Persistent Aura with Small Occipital Cortical Infarction: Implications for Migraine Pathophysiology

Thissen, Sam; Koehler, Peter J.

doi:10.1159/000366409

Cited by 4 publications

(5 citation statements)

References 13 publications

(18 reference statements)

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“…It is worth noting that the International Classification of Headache Disorders, third version ( 71 ) lists features for other less frequent migraine disorders, such as status migrainosus, persistent aura without infarction, and migrainous infarction ( 71 ). The aforementioned SD mechanisms may play a significant role in these conditions, as demonstrated specifically in migrainous infarction, a condition that may lie on a continuum with cerebral ischemia (see below) ( 112 – 114 ). It has been shown that FHM1 mutations may share genetic determinants of migraine with aura and stroke; indeed, these mutations, typically associated with migraine with aura, increase stroke vulnerability and also accelerate stroke evolution ( 115 ) by enhancing the susceptibility to ischemic depolarizations, a process akin to SD.…”

Section: Sd In Disease Conditionsmentioning

confidence: 99%

Understanding Spreading Depression from Headache to Sudden Unexpected Death

et al. 2018

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Spreading depression (SD) is a neurophysiological phenomenon characterized by abrupt changes in intracellular ion gradients and sustained depolarization of neurons. It leads to loss of electrical activity, changes in the synaptic architecture, and an altered vascular response. Although SD is often described as a unique phenomenon with homogeneous characteristics, it may be strongly affected by the particular triggering event and by genetic background. Furthermore, SD may contribute differently to the pathogenesis of widely heterogeneous clinical conditions. Indeed, clinical disorders related to SD vary in their presentation and severity, ranging from benign headache conditions (migraine syndromes) to severely disabling events, such as cerebral ischemia, or even death in people with epilepsy. Although the characteristics and mechanisms of SD have been dissected using a variety of approaches, ranging from cells to human models, this phenomenon remains only partially understood because of its complexity and the difficulty of obtaining direct experimental data. Currently, clinical monitoring of SD is limited to patients who require neurosurgical interventions and the placement of subdural electrode strips. Significantly, SD events recorded in humans display electrophysiological features that are essentially the same as those observed in animal models. Further research using existing and new experimental models of SD may allow a better understanding of its core mechanisms, and of their differences in different clinical conditions, fostering opportunities to identify and develop targeted therapies for SD-related disorders and their worst consequences.

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Section: Sd In Disease Conditionsmentioning

confidence: 99%

Understanding Spreading Depression from Headache to Sudden Unexpected Death

et al. 2018

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“…Migraine aura is generally attributed to CSD, which is a brief depolarizing wave moving at 3–5 mm/min across the cortex followed by sustained neuronal depression. During prolonged aura, long-lasting cortical neuronal hyperexcitability can result in reverberating CSD 25. Thus, inhibitory control may be lost in the primary visual cortex due to perturbation of the GABAergic system.…”

Section: Discussionmentioning

confidence: 99%

“…One group proposed that migraine-related neuronal injury causes glial cell multiplication and accumulation of protein and fat macrophages, which restricts the motion of water molecules in MRI and yields hyperintensities in the T1-weighted image of the affected cerebral region;23 this is supported by a recent report 24. Others have demonstrated cortical hyperexcitability in the primary visual cortex, possibly due to impairment of the γ-aminobutyric acid (GABA)ergic inhibitory network and hypoactivity of thalamo-cortical circuits 25. Cortical hypermetabolism was also proposed in a case of MI with laminar necrosis 26.…”

Section: Systematic Reviewmentioning

confidence: 92%

“…In another patient with MI and vasospasm, a biochemical origin was suggested for the latter based on evidence of enhanced intracellular calcium concentration and vasoactive agents such as serotonin, angiotensin II, hydroperoxides, adenosine diphosphate, and prostaglandins 16Table 2Biochemical Implications Proposed In Migrainous InfarctionMorais et al 201824Deposition of fat laden macrophages, higher protein concentration and glial cell proliferation in the cortical area affectedThissen and Koehler 201425Damage to inhibitory GABAergic cells in the occipital lobe and low cortical preactivation in thalamocortical tractArboix et al 201323Fat macrophages and glial proliferation due to selective neuronal damageSchulz et al 200936Phosphocreatine/inorganic phosphate ratio lower in patients with persistent aura than in Migrainous infarction and controlsLiang and Scott 200726Blood-brain barrier disruption, cytotoxic edema secondary to focal hypermetabolismSolomon et al 199016Intracellular calcium increase, catecholamines and prostaglandins release leading to vasoconstriction …”

Section: Systematic Reviewmentioning

confidence: 99%

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<p>Migrainous Infarction And Cerebral Vasospasm: Case Report And Literature Review</p>

Vinciguerra¹,

Cantone²,

Lanza³

et al. 2019

JPR

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Migrainous infarction (MI) is a rare complication of migraines that accounts for 0.5–1.5% of all ischemic strokes. Although the pathogenesis of MI is still debated, cortical spreading depression and the consequent biochemical cascade and hemodynamic changes are presumed to play an important role. Here we describe a case of MI and systematically review the literature on the complex and possibly bidirectional relationship between migraine and stroke. A 44-year-old female with history of migraine with visual aura presented at the Emergency Department due to a sudden onset of left limb paresis and hypoesthesia. Brain magnetic resonance imaging revealed right fronto-parietal ischemic stroke. Two days after hospitalization, the patient experienced a prolonged visual aura and showed ultrasound evidence of intracranial artery vasospasm. To date, there have been 33 published articles on a total 119 patients with MI, although intracranial vasospasm has rarely been reported. Sustained hyperexcitability of cortical neurons, impairment of γ-aminobutyric acid inhibitory circuitry, altered serotonergic transmission, release of vasoconstrictive molecules, and cerebral blood flow changes have been proposed as pathogenic mechanisms of MI. The present case provides insight into the pathophysiological link between stroke and migraine, thus aiding clinicians in therapeutic decision-making although additional studies are needed to clarify the clinical, neuroradiological, and ultrasound findings that link MI and stroke-related migraine.

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“…Eine persistierende Aura kann Ausdruck einer fokalen Hirnschädigung [17], z. B. eines Infarkts [18] oder einer arteriovenösen Malformation sein [19]. In derartigen Fällen ist die Abgrenzung zu einer Epilepsie erforderlich, die auraähnliche visuelle Phänomene auslösen kann [20].…”

Section: Migräneunclassified

Das Visual-Snow-Syndrom: Symptome und ophthalmologische Befunde

Tegetmeyer

2016

Klin Monatsbl Augenheilkd

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The symptom "visual snow" describes the continuous perception of tiny flickering dots within the whole visual field of both eyes. The diagnosis of a visual snow syndrome requires the appearance of typical additional visual symptoms and the exclusion of ophthalmological or neurological causes, or pharmacological influences. Three male and four female subjects between 13 and 36 years of age referred with visual snow were investigated and asked about their symptoms. A complete ophthalmological investigation, including binocular fundoscopy, was performed in all patients. Furthermore, best corrected visual acuity, perimetry, binocular functions, colour vision (D15-test), full-field ERG, pattern-reversal VEP and SD-OCT images of macula and optic nerve (RNFL) were analysed. Visual acuity of at least 1.0 and normal findings for all further investigations were observed in all patients. The following additional visual symptoms were identified: illusionary palinopsia (n = 6), disturbance of night vision (n = 5), positive light phenomena (n = 7). A history of migraine with aura was reported in five patients. The intake of hallucinogenic drugs or centrally active pharmaceuticals was denied by all patients. The findings of available or initiated neurological investigations were normal. The visual snow syndrome has to be regarded as a diagnosis of exclusion. Visual function parameters are not impaired. Apart from eye diseases, a persistent migraine aura as well as neurological diseases or the intake of hallucinogenic drugs must be excluded as possible causes of visual snow and palinopsia.

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Persistent Aura with Small Occipital Cortical Infarction: Implications for Migraine Pathophysiology

Cited by 4 publications

References 13 publications

Understanding Spreading Depression from Headache to Sudden Unexpected Death

Understanding Spreading Depression from Headache to Sudden Unexpected Death

<p>Migrainous Infarction And Cerebral Vasospasm: Case Report And Literature Review</p>

Das Visual-Snow-Syndrom: Symptome und ophthalmologische Befunde

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