Are Classical and Common Migraine Different Entities?

Marcia Wilkinson, D.M., F.R.C.P and J.N. Blau, M.D., F.R.C.P

From the City of London Migraine Clinic, 22 Charterhouse Square, London, EC1, England.

Accepted for Publication: August 15, 1984

SYNOPSIS

Classical migraine has been described as a familial disorder characterized by recurrent attacks of headachewidely variable in intensity, frequency and duration.1 Attacks are commonly unilateral and are usually associatedwith anorexia, nausea and vomiting. In classical migraine the headache is preceded or accompanied by transientfocal neurological phenomena e.g. visual, sensory or speech disturbances. Nonclassical or common migraine isnot associated with sharply defined focal neurological disturbances and occurs more frequently.

Are these two conditions the same or do they differ in some fundamental way? The evidence for and againsttheir being a single entity is discussed. The conclusion reached is that common and classical migraine areprobably different aspects of the same disorder.

(Headache 25:211-212, 1985)

INTRODUCTION

Good research is often thought provoking and can make us re-examine accepted ideas. At times it poses new questions.Falling into this category are the cerebral blood flow studies of Olesen and his colleagues.2,3,4 Their results showed that inclassical migraine a wave of diminished blood flow sweeps across the brain at approximately 2 mm per minute, very similar tothe rate of progression found by Leao5,6,7 after stimulating the cerebral cortex in different ways and now called after him -Leao's spreading depression.

However, in common migraine, Olesen et al2 did not find these alterations of blood flow, and concluded that there werefundamental differences between classical and common migraine.

It is this conclusion that we wish to consider from the clinical and experimental point of view.

Examination of the clinical evidence. Wolfson and Graham8 reported a patient with common and classical migraine.This combination is well known and seen by all in clinical practice. It would be surprising for two different entitites to bepresent in the same patient.

In our clinical experience patients fall into three groups:

1. Patients who have an aura before every attack.

2. Patients who have an aura once or twice in their life.

3. Patients who fall between these two categories and who may have an aura in perhaps two or three attacks out of ten.Should all these groups be said to be suffering from classical migraine and if so what do we call the headaches that groups 2and 3 have without an aura?

We have studied 14 patients with migraine, all of whom have auras either before every attack or before some attacks. Weasked them to record their experiences and in particular to see if there was any difference between the headache that followsan aura and a headache that occurs without a preceding aura.

The patients recorded that there was no difference between the two kinds of headaches in duration, quality or severity Atypical story is that of a boy of twelve who has had migraine for five years. The pain always starts in the left temple andspreads across the forehead. He gets between one and four headaches a month. In two out of five attacks he has visualdisturbances which he describes as bright flashes of light or blanknesses. He is quite sure that the headache is the samewhether or not he has the lights.

One of us (MW) has suffered from migraine attacks since the age of five. Most attacks are not preceded by an aura;perhaps once in 2-5 years a classical aura is present. The rest of the attacks, occurring at approximately 3-weekly intervals,have no warning. However, the headaches, with or without an aura, have exactly the same quality, duration and associatedsymptoms of nausea and vomiting. It is difficult to accept that there are different pathophysiological processes going on in thesame patient, although some attacks are mild, others moderate and some occasionally severe.

Both classical and common migraine respond to ergotamine tartrate, and other therapies including metoclopramide andanalgesics.

A review of the experimental evidence. 1. Numbers. The initial reports by Olesen and his colleagues2 related to eightpatients. Six had classical migraine, one (case 234) had migraine but whether classical or common was uncertain, and one(case 109) did not suffer from migraine but from chronic headache and dementia. In the ensuing four years the numbershave increased to 42 in total. This, in our opinion, is an adequate number on which to

base conclusions.

2. Red wine precipitation. Olesen and his colleagues3 studied twelve patients with common migraine who could reliably induce attacks withinone hour. These twelve were given 150 ml of red wine and one in addition dark chocolate. Successful measurements were obtained eight times insix patients; the others did not develop headache. In none of the eight was any significant focal or global reduction of cerebral blood flow found atany time. It is possible that these headaches may be different from naturally occurring migraine. However, they also report twelve cases ofspontaneously occurring common migraine in which no change was found.9 It would be interesting to see a control study of red wine precipitatingclassical migraine. It is possible that the alcohol induced vasodilatation could be responsible for the CBF response.

3. Facial color. We know from clinical experience that patients with mild migraine attacks do not change in color, but when the attacks aremore severe, with vomiting, they go pale. It has been suggested that the facial color is a reflection of the meningeal color and perhaps of the braintoo. Hence it would be helpful in future papers to record the severity of the attacks, and any variation in facial appearance-the occasional patientflushing during attacks.

4. Pain and spreading depression. We know that the aura of migraine is painless and if the remaining symptoms were due to the spreadingdepression then the cortical changes, as would be expected, should also be painless. Therefore spreading depression cannot account for theheadache.

5. Cortical topography and symptoms. If the spreading depression is responsible for the aura, as the cortical changes progress anteriorlywe would have expected, by the time they reached the Sylvian fissure, they would have produced hemianaesthesia and when they reached thefrontal cortex, hemi-plegia. This progression of hemianopia, hemianaesthesia, hemiplegia, was not recorded and we have not seen it in practice,the aura seeming to remain visual. The changes recorded by the Copenhagen workers progress anteriorly and it is odd that these additionalsymptoms did not apparently occur.

6. Duration of the oligaemia. Lauritzen9 states "the hypoperfusion outlasts the focal symptoms by several hours, thereby indicating theabsence of a cause or relationship". We agree with this conclusion, implying that the cortical perfusion changes are correlated and not causal.

7. Spreading depression in humans. Leao's spreading depression has not been encountered in man by four experienced neurosurgeons.One of these, Professor Lindsay Symon (personal communication), a world authority on CBF who has specifically studied this phenomenon, hasnot seen spreading depression in man or in monkeys, nor has Dr. J. Stirling Meyer (personal communication).

8. Spreading depression and vasodilatation. Leao's spreading depression in animals is accompanied by vasoconstriction but is followed in10-15 minutes by intense vasodilatation - arterial dilatation of the order of 50% and arteriolization of venous blood. Hence the analogy is incompletebecause Olesen10 stated that patients with classic migraine "did not develop reactive hyperaemia at any point in time".

CONCLUSIONS

1. A comparison between spontaneous classical migraine and red wine induced common migraine is not necessarily valid.

2. Clinically the headache of migraine is the same in common and classical varieties.

3. CBF observations in classic migraine correspond only partially with vascular changes observed after Leao's depression: - in migraine thevaso-constriction lasted much longer, and a vasodilatory phase was absent.

4. In migraine the clinical picture did not correspond with the vascular changes - hemisensory, motor and speech disturbances were absent.

5. We are most grateful to Dr. Olesen and his colleagues for their major contributions to the study of migraine because, as a result of theirscientific investigations, we know more about what happens in attacks but there are still facets - prodromal and resolution11 - left to explain.

REFERENCES

1. Definition of Migraine. Background to Migraine. Third Migraine Symposium, 1969 p 181-2 Ed: Cochrane A. L Heinemann Medical BooksLtd. London.

2. Olesen J, Larsen B, Lauritzen M: Focal hyperemia followed by spreading oligemia and impaired activation of RCBF in classic migraine. AnnNeurol 9:344-352, 1981.

3. Olesen J, Tfelt-Hensen P, Henriksen L, Larsen B: The common migraine attack may not be initiated by cerebral is-chaemia. Lancet2:438-440, 1981.

4. Olesen J, Lauritzen M, Tfelt-Hansen P, Henriksen L, Larsen B: Spreading cerebral oligemia in classical and normal cerebral blood flow incommon migraine. Headache 22:242- 248, No. 6, 1982.

5. Leao AAP: Spreading depression of activity in the cerebral cortex. J Neurophysiol 7:359-390, 1944.

6. Leao AAP: Pial circulation and spreading depression of activity in cerebral cortex. J Neurophysiol 7:391-396, 1944.

7. Leao AAP, Morrison RS: Propagation of spreading cortical depression. J Neurophysiol 8:33-45, 1945.

8. Wolfson W, Graham JR: Development of tolerance to ergot alkaloids in a patient with unusually severe migraine. New England Journal ofMedicine 241:296-298, 1949.

9. Lauritzen M: Spreading cortical depression in migraine. The pharmacological basis of migraine therapy. Ed. by WK Amery, JM Van Nueten& A Wauquier. Pitman Publishing Ltd Bath 149-170, 1984.

10. Olesen J, Lauritzen M: The role of vasoconstriction in the pathogenesis of migraine. The pharmacological basis of migraine therapy. Ed. byWK Amery, JM Van Nueten & A Wauquier. Pitman Publishing Ltd Bath 7-19, 1984.

11. Blau JN: Migraine Pathogenesis. The neural hypothesis re-examined. J Neurol Neurosurg & Psychiatry 47:437-442, 1984.