Migraines and Chronic Pain

Migraine is a brain experience. It shares brain space and function with other experiences, those of thought and mood and then vegetative behaviors of sleep and appetite. Migraine is not a free-standing entity. It is interrelated and comorbid with other diseases, and in the last analysis, subject to their persuasion. It could not be otherwise.

Let’s create a hypothetical patient, a female because migraine is predominant in that gender. Let’s introduce a stressor, say the death of a loved one. In doing so, let’s be aware that the stressor need not be nearly so dramatic. It may be trivial, perhaps some minor personal rejection, or it may even be indiscernible, perhaps some disruption of biologic rhythms. Regardless, our patient, genetically endowed with migraine, possesses a neural system readily available for exhibition. This is recruited—and quickly.

The migraine machinery is there. No reconfiguration is necessary. With the appearance of stress, she experiences an increase in the frequency and severity of headache. This sudden worsening of migraine is a certain indicator that the infrastructure is being challenged. Our patient may recover spontaneously. Recovery is the rule, not the exception, as most of our brain’s unravelings are transient experiences. If, however, we fail to recover, the subcortical brain, the mastermind of our behavior, disassembles into multiple expressions. This happens slowly. It takes time for the neural axis to reconfigure into maladaptive functioning, just as it takes time for drug therapy to reconfigure the axis into effective functioning.

Which maladaptation should appear first and which later is quite variable, but it usually begins with disordered sleep. As our patient suffers an increased frequency of her headaches, she will likely experience insomnia. Her appetite will change, perhaps with sweet cravings and weight gain or, on the other side of the scale (there is no way to predict), she will become anorectic. Mood will disfigure with despondency and apathy. Temperament will be disordered with anxiety and restlessness, and perhaps even mind-too-busy obsessions.

Migraine, now under the pervasive influence of other brain forces, loses its identity and transmogrifies into another state of illness. The characteristic spatial and temporal dimensions of headache change. Periodicity is lost. Pain is no longer occasional. It is constant. Its unilaterality disappears. Pain crosses the midline in a mirror image manner and becomes generalized. The exotic sensory effects, visual and otherwise, go away. No longer are there intervals of hemianopia or scotoma. They vanish, leaving only a trace of their legacy, the occasional appearance of vague scintillations in the periphery of the visual field. Our patient has transformed migraine, a hybrid, a mix of fragments and comorbidities—part depression, part migraine, and probably part a host of other derangements.

Her pain no longer responds to anti-migraine drugs, and her depression does not respond to SSRIs. She doesn’t have either of those diseases. She has chronic pain. And that disease responds rather predictably to the tricyclic drugs. These agents, as I surmised early on, are useful and perhaps exclusively useful in the sleep-disordered, and the most certain attribute of chronic pain is impaired sleep. It is a clear identifier of the disease. It is not an identifier of migraine. That disease, remember, is characterized by intervals of wellness, and wellness is not sleep-disturbed.

When, exactly, does migraine become chronic pain? It is quite impossible to say because it happens slowly and gradually. Nature does not draw straight lines in time or space. They are irregular, and curvilinear, and the evolution of migraine into chronic pain (or vice versa) does not occur at a precise point in time. Indeed, in the natural history of the diseases, and they both have a discernible natural history, their display may shift from predominant migraine for one interval and for another, chronic pain.

The distinction between migraine and chronic pain can challenge the resources of the most skillful physician. It is never simple. Perhaps our hypothetical patient is drinking too much. Substance abuse certainly weighs heavily in the scales. Perhaps our patient is bipolar, or perhaps she was abused in her youth. All these must befactored in. They invite the use of a variety of drugs for the treatment of a disease that we often presume to be migraine, but it is really not.

Transformed migraine is the disease that for so many years was, and unfortunately still is, misidentified as tension headaches—an egregious example of our proclivity to ascribe a state of pain to an inability to deal emotionally with the environment. Nothing really wrong with that, so long as we remember that many diseases are the product of inability to deal with the environment. No reason to single out headache for special treatment. We would hardly employ the phrases tension schizophrenia, or tension depression, or tension heart attack. These are nonsensical because we recognize that each of these disorders has a certain biologic substrate. We don’t afford headaches that dignity. It is too convenient to blame the patient.

Dr. Robert T. Cochran Jr., M.D.uniquely incorporates the fields of neurology, internal medicine, and psychiatry in deriving insightful - sometimes, disturbing - yet hopeful conclusions for the chronic pain sufferer. He brings to light intriguing new treatment strategies that should be of interest to the medical community and chronic pain sufferers alike. http://www.understandingpain.com