How caloric vestibular irritation influences migraine attacks
Ognyan Kolev
CEPHALALGIA Kolev O. How caloric vestibular irritation influences migraine attacks. Cephalalgia 1990; 10: 167-9. Oslo. ISSN 0333-1024 Stimulation of the vestibular system by cold irritation of the ear was performed in 12 patients during a migraine attack. In eleven of the subjects the headache was changed. The changes varied from completely disappeared to a slight decrease. The duration of the changes was either several minutes, during the vestibular irritation, or days. All changes were related to the induced sensation of vertigo. We discuss the probable mechanisms of these vestibular influences. • Caloric probe, migraine attack, vertigo, vestibular system O Kolev, Otoneurology Department, Institute of Neurology, Psychiatry and Neurosurgery, Medical Academy, Lenin Boulevard 4-th km, 1113 Sofia, Bulgaria; Accepted 27 April 1990 It is well known that one of the possible symptoms of vestibular irritation is headache (1). On the other hand, vertigo may occur as part of a migraine attack (2, 3). However, there are no reports on how the artificial vestibular irritation influences a subject during a migraine attack. During vestibular testing of several patients during a migraine attack with the strong irritating Barany probe, patients informed us that their headache disappeared. Materials and method
The vestibular system of 12 patients with migraine without aura (3) during a migraine attack (age, sex, location and degree of headache is shown in Table 1) was irritated by a caloric probe-irrigation of the right and the left ear consecutively with 100 cc water per 20 sec at 10ºC. The interval between irrigations was 10 min. During the calorization the patients were supine, with closed eyes and head raised about 30º above the horizontal. The subjects were asked (avoiding any suggestion) for appearance of any change (if any) in their headache, its degree, duration and relationship with the provoked vertigo. The vestibular reaction was measured using electronystagmographic records with Toennies (BRD) recorder and analyser. All patients were subjected to Table 1. Age, sex, location and degree of headache for each patient. Strength Subject Side of of no. Age Sex headache headache 1 28 male left severe 2 40 female left severe 3 33 female right moderate 4 41 female left severe 5 29 female right severe 6 30 female left moderate 7 37 female left moderate 8 33 female left moderate 9 38 male right moderate 10 30 female left moderate 11 36 female right moderate 12 29 female right severe
caloric irrigation at body temperature before the cold irrigations as a control measure to reduce the placebo effect. Before calorization, the vestibular system of the patients was stimulated by a rotatory chair which is programmed only for low accelerations with a maximal stimulation of 60° stop stimulus. Results
The results are shown in Table 2. The patients were divided into four groups as follows: Group I. Patient Nos. 3, 4, and
Table 2. Effect of irritation on pain and duration of headache. Max. Degree of pain after Subject SPV o/sec Vertigo irritation no. RI LI RI LI RI LI 1 52 54 ++ ++ no pain no pain 2 43 43 ++ ++ mild mild 3 58 56 ++ ++ no pain no pain 4 55 60 ++ ++ no pain no pain 5 46 48 ++ ++ mild mild 6 53 49 ++ ++ no pain no pain 7 30 33 + + moderate moderate 8 51 55 ++ ++ no pain no pain 9 44 43 ++ ++ mild mild 10 57 60 ++ ++ no pain no pain 11 45 46 ++ ++ no pain no pain 12 49 47 ++ ++ mild mild
Duration of change in headache RI LI 3 min 3 min 2 min 2 min 8 days 1 day 2.5 min 2.5 min 3 min 3 min 3 min 3 min 2.5 min 2.5 min 4 days 2 min 2 min 3 min 3 min
Max SPV-slow nystagmic phase velocity in the culmination; RI-right irrigation; LI-left irrigation; ++-strong vertigo; +- 3/4weak vertigo; In subjects Nos. 3, 4 and 10 the second calorization was performed in the absence of headache and no change was found. 10. Their headache disappeared during the vertigo period and continued for varying durations. The subjects reported strong vertigo and had severe nystagmus. Group II. Patient Nos. 1, 6, 8, and 11. Their headache disappeared completely during the sensation of vertigo. In patient Nos. 6 and 8 the headache gradually returned to its initial intensity after the period of vertigo. In patient Nos. 1 and 11 the headache gradually appeared again but before the end of the vertigo, as it was decreasing. All had severe nystagmus and vertigo. Group III. Patient Nos. 2, 5, 9 and 12. Their headache did not disappear but decreased in intensity during the period of vertigo. At the end of the period of vertigo it gradually returned to the initial intensity. Their nystagmus was relatively weaker. Group IV. Patient No. 7. There was no change in headache. This patient reported weak sensations of vertigo after the calorizations. The nystagmus responses were also weak. There was no change in the headache of patients after irrigation with water at body temperature and no nystagmus was noted. No relationship was established between the side of stimulation and the side of the headache. There was a relationship noted between the strength of the vestibulo-ocular reflex and changes in the headache. The rotatory stimulation did not provoke any change in the headache. Discussion
We propose the following mechanisms of vestibular influences on headache: (i) The vestibular irritations act on vasomotor regulating centres located in different levels of the brain (medulla, pons mesencephalon, diencephalon, cortex) (4), which can alter the tone of the cephalic vessels in two ways: (a) neuroreflexive-reflex arc reaching to the vessels; (b) by release of vasoactive substances (substance P, prostaglandins etc.) from brain (or other tissue) cells. (ii) The vestibular irritation acts on nociceptive centres (locus coeruleus, centrus median Luys, nuclei suband parafascicularis, nucleus raphe magnus, areas reticularis magno- and gigantocellularis etc.) (5) by means of; (a) axonal projections (such projections are established) (5); or (b) via
induced release of substances (e.g. regulatory peptides etc.) decreasing sensitivity to pain. Possibly the calorization normalizes a supposed disinhibition of the nociceptive neurons in the trigemino-cervical nucleus by aminergic neurons from nociceptive brain-stem centres (7). (iii) The responses of the centres in the brain involved in headache may be temporarily reduced as the focus is on the sensation of vertigo during vestibular irritation. Indirect confirmative data have been shown by experiments on cats showing diminished responses of the cochlear nuclei to the auditory irritations of the attention by other sensory information when the animal is stimulated by other sensory input (5). (iv) Combination of the above mechanisms. In group I the results are explained by the long term normalization of the tone of the cephalic vessels caused by mechanisms (i)a and,/or (i)b. The results from group II can be explained by mechanisms (i)a and (i)b-the impulses from the vestibular centres or the changed level of vasoactive substances temporarily (while the vestibular irritation is over a sufficiently high level) neutralize the mechanisms leading to dilatation of the regional cephalic vessels; or mechanisms (ii)a and (ii)b are switched on in the same way. In group III the mechanisms (i), (ii) and (iii) could be suspected, but the strength of action of these mechanisms is weaker. Probably mechanism (iii) is most responsible. The absence of any changes in headache in group IV can be explained by an insufficient vestibular irritation which can not switch on the described mechanisms. The absence of any change in the headache during the rotation is the result of the weak vestibular irritation. The question arises: Why do migraine patients have phono- and photophobia during attack, while increased vestibular sensory input should give rise to improvement of symptoms? (Personal communication with Ottar Sjaastad). Our explanation is the following: The sense of balance is one of the most primitive faculties in man's development, appearing in the biological scale before the sense of sight and hearing (7). Therefore, probably the vestibular system has wider connections with the nonspecific brain systems and the vestibulo-vegetative reflex has a low threshold. This, we think, is the reason that the vestibular system differs, in its effect on the migraine attack, from the visual and the acoustic systems. References
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