Are Cortical Spreading Depression and Headache in Migraine Causally Linked?

Cephalalgia ◽  
2009 ◽  
Vol 29 (2) ◽  
pp. 244-249 ◽  
Author(s):  
J Wolthausen ◽  
S Sternberg ◽  
C Gerloff ◽  
A May

During the past few decades, much controversy has surrounded the pathophysiology of migraine. Cortical spreading depression (CSD) is widely accepted as the neuronal process underlying visual auras. It has been proposed that CSD can also cause the headaches, at least in migraine with aura. We describe three patients, each fulfilling the International Headache Society criteria for migraine with aura, who suffered from headaches 6–10 days per month. Two patients were treated with flunarizine and the third patient with topiramate for the duration of 4 months. All patients reported that aura symptoms resolved completely, whereas the migraine headache attacks persisted or even increased. These observations question the theory that CSD (silent or not) is a prerequisite for migraine headaches.

Cephalalgia ◽  
2008 ◽  
Vol 28 (5) ◽  
pp. 558-562 ◽  
Author(s):  
M Berger ◽  
E-J Speckmann ◽  
HC Pape ◽  
A Gorji

Cortical spreading depression (CSD) plays a role in migraine with aura. However, studies of the neuronal effects of CSD in human cortex are scarce. Therefore, in the present study, the effects of CSD on the field excitatory postsynaptic potentials (fEPSP) and the induction of long-term potentiation (LTP) were investigated in human neocortical slices obtained during epilepsy surgery. CSD significantly enhanced the amplitude of fEPSP following a transient suppressive period and increased the induction of LTP in the third layer of neocortical tissues. These results indicate that CSD facilitates synaptic excitability and efficacy in human neocortical tissues, which can be assumed to contribute to hyperexcitability of neocortical tissues in patients suffering from migraine.


Cephalalgia ◽  
2004 ◽  
Vol 24 (11) ◽  
pp. 960-966 ◽  
Author(s):  
W Dent ◽  
HK Spiss ◽  
R Helbok ◽  
WBP Matuja ◽  
S Scheunemann ◽  
...  

We set out to assess the prevalence during the previous year of migraine in a rural area surrounding the Mnero Diocesan Hospital in Southern-Tanzania. A door-to-door survey from August until December 1999 using a questionnaire based on the criteria of the International Headache Society (IHS), including 1047 households with 3351 persons, was done, consisting of a screening dialogue with a representative family member followed by a face-to-face interview with the affected subject. Of the 3351 participants (female 1876; male 1475; age > 10 years), 23.1% had suffered from headache during the past year; overall prevalence of migraine was 5.0% (female 7.0%; male 2.6%); 1.4% reported migraine without aura (female 1.8%; male 0.9%); and 3.6% reported migraine with aura (female 5.2%, male 1.6%). The peak prevalence was found in female persons in the fourth (11.1%), in male persons in the third decade of life (3.8%). Compared with other African surveys, the prevalence rate of migraine headache in South Tanzania is slightly higher than among Ethiopian and Zimbabwean Africans.


Cephalalgia ◽  
1999 ◽  
Vol 19 (7) ◽  
pp. 660-667 ◽  
Author(s):  
I Christiansen ◽  
LL Thomsen ◽  
D Daugaard ◽  
V Ulrich ◽  
J Olesen

Migraine with aura and migraine without aura have the same pain phase, thus indicating that migraine with aura and migraine without aura share a common pathway of nociception. In recent years, increasing evidence has suggested that the messenger molecule nitric oxide (NO) is involved in pain mechanisms of migraine without aura. In order to clarify whether the same is true for migraine with aura, in the present study we examined the headache response to intravenous infusion of glyceryl trinitrate (GTN) (0.5 μg/kg/min for 20 min) in 12 sufferers of migraine with aura. The specific aim was to elucidate whether an aura and/or an attack of migraine without aura could be induced. Fourteen healthy subjects served as controls. Aura symptoms were not elicited in any subject. Headache was more severe in migraineurs than in the controls during and immediately after GTN infusion ( p=0.037) as well as during the following 11 h ( p=0.008). In the controls, the GTN-induced headache gradually disappeared, whereas in migraineurs peak headache intensity occurred at a mean time of 240 min post-infusion. At this time the induced headache in 6 of 12 migraineurs fulfilled the diagnostic criteria for migraine without aura of the International Headache Society. The results therefore suggest that NO is involved in the pain mechanisms of migraine with aura. Since cortical spreading depression has been shown to liberate NO in animals, this finding may help our understanding of the coupling between cortical spreading depression and headache in migraine with aura.


Author(s):  
Julio R Vieira ◽  
Richard B Lipton

This chapter examines migraine. The incidence of migraine varies depending on multiple aspects, including age, sex, and the presence of aura. At an earlier age (younger than age ten), migraine initially affects more boys than girls, with migraine with aura (MA) occurring at a younger age than migraine without aura (MO). Later in life, when puberty starts, this relationship changes and it becomes more common in women than men. Migraine aura are focal neurological symptoms that typically occur prior to the onset of a headache due to a phenomenon called cortical spreading depression. The prevalence of migraine with aura vary between visual, sensory, or motor symptoms. It can also present as diplopia, slurred speech, aphasia, dizziness, vertigo, and hemiparesis. Moreover, the prevalence of migraine varies according to headache frequency. The chapter then looks at chronic migraine and menstrual migraine. It also explores several comorbidities associated with migraine, including many neurologic, medical, and psychiatric conditions.


Cephalalgia ◽  
2018 ◽  
Vol 39 (6) ◽  
pp. 711-721 ◽  
Author(s):  
Claire Carpenet ◽  
Elie Guichard ◽  
Christophe Tzourio ◽  
Tobias Kurth

Objectives The aim was to evaluate the association of self-perceived levels of attention deficit and hyperactivity symptoms with non-migraine and migraine headaches among university students. We also evaluated their association with migraine aura. Methods Study subjects were all participants in the internet-based Students Health Research Enterprise. Scores were built to evaluate global attention and hyperactivity symptom levels, self-perceived attention deficit levels and self-perceived hyperactivity symptom levels based on the Adult Attention Deficit and Hyperactivity Disorder Self-Report Scale (ASRS v1.1.). We used standardised questions to classify headache and group participants into “no headache,” “non-migraine headache,” “migraine without aura” or “migraine with aura”. Results A total of 4816 students were included (mean age 20.3 ± 2.8 years; 75.5% women). Compared with participants without headache, we found significant associations between global ADHD scores and migraine. Students in the highest quintile of global ASRS scores had adjusted odds ratio (aOR) of 1.95 (95% CI 1.56–2.45) when compared to the lowest. This association was mainly driven by an association between self-perceived hyperactivity and migraine with aura. The aOR for migraine with aura was 2.83 (95% CI 2.23–3.61) for students in the highest quintile of hyperactivity. No significant association was found for any attention and hyperactivity symptom level measure and non-migraine headache and between self-perceived levels of attention deficit and migraine. Conclusions Among students in higher education in France, self-perceived levels of attention deficit and hyperactivity symptoms were selectively associated with migraine. The association was strongest for the hyperactivity domain and migraine with aura.


Cephalalgia ◽  
1993 ◽  
Vol 13 (3) ◽  
pp. 180-183 ◽  
Author(s):  
Richard D Piper ◽  
Lars Edvinsson ◽  
Rolf Ekman ◽  
Geoffrey A Lambert

There is circumstantial evidence that cortical spreading depression (SD) may account for the scotoma and the “spreading cortical oligemia” seen during migraine with aura. It has been shown that calcitonin gene-related peptide (CGRP) is increased in blood taken from the external jugular vein (EJV) in humans during migraine and after stimulation of the trigeminal ganglion. To test the hypothesis that cortical SD may elevate the concentration of this vasoactive peptide in the EJV during migraine, we have measured its concentration in the external jugular vein of cats during cortical SD. This study demonstrates that SD has no effect on the concentration of CGRP either during the passage of a wave of spreading depression across the cortex or, 60 min later, during the period of post-SD cortical oligemia.


Cephalalgia ◽  
1993 ◽  
Vol 13 (2) ◽  
pp. 132-134 ◽  
Author(s):  
Leo Goldhammer

This is a case history of a 38–year-old woman with a dumbbell-shaped C2 neurofibroma associated with right-sided classic migraine headaches (migraine with aura) and cervical trigeminal signs on the affected side. Surgical removal of the tumor was followed by resolution of the migraine headaches and persistence of the signs of cervicotrigeminal involvement.


Cephalalgia ◽  
1992 ◽  
Vol 12 (6) ◽  
pp. 356-359 ◽  
Author(s):  
PA Keenan ◽  
LA Lindamer

Fluctuation of estrogen levels across the menstrual cycle influences migraine headache. In this study, 53 women documented prospectively the incidence and severity of headache daily for an average of three menstrual cycles. Seven of the women met the criteria established by the International Headache Society for migraine with or without aura, while the remaining 46 women failed to do so. Chi-square analysis revealed that, overall, the incidence of non-migraine headache was dependent on day of the cycle (χ2 [1,66] = 247.7, p < 0.001), with more headaches occurring during the perimenstrual phase. The 46 women without migraine were further classified according to NIMH criteria into PMS ( N= 26) and non-PMS groups (n = 26). An association between headache and menstrual cycle phase was noted for both groups ( p < 0.001), although the incidence of severe headache was greater for the PMS women, during both the perimenstrual and intermenstrual phases. Both groups experienced an increase in severe headaches during the perimenstrual phase. The PMS women peaked on the day prior to menstruation, while the non PMS women peaked on the first day of menstruation. There did not appear to be an overall difference in the reporting of mild headache across the cycle between women with or without PMS. These findings suggest that (a) severe headache which does not meet the criteria for migraine with or without aura also may be menstrually related in women with and without PMS and; (b) the as yet unidentified physiological mechanism predisposing some women to PMS may also render them susceptible to more frequent, severe, non-migraine headaches both during the perimenstrual phase and throughout the entire menstrual cycle.


Cephalalgia ◽  
2007 ◽  
Vol 27 (5) ◽  
pp. 456-460 ◽  
Author(s):  
OD San-Juan ◽  
PF Zermeño

Persistent aura symptoms in patients with migraine are rare but well documented. The International Headache Society defines persistent aura without infarction as when the aura symptoms persist for >1 week without radiographic evidence of infarction. The visual aura of migraine attacks has been explained by cortical spreading depression. We describe a case of a 28-year-old Mexican woman, who presented with persistent aura symptoms, and a literature review. The patient had a 24-year history of migraine headache. In November 2005 the patient had an attack which started with scintillating scotomas bilaterally associated with photopsias and amaurosis followed by migraine headache. All imaging studies were negative. The episode lasted 35 days and probably resolved with nimodipine therapy. Persistent aura symptoms are rare entities. This is the first case documented of a Mexican patient with persistent aura without infarction and probably resolved with nimodipine therapy.


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