The ACOMM Aneurysm: Balloons and Blood

In order to understand the anterior communicating artery, we have to first appreciate the anatomy of the anterior cerebral arteries. The anterior cerebral arteries are one of the two terminal branches of each internal carotid artery (the other being the middle cerebral artery). Each anterior cerebral artery has several sections from A1 to A5.

Each A1 segment branches into an A2 segment and into the anterior communicating artery. The anterior communicating artery connects each anterior cerebral arteries’ A1 segment together to form a circle (see schematic below).

The anterior communicating artery is one of the most common sites for intracranial aneurysm formation. Patients at risk for developing aneurysms include those with atherosclerosis, those with a family history of intracranial aneurysms, those with a history of hypertension or collagen vascular disease, and those with polycystic kidney disease. Smokers are also at a higher risk of developing aneurysms.

Basilar Tip Schematic Drawing
Anterior communicating artery aneurysms form when the lining of the vessel wall is thinned and the muscular layer of the blood vessel (tunica media) becomes weakened.

This thinning allows turbulent blood flow to form out-pouchings in the vessel wall. Typically these out-pouchings occur at points where blood vessels branch.

Signs and Symptoms

Anterior communicating artery aneurysms commonly present after a subarachnoid hemorrhage, which can cause a variety of signs and symptoms. The most common being a severe headache, although cranial nerve dysfunction, stroke, coma, and death can also occur.

Less commonly, aneurysms in this location can compress the optic chiasm or optic nerves leading to problems with vision.

How Do You Diagnose Aneurysms

Anterior cerebral artery aneurysms are most commonly diagnosed after a subarachnoid hemorrhage when a patient presents with the "worst headache of their life". The best imaging methods for diagnosing these aneurysms are CT angiograms (see image below), MR angiograms, and formal cerebral angiograms.


Like other intracranial aneurysms, anterior communicating artery aneurysms may be clipped or coiled. Clipping of an aneurysm involves an open surgical procedure where the surgeon dissects down to the aneurysm and places a clip across its neck. This excludes it from the circulation and prevents it from rupturing.

Anterior Communicating Artery Aneurysm CT Angiogram

Aneurysms may also be treated from inside the blood vessel. In this procedure a catheter is threaded from the femoral artery in the groin up towards the location of the aneurysm. Small metallic coils are placed within the dome of the aneurysm, which also excludes it from the normal circulation.

Regardless of how the aneurysm is treated – either with clipping or coiling – the end result is that the aneurysm is excluded from the normal circulation. This prevents it from rupturing.

The merits of clipping versus coiling are still under debate. Ultimately, the treatment depends on the size and location of the aneurysm, as well as other medical problems that the patient may have.

The Highlights…

Anterior communicating artery aneurysms are the most common intracranial aneurysm. They typically present after rupturing into the subarachnoid space and/or adjacent frontal lobes. They are diagnosed using CT angiograms or formal cerebral angiography. Treatment is with clipping and/or coiling.

Related Readings

Not Satisfied? More Reading on the Subject…

  • Bederson JB, Awad IA, Wiebers DO, et al. Recommendations for the management of patients with unruptured intracranial aneurysms. Stroke 2000;31:2742-2750.
  • li>Hunt WE, Hess RM. Surgical Risk as Related to Time of Intervention in the Repair of Intracranial Aneurysms. Journal of Neurosurgery 1968; 28:14-20.
  • Brisman JL, Song JK, Newell DW. Cerebral Aneurysms. NEJM 2006; 355:928-939.
  • Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.
  • Frontera JA. Decision Making in Neurocritical Care. First Edition. New York: Thieme, 2009.
  • Greenberg MS. Handbook of Neurosurgery. Sixth Edition. New York: Thieme, 2006. Chapter 25.

Middle Cerebral Artery: A Common Site for Stroke

Middle cerebral artery (MCA) strokes occur when the MCA or its branches are occluded. With occlusion, blood, and along with it, oxygen and nutrients fail to reach the brain. If blood flow is not restored quickly the affected brain tissue dies leading to permanent neurological injury.

Risk factors for MCA strokes are the same for other strokes. They include hypertension, diabetes, smoking, atrial fibrillation, and a whole slew of hypercoagulable states (ie: pathologic increases in the bodies’ propensity to form blood clots).

In order to understand MCA strokes we have to first appreciate the anatomy of the MCAs, as well as the brain that they serve. The MCAs are subdivided into four parts. The M1 segment is one of the terminal branches of the internal carotid artery. The MCAs then become progressively more narrow and form more and more branches as they reach out towards the cortical surfaces of the brain. The most distal portions of the MCA are deemed the M4 branches. The lateral lenticulostriate arteries are small branches that branch from the M1 segments; these small arteries feed some of the deeper structures of the brain.

Importantly, the MCAs and their branches provide blood flow to an extremely large portion of the brain. These areas include the lateral and inferior frontal lobes, superior portion of the temporal lobes, insula, and lateral parietal lobes. Branches of the first portion of the MCAs (aka: the lateral lenticulostriate arteries) also provide blood flow to the deep sections of the brain including the putamen, head and body of the caudate, external globus pallidus, and parts of the posterior limb of the internal capsule.

The segmental anatomy of the MCAs is important because strokes that occur in the outer segments (ie: M3 and M4) cause less neurological injury than the inner MCA segments (ie: M1 and M2). This is because less total brain volume is affected by outer segment strokes.

The most common cause of MCA strokes are clots that break off and travel from the heart or the carotid arteries to the MCA (aka: emboli). Less commonly, a blood clot will form directly in the MCA itself (aka: thrombus). Atherosclerotic disease is the most common cause of thrombus formation in the MCA and atrial fibrillation (an abnormal heart rhythm) is the most common cause of emboli from the heart.

Signs and Symptoms

Middle cerebral artery strokes present with one of two types of syndromes depending on which MCA – right or left – is involved, as well as which segments of the MCA are involved.

In the worst case scenario, a stroke of the right or left M1 segment of the MCA causes weakness of the opposite side of the body. This is a result of cortical damage to the primary motor cortex as well as possible infarction of the posterior limb of the internal capsule (ie: the location of descending motor tracts). MCA strokes usually present with face and arm weakness that is worse than leg weakness. Remember that the motor cortex that controls leg function is served by the anterior cerebral arteries.

M1 strokes also cause decreased ability to feel sensation on the opposite side of the body as a result of damage to the parietal lobes.

Damage to the optic radiations, which course in the parietal (Baum’s loop) and temporal lobes (Meyer’s loop) can cause problems with vision. Finally, injuries to the frontal eye fields cause the eyes to deviate towards the side of the stroke (ie: the frontal eye fields normally allow you to make fast eye movements in the opposite direction, therefore damage prevents patients from looking to the non-affected side).

Right and left sided M1 strokes will give you all of the above symptoms; however, laterality can be determined based on specific symptoms caused by only a left or a right sided strokes.

The poor patients with left M1 strokes have a decreased ability to speak and/or understand language because of damage to Broca’s area in the left frontal lobe (speech production) and Wernicke’s area in the left temporal lobe (speech comprehension). Remember this is in addition to all the other stuff above.

Right M1 strokes can cause "anosognosia", in which the patient is unaware of certain deficits they may have; these patients also often fail to recognize the left side of their body (ie: they "neglect" or fail to appreciate the entire left side of the world) and may have difficulty appreciating people or objects presented in their left visual field.

Right MCA stroke
Less "severe" cases, in which M2, M3 or M4 branches are affected can produce a variety of signs and symptoms depending on the specific branches involved.


Diagnosis of MCA strokes are based on symptoms, CT scans, and MRI images. CT and MR angiograms frequently show the blocked blood vessel causing the stroke. CT perfusion scans are a newer technology that give information regarding the amount of blood flow to affected brain tissue.


Treatment depends on the timing of the stroke. If the patient presents within 3 hours of symptom onset, and the head CT reveals no bleeding, than intravenous tissue plasminogen activator (tPA) may be given to help "break" up the blood clot causing the stroke.

Other treatments using catheter based approaches are frequently used in patients who are unable to receive tPA. Such treatments include mechanical clot removal with special catheter and wire devices. In addition, in patients more than 3 hours, but less than 6 hours out from symptom onset intra-arterial (not to be confused with intravenous) tPA may be used.

Less commonly, large "malignant" MCA strokes may cause significant swelling, which can put pressure on the brainstem. These patients sometimes undergo an open surgical procedure known as a "craniectomy", in which the bone overlying the affected brain tissue is removed. This surgery allows the edematous brain tissue to swell outwards preventing it from herniating downwards towards vital brainstem structures.


Middle cerebral artery strokes are most commonly caused by blood clots that break off from the heart or carotid artery. Symptoms of MCA strokes depend on the segment involved, as well as which MCA (right versus left) is involved. Diagnosis is made with a combination of MRI, CT, and symptomatology. Treatment consists of intravenous or intra-arterial tPA and/or mechanical clot removal depending on the time frame of the symptoms.

Related Articles

References and Resources

Brain Boo-Boos: Cerebrovascular Accidents (Stroke)

MCA Stroke CT Scan

Stroke - ADC Map

Stroke - Diffusion Weighted
A cerebrovascular accident, commonly known as a stroke, occurs when blood flow stops reaching brain tissue. If the entire brain is involved it is referred to as a "global" stroke; if a specific region of brain is involved it is referred to as a "focal" or "territorial" stroke. There are three broad causes of territorial strokes: thrombotic, embolic, and hemorrhagic.

A thrombotic stroke occurs when a blood clot forms in a blood vessel that supplies brain tissue. This is similar to what happens in cardiac infarction (ie: heart attacks). Thrombi are most commonly caused by atherosclerotic disease of the cerebral blood vessels. Thrombi usually form at areas of turbulent blood flow and at locations where vessels form branch points.

Embolic strokes are similar because they are technically blood clots. However, an embolus is a fragment of a clot (thrombus) that formed in another part of the body. Those fragments break free from the original clot and travel to blood vessels in the brain. They get lodged at some point and prevent blood from flowing resulting in a stroke if treatment is not obtained quickly.

Strokes can also be caused by bleeding into brain tissue. These type of strokes are called “hemorrhagic stroke”. Bleeding can occur in people with long standing untreated high blood pressure, or in those that have underlying structural disorders of the blood vessels in the brain (ie: aneurysms or arteriovenous malformations).


Speedy diagnoses of stroke is extremely important because brain tissue dies quickly if it doesn’t receive adequate oxygen.

The first test that is done in cases of suspected stroke is a CT scan of the head. The purpose of the CT scan is not necessarily to "see" the stroke, but rather to rule out some other cause (ie: tumor, subdural hematoma, etc) for the symptoms. If bleeding is present on the CT scan the treatment algorithm becomes much different. If no bleeding is seen on CT then the second scan is usually an MRI.

An MRI takes longer than a CT scan, but it gives a much more detailed picture of the brain. In addition, it can pick up ischemia (ie: cell death related to decreased blood flow) much earlier than CT.

The best sequences to detect a stroke on an MRI are the diffusion weighted images and apparent diffusion coefficient maps. Stroked brain tissue will appear “bright” on diffusion weighted imaging and “dark” on the apparent diffusion coefficient map (see images to the left).

In addition, the carotid arteries are scanned using ultrasound in order to detect potential narrowing from atherosclerotic disease. Atherosclerotic carotid arteries are a potential source of emboli.

Sometimes a procedure known as transcranial doppler, which also uses ultrasound technology, is used to detect blood flow in the individual blood vessels of the brain. This can sometimes help determine the specific location of the thrombus/embolus.

Cerebral angiograms are much more invasive tests, but give a detailed view of which vessels are blocked. Cerebral angiograms can also be used to treat some strokes by directly removing clot from the affected blood vessel.

Most patients should undergo a thorough work up for atherosclerotic disease including a fasting lipid panel and hemoglobin A1C levels (a marker of diabetes).

If the heart is a suspected source of emboli than transthoracic echocardiography (ie: an ultrasound of the heart) is often done as well.

Signs and Symptoms

Cerebrovascular accidents present with a wide variety of signs and symptoms. It is entirely dependent on the blood vessel, and therefore, region of the brain involved. For example, strokes in the left middle cerebral artery will often cause significant language impairments if left untreated. Middle cerebral artery strokes usually cause contralateral paresis as well (usually the face and arm are more affected than the leg). Strokes in the frontal lobes caused by blockage of the anterior cerebral arteries can cause personality changes, as well as paresis/paralysis of the contralateral lower extremity.

Suffice it to say that there are a variety of possible clinical presentations in patients suffering from stroke. These presentations generally correlate with our understanding of brain anatomy and function.


Prompt treatment of stroke is critical for preserving viable brain tissue. If a stroke is due to a blood clot (ie: thrombus or embolus) the treatment is with a drug known as tissue plasminogen activator (tPA). tPA is a medication that helps break up the clot.

It can be a dangerous medication because it can cause serious bleeding, but if given early enough, and in the right patient, it can completely prevent brain tissue death. There are numerous contraindications to giving tPA so caution must be used. The traditional teaching is that is should be given within three hours of symptom onset (this is the FDA approved indication); however, up to 4.5 hours from symptom onset has become common in clinical practice (but this is not FDA approved).

Endovascular therapies that mechanically remove the clot are becoming more common, especially for large vessel disease. However, this type of treatment requires specialized interventional neuro-radiologists and is not available in all medical centers. Endovascular therapy with a clot retrieving device is usually indicated up to 6 hours post symptom onset for large vessel occlusions. More distal (ie: further out) occlusions are not candidates for this type of procedure yet.

If a patient survives their first stroke, they are often started on medications to decrease their risk of having a second stroke. One of the most common medications used to prevent a second stroke is aspirin.

However, other medications like ticlopidine and clopidogrel (Plavix®) are also frequently used. All three of these medications prevent platelets (ie: one of the bodies natural ways of forming blood clots) from clumping together. In addition, aspirin is often mixed with another medication called dipyridamole (dipyridamole + aspirin = Aggrenox® in the United States). Patients who have suffered a minor stroke or have high risk transient ischemic attacks should be started on aspirin and clopidogrel and then transitioned to aspirin alone at 21 days.

If atherosclerosis is believed to be the cause of the stroke patients are often started on a statin. This helps slow the process of atherosclerosis and can help prevent another stroke from occurring.

If an embolus was the cause of the stroke patients are often started on an anticoagulant. The most common one used is warfarin (although there are many others). Warfarin is also used to treat a common cause of embolic stroke, an abnormal heart rhythm known as atrial fibrillation.


Strokes can be caused by thrombi or emboli which are blood clot that block blood flor, or from hemorrhage into brain tissue. Diagnosis is made by CT and MRI scans. Additional studies including carotid ultrasound, cerebral angiography, echocardiography, fasting lipid profiles, and tests for diabetes are also frequently performed.

Treatment depends on the etiology. Tissue plasminogen activator (tPA) is given if thrombi or emboli are the cause, and symptoms began less than 3 hours prior to presentation (4.5 hours is becoming the standard of care). Mechanical endovascular removal of the clot is also possible in some medical centers with specialized equipment.

Prevention of secondary strokes involve the use of anti-platelet (ie: aspirin, clopidogrel), anti-coagulant (ie: warfarin), and anti-atherosclerotic medications depending on the etiology of the previous stroke.

Related Articles

References and Resources

The Anterior Choroidal Artery: Small but Mighty

The anterior choroidal arteries are small, but vital blood vessels in the brain. They are branches of the internal carotid arteries. They arise proximal to the splitting of the internal carotid into the anterior and middle cerebral arteries.

The anterior choroidal arteries deliver blood to vital brain structures. These structures include the posterior limbs of the internal capsules, portions of the thalami, optic tracts, middle third of the cerebral peduncles, portions of the temporal lobes (ie: parts of the pyriform cortex, uncus, and amygdala), substantia nigra, portions of the globus pallidus, as well as the choroid plexus in the lateral ventricles.

The anterior choroidal artery forms connections (anastamoses) with the posterior lateral choroidal arteries. Cerebral angiograms are the best way to visualize the anterior choroidal arteries.

Importance in Disease

Blockage of the anterior choroidal artery can cause a stroke. The most common symptoms of an anterior choroidal stroke are hemiparesis (weakness on the opposite side of the body), hemianesthesia (decreased sensation on the opposite side of the body), and a homonymous hemianopsia (loss of a portion of the visual field of both eyes). High blood pressure is the most common underlying factor in people with anterior choroidal artery strokes.

The hemiparesis is a result of damage to the posterior limb and genu of the internal capsule. The posterior limb contains the corticospinal tracts, which send information about movement from the brain to the spinal cord.

The hemianesthesia is a result of damage to the ventral posterolateral nucleus of the thalamus. This nucleus contains neurons that receive information from the spinal cord about sensation from the body. This symptom is less common than weakness, and occurs in roughly half of patients with an anterior choroidal stroke.

Cerebral angiogram showing anterior choroidal artery.

The final symptom, homonymous hemianopsia, is caused by damage to the optic tracts and lateral geniculate nucleus of the thalamus. Patients lose the ability to see objects on the left or right side (depending on which anterior choroidal artery is involved) in both eyes. This is an even more uncommon symptom, which occurs in less than 10% of patients with an anterior choroidal artery stroke.

Strokes of the anterior choroidal artery rarely cause all three symptoms. This is because the brain tissue served by the anterior choroidals also receives blood flow from other arteries.

Aneurysms of the anterior choroidal arteries are rare and will not be discussed in this article.


The anterior choroidal arteries are paired structures that arise from the internal carotid arteries. They supply blood to many important structures within the brain. Stroke is the most common pathological disease related to this blood vessel and frequently causes weakness of the opposite side of the body. High blood pressure is the most common underlying disease seen in people who have a stroke in this vascular distribution.

Other Stuff Worth Looking At…

References and Resources

  • Pezzella FR, Vadalà R. Anterior choroidal artery territory infarction. Front Neurol Neurosci. 2012;30:123-7. Epub 2012 Feb 14.
  • Bruno A, Graff-Radford NR, Biller J, et al. Anterior choroidal artery territory infarction: a small vessel disease. Stroke. 1989 May;20(5):616-9.
  • Baehr M, Frotscher M. Duus’ Topical Diagnosis in Neurology: Anatomy, Physiology, Signs, Symptoms. Fourth Edition. Stuttgart: Thieme, 2005.
  • Nolte J. The Human Brain: An Introduction to its Functional Anatomy. Sixth Edition. Philadelphia: Mosby, 2008.
  • Baskaya MK, Coscarella E, Gomez F, et al. Surgical and angiographic anatomy of the posterior communicating and anterior choroidal arteries. Neuroanatomy (2004) v3:38-42.

Subarachnoid Hemorrhage: Aneurysms, Vasospasm, and Hyponatremia

In order to understand subarachnoid hemorrhage we have to first appreciate the layers that make up the brain and its surrounding tissues. The brain itself has three protective layers: dura mater, the arachnoid, and the pia.

The dura is a thick layer of fibrous tissue immediately below the skull. Below the dura is the arachnoid, which is a layer of delicate web-like tissue (hence the name "arachnoid"). Finally, below the arachnoid is the pia mater. The pia is a very thin layer that is directly adjacent to brain tissue.

The subarachnoid space, or the region between the arachnoid tissue and the pia contains cerebrospinal fluid, which acts like a liquid shock absorber for the brain. Also contained within the subarachnoid space are blood vessels that penetrate down into the brain tissue. Sometimes these blood vessels "leak", which can cause a "sub-arachnoid" hemorrhage.

Brain Layers

The most common cause of subarachnoid hemorrhage is traumatic injury; the most common non-traumatic cause is a ruptured aneurysm.

An aneurysm is an abnormal ballooning out of a blood vessel’s wall. The balloon’s dome is much weaker than the rest of the vessel wall. These weak areas can rupture allowing blood to leak out of into the subarachnoid space.

Other causes of subarachnoid hemorrhage include idiopathic (ie: unknown) causes, arteriovenous malformations, vessel dissections, and very rarely tumors. Regardless of the cause, blood will pool in the subarachnoid space.

The remainder of this article will focus on the most common non-traumatic cause of subarachnoid hemorrhage – aneurysm rupture.

Signs and Symptoms

The classic symptom of a subarachnoid hemorrhage is a horrific headache described as the “worst headache of their life". Photophobia, nausea, vomiting, and nuchal rigidity are also common. Seizures may also occur. In addition, depending on how severe the subarachnoid hemorrhage is, patients may have decreased levels of consciousness; some patients become comatose, and many die before reaching medical attention.

The patient’s clinical status is graded according to the Hunt and Hess system. It only applies to patients in whom subarachnoid hemorrhage is caused by rupture of an aneurysm. This grading system was initially established to help determine mortality and clinical outcomes. In modern practice, these numbers are likely high given modern improvements in critical care and neurosurgical intervention since Hunt and Hess first developed their grading system.

Hunt and Hess Clinical Grading Scale
Grade Patient’s Clinical Status Associated Mortality
1 Mild headache and/or nuchal rigidity 1%
2 Cranial nerve dysfunction, moderate to severe headache and/or nuchal rigidity 5%
3 Mild focal neurological deficit, lethargic, confused 19%
4 Stuporous, moderate to severe hemiparesis, early decerebrate posturing 40%
5 Coma, decerebrate posturing 77%

The world federation of neurological surgeons also has a clinical score based on the Glasgow Coma Scale (GCS). It associates the patient’s GCS with the likelihood of death.

World Federation of Neurological Surgeons Grading System
  GCS Major focal deficit Mortality
1 15 No 5%
2 13-14 No 9%
3 13-14 Yes or No 20%
4 7-12 Yes or No 33%
5 3-6 Yes or No 77%

It is very important to think about the possibility of subarachnoid hemorrhage in patients presenting with these signs and symptoms. Prompt diagnosis and treatment is necessary in order to prevent devastating consequences!


Blood in the subarachnoid space is very irritating to the brain and cerebral blood vessels. Because of this, several complications can occur.

One of the most common complications is known as "vasospasm." Vasospasm occurs when the blood vessels of the brain spasm several days after the initial hemorrhage. When this occurs blood is no longer able to flow past the blockage; if this occurs for a long enough period of time a stroke can occur. The peak period for vasospasm occurs between 3 and 14 days after the initial bleed.

Another complication of subarachnoid hemorrhage is known as cerebral salt wasting. This occurs when a patient urinates excessive amounts of sodium causing the blood level of sodium to drop precipitously. Because of the excessive urination the patient also becomes dehydrated. Aggressive fluid and salt resuscitation must be given to prevent profound hyponatremia (ie: decreased sodium levels in the blood), which can cause seizures, coma, and death.

In addition, for unknown reasons, many patients with subarachnoid hemorrhage also shower their cerebral hemispheres with micro-thrombi (ie: clots), which can lead to many small strokes. The reason why patients with subarachnoid hemorrhage become coagulopathic is still an area of intense research.


Subarachnoid hemorrhage is most commonly diagnosed by head CT. CT scans are fast and readily pick up the extravasated blood, which layers in the subarachnoid space (see image below). If there is a high clinical index of suspicion but CT of the head is negative than a lumbar puncture should be performed. If the spinal fluid has xanthochromima (a product of red blood cell breakdown) this is highly concerning for subarachnoid hemorrhage.

CT Scan of Subarachnoid Hemorrhage

Subarachnoid hemorrhage is not a diagnosis per say, but rather the result of some underlying pathology (ie: aneurysm, trauma, etc.). Many of these pathologies are treatable; therefore, it is important to figure out what caused the subarachnoid hemorrhage.

Since many are the result of ruptured aneurysms there are several other tests that are often done. The first test is a CT angiogram (CTA). In this test a radio-opaque material is injected into the blood vessels and a CT is performed.

Cererbral Angiogram with Aneurysm
Dye in the dome of the aneurysm will appear as an abnormality helping to confirm the presence, and more importantly the location of the aneurysm.

A more invasive procedure known as a "cerebral angiogram" (image to the right) is also often performed.

In this test, a catheter is inserted into blood vessels in the groin and then threaded up into the blood vessels of the brain. Radio-opaque material is injected and x-rays can pick up abnormalities in the vessel.

The benefit of doing a cerebral angiogram is that it is diagnostic, and treatment can frequently be offered through the catheter itself.


There are three main components of treating a subarachnoid hemorrhage: treating the underlying cause, preventing a "re-bleed", and preventing secondary complications.

Since many subarachnoid hemorrhages are caused by aneurysm rupture we’ll discuss the treatment for this common cause. Aneurysms are treated either “open” or “closed”.

“Open” refers to a surgical procedure in which part of the skull is removed. The surgeon then dissects down to the aneurysm. Once identified, a clip is placed around the neck of the aneurysm (ie: you can think of the clip as putting a knot in the neck of a balloon). This stops blood from flowing into the aneurysm, and therefore prevents re-rupture.

“Closed” treatment refers to endovascular technology in which a small micro-catheter is threaded from the blood vessels in the groin into the cerebral vasculature. The aneurysm is located via angiogram. Through a hole in the microcatheter tip the physician then fills the aneurysm dome with small metallic coils.

Once blood is in the subarachnoid space secondary complications often result. One of these complications is referred to as "vasospasm". Medications such as oral nimodipine and intra-arterial nifedipine are used to reduce the amount of vasospasm by inhibiting smooth muscle contraction in the wall of the blood vessel.


Subarachnoid hemorrhage occurs most commonly after an intracerebral aneurysm ruptures, although other causes exist. Regardless of the cause, blood spills out into the subarachnoid space. Symptoms include a horrible headache, focal neurological deficits (ie: weakness, difficulty speaking, etc.), and coma. If an aneurysm is the cause, it is secured with clipping or coiling. Preventing secondary complications such as vasospasm is also an important component of treatment.

References and Resources

Carotid Stenosis: TIAs, Strokes, and Amaurosis Fugax

Carotid stenosis is narrowing of the carotid arteries. This is usually due to atherosclerotic disease present in the internal carotid arteries.

The internal carotid arteries supply a significant portion of the brain with blood, nutrients, and oxygen. If carotid stenosis is present it can result in transient ischemic attacks and possibly stroke.

Signs and Symptoms

Carotid stenosis may be either symptomatic or asymptomatic. Symptomatic carotid stenosis presents in one of three ways: transient ischemic attacks, stroke, or amaurosis fugax.

Transient ischemic attacks (TIA) occur when blood to the brain is blocked temporarily. TIAs cause the same symptoms as a stroke, but the symptoms resolve over 24 hours and there is no permanent brain injury.

A sub-category of TIA is a symptom known as amaurosis fugax, which is a temporary loss in vision, usually in one eye. It is described by patients as a curtain being drawn over the affected eye. It is caused by a small blood clot that breaks off from an atherosclerotic plaque present in the internal carotid artery. This small clot enters the retinal artery and occludes blood flow causing temporary blindness.

Stroke is by far the scariest problem associated with carotid stenosis. When a stroke occurs it can cause severe and irreversible brain injury. Strokes can cause life changing symptoms such as paralysis, aphasia (inability to speak or understand language), and even death!

Carotid Stenosis


Diagnosis of carotid stenosis is based on imaging studies. The most commonly employed studies are carotid ultrasound, CT angiogram, MR angiogram, and formal angiography.


Treatment is dependent on the location and degree of stenosis. Lesions that are near the origin of the internal carotid artery are frequently fixed with surgery in a procedure known as an endarterectomy. In a carotid endarterectomy the artery is surgically opened and the atherosclerotic material is "scooped" out.

The benefit of carotid endarterectomy on stroke risk for symptomatic patients is dependent on the degree of narrowing in the vessel. A landmark study in 1991 showed that carotid endarterectomy was very beneficial in preventing stroke in already symptomatic patients when the degree of narrowing was high (defined as 70 to 99%). A different study looked at lesser degrees of stenosis (50 to 69%) and found a benefit, albeit less robust. There is no clear benefit to having surgery in patients who have narrowing that is 50% or less. Surgery in asymptomatic patients with higher degrees of stenosis follows a more complicated algorithm.

If the diseased segment is higher up on the internal carotid, and surgical access is anatomically difficult, then procedures like carotid stenting or angioplasty can be performed. Stenting is a procedure in which a tiny metal tube-like device is threaded up through the femoral artery in the groin and then opened to “re-expand” the diseased arterial segment.

Patients who may not tolerate a procedure are often managed medically with antiplatelet medications such as aspirin, aspirin/dipyridamole combo (Aggrenox®), ticlopidine (Ticlid®) or clopidogrel (Plavix®). Currently there is no "best" medication to prescribe; the choice is highly dependent on the individual patient and physician.


Carotid stenosis refers to narrowing of the internal carotid artery. It is usually due to atherosclerotic disease. It can cause transient ischemic attacks, stroke, and amaurosis fugax. Diagnosis is with CT angiogram, carotid ultrasound, and/or formal invasive angiography. Treatment is highly variable, but usually involves a combination of surgery (endarterectomy), stenting, angioplasty, and antiplatelet medications like aspirin.

References and Resources

  • Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med. 1998 Nov 12;339(20):1415-25.
  • Chambers BR, Donnan GA. Carotid endarterectomy for asymptomatic carotid stenosis. Cochrane Database Syst Rev. 2005 Oct 19;(4):CD001923.
  • [No authors listed]. Beneficial effect of carotid endarterectomy in symptomatic patients wth high-grade carotid stenosis. North American symptomatic carotid endarterectomy trial collaborators. N Eng J Med. 1991 Aug 15;325(7):445-53.
  • Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation. 1998 Feb 10;97(5):501-9.

Atherosclerosis: Gruel and Hardening


What does the term atherosclerosis mean? If we break the term down into its components, "athero" is Greek for a gruel or paste, and sclerosis means hardening. This is precisely what is happening in the blood vessels of people with this disease; a paste-like material hardens to form a plaque. The specifics of how that paste-like material forms are much more complicated.

The paste-like material is composed of several different elements. The first, and perhaps most important element, is low density lipoprotein (ie: LDL). LDL, or the “bad cholesterol” as it is commonly referred, is a mixture of lipid (ie: fat and cholesterol) and protein. These molecules are highly atherogenic, which means they accelerate the plaque forming process.

How does LDL lead to a plaque? The first step involves disruption of part of the blood vessel known as the intima. Blood vessels have three layers: intima, media, and adventitia. The intimal layer is the portion of the vessel directly in contact with blood flow. It is composed of endothelial cells, which have numerous important functions. The medial layer is smooth muscle that controls the diameter of the blood vessel; the adventitial layer is a connective tissue coating (ie: similar to the plastic coating surrounding an electrical wire) that anchors the vessel to adjacent structures in the body.

Blood Vessel with Plaque

When the intimal layer is disrupted, LDL particles floating in the blood get trapped in the vessel wall. Once trapped, they start an inflammatory reaction. White blood cells (a key component of inflammation) known as macrophages are recruited to the vessel’s walland gobble up the intruding LDL particles. At this point the macrophages are known as “foam cells”. Foam cells get enmeshed in a web of scar and smooth muscle. All of this together becomes a "plaque".


The symptoms of atherosclerosis depend on how large the plaques are, and where they are located. The three common symptoms associated with atherosclerosis:

(1) Angina (chest pain) – read about acute coronary syndromes
(2) Transient ischemic attacks (TIA)
(3) Vascular claudication

Angina refers to chest pain that occurs with exercise (by exercise we refer to any activity above normal daily activity). The pain is a result of atherosclerotic plaque blocking the increased blood flow needed to supply the heart during strenuous activities. In essence, what is happening is that the heart is "starving" for oxygen, which results in chest pain. When the patient stops exercising the heart no longer needs as much oxygen; the amount of blood flow is again adequate, and the chest pain ceases. Angina is a harbinger of a potential heart attack.

Transient ischemic attacks are due to atherosclerosis in the blood vessels leading to the brain. The temporary decrease in blood flow to the brain caused by the blockages can result in stroke-like symptoms that resolve within twenty-four hours. TIAs are harbingers of potential strokes in the future.

If atherosclerosis develops in the vessels going to the lower extremities, vascular claudication occurs. Claudication refers to pain in the legs that worsens while walking (or running). Similar to angina, the pain is due to blocked blood flow to the legs secondary to the plaques. A condition known as "Leriche’s syndrome" occurs when there is decreased blood flow to not only the legs, but also the vessels leading to the penis. This causes not only lower extremity claudication, but also impotence.

The complications of atherosclerosis stem from the symptoms. They include myocardial infarction (eg: heart attack), of which angina is a warning sign; as well as cerebrovascular accidents (eg: strokes), of which transient ischemic attacks serve as a warning. Worsening disease in the lower extremities can lead to gangrenous limbs and the need for potential amputation.

(1) Myocardial infarction (eg: heart attack)
(2) Cerebrovascular accidents (eg: stroke)
(3) Worsening lower extremity disease -> amputations


Diagnosis of atherosclerotic disease depends on the location of symptoms. If anginal chest pain is the main symptom several different studies can be done. One such study is the “stress test”. There are several different permutations of the stress test.

All of them include two components. The first is a method of "visualizing" the heart. This can be done by ECG, echocardiography (ie: ultrasound of the heart), or nuclear/radioactive scans. The second component involves "stressing" the heart. This is most commonly done by exercising on a treadmill, but medications like dobutamine can also be used if the patient cannot exercise for whatever reason.

Stress Testing
Methods for visualizing the heart’s function – Electrocardiogram (ECG)
– Echocardiogram (echo)
– Nuclear studies
Methods for stressing the heart – Exercise (ie: treadmill)
– Medications (ie: dobutamine, persantine, etc.)

If the stress test is positive, or there is a high index of suspicion for atherosclerosis involving the coronary arteries, the next test performed is an angiogram. This involves injecting radio-opaque contrast material into the coronary arteries through a tiny catheter. The coronary arteries can then be visualized using x-rays. Areas where there is less contrast in the vessel indicate coronary atherosclerotic disease. The image below is an example of narrowing in the circumflex artery (indicated by the arrow).

Angiogram Circumflex Atherosclerosis

If the involved areas are the carotid arteries, a test known as "carotid artery duplex scanning" can be done. This involves using ultrasound to detect the amount of blood flow present in the vessel(s). Decreased rates are often attributable to atherosclerotic disease.

Finally, if disease is thought to be present in the lower extremities, a test known as the arterial brachial-ankle index (ABI) is obtained. This test involves taking the blood pressure in the arm and the leg and comparing the results. Blood pressure should be about equal in the upper and lower extremities resulting in a brachial to ankle ratio of 1.0. However, if there is atherosclerotic diseases in the lower extremities the ABI decreases to less than 1.0.

Location of suspected atherosclerotic disease: Initial test performed:
– Coronary arteries – Stress test
– Carotid arteries – Duplex scanning
– Arteries of lower extremities – Ankle-Brachial index (ABI)

Occasionally cardiologists or vascular surgeons will recommend a more invasive procedure known as a "catheterization". In this procedure a small catheter is threaded from a blood vessel in the groin to the area of interest (ie: the heart, carotids, vessels of the lower extremities). From there radio-opaque dye is injected. A fancy X-ray machine can then pick up locations of significant plaque formation.


Treatment is designed to prevent further plaque formation. Since LDL plays a crucial role in this process, it is a target of medical therapy, but in order to understand treatment we have to first understand how cholesterol gets into the body. Cholesterol is either (a) absorbed by the gut from your diet, or (b) produced naturally by your body through a series of biosynthetic reactions.

The first interventions for decreasing cholesterol in the body are, you guessed it, dietary modifications. By decreasing the amount of cholesterol in the diet it is possible to decrease the amount of cholesterol, either free or in the form of LDL, that is in the blood stream. There is also some evidence that replacing saturated fats with polyunsaturated fats (ie: α-linolenic acid, an ω-3 fatty acid) can decrease atherosclerotic plaque formation.

Unfortunately, diet and exercise are not always enough to decrease blood cholesterol levels to acceptable limits. Several medications have been developed, and as one could imagine, they target either cholesterol in the gut, or the biosynthetic machinery that produces cholesterol naturally.

There are several types of drugs that bind cholesterol in the gut to keep it from being absorbed. They are referred to as "bile acid binding medications" or "bile acid sequestrants". It is important to realize that bile acids, which are secreted by the liver and gallbladder, are rich in cholesterol.

Under normal circumstances they are reabsorbed by the gut and recycled back into the bile pathway. By inhibiting their re-absorption, cholesterol from the blood stream is recruited by the liver to replace the bile acids that were previously being recycled. The ultimate effect is that these drugs decrease the amount of cholesterol in the blood stream. There are three common medications in this category: colesevelam, cholestyramine, and colestipol.

Another medication, ezetimibe, directly binds to free cholesterol in the gut. As a result, less cholesterol is delivered to the liver. To compensate, the liver increases its ability to absorb LDL and other forms of cholesterol from the blood resulting in decreased plasma levels.


(1) diet and
(2) bile acid
(3) statins
(4) niacin
(5) fibrates
Perhaps the most widely used class of medications used to treat atherosclerosis are known as “statins.” Statins such as atorvastatin and pravastatin inhibit an enzyme (ie: HMG-CoA reductase) that normally produces cholesterol in the body. These medications dramatically reduce the risk of stroke and heart attack in patients with atherosclerotic disease.

A vitamin, niacin (ie: vitamin B3), can also lead to favorable effects on the lipid profile of the blood. It increases "good" cholesterol (ie: HDL). It is believed to perform these feats by increasing the activity of an enzyme, lipoprotein lipase, which normally breaks down VLDL particles (a precursor of LDL).

A final category of medications known as the "fibrates" decrease fat content in the blood. They do not necessarily affect LDL levels significantly, but they do decrease another atherosclerotic forming fat type known as triglycerides. The two common fibrates in use today are gemfibrozil and fenofibrate.


Atherosclerosis is due to LDL trapping in blood vessel walls. This trapping results in inflammation and the formation of a fibromuscular plaque. Symptoms include angina (ie: chest pain), lower extremity claudication, and transient ischemic attacks. Diagnosis is made by stress testing, carotid ultrasound, and ankle-brachial index; more invasive testing with groin catheters can be performed as well. Treatment is based on decreasing cholesterol absorption from the gut, or decreasing the bodies natural mechanism for creating cholesterol.

References and Resources

  • Negi S, Nambi V. Coronary heart disease risk stratification: pitfalls and possibilities. Methodist Debakey Cardiovasc J. 2010 Dec;6(4):26-32.
  • Amarenco P, Lavallée PC, Labreuche J, et al. Prevalence of Coronary Atherosclerosis in Patients With Cerebral Infarction. Stroke. 2010 Nov 18. [Epub ahead of print].
  • Kumar V, Abbas AK, Fausto N. Robbins and Cotran Pathologic Basis of Disease. Seventh Edition. Philadelphia: Elsevier Saunders, 2004.
  • Lilly LS, et al. Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty. Fourth Edition. Lippincott Williams and Wilkins, 2006.
  • Flynn JA. Oxford American Handbook of Clinical Medicine (Oxford American Handbooks of Medicine). First Edition. Oxford University Press, 2007.

Hypertension: Understanding and Managing High Blood Pressure

The pathology of essential hypertension is not well understood. However, there are numerous theories, each with supporting evidence.

Genetic causes are supported by the fact that children of hypertensive parents have an increased risk of developing the disease. However, specific known genetic mutations are not common. When mutations are responsible for essential hypertension they often involve the sodium and chloride channels in kidney cells, or mutations in the genes responsible for producing the proteins of the renin-angiotensin-aldosterone system. Sodium, renin, angiotensin, and other molecules play a vital role in blood pressure. In some hypertensive patients these systems are abnormal and can lead to elevated blood pressure.

Some patients with essential hypertension appear to be “salt sensitive”. Salt, or more specifically sodium, appears to play a role in the development of hypertension. Some patients likely have a genetic predisposition to retain sodium. Excess sodium enters the blood stream where it exerts an osmotic pull on water in adjacent tissues. Fluid from body tissues is "sucked" into the blood stream resulting in increased blood volumes. The expanded blood volume increases the pressure within the blood vessel causing hypertension. Although salt plays a role in hypertension, new research has shown its importance may not be as clear as once thought.

There are other known causes of hypertension, but they constitute a relatively small proportion of cases. They are discussed in separate articles.

Signs and Symptoms

Essential hypertension in its earliest stages does not cause any signs or symptoms. Many people do not know they have high blood pressure. However, if left untreated hypertension can cause serious long term consequences.

One such consequence is an increase in the risk of cardiovascular disease. The risk of cardiovascular disease doubles with each 20/10 mmHg increase in blood pressure beyond a "baseline" of 115/75 mmHg! After years of pumping at elevated pressures the heart undergoes physical changes. Like any good muscle, it becomes larger because it is having to pump harder than normal. The result is a process known as concentric hypertrophy. The added muscle mass of the heart results in increased oxygen demand and the potential for heart attacks and heart failure.

Overall, nearly a third of heart attacks are attributable to high blood pressure. In addition, the risk of stroke is also dramatically higher in untreated hypertensive patients. The small blood vessels in the kidney and retina can also be damaged by years of high blood pressure resulting in kidney failure (hypertensive nephropathy) and blindness (hypertensive retinopathy).


The diagnostic parameters of hypertension are constantly shifting. Currently the diagnosis can be made if a patient presents with a severely elevated blood pressure (systolic blood pressure > 200 and/or a diastolic blood pressure > 120) and/or signs or symptoms referable to the elevated blood pressure.

Severity Classification:
(1) Pre-hypertensive:
(2) Grade 1:
(3) Grade 2:
In patients with less severe elevations, it is generally recommended that the blood pressure be measured several times over a period of multiple weeks. If the average of these readings is a systolic blood pressure of 140 or greater, or a diastolic blood pressure of 90 or greater than the diagnosis can be made. If the blood pressue stays between 120 and 130 systolic, and 80 to 90 diastolic the diagnosis of "pre-hypertension" is made meaning the patient is at risk of becoming hypertensive.

Some patients may have "white coat" hypertension simply by being in a doctor’s office (and the anxiety that this can provoke! Gosh, I hate going to the doctor’s office!). If this is the case the patient should be instructed to take their blood pressure at home and keep a log of the results.


Treatment of hypertension consists of lifestyle modifications and/or using medications from several different pharmacologic categories. These medications may be used alone, or in combination, depending on each individual patient’s needs.

Patients who are pre-hypertensive or have stage 1 hypertension should be started on “lifestyle” modification therapy for at least 6 months prior to starting medicines (assuming there are no other health issues like diabetes or coronary artery disease). Lifestyle therapy consists of increasing aerobic exercise, as well as adhering to the “DASH” diet. DASH stands for "dietary approaches to stop hypertension" and consists of eating fruits, vegetables, low-fat dairy, whole grains, poultry and fish while reducing (or eliminating) red meat and sugars. This intervention alone can decrease systolic pressures over 10 mmHg and diastolic pressures over 5 mmHg.

Sometimes diet and exercise aren’t enough so we may have to resort to medications to control blood pressure. The first category of medications are known as diuretics, most commonly of the thiazide class. Thiazide diuretics work by inhibiting the re-absorption of sodium at the distal convoluted tubule of the kidney. Less sodium means less circulating blood volume, and therefore decreased blood pressure. Hydrochlorothiazide is a commonly used thiazide diuretic.

The second category of medications is known as β-blockers. β-blockers lower blood pressure by slowing the heart rate and indirectly lowering the amount of angiotensin II (angiotensin II is a potent natural blood vessel constrictor produced by the body). β-blockers reduce renin synthesis by specialized cells in the kidney.

A third category of medications known as angiotensin converting enzyme inhibitors (ACEIs) interfere with the formation of angiotensin II. ACEIs inhibit an enzyme present in the lung, which converts angiotensin I into the more potent vasoconstrictor angiotensin II. Interestingly, ACEIs also increase the level of bradykinin; this molecule causes blood vessels to dilate, which helps to further lower pressure.

There are also medications called direct angiotensin receptor blockers (ARBs), which inhibit the actions of angiotensin II. They do this by blocking angiotensin IIs ability to bind to its normal receptor sites.

Some medications, the calcium channel blockers (CCBs), lower blood pressure by inhibiting the contraction of smooth muscle cells that line the blood vessel walls. A specific subcategory of calcium channel blockers known as dihydropyridines block calcium from flowing into vascular smooth muscle cells. This results in decreased contraction of the muscle surrounding the vessel. As a result the vessel remains dilated, which lowers pressure.


The pathology of essential hypertension is not well understood. Several theories have been postulated, but it is likely a combination of genetic predispositions that result in this type of high blood pressure. Years of elevated blood pressure lead to cardiovascular disease including heart failure, heart attacks, and stroke, as well as damage to the kidneys and retinas. Treatment is with lifestyle modifications, diuretics, β-blockers, calcium channel blockers, angiotensin converting enzyme inhibitors, and angiotensin receptor blockers.

References and Resources