increase
in the rate of rebleeding, and show a persistent 7% lower mortality rate in subarachnoid hemorrhage patients who have been
treated with coiling. In ISAT, the need for late retreatment of aneurysms was 6.9 times more likely for endovascular coiling as
compared to surgical clipping. [9]
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. The long-term data for unruptured aneurysms are still
being gathered.
Patients who undergo endovascular coiling need to have several serial studies (such as MRI/MRA, CTA, or angiography) to detect
early recurrences. If a recurrence is identified, the aneurysm may need 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.
[ edit] 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. [10][11]
Decompressive craniectomy is a neurosurgical procedure in which part of the skull is removed to allow a swelling brain room to
expand without being squeezed. It is performed on victims of traumatic brain injury and stroke. Use of the surgery is

Reduction of intracranial pressure

Though the procedure is considered a last resort, some evidence suggests that it does improve outcomes by lowering intracranial
pressure (ICP), the pressure within the skull.[1][2][3] Raised intracranial pressure is very often debilitating or fatal because it
causes compression of the brain and restricts cerebral blood flow. The aim of decompressive craniectomy is to reduce this pressure.
The part of the skull that is removed is called a bone-flap. A study has shown that the larger the removed bone-flap is, the more ICP
is reduced.[4]
In addition to reducing ICP, studies have found decompressive craniectomy to improve cerebral perfusion pressure[1][3] and
cerebral blood flow in head injured patients.[1]
Decompressive craniectomy is also used to manage major strokes, associated with "malignant" edema and intracranial
hypertension. The pooled evidence from three randomised controlled trials in Europe supports the retrospective observations that
early (within 48 hours) application of decompressive craniectomy after "malignant" stroke may result in improved survival and
functional outcome in patients under the age of 55, compared to conservative management alone. [5]
The procedure is recommended especially for young patients in whom ICP is not controllable by other methods. [1] Age of greater than
50 years is associated with a poorer outcome after the surgery.[3]
Infections such as meningitis or brain abscess can occur after decompressive craniectomy.[6]
In severely head injured children, a study has shown that decompressive craniectomy resulted in good recovery in all children in the
study, suggesting the procedure has an advantage over non-surgical treatment in children.[7] In one of the largest studies on pediatric
patients, Jagannathan et al. found a net 65% favorable outcomes rate in pediatric patients for accidental trauma after craniectomy when
followed for more than five years. Only three patients were dependent on caregivers.[8] This is the only prospective randomised
controlled study to date to support the potential benefit of decompressive craniectomy following traumatic brain injury. [9]
After a craniectomy, the risk of brain injury is increased, particularly after the patient heals and becomes mobile again. Therefore,
special measures must be taken to protect the brain, such as a helmet or a temporary implant in the skull [10].
When the patient has healed sufficiently, the opening in the skull is usually closed with a cranioplasty. If possible, the original skull
fragment is preserved after the craniectomy in anticipation of the cranioplasty[11].
Two prospective randomised controlled trials are currently being run in an attempt to provide Class I evidence on the role of
surgical decompression in the treatment of raised intracranial pressure after severe head injury. The RESCUEicp study [1] is an
international multicentre trial, coordinated by the University of Cambridge Academic Neurosurgery Unit [2] and the European Brain
Injury Consortium (EBIC)[3] and the DECRA trial[4] is run and coordinated by the Australian centres[5].

Cerebral angiography is a form of angiography which provides images of blood vessels in and around the brain, thereby allowing
detection of abnormalities such as arteriovenous malformations and aneurysms. The technique was pioneered by Egas Moniz
in 1927.
Typically a catheter is inserted into a large artery (such as the femoral artery) and threaded through the circulatory system to the
carotid artery, where a contrast agent is injected. A series of radiographs is taken as the contrast agent spreads through the
brain's arterial system, then a second series as it reaches the venous system.
For some applications[citation needed] this method may yield better images than less invasive methods such as computed
tomography angiography and magnetic resonance angiography. In addition, cerebral angiography allows certain treatments
to be performed immediately, based on the its findings. If, for example, the images reveal an aneurysm, metal coils may be
introduced through the catheter already in place and maneuvered to the site of aneurysm; over time these coils encourage formation of
connective tissue at the site, strengthening the vessel walls.
In some jurisdictions, cerebral angiography is required to confirm brain death.[citation needed]

reliminary Experience with Intra-Arterial Nicardipine as a Treatment for Cerebral Vasospasm

Neeraj Badjatiaa, Mehmet A. Topcuoglua, Johnny C. Pryorb,c, James D. Rabinovb, Christopher S.

Ogilvyc, Bob S. Carterc and Guy A. Rordorfa
a Department of Neurology, Massachusetts General Hospital, Boston
b Department of Interventional Neuroradiology, Massachusetts General Hospital, Boston
c Department of Neurosurgery, Massachusetts General Hospital, Boston
Address reprint requests to Neeraj Badjatia, MD, Neurocritical Care Service, Blake 1291, Department of
Neurology, Massachusetts General Hospital, Boston, Massachusetts 02114
BACKGROUND AND PURPOSE: Papaverine is the primary intra-arterial (IA) treatment for vasospasm after
aneurysmal subarachnoid hemorrhage (SAH); however, is it limited in effect and by adverse effects. We
prospectively studied the use of IA nicardipine as a treatment for vasospasm.
METHODS: Over 12 months, all patients with SAH who required interventional treatment for vasospasm were
given IA nicardipine with or without angioplasty. Vasospasm was determined by serial clinical assessments
and/or daily transcranial Doppler (TCD) imaging and confirmed by angiography. Doses of IA nicardipine per
vessel were 0.5–6 mg. All patients were monitored for increased intracranial pressure (ICP) and change in
cardiovascular or neurologic status.
RESULTS: Forty-four vessels in 18 patients with vasospasm were treated with IA nicardipine alone. TCD data
for 38 vessels (15 cases) were available. All vessels demonstrated immediate angiographic dilatation after IA
nicardipine. No sustained cardiovascular changes were after treatment. ICP was transiently elevated in five
patients and persistently elevated in one. Mean peak systolic velocities at TCD imaging were significantly
reduced from pretreatment values in all treated vessels for 4 days after infusion (268.9 ± 77.8 vs 197.6 ± 74.1
cm/s, P < .001). Neurologic improvement after IA nicardipine occurred in eight (42.1%) patients. No clinical
deterioration was noted.
CONCLUSION: As shown by TCD imaging, IA nicardipine has an immediate and sustained effect on
vasospasm. It does not appear to have sustained effect on ICP or cardiovascular status. This treatment warrants
further study to determine its safety and efficacy.

Safety and Feasibility of Intra-Arterial Nicardipine for the Treatment of Subarachnoid Hemorrhage-Associated Vasospasm:
Initial Clinical Experience with High-Dose Infusions

J.G. Tejadaa, R.A. Taylora, M.S. Ugurela, M. Hayakawaa, S.K. Leea and J.C. Chaloupkaa
a From the Department of Radiology, University of Iowa College of Medicine, Iowa City, Iowa
Address correspondence to Juan G. Tejada, MD, Department of Radiology, 550 N. University Blvd, Room 0279,
Indianapolis, IN 46202; e-mail: jtejada{at}
BACKGROUND AND PURPOSE: Delayed cerebral ischemia from vasospasm is a major complication after
aneurysmal subarachnoid hemorrhage (SAH), but complications and/or low efficacy are associated with current
therapy. We report our initial experience with intra-arterial use of a calcium channel blocker, nicardipine.
MATERIALS AND METHODS: A retrospective review of a consecutive series of patients with clinical and
angiographic vasospasm treated with intra-arterial nicardipine was performed. Standard criteria for definition of
significant, intractable vasospasm after aneurysmal SAH were used. After catheter angiographic confirmation of
vasospasm, arteries showing severe narrowing were targeted for superselective catheterization. Nicardipine was
infused at a high dose rate (0.415–0.81 mg/min). Contrast injections were performed at 2–5-mg intervals to
assess effective response (a 60% increase in arterial diameter of the most severely decreased in caliber vessel
compared with the very first angiographic run).
RESULTS: Eleven consecutive patients underwent a total of 20 procedures; most had SAH with high Hunt and
Hess grades (III or IV). All had depressed level of consciousness; others had paresis (7/20, 35%), aphasia (1/20,
5%), and facial nerve palsy (1/20, 5%). Between 10 and 40 mg of nicardipine was used. A 60% increase in
diameter of the main affected artery compared with the initial diameter measured in the initial angiographic run
was achieved in all procedures. Clinical improvement (resolved focal symptoms or increased Glasgow Coma
Score) occurred in 10 of 11 patients (91%). One patient died from complications of the initial hemorrhage. No
complications occurred after 16 of 20 procedures (80%); minor complications without sequelae occurred after
the remaining procedures. Follow-up of at least 2 months in 10 survivors revealed minor or no deficits in most
patients with a Glasgow Outcome Score of 1 or 2 in 9 of 10 patients (90%).
CONCLUSION: In this small series, high-dose intra-arterial nicardipine infusion to treat SAH-associated
vasospasm seems to be safe and effective.
Embolization is a non-surgical, minimally-invasive procedure performed by an interventional radiologist and interventional
neuroradiologists. It involves the selective occlusion of blood vessels by purposely introducing emboli. Embolisation is
used to treat a wide variety of conditions affecting different organs of the human body.

The treatment is used to occlude:
• Arteriovenous malformations (AVMs)
• Cerebral aneurysm
• Gastrointestinal bleeding
• Epistaxis
• Primary post-partum hemorrhage[1]

The treatment is used to slow or stop blood supply thus reducing the size of the tumour:
• Liver lesions, typically hepatocellular carcinoma (HCC). Either by partical infarction or transcatheter
arterial chemoembolization (TACE).
• Kidney lesions
• Uterine fibroids

• Portal vein

The procedure is a minimally-invasive alternative to surgery. The purpose of embolization is to prevent blood
flow to an area of the body, which effectively can shrink a tumour or block an aneurysm.
The procedure is carried out as an endovascular procedure, by a consultant radiologist in an interventional suite.
It is common for most patients to have the treatment carried out with little or no sedation, although this depends
largely on the organ to be embolized. Patients who undergo cerebral embolization or portal vein embolization
are usually given a general anesthetic.
Access to the organ in question is acquired by means of a guidewire and catheter(s). Depending on the organ this
can be very difficult and time consuming. The position of the correct artery or vein supplying the pathology in
question is located by digital subtraction angiography (DSA). These images are then used as a map for the
radiologist to gain access to the correct vessel by selecting an appropriate catheter and or wire, depending on the
'shape' of the surrounding anatomy.
Once in place, the treatment can begin. The artificial embolus used is usually one of the following:
• Coils: Guglielmi Detachable Coil or Hydrocoil
• Particles
• Foam
• Plug
Once the artificial emboli have been successfully introduced, another set of DSA images are taken to confirm a
successful deployment.

liquid embolic agents - used for AVM. these agents are able to flow through complex vascular structures so the
surgeon does not need to target his catheter to every single vessel.
nbca - n-butyle-2-cyanoacrylate: this agent is a permanent rapidly acting liquid that will polymeraize
immediately on contact with ions. aka superglue. it also has an exothermic reaction which destroys the vessel
wall. since the polymerization is so rapid, it requires skill of the surgeon when using. during the procedure, the
surgeon must flush the catheter before and after injecting the nbca or the agent will polymerize within the
catheter. also the catheter must be withdrawn quickly or it will be stuck to the vessel. oil can be mixed with nbca
to slow the rate of polymerization
ethiodol - made from iodine and poppyseed oil, this is a highly viscous agent. it is usually used for
chemembolizations, especially for hepatomas. this is because these types of tumors have a characteristic of
absorbing iodine. half life is 5 days so it only temporarily embolizes vessels
sclerosing agents - these will harden the endothelial lining of vessels. they have been around for a long time and
need more time to react than the liquid embolic agents. therefore you can't use them for high flow vessels or
large vessels.
ethanol - this permanent agent is very good for treating AVM. the alcohol does need some time to denaturize
proteins of the endothelium and activate the coagulation system which causes a blood clot. therefore, some
surgeons will use a balloon occlusion catheter to stop the blood flow and allow time for ethanol to work. the
disadvantage of this is that it is toxic to the system in large quantities and may cause compartment syndrome.
also the injections are painful
ethanolamine oleate - this permanent agent is used for sclerosing esophageal varices. it is made of 2% benzyl
alcohol so it is less painful than ethanol. however it does cause hemolysis and renal failure in large doses.
sotradecol - is used for superficial lower extremity varicose veins. it has been around for a very long time and is
a proven remedy. however, it does cause hyperpigmentation of the region in 30% of patients. it is less painful
than ethanol.
particulate embolic agents - only used for precapillary arterioles or small arteries. these are also very good for
AVM deep within the body. the disadvantage is that they are not easily targeted in the vessel. none of these are
radioopaque so it makes radiologic imaging difficult to see them unless they were soaked in contrast prior to
gelfoam - temporarily occludes vessels for 5 weeks. they work by absorbing liquid and plugging up the vessel.
these are water insoluble gelatin so the particles may travel distally and occlude smaller capillaries. a way to
localize the injection of gelfoam is to make a gelfoam sandwich. a coil is placed at a precise location. then
gelfoam is injected and lodged into the coil.
polyvinyl alcohol (PVA) - these are permanent agents. they are tiny balls 50-1200 um in size. the particles are
not meant to mechanically occlude a vessel. instead they cause an inflammatory reaction. unfortunately they
have a tendency to clump together since the balls are not perfectly round. the clump can separate a few days later
failing as an embolic agent.
acrylic gelatin microspheres - this is a superior form of permanent particulate embolic agent. they are similar to
PVA but they are perfectly round. thus they do not clump together. the balls are fragile so they may crack inside
small catheters.
mechanical occlusion devices - these fit in all vessels. they also have the advantage of accuracy of location (they
are deployed exactly where the catheter ends).
coils - used for AVF, aneurysms, or trauma. they are very good for fast flowing vessels because they
immediately clot the vessel. made from platinum or stainless steel. they induce clot because of the dacron wool
tails around the wire. the coil itself will not cause mechanical occlusion. because it is made of metal, it is easily
seen in radiographic images. the disadvantage is that large coils can disrupt the radiographic image. the coil may
also lose its shape if the catheter is kinked. also there is a small risk of dislodging from the deployed location.
detachable balloon - treat AVF and aneurysms. these balloons are simply implanted in a target vessel then filled
with saline through a one-way valve. the blood stops and endothelium grows around the balloon until the vessel
fibroses. unfortunately, the balloon may be hypertonic relative to blood and cause the balloon to rupture and fail.
or the balloon may be hypotonic and cause the balloon to shrink and migrate somewhere else.

• Minimally invasive
• No scarring
• Minimal risk of infection
• No or rare use of general anesthetic
• Faster recovery time
• High success rate compared to other procedures

• User dependent success rate
• Risk of emboli reaching healthy tissue
• Not suitable for everyone
• Recurrence more likely
Endovascular surgery is a form of minimally invasive surgery that was designed to access many regions of the body via major blood
Endovascular techniques were originally designed for diagnostic purposes. Basic techniques involve the
introduction of a catheter percutaneously or through the skin, into a large blood vessel. Typically the blood
vessel chosen is the femoral artery or vein found near the groin. Access to the femoral artery for example, is
required for coronary, carotid, and cerebral angiographic procedures. The catheter is injected with a radio-
opaque dye that can be seen on live X-ray or fluoroscopy. As the dye courses through the blood vessels,
characteristic images are seen by experienced viewers and can assist in the diagnosis of diseases such as
atherosclerosis, vascular trauma, or aneurysms.
In recent years, however, the development of intravascular balloons, stents and coils have allowed for new
therapies as alternatives to traditional surgeries such as Coronary artery bypass surgery (CABG), carotid
endarterectomy and aneurysm clipping. Stents and coils are composed of fine wire materials such as platinum,
that can be inserted through a thin catheter and expanded into a predetermined shape once they are guided into
Endovascular surgery is performed by radiologists, neurologists, neurosurgeons, cardiologists, and vascular
surgeons. The field is rapidly growing as its minimally invasive techniques offer an immediate advantage over
more traditional, yet highly invasive surgeries. However, the science of endovascular surgery and its developing
techniques are so new that it is currently difficult to compare the long term outcomes and complications of these
patients. Several trials are underway, including Carotid Revascularization Endarterectomy versus Stent Trial
(CREST), and International Subarachnoid Aneurysm Trial (ISAT), among others.
The most common and advanced form of endovascular surgery taking place today is an EVAR. This is a new
technique developed to treat aortic aneurysms, that was developed by Juan C. Parodi from Argentina.
Arteriovenous malformation or AVM is an abnormal connection between veins and arteries, usually congenital. This pathology is
widely known because of its occurrence in the central nervous system, but can appear in any location.
The genetic transmission patterns of AVM, if any, are unknown. AVM is not generally thought to be an inherited
disorder, unless in the context of a specific hereditary syndrome.

Signs and symptoms

Symptoms of AVM vary according to the location of the malformation. Roughly 88% [1] of people affected with
AVM are asymptomatic; often the malformation is discovered as part of an autopsy or during treatment of an
unrelated disorder (called in medicine an incidental finding); in rare cases its expansion or a micro-bleed from an
AVM in the brain can cause epilepsy, deficit or pain.
The most general symptoms of a cerebral AVM include headache and epilepsy, with more specific symptoms
occurring that normally depend on the location of the malformation and the individual. Such possible symptoms
• Difficulties with movement or coordination, including muscle weakness and even paralysis;
• vertigo (dizziness);
• Difficulties of speech (dysarthria) and communication, such as alogia;
• Difficulties with everyday activities, such as apraxia;
• Abnormal sensations (numbness, tingling, or spontaneous pain);
• Memory and thought-related problems, such as confusion, dementia or hallucinations.


Arteries and veins are part of the human cardiovascular system. Normally, the arteries in the vascular system
carry oxygen-rich blood, except in the case of the pulmonary artery. Structurally, arteries divide and sub-divide
repeatedly, eventually forming a sponge-like capillary bed. Blood moves through the capillaries, giving up
oxygen and taking up waste products, including CO2, from the surrounding cells. Capillaries in turn successively
join together to form veins that carry blood away. The heart acts to pump blood through arteries and uptake the
venous blood.
An AVM lacks the dampening effect of capillaries on the blood flow; it also causes the surrounding area to be
deprived of the functions of the capillaries - removal of CO2 and delivery of nutrients to the cells. The resulting
tangle of blood vessels, often called a nidus (Latin for "nest") has no capillaries and abnormally direct
connections between high-pressure arteries and low-pressure veins. It can be extremely fragile and prone to
bleeding. The resultant sign, audible via stethoscope, is a rhythmic, whooshing sound caused by excessively
rapid blood flow through the arteries and veins. It has been given the term "bruit", French for noise. On some
occasions a patient with a brain AVM may become aware of the noise, which can compromise hearing and
interfere with sleep in addition to causing psychological distress.

AVMs can occur in various parts of the body
• brain, causing a cerebral arteriovenous malformation
• spleen[3]
• lung[4]
• kidney[5]
• spinal cord[6]
• liver[7]
• intercostal space[8]
• iris[9]
• spermatic cord[10]
AVMs may occur in isolation or as a part of another disease (e.g. Von Hippel-Lindau disease or hereditary
hemorrhagic telangiectasia).
Bleeding from an AVM can be devastating, particularly in the brain. It can cause severe and often fatal strokes.
If a cerebral AVM is detected before a stroke occurs, usually the arteries feeding blood into the nidus can be
closed off to avert the danger.

Treatment can be symptomatic, or it can involve surgery or radiation therapy.[2] Embolization, that is, cutting
off the blood supply to the AVM with coils or particles or glue introduced by a radiographically guided catheter,
can be used in addition to either, but is rarely successful in isolation except for in smaller AVMs.

An estimated 300,000 Americans have AVMs, of whom 12% (approximately 36,000) will exhibit symptoms of
greatly varying severity.[2]
Society and culture

• On December 13, 2006, Senator Tim Johnson was diagnosed with AVM and treated at George
Washington University Hospital.[11]
• In the United Kingdom, Sky3 aired a documentary about Pete Nash and his fight with the NHS to operate
on the AVM in his brain.

Cases in fiction
• The plot of William Finn's 1998 Off-Broadway musical A New Brain revolves around the main
character's battle with AVM.
• The character Nate Fisher on the HBO television show Six Feet Under suffers from AVM.
• Patients with AVM appeared in an episode of the series House entitled "DNR" as well as in a fictional
British medical show called Harley Street.
• The protagonist of Robert J. Sawyer's novel Mindscan suffers from an AVM that threatens to reduce him
to a permanent vegetative state.
• In an episode of TNT's HawthoRNe entitled "The Sense of Belonging" patient Amy Johnson suffers from
this disorder, as well as an unspecified congenital heart defect.