150
ASAA
Sousa-Santos PEM, Pucci GF, Akita J
Vertebral artery hypoplasia and chronic migraine: is there an association or just an incidental finding?
subtraction angiography (DSA), considered the gold
standard for studying cerebral circulation. However, since
DSA is an invasive procedure, and the risk of developing
neurological complications can be as high as 1%
4
, we
decided not to perform it in this patient, as no additional
benet would be obtained for her diagnosis or treatment.
An association between migraine and VAH emerged
in a study done by Laurevic and colleagues, in 1998
5
,
which showed a prevalence of 29% of VAH in patients
with migraine with aura comparing to 7% in patients with
migraine without aura. In this article, a pathophysiological
model was proposed, in which VAH was related to
decreased posterior circulatory ow during migraine
attacks, thus contributing to the manifestation of the aura.
Later, Chung et al.
1
found a similar prevalence of VAH in
migraine with aura (28.26%), 14 times higher compared
to controls. However, no decrease in vertebral artery ow
was found in patients with VAH during migraine attacks.
Wherefore, the role of the VAH in migraine may not
involve hypoperfusion during the attack phase but yet may
contribute to migraine through complex neurovessels pain-
producing trigeminovascular pathways mechanisms.
1,3
Thus, it is plausible that VAH could be a contributing factor
to the process of chronication of episodic migraine (Figure
3).
Figure 3. The role of VAH and Migraine. VAH, vertebral arteria
hypoplasia; TVP, trigeminovascular pathways; BMI, body mass
index.
Chronic migraine (CM) is dened as frequent headache
attacks with at least 15 headache days per month for
more than 3 months, and in at least 8 days per month with
migraine characteristics.
6
There are several predisposing
factors to the chronication of a migraine, such as overuse
of analgesics, inadequate prophylactic treatment for
migraine and stressful events, high BMI, in addition to
sensitization of the trigeminal system and various molecular
mechanisms, such as calcitonin gene-related peptide
(CGRP) and serotonin (5-HT).
7
Our patient presented some
predisposing factors for CM associated with obesity and
psychiatric comorbidities.
Therefore, management of CM includes a rigorous control
of risk factors, acute pain relief, and effective prophylactic
treatment of migraine.
7
Another fundamental step in
CM is the treatment of psychiatric disorders and other
comorbidities. The overlapping symptoms of migraine,
anxiety, and mood disorders make the treatment very
challenging. Once the concept of migraine/tension-
type headache and depression/anxiety are continuum
pathologies, it is reasonable to think of a possible spectrum
or continuum between migraine and anxiety/mood
disorders.
8
Few studies have analyzed the most effective
medications for patients with these three conditions, and
a rational approach based on the main symptoms may be
an option.
8
Topiramate, at a daily dose of 100 mg, is generally an
effective and tolerable prophylactic drug to CM.
9
Other
preventive medications, such as amitriptyline, valproate, and
pregabalin, have also been shown to be effective in some
studies.
9
Considering pain relief, tricyclic antidepressants
(amitriptyline, nortriptyline) seem to be more effective
than SNRIs selective serotonin/norepinephrine reuptake
inhibitor) and SSRIs (selective serotonin reuptake inhibitor).
However, the treatment of anxiety and depression has
better responses to SNRIs and SSRIs, and doses of tricyclic
antidepressants are often higher than those used for the
preventive treatment of migraine, making it difcult to be
tolerated.
10
In our patient, we chose to start topiramate
for migraine prophylaxis and maintain uoxetine, as she
showed an adequate response to anxiety and depression.
Conclusion
Despite the role of VAH in migraine being unclear, VAH
may contribute to the chronication of migraine through
complex pain-producing trigeminovascular pathways
mechanisms. However, it is important to be aware of factors
such as overuse of analgesics and psychiatry comorbidities
for the adequate treatment of chronic migraine.
Declaration of conflicting interests: The authors declared
no potential conicts of interest with respect to the research,
authorship, and/or publication of this article.
Funding: The authors received no nancial support for the
research, authorship, and/or publication of this article.
Author's Contribution: PEMSS, conceptualization, data
curation, writing – original draft; GFP, data curation,