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Migraine-related vertigo: The challenge of the basic sciences
Clinical Neurology and Neurosurgery 108 (2005) 109–110
Letter to the Editor
Migraine-related vertigo: The challenge of the basic sciences Dear Sir, Crevits and Bosman present a balanced clinical overview of recurrent vestibular symptoms related to migraine [1]. These authors underscore the temporal association of imbalance and motion intolerance to the headache, dissociating the putative abnormal central processing from both cerebral ischemia as well as spreading depression. The source of augmented vestibular/brain stem input in migraine-related vertigo (MRV), however, remains uncertain; the belief that antidromic sterile neurogenic inflammation (NI) might contribute to vestibular stimulation is debatable. Whereas NI is probably a constant feature of migraine headache, MRV can occur either with or without headache; in some patients, headache and vertigo never occur together [1]. The characteristic delay between onset of migraine and onset of MRV [1] also indicates that NI is not, by itself, the critical factor in precipitation of MRV. MRV appears to be the outcome of a peculiarly gradual setting up of neuronal traffic (mis)direction. Motion sickness, to which migraine patients have a particular predisposition, involves nausea or vomiting or both with or without vertigo. The distinction between motion sicknessrelated vertigo and MRV [1] is more semantic than practical; both clinical circumstances essentially reflect the same underlying disease propensity and are managed on similar lines. The susceptibility of the individual to motion sickness is likely related to jerk nystagmus induced by both optokinetic and vestibular stimulation, involving proprioceptive and nociceptive afferent brain stem input [2]. Elimination of optokinetic nystagmus, as by closure of eyes or by gaze fixation, generally prevents motion sickness. Vestibular otolithic function is eliminated in microgravity; motion sickness in space also indicates a predominant pathogenetic role for visuo-sensory input [2]. Scopolamine, dimenhydrinate, and promethazine do not influence NI but reduce motion-related nystagmus [2,3]. Motion-induced nystagmus – whether optokinetic or vestibular in origin – is the likely source of sudden augmentation of brain stem afferent input that culminates in either vomiting in motion sickness [2] or DOI of original article:10.1016/j.clineuro.2005.08.006. 0303-8467/$ – see front matter © 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2005.08.005
vertigo in MRV. Since vomiting is central to motion sickness and a very frequent accompaniment of migrainous or nonmigrainous vertigo, the neurohumoral role of vasopressin also merits attention [4]. Nausea and emesis are clearly linked to increased arginine vasopressin (AVP) release [5,6]. Nausea itself – even without vomiting – is accompanied by intense and rapid AVP release. AVP release is fundamentally adaptive and operates in a wide variety of clinical circumstances; AVP promotes vasomotor control, antinociception, and behavioral adaptation and can abort migraine attacks and maintain remissions [7]. The concept that migraine or MRV is central in origin is also challenged by the fact that drugs that do not freely cross the intact blood–brain barrier (BBB) or significantly influence brain neuronal function such as atenolol, nadolol, or verapamil can prevent migraine [8]. Also, the fact that nifedipine or isoproterenol have negligible BBB permeability but can instantaneously abort the migraine aura presents another formidable pharmacological absolute against the central origin of migraine [9] or MRV. Finally, precipitation of migraine by fronto-temporal application of nitroglycerine argues for a peripheral rather than a central origin [10]. Against this background, it seems logical to conclude that the source of abnormal afferent brain stem neural traffic responsible for migraine [8] or MRV lies outside the central nervous system. Further, in contrast to the more common variants of migraine, with or without aura, basilar-type migraine is more consistently associated with vertigo [1]. Three features bear emphasis: (i) the posterior cerebral artery is particularly susceptible to any vasospastic influence [11]. In this context, cerebral hypoperfusion in patients susceptible to motion sickness should be regarded as an adaptive or protective neurophysiological alteration to an unusual situation; the rare occurrence of posterior circulation infarcts in migraine patients might then be viewed as an unfortunate concomitant complication of a usually beneficial physiological adaptation [4,11]. (ii) The fortification spectrum (scintillating scotoma) is a distinctively rare occurrence in basilar-type migraine, attenuating the role of posterior circulation ischemia in the pathogenesis of this typical migraine aura. (iii) Headache-associated posterior circulatory ischemia in basilar-type migraine possibly reduces the ability of the brain stem to handle sudden surges in afferent neuronal traffic thereby resulting frequently in dizziness or vertigo.
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Letter to the Editor / Clinical Neurology and Neurosurgery 108 (2005) 109–110
Additionally, the positional component of vertigo in MRV [1] may also be related to a positional aggravation of the underlying nystagmus. The usefulness of MRV as a distinctive clinical or pathophysiological entity [1] needs to be substantiated. Restraint is the key watchword that should determine use of the term ‘new’ or ‘distinctive’ in describing any migraine-related symptom-complex [12]. In the elucidation of the link between visual cues and migraine symptoms, including space and motion discomfort, nystagmus-associated neurophysiological phenomena may well represent the final common pathway [12].
References [1] Crevits L, Bosman T. Migraine-related vertigo: towards a distinctive entity. Clin Neurol Neurosurg 2005;107:82–7. [2] Gupta VK. Motion sickness is linked to nystagmus-related trigeminal brain input: a new hypothesis. Med Hypotheses 2005;64:1177– 81. [3] Pykko I, Schalen L, Jantti V, Magnusson M. A reduction of vestibulo-visual integration during transdermally administered scopolamine and dimenhydrinate. A presentation of gain control theory in motion sickness. Acta Otolaryngol Suppl 1984;406:167– 73. [4] Gupta VK. Vasopressin: neurohumoral link between nausea and motion sickness. Aviat Space Environ Med 2005;76:805.
[5] Rowe JW, Shelton RL, Helderman JH, Vetal RE, Robertson GL. Influence of the emetic reflex on vasopressin release in man. Kidney Int 1979;16:729–35. [6] Faull CM, Rooke P, Bayliss PH. The effect of a highly specific serotonin agonist on osmoregulated vasopressin secretion in healthy man. Clin Endocrinol 1991;35:423–30. [7] Gupta VK. A clinical review of the adaptive potential of vasopressin in migraine. Cephalalgia 1997;17:561–9. [8] Gupta VK. Non-lateralizing brain PET changes in migraine: phenomenology versus pharmacology? Brain 2004;127:E12. [9] V.K. Gupta. Management of migraine aura: basic theoretical and clinical reconsiderations. Headache, in press. [10] Bonuso S, Marano E, Stasio ED, Sorge F, Barbieri F, Ullucci E. Source of pain and primitive dysfunction in migraine: an identical site? J Neurol Neurosurg Psychiatry 1989;52:1351–4. [11] Gupta VK. Regional cerebral blood flow patterns in migraine: what is the contribution to insight into disease mechanisms? Eur J Neurol 1995;2:586–7. [12] V.K. Gupta. Migraine: searching for pathophysiology in semantics and nosology. J Neurol Neurosurg Psychiatry. Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/1/1-a (17 January 2005).
Vinod K. Gupta ∗ Dubai Police Medical Services, P.O. Box 12005, Dubai, United Arab Emirates ∗ Tel.:
+971 50 4647556; fax: +971 4 2683701. E-mail address: dr [email protected] 30 June 2005
Letter to the Editor
Migraine-related vertigo: The challenge of the basic sciences Dear Sir, Crevits and Bosman present a balanced clinical overview of recurrent vestibular symptoms related to migraine [1]. These authors underscore the temporal association of imbalance and motion intolerance to the headache, dissociating the putative abnormal central processing from both cerebral ischemia as well as spreading depression. The source of augmented vestibular/brain stem input in migraine-related vertigo (MRV), however, remains uncertain; the belief that antidromic sterile neurogenic inflammation (NI) might contribute to vestibular stimulation is debatable. Whereas NI is probably a constant feature of migraine headache, MRV can occur either with or without headache; in some patients, headache and vertigo never occur together [1]. The characteristic delay between onset of migraine and onset of MRV [1] also indicates that NI is not, by itself, the critical factor in precipitation of MRV. MRV appears to be the outcome of a peculiarly gradual setting up of neuronal traffic (mis)direction. Motion sickness, to which migraine patients have a particular predisposition, involves nausea or vomiting or both with or without vertigo. The distinction between motion sicknessrelated vertigo and MRV [1] is more semantic than practical; both clinical circumstances essentially reflect the same underlying disease propensity and are managed on similar lines. The susceptibility of the individual to motion sickness is likely related to jerk nystagmus induced by both optokinetic and vestibular stimulation, involving proprioceptive and nociceptive afferent brain stem input [2]. Elimination of optokinetic nystagmus, as by closure of eyes or by gaze fixation, generally prevents motion sickness. Vestibular otolithic function is eliminated in microgravity; motion sickness in space also indicates a predominant pathogenetic role for visuo-sensory input [2]. Scopolamine, dimenhydrinate, and promethazine do not influence NI but reduce motion-related nystagmus [2,3]. Motion-induced nystagmus – whether optokinetic or vestibular in origin – is the likely source of sudden augmentation of brain stem afferent input that culminates in either vomiting in motion sickness [2] or DOI of original article:10.1016/j.clineuro.2005.08.006. 0303-8467/$ – see front matter © 2005 Elsevier B.V. All rights reserved. doi:10.1016/j.clineuro.2005.08.005
vertigo in MRV. Since vomiting is central to motion sickness and a very frequent accompaniment of migrainous or nonmigrainous vertigo, the neurohumoral role of vasopressin also merits attention [4]. Nausea and emesis are clearly linked to increased arginine vasopressin (AVP) release [5,6]. Nausea itself – even without vomiting – is accompanied by intense and rapid AVP release. AVP release is fundamentally adaptive and operates in a wide variety of clinical circumstances; AVP promotes vasomotor control, antinociception, and behavioral adaptation and can abort migraine attacks and maintain remissions [7]. The concept that migraine or MRV is central in origin is also challenged by the fact that drugs that do not freely cross the intact blood–brain barrier (BBB) or significantly influence brain neuronal function such as atenolol, nadolol, or verapamil can prevent migraine [8]. Also, the fact that nifedipine or isoproterenol have negligible BBB permeability but can instantaneously abort the migraine aura presents another formidable pharmacological absolute against the central origin of migraine [9] or MRV. Finally, precipitation of migraine by fronto-temporal application of nitroglycerine argues for a peripheral rather than a central origin [10]. Against this background, it seems logical to conclude that the source of abnormal afferent brain stem neural traffic responsible for migraine [8] or MRV lies outside the central nervous system. Further, in contrast to the more common variants of migraine, with or without aura, basilar-type migraine is more consistently associated with vertigo [1]. Three features bear emphasis: (i) the posterior cerebral artery is particularly susceptible to any vasospastic influence [11]. In this context, cerebral hypoperfusion in patients susceptible to motion sickness should be regarded as an adaptive or protective neurophysiological alteration to an unusual situation; the rare occurrence of posterior circulation infarcts in migraine patients might then be viewed as an unfortunate concomitant complication of a usually beneficial physiological adaptation [4,11]. (ii) The fortification spectrum (scintillating scotoma) is a distinctively rare occurrence in basilar-type migraine, attenuating the role of posterior circulation ischemia in the pathogenesis of this typical migraine aura. (iii) Headache-associated posterior circulatory ischemia in basilar-type migraine possibly reduces the ability of the brain stem to handle sudden surges in afferent neuronal traffic thereby resulting frequently in dizziness or vertigo.
110
Letter to the Editor / Clinical Neurology and Neurosurgery 108 (2005) 109–110
Additionally, the positional component of vertigo in MRV [1] may also be related to a positional aggravation of the underlying nystagmus. The usefulness of MRV as a distinctive clinical or pathophysiological entity [1] needs to be substantiated. Restraint is the key watchword that should determine use of the term ‘new’ or ‘distinctive’ in describing any migraine-related symptom-complex [12]. In the elucidation of the link between visual cues and migraine symptoms, including space and motion discomfort, nystagmus-associated neurophysiological phenomena may well represent the final common pathway [12].
References [1] Crevits L, Bosman T. Migraine-related vertigo: towards a distinctive entity. Clin Neurol Neurosurg 2005;107:82–7. [2] Gupta VK. Motion sickness is linked to nystagmus-related trigeminal brain input: a new hypothesis. Med Hypotheses 2005;64:1177– 81. [3] Pykko I, Schalen L, Jantti V, Magnusson M. A reduction of vestibulo-visual integration during transdermally administered scopolamine and dimenhydrinate. A presentation of gain control theory in motion sickness. Acta Otolaryngol Suppl 1984;406:167– 73. [4] Gupta VK. Vasopressin: neurohumoral link between nausea and motion sickness. Aviat Space Environ Med 2005;76:805.
[5] Rowe JW, Shelton RL, Helderman JH, Vetal RE, Robertson GL. Influence of the emetic reflex on vasopressin release in man. Kidney Int 1979;16:729–35. [6] Faull CM, Rooke P, Bayliss PH. The effect of a highly specific serotonin agonist on osmoregulated vasopressin secretion in healthy man. Clin Endocrinol 1991;35:423–30. [7] Gupta VK. A clinical review of the adaptive potential of vasopressin in migraine. Cephalalgia 1997;17:561–9. [8] Gupta VK. Non-lateralizing brain PET changes in migraine: phenomenology versus pharmacology? Brain 2004;127:E12. [9] V.K. Gupta. Management of migraine aura: basic theoretical and clinical reconsiderations. Headache, in press. [10] Bonuso S, Marano E, Stasio ED, Sorge F, Barbieri F, Ullucci E. Source of pain and primitive dysfunction in migraine: an identical site? J Neurol Neurosurg Psychiatry 1989;52:1351–4. [11] Gupta VK. Regional cerebral blood flow patterns in migraine: what is the contribution to insight into disease mechanisms? Eur J Neurol 1995;2:586–7. [12] V.K. Gupta. Migraine: searching for pathophysiology in semantics and nosology. J Neurol Neurosurg Psychiatry. Available at: http://jnnp.bmjjournals.com/cgi/eletters/76/1/1-a (17 January 2005).
Vinod K. Gupta ∗ Dubai Police Medical Services, P.O. Box 12005, Dubai, United Arab Emirates ∗ Tel.:
+971 50 4647556; fax: +971 4 2683701. E-mail address: dr [email protected] 30 June 2005