Unilateral Cortical Spreading Depression Affects Sleep Need and Induces Molecular and Electrophysiological Signs of Synaptic Potentiation In Vivo

Faraguna, Ugo; Nelson, Aaron; Vyazovskiy, Vladyslav V.; Cirelli, Chiara; Tononi, Giulio

doi:10.1093/cercor/bhq041

Cited by 46 publications

(20 citation statements)

References 54 publications

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“…Changes consistent with both LTP and LTD have been induced by CSD in slice models (Footitt and Newberry, 1998; Berger et al, 2008); both potentiation and suppression of evoked responses have been observed in different in vivo studies (Guiou et al, 2005; Piilgaard and Lauritzen, 2009; Faraguna et al, 2010; de Souza et al, 2011). Our results reconcile these apparently contradictory findings by showing that potentiation and suppression depend on location relative to stimulated receptive field.…”

Section: Discussionmentioning

confidence: 86%

Cortical Sensory Plasticity in a Model of Migraine with Aura

et al. 2012

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The migraine attack is characterized by alterations in sensory perception, such as photophobia or allodynia, which have in common an uncomfortable amplification of the percept. It is not known how these changes arise. We evaluated the ability of cortical spreading depression (CSD), the proposed mechanism of the migraine aura, to shape the cortical activity that underlies sensory perception. We measured forepaw- and hindpaw-evoked sensory responses in rat, before and after CSD, using multi-electrode array recordings and 2-dimensional optical spectroscopy. CSD significantly altered cortical sensory processing on a timescale compatible with the duration of the migraine attack. Both electrophysiological and hemodynamic maps had a reduced surface area (were sharpened) after CSD. Electrophysiological responses were potentiated at the receptive field center, but suppressed in surround regions. Finally, the normal adaptation of sensory evoked responses was attenuated at the receptive field center. In summary, we show that CSD induces changes in the evoked cortical response that are consistent with known mechanisms of cortical plasticity. These mechanisms provide a novel neurobiological substrate to explain the sensory alterations of the migraine attack.

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Section: Discussionmentioning

confidence: 86%

Cortical Sensory Plasticity in a Model of Migraine with Aura

et al. 2012

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“…These increases in neural activity and blood flow should raise production of BDNF by neurons and the endothelium, respectively. In fact, BDNF mRNA and protein levels are markedly increased in the rat brain, and long‐term synaptic potentiation is strengthened, following CSD.…”

Section: Components Of Migraine Through the Lens Of Neuroprotectionmentioning

confidence: 99%

The Migraine Attack as a Homeostatic, Neuroprotective Response to Brain Oxidative Stress: Preliminary Evidence for a Theory

Borkum

2017

Headache

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Background.-Previous research has suggested that migraineurs show higher levels of oxidative stress (lipid peroxides) between migraine attacks and that migraine triggers may further increase brain oxidative stress. Oxidative stress is transduced into a neural signal by the TRPA1 ion channel on meningeal pain receptors, eliciting neurogenic inflammation, a key event in migraine. Thus, migraines may be a response to brain oxidative stress.Results.-In this article, a number of migraine components are considered: cortical spreading depression, platelet activation, plasma protein extravasation, endothelial nitric oxide synthesis, and the release of serotonin, substance P, calcitonin gene-related peptide, and brain-derived neurotrophic factor. Evidence is presented from in vitro research and animal and human studies of ischemia suggesting that each component has neuroprotective functions, decreasing oxidant production, upregulating antioxidant enzymes, stimulating neurogenesis, preventing apoptosis, facilitating mitochondrial biogenesis, and/or releasing growth factors in the brain. Feedback loops between these components are described. Limitations and challenges to the model are discussed.Conclusions.-The theory is presented that migraines are an integrated defensive, neuroprotective response to brain oxidative stress.

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“…Indeed, local neuronal hyperactivity that progressively recruits a synchronous discharge via recurrent excitatory collaterals and (K + ) accumulation has been hypothesized to initiate epileptic discharge in slice models (Pinto et al 2005). CSD, experimentally induced in rats, increases cortico-cortical evoked responses and strongly induces "brain-derived neurotrophic factor" with synaptic potentiation in vivo (Faraguna et al 2010), while the induction of a "long-term potentiation-like" (LTP-like) phenomenon by CSD receives support from experimental evidence. In vivo data that lend support to the idea of a CSD-induced LTP-like phenomenon also exist (De Souza et al 2011).…”

Section: Sunset Of the "Migralepsy" Conceptmentioning

confidence: 99%

The Complex Relationship Between Epilepsy and Headache and the Concept of Ictal Epileptic Headache

Parisi

2014

Contemporary Clinical Neuroscience

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Key Points-Headache/migraine is often associated with epilepsy in children, as a pre-ictal, ictal, post-ictal or inter-ictal phenomenon.-Epidemiological aspects of the co-morbidity between epilepsy and headache are clearly different in children and adults.-Headache as a symptom, with migraine characteristics and/or tension-type headache characteristics, may be the only clinical ictal manifestation of an epileptic seizure: this condition is now classified as "ictal epileptic headache".-In particular, according to published criteria, the term "ictal epileptic headache" must be used in cases of a headache/migraine attack as the sole clinical ictal symptom of epileptic origin, confirmed by ictal-EEG recording and clinical-EEG responsiveness to intravenous antiepileptic drugs.-EEG is not recommended as a routine examination for children diagnosed with headache, but is mandatory and must be carried out promptly in cases of prolonged migraine/headache that does not respond to antimigraine drugs and in which epilepsy is suspected.-This is not a marginal question, because these possible, isolated, non-motor, ictal manifestations (i.e. ictal epileptic headache) should be taken into account before declaring an epileptic patient as "seizure free" so as to be able to suspend anticonvulsant therapy safely. SummaryThe possible link/comorbidity (causal or not causal) between epilepsy and headaches has been a topic of debate for over a hundred years, ever Since William Richard Gowers's time. In recent decades, new data have emerged in favor of a non-random relationship between these two entities. They are both characterized by transient attacks of altered brain function with a clinical, pathophysiological, genetic and therapeutic overlap, and may thus mimic each other. Indeed, the clinical distinction between headache and epilepsy may make the differential diagnosis a highly challenging task. Both are common and often co-morbid, with headache attacks in epilepsy being temporally related to the occurrence of epileptic seizures as a pre-ictal, ictal, post-ictal or inter-ictal event. Yet, they are both paroxysmal and chronic neurological disorders that share many clinical and epidemiological aspects, and they may both present with visual, cognitive, sensitive-sensorial and motor signs/symptoms; these neurophysiologicl phenomena arise from the cerebral cortex and are modulated by sub-cortical connections. Even from an epidemiological point of view, data in the literature regarding the co-morbidity between headache and epilepsy appear to be quite distinct in children. What makes this scenario even more variegated and complex are new data suggesting that a headache may, in some cases, even be the only ictal manifestation of an epileptic seizure. The latter condition, the so-called "ictal epileptic headache", is a new entity that has recently been cited in the new classification of headache disorders (ICHD-III), whose diagnostic criteria have very recently been defined and published. The data that have led, over the last decade, to the...

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Unilateral Cortical Spreading Depression Affects Sleep Need and Induces Molecular and Electrophysiological Signs of Synaptic Potentiation In Vivo

Cited by 46 publications

References 54 publications

Cortical Sensory Plasticity in a Model of Migraine with Aura

Cortical Sensory Plasticity in a Model of Migraine with Aura

The Migraine Attack as a Homeostatic, Neuroprotective Response to Brain Oxidative Stress: Preliminary Evidence for a Theory

The Complex Relationship Between Epilepsy and Headache and the Concept of Ictal Epileptic Headache

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