Neuronal injuries evidenced by transient cortical magnetic resonance enhancement in hemiplegic migraine: A case report

Pellerin, A.; Marois, Clémence; Mezouar, Nicolas; Mokhtari, Karima; Leclercq, Delphine; Law-Ye, Bruno

doi:10.1177/0333102418794481

Cited by 13 publications

(10 citation statements)

References 5 publications

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“…Cerebral hypoperfusion has been shown to be linked to SHM in some patients, whereas arterial dilation and focal hyperemia may also play a role in causing SHM . Severe SHM attacks may result in brain atrophy due to diffuse vasospasm without ischemia and blood‐brain barrier disruption . However, many researchers believe that the pathogenesis of SHM lies at the cellular level.…”

Section: Discussionmentioning

confidence: 99%

Interrelated Pathogenesis? Neuronal Intranuclear Inclusion Disease Combining With Hemiplegic Migraine

Wang

Nie

et al. 2019

Headache

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Background.-Neuronal intranuclear inclusion disease (NIID) is considered a heterogeneous disease because of its highly variable clinical manifestations. To date, there are no reports of NIID patients presenting with hemiplegic migraine (HM)-like headache, or of HM and NIID co-occurring as comorbidity, and the connection between these 2 seemingly unrelated clinical conditions has yet to be established.Method.-We present a patient with NIID who was previously diagnosed with HM. To determine the pathogenesis of HM in this NIID patient, we systematically reviewed published NIID and HM cases and cataloged them based on their clinical manifestations.Result.-The clinical manifestations of NIID is highly various; however, there is no case reported to date that shows HMlike symptoms or cerebral edema. All documented symptomatic HM cases show vascular dysfunction to various degrees, but none of them has been shown to be correlated with NIID. Conclusion.-Our patient is the first documented case in which HM and NIID occur simultaneously. Vascular dysfunctions that cause cerebral hypoperfusion and glucose hypometabolism, two of the dominant causes of symptomatic HM, may be associated with the accumulation of eosinophilic hyaline inclusions that cause NIID. However, the existence of inclusions may also alter neuronal behavior and indirectly cause cerebral hypoperfusion and glucose hypometabolism. Further research andobservations are needed to examine the relationship between HM and NIID. Key words: hemiplegic migraine, sporadic hemiplegic migraine, neuronal intranuclear inclusion disease Abbreviations: CNS central nervous system, CSF cerebrospinal fluid, CT computed tomography, DWI diffusion-weighted imaging, EEG electroencephalography, FHM familial hemiplegic migraine, HM hemiplegic migraine, ICHD International Classification of Headache Disorders, MRA magnetic resonance angiography, MRI magnetic resonance imaging, NIID neuronal intranuclear inclusion disease, PET positron emission tomography, PWI perfusion-weighted imaging, SHM sporadic hemiplegic migraine, SWI susceptibility weighted imaging (Headache 2020;60:382-395) Headache

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Section: Discussionmentioning

confidence: 99%

Interrelated Pathogenesis? Neuronal Intranuclear Inclusion Disease Combining With Hemiplegic Migraine

Wang

Nie

et al. 2019

Headache

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“…Four case reports have observed gadolinium-contrast MR enhancement of the meninges which could be accompanied by cortical edema [ 22 , 23 , 25 , 26 ]. These findings revealed permeability changes, that repeatedly occurred in the gyri, but were also present in the dura matter (Table 2 ) [ 22 ].…”

Section: Resultsmentioning

confidence: 99%

“…Contrast agent extravasated in 5 out of 13 hemiplegic migraine attacks. These were always prolonged auras, and the extravasation of contrast agent was extensive, sometimes associated with cortical oedema, and was seen in a phase of hyperemia [ 22 – 26 ].…”

Section: Discussionmentioning

confidence: 99%

Imaging the inflammatory phenotype in migraine

et al. 2022

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Several preclinical and clinical lines of evidence suggest a role of neuroinflammation in migraine. Neuroimaging offers the possibility to investigate and localize neuroinflammation in vivo in patients with migraine, and to characterize specific inflammatory constituents, such as vascular permeability, and macrophage or microglia activity. Despite all imaging data accumulated on neuroinflammation across the past three decades, an overview of the imaging evidence of neuroinflammation in migraine is still missing.We conducted a systematic review in the Pubmed and Embase databases to evaluate existing imaging data on inflammation in migraine, and to identify gaps in the literature. We included 20 studies investigating migraine without aura (N = 4), migraine with aura (N = 8), both migraine with and without aura (N = 3), or hemiplegic migraine (N = 5).In migraine without aura, macrophage activation was not evident. In migraine with aura, imaging evidence suggested microglial and parameningeal inflammatory activity. Increased vascular permeability was mostly found in hemiplegic migraine, and was atypical in migraine with and without aura. Based on the weight of existing and emerging data, we show that most studies have concentrated on demonstrating increased vascular permeability as a marker of neuroinflammation, with tools that may not have been optimal. In the future, novel, more sensitive techniques, as well as imaging tracers delineating specific inflammatory pathways may further bridge the gap between preclinical and clinical findings.

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“…49,52,53 In one of the cases, the patient had not yet been diagnosed with HM and ultimately underwent cortical biopsy, which showed "advanced neuronal suffering, ballooned cells, neoangiogenesis with fibrohyalinosis suggestive of noninflammatory vasculopathy." 52 This pathologic finding may explain cortical atrophy that has been reported in HM.…”

Section: Hemiplegic Migrainementioning

confidence: 99%

“…In contrast to diffusion restriction and focal T2 Three case reports demonstrated contrast enhancement in addition to cortical edema in the affected hemisphere during an HM attack, demonstrative of blood-brain barrier breakdown. 49,52,53 In one of the cases, the patient had not yet been diagnosed with HM and ultimately underwent cortical biopsy, which showed "advanced neuronal suffering, ballooned cells, neoangiogenesis with fibrohyalinosis suggestive of noninflammatory vasculopathy." 52 This pathologic finding may explain cortical atrophy that has been reported in HM.…”

Section: Hemiplegic Migrainementioning

confidence: 99%

Narrative review of neuroimaging in migraine with aura

2021

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Objective To improve the understanding of the role and utility of various neuroimaging modalities (clinical and research) for the evaluation of migraine aura (MA) and hemiplegic migraine during the ictal and interictal phases. Background MA is defined by reversible neurologic symptoms and is considered a manifestation of a primary condition. As such, most patients with MA do not require imaging. However, if there are atypical features, change in symptom pattern, or it is a first‐time presentation, neuroimaging may be used to evaluate for secondary conditions. Neuroimaging includes many modalities, and it is important to consider what information is being captured by these modalities (i.e., structural vs. functional). Imaging abnormalities may be noted both during (ictal) and between (interictal) MA attacks, and it is important for clinicians to be familiar with neuroimaging findings reported in migraine with aura (MWA) compared with other conditions. Methods With the assistance of a medical librarian, we performed a review of the literature pertaining to MWA and neuroimaging in PubMed. Search terms included were magnetic resonance imaging, positron‐emission tomography, single photon‐emission computed tomography, functional magnetic resonance imaging, and migraine with aura. We hand‐searched these references to inform our subsequent literature review. Results Acute MA can be associated with several unique neuroimaging findings—reversible cortical diffusion restriction, cortical venous engorgement, and a “biphasic” transition from hypoperfusion to hyperperfusion. Imaging findings during MA tend to span more than one vascular territory. Between acute attacks, neuroimaging in people with MWA can resemble migraine without aura in terms of white matter abnormalities and “infarct‐like lesions.” Research imaging modalities such as volumetric analysis and functional imaging have demonstrated unique findings in migraine with aura. Conclusion Although migraine is a clinical diagnosis, understanding of neuroimaging findings in MWA can help clinicians interpret imaging findings and improve patient care.

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Neuronal injuries evidenced by transient cortical magnetic resonance enhancement in hemiplegic migraine: A case report

Cited by 13 publications

References 5 publications

Interrelated Pathogenesis? Neuronal Intranuclear Inclusion Disease Combining With Hemiplegic Migraine

Interrelated Pathogenesis? Neuronal Intranuclear Inclusion Disease Combining With Hemiplegic Migraine

Imaging the inflammatory phenotype in migraine

Narrative review of neuroimaging in migraine with aura

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