scholarly journals Clinical Study of Chronic Heredofamilial Migraine with Aura

2020 ◽  
pp. 1-8
Author(s):  
Orlando J Castejón ◽  
◽  
Galindez P ◽  
De Castejón Salones M ◽  
Torres IA ◽  
...  

Sixteen patients ranging from 19 to 68 years-old were studied with Chronic Heredofamilial Migraine with Aura. The following symptoms were associated to chronic heredofamilial migraine: dizziness, vertigo, syncope, redness eye, photophobia, blurred vision and reduced and loss of vision, scintillant scotomas, dizziness, ears noise, temporospatial disorientation, memory disorders, effort dyspnea, asthenia, son phobia, nausea, vomits, and social, labor and home stress. The followings symptoms were interpreted as migraine auras: Blurred vision and reduced and loss of vision, scintillant scotomas, dizziness, ears noise. The following comorbidities were found: syncope, bradycardia, mitral prolapse and tachycardia, effort dyspnea, asthenia, seizures, environment, labor and home stress, sleep disorders or insomnia and constipation. The followings aspects were discussed: migraine and prodroms, migraine and vascular diseases, migrainous vertigo and dizziness, symptoms related to the visual system in migraine, migraine and sleep disorders, hemiplegic migraine, neural correlates of migraine, histamine and migraine, the calcitonin gene-related peptide in migraine and its role in migraine physiopathology, and migraine genetic

2021 ◽  
Vol 22 (5) ◽  
pp. 2688
Author(s):  
Marta Kowalska ◽  
Michał Prendecki ◽  
Thomas Piekut ◽  
Wojciech Kozubski ◽  
Jolanta Dorszewska

Migraine is a common neurological disease that affects about 11% of the adult population. The disease is divided into two main clinical subtypes: migraine with aura and migraine without aura. According to the neurovascular theory of migraine, the activation of the trigeminovascular system (TGVS) and the release of numerous neuropeptides, including calcitonin gene-related peptide (CGRP) are involved in headache pathogenesis. TGVS can be activated by cortical spreading depression (CSD), a phenomenon responsible for the aura. The mechanism of CSD, stemming in part from aberrant interactions between neurons and glia have been studied in models of familial hemiplegic migraine (FHM), a rare monogenic form of migraine with aura. The present review focuses on those interactions, especially as seen in FHM type 1, a variant of the disease caused by a mutation in CACNA1A, which encodes the α1A subunit of the P/Q-type voltage-gated calcium channel.


Cephalalgia ◽  
2010 ◽  
Vol 30 (10) ◽  
pp. 1179-1186 ◽  
Author(s):  
Jakob Møller Hansen ◽  
Anne Werner Hauge ◽  
Jes Olesen ◽  
Messoud Ashina

Introduction: Calcitonin gene-related peptide (CGRP) is a key molecule in migraine pathogenesis. Intravenous CGRP infusion triggers delayed migraine-like attacks in patients with migraine without aura (MO). In contrast to patients with MO, in prior studies patients with familial hemiplegic migraine (FHM) did not report more migraine-like attacks compared to controls. Whether CGRP triggers migraine in patients with typical (non-hemiplegic) migraine with aura is (MA) unknown. In the present study we examined the migraine inducing effect of CGRP infusion in patients suffering from MA and healthy controls. Methods: Fourteen patients suffering exclusively from migraine with typical aura (MA) and 11 healthy volunteers received a continuous intravenous infusion of 1.5 µg/min CGRP over 20 minutes. Headache and other migraine symptoms were scored every 10 minutes for one hour and self recorded hourly thereafter and until 13 hours post-infusion. Results: CGRP infusion induced significantly more delayed headaches in MA patients (12 out of 14) than in controls (2 out of 11) ( p = 0.001). Furthermore, significantly more MA patients (57%; 8 out of 14) fulfilled criteria for an experimentally induced migraine attack after CGRP than controls (0%; 0 out of 11) ( P = 0.003). Four patients (28%) reported aura symptoms after CGRP infusion. Conclusion: CGRP triggered migraine-like attacks without aura in patients suffering exclusively from MA. It also triggered a typical aura in 28% of the patients. These data indicate similar neurobiological pathways responsible for triggering migraine headache in MA and MO patients, and suggest differences between MA/MO and FHM.


Neurology ◽  
2003 ◽  
Vol 60 (4) ◽  
pp. 595-601 ◽  
Author(s):  
Lise L. Thomsen ◽  
Elsebet Ostergaard ◽  
Jes Olesen ◽  
Michael B. Russell

Objective: To compare clinical characteristics of patients with sporadic hemiplegic migraine (SHM) with those of patients with migraine with typical aura (MA) and patients with familial hemiplegic migraine (FHM).Methods: The authors used a computer search of Denmark’s National Patient Register to screen the population for patients with migraine with aura with motor weakness, and also examined case records from headache clinics and private practicing neurologists and placed advertisements. The authors screened patients and their relatives with a semi-structured validated telephone interview. All recruited patients were then interviewed by a physician and given a neurologic examination.Results: A total of 105 patients with SHM were identified. Seventy-two percent had four typical aura symptoms: visual, sensory, aphasic, and motor. All had at least two symptoms present during SHM attacks. A gradual progression and sequential appearance of aura symptoms was typical; compared with MA, the duration of each aura symptom was usually prolonged and bilateral motor symptoms were more frequent. Of the patients with SHM, 72% fulfilled the criteria for basilar migraine during SHM attacks. The aura was usually followed by headache, as is common in FHM but not MA.Conclusions: Patients with sporadic hemiplegic migraine had clinical symptoms identical to familial hemiplegic migraine and significantly different from migraine with typical aura. Sporadic hemiplegic migraine is a separate entity, and should be classified with familial hemiplegic migraine.


Cephalalgia ◽  
2011 ◽  
Vol 31 (12) ◽  
pp. 1274-1281 ◽  
Author(s):  
Jakob Møller Hansen ◽  
Anne Werner Hauge ◽  
Messoud Ashina ◽  
Jes Olesen

Objective: The aim was to identify and describe migraine trigger factors in patients with familial hemiplegic migraine (FHM) from a population-based sample. Methods: 127 FHM patients were sent a questionnaire listing 16 trigger factors. Distinction was made between attacks of hemiplegic migraine (HM) and migraine with aura (MA) or without aura (MO) within each patient. Results: The response rate was 59% (75/127) of whom 57 (76%) had current HM attacks. Sixty-three per cent (47/75) reported at least one factor triggering HM, and 36% (27/75) reported at least one factor that often or always caused HM. Twenty per cent (15/75) reported only HM, whereas FHM in combinations with MA and MO were reported by 80% (60/75). Stress (with attacks either following or during the stress), bright light, intense emotional influences and sleeping too much or too little were the trigger factors mentioned by most. Conclusion: Many FHM patients report trigger factors and one-third reported at least one trigger factor often or always triggering FHM. The typical triggers are the same as for MA. Patients should be educated to avoid these factors. The role of trigger factors in the onset of new or first attacks of FHM remains unknown.


Cephalalgia ◽  
2011 ◽  
Vol 31 (16) ◽  
pp. 1652-1658 ◽  
Author(s):  
Luiz Paulo Queiroz ◽  
Deborah Isa Friedman ◽  
Alan Mark Rapoport ◽  
R Allan Purdy

Background: Migraine aura, made up of one or more neurological symptoms arising from the cortex or brainstem, is a complex neurological phenomenon. Visual aura is the most frequent aura manifestation. Studying the subjective components of visual aura makes it possible to identify common characteristics. Objective: To thoroughly describe the characteristics of migraine visual aura in patients with migraine with aura. Methods: We performed a retrospective, descriptive study of the visual aura of 122 migraine patients collected at two headache clinics in the Americas. This study was designed to determine the characteristics of a typical visual aura. Results: The most common features of the visual aura in our study are that it occurs before the headache with a gap of less than 30 minutes, lasts 5 to 30 minutes, has a gradual onset, usually begins peripherally, is unilateral, and shimmers. Furthermore, the location of typical visual aura in the visual field has no fixed relationship to headache laterality, is slightly more often without color, and is often described as small bright dots and zigzag lines. Blurred vision, not typically considered to be an aura phenomenon of cortical origin, is in fact the most frequently reported visual symptom. Conclusions: Migraine visual aura is heterogeneous and pleomorphic, and some of our findings run contrary to common beliefs.


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 ◽  
2008 ◽  
Vol 28 (10) ◽  
pp. 1039-1047 ◽  
Author(s):  
E Cuenca-León ◽  
R Corominas ◽  
N Fernàndez-Castillo ◽  
V Volpini ◽  
M del Toro ◽  
...  

Familial hemiplegic migraine (FHM) is a rare type of migraine with aura. Mutations in three genes have been described in FHM patients: CACNA1A (FHM1), ATP1A2 (FHM2) and SCN1A (FHM3). We screened 27 Spanish patients with hemiplegic migraine (HM), basilar-type migraine or childhood periodic syndromes (CPS) for mutations in these three genes. Two novel CACNA1A variants, p.Val581Met and p.Tyr1245Cys, and a previously annotated change, p.Cys1534Ser, were identified in individuals with HM, although they have not yet been proven to be pathogenic. Interestingly, p.Tyr1245Cys was detected in a patient displaying a changing, age-specific phenotype that began as benign paroxysmal torticollis of infancy, evolving into benign paroxysmal vertigo of childhood and later becoming HM. This is the first instance of a specific non-synonymous base change being described in a subject affected with CPS. The fact that the molecular screen identified non-synonymous changes in< 15± of our HM patients further stresses the genetic heterogeneity underlying the presumably monogenic forms of migraine.


Cephalalgia ◽  
2014 ◽  
Vol 34 (10) ◽  
pp. 725-744 ◽  
Author(s):  
Philip R Holland

Objective The objective of the current article is to review the shared pathophysiological mechanisms which may underlie the clinical association between headaches and sleep disorders. Background The association between sleep and headache is well documented in terms of clinical phenotypes. Disrupted sleep-wake patterns appear to predispose individuals to headache attacks and increase the risk of chronification, while sleep is one of the longest established abortive strategies. In agreement, narcoleptic patients show an increased prevalence of migraine compared to the general population and specific familial sleep disorders have been identified to be comorbid with migraine with aura. Conclusion The pathophysiology and pharmacology of headache and sleep disorders involves an array of neural networks which likely underlie their shared clinical association. While it is difficult to differentiate between cause and effect, or simply a spurious relationship the striking brainstem, hypothalamic and thalamic convergence would suggest a bidirectional influence.


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