Clipping the wings of cerebral aneurysms: is the pendulum swinging back?

This is a follow up to my previous blog post, What should we really know about cerebral aneurysms? In that post, I discussed the nature and presentations of cerebral aneurysms. In this post I will look at the two major treatments for cerebral aneurysms, exploring their pros and cons, and looking at some emerging challenges to the conventional wisdom. 

By Tiago Etiene QueirozOwn work, CC BY-SA 3.0, Link

The first question to answer regarding treatment of aneurysms is whether they need any treatment at all. In other words, are they best left well alone? In principle, aneurysms that have ruptured require treatment, irrespective of their size. On the other hand, aneurysms that are discovered incidentally, before they rupture, may not need surgical treatment unless they are large (usually 7mm or more in diameter), or they are associated with high-risk features/locations. Low-risk aneurysms that do not require treatment however need long-term surveillance with intermittent brain imaging. To limit the growth of such aneurysms, people harbouring them are advised to stop smoking, and if they have hypertension, to ensure that this is well-controlled.

By Professor Dr. O. Bollinger. – LEHMANN’S MEDICIN. HAND ATLANTEN Atlas und Grundrissder PATHOLOGISCHENANATOMIE 1901, Public Domain, Link

There are two treatment approaches to ruptured aneurysms and high-risk unruptured aneurysms. The first is invasive and neurosurgical; the cranium is opened, the aneurysm located, and a surgical clip is put around its neck, sequestering it from its parent vessel. In this way, with its wing literally clipped, the aneurysm is disarmed, its potential for growth and rupture severely restricted. 

By Roberto Stefini – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=47226273

The other procedure, younger and safer than clipping, is endovascular coiling or coil embolisation. This procedure, performed by an interventional neuroradiologist, involves tunnelling a fine wire or coil through blood vessels until it reaches the aneurysm. The aneurysm space is then filled up with the coil until it is totally obliterated. Unable to fill up with blood or expand, the aneurysm is rendered impotent. Both coiling and clipping however carry a small failure risk, resulting in aneurysm recurrence or re-rupture.

By 77giallo77 – Own work, CC BY-SA 4.0, Link

This is the conventional wisdom of cerebral aneurysm treatment. But there are advocates out there who are pushing the case for clipping over coiling. One reason they put forward is the emerging observation that clipping results in better recovery of function of the third cranial or oculomotor nerve. The oculomotor nerve is critical to the movement of the eye and eyelid, and it is vulnerable to compression by the posterior communicating artery (PCOM) aneurysm. A compressed third cranial nerve results in a droopy eyelid (ptosis) and double vision (diplopia); recovery of function of the oculomotor nerve is therefore an important goal in the treatment of aneurysms.

Автор: Patrick J. Lynch, medical illustrator – Patrick J. Lynch, medical illustrator, CC BY 2.5, Посилання

There are now at least four systematic reviews and/or meta-analyses that show that recovery of the oculomotor nerve function is better achieved by clipping than by coiling. These are:

Another meta-analysis, titled Clinical outcome after surgical clipping or endovascular coiling for cerebral aneurysms, goes further to argue that clipping results in better chances of survival and independent living than coiling. 

By HellerhoffOwn work, CC BY-SA 3.0, Link

These may be the last-gasp attempts of clippers to have one up over coilers, but the consensus still remains dominantly in favour of endovascular coiling. We however need to keep a close eye on this pendulum-it may just swing back unexpectedly.

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Why not check out these related blog posts:

How does aspirin influence the rupture risk of cerebral aneurysms?

Is the growth of cerebral aneurysms predictable?

What should we really know about cerebral aneurysms?

Cerebral aneurysms are scary things. It is alarming enough that they exist, but it is more spine-chilling that they enlarge with time. The most infamous aneurysm arises from the posterior communicating artery, the so-called PCOM aneurysm. And it signifies its sinister intent when it gradually enlarges and compresses its vascular neighbour, the third cranial nerve, otherwise known as the oculomotor nerve. A dysfunctional third nerve manifests with a droopy eyelid (ptosis) and double vision (diplopia). The reason for the double vision becomes obvious when the neurologist examines the eyes; one eyeball is out of kilter and is deviated downwards and outwards; it is indeed down and out! The pupil is also very widely dilated (mydriasis). These are among the most worrying red flags in medicine, and a very loud call to arms. Cerebral aneurysms however often wave no flags, red or otherwise. Indeed the most malevolent of them will expand quietly until they reach horrendous proportions, and then, without much ado, just rupture. They are therefore veritable time bombs…just waiting to go off.

By Tiago Etiene Queiroz – Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=24418848

Cerebral aneurysm however do not need to reach large proportions to rupture; some just rupture when they feel like. Aneurysms under 7mm in diameter however are less prone to rupture. A rupturing aneurysm presents with very startling symptoms. The most ominous is a sudden onset thunderclap headache (TCH), subjects reporting feeling as if they have been hit on the back of the head with a baseball or cricket bat. It is not quite known what non-sporting patients experience-for some reason they never get aneurysms in neurology textbooks! More universally appropriate, a ruptured aneurysm may manifest as sudden loss of consciousness. Both symptoms result from leakage of blood into the cerebrospinal fluid (CSF) space, a condition known as a subarachnoid haemorrhage (SAH).

By Lipothymia – Anonymised CT scan from my own practice, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=787177

You may breath a small sigh of relief here because the vast majority of people with thunderclap headaches do not have subarachnoid haemorrhage. Unfortunately, every person who presents with a thunderclap headache must be investigated- to exclude (hopefully), or confirm (ruefully), this catastrophic emergency. The first test is a CT head scan which identifies most head bleeds. The relief of a normal scan is however short-lived because some bleeds do not show on the CT. The definitive test to prove the presence or absence of a bleed is less high tech, but more invasive: the humble spinal tap or lumbar puncture (LP). This must however wait for least 12 hours after the onset of headache or blackout. This is the time it takes for the haemoglobin released by the red blood cells to be broken down into bilirubin and oxyhaemoglobin. These breakdown products are readily identified in the biochemistry lab, and they also impart on the spinal fluid a yellow tinge called xanthochromia. The test may be positive up to 2 weeks after the bleed, but the sensitivity declines after this time. A positive xanthochromia test is startling and sets off an aggressive manhunt for an aneurysm-the culprit in most cases. 

By Ben Mills – Own work, Public Domain, https://commons.wikimedia.org/w/index.php?curid=13051957

Many people with cerebral aneurysms have a family history of these, or of subarachnoid haemorrhage. Some others may have connective tissue diseases such as Ehler’s Danlos syndrome (EDS), adult polycystic kidney disease (APCKD), or the rare Loeys-Dietz syndrome. This family history is a window of opportunity to screen family members for aneurysms. The screening is usually carried out with a CT angiogram (CTA) or MR angiogram (MRA). People are often not born with aneurysms, but tend to develop them after the age of 20 years. Aneurysm surveillance therefore starts shortly after this age, and many experts advocate repeating the screening test every 5-7 years until the age of 70-80 years.

By Nicholas Zaorsky, M.D. – Nicholas Zaorsky, M.D., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=15533196

How are aneurysms treated? This will be the subject of a future blog post so watch this space!

 

Migraine and the challenge of white matter lesions in the brain

Neurologists often refer their patients with headache for a brain MRI scan. Quite often the reason for this is to reassure their patients who are worried about a sinister cause for their headache…and the anxiety provoking culprit is usually a brain tumour. The headache is often a migraine which has recently changed in character, or which is defying conventional treatment.

The neurologist is often ambivalent when requesting such scans. On the one hand, she expects the scan to be normal. On the other hand, she can not be certain there is indeed no sinister cause for the headaches. Another thing also bothers the neurologist, beyond the chance of detecting a brain tumour. And this is the ‘risk’ that the brain scan detects ‘incidental’ findings called white matter lesions (WML). Alas, these reassurograms frequently pick up these less sinister, but nevertheless unexplained, findings.

By Xavier Gigandet et. al. - Gigandet X, Hagmann P, Kurant M, Cammoun L, Meuli R, et al. (2008) Estimating the Confidence Level of White Matter Connections Obtained with MRI Tractography. PLoS ONE 3(12): e4006. doi:10.1371/journal.pone.0004006, CC BY 2.5, Link
By Xavier Gigandet et. al. – Gigandet X, Hagmann P, Kurant M, Cammoun L, Meuli R, et al. (2008) Estimating the Confidence Level of White Matter Connections Obtained with MRI Tractography. PLoS ONE 3(12): e4006. doi:10.1371/journal.pone.0004006, CC BY 2.5, Link

White matter lesions are often just age-related, ‘wear and tear’ changes, and they are more common in people with vascular risk factors such as hypertension, smoking and raised cholesterol levels. Neurologists generally believe migraine is also a risk factor for white matter lesions. And there are several studies to support this belief.

An example is a paper by the headache gurus Marcelo Bigal and Richard Lipton, published in the journal Cephalalgia, titled migraine as a risk factor for deep brain lesions and cardiovascular disease. Another is a paper by Kruit and colleagues in the Journal of the American Medical Association (JAMA) titled migraine as a risk factor for subclinical brain lesions. If you are still not convinced, try this article in the Archives of Neurology by Swartz and colleagues, with the unequivocal title-migraine is associated with magnetic resonance imaging white matter abnormalities.

MIGRAINE. aka TMan on Flikr. https://www.flickr.com/photos/rundwolf/331545021
MIGRAINE. aka TMan on Flikr. https://www.flickr.com/photos/rundwolf/331545021

With this strong evidence, neurologists are able to convince themselves there is nothing to these MRI high signal changes in their patients with migraine. No ‘chicken and egg’ philosophical equivocation is entertained. The scans are sometimes discussed at neuroradiology meetings where everybody murmurs ‘migraine white matter lesions’. All doubt dispelled, the neurologist reassures the patient, and hurriedly closes the chapter.

https://pixabay.com/en/book-closed-bookmark-close-section-2159519/

It is therefore with a strong jolt that neurologists read a recent article in the prestigious journal, Brain, greatly upsetting this cosy neurological consensus. In the paper titled migraine with aura and risk of silent brain infarcts and white matter hyperintensities, the authors found no association between migraine and brain white matter lesions. Shocking!

Shocked girl. Bixendro on Flikr. https://www.flickr.com/photos/bixentro/6360922151
Shocked girl. Bixendro on Flikr. https://www.flickr.com/photos/bixentro/6360922151

The authors studied female twin pairs aged between 30–60 years. The twins were  identified through the population-based Danish Twin Registry. The authors compared the MRI scans of the subjects with and without migraine, and found no difference in the frequency of white matter changes between the two groups. They proudly, and disconcertingly, declare that ‘we found no evidence of an association between silent brain infarcts, white matter hyperintensities, and migraine with aura‘.

Migraine with aura. Joana Roja on Flikr. https://www.flickr.com/photos/cats_mom/2761999058
Migraine with aura. Joana Roja on Flikr. https://www.flickr.com/photos/cats_mom/2761999058

Oh dear-what do neurologists tell their patients now? I shudder to think!

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What unconventional stroke risk factors are out there?

Stroke is a terrible disease. It comes unexpectedly out of the blue, strikes quickly, and leaves devastation in its wake.

Ischemic stroke. NIH Image Gallery on Flikr. https://www.flickr.com/photos/nihgov/24964721940
Ischemic stroke. NIH Image Gallery on Flikr. https://www.flickr.com/photos/nihgov/24964721940

 

Stroke treatment is advancing in leaps and bounds, but the best approach remains preventative. We are all aware of the need to guard against the conventional harbingers of stroke: hypertension, high cholesterol, diabetes mellitus, and smoking. We are also aware of the benefits of a healthy diet and exercise.

There are of course stroke risk factors we can do nothing about: age is one, and there is of course a long list of genetic stroke risk factors.

DNA rendering. ynse on Flikr. https://www.flickr.com/photos/ynse/542370154
DNA rendering. ynse on Flikr. https://www.flickr.com/photos/ynse/542370154

 

Just as we are getting used to monitoring our blood pressures and heading to the park, some neurologists are bent on making our task a little bit harder. It’s no longer enough to flex those biceps or stamp out that stub; we now have to take notice of unconventional stoke risk factors. The first of these is infection.

3D model of influenza virus
3D model of influenza virus

This paper in Neurology titled Infection, vaccination, and childhood arterial ischemic stroke establishes the association between infection and stroke. The authors showed that 18% of children with stroke had an infection in the preceding week, compared to only 3% of those that did not have a stroke. Adults should not count themselves lucky going by another paper in the journal Vaccine titled Influenza vaccination and risk of stroke: Self-controlled case-series study. Both papers reassure us that immunisation helps to counter the stroke hazard of infections- one strong reason not to skip the next round of flu vaccinations.

By LaurMG. - Cropped from "File:Frustrated man at a desk.jpg"., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20367001
By LaurMG. – Cropped from “File:Frustrated man at a desk.jpg“., CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=20367001

 

Beyond infection come more bizarre unconventional stroke risk factors. We have always known that stress is no good; now we have some evidence to back this up. Just take the following factors now linked to stroke:

Add depression to this and you have a dangerous trio.

 

By BruceBlaus - Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=44968538
By BruceBlaus – Own work, CC BY-SA 4.0, https://commons.wikimedia.org/w/index.php?curid=44968538

 

Some medical risk factors are difficult to relate with stroke. Take for example

By M. Adiputra - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11602220
By M. AdiputraOwn work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11602220

 

Another risk factor to watch out for is air pollution. And to cap it off, being bilingual improves the chances of recovery from stroke. How unconventional is that!

Addendum

And straight off the press, you can now add sleep apnoea and insomnia to the list of stroke risk factors.