Presentation, diagnosis, and management of an unusual parasagittal ependymoma, radiographically resembling a falcine meningioma, are described. Despite its radiographic appearance, pathologic evaluation revealed classic features of an ependymoma. The radiographic and pathologic characteristics of this unusual lesion are briefly examined, and the literature is reviewed. Although extraaxial ependymomas are rare, they should be considered in the radiographic differential diagnosis of dural-based lesions, especially for patients within the first 3 decades of life. (+info)
Role of opioid receptors in neurogenic dural vasodilation and sensitization of trigeminal neurones in anaesthetized rats.
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Migraine headache is thought to be caused by a distension of meningeal blood vessels, the activation of trigeminal sensory neurones and the the development of a central sensitization within the trigeminal nucleus caudalis (TNC). It has been proposed that clinically effective 5-HT(1B/1D) agonists act peripherally to inhibit the release of calcitonin gene-related peptide (CGRP) and neurogenic dural vasodilation, and to attenuate nociceptive neurotransmission within the TNC. Since opioids are also effective anti-migraine agents the present studies investigated the role of opioids within the trigemino-vascular system in anaesthetised rats. Electrical stimulation of the dura mater evoked neurogenic dural vasodilation which was significantly inhibited by morphine (1 mg kg(-1)) the selective mu-opioid agonist DAGO (10 microg kg(-1)) and the mixed agonist/antagonist butorphanol (1 mg kg(-1)) but not by the kappa- and delta-opioid agonists (+/-) U50488H (100 microg kg(-1)) and DPDPE (1 mg kg(-1)). Morphine had no effect on CGRP-evoked dural vasodilation. In electrophysiological studies morphine (1 - 10 mg kg(-1)) significantly attenuated brainstem neuronal activity in response to electrical stimulation of the dura by 65% at 10 mg kg(-1). Morphine (3 mg kg(-1)) also inhibited the TNC neuronal sensitization following CGRP-evoked dilation. The present studies have demonstrated that opioids block the nociceptive neurotransmission within the trigeminal nucleus caudalis and in addition inhibit neurogenic dural vasodilation via an action on mu-opioid receptors located on trigeminal sensory fibres innervating dural blood vessels. These peripheral and central actions are similar to those of the 'triptan' 5-HT(1B/1D) agonists and could account for the anti-migraine actions of opioids. (+info)
The anti-migraine 5-HT(1B/1D) agonist rizatriptan inhibits neurogenic dural vasodilation in anaesthetized guinea-pigs.
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These studies investigated the pharmacology of neurogenic dural vasodilation in anaesthetized guinea-pigs. Following introduction of a closed cranial window the meningeal (dural) blood vessels were visualized using intravital microscopy and the diameter constantly measured using a video dimension analyser. Dural blood vessels were constricted with endothelin-1 (3 microg kg(-1), i.v.) prior to dilation of the dural blood vessels with calcitonin gene-related peptide (CGRP; 1 microg kg(-1), i.v.) or local electrical stimulation (up to 300 microA) of the dura mater. In guinea-pigs pre-treated with the CGRP receptor antagonist CGRP((8-37)) (0.3 mg kg(-1), i.v.) the dilator response to electrical stimulation was inhibited by 85% indicating an important role of CGRP in neurogenic dural vasodilation in this species. Neurogenic dural vasodilation was also blocked by the 5-HT(1B/1D) agonist rizatriptan (100 microg kg(-1)) with estimated plasma levels commensurate with concentrations required for anti-migraine efficacy in patients. Rizatriptan did not reverse the dural dilation evoked by CGRP indicating an action on presynaptic receptors located on trigeminal sensory fibres innervating dural blood vessels. In addition, neurogenic dural vasodilation was also blocked by the selective 5-HT(1D) agonist PNU-142633 (100 microg kg(-1)) but not by the 5-HT(1F) agonist LY334370 (3 mg kg(-1)) suggesting that rizatriptan blocks neurogenic vasodilation via an action on 5-HT(1D) receptors located on perivascular trigeminal nerves to inhibit CGRP release. This mechanism may underlie one of the anti-migraine actions of the triptan class exemplified by rizatriptan and suggests that the guinea-pig is an appropriate species in which to investigate the pharmacology of neurogenic dural vasodilation. (+info)
Rosai-Dorfman disease presenting with isolated bilateral orbital masses: report of two cases.
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Rosai-Dorfman disease (sinus histiocytosis with massive lymphadenopathy) is a rare benign idiopathic proliferative disease of phagocytic histiocytes. Approximately 80% of patients present with painless massive cervical lymphadenopathy. Isolated extranodal involvement is relatively uncommon. Two cases of Rosai-Dorfman disease are reported: one with isolated bilateral orbital involvement and one with marked cervical lymphadenopathy and multiple dural-based and intraventricular masses. (+info)
Treatment of a giant orbitofacial vascular malformation and ophthalmic artery aneurysms with intralesion glue injections: case report.
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We describe a giant left orbital vascular malformation that was treated with both percutaneous and transarterial embolization. Feeder artery aneurysms thrombosed as a result of retrograde reflux of embolic material into the distal ophthalmic artery. In this presentation, we emphasize the efficacy of percutaneous embolization and retrograde thromboses of two intradural saccular ophthalmic artery aneurysms. (+info)
A neurohistochemical blueprint for pain-induced loss of appetite.
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A common complaint among pain patients is that they lose their appetite. These accounts are anecdotal, however, and the neural mechanism underlying pain-induced loss of appetite remains unknown. In this study, we documented the occurrence of appetite loss in patients under migraine attack and investigated the neuronal substrate of pain-induced anorexia in our animal model of intracranial pain. We found that loss of appetite during the migraine attack in humans coincided strongly with the onset and duration of the head pain in 32/39 cases, and that brief noxious stimulation of the dura in conscious rats produced a transient suppression of food intake. Mapping of neuronal activation in the rat showed that noxious dural stimulation induced a 3- to 4-fold increase in the number of Fos-positive neurons in medullary dorsal horn areas that process nociceptive signals (laminae I, V) and in parabrachial and hypothalamic neurons positioned to suppress feeding behavior. In the parabrachial area, activated neurons were localized in the superior-lateral subnucleus, and 40% of them expressed the mRNA encoding the anorectic neuropeptide cholecystokinin. In the hypothalamus, activated Fos-positive neurons were found in the dorsomedial area of the ventromedial nucleus, and 76% of them expressed the mRNA for cholecystokinin type-B receptor. Based on these findings, we suggest that at least one of several groups of hypothalamic neurons that normally inhibit appetite in response to metabolic cues is positioned to mediate the suppression of food intake by pain signals. (+info)
Effectiveness of epidural blood patch in the management of post-dural puncture headache.
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BACKGROUND: Lumbar epidural blood patch (EBP) is a common treatment of post-dural puncture headache, but its effectiveness and mode of action remain a matter of debate. The aim of this study was to assess both the effectiveness and the predictive factors of failure of EBP on severe post-dural puncture headache. METHODS: This prospective observational study includes all patients treated in the authors' hospital with EBP for incapacitating post-dural puncture headache, from 1988 to 2000. The EBP effect was classified into complete relief (disappearance of all symptoms), incomplete relief of symptoms (clinically improved patients who recovered sufficiently to perform normal daily activity), and failure (persistence of severe symptoms). The following data were analyzed using a logistic regression to identify predictive factors of failure of EBP: (1) patient characteristics; (2) circumstances of dural puncture; (3) delay between dural puncture and EBP; and (4) the volume of blood injected for EBP. RESULTS: A total of 504 patients were analyzed. The frequency rates of complete relief, incomplete relief of symptoms, and failure after EBP were 75% (n = 377), 18% (n = 93), and 7% (n = 34), respectively. In a multivariate analysis, only the diameter of the needle used to perform dura mater puncture (odds ratio = 5.96; 95% confidence interval, 2.63-13.47; P < 0.001) and a delay in EBP less than 4 days (odds ratio = 2.63; 95% confidence interval, 1.06-6.51; P = 0.037) were independent significant risk factors for a failure of EBP. CONCLUSIONS: Epidural blood patch is an effective treatment of severe post-dural puncture headache. Its effectiveness is decreased if dura mater puncture is caused by a large bore needle. (+info)
Spontaneous extradural haematomas.
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Spontaneous extradural haemorrhage may be due to neighbourhood infections, vascular malformations of the dura mater, and disorders of blood coagulation. Two cases are described here: in one, infection was present; in the other, there was a berry aneurysm of the middle meningeal artery with a small parietal dural angioma. Operation was successful in both patients. (+info)