Inhalational Anesthetics Inhibit Spreading Depression: Relevance to Migraine

Piper, R. Hunt; Lambert, Geoffrey

doi:10.1046/j.1468-2982.1996.1602087.x

Cited by 37 publications

(31 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, Saito et al found a complete suppression of KCl-evoked CSDs in cats under 0.7 MAC halothane when compared to α-chloralose, although both groups received 70% N 2 O, which may have potentiated the CSD suppression by halothane as observed in our study (Saito, et al, 1995). In another study, halothane (1-1.5 MAC) was more effective in suppressing pinprick-induced CSDs compared to isoflurane (1.5 MAC); at this concentration, however, isoflurane still suppressed CSDs compared to α-chloralose (Piper and Lambert, 1996). Using a continuous topical 3M KCl application similar to ours, the frequency of evoked CSDs was suppressed in a concentration-dependent manner by halothane, isoflurane and sevoflurane; the lowest isoflurane concentration that suppressed CSDs was 1 MAC, while CSD frequency under 0.5 MAC isoflurane did not differ from pentobarbital (Kitahara, et al, 2001).…”

Section: Discussionsupporting

confidence: 43%

“…General anesthetics modulate CSD susceptibility (Guedes and Barreto, 1992, Kitahara, et al, 2001, Piper and Lambert, 1996, Saito, et al, 1997, Saito, et al, 1995, Sonn and Mayevsky, 2006, Verhaegen, et al, 1992. Interestingly, nitrous oxide (N 2 O), an inhalational anesthetic frequently used as an adjunct with other general anesthetics in experimental models, reportedly shows clinical efficacy in aborting acute migraine (Triner, et al, 1999), whereas normobaric hyperoxia (100% O 2 ) is ineffective (Myers and Myers, 1995).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The impact of anesthetics and hyperoxia on cortical spreading depression

Kudo

Nozari

Moskowitz

et al. 2008

Experimental Neurology

View full text Add to dashboard Cite

Cortical spreading depression (CSD), a transient neuronal and glial depolarization that propagates slowly across the cerebral cortex, is the putative electrophysiological event underlying migraine aura. It negatively impacts tissue injury during stroke, cerebral contusion and intracranial hemorrhage. Susceptibility to CSD has been assessed in several experimental animal models in vivo, such as after topical KCl application or cathodal stimulation. Various combinations of anesthetics and ambient conditions have been used by different laboratories making comparisons problematic and differences in data difficult to reconcile. We systematically studied CSD susceptibility comparing commonly used experimental anesthetics (isoflurane, α-chloralose, urethane) with or without N 2 O or normobaric hyperoxia (100% O 2 inhalation). The frequency of evoked CSDs, and their propagation speed, duration, and amplitude were recorded during 2 hour topical KCl (1M) application. We found that N 2 O reduced CSD frequency when combined with isoflurane or urethane, but not α-chloralose; N 2 O also decreased CSD propagation speed and duration. Urethane anesthesia was associated with the highest CSD frequency that was comparable to pentobarbital. Inhalation of 100% O 2 did not alter CSD frequency, propagation speed or duration in combination with any of the anesthetics tested. Our data show anesthetic modulation of CSD susceptibility in an experimental model of human disease, underscoring the importance of proper study design for hypothesis testing as well as for comparing results between studies.

show abstract

Section: Discussionsupporting

confidence: 43%

Section: Introductionmentioning

confidence: 99%

The impact of anesthetics and hyperoxia on cortical spreading depression

Kudo

Nozari

Moskowitz

et al. 2008

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…Our data suggest that FHM1 mutations facilitate corticostriatal SD propagation. The anesthetic regimen used in our model may explain the complete lack of corticostriatal SD propagation in WT mice (63,64).…”

Section: Figurementioning

confidence: 99%

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Eikermann-Haerter¹,

Dileköz²,

Kudo³

et al. 2008

J. Clin. Invest.

187

290

View full text Add to dashboard Cite

Familial hemiplegic migraine type 1 (FHM1) is an autosomal dominant subtype of migraine with aura that is associated with hemiparesis. As with other types of migraine, it affects women more frequently than men. FHM1 is caused by mutations in the CACNA1A gene, which encodes the α 1A subunit of Ca v 2.1 channels; the R192Q mutation in CACNA1A causes a mild form of FHM1, whereas the S218L mutation causes a severe, often lethal phenotype. Spreading depression (SD), a slowly propagating neuronal and glial cell depolarization that leads to depression of neuronal activity, is the most likely cause of migraine aura. Here, we have shown that transgenic mice expressing R192Q or S218L FHM1 mutations have increased SD frequency and propagation speed; enhanced corticostriatal propagation; and, similar to the human FHM1 phenotype, more severe and prolonged post-SD neurological deficits. The susceptibility to SD and neurological deficits is affected by allele dosage and is higher in S218L than R192Q mutants. Further, female S218L and R192Q mutant mice were more susceptible to SD and neurological deficits than males. This sex difference was abrogated by ovariectomy and senescence and was partially restored by estrogen replacement, implicating ovarian hormones in the observed sex differences in humans with FHM1. These findings demonstrate that genetic and hormonal factors modulate susceptibility to SD and neurological deficits in FHM1 mutant mice, providing a potential mechanism for the phenotypic diversity of human migraine and aura.

show abstract

“…1 Clinically, CSD is postulated to play a role in the pathogenesis of stroke, 2 traumatic cortical injury, 3 cerebral ischemia, 4,5 migraine, 6 and transient global amnesia. 7 CSD can be induced by a variety of stimuli including pinprick or needle stab, 8,9 elevated potassium, 5,10 electrical stimulation, 1,11 or glutamate application. On a cellular level, electrophysiological changes are accompanied by significant shifts in intra-and extracellular ion concentrations, 12 cellular swelling, 13 dendritic beading, 14 and changes in gene expression.…”

Section: Introductionmentioning

confidence: 99%

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

et al. 2005

View full text Add to dashboard Cite

Abstract. Cortical spreading depression (CSD) is a pronounced depolarization of neurons and glia that spreads slowly across the cortex followed by a period of depressed electrophysiological activity. The vascular changes associated with CSD are a large transient increase in blood flow followed by a prolonged decrease lasting greater than 1 h. Currently, the profile of functional vascular activity during this hypovolemic period has not been well characterized. Perfusion-based imaging techniques such as functional magnetic resonance imaging (fMRI) assume a tight coupling between changes in neuronal and vascular activity. Under normal conditions, these variables are well correlated. Characterizing the effect of CSD on this relationship is an important step to understand the impact acute pathophysiological events may have on neurovascular coupling. We examine the effect of CSD on functional changes in cerebral blood volume (CBV) evoked by cortical electrophysiological activity for 1 h following CSD induction. CBV signal amplitude, duration, and time to peak show little recovery at 60 min post-induction. Analysis of spontaneous vasomotor activity suggests a decrease in vascular reactivity may play a significant role in the disruption of normal functional CBV responses. Electrophysiological activity is also attenuated but to a lesser degree. CBV and evoked potentials are not well correlated following CSD, suggesting a breakdown of the neurovascular coupling relationship.

show abstract

Inhalational Anesthetics Inhibit Spreading Depression: Relevance to Migraine

Cited by 37 publications

References 12 publications

The impact of anesthetics and hyperoxia on cortical spreading depression

The impact of anesthetics and hyperoxia on cortical spreading depression

Genetic and hormonal factors modulate spreading depression and transient hemiparesis in mouse models of familial hemiplegic migraine type 1

Cortical spreading depression produces long-term disruption of activity-related changes in cerebral blood volume and neurovascular coupling

Contact Info

Product

Resources

About