Capsaicin-insensitive sensory-efferent meningeal vasodilatation evoked by electrical stimulation of trigeminal nerve fibres in the rat.
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1. Antidromic vasodilatation and plasma extravasation to stimulation of the trigeminal ganglion or its perivascular meningeal fibres was investigated by laser-Doppler flowmetry and 125I-labelled bovin serum albumin in the dura mater and in exteroceptive areas (nasal mucosa, upper eyelid) of anaesthetized rats pretreated with guanethidine and pipecuronium. 2 Trigeminal stimulation at 5 Hz for 20 s elicited unilateral phasic vasodilatation in the dura and lasting response in the nasal mucosa. Resiniferatoxin (1-3 microg kg(-1) i.v.), topical (1%) or systemic capsaicin pretreatment (300 mg kg(-1) s.c. plus 1 mg kg(-1) i.v.) did not inhibit the meningeal responses but abolished or strongly inhibited the nasal responses. Administration of vinpocetine (3 mg kg(-1) i.v.) increased both basal blood flow and the dural vasodilatation to perivascular nerve stimulation. 3. Dural vasodilatation to trigeminal stimulation was not inhibited by the calcitonin gene-related peptide-1 receptor (CGRP-1) antagonist hCGRP8-37 (15 or 50 microg kg(-1) i.v), or the neurokinin-1 receptor antagonist RP 67580 (0.1 mg kg(-1) i.v.) although both antagonists inhibited the nasal response. Neither mucosal nor meningeal responses were inhibited by atropine (5 mg kg(-1) i.v.), hexamethonium (10 mg kg(-1) i.v.) or the vasoactive intestinal polypeptide (VIP) antagonist (p-chloro-D-Phe6-Leul7)VIP (20 microg kg(-1) i.v.). 4. Plasma extravasation in the dura and upper eyelid elicited by electrical stimulation of the trigeminal ganglion was almost completely abolished in rats pretreated with resiniferatoxin (3 microg kg(-1) i.v.). 5. It is concluded that in the rat meningeal vasodilatation evoked by stimulation of trigeminal fibres is mediated by capsaicin-insensitive primary afferents, while plasma extravasation in the dura and upper eyelid and the vasodilatation in the nasal mucosa are mediated by capsaicin-sensitive trigeminal fibres. (+info)
Detection of meningeal fibrosis after subarachnoid haemorrhage by assaying procollagen propeptides in cerebrospinal fluid.
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OBJECTIVE: To study whether meningeal collagen synthesis under normal conditions is reflected in the CSF and whether a meningeal fibroproliferative reaction or fibrosis after subarachnoid haemorrhage can be detected by measuring markers of collagen synthesis in the CSF. METHODS: Serum samples and CSF were collected from 56 patients with various neurological symptoms and from nine patients with a recent subarachnoid haemorrhage. The concentrations of the carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) were measured using radioimmunoassays. RESULTS: The mean(SD) concentration of PICP was 75.2 (SD 13.6) microgram/l and that of PIIINP 3.56 (SD 0.91) microgram/l in the CSF of the controls, and the CSF/serum ratios were 0.74 (SD 0.24) for PICP and 1.34 (SD 0.48) for PIIINP. A 1.4-fold increase in both the PICP (p=0.001) and the PIIINP (p=0.001) concentration was found in patients with a neurological disease and with an abnormal CSF leucocyte count or protein concentration. In eight patients with a recent subarachnoid haemorrhage the PICP was 5.9-fold higher (p<0.001) and the PIIINP concentration 7.7-fold higher (p<0.001) than that in the controls, whereas no difference was found in the serum values. Similar high concentrations were also found in a patient from whom the CSF sample was obtained before operation for aneurysm. CONCLUSIONS: The intrathecal compartment is a site for active collagen synthesis under normal conditions. The synthesis rate is markedly increased in patients with a recent subarachnoid haemorrhage, suggesting a fibroproliferative reaction or fibrosis. Assays of procollagen propeptides may be useful in the clinical diagnosis of meningeal fibrosis and their use may enable the identification of diseases and symptoms aetiologically related to meningeal fibrosis. (+info)
Presenilin-1 deficiency leads to loss of Cajal-Retzius neurons and cortical dysplasia similar to human type 2 lissencephaly.
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BACKGROUND: Presenilin-1 (PS1) is a transmembrane protein that is located in the endoplasmic reticulum and the cis Golgi apparatus. Missense mutations of PS1 that modify gamma-secretase function, leading to a pathologic processing of amyloid precursor protein, are an important cause of familial Alzheimer's disease. Physiologically, the presenilins are involved in the Notch and Wnt-beta-catenin signaling pathways. RESULTS: PS1-deficient mice develop a cortical dysplasia resembling human type 2 lissencephaly, with leptomeningeal fibrosis and migration of cortical-plate neurons beyond their normal position into the marginal zone and subarachnoid space. This disorder of neuronal migration is associated with the disappearance of the majority of the cells of the marginal zone, notably most of the Cajal-Retzius pioneer neurons, between embryonic days E14 and E18, and is preceded and accompanied by disorganization of Notch-1 immunoreactivity on the neuronal cell membranes. The marginal zone also becomes depleted of the extracellular matrix protein reelin and chondroitin sulfate proteoglycans. At that stage PS1 is transiently expressed in leptomeningeal fibroblasts, which are mandatory for the trophic support of Cajal-Retzius neurons. CONCLUSIONS: In agreement with models in which neuronal migration disorders have been linked to a defect in Cajal-Retzius cells, the loss of most of these cells in PS1-deficient mice leads to cortical dysplasia. Because PS1 is normally expressed in the leptomeninges, and these become fibrotic in the PS1-knockout mice, we favor the hypothesis that the loss of Cajal-Retzius cells is caused by a defective trophic interaction with leptomeningeal cells, possibly involving disruption of Notch signaling. (+info)
Embolization of meningohypophyseal and inferolateral branches of the cavernous internal carotid artery.
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BACKGROUND AND PURPOSE: Despite the continued improvements in endovascular techniques this decade, few dedicated studies addressing the feasibility of such procedures or their efficacy relative to risk have been conducted. The purpose of this study was to use current endovascular techniques to assess the feasibility, effectiveness, and safety of direct selective catheterization and embolization of the small branches of the cavernous segment of the internal carotid artery. METHODS: We retrospectively reviewed the findings in 10 patients with lesions (five meningiomas and five arteriovenous malformations) primarily or partly supplied by branches of the meningohypophyseal trunk or inferolateral trunk who had undergone endovascular embolization of the feeding arteries during the period from 1991 to 1997. In each case, the artery was selectively catheterized with a microcatheter/microguidewire system and embolized with polyvinyl alcohol particles (n = 5), n-butyl cyanoacrylate tissue adhesive (n = 4), or both (n = 1). RESULTS: In all 10 patients, the feeding artery from the meningohypophyseal trunk (eight patients) or inferolateral trunk (three patients; one patient with both) was successfully catheterized and embolized. In nine patients, embolization resulted in complete obliteration of the vascular territory; in the remaining patient, blood supply was decreased by an estimated 80%. No immediate or delayed complications occurred. CONCLUSION: Advances in microcatheter and microguidewire technology allow more efficient and safer selective catheterization and embolization of branches of the cavernous segment of the internal carotid artery than in the recent past. Meticulous technique and detailed knowledge of the vascular anatomy of the cavernous sinus region are necessary to maximize lesion devascularization and to minimize the risk of stroke, cranial nerve palsies, and blindness. (+info)
Embolization of the meningohypophyseal trunk as a cause of diabetes insipidus.
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We present an unusual case of diabetes insipidus occurring after selective embolization of 50% dextrose and pure ethanol into an enlarged left meningohypophyseal trunk (MHT) supplying a dural carotid cavernous fistula. The inferior hypophyseal artery was not opacified during the selective preembolization MHT injection; however, diabetes insipidus developed abruptly a few hours after the procedure. The patient required intranasal 1-deamino-(8-D-arginine)-vasopressin for approximately 3 months, after which his symptoms resolved. The hazards of using liquid embolic agents, especially ethanol, in the cavernous branches of the internal carotid artery should always be borne in mind. (+info)
Increase of collagen synthesis and deposition in the arachnoid and the dura following subarachnoid hemorrhage in the rat.
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Arachnoidal fibrosis following subarachnoid hemorrhage (SAH) has been suggested to play a pathogenic role in the development of late post-hemorrhagic hydrocephalus in humans. The purpose of this study was to investigate the rate of collagen synthesis in the arachnoid and the dura in the rat under normal conditions and to study the time schedule and the localization of the increased collagen synthesis following an experimental SAH. We found that the activity of prolyl 4-hydroxylase, a key enzyme in collagen synthesis, was 3-fold higher in the dura than that in the arachnoid and was similar to the activity in the skin. We then induced SAH in rats by injecting autologous arterial blood into cisterna magna. After SAH, we observed an increase in prolyl 4-hydroxylase activity of the arachnoid and the dura at 1 week. At this time point the enzyme activity in both tissues was 1.7-1.8-fold compared to that in the controls and after this time point the activities declined but remained slightly elevated at least till week 4. The rate of collagen synthesis was measured in vitro by labeling the tissues with [(3)H]proline. The rate increased to be 1.7-fold at 1 to 2 weeks after the SAH in both of the tissues. Immunohistochemically we observed a deposition of type I collagen in the meninges at 3 weeks after the SAH. SAH is followed by a transient increase in the rate of collagen synthesis in the arachnoid and, surprisingly, also the dura. Increased synthesis also resulted in an accumulation of type I collagen in the meningeal tissue, suggesting that the meninges are a potential site for fibrosis. The time schedule of these biochemical and histological events suggest that meningeal fibrosis may be involved in the pathogenesis of late post-hemorrhagic hydrocephalus. (+info)
Sonographic nomogram of the leptomeninges (pia-glial plate) and its usefulness for evaluating bacterial meningitis in infants.
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BACKGROUND AND PURPOSE: To our knowledge, the upper limits of the thickness of normal meninges on neurosonograms are not known. We therefore established a nomogram for sonographic measurements of the leptomeninges (pia-glial plate) and assessed its usefulness in neurosonographic examinations of children with bacterial meningitis. METHODS: The pia mater-cortical glia limitans complex on the surface of the brain and in the sulcus of a frontal gyrus was measured on neurosonograms in 100 infants without meningeal disease in order to establish a nomogram of the thickness of this pia-glial plate, referred to as the leptomeninx. Effects of prematurity, age, sex, and single-layer (surface) versus double-layer (sulcus) measurements were analyzed. Meningeal thicknesses derived from a retrospective analysis of the neurosonograms of 33 patients with purulent meningitis and a prospective study of 22 patients with bacterial meningitis were compared with the nomograms. Clinical outcomes of children with meningeal thickening were compared with those of affected children with normal meninges. RESULTS: The distribution of sulci measurements was significantly asymmetrical around the mean. Statistical data showed no influence of prematurity and sex, but showed surface measurements to be more consistent than sulcal measurements. Older chronological age was related to slightly larger sulci, but did not influence the surface measurements. In children with bacterial meningitis, the surface meninges were less frequently thickened than were the sulci. Sulcal enlargement occurred often in combination with echogenic deposits in the sub-arachnoid space. CONCLUSION: Leptomeninges are best measured on the surface of a gyrus rather than in a sulcus, as the normal thickness of the sulci shows much more variability. Clinical outcome of bacterial meningitis cannot be predicted by presence or absence of meningeal thickening as the only sonographic abnormality. (+info)
Ehlers-Danlos syndrome associated with multiple spinal meningeal cysts--case report.
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A 40-year-old female with Ehlers-Danlos syndrome was admitted because of a large pelvic mass. Radiological examination revealed multiple spinal meningeal cysts. The first operation through a laminectomy revealed that the cysts originated from dilated dural sleeves containing nerve roots. Packing of dilated sleeves was inadequate. Finally the cysts were oversewed through a laparotomy. The cysts were reduced, but the postoperative course was complicated by poor wound healing and diffuse muscle atrophy. Ehlers-Danlos syndrome associated with spinal cysts may be best treated by endoscopic surgery. (+info)