De-coupling of blood flow and metabolism in the rat brain induced by glutamate

Currently available drugs for the acute treatment of migraine, i.e. ergot alkaloids and triptans, are cranial vasoconstrictors. Although cranial vasoconstriction is likely to mediate-at least a part of-their therapeutic effects, this property also causes vascular side-effects. Indeed, the ergot alkaloids and the triptans have been reported to induce myocardial ischemia and stroke, albeit in extremely rare cases, and are contraindicated in patients with known cardiovascular risk factors. In view of these limitations, novel antimigraine drugs devoid of vascular (side) effects are being explored. Currently, calcitonin gene-related peptide (CGRP) receptor antagonists, which do not have direct vasoconstrictor effects, are under clinical development. Other classes of drugs, such as 5-HT(1F) receptor agonists, glutamate receptor antagonists, nitric oxide synthase inhibitors, VPAC/PAC receptor antagonists and gap junction modulators, have also been proposed as potential targets for acute antimigraine drugs. Although these prospective drugs do not directly induce vasoconstriction, they may well induce indirect vascular effects by inhibiting or otherwise modulating the responses to endogenous vasoactive substances. These indirect vascular effects might contribute to the therapeutic efficacy of the previously mentioned compounds, but may alternatively also lead to vascular side-effects. As described in the current review, some of the prospective antimigraine drugs with a proposed non-vascular mechanism of action may still have direct or indirect vascular effects.

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A Case of Creutzfeldt-Jakob Disease Mimicking Corticobasal Degeneration

Zhang

Minoshima²,

Vesselle³

et al. 2012

Clinical Nuclear Medicine

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A 58-year-old woman was admitted with left-sided decreased sensation, ataxia, and left "alien" hand and leg. Brain SPECT and PET showed hypoperfusion and hypometabolism in the right frontoparietal cortices, including the primary sensorimotor cortex, and temporal cortex. MRI demonstrated matching-restricted diffusion and fluid-attenuated inversion recovery hyperintensity. Corticobasal degeneration was suspected initially. The patient declined rapidly, and the diagnosis of sporadic Creutzfeldt-Jakob disease (CJD) was made based on cerebrospinal fluid biomarkers. CJD can present with symptoms similar to other disorders. This case illustrates that CJD can mimic a rare neurodegenerative disorder, cortico-basal degeneration, both clinically and by neuroimaging.

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De-coupling of blood flow and metabolism in the rat brain induced by glutamate

Cited by 3 publications

References 35 publications

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PK11195 might selectively suppress the quinolinic acid-induced enhancement of anaerobic glycolysis in glial cells

Potential mechanisms of prospective antimigraine drugs: A focus on vascular (side) effects

A Case of Creutzfeldt-Jakob Disease Mimicking Corticobasal Degeneration

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