Aura and Head pain: relationship and gaps in the translational models

Bolay, Hayrünnisa; Vurallı, Doğa; Goadsby, PJ

doi:10.1186/s10194-019-1042-8

Cited by 40 publications

(45 citation statements)

References 136 publications

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“…During CSD, the cerebral cortex involved in aura symptom generation presents a prolonged depolarization status which overcomes the duration of a usual membrane action potential, thus explaining aura typical duration (5‐60 minutes). Recently, it has been acutely observed that canonical CSD does explain the typical migraine aura manifestations, for example, visual aura followed by contralateral pain, whereas less common migraine aura scenarios, such as pain ipsilateral to aura symptoms, led to the hypothesis that spreading depression can occur in other brain areas 12 …”

Section: Clinical Evidencementioning

confidence: 99%

Migraine as a Cortical Brain Disorder

et al. 2020

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Purpose Migraine is an exclusively human chronic disorder with ictal manifestations characterized by a multifaceted clinical complexity pointing to a cerebral cortical involvement. The present review is aimed to cover the clinical, neuroimaging, and neurophysiological literature on the role of the cerebral cortex in migraine pathophysiology. Overview Converging clinical scenarios, advanced neuroimaging data, and experimental neurophysiological findings, indicate that fluctuating excitability, plasticity, and metabolism of cortical neurons represent the pathophysiological substrate of the migraine cycle. Abnormal cortical responsivity and sensory processing coupled to a mismatch between the brain’s energy reserve and workload may ignite the trigeminovascular system, leading to the migraine attack through the activation of subcortical brain trigeminal and extra‐trigeminal structures, and driving its propagation and maintenance. Discussion The brain cortex emerges as the crucial player in migraine, a disorder lying at the intersection between neuroscience and daily life. Migraine disorder stems from an imbalance in inhibitory/excitatory cortical circuits, responsible for functional changes in the activity of different cortical brain regions encompassing the neurolimbic‐pain network, and secondarily allowing a demodulation of subcortical areas, such as hypothalamus, amygdala, and brainstem nuclei, in a continuous mutual crosstalk.

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Section: Clinical Evidencementioning

confidence: 99%

Migraine as a Cortical Brain Disorder

et al. 2020

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“…TBI, including mTBI, might trigger cortical spreading depression (CSD) at the time of injury and be associated with the extent of brain tissue injury and functional outcomes (35). As has been theorized for migraine, CSD might directly activate the trigeminocervical system resulting in headache (36)(37)(38). In fact, some patients with PTH are reported to experience auras with their PTH (12,18,39).…”

Section: Pathophysiologymentioning

confidence: 99%

Post-traumatic headache due to mild traumatic brain injury: Current knowledge and future directions

Schwedt

2020

Cephalalgia

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Background/objective Post-traumatic headache is one of the most common and persistent symptoms following mild traumatic brain injury. The objective of this narrative review is to provide an update on the diagnostic criteria, clinical presentation, epidemiology, pathophysiology, and treatment of post-traumatic headache, and to identify future research priorities. Methods This is a narrative review of the literature regarding post-traumatic headache attributed to mild traumatic brain injury. Results Onset of post-traumatic headache within 7 days of injury is the only evidence for a causal relationship between the injury and the headache included in the diagnostic criteria. Post-traumatic headache often resolves within the first few days of onset, whereas it persists for at least 3 months in 30–50%. The majority of insights into post-traumatic headache pathophysiology come from pre-clinical animal studies and human imaging studies, which implicate structural, functional, metabolic, and neuroinflammatory mechanisms for post-traumatic headache. There is a paucity of quality evidence for how to best treat post-traumatic headache. Conclusions Although meaningful progress has been made in the post-traumatic headache field, priorities for future research are numerous, including the optimization of diagnostic criteria, a greater understanding of post-traumatic headache pathophysiology, identifying mechanisms and predictors for post-traumatic headache persistence, and identifying safe, well-tolerated, effective therapies.

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“…Visual aura symptoms are traditionally attributed to the depolarization phase of CSD and/or CSD-induced hemodynamic changes. However, some features of CSD do not match clinical symptoms of aura; for example, the pre-CSD excitation of cortical neurons, which is thought to underlie positive aura symptoms, seems to be very brief (2–4 sec) to explain the symptoms (6). Our study in awake rats shows that CSD is followed by aberrant cortical activation and hemispheric functional disconnection that last several minutes.…”

Section: Discussionmentioning

confidence: 99%

“…It is thought that a brief burst of neuronal firing before CSD onset produces positive visual symptoms (flashing lights, scintillations) and subsequent depression of neuronal activity underlies negative symptoms (scotoma, blurring of vision). Despite the widely accepted link between CSD and migraine aura, there are several gaps in translating CSD features to clinical aura symptoms and some patterns of aura described in migraine patients cannot be explained based on the known properties of CSD (6). This may be in part due to the fact that most information about CSD and its electrophysiological characteristics has been obtained in anesthetized animals and acute slice preparations.…”

Section: Introductionmentioning

confidence: 99%

Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

2020

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Objective Growing evidence shows a critical role of network disturbances in the pathogenesis of migraine. Unilateral pattern of neurological symptoms of aura suggests disruption of interhemispheric interactions during the early phase of a migraine attack. Using local field potentials data from the visual and motor cortices, this study explored effects of unilateral cortical spreading depression, the likely pathophysiological mechanism of migraine aura, on interhemispheric functional connectivity in freely behaving rats. Methods Temporal evolution of the functional connectivity was evaluated using mutual information and phase synchronization measures applied to local field potentials recordings obtained in homotopic points of the motor and visual cortices of the two hemispheres in freely behaving rats after induction of a single unilateral cortical spreading depression in the somatosensory S1 cortex and sham cortical stimulation. Results Cortical spreading depression was followed by a dramatic broadband loss of interhemispheric functional connectivity in the visual and motor regions of the cortex. The hemispheric disconnection started after the end of the depolarization phase of cortical spreading depression, progressed gradually, and terminated by 5 min after initiation of cortical spreading depression. The network impairment had region- and frequency-specific characteristics and was more pronounced in the visual cortex than in the motor cortex. The period of impaired neural synchrony coincided with post-cortical spreading depression electrographic aberrant activation of the ipsilateral cortex and abnormal behavior. Conclusion The study provides the first evidence that unilateral cortical spreading depression induces a reversible loss of functional hemispheric connectivity in the cortex of awake animals. Given a critical role of long-distance cortical synchronization in sensory processing and sensorimotor integration, the post-cortical spreading depression breakdown of functional connectivity may contribute to neuropathological mechanisms of aura generation.

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Aura and Head pain: relationship and gaps in the translational models

Cited by 40 publications

References 136 publications

Migraine as a Cortical Brain Disorder

Migraine as a Cortical Brain Disorder

Post-traumatic headache due to mild traumatic brain injury: Current knowledge and future directions

Transient loss of interhemispheric functional connectivity following unilateral cortical spreading depression in awake rats

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