EXPERT OPINION
or hyposexuality. The real issue is that patients don’t recognize these
things for what they are, so the physician must specifically ask about
prodrome symptoms. If recognized, treatment can begin soon after
the onset of headache.15
WHeN THe MiGRAiNe
BeCOMeS SeVeRe,
SOMe PATieNTS DeVeLOP
ALLODYNiA, OR
PAiN FROM NONPAiNFUL
STiMULi. THeiR HAiR
MA HURT (CePHALGiC)
Y
AND/OR THeY
MAY DeVeLOP
eXTRACePHALGiC
PAiN iN THe CHeST,
eXTReMiTieS,
OR BACK
MUSCLeS.
The headache can last 4 to 72 hours if it isn’t aborted by an appropriate medication (ie, a triptan or ergot). The pain can begin as mild and
diffuse and become moderate to severe. Typical associated symptoms
include nausea, vomiting, photophobia, and phonophobia. While the
typical adult migraine is unilateral, it may be bilateral in some migraineurs who experienced bilateral migraine as children and who
did not develop unilateral migraine as they grew older. It is most
important to begin treatment as soon as possible.16,17
migraine-pain free with triptan treatment. Burstein, who demonstrated sensitization of the trigeminovascular pathway, showed that
the use of an NSAID preceding triptans by an hour optimizes triptan
treatment if CA exists.20,21
The migraine postdrome, or postheadache period, is described by
most patients as a “hangover” with symptoms including cognitive difficulties, dizziness, fatigue, and concern that the headache may recur.
The postdrome may last 24 to 48 hours.
There are some forms of migrainous aura that indicate the need for a
full neurologic workup, at least the first time they occur. These may
include motor symptoms/hemiplegic aura, brain symptoms (such as
severe dysarthria, vertigo, syncope, bilateral sensory changes), prolonged aura (>60 minutes), atypical aura (such as “Alice-in-Wonderland” or hallucinatory changes), changes in perception of time and
space, as well as migralepsy or a seizure associated with migraine.
There appears to be a relationship between migraine and epilepsy.
Patients with one disorder are at least twice as likely to have the other.22 In the Epilepsy Family Study, 44% of patients reported physician diagnosed migraine, higher than the prevalence in the general
population. In another study, 14% of adult patients with seizures had
identified diagnoses of migraine, with migraine induced seizures in
1.7%.23 Some of these patients had better treatment results with a
combination of antimigraine and anticonvulsant medications.
A genetically determined dysfunction of ion channels (calcium, sodium/potassium) seems to point to a common underlying mechanism
for both paroxysmal disorders. There are mutations in the 3 known
genes for familial hemiplegic migraine that can cause epilepsy.24 Alterations of cortical hyperexcitability as a possible pathologic mechanism underlying the onset of migraine and epileptic attacks has been
noted.25
PATHOPHYSiOLOGY
igraine is primarily a neurogenic process with
secondary vascular changes (via cortical-spreading
depression [CSD]).26 The interictal migraineur has
a state of neuronal hyperexcitability in the cerebral
(primarily occipital) cortex, which has been demonstrated by functional magnetic resonance imaging (fMRI).27 Patients
with epilepsy have similar interictal neuronal irritability, which may
help explain the increased susceptibility of the migrainous brain to
headaches.28
When the migraine becomes severe, some patients develop allodynia,
or pain from nonpainful stimuli. Their hair may hurt (cephalgic) and/
or they may develop extracephalgic pain in the chest, extremities, or
back muscles. The development of allodynia suggests or even indi- The brain of the migraineur is genetically more excitable and more
cates central sensitization, a physiologic state in which central neu- vigilant than the brain of a person without migraine. The brain of the
rons transmit noxious sensory signals independent of sensory signals migraineur is genetically more excitable and more vigilant than the
from the periphery.18
brain of a person without migraine.29,30 The brain of a migraineur
doesn’t extinguish sensory stimuli as rapidly or as completely as
Guy et al19 found that modalities of cephalgic and extracephalgic the brain of those without migraine.18,31 In one study, fMRI of
cutaneous allodynia (CA) were different, with extracephalgic CA be- 12 patients with migraine compared with that of 12 healthy controls
ing mostly thermal and cephalgic CA mostly mechanical, suggest- demonstrated that patients with migraine, but not controls, had
ing different mechanisms for the two. Further, whether a patient highly significant hypoactivity in the nucleus cuneiformis, part of the
shows signs of CA is a predictor of whether that patient can become descending pathway for pain signals.32
34 | PWJ | www.painweek.org
Q3 | 2013