‘Robot Mouse’ Marks New Step Forward in Neuroscience

The mouse walked, the mouse stopped; the mouse ignored a bowl of food, then scampered back and gobbled it up, and it was all controlled by neuroscientists, researchers reported on Thursday.

The study, describing a way to manipulate a lab animal’s brain circuitry accurately enough to turn behaviors both on and off, is the first to be published under President Barack Obama’s 2013 BRAIN Initiative, which aims to advance neuroscience and develop therapies for brain disorders.

The point of the remote-control mouse is not to create an army of robo-rodents. Instead, neuroscientists hope to perfect a technique for identifying brain wiring underlying any behavior, and control that behavior by activating and deactivating neurons.

If scientists are able do that for the circuitry involved in psychiatric or neurological disorders, it may lead to therapies. That approach reflects a shift away from linking such illnesses to “chemical imbalances” in the brain, instead tracing them to miswiring and misfiring in neuronal circuits.

“This tool sharpens the cutting edge of research aimed at improving our understanding of brain circuit disorders, such as schizophrenia and addictive behaviors,” said Dr. Francis Collins, director of the National Institutes of Health, which funded the $1 million study.

The technique used to control neurons is called DREADDs (designer receptors exclusively activated by designer drugs).

Brain neurons are genetically engineered to produce a custom-made — “designer” — receptor. When the receptor gathers in a manmade molecule that fits like a key in a lock, the neuron is activated.

Because the receptor does not respond to other molecules, including natural ones in the brain, the only way to activate the neurons is via the manmade one. DREADDs allow scientists to manipulate neurons without implanting anything in the brain.

DREADDs, invented about a decade ago, had been used to turn neurons on or off, but not both. DREADDs 2.0 are the first to do that, scientists led by Bryan Roth of the University of North Carolina reported April 30 in the journal Neuron.

Targeting hunger-promoting neurons, the scientists made mice ignore food bowls or dive into them. Targeting movement neurons, they made mice scamper or stop.

In a competing remote-control technique called optogenetics, engineered neurons are activated upon receiving a pulse of light. That turns them on and off more quickly than with DREADDs, but the hardware required for delivering light to a spot in the brain is invasive and cumbersome.

MIT Researchers Think They Can Spot Early Signs of Parkinson’s in the Way People Type.

It may be possible to detect neurological diseases years before other symptoms appear by monitoring how long we hold down keystrokes


From the physical keys on our laptops to the software buttons on our smartphones, most of us rely on keyboards as the primary way of entering data into the digital world. But it turns out that our keyboards can also tell us quite a bit about ourselves, detecting when we’re tired, drunk, and even when we’re showing early signs of neurological disorders like Parkinson’s disease—perhaps years before more recognizable symptoms surface.

Researchers at the Madrid-MIT M+Visión Consortium, a network dedicating to healthcare innovation in Madrid, are gathering and analyzing the keystrokes of volunteers with software and studying the patterns that emerge through machine learning. Individual typing patterns have already been used to identify individuals; some banks have used them to increase security when logging into accounts. But according to a soon-to-be-published paper in Scientific Reports, the M+Visión team was able to take the same typing data, combined with pattern recognition techniques, to distinguish between typing done when fully rested and when volunteers were tasked to type when woken up in the night. That data could also be used to detect neurological conditions much earlier than existing methods.

To be clear, the team is only gathering information about the timing of key presses, not which keys are being pressed. The researchers developed software that could be applied to a web browser to track how long a typist holds down each key. There’s no need to use specialized keyboards, and little cause for privacy concerns. In fact, many third-party smartphone keyboards gather much more data about what we type.

But it’s clear from the group’s work that we leave behind a trove of information when we interact with electronic devices in our daily lives.

“Every time we touch something that has a microprocessor in it, the microprocessor is able to measure the timing with sub-millisecond accuracy,” Luca Giancardo, a M+Vision fellow and the paper’s first author says. “You can get potential information from a microwave, but changing the software in a microwave is much harder.”

Watch the video. URL: https://youtu.be/pthM_gR6VbQ


Stroke Warning Signs and Symptoms.


Epilepsy Risk for Men Reduced with Exercise.

Story at-a-glance

  • Men who had a high level of fitness when they were young were 79 percent less likely to develop epilepsy later in life compared to those with low fitness levels
  • Compared to young men with average fitness levels, the high-fitness group was still 36 percent less likely to develop epilepsy
  • Exercise may protect the brain and create a stronger brain reserve, which may reduce epilepsy risk
  • If you have epilepsy, exercising may help to reduce the frequency of seizures.


The next time you work out, take a moment to think about all of the wonderful ways it is benefitting your body. And I’m not only talking about your muscles or your six-pack abs… I’m referring to you brain.

Exercise is emerging as a key player in brain health at various stages of life and has been shown to prevent cognitive decline, moderate brain damage caused by drinking and even lower your risk of brain diseases like Alzheimer’s. Now, researchers have uncovered yet another brain benefit of exercise – a reduced risk of epilepsy.

Vigorous Exercise May Reduce Epilepsy Risk by Up to 80 Percent

In a study involving more than 1.1 million men who were followed for an average of 25 years, those who had a high level of fitness when they were young were 79 percent less likely to develop epilepsy later in life compared to those with low fitness levels.1

Compared to young men with average fitness levels, the high-fitness group was still 36 percent less likely to develop epilepsy. This is the first study in humans to reveal that exercise may impact epilepsy risk. One of the study’s researchers noted:2

Exercise may affect epilepsy risk in two ways. It may protect the brain and create stronger brain reserve, or it may simply be that people who are fit early in life tend to also be fit later in life, which in turn affects disease risk.”

Exercise May Reduce Seizure Frequency in People with Epilepsy

Epilepsy is a neurological disorder involving disturbed nerve cell activity in your brain. This results in seizures that may include a staring spell, confusion, uncontrollable jerking movements and loss of consciousness or awareness. Obviously, this presents risks of falls and injuries that may occur if you have a seizure while driving or even exercising.

For this reason, people with epilepsy have previously been discouraged from participating in physical activity, and this stigma remains today even though medical recommendations have long since changed.

Now, exercise is highly recommended for people with epilepsy, for starters because it helps to reduce stress levels, which can sometimes trigger seizures. In fact, physical activity has been shown to decrease seizure frequency,3 as well as lead to improved cardiovascular and psychological health in people with epilepsy.4

Tips for Exercising if You Have Seizures

If you have epilepsy, make sure you exercise with a buddy or a personal trainer who knows what to do if you have a seizure. A medical alert bracelet can also be worn.

Try to exercise in a safe area, such as a grassy field or on a gym mat, and wear elbow and knee pads. If you’ll be swimming, be sure you wear a life vest and never go swimming alone (a strong swimmer should be with you at all times in case you need help).

If you’ll be exercising on a bicycle, stay away from busy streets (and wear a helmet)… likewise if you’ll be hiking — stick to simpler trails, not those with steep drop-offs or cliffs. If you have epilepsy, you’ll need to take special care during activities that pose a risk of a blow to your head, such as football; if you do engage in such sports be sure to wear a helmet.

Generally speaking, however, you can exercise normally if you have epilepsy, but do use commonsense precautions – avoid getting over-tired or overheated, and avoid exercising when it’s very hot. As an aside, if you have epilepsy, be sure to get your vitamin D levels checked. When epileptic patients improved their vitamin D levels, their seizures were reduced by an average of 40 percent in one study.5

What Else Can Exercise Do for Your Brain?

Along with potentially reducing your risk for epilepsy quite significantly, scientific evidence shows that physical exercise helps you build a brain that not only resists shrinkage, but also increases cognitive abilities.6 In one review of more than 100 studies, both aerobic and resistance training were found to be important for maintaining cognitive and brain health in old age.7 Moderate exercise may even reverse normal brain shrinkage by 2 percent, effectively reversing age-related hippocampus degeneration, which is associated with dementia and poor memory, by one to two years.8

Not to mention, other contributing factors to brain disease caused by the normal aging process may also include a decrease in blood flow to your brain, and the accumulation of environmental toxins in your brain. Exercise can help ameliorate both of these conditions by increasing blood flow to your brain, thereby increasing oxygen supply to your brain and encouraging a more vigorous release and removal of accumulated toxins through better blood circulation.

You’ve Got to Move It… Or You Might Lose It

If you work out religiously for three months, then suddenly stop for an extended period, your muscle tone will definitely suffer. This is one of the more obvious examples that your body is designed for regular exercise, not sporadic or infrequent activity.

Likewise, research suggests that the brain benefits of exercise also quickly fade if your exercise program stops. The silver lining is that the opposite also appears to hold true. While the benefits of exercise might fade fast, they can also be achieved relatively quickly.

Exercising – even briefly – can change your DNA in a way that readies your body for increased muscle strength and fat burning. It also boosts your natural human growth hormone (HGH) production, which is important for maintaining muscle mass as you age. If you’re approaching middle-age or beyond, you might be thinking that it’s too late for you to get in shape, but this is not the case. Remember, you are never too old to start exercising and start reaping the mental and physical benefits that physical activity has to offer.


If you have epilepsy and are unable to control the seizures, or have refractory epilepsy – or know someone who is affected – please view the video above, which is my interview with Dr. Thomas Seyfried about the ketogenic diet. The ketogenic diet has been used for managing seizures for quite some time, and is now recognized as an important component for the management of refractory seizures in children. A ketogenic diet calls for eliminating all but non-starchy vegetable carbohydrates, and replacing them with healthy fats and high-quality protein.

Eating this way will help you convert from carb-burning mode to fat burning, as well, so it provides many benefits beyond seizure control. According to Dr. Seyfried, the mechanism by which the ketogenic diet manages seizures is not clear, but the results speak for themselves. You can learn more about the ketogenic diet here.

Want to Boost Your Brainpower? Try This Exercise ‘Prescription’

The more active you stay, the better your brain (and overall health) is likely to be. This includes not only specifically engaging in exercise and other physically demanding activities but also making an effort to sit less. To get all the benefits exercise has to offer, you’ll want to strive for a varied and well-rounded fitness program that incorporates a variety of exercises. I recommend incorporating the following types of exercise into your program:

    • High-Intensity Interval (Anaerobic) Training: This is when you alternate short bursts of high-intensity exercisewith gentle recovery periods. The HIIT approach I personally prefer and recommend is the Peak Fitness method of 30 seconds of maximum effort followed by 90 seconds of recuperation.

I personally modified the number of repetitions from 8 to 6 this year, as it was sometimes just too strenuous for me to do all 8. So by listening to my body and cutting it back to 6 reps, I can now easily tolerate the workout and go full out. You can see a demonstration of Peak Fitness in the video I did.

    • Strength Training: If you want, you can increase the intensity by slowing it down. You need enough repetitions to exhaust your muscles. The weight should be heavy enough that this can be done in fewer than 12 repetitions, yet light enough to do a minimum of four repetitions. It is also important NOT to exercise the same muscle groups every day. They need at least two days of rest to recover, repair and rebuild. For more information about using super slow weight training as a form of HIIT, please see my interview with Dr. Doug McGuff.
    • Core Exercises: Your body has 29 core muscles located mostly in your back, abdomen and pelvis. This group of muscles provides the foundation for movement throughout your entire body, and strengthening them can help protect and support your back, make your spine and body less prone to injury and help you gain greater balance and stability.

Exercise programs like Pilates, yoga and Foundation Training are great for strengthening your core muscles, as are specific exercises you can learn from a personal trainer.

    • Stretching: My favorite type of stretching is Active Isolated Stretching (AIS) developed by Aaron Mattes. With AIS, you hold each stretch for only two seconds, which works with your body’s natural physiological makeup to improve circulation and increase the elasticity of muscle joints. This technique also allows your body to repair itself and prepare for daily activity. You can also use devices like the Power Plate to help you stretch.
    • Non-Exercise Activity: One of the newest recommendations I have is based on information from NASA scientist Dr. Joan Vernikos, who I recently interviewed: simply set a timer when you are sitting and stand up every 10 minutes. I even modify this further by doing jump squats at times in addition to standing up. This will help counteract the dangerous consequences of excessive sitting.

Going to the gym a few times a week for an hour simply isn’t going to counteract hours upon hours of chronic uninterrupted sitting, which essentially mimics a microgravity situation, i.e. you’re not exerting your body against gravity. Only frequent non-exercise movement will do that. The key point is to move and shift position often, when you’re sitting down. Meaning, you want to interrupt your sitting as often as possible.

Multiple sclerosis patients are missing out on drugs.

Only 40% of people eligible for drugs to combat multiple sclerosis in the UK are actually taking them, says a report from the MS Society.

A survey of more than 10,000 adults with MS showed that many were missing out on the seven licensed medicines approved for use.

The charity said a lack of information and access to specialists was to blame.


It is calling for the government to provide a personalised care plan to every person with MS.

The MS Society’s survey and accompanying report showed that there were differences in access to disease-modifying treatments (DMTs) across the four nations of the UK.

These are medicines that can reduce the frequency and severity of MS attacks, and in some cases can slow the progression of the disabling condition.

Someone living in Northern Ireland with MS was twice as likely to be taking a DMT (68%) than someone with the condition in Wales (30%), for example.

Access to treatment in Scotland and England was only a little higher at 36% and 40%.

What is multiple sclerosis?

Multiple sclerosis (MS) is a neurological condition that affects around 100,000 people in the UK.

Most patients have it diagnosed between the ages of 20 and 40, but it can affect younger and older people too.

Almost three times as many women as men have MS.

In Europe, additional research shows that only Poland and Romania have a smaller proportion of people with MS taking licensed medicines.

Routine assessment

The charity’s report said that being well informed about the medicines available was crucial.

Those who felt they had enough information about medicines were 32% more likely to be taking a DMT, the survey found, and those with access to a specialist MS nurse or neurologist were more than twice as likely to be taking the appropriate drugs.

Northern Ireland is the only place in the UK where most people with MS are routinely invited every six months to see a neurologist or MS nurse for a review.

This means that people with MS are constantly having their treatment options assessed, the report says.

As a result, they are more likely to get the information they need and discuss issues such as side-effects.

UK licensed medicines for MS

  • Avonex, Betaferon, Rebif and Copaxone were all made available on the NHS in 2002 throughout the UK.
  • Extavia was licensed in 2009 and reduces relapses by a third.
  • Tysabri is a monthly infusion administered by a healthcare professional. It can reduce the number of relapses by an estimated 67% and slow disability. It was approved for use on the NHS across the UK in 2007.
  • Gilenya, the first pill for MS, is said to reduce relapse rates by 54-60% and slows disability progression by around 30%. It was approved in 2012.

Yet this may not be the only solution. Forty-one per cent of those who said they did have enough information about drug treatments still did not take a disease-modifying treatment.

The report concluded: “This could be due to barriers to accessing medicines; because individuals make an informed decision not to take them; or because they don’t know what information is out there that they could have access to, such as around new treatments or new evidence of efficacy.”

New policy

Nick Rijke, director for policy and research at the MS Society, said people with multiple sclerosis were facing a lottery.

“These findings worryingly suggest that the likelihood of someone receiving a life-changing treatment is often based on luck – like where they live or how helpful their healthcare professional is – rather than their genuine clinical need.

“When it comes to prescription rates, the UK ranks 25th out of 27 European countries. Given the relative wealth of the UK this is simply unacceptable.”

The MS Society is now calling on all four governments in the UK to ensure every person with MS has a personalised treatment, care and support plan, with two comprehensive reviews each year.

Ed Holloway, head of care and services research at the MS Society, said that because some MS drugs were costly, they were often not offered when they should be because of restricted NHS budgets.

A spokesman for NHS England, which has recently taken on the commissioning of treatment for MS from primary care trusts, said a new policy from 1 April would mean that people across England would have the same access to treatment.

“By making decisions nationally about specialist treatments, we are confident that patients will now be able to receive the treatment they need, irrespective of where they live.

“As with all policies, we will continue to collect and review the outcome of treatments for patients and consider them when our policy is reviewed.

“If a patient has concerns about the treatment they are receiving we would urge them to speak to their GP or consultant.”





Poststroke Seizures.

Stroke is the most common cause of seizures in the elderly, and seizures are among the most common neurologic sequelae of stroke. About 10% of all stroke patients experience seizures, from stroke onset until several years later. This review discusses current understanding of the epidemiology, pathogenesis, classification, clinical manifestations, diagnostic studies, differential diagnosis, and management issues of seizures associated with various cerebrovascular lesions, with a focus on anticonvulsant use in the elderly.

Poststroke seizures are a common and treatable phenomenon, whereas the development of epilepsy is relatively rare. Cerebrovascular lesions associated with the development of seizures include the following: intracerebral (parenchymal) and subarachnoid hemorrhage and cerebral venous thrombosis, with or without venous infarction; lesions involving the cerbral cortex; larger neurologic deficits or disability at presentation; and revascularization procedures involving the extracranial internal carotid artery. The treatment of poststroke seizures is no different than the approach to treatment of partial-onset seizures due to other cerebral lesions, and poststroke seizures usually respond well to a single antiepileptic drug. Given their tolerability, the newer generations of anticonvulsant agents hold promise in treating older patients. Given the low incidence of poststroke epilepsy, there is no indication for seizure prophylaxis in patients with acute ischemic stroke who have not had a well-documented first event. The need for chronic anticonvulsant use should be evaluated periodically, perhaps every 6 months. Despite the absence of clinical data documenting effectiveness, most patients presenting with intracerebral or subarachnoid hemorrhage should receive short-term antiepileptic prophylaxis.45– 46

Future areas of research regarding poststroke seizures include assessing their impact on initial lesion size and on delayed patient outcomes, determining the appropriateness of chronic antiepileptic therapy after a single seizure, and establishing risk factors for the reperfusion syndrome. Poststroke epilepsy may also become an important basic model in research that aims to prevent the transformation of injured cerebral tissue into an epileptic focus.


Source: JAMA


New experimental and clinical links between the hippocampus and the dopaminergic system in Parkinson’s disease.

Parkinson’s disease is a common progressive neurodegenerative disease, of which the main neuropathological hallmark is dopaminergic neuronal loss. Increased attention has been directed towards non-motor symptoms in Parkinson’s disease, such as cognitive impairment and behavioural disorders. Clinical and experimental findings support the view that the hippocampus, a temporal lobe structure involved in physiological learning and memory, is also implicated in the cognitive dysfunction seen in some patients with Parkinson’s disease. Moreover, emerging data suggest interactions between the dopaminergic systems and the hippocampus in synaptic plasticity, adaptive memory, and motivated behaviour. This structure is also implicated in the pathophysiology of other non-motor symptoms, such as impulse control disorders, anosmia, and fatigue. Evidence from clinical observations and experimental studies suggest a complex hippocampal cross-talk among the dopaminergic and other transmitter systems. Furthermore, neurotrophic factors might interact with the hippocampal dopaminergic system having possible implications on the non-motor symptoms seen in patients with Parkinson’s disease.

Source: Lancet


P-glycoprotein expression and function in patients with temporal lobe epilepsy: a case-control study.


Studies in rodent models of epilepsy suggest that multidrug efflux transporters at the blood—brain barrier, such as P-glycoprotein, might contribute to pharmacoresistance by reducing target-site concentrations of antiepileptic drugs. We assessed P-glycoprotein activity in vivo in patients with temporal lobe epilepsy.


We selected 16 patients with pharmacoresistant temporal lobe epilepsy who had seizures despite treatment with at least two antiepileptic drugs, eight patients who had been seizure-free on antiepileptic drugs for at least a year after 3 or more years of active temporal lobe epilepsy, and 17 healthy controls. All participants had a baseline PET scan with the P-glycoprotein substrate (R)-[11C]verapamil. Pharmacoresistant patients and healthy controls then received a 30-min infusion of the P-glycoprotein-inhibitor tariquidar followed by another (R)-[11C]verapamil PET scan 60 min later. Seizure-free patients had a second scan on the same day, but without tariquidar infusion. Voxel-by-voxel, we calculated the (R)-[11C]verapamil plasma-to-brain transport rate constant, K1 (mL/min/cm3). Low baseline K1 and attenuated K1 increases after tariquidar correspond to high P-glycoprotein activity.


Between October, 2008, and November, 2011, we completed (R)-[11C]verapamil PET studies in 14 pharmacoresistant patients, eight seizure-free patients, and 13 healthy controls. Voxel-based analysis revealed that pharmacoresistant patients had lower baseline K1, corresponding to higher baseline P-glycoprotein activity, than seizure-free patients in ipsilateral amygdala (0·031 vs 0·036 mL/min/cm3; p=0·014), bilateral parahippocampus (0·032 vs 0·037; p<0·0001), fusiform gyrus (0·036 vs 0·041; p<0·0001), inferior temporal gyrus (0·035 vs 0·041; p<0·0001), and middle temporal gyrus (0·038 vs0·044; p<0·0001). Higher P-glycoprotein activity was associated with higher seizure frequency in whole-brain grey matter (p=0·016) and the hippocampus (p=0·029). In healthy controls, we noted a 56·8% increase of whole-brain K1 after 2 mg/kg tariquidar, and 57·9% for 3 mg/kg; in patients with pharmacoresistant temporal lobe epilepsy, whole-brain K1 increased by only 21·9% for 2 mg/kg and 42·6% after 3 mg/kg. This difference in tariquidar response was most pronounced in the sclerotic hippocampus (mean 24·5% increase in patients vs mean 65% increase in healthy controls, p<0·0001).


Our results support the hypothesis that there is an association between P-glycoprotein overactivity in some regions of the brain and pharmacoresistance in temporal lobe epilepsy. If this relation is confirmed, and P-glycoprotein can be identified as a contributor to pharmacoresistance, overcoming P-glycoprotein overactivity could be investigated as a potential treatment strategy.

Source: Lancet

Siponimod for patients with relapsing-remitting multiple sclerosis (BOLD): an adaptive, dose-ranging, randomised, phase 2 study.


Siponimod is an oral selective modulator of sphingosine 1-phosphate receptor types 1 and type 5, with an elimination half-life leading to washout in 7 days. We aimed to determine the dose-response relation of siponimod in terms of its effects on brain MRI lesion activity and characterise safety and tolerability in patients with relapsing-remitting multiple sclerosis.


In this double-blind, adaptive dose-ranging phase 2 study, we enrolled adults (aged 18—55 years) with relapsing-remitting multiple sclerosis at 73 medical centres in Europe and North America. We tested two patient cohorts sequentially, separated by an interim analysis at 3 months. We randomly allocated patients in cohort 1 (1:1:1:1) to receive once-daily siponimod 10 mg, 2 mg, or 0·5 mg, or placebo for 6 months. We randomly allocated patients in cohort 2 (4:4:1) to siponimod 1·25 mg, siponimod 0·25 mg, or placebo once-daily for 3 months. Randomisation was done with a central, automated system and patients and investigators were masked to treatment assignment. The primary endpoint was dose-response, assessed by percentage reduction in monthly number of combined unique active lesions at 3 months for siponimod versus placebo; this endpoint was analysed by a multiple comparison procedure with modelling techniques in all patients with at least one MRI scan up to 3 months. We assessed safety in all patients who received at least one dose of study drug. This study is registered with ClinicalTrials.gov, number NCT00879658.


Between March 30, 2009, and Oct 22, 2010, we recruited 188 patients into cohort 1 and 109 patients into cohort 2. We showed a dose-response relation (p=0·0001) across the five doses of siponimod, with reductions in combined unique active lesions at 3 months compared with placebo of 35% (95% CI 17—57) for siponimod 0·25 mg (51 patients included in the primary endpoint analysis), 50% (29—69) for siponimod 0·5 mg (43 patients), 66% (48—80) for siponimod 1·25 mg (42 patients), 72% (57—84) for siponimod 2 mg (45 patients), and 82% (70—90) for siponimod 10 mg (44 patients). In patients treated for 6 months, 37 (86%) of 43 patients who received siponimod 0·5 mg had adverse events (eight serious), as did 48 (98%) of 49 patients who received siponimod 2 mg (four serious), 48 (96%) of 50 patients who received siponimod 10 mg (three serious), and 36 (80%) of 45 controls (none serious). For individuals treated to 3 months, 38 (74%) of 51 patients who received siponimod 0·25 mg had adverse events (none serious), as did 29 (69%) of 42 patients who received siponimod 1·25 mg (two serious) and 13 (81%) of 16 controls (none serious).


Therapeutic effects of siponimod on MRI lesion activity in model-based analyses and its tolerability in relapsing-remitting multiple sclerosis warrant investigation in a phase 3 trial.

Source: Lancet

Magnetic resonance angiography of intracranial and extracranial arteries in patients with spontaneous migraine without aura: a cross-sectional study.



Extracranial arterial dilatation has been hypothesised to be the cause of pain in patients who have migraine without aura. To test that hypothesis, we aimed to measure extracranial and intracranial arteries during attacks of migraine without aura.


In this cross-sectional study, we recruited patients aged 18–60 years from the Danish Headache Centre and via announcements on a Danish website. We did magnetic resonance angiography during spontaneous unilateral migraine attacks. Primary endpoints were difference in circumference of extracranial and intracranial arterial segments comparing attack and attack-free days and the pain and the non-pain side. The extracranial arterial segments measured were the external carotid (ECA), the superficial temporal (STA), the middle meningeal (MMA), and the cervical part of the internal carotid (ICAcervical) arteries. The intracranial arterial segments were the cavernous (ICAcavernous) and cerebral (ICAcerebral) parts of the internal carotid, the middle cerebral (MCA), and the basilar (BA) arteries. This study is registered at Clinicaltrials.gov, numberNCT01471314.


Between Oct 12, 2010, and Feb 8, 2012, we recruited 78 patients, of whom 19 women had a scan during migraine and were included in the final analysis. On migraine compared with non-migraine days, we detected no statistically significant dilatation of the extracranial arteries on the pain side (ECA, mean difference 1·2% [95% CI −5·7 to 8·2] p=0·985, STA 3·6% [–3·7 to 11·0] p=0·532, MMA 1·7% [–1·7 to 5·2] p=0·341, and ICAcervical 2·3% [–0·3 to 4·9] p=0·093); the intracranial arteries were more dilated during attacks (MCA, 13·0% [6·4 to 19·6] p=0·001, ICAcerebral 11·5% [5·6 to 17·3] p=0·0004, and ICAcavernous 11·4% [5·3 to 17·5] p=0·001), except for the BA (1·6% [–2·7 to 5·9] p=0·621). Compared with the non-pain side, during attacks we detected dilatation on the pain side of the intracranial arteries (MCA, mean difference 10·5% [0·7–20·3] p=0·044, ICAcerebral (14·4% [4·6–24·1] p=0·013), and ICAcavernous (9·1% [3·9–14·4] p=0·003) but not of the extracranial arteries (ECA, 2·1% [–3·8 to 9·2] p=0·238, STA, 3·6% [–3·7 to 10·8] p=0·525, MMA, 2·7% [–1·3 to 5·6] p=0·531, and ICAcervical, 5·0% [–0·5 to 10·4] p=0·119).


Migraine pain was not accompanied by extracranial arterial dilatation, and by only slight intracranial dilatation. Future migraine research should focus on the peripheral and central pain pathways rather than simple arterial dilatation.

Source: http://www.sciencedirect.com

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