Migraine PDF

Preface

Headache is the commonest of all human maladies. For most of us, it is an infrequent and relatively minor inconvenience but for a substantial minority, recurrent or persistent headache is a serious disability and handicap, with significant consequences for the wider community in terms of time lost from work and treatment costs, in addition to the suffering of affected individuals.

This, however, is not just another book about headache, although inevitably this aspect is covered in depth. Rather, we have focussed on the ‘‘migraine mechanism,'' its clinical manifestations, and the occasional serious consequences that it can cause. Our observations and conclusions are based on the case histories of over 250 headache patients seen in a general neurology outpatient clinic between 1990 and 2004. Based on these observations and the extensive scientific literature on migraine, we propose two main hypotheses.

First, we believe that migraine is a fundamental property of the normal human brain; we are all potential migraineurs. Migraine is not a disease but a pathophysiological process. Anyone can experience the symptoms of migraine if their genetically determined threshold for initiation of the migraine mechanism is breached. Indeed, we would predict that almost all of us will sooner or later experience some manifestation of this process, although many may not realize the origin of the symptoms. In particular, the symptoms may not include headache. Thus, while migraine attacks are thought to afflict ‘only' 15% to 20% of the population, and most people will deny they ‘‘suffer from migraine,'' we suspect that symptoms of migrainous origin are frequently ignored or attributed to other causes. For example, one of the authors had his first migraine aura while conducting an outpatient clinic in Liverpool about twenty years ago. He felt increasingly strange and ‘‘distant'' over a number of minutes and then became aware of a bright, shimmering, partly-colored, snake-like hallucination that migrated to the left for about thirty minutes before disappearing. There was a little nausea but no headache. The cause was immediately recognized but might well have caused consternation to someone unfamiliar with such symptoms. He had a further identical attack about eight years later at a medical conference and took the opportunity to confirm that the newly developed medication sumatriptan had no effect on the aura. He has since had one or two minor headaches with some migrainous qualities, but if asked, ‘‘Do you suffer from migraine?'' the author would respond, ‘‘No.'' No doubt many readers will have had similar experiences. It is interesting to note that the ‘‘prevalance'' of migraine is substantially higher among physicians than the general population and higher still among neurologists and headache specialists.

The migraine mechanism can produce a wide range of neurological symptoms in addition to the classical visual, somasthetic, and dysphasic auras. These can be as non-descript as vague episodic visual blurring or shimmering, which might be attributed to the effects of bright lights or the ‘‘wrong glasses''; funny turns, faints, and episodes of amnesia, often erroneously ascribed to ‘‘blood pressure'' or ‘‘transient ischemia''; recurrent attacks of vertigo without evidence of underlying vestibular dysfunction; and episodic non-specific headaches or head pains, which may be attributed to ‘‘sinus'' or ‘‘arthritis in the neck.'' We suspect that many unnecessary visits to opticians, dentists, and ear, nose, and throat surgeons are made because the many manifestations of the migraine mechanism are not widely appreciated.

Our second contention is that all primary headaches are caused by the same fundamental migraine mechanism. While we are firm supporters of the attempts by the International Headache Society to provide detailed definitions of individual forms of primary headache, it must be realized that many patients do not conform to these stereotypes. ‘‘Overlap'' cases are very common, and we have seen many examples of patients with typical migraine who subsequently develop features of other primary headache disorders.We have also seen examples of aura in cluster headache, and features of trigeminal autonomic dysfunction, and Horner's syndrome, in otherwise typical migraine. While most patients certainly experience stereotyped headache attacks conforming to a particular primary headache syndrome, transformation to another form is not uncommon, and there is probably no clinical symptom that is exclusive to any particular headache syndrome. We think it is unlikely that an individual who experiences different forms of primary headache actually has several different disorders; rather, the symptoms result from the same basic process, which varies in output characteristics at different times.

All recurrent, episodic, and stereotyped primary headaches probably begin with neural activation in the brain, although whether this occurs first in the cortex or brainstem remains unclear and it is likely that the cortex and brainstem activations occur independantly. If the process starts in the cortex, the patient may experience an aura. The neural activation leads to a complex sequence of events involving principally the trigeminocervical complex and its outflow pain pathways, resulting in a headache or head pain, with characteristics depending on the specific pathways involved and the extent of autonomic activation via the trigeminal-autonomic reflex. Presumably the neural activation sometimes fails to excite the pain pathways, resulting in aura symptoms without headache (acephalalgic migraine). This is hardly a new idea but rather a modern restatement of Edward Liveing's 19th century thesis of ‘‘nerve-storms.'' The process underlying aura is almost certainly cortical spreading depression. From observations on migrainous ventigo, increasingly recognized as a common manifestion of the migraine mechanism, we speculate that brainstem neural activation demonstrated during migraine attacks is also caused by spreading depression.

The book starts with a review of the historical development of our understanding of the migraine mechanism, and then explores the current views of migraine pathogenesis, based largely on recent revelations from neuroimaging. Chapter 3 deals with auras, the clinical manifestations of the migraine mechanism, including what we refer to as ‘‘atypical auras,'' which include a number of common neurological symptoms not usually considered to be of migrainous origin. Chapter 4 deals with the neurological complications of the migraine mechanism. Current evidence suggests that no matter how severe the symptoms, the migraine mechanism normally does not damage the brain. Conversely, however, migraine attacks can sometimes lead to blackouts, amnesic attacks, and stroke, and the reasons for this are considered.

The chapter on ‘‘Variants'' deals with the relationship between migraine and other primary headache disorders. We begin with a review of the history of headache classification, and then give illustrative examples of typical cases of migraine variants and other primary headache syndromes. In each instance, however, we also give examples of ‘‘overlap'' cases in which symptoms of one or more additional primary headache disorders have occurred in association with, or instead of, the habitual headache syndrome to another and also provide illustrative cases of ‘‘transformation'' of one primary headache syndrome in individual patients. We then consider the difficult clinical problem of ‘‘symptomatic migraine,'' in which the migraine mechanism is provoked by systemic diseases or structural lesions in the brain. The final chapters include an overview of our findings and conclusions and our current strategies for managing headache.

Our hypotheses are simple.All primary headaches are ‘‘migraine'' and the migraine mechanism is responsible for many other recurrent and stereotypical neurological symptoms. Secondly, everyone has migraine-we are all susceptible. Finally, we suggest that the migraine mechanism is fundamentally, spreading depression. We appreciate that some of our views are likely to prove controversial, perhaps even heretical, but we trust they are at least thought provoking. Criticism will no doubt encourage debate and further experiment.