Neurovascular changes in prolonged migraine aura in FHM with a novel ATP1A2 gene mutation

Iizuka, Takahiro; Takahashi, Yūji; Sato, Minoru; Yonekura, Junko; Miyakawa, Saori; Endo, M; Hamada, Junichi; Kan, Shinichi; Mochizuki, Hideki; Momose, Yoshika; Tsuji, Shoji; Sakai, Fumihiko

doi:10.1136/jnnp-2011-300843

Cited by 39 publications

(44 citation statements)

References 41 publications

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“…Imaging FHM patients with prolonged symptoms (lasting 4 to 12 days) on days 1 to 4 most frequently evidenced hyperperfusion in the "predominantly affected hemisphere" contralateral to hemiplegia, although hypoperfusion was also noted. 25,26 The "non-predominantly affected" hemisphere exhibited only hypoperfusion. in 2 patients with signs of acute ischemic stroke who turned out to suffer from FHM, Hansen and colleagues 27 recorded the early phase of the hemiplegic aura using computed tomography with perfusion sequences and MRI.…”

Section: This Review Was Initiated With a Pubmed Search Of The Us Natmentioning

confidence: 99%

Structural and Functional Neuroimaging in Migraine: Insights From 3 Decades of Research

Lakhan

Avramut

Tepper³

2012

Headache

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Modern imaging methods provide unprecedented insights into brain structure, perfusion, metabolism, and neurochemistry, both during and between migraine attacks. Neuroimaging investigations conducted in recent decades bring us closer to uncovering migraine as a multifaceted, primarily central nervous system disorder. Three main categories of structural and functional brain changes are described in this review, corresponding to the migrainous aura, ictal headache, and interictal states. (Headache 2013;53:46-66)

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Section: This Review Was Initiated With a Pubmed Search Of The Us Natmentioning

confidence: 99%

Structural and Functional Neuroimaging in Migraine: Insights From 3 Decades of Research

Lakhan

Avramut

Tepper³

2012

Headache

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“…7 Single-photon emission computed tomography (SPECT) data indicate that clustering of CSD may also develop in hemiplegic migraine, a special subtype of migraine characterized by prolonged aura with motor weakness. 8,9 Nevertheless, to the best of our knowledge, the pathophysiological difference between single and clustering spreading depression/ depolarization has not been fully explored.…”

Section: Introductionmentioning

confidence: 99%

High-mobility group box 1 is an important mediator of microglial activation induced by cortical spreading depression

Takizawa

Shibata

Kayama

et al. 2016

J Cereb Blood Flow Metab

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Single episodes of cortical spreading depression (CSD) are believed to cause typical migraine aura, whereas clusters of spreading depolarizations have been observed in cerebral ischemia and subarachnoid hemorrhage. We recently demonstrated that the release of high-mobility group box 1 (HMGB1) from cortical neurons after CSD in a rodent model is dependent on the number of CSD episodes, such that only multiple CSD episodes can induce significant HMGB1 release. Here, we report that only multiple CSD inductions caused microglial hypertrophy (activation) accompanied by a greater impact on the transcription activity of the HMGB1 receptor genes, TLR2 and TLR4, while the total number of cortical microglia was not affected. Both an HMGB1-neurtalizing antibody and the HMGB1 inhibitor glycyrrhizin abrogated multiple CSD-induced microglial hypertrophy. Moreover, multiple CSD inductions failed to induce microglial hypertrophy in TLR2/4 double knockout mice. These results strongly implicate the HMGB1-TLR2/4 axis in the activation of microglia following multiple CSD inductions. Increased expression of the lysosomal acid hydrolase cathepsin D was detected in activated microglia by immunostaining, suggesting that lysosomal phagocytic activity may be enhanced in multiple CSDactivated microglia.

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“…Fedak et al reported four pediatric cases of SHM where these flow abnormalities spontaneously resolved within 24 h after hospital presentation [23]. Other authors have reported similar findings [24][25][26]. Sugrue et al described a case wherein evidence of cerebral edema without evidence of infarction was documented in a patient with persistent hemiplegia following headache [27].…”

Section: Sporadic Hemiplegic Migrainementioning

confidence: 72%

Hemiplegia and Headache: a Review of Hemiplegia in Headache Disorders

Lopez

Holdridge

Rothrock

2014

Curr Pain Headache Rep

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The most common scenario wherein the practicing neurologist is likely to encounter a patient with headache and hemiplegia will vary depending on his/her specific type of practice. A neurologist providing consultative service to an emergency department is far more likely to see patients with "secondary" headache and hemiplegia in the setting of either ischemic or hemorrhagic stroke than hemiplegia as a transient feature of a primary headache disorder. Neurologists subspecializing in headache medicine who practice in a tertiary referral headache clinic are more likely to encounter hemiplegic migraine, but even in that clinical setting hemiplegic migraine is by no means a frequent diagnosis. The acute onset of hemiplegia can be very frightening not only to the patient but also to the medical personnel. Given the abundance of mimicry, practitioners must judiciously ascertain the correct diagnosis as treatment may greatly vary depending on the cause of both headache and hemiplegia. In this review, we will address the most common causes of hemiplegia associated with headache.

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Neurovascular changes in prolonged migraine aura in FHM with a novel ATP1A2 gene mutation

Cited by 39 publications

References 41 publications

Structural and Functional Neuroimaging in Migraine: Insights From 3 Decades of Research

Structural and Functional Neuroimaging in Migraine: Insights From 3 Decades of Research

High-mobility group box 1 is an important mediator of microglial activation induced by cortical spreading depression

Hemiplegia and Headache: a Review of Hemiplegia in Headache Disorders

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