Thursday, January 10, 2008

Tata Nano- The New Peoples' Millennial Car

Re: Millenial Tata Nano Technology Car: Making Technology Serve the Majority

10 January 2007* Thursday, 10 Hours Ago

The Tata Nano is an Oxidation Catalytic Converter driven care emitting 120 grams of Carbon Dioxide per kilometer, Is this a new source of Noise and Carbon Pollution!

As cheap as $2500, where the nearest motorcyle costs about $1000. It might be safe!
The car has seat belts, but no air bags. The Nano is about 10 feet long, 5 feet wide. The 2-cylinder petrol engine delivers 33 horsepower and a top speed of just over 60 mph. Can run at 50 miles per gallon!

Ford's Model T, which debuted in 1909 for $825, had a 4-cylinder, 20 horsepower engine with a top speed of 45 mph. The Model T had fuel economy between 13 to 21 miles per gallon

In 2005, Indian vehicles released 219 million tons of carbon dioxide, the leading greenhouse gas blamed for global warming.

By 2035, that number is projected to increase to 1,467 million tons, due largely to the expanding middle-class and the expected rise of low-cost cars, according to the Asian Development Bank.

"The cheaper and cheaper vehicles become, the quicker those pollution levels will increase," Leather said.


Tata unveils world's cheapest car By GAVIN RABINOWITZ, Associated Press Writer
40 minutes ago

India's Tata Motors on Thursday unveiled the world's cheapest car, bringing new mobility within the reach of tens of millions of people and nightmares to environmentalists, traffic engineers and safety advocates.

Company Chairman Ratan Tata, introducing the Nano — price tag $2,500 — during India's main auto show, drove onto a stage in a white version of the tiny four-door subcompact, his head nearly scraping the roof.

With a snub nose and a sloping roof, it can fit five people — if they squeeze. And the basic version is spare: there's no radio, no passenger-side mirror and only one windshield wiper. If you want air conditioning to cope with India's brutal summers, you need to get the deluxe version.

But it's cheap. The Nano's closest competitor here is the Maruti 800, a four-door that sells for nearly twice as much.

Tata, however, is targeting people moving up from the lower ends of India's transportation spectrum, where two-wheeled scooters selling for as little as $900 are often crammed with entire families.

While the price has created a buzz, critics say the Nano could lead to possibly millions more automobiles hitting already clogged Indian roads, adding to mounting air and noise pollution problems. Others have said Tata will have to sacrifice quality and safety standards to meet the target price.

The chairman, though, insists the car will meet safety standards and pollute even less than motorcycles, passing domestic and European emission standards and averaging about 50 miles per gallon. Girish Wagh, who headed the design team, said it had an oxidation catalytic convertor and it emitted 120 grams of carbon dioxide per kilometer.

Chief U.N. climate scientist Rajendra Pachauri, who shared last year's Nobel Peace Prize, said last month that "I am having nightmares" about the prospect of the low-cost car.

"Dr. Pachauri need not have nightmares," Ratan Tata said at the unveiling. "For us it's a milestone and I hope we can make a contribution to the country."

The basic model will sell for 100,000 rupees, but analysts estimate that customers could pay 20 percent to 30 percent more than that to cover taxes, delivery and other charges.

Tata has long promised that he'd create a 100,000-rupee car, a vow that was much-derided in the global industry but created a frenzy in India. On Thursday, nearly every media outlet in India focused on the live unveiling.

"A promise is a promise," Tata told the crowd.

The car has seat belts, but no air bags. The Nano is about 10 feet long, 5 feet wide. The 2-cylinder petrol engine delivers 33 horsepower and a top speed of just over 60 mph.

Ford's Model T, which debuted in 1909 for $825, had a 4-cylinder, 20 horsepower engine with a top speed of 45 mph. The Model T had fuel economy between 13 to 21 miles per gallon.

Tata has said they expect the car to revolutionize the auto industry, and analysts believe the Nano may force other manufacturers to lower their own pricing. French auto maker Renault SA and its Japanese partner, Nissan Motor Co., are trying to determine if they can sell a compact car for less than $3,000.

For now, the car will be sold only in India, but Tata eventually hopes to export it. The Nano could become the basis for other similar super-cheap models in developing markets around the world.

As rising middle class incomes drive demand for cars in India, automakers expect the ranks of car owners in the country to expand dramatically in coming years.

But for some, a huge influx of cars is a terrifying prospect of traffic jams at midnight, hours-long commutes and increasing pollution.

"If you're talking about urban environment, it will cause serious problems," said Jamie Leather, a transport specialist with the Asian Development Bank. "It's a major concern."

In 2005, Indian vehicles released 219 million tons of carbon dioxide, the leading greenhouse gas blamed for global warming.

By 2035, that number is projected to increase to 1,467 million tons, due largely to the expanding middle-class and the expected rise of low-cost cars, according to the Asian Development Bank.

"The cheaper and cheaper vehicles become, the quicker those pollution levels will increase," Leather said.

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Wednesday, January 09, 2008

Aneurisms: Defective blood vessel walls and their impact

Anterior communicating artery
Artery: Anterior communicating artery

The cerebral arterial circle and arteries of the brain. The anterior communicating arteries (top of figure) connect the left and right anterior cerebral arteries.
Latin arteria communicans anterior Gray's subject #146 572

In human anatomy, the anterior communicating artery is a blood vessel of the brain that connects the left and right anterior cerebral arteries.

The anterior communicating artery connects the two anterior cerebral arteries across the commencement of the longitudinal fissure. Sometimes this vessel is wanting, the two arteries joining together to form a single trunk, which afterward divides; or it may be wholly, or partially, divided into two.

Its length averages about 4 mm, but varies greatly. It gives off some of the anteromedial ganglionic vessels, but these are principally derived from the anterior cerebral artery.

It is part of the cerebral arterial circle, also known as the circle of Willis.

Aneurysms of the anterior communicating artery are the most common circle of Willis aneurysm[1] and can cause visual field defects such as bitemporal hemianopsia,[2] psychopathology and frontal lobe pathology.[3]

The arteries of the base of the brain. Anterior communicating artery at top. The temporal pole of the cerebrum and a portion of the cerebellar hemisphere have been removed on the right side. Inferior aspect (viewed from below).

[edit] References
^ Beck J, Rohde S, Berkefeld J, Seifert V, Raabe A. Size and location of ruptured and unruptured intracranial aneurysms measured by 3-dimensional rotational angiography. Surg Neurol. 2006 Jan;65(1):18-25; discussion 25-7. PMID 16378842.
^ Aoki N. Partially thrombosed aneurysm presenting as the sudden onset of bitemporal hemianopsia. Neurosurgery. 1988 Mar;22(3):564-6. PMID 3362325.
^ Johnson MK, O'Connor M, Cantor J. Confabulation, memory deficits, and frontal dysfunction. Brain Cogn. 1997 Jul;34(2):189-206. PMID 9220085.

[edit] External links
MedEd at Loyola Neuro/neurovasc/navigation/aca.htm
SUNY Labs 28:09-0221
Roche Lexicon - illustrated navigator, at Elsevier 13048.000-1
Roche Lexicon - illustrated navigator, at Elsevier 13048.000-3
This article was originally based on an entry from a public domain edition of Gray's Anatomy. As such, some of the information contained herein may be outdated. Please edit the article if this is the case, and feel free to remove this notice when it is no longer relevant.

v • d • eList of arteries of head and neck
Anterior: CC/EC superior thyroid (superior laryngeal) - lingual (sublingual)
facial: cervical branches (ascending palatine, tonsillar, submental, glandular) - facial branches (inferior labial, superior labial, lateral nasal, angular)

Posterior and ascending: CC/EC occipital - posterior auricular (stylomastoid) - ascending pharyngeal (meningeal branches)
Terminal, superficial temporal: CC/EC transverse facial - middle temporal (zygomaticoörbital) - anterior auricular - frontal - parietal

Terminal, maxillary: CC/EC 1st part: anterior tympanic - deep auricular - middle meningeal (superior tympanic) - accessory meningeal - inferior alveolar (mylohyoid)

2nd part: deep temporal - pterygoid branches - masseteric - buccal

3rd part: posterior superior alveolar - infraorbital (anterior superior alveolar) - descending palatine - artery of the pterygoid canal - sphenopalatine
portions #1 and 2: CC/IC cervical portion (carotid sinus) - petrous portion (Vidian, caroticotympanic)
cavernous portion/ophthalmic: CC/IC orbital group: lacrimal (lateral palpebral) - supraorbital - posterior ethmoidal - anterior ethmoidal - medial palpebral - supratrochlear - dorsal nasal
ocular group: central retinal - ciliary (short posterior, long posterior, anterior) - superior hypophysial - inferior hypophysial

cerebral portion: CC/IC ACA - anterior communicating - MCA (anterolateral central) - posterior communicating - anterior choroidal - circle of Willis
vertebral artery: SC meningeal branches - posterior spinal - anterior spinal - PICA - basilar (pontine, labyrinthine, AICA, SCA, PCA)
thyrocervical trunk: SC inferior thyroid (inferior laryngeal, tracheal, esophageal, ascending cervical) - suprascapular - transverse cervical - dorsal scapular


Classification & external resources
ICD-10 I72.
ICD-9 442
DiseasesDB 15088
MedlinePlus 001122

An aneurysm (or anneurism) is a localized, blood-filled dilation (bulge) of a blood vessel caused by disease or weakening of the vessel wall.[1]

Aneurysms most commonly occur in arteries at the base of the brain (the circle of Willis) and in the aorta (the main artery coming out of the heart), a so-called aortic aneurysm.

The bulge in a blood vessel can burst and lead to death at any time. The larger an aneurysm becomes, the more likely it is to burst. Aneurysms can usually be treated.

Look up Aneurysm in
Wiktionary, the free dictionary.Contents [hide]
1 Classification
1.1 Shape
1.2 Structure
1.3 Location
2 Risks
3 Formation
4 Treatment
4.1 Treatment of brain aneurysms
4.2 Treatment of peripheral aneurysms
5 See also
6 References
7 External links

[edit] Classification
Aneurysms may involve arteries or veins and have various causes. They are commonly further classified by shape, structure and location.


A saccular aneurysm resembles a small bubble that appears off the side of a blood vessel. The innermost layer of an artery, in direct contact with the flowing blood, is the tunica intima, commonly called the intima. Adjacent to this layer is the tunica media, known as the media and composed of smooth muscle cells and elastic tissue.

The outermost layer is the tunica adventitia or tunica externa. This layer is composed of tougher connective tissue. A saccular aneurysm develops when fibers in the outer layer separate allowing the pressure of the blood to force the two inner layers to balloon through.

A fusiform aneurysm is a bulging around the entire circumference of the vessel without protrusion of the inner layers. It is shaped like a football or spindle.

These aneurysms can result from hypertension in conjunction with atherosclerosis that weakens the tunica adventitia, from congenital weakness of the adventitial layer (as in Marfan syndrome) or from infection.


In a true aneurysm the inner layers of a vessel have bulged outside the outer layer that normally confines them. The aneurysm is surrounded by these inner layers.

A false- or pseudoaneurysm does not primarily involve such distortion of the vessel. It is a collection of blood leaking completely out of an artery or vein, but confined next to the vessel by the surrounding tissue.

This blood-filled cavity will eventually either thrombose (clot) enough to seal the leak or it will rupture out of the tougher tissue enclosing it and flow freely between layers of other tissues or into looser tissues.

Pseudoaneurysms can be caused by trauma that punctures the artery and are a known complication of percutaneous arterial procedures such as arteriography or of arterial grafting or of use of an artery for injection, such as by drug abusers unable to find a usable vein. Like true aneurysms they may be felt as an abnormal pulsatile mass on palpation.


Most non-intracranial aneurysms (94%) arise distal to the origin of the renal arteries at the infrarenal abdominal aorta, a condition mostly caused by atherosclerosis. The thoracic aorta can also be involved.

One common form of thoracic aortic aneurysm involves widening of the proximal aorta and the aortic root, which leads to aortic insufficiency.

Aneurysms occur in the legs also, particularly in the deep vessels (e.g., the popliteal vessels in the knee). Arterial aneurysms are much more common, but venous aneurysms do happen (for example, the popliteal venous aneurysm).

While most aneurysms occur in an isolated form, the occurrence of berry aneurysms of the anterior communicating artery of the circle of Willis is associated with autosomal dominant polycystic kidney disease (ADPKD).

The third stage of syphilis also manifests as aneurysm of the aorta, which is due to loss of the vasa vasorum in the tunica adventitia.

Rupture and blood clotting are the risks involved with aneurysms. Rupture leads to drop in blood pressure, rapid heart rate, and lightheadedness. The risk of death is high except for rupture in the extremities.

Blood clots from popliteal arterial aneurysms can travel downstream and suffocate tissue. Only if the resulting pain and/or numbness are ignored over a significant period of time will such extreme results as amputation be needed.

Clotting in popliteal venous aneurysms are much more serious as the clot can embolise and travel to the heart, or through the heart to the lungs (a pulmonary embolism). Risk factors for an aneurysm are diabetes, obesity, hypertension, tobacco smoking, alcoholism, and Copper deficiency.

Aneurysms are caused by a copper deficiency. Numerous animal experiments have shown that a copper deficiency can cause diseases affected by elastin [2] tissue strength [Harris].

The lysyl oxidase that cross links connective tissue is secreted normally, but its activity is reduced [3], due, no doubt, to some of the initial enzyme molecules (apo-enzyme or enzyme without the copper) failing to contain copper [4] [5].

Aneurysms of the aorta are the chief cause of death of copper deficient chickens, and also depleting copper produces aneurysms in turkeys [6]. Men who die of aneurysms have a liver content which can be as little as 26% of normal [7]. The median layer of the blood vessel (where the elastin is) is thinner but its elastin copper content is the same as normal men.

The overall thickness is not different [8]. The body must therefore have some way of preventing elastin tissue from growing if there is not enough activated lysyl oxidase for it. Men are more susceptible to aneurysms than young women, probably because estrogen increases the efficiency of absorption of copper.

However, women can be affected by some of these problems after pregnancy, probably because women must give the liver of their babies large copper stores in order for them to survive the low milk copper.

A baby’s liver has up to ten times as much copper as adult livers [9]. Elastin is about as flexible as a rubber band and can stretch to two times its length [10]. Collagen is about 1000 times stiffer. A healthy artery requires about 1000 mm of mercury or 10 times the normal mean blood pressure in order to rupture [11]. Therefore keeping strength of arteries up would seem to be even more important than keeping blood pressure down.

Most frequent site of occurrence is in the anterior cerebral artery from the circle of Willis. The occurrence and expansion of an aneurysm in a given segment of the arterial tree involves local hemodynamic factors and factors intrinsic to the arterial segment itself.

The human aorta is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation.

Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment.

Hemodynamically, the coupling of aneurysmal dilation and increased wall stress is approximated by the law of Laplace. Specifically, the Laplace law states that the (arterial) wall tension is proportional to the pressure times the radius of the arterial conduit (T = P X R).

As diameter increases, wall tension increases, which contributes to increasing diameter. As tension increases, risk of rupture increases. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture.

In addition, the vessel wall is supplied by the blood within its lumen in humans. Therefore in a developing aneurysm, the most ischemic portion of the aneurysm is at the farthest end, resulting in weakening of the vessel wall there and aiding further expansion of the aneurysm. Thus eventually all aneurysms will, if left to complete their evolution, rupture without intervention. In dogs, collateral vessels supply the vessel and aneurysms are rare.


Historically, the treatment of arterial aneurysms has been surgical intervention, or watchful waiting in combination with control of blood pressure. Recently, endovascular or minimally invasive techniques have been developed for many types of aneurysms.

Treatment of brain aneurysms

Currently there are two treatment options for brain aneurysms: surgical clipping or endovascular coiling. 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. The surgical technique has been modified and improved over the years.

Surgical clipping remains the best method to permanently eliminate aneurysms. 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. In the case of broad-based aneurysms, a stent is passed first into the parent artery to serve as a scaffold for the coils ("stent-assisted coiling").

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. The major problem associated with endovascular coiling, however, is the high recurrence rate and subsequent bleeding of the aneurysms.

For instance, the most recent 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. (Piotin M et al., Radiology 243(2):500-508, May 2007)

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. (Raymond J et al., Stroke 34(6):1398-1403, June 2003)

The long-term coiling results of one of the two prospective, randomized studies comparing surgical clipping versus endovascular coiling, namely the International Subarachnoid Aneurysm Trial (ISAT) are turning out to be similarly worrisome.

In ISAT, the need for late retreatment of aneurysms was 6.9 times more likely for endovascular coiling as compared to surgical clipping. (Campi A et al., Stroke 38(5):1538-1544, May 2007)

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 and bleeding rate after treatment.

Patients who undergo endovascular coiling need to have annual studies (such as MRI/MRA, CTA, or angiography) indefinitely to detect early recurrences.

If a recurrence is identified, the aneurysm needs 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.

At present it appears that only older patients with aneurysms that are difficult to reach surgically are more likely to benefit from endovascular coiling. These generalizations, however, are difficult to apply to every case, which is reflected in the wide variability internationally in the use of surgical clipping versus endovascular coiling.

Treatment of peripheral aneurysms

For aortic aneurysms or aneurysms that happen in the vessels that supply blood to the arms, legs, and head (the peripheral vessels), surgery involves replacing the weakened section of the vessel with an artificial tube, called a graft. More recently, covered metallic stent grafts can be inserted through the arteries of the leg and deployed across the aneurysm.

[edit] See also
Aortic aneurysm
Aortic dissection
Cerebral aneurysm
Charcot-Bouchard aneurysms
Rasmussen aneurysm
Aneurysm of sinus of Valsalva

[edit] References

^ The American Heritage Stedman's Medical Dictionary. KMLE Medical Dictionary Definition of aneurysm.
^ elastin review.
^ Kosonen T Uriu-Hare JY Clegg MS Keen CL Rucker RB 1996 Copper incorporation into lysyl oxidase. FASEB Journal; 10; A293,
^ Rucker RB, Kosonen T, Clegg MS, Mitchell AE, Rucker BR, Uriu-Hare JY, Keen CL 1998 Copper, lysyl oxidase, and extracellular matrix protein cross-linking.; Am J Clin Nutr. May;67(5 Suppl):996S-1002S.
^ Smith-Mungo LI, Kagan HM.: Lysyl oxidase 1998 properties, regulation and multiple functions in biology; Matrix Biol. Feb;16(7); 387-98.
^ Guenther E Carlson CW Emerick RJ 1978 Copper salts for growth stimulation and alleviation of aortic rupture losses in turkeys., Poult. Sci. Sep;57(5):1313-24.
^ Tilson MD 1983 Decreased hepatic copper levels. Arch. Surgery 117; 1212.-1213
^ Senapati A Carlsson LK Fletcher CDM Browse NL & Thompson RPH 1995 Is tissue copper deficiency associated with aortic aneuryzms? British Journal of Surgery 72; 352-353.
^ Dorea JG, Brito M, Araujo MO. 1987 Concentration of copper and zinc in liver of fetuses and infants. J Am Coll Nutr. Dec;6(6):491-5.
^ Carnes 1971 WH Role of copper connective tissue metabolism. Fed. Proc. 30; 995.
^ Shadwick RE 1998 Elasticity in arteries. American Scientist 86; 535-551.

[edit] External links
Cerebral Aneurysms
Dr. Solomon on Cerebral Aneurysms
Addressing the Challenges Faced as a Result of Brain Haemorrhage
Brain Blood Vessel Disorder Help & Info Site
@neurIST - Integrated Biomedical Informatics for the Management of Cerebral Aneurysms
Story of Aneurysm Survival
v • d • eCirculatory system pathology (I, 390-459)
Hypertension Hypertensive heart disease - Hypertensive nephropathy - Secondary hypertension (Renovascular hypertension)
Ischaemic heart disease Angina pectoris (Prinzmetal's angina) - Myocardial infarction - Dressler's syndrome
Pulmonary circulation Pulmonary embolism - Cor pulmonale
Pericardium Pericarditis - Pericardial effusion - Cardiac tamponade
Endocardium/heart valves Endocarditis - mitral valves (regurgitation, prolapse, stenosis) - aortic valves (stenosis, insufficiency) - pulmonary valves (stenosis, insufficiency) - tricuspid valves (stenosis, insufficiency)
Myocardium Myocarditis - Cardiomyopathy (Dilated cardiomyopathy, Hypertrophic cardiomyopathy, Loeffler endocarditis, Restrictive cardiomyopathy) - Arrhythmogenic right ventricular dysplasia
Electrical conduction system
of the heart Heart block: AV block (First degree, Second degree, Third degree) - Bundle branch block (Left, Right) - Bifascicular block - Trifascicular block
Pre-excitation syndrome (Wolff-Parkinson-White, Lown-Ganong-Levine) - Long QT syndrome - Adams-Stokes syndrome - Cardiac arrest - Sudden cardiac death
Arrhythmia: Paroxysmal tachycardia (Supraventricular, AV nodal reentrant, Ventricular) - Atrial flutter - Atrial fibrillation - Ventricular fibrillation - Premature contraction (Atrial, Ventricular) - Ectopic pacemaker - Sick sinus syndrome
Other heart conditions Heart failure - Cardiovascular disease - Cardiomegaly - Ventricular hypertrophy (Left, Right)
Cerebrovascular diseases Intracranial hemorrhage/cerebral hemorrhage: Extra-axial hemorrhage (Epidural hemorrhage, Subdural hemorrhage, Subarachnoid hemorrhage)
Intra-axial hematoma (Intraventricular hemorrhages, Intraparenchymal hemorrhage) - Anterior spinal artery syndrome - Binswanger's disease - Moyamoya disease
Arteries, arterioles
and capillaries Atherosclerosis (Renal artery stenosis) - Aortic dissection/Aortic aneurysm (Abdominal aortic aneurysm) - Aneurysm - Raynaud's phenomenon/Raynaud's disease - Buerger's disease - Vasculitis/Arteritis (Aortitis) - Intermittent claudication - Arteriovenous fistula - Hereditary hemorrhagic telangiectasia - Spider angioma
Veins, lymphatic vessels
and lymph nodes Thrombosis/Phlebitis/Thrombophlebitis (Deep vein thrombosis, May-Thurner syndrome, Portal vein thrombosis, Venous thrombosis, Budd-Chiari syndrome, Renal vein thrombosis, Paget-Schroetter disease) - Varicose veins / Portacaval anastomosis (Hemorrhoid, Esophageal varices, Varicocele, Gastric varices, Caput medusae) - Superior vena cava syndrome - Lymph (Lymphadenitis, Lymphedema, Lymphangitis)
Other Hypotension (Orthostatic hypotension)
See also congenital (Q20-Q28, 745-747)


Anterior Communicating Artery

The anterior communicating artery (abbreviated ACoA) is a small blood vessel which bridges the two larger anterior cerebral arteries. Together with the posterior cerebral arteries and posterior communicating artery, these arteries form a ring, sometimes called the Circle of Willis, lying at the base of the brain.

Normal variations in this layout are so common that only about 50% of the population has a "complete" Circle of Willis. The ACoA gives rise to a number of small branches, called collaterals. The number of collaterals is also variable, and can range from about 5 to 9. These collaterals supply blood to brain areas including the frontal lobes and the basal forebrain.

The ACoA is one of the most common sites of aneurysm in the brain. About 85% of people who survive ACoA aneurysm recover well enough to return to their normal life; but about 5-15% have long-lasting impairments.

These can include memory impairments (such as amnesia), personality changes (such as loss of self-control, unpredictable aggression, or apathy), or a combination of the two. The precise symptoms depend on which parts of the brain have been damaged by the aneurysm - and since the ACoA branches vary from individual to individual, the impairments do too.

It is believed that memory problems occur if the aneurysm damages the basal forebrain, while personality and judgment problems occur if the aneurysm damages the frontal lobes. If both basal forebrain and frontal lobes are damaged, the individual may show a syndrome called confabulation, in which the individual may report detailed memories of events which never occurred (or which occurred at a different time or place).

Further Reading:


The Truth About Confabulation
The rupture of a tiny blood vessel in the brain can produce distorted or erroneous memories.

by Daniel Pendick
Copyright © 2000 Memory Loss and the Brain

If someone asked you what you did yesterday, you would probably recite a list of mundane facts: what time you woke, what you ate for breakfast, when you left for work.

You would know these facts to be true simply because you remember them. But what if the day-to-day facts of your life proved to be utterly erroneous?

This is the predicament faced by many of the patients seen by neuropsychologist John DeLuca, Ph.D., director of neuroscience research at the Kessler Medical Rehabilitation Research and Education Corporation in West Orange, New Jersey. Dr. DeLuca studies people for whom the line between fact and fiction can sometimes become obscured.

These patients suffer from a disorder called confabulation, which produces inaccurate memories ranging from "subtle alternations to bizarre fabrications," DeLuca says.

Dr. DeLuca

The patients that DeLuca works with confabulate because of a rupture in a tiny blood vessel in the brain called the anterior communicating artery (ACoA).

The rupture of this tiny artery temporarily cuts off the normal flow of oxygenated blood to areas of the brain that are essential to the proper recall of memories.

The damage caused by an ACoA rupture can vary from one person to another, both in the location and the degree of damage. And the symptoms are also diverse: the person can suffer memory impairment alone, or memory impairment accompanied by confabulation.

When the ACoA balloons into an aneurysm and bursts, part of the frontal lobe–the region of the brain behind the forehead–is starved of oxygenated blood. This condition, known as hypoxia, can lead to the death of brain cells.

An area at the bottom of the brain, the basal forebrain, can also suffer damage. For reasons not entirely clear, damage to the basal forebrain can impair the ability to form lasting memories from recent experiences, a condition known as anterograde amnesia.

Confabulation in ACoA patients takes two forms. One involves distortions of when a particular remembered event actually occurred–what DeLuca calls its "temporal context." The other type of confabulation is marked by distortions in what actually occurred–the actual content of a memory.

For instance, when asked what he did the previous weekend, one of DeLuca's ACoA patients said that he spent time with an old friend, visited New York City, and stopped by his store.

Then the patient mentioned that the store was no longer in operation, contradicting himself. Furthermore, since the man had not left the hospital in the previous three weeks, much less traveled to New York City, the whole story was a confabulation. He had distorted both the when and the what of his memory.

Yet this patient was totally unaware of the errors in his memory of the weekend. This reflects an aspect of confabulation known as impaired self monitoring.

"Normally we're able to filter out what doesn't fit with the context of what we're doing or saying," DeLuca says. "But apparently, people who confabulate are having a breakdown in that. The system that tells them it's not right isn't working. That’s the frontal lobes."

The frontal lobes are important to the "executive" functions of the mind, including self monitoring, or awareness of one’s own behavior. In confabulation, self monitoring is crippled. This is what allows a confabulating ACoA patient to recall impossible or improbable events without realizing it.

The picture of human memory emerging from research on confabulation doesn’t match the popular misconception of memory as a computerlike system that simply stores and retrieves information.

Instead, DeLuca emphasizes, memory is a "reconstructive process" that pieces together rough drafts of an event based on a lifetime of experiences and perceptions. And being imperfect, human memory needs something to check up on it: call it the executive within.

Deprived of this executive within, the confabulating patient mixes fact and fiction and the order of particular events.

DeLuca is quick to emphasize, however, that ACoA patients who confabulate are not deliberately attempting to deceive anyone. Some psychiatrists, he says, still assume that confabulation is an amnesic patient’s way of filling in lost details to save face. However, DeLuca sees little evidence for that in his research. "They really believe with conviction that what they're saying is absolutely true," he says.

At the Kessler Medical Rehabilitation Research and Education Corporation, where DeLuca and his colleagues conduct their research, neuropsychologists, physicians, and therapists help people with confabulation to become aware that some of the memories they recall, believe, and even passionately defend are inaccurate.

As awareness of the confabulation grows, the person confabulates less. Just how and why this happens is unknown. But gradually, over a period of weeks to months, most patients stop reporting inaccurate memories. The amnesia generally persists, but the executive within has returned to his desk.

Would you like to participate in research on memory loss? Please go to Getting Involved