Migraine with Aura
According to ICDH Migraine with aura has the following characteristics:
Migraine with aura:
A. At least 2 attacks fulfilling criteria B-D
B. Aura consisting of at least one of the following, but no motor weakness:
1. fully reversible visual symptoms including positive features (e.g., flickering lights, spots or lines) and/or negative features (i.e., loss of vision)
2. fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (i.e., numbness)
3. fully reversible dysphasic speech disturbance
C. At least two of the following:
1. homonymous visual symptoms and/or unilateral sensory symptoms
2. at least one aura symptom develops gradually over 5 minutes and/or different aura symptoms occur in succession over 5 minutes
3. each symptom lasts 5 and 60 minutes
D. Headache fulfilling criteria B-D for 1.1 Migraine without aura begins during the aura or follows aura within 60 minutes.
E. Not attributed to another disorder.
Migraine with aura comes in attacks of reversible focal neurological symptoms that usually develop gradually over 5-20 minutes and last for less than 60 minutes. The headache that comes with these attacks has the features of migraine without aura, although sometimes there is an accompanying headache which lacks migrainous features or even no headache at all. Migraine with aura was called “Classical Migraine” in the 1962 Classification of Headache[ii], an earlier classification and it comprises about 30 % of migraine attacks.
In many cases these patients know exactly what their diagnosis is and have known it since they were a child or a teenager and they had their first visual attack which resulted in a hurried, dramatic visit to a reassuring ophthalmologist or neurologist. These patients usually come in later for treatment and sometimes for MRI scanning to be certain that the diagnosis is truly migraine and not something else more worrisome like an aneurysm, a TIA, which is a warning of a stroke, or a stroke. Occasionally patients have both migraine with and without aura where the predominant headache is usually migraine without aura.
Some patients have only the aura symptoms and no headache so they are not aware that migraine is the problem they have been having. This used to be called “migraine sine hemicrania” where sine is Latin for “without” but ICDH-II calls this ”Typical aura without headache.”[iii] A large portion of these patients are middle aged women who swear they have never had a migraine or any other significant headache in their life. Sometimes they may admit they also have “sinus headaches” which on close analysis resemble migraine without aura and they may have a number of migraine links--like motion sickness, hungry headache, menstrual headaches, and the like.
The visual images which slowly trace across the patient’s visual field come from migraine induced spreading waves of depolarization occurring in the occipital cortex of the brain. This statement requires some explanation. Light enters the eye through the pupil, is focused as it passes through the lens, and then it impacts on the light sensitive tissue of the rods and cones in the retina. Next the signal, much like electricity passing through a circuit, passes through the optic nerve, to the optic chiasm where it is split in half. Then in a microsecond the signal goes through the optic radiations to the occipital cortex in the back of the brain on both sides. So light comes in the eye in front and is quickly sent to the occipital cortex in the back of the brain where it is perceived.
Spreading waves of depolarization are created in the occipital cortex in the migraine with aura sensitive brain which travel outward in concentric circles, much like the waves of water at a pond after one throws a rock in its surface. Neural tissue is made up on the cellular level by neurons which quickly fire off, or depolarize, as they release energy and then recharge
These spreading waves were discovered and written about by Aristides Leão[v] in 1944 in an article he published in the Journal of Neurophysiology.
Originally, Leão intended to study "experimental epilepsy," specifically the propagation of electrically provoked seizure discharges in the cerebral cortex. To this end, he opened the skull of rabbits under anesthesia and arranged a row of chlorided silver wire electrodes in contact with the cortical surface. Of these electrodes, one pair served for stimulation and the others, connected in six staggered pairs, for bipolar recording of the electrocorticogram (ECoG) at increasing distance from the stimulated points. Unexpectedly, instead of seizure-like discharge, the stimulation was frequently followed by a flattening of the spontaneous ECoG waves traced by the Grass oscillograph. The ECoG activity in the electrodes nearest to the stimulated area was silenced first, and then the extinction spread in orderly sequence from one electrode pair to the next, eventually covering almost all the cortex. Recovery of the ECoG waves occurred in the same sequence as their previous depression.
Patients report spots or holes or seeing half of things. Sometimes they see images with jagged borders bent in the shape of a large letter C. A spot or hole in the visual field is called a scotoma. They may have negative visual effects where they lose vision or positive visual effects where they see something not of this world or part of normal vision. The positive effects are noted with the eyes closed and many patients through the centuries have drawn pictures of what they have seen during their migraine experiences. I have some of these pictures in my office and show them to patients to see if they strike a chord and most of the time they do. Usually I like the patient to draw what they see and they can almost always do this, sometimes quite well and with vivid detail, as if the images had been burned into their memory.
Representative images of migrainous images follow:
[i] The International Classification of Headache, 2nd Edition. Migraine with Aura. Cephalalgia 2004. 24; (Supplement 1): 25-27.
[ii] Classification of Headache. JAMA. 1962;179(March 3):717-718.
[iii] The International Classification of Headache, 2nd Edition. Typical aura without headache. Cephalalgia 2004. 24;(Supplement 1):28.
[iv] Lauritzen M. Cortical spreading depression as a putative migraine mechanism. Trends Neurosci, 1987;10:8-13.
[v] Leao AAP, Spreading depression of activity in the cerebral cortex. J Neurophysiol. 1944;7:359-390.