The relation between depression and headache is
complex. In clinical practice depressive mood is frequently
encountered in patients with frequent headaches, including
tension-type headache (TTH), but overt major depression is
rather rare. In a cohort of subjects with TTH of any severity
the incidence of depression was not increased (Merikangas
et al., 1994). There is a bidirectional relationship in lifetime
prevalence between migraine and major depression,
suggesting a shared cause. Severe non-migrainous headaches
(most of which were frequent tension-type headaches),
however, were not predicted by major depression,
while they were themselves predictive of first-onset major
depression (Breslau et al., 2000). It was therefore felt by
some that depression was merely a secondary phenomenon
in disabling TTH, the more so that such headaches can be
ameliorated by tricyclics at low doses supposed to have little
or no antidepressant effect.
The study by Janke et al. (2004) in this issue is of
paramount importance for this discussion as it shows for the
first time that major depression favours the occurrence of
stress-induced headache in subjects suffering from frequent
TTH and that this is associated with increased pericranial
palpation tenderness. Pressure-pain thresholds were also
decreased at an extracephalic site in the depressed TTH
sufferers. The neurobiological mechanisms through which
depression promotes TTH are likely to be central sensitisation
and dysfunctioning of descending pain control pathways.
It cannot be concluded from the study whether
depression per se or increased stress in the depressed subjects
are responsible for the observed changes. From findings with
brain stem reflexes we have previously hypothesised that the
limbic control of descending pain control systems might be
abnormal in chronic TTH patients (Schoenen, 1990).
Fortunately for our PhD students, the study by Janke
et al. (2004) does not answer all questions. For instance,
they were not able to recruit depressed subjects with less
than 12 headaches per year, which by itself suggests that
depression may cause TTH, but leaves open the question
whether depression is able to favour TTH by itself.
Although the study convincingly shows that depression
predisposes to stress-induced headache episodes, it does not
prove that it is the major culprit in frequent or chronic TTH.
It could only be an aggravating factor like for instance
hormonal changes in the perimenstrum (which was not
taken into account in the present study). The fact that
specific serotonin reuptake blockers, though effective
antidepressants, are not useful for chronic TTH (Schoenen,
2000) would not favour a primary pathogenic role for
depression. The subjects recruited by Janke et al. (2004) had
major depression which is not the rule in clinical samples of
TTH patients. It would be interesting to know whether
depressive mood (scores !18 on Beck’s inventory) also
increases onset of TTH following laboratory stress. Finally,
considering the abovementioned bidirectional relationship
between migraine and depression, it seems worthwhile to
perform a similar study in migraineurs in order to determine
if depression favours migraine attacks or certain interval
headaches which can be indistinguishable from TTH.
In summary, despite its limitations this study is a
milestone in headache research as it provides experimental
evidence that depression may be the villain in tension-type
headache, and not just a bystander.
J. Schoenen
Departments of Neuroanatomy and Neurology,
University of Liege, 20,
complex. In clinical practice depressive mood is frequently
encountered in patients with frequent headaches, including
tension-type headache (TTH), but overt major depression is
rather rare. In a cohort of subjects with TTH of any severity
the incidence of depression was not increased (Merikangas
et al., 1994). There is a bidirectional relationship in lifetime
prevalence between migraine and major depression,
suggesting a shared cause. Severe non-migrainous headaches
(most of which were frequent tension-type headaches),
however, were not predicted by major depression,
while they were themselves predictive of first-onset major
depression (Breslau et al., 2000). It was therefore felt by
some that depression was merely a secondary phenomenon
in disabling TTH, the more so that such headaches can be
ameliorated by tricyclics at low doses supposed to have little
or no antidepressant effect.
The study by Janke et al. (2004) in this issue is of
paramount importance for this discussion as it shows for the
first time that major depression favours the occurrence of
stress-induced headache in subjects suffering from frequent
TTH and that this is associated with increased pericranial
palpation tenderness. Pressure-pain thresholds were also
decreased at an extracephalic site in the depressed TTH
sufferers. The neurobiological mechanisms through which
depression promotes TTH are likely to be central sensitisation
and dysfunctioning of descending pain control pathways.
It cannot be concluded from the study whether
depression per se or increased stress in the depressed subjects
are responsible for the observed changes. From findings with
brain stem reflexes we have previously hypothesised that the
limbic control of descending pain control systems might be
abnormal in chronic TTH patients (Schoenen, 1990).
Fortunately for our PhD students, the study by Janke
et al. (2004) does not answer all questions. For instance,
they were not able to recruit depressed subjects with less
than 12 headaches per year, which by itself suggests that
depression may cause TTH, but leaves open the question
whether depression is able to favour TTH by itself.
Although the study convincingly shows that depression
predisposes to stress-induced headache episodes, it does not
prove that it is the major culprit in frequent or chronic TTH.
It could only be an aggravating factor like for instance
hormonal changes in the perimenstrum (which was not
taken into account in the present study). The fact that
specific serotonin reuptake blockers, though effective
antidepressants, are not useful for chronic TTH (Schoenen,
2000) would not favour a primary pathogenic role for
depression. The subjects recruited by Janke et al. (2004) had
major depression which is not the rule in clinical samples of
TTH patients. It would be interesting to know whether
depressive mood (scores !18 on Beck’s inventory) also
increases onset of TTH following laboratory stress. Finally,
considering the abovementioned bidirectional relationship
between migraine and depression, it seems worthwhile to
perform a similar study in migraineurs in order to determine
if depression favours migraine attacks or certain interval
headaches which can be indistinguishable from TTH.
In summary, despite its limitations this study is a
milestone in headache research as it provides experimental
evidence that depression may be the villain in tension-type
headache, and not just a bystander.
J. Schoenen
Departments of Neuroanatomy and Neurology,
University of Liege, 20,
No comments:
Post a Comment