Posts Tagged ‘aura’

h1

Open Journal Article: Patients with migraine with aura have increased flow mediated dilation

2010 March 16

Fabrizio Vernieri, Leo Moro, Claudia Altamura, Paola Palazzo, Raffaele Antonelli Incalzi, Paolo Maria Rossini and Claudio Pedone.

BMC Neurology 2010, 10:18doi:10.1186/1471-2377-10-18
Published:     10 March 2010
Abstract (provisional):

Background

Endothelium-derived nitric oxide (NO) mediates the arterial dilation following a flow increase (i.e. flow-mediated dilation, FMD), easily assessed in the brachial artery. NO is also involved in cerebral hemodynamics and it is supposed to trigger vascular changes occurring during migraine. This study aimed at investigating whether migraine patients present an altered response to NO also in the peripheral artery system.

Methods

We enrolled 21 migraineurs (10 with aura [MwA], 11 without aura [MwoA]), and 13 controls. FMD was evaluated with ultrasound in all subjects by measuring the percentage increase of the brachial artery diameter induced by hyperaemia reactive to sustained cuff inflation around the arm above systolic pressure. FMD values were then normalized for shear stress.

Results

Normalized FMD values were higher in patients with MwA (28.5 10-2%.s) than in controls (9.0 10-2%.s) and patients with MwoA (13.7 10-2%.s) (p<0.001). FMD was over the median value (19%) in 23.1% of controls, in 45.5% of the MwoA patients, and in 90% of the MwA patients.

Conclusions

Migraineurs with aura present an excessive arterial response to hyperaemia, likely as an effect of an increased sensitivity to endothelium-derived nitric oxide. This phenomenon observed peripherally might reflect similar characteristics in the cerebral circulation.

You can read the full article here: http://www.biomedcentral.com/content/pdf/1471-2377-10-18.pdf

Advertisements
h1

Migraines (Part 3) (Last Edited: 2009 Nov 19)

2008 August 16

Go back to Part 2 | Go on to Part 4

This is part three of a four part series about migraine. You can use the links above or at the end of this page to go back or forward. Or you can jump to any part from the Migraine FAQs page link.


The exact triggers for migraine attack are uncertain, and may vary widely. Sufferers usually keep a diary to try to identify:

  1. Triggers,
  2. Other things affecting migraine frequency,
  3. Things that may prevent attacks,
  4. Things that might predict impending attack.

Commonly suggested triggers include: allergies, things in the environment like lighting, noise or scents, stress, changes in sleep patterns, cigarette smoke, alcohol, certain foods, and weather or seasonal changes.

All auras are the results of “cortical spreading depression”. This is a self-propagating wave of cell depolarisation that travels through the cortex. The cortex is the crinkled outer or “higher” part of the brain. During this phase, the affected neurons go into a kind of hibernation. The exact mechanism of neuronal “firing” depends on a critical flow of sodium, potassium and calcium ions. During the depressed state, neurons rest high in potassium, and low in sodium and calcium. Cell “firing”, releases neurotransmitter chemicals, when the inside of the cell is positively charged relative to the outside. After firing the cells become strongly negatively charged on the inside by allowing potassium ions to flow out. This returns the neurons to their resting states. But neurons can become hyper-polarised, or inhibited, for some time after intense stimulation.

The phase of hyper-excitability followed by inhibition in cortical spreading depression may explain the changes in blood blow recorded before the pain phase of migraine. Active neurons need energy, which is transported by blood. When inhibited, they need less blood.

Further studies link cortical spreading depression with description of visual aura. The wave travels across the cortex at between two and three millimetres per minute. The visual aura match with those expected given that rate of spread. The change of sensations also match observed spreading depressions.

Migraine is a complex disorder that shows a strong genetic component. But studies show that it is a range of genetic mutations that affect migraine rather than a single gene. This is called a poly-genetic disorder. There is also evidence of non-genetic parts. The strongest evidence for both comes from identical twin studies. These show that identical twins are more likely to share migraine that non-identical twins. But even identical twins do not necessarily both share migraine. One may suffer migraine, while the other does not.

Recent evidence also supports the view that at least one type of migraine is caused by faulty genes. These govern the ion channels talked about earlier. This is a newly recognised condition called “channelopathy”, which is also responsible for other conditions like cardiac arrhythmia and seizures. But it is not yet known whether this mechanism is common to all forms of migraine.

There is also another controversial theory about a common heart defect. It is called “patent foramen ovale” or PFO. It is where a small hole in the heart allows oxygen-rich and oxygen-poor blood to mix. It is controversial because the way PFO may cause migraine is unclear. Closing the hole in migraine patients has shown some results, but they are not statistically significant.

Go back to Part 2 | Go on to Part 4

h1

Migraines (Part 2) (Last Edited: 2009 Nov 19)

2008 August 9

Go back to Part 1 | Go on to Part 3

This is part two of a four part series about migraine. You can use the links above or at the end of this page to go back or forward. Or you can jump to any part from the Migraine FAQs page link.


Migraine can occur with what are called “aura”. These are mild hallucinations that vary from person to person, or between attacks. Not all sufferers have aura. In those that do, not all migraine attacks have aura. They can occur at different stages of migraine: before, during or after the pain phase. Some migraines, and some migraine sufferers, do not get headache even though they get aura. And some migraine sufferers can have permanent aura.

Typical precursory auras include a variety of “scintillating scotoma”. These appear as a small spot of flashing light that generally expands into the visual field. They can take on several forms; the most typical is a zigzag line. Other aura can include “paresthesia”: pins-and-needles sometimes followed by numbness, which spreads through certain parts of the body. Some form of “aphasia” can also follow: ranging from problems speaking, through to whole loss of language comprehension. All auras are temporary.

Migraine can occur with or without aura, and with or without headache. Migraines typically last from seven hours to a day or so, passing through four distinct phases. The first, or “prodrome”, phase can occur hours or sometimes days before the pain phase. This occurs in forty to sixty percent of sufferers. It may manifest as altered mood, irritability, depression, fatigue, food cravings, muscle stiffness, and so on.

The second, or “aura”, phase occurs before the pain phase. Twenty to thirty percent of sufferers have migraine with aura. The aura can include visual disturbance, pins-and-needles, numbness, phantom smells, problems speaking, and so on. This phase usually lasts less than sixty minutes. The pain phase manifests as moderate to sever head pain. It is usually on one side of the head and worsened by physical activity. This phase can last between four and seventy-two hours in adults. Children generally have shorter pain phases.

The pain itself has been compared to being worse than childbirth or a gun-shot wound. It is usually accompanied by other symptoms like nausea and (if untreated) vomiting. Sensitivity to light and sound are commonplace.

The final phase of migraine, or “postdrome”, may last a similar length of time to the headache phase. Usually a good night’s rest ends the attack. The postdrome phase may leave the sufferer “washed out”, listless, irritable or moody, whereas others may feel refreshed or euphoric.

Go back to Part 1 | Go on to Part 3

h1

Welcome

2008 June 27

Thanks for visiting today.

I will be starting my new blog on Friday 1st August.

I will be writing on a number of topics. I hope you will feel able to contribute constructively with your own experiences or questions.

1. Inability or Limited Ability to Visualise (“Cannot visualise”, “unable to visualise”).

For many years now I have noticed that I can no longer bring forward detailed images in my mind’s eye. I can provide some descriptive details about things, but cannot actually picture the image clearly. For example, I can describe a ripe banana as a curved yellow fruit often with a polygonal shape in cross-section with a tough outer blotchy skin and soft interior, and the fruit tapering at either end.

The variation is ability to visualise seems only recently to have been acknowledged medically. So far I have found only one study, but this has found correlations between both functional magnetic resonance imaging (fMRI) and novel psychophysiological test and test subjects’ subjective appraisal of their ability to visualise.

I offer a forum to others who experience this or who wish to understand more about the phenomenon. I especially would like to hear from researchers or medical practitioners who know more about it.

2. Poor Visual Memory Recall (With Poor Episodic Memory).

I think, though ironically cannot be certain, that before I first encountered the visualisation problem described above, I had near-photographic memory. Since then my memory also deteriorated. I can best describe the situation now as like having a photo album in which someone else wrote vague descriptions on my life events such as “I think that was so-and-so”, or “I think I was in such-and-such place”, or “This would be about 1994”, and then removed all the photographs. As such when asked to rely on episodic memory recall this can be unreliable. Linguistically descriptive recollection can take me so far. In work environments I compensate by taking organised notes (and making use of any supplied software). In social environments it makes small-talk difficult, since I cannot so easily organise the things others have said and the time to recall past events by other routes often means the conversation has moved on. It also makes finding questions to ask others about themselves difficult. As a result, I find many friendships don’t last.

The memory problem also does not appear to be described at all in medical literature. This may explain why I have had no luck in getting any kind of response at all from doctors on this. I do know of two other people who say they have this problem, both of which also report inability to visualise.

I note that the memory must exist in order for the description to be possible, and because I have vivid dreams. But places visited or lived in after the problem first started are substituted by others that have some contextual similarity. For example, the university I recently worked at may appear as my high school from before the start of this condition.

I offer a forum to others who experience this or who wish to understand more about the phenomenon. I especially would like to hear from researchers or medical practitioners who know more about it.

3. Migraine.

I am currently unable to work because of migraine attacks (usually with aura) between 1 and 2 per week, with significant variation. The memory problem above, and lack of medical recognition, also means that it is difficult to help my consultant diagnostically when he asks such questions as “Do your migraine attacks favour the left or right side of your head?”

The problem is complicated because I also have 10% mobility in my neck and shoulder muscles that itself causes chronic (and possibly acute) head pain. At present I am unclear whether this is related to an underlying migraine cause, or is a distinct condition. I have noted one classical migraine attack after which my neck movement freed up for a short while, though. Chronic pain is that which persists over a long period, acute is usually much shorter (though acute migraine pain can last up to 72 hours in rare occurrences).

Migraine aura mean neurological phenomena usually of a subjective nature that the sufferer can observe but is not observable to another (with certain exceptions, such as vomiting). Common acute examples include:

  • Nausea,
  • Pins and needles followed by numbness,
  • Scintillating scotoma – a visual effect characterised by flickering bright light.

Other aura that seem to be chronic include:

  • “Visual snow” – an appearance like dancing fireflies but in bright light such as when looking at blue sky (not entirely sure if this is the right name),
  • Palinopsia – a variation of the normal “afterimages” seen to persist after looking at a bright light,
  • “Spontaneous afterimages” in which such afterimages appear without stimulus,
  • “Pinpoint flashes” – brief, tiny and infrequent flashes of light in a dark environment,
  • “Twitches” – twitching of individual muscle fibres or nerves.

These are examples of chronic aura that I have. The first two are described medically and associated with a variant of migraine called “persistent aura without infarction”, in which the sufferer basically has a prolonged aura state. This is poorly understood at present. The latter three are examples I gave other sufferers in a forum, which some agreed they also have. I have been unable to find specific medical descriptions for these.

I offer a forum to others who experience this or who wish to understand more about the phenomenon.

4. Dynamical Systems.

These relate to a certain class of systems across many scientific disciplines (such as physics, chemistry, biology and so on), that display self-organising behaviour. Strictly, though, the mathematical description relates to the mathematical description of systems’ behaviour in its ambient space. This relates to an area of mathematics and interrelated disciplines called complexity theory.

One theory of migraine causation suggests that scintillating scotoma are the sufferer’s observed result of a cortical spreading depression. This is an example of a self-propagating wave of cellular depolarisation in the structure in the brain concerned with memory, attention, awareness and so on called the cortex.

I believe much of the work in this field may have application in sociology and psychology also, and be translatable into a new approach to philosophy. I would like to have taken up research on this and had a place at Warwick University in England, a leading university in psychological research. But health problems and employment instability have meant I could not afford to take up the place. But I have maintained an amateur interest.

5. Buddhism.

I am also a practising Buddhist, though not member of a geographical sangha at present because of health constraints.

6. Creative Writing and Writing Novels and Screenplays.

In the past I have enjoyed writing short stories, within the limitations imposed by my problems with visualisation and memory. With the availability of the Internet and sites such as Flickr, I can now search for and find information and images to describe that overcome the handicap.

I am working on a theory of the story, and am working on a screenplay and on a novel. I swap between the two whenever I get stuck on one of them! I will share the ups and downs of this process.

I look forward to meeting you.