Neurology -- Correspondence for Deprez et al., 68 (23) 1995-2002

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Correspondence published:

Familial occipitotemporal lobe epilepsy and migraine with visual aura: Linkage to chromosome 9q: Helio A. Teive, MD, PhD, Elcio J. Piovesan, MD, Pedro A. Kowacs, MD, Lineu C. Werneck, MD, PhD (3 October 2007)

Reply from the editorialist: Melodie R. Winawer, MD MS (3 October 2007)

Reply from the authors: Peter De Jonghe, MD, PhD, L. Deprez, MSc, K. Peeters, MD, W. Van Paesschen, FRCP, PhD, K. G. Claeys, MD, PhD, L.R.F. Claes, PhD, A. Suls, MSc, D. Audenaert, PhD, T. Van Dyck, BSc, D. Goossens, PhD, J. Del-Favero, PhD (3 October 2007)

Familial occipitotemporal lobe epilepsy and migraine with visual aura: Linkage to chromosome 9q 3 October 2007

Helio A. Teive, MD, PhD,
Federal University of Parana
Curitiba, PR, Brazil,
Elcio J. Piovesan, MD, Pedro A. Kowacs, MD, Lineu C. Werneck, MD, PhD
Send Correspondence to journal:
Re: Familial occipitotemporal lobe epilepsy and migraine with visual aura: Linkage to chromosome 9q

hagteive{at}mps.com.br Helio A. Teive, MD, PhD, et al.

We read the article by Deprez et al [1] and the accompanying editorial by Dr. Winawer [2] with great interest. Deprez et al present a family with occipitotemporal lobe epilepsy and migraine with visual aura and the linkage to a single locus in the chromosome 9q. [1]
The relationship between epilepsy and migraine is described, including data on evidence regarding the comorbidity of migraine and epilepsy. [1,2] Neither Deprez nor Winawer commented on the important contributions of Leão in this topic. Cortical spreading depression was discovered in 1943 by Aristides Leão while experimentally studying epilepsy in the cortex of rabbits, and for several years it was considered an unexplained, serendipitous, and experimental event. [3]
Many studies have confirmed the relevance of Leão´s cortical spreading depression (LCSD) in the mechanism of several neurological diseases, particularly in migraine. [3] In the seminal article by Leão, he said that his study “originated in an attempt to secure more data for the understanding of the cortical electrogram” which occurs in “experimental epilepsy” or “cortical epilepsy”. [4]
In 1945, Leão and Morrison studied the propagation of cortical depression and suggested for the first time that this phenomenon could be involved in the pathophysiology of migraine, since the slow march of scotomata in the visual or somatic sensory areas was similar to LCSD. [3]
Several others authors, including Milner, Basser, Garner-Medwin and Lauritzen stressed the relationship between LCSD and the seminal article of Lashley on migraine. [3] Years later Leão commented on the relationship between epilepsy in a book chapter. [5] Leão described among the most important characteristics of LCSD: “Although all intrinsic and evoked neuronal activity are depressed, abnormal activity may occur locally in the course of cortical spreading depression. At any site, at the onset of the depression, the neurons usually generate a brief (1-3 s) burst of discharges, and within some 30s of this burst, abnormal activity of the same kind as cortical seizure activity may erupt, and last more than 20s. This eruption depends on the local conditions, and in a single cortical spreading depression it may occur at some sites and not at others”. [5]
The relevance of LCSD should be considered, especially when the relationship between epilepsy and migraine became more clear and biologically linked.
References
1. Deprez L, Peeters K, Van Paesschen W et al. Familial occipitotemporal lobe epilepsy and migraine with visual aura: linkage to chromosome 9q. Neurology 2007;68:1995-2002.
2. Winawer M. New evidence for a genetic link between epilepsy and migraine. Neurology 2007;68:1969-1970.
3. Teive HA, Kowacs PA, Maranhão Filho P, Piovesan EJ, Werneck LC. Leao´s cortical spreading depression: from experimental “artifact” to physiological principle. Neurology 2005;65:1455-1459.
4. Leao AA. Spreading depression of activity in the cerebral cortex. J. Neurophysiol 1944;7:359-390.
5. Leao AA. On the inferred relantionship of migraine and spreading depression. In: F. Clifford Rose, ed. Advances in headache research. London: John Libbey & Co., 1987;19-24.
Disclosure: The authors report no conflicts of interest.

Reply from the editorialist 3 October 2007

Melodie R. Winawer, MD MS,
Department of Neurology, Columbia University
GH Sergievsky Center, Columbia University 630 W. 168th Street, PH 19 New York, NY 10032
Send Correspondence to journal:
Re: Reply from the editorialist

mw211{at}columbia.edu Melodie R. Winawer, MD MS

Teive et al raise interesting points in their letter regarding the potential role of Leão’s cortical spreading depression (LCSD) in both migraine and epilepsy pathophysiology.
The role of LCSD in migraine, particularly migraine aura, is well-established. (3,6,7) Several findings suggest LCSD as a mechanistic link between migraine and epilepsy. First, described by Teive et al in their letter and in the paper to which they refer [3] is Leão’s own observation of abnormal cortical seizure activity occurring concurrently with LCSD.
More recently, spreading depression has been shown to enhance spontaneous epileptiform activity in slice preparations from human epilepsy surgical patients. [8] Spreading depression has also been found to occur early in audiogenic kindling of genetically susceptible rats. [9] A clinical perspective comes from findings that patients with migraine and epilepsy comorbidity have a higher frequency of migraine with aura than migraine without aura, supporting the role of LSCD in the shared pathophysiology of the two disorders. [10]
Finally, as recently reviewed by Aguggia et al [7], a number of anti-convulsants have been shown to be effective in the treatment of migraine, implicating neuronal hyperexcitability as a possible common mechanism.
References
6. Pietrobon D. Migraine: new molecular mechanisms. Neuroscientist 2005;11:373-386.
7. Aguggia M, D'Andrea G, Bussone G. Neurophysiology and neuromodulators. Neurol Sci 2007;28 Suppl 2:S97-S100.
8. Gorji A, Speckmann EJ. Spreading depression enhances the spontaneous epileptiform activity in human neocortical tissues. Eur J Neurosci 2004;19:3371-3374.
9. Vinogradova LV, Vinogradov VY, Kuznetsova GD. Unilateral cortical spreading depression is an early marker of audiogenic kindling in awake rats. Epilepsy Res 2006;71:64-75.
10. Leniger T, von den Driesch S, Isbruch K, Diener HC, Hufnagel A. Clinical characteristics of patients with comorbidity of migraine and epilepsy. Headache 2003;43:672-677.
Disclosure: The author reports no conflicts of interest.

Reply from the authors 3 October 2007

Peter De Jonghe, MD, PhD,
University of Antwerp
Universiteitsplein 1, BE-2610 Antwerpen, Belgium,
L. Deprez, MSc, K. Peeters, MD, W. Van Paesschen, FRCP, PhD, K. G. Claeys, MD, PhD, L.R.F. Claes, PhD, A. Suls, MSc, D. Audenaert, PhD, T. Van Dyck, BSc, D. Goossens, PhD, J. Del-Favero, PhD
Send Correspondence to journal:
Re: Reply from the authors

peter.dejonghe{at}ua.ac.be Peter De Jonghe, MD, PhD, et al.

We agree with Teive et al that Leão made major contributions to the study of migraine by the discovery of cortical spreading depression in 1943. [4]
It is also evident that many years ago he perceived the importance of this mechanism suggesting a close relationship between migraine and some forms of epilepsy.
In the original draft of our manuscript, cortical spreading depression was extensively discussed but due to space limitations we had to omit this section in the final version. We hope that the eventual identification of the gene defect in our extended family may shed more light on the molecular basis of cortical spreading depression.
Disclosure: The authors report no conflicts of interest.