In the article by Shechter et al. [1], the authors do not seem to
know that systolic and diastolic blood pressure values in the sitting
position are the result of the interaction of different systems and do not
provide information on the sympathetic nervous system which may be used
for autonomic nervous system assessment. Although a "marginally" (with no
statistical significance) increase in diastolic blood pressure was found
in patients with disabling migraine, the authors dwell extensively with
this point in the discussion. They state that "increased diastolic blood
pressure in migraine cases could be secondary to sympathetic hyperfunction
or reflex response to sympathetic hypofunction" and conclude that this
finding is indicative of autonomic nervous system dysfunction.
Among the tests that can provide information on sympathetic function
[2, 3, 4, 5], the authors used only one mental stressor test, the "mirror
star-tracing test" which did not reveal any significant abnormality in
migraine patients. However, as this test may have individual variability
and low reproducibility, it should have been associated with at least one
other test such as the cold pressor test or handgrip.
The authors performed Valsalva maneuver, but state that 40% of
patients and 39% of controls not a negligible number of subjects, were
unable to complete a valid test. Since both patients and controls were
young and did not suffer from any disease that might have impaired their
physical performance, I wonder why the test was not repeated to obtain
"the power to detect differences" as the author claim at the end of the
discussion.
In this paper, the only significant finding indicative of autonomic
nervous system involvement is the decrease in deep breathing response
found in migraine patients with disabling migraine.
Heart rate is controlled by the inhibitory tonus of the vagus. In
deep breathing, the activity of the cardiohinibitory center is directly
inhibited by the respiratory center neurons during the inspiration phase
(tachycardia), before returning to its basal tonus during the expiration
phase (bradycardia). A decrease in deep breathing ratio is, therefore,
indicative of parasympathetic hypofunction. [2, 3, 4, 5]
In the discussion, the authors claim that "sympathetic stimulation
increases heart rate and parasympathetic stimulation decreases heart rate
during deep breathing". This statement is incorrect, because the
sympathetic system has inotropic and a cronotropic effect on the heart and
the tachycardia that occurs during deep breathing is the result of the
inhibition of vagal cardioinhibitory activity on the heart. [2, 3, 4, 5]
References
1) Shechter A, Stewart WF, Silberstein SD, Lipton RB. Migraine and
autonomic nervous system function. A population-based, case-control study.
Neurology 2002;58:422-427.
2) Ewing DJ. Analysis of heart rate variability and other non-
invasive tests with special reference to diabetes mellitus. In: Bannister
R, Mathias CJ, eds. Autonomic failure. A textbook of clinical disorders of
the autonomic nervous system. Oxford: Oxford University Press, 1992:312-
333.
3) Mathias CJ, Bannister R. Investigation of autonomic disorders. In:
Bannister R, Mathias CJ, eds. Autonomic failure. A textbook of clinical
disorders of the autonomic nervous system. Oxford: Oxford University
Press, 1992:255-290.
4) Gilbey MP, Spyer KM. Physiological aspects of autonomic nervous
system function. Curr Opinion Neurol Neurosurg 1993;6:518-523.
5) Appenzeller O, Oribe E. Testing autonomic reflexes. In:
Appenzeller O and Oribe E eds. The autonomic nervous system. An
introduction to basic and clinical concepts. Amsterdam: Elsevier, 1997:671
-710.