Delayed Hyperperfusion Following Migraine With a Prolonged Aphasic Aura in a Patient With CADASIL

Tfelt-Hansen, P.; Jensen, Lars Thorbjørn; Olesen, Jes

doi:10.1111/j.1468-2982.2008.01626.x

Cited by 7 publications

(9 citation statements)

References 17 publications

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“…The hyperperfusion revealed by perfusion CT on day 7 is a more interesting finding with respect to migraine pathophysiology: the concept of 'delayed hyperperfusion' in MA has been suggested already by early studies [18,19], and some authors have hypothesized that it may reflect a loss of neurogenic control of cerebrovascular tone caused by CSD. Apparently, the duration and extent of hyperperfusion do correlate with the severity of aura symptoms [19]: in a recently reported case of prolonged aphasic aura in the setting of CADASIL, delayed hyperperfusion was recorded on day 5 [20]. Along these lines, several authors have demonstrated delayed unilateral hyperperfusion 48 h up to several days after symptom onset also in cases of prolonged aura in patients with hemiplegic migraine [21][22][23][24].…”

Section: Discussionmentioning

confidence: 88%

A case of Sturge–Weber syndrome with symptomatic hemiplegic migraine: Clinical and multimodality imaging data during a prolonged attack

Freilinger

Peters

Rémi

et al. 2009

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 88%

A case of Sturge–Weber syndrome with symptomatic hemiplegic migraine: Clinical and multimodality imaging data during a prolonged attack

Freilinger

Peters

Rémi

et al. 2009

Journal of the Neurological Sciences

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“…It is possible that a similar mechanism occurs in CADASIL patients since these patients have a decreased baseline level of cerebral blood flow (26,27). A more pronounced hypoperfusion phase, or a prolonged hyperperfusion phase, as has been observed in a CADASIL patient (28), could affect the type and intensity of the aura. Since hypoperfusion as well as prolonged hyperperfusion has been associated with prolonged duration of migraine aura (28,33), it is possible that these flow changes lead to more impairment of cortical function during the attack.…”

Section: Possible Mechanisms Of Migraine In Cadasilmentioning

confidence: 94%

“…A more pronounced hypoperfusion phase, or a prolonged hyperperfusion phase, as has been observed in a CADASIL patient (28), could affect the type and intensity of the aura. Since hypoperfusion as well as prolonged hyperperfusion has been associated with prolonged duration of migraine aura (28,33), it is possible that these flow changes lead to more impairment of cortical function during the attack. For example, normal CSDs, which usually leads to typical visual aura in the general migraineurs, may cause atypical prolonged hemiplegic aura in CADASIL, because of the pronounced flow changes (23).…”

Section: Possible Mechanisms Of Migraine In Cadasilmentioning

confidence: 97%

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CADASIL and migraine: A narrative review

et al. 2010

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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is caused by mutations in the NOTCH3 gene and is clinically characterized by recurrent stroke, cognitive decline, psychiatric disturbances and migraine. The prevalence of migraine in CADASIL is slightly higher than in the general population, and the proportion of migraine with aura is much higher. The pathophysiological mechanism that leads to increased aura prevalence in CADASIL is unknown. Possible mechanisms of the excess of migraine with aura are an increased susceptibility to cortical spreading depression (CSD) or a different expression of CSD. It is also possible that the brainstem migraine area is involved in CADASIL. Last, it is possible that the NOTCH3 mutation acts as a migraine aura susceptibility gene by itself. In this narrative review we summarize the literature about migraine in CADASIL, with a special focus on what CADASIL might teach us about the pathophysiology of migraine.

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“…10 Those with CADASIL are known to have a reduced baseline total cerebral blood flow when compared with the general population. 11 In one case report involving a patient with CADASIL, ictal perfusion imaging showed a delayed cerebral hyperperfusion following a prolonged migrainous aura. 12 Calcitonin gene-related peptide (CGRP), a potent vasoactive nociceptive peptide important in migraine pathology and cortical spreading depression, may be a contributor to migrainous perfusion changes in the general population.…”

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confidence: 99%

CGRP, Migraine, and Brain MRI in CADASIL

et al. 2022

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Background: Migraine is associated with neuroimaging differences in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). However, it is unknown if migraine-related disability (MRD) or if calcitonin gene-related peptide (CGRP), a vasoactive peptide important in migraine pathology, have radiographic implications. The aims of this study were to identify whether MRD or interictal serum CGRP levels impacted neuroimaging findings for those with CADASIL. Materials and Methods: A cross-sectional analysis was performed. The primary outcomes were neuroimaging differences associated with MRD among those with migraine or interictal serum CGRP levels of those with and without migraine. MRD was defined by 2 migraine disability scales (Migraine Disability Assessment, Headache Impact Test-6). Retrospective brain magnetic resonance imaging was reviewed (average 1.7 ± 2.0 y before enrollment). Rank-sum and χ2 tests were used. Results: Those with migraine (n=25, vs. n=14 without) were younger [median 49 (25 to 82) y vs. 60 (31 to 82) y, P<0.007], had fewer cerebral microbleeds (0 to 31 vs. 0 to 50, P=0.02) and less frequently had anterior temporal lobe T2 hyperintensities [68% (17/25) vs 100% (14/14), P=0.02]. MRD scale outcomes had no significant radiographic associations. Interictal serum CGRP did not differ (migraine: n=18, 27.0±9.6 pg/mL vs. no migraine: n=10, 26.8±15.7 pg/mL, P=0.965). Conclusions: Migraine may forestall microangiopathy in CADASIL, though possibly independent of severity as measured by MRD. Interictal serum CGRP did not differ in our cohort suggesting CGRP may not be vital to migraine pathophysiology in CADASIL. Larger studies are needed to account for age differences.

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Delayed Hyperperfusion Following Migraine With a Prolonged Aphasic Aura in a Patient With CADASIL

Cited by 7 publications

References 17 publications

A case of Sturge–Weber syndrome with symptomatic hemiplegic migraine: Clinical and multimodality imaging data during a prolonged attack

A case of Sturge–Weber syndrome with symptomatic hemiplegic migraine: Clinical and multimodality imaging data during a prolonged attack

CADASIL and migraine: A narrative review

CGRP, Migraine, and Brain MRI in CADASIL

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