Posts Tagged ‘pfo’


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