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      Cardiac cephalalgia: one case with cortical hypoperfusion in headaches and literature review.

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          Abstract

          Cardiac cephalalgia (CC) is a rare disease occurring during an episode of myocardial ischemia and relieved by nitroglycerine. Though more than 30 cases of CC have been reported since 1997, the mechanism is yet obscure. Herein, a case of CC is presented and discussed in relevance with previous literature to propose a novel hypothesis about the mechanism of CC.

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          The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. A prospective series of 67 patients.

          Anne Ducros, Monique Boukobza, Raphael Porcher … (2007)
          Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by the association of severe headaches with or without additional neurological symptoms and a 'string and beads' appearance on cerebral arteries, which resolves spontaneously in 1-3 months. We present the clinical, neuroimaging and outcome data of 67 consecutive patients prospectively diagnosed over 3 years in our institution with an angiographically confirmed RCVS. There were 43 females and 24 males with a mean age of 42 years (19-70). RCVS was spontaneous in 37% of patients and secondary in the 63% others, to postpartum in 5 and to exposure to various vasoactive substances in 37, mainly cannabis, selective serotonin-recapture inhibitors and nasal decongestants. The main pattern of presentation (94% of patients) was multiple thunderclap headaches recurring over a mean period of 1 week. In 51 patients (76%), headaches resumed the clinical presentation. Various complications were observed, with different time courses. Cortical subarachnoid haemorrhage (cSAH) (22%), intracerebral haemorrhage (6%), seizures (3%) and reversible posterior leukoencephalopathy (9%) were early complications, occurring mainly within the first week. Ischaemic events, including TIAs (16%) and cerebral infarction (4%), occurred significantly later than haemorrhagic events, mainly during the second week. Significant sex differences were observed: women were older, had more frequent single-drug exposure and a higher rate of stroke and cSAH. Sixty-one patients were treated by nimodipine: 36% had recurrent headaches, 7% TIAs and one multiple infarcts. The different time courses of thunderclap headaches, vasoconstriction and strokes suggest that the responsible vasospastic disorder starts distally and progresses towards medium sized and large arteries. No relapse was observed during the 16 +/- 12.4 months of follow-up. Our data suggest that RCVS is more frequent than previously thought, is more often secondary particularly to vasoactive substances, and should be considered in patients with recurrent thunderclap headaches, cSAH or cryptogenic strokes with severe headaches.
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            Activation of central trigeminovascular neurons by cortical spreading depression.

            Xichun Zhang, Dan Levy, Vanessa Kainz … (2011)
            Cortical spreading depression (CSD) has long been implicated in migraine attacks that begin with visual aura. Having shown that a wave of CSD can trigger long-lasting activation of meningeal nociceptors--the first-order neurons of the trigeminovascular pathway thought to underlie migraine headache--we now report that CSD can activate central trigeminovascular neurons in the spinal trigeminal nucleus (C1-2). Stimulation of the cortex with pinprick or KCl granule was used to induce CSD in anesthetized rats. Neuronal activity was monitored in C1-2 using single-unit recording. In 25 trigeminovascular neurons activated by CSD, mean firing rate (spikes/s) increased from 3.6 ± 1.2 before CSD (baseline) to 6.1 ± 1.8 after CSD (p 13 minutes. Neuronal activity returned to baseline level after 30.0 ± 3.1 minutes in 14 units, and remained elevated for 66.0 ± 8.3 (22-108) minutes through the entire recording period in the other 11 units. Neuronal activation began within 0.9 ± 0.4 (0-2.5) minutes after CSD in 7 neurons located in laminae I-II, or after a latency of 25.1 ± 4.0 (7-75) minutes in 9 neurons located in laminae I-II, and 9 neurons located in laminae III-V. In 27 trigeminovascular neurons not activated by CSD, mean firing rate was 2.0 ± 0.7 at baseline and 1.8 ± 0.7 after CSD. We propose that CSD constitutes a nociceptive stimulus capable of activating peripheral and central trigeminovascular neurons that underlie the headache of migraine with aura. Copyright © 2011 American Neurological Association.
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              Activation of meningeal nociceptors by cortical spreading depression: implications for migraine with aura.

              Moshe Jakubowski, Rami Burstein, Rodrigo Noseda … (2010)
              Attacks of migraine with aura represent a phenomenon in which abnormal neuronal activity in the cortex produces sensory disturbances (aura) some 20-40 min before the onset of headache. The purpose of this study was to determine whether cortical spreading depression (CSD)--an event believed to underlie visual aura--can give rise to activation of nociceptors that innervate the meninges--an event believed to set off migraine headache. CSD was induced in anesthetized male rats by stimulation of the visual cortex with electrical pulses, pin prick, or KCl; single-unit activity of meningeal nociceptors was monitored in vivo in the rat before and after CSD. Regardless of the method of cortical stimulation, induction of CSD was recorded in 64 trials. In 31 of those trials, CSD induced a twofold increase in meningeal nociceptor firing rate that persisted for 37.0 +/- 4.6 min in trials in which activity returned to baseline, or >68 min in trials in which activity remained heightened at the time recording was interrupted. In two-thirds of the trials, onset of long-lasting neuronal activation began approximately 14 min after the wave of CSD. The findings demonstrates for the first time that induction of CSD by focal stimulation of the rat visual cortex can lead to long-lasting activation of nociceptors that innervate the meninges. We suggest that migraine with aura is initiated by waves of CSD that lead up to delayed activation of the trigeminovascular pathway.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): J Headache Pain
                Title: The journal of headache and pain
                Publisher: Springer Nature
                ISSN (Electronic): 1129-2377
                ISSN (Print): 1129-2369
                Publication date (Electronic): Dec 2017
                Volume: 18
                Issue: 1
                Affiliations
                [1 ] The Department of Geriatric Neurology, Chinese PLA General Hospital, Beijing, China.
                [2 ] The Outpatient Department of Fuxing Road No. 7, the First Affiliated Hospital of PLA General Hospital, Beijing, China.
                [3 ] The Department of of Cardiology, Chinese PLA General Hospital, Beijing, China.
                [4 ] The Department of of Radiology, Chinese PLA General Hospital, Beijing, China.
                [5 ] Department of Neurology, Chinese PLA General Hospital, Fuxing Road 28, Haidian District, Beijing, 100853, China. dong_zhaozhao@126.com.
                [6 ] Department of Neurology, Chinese PLA General Hospital, Fuxing Road 28, Haidian District, Beijing, 100853, China.
                Article
                Publisher Item ID: 10.1186/s10194-017-0732-3
                DOI: 10.1186/s10194-017-0732-3
                PMC ID: 5318311
                PubMed ID: 28220375
                SO-VID: 733cff42-ec9e-427c-94e1-80a39620df8a
                History

                Keywords: Cardiac cephalalgia,Clinical features,Neuroimages,Pathophysiology
                Data availability:
                Keywords: Cardiac cephalalgia, Clinical features, Neuroimages, Pathophysiology

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