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Query: UMLS:C0018681 (headache)
 56,091 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The headache in migraine is thought to result from neuronal nociceptive activity in the trigeminovascular system, that is, the meninges. In addition, trigeminal axons projecting to the meninges contain vasoactive neuropeptides, such as substance P, calcitonin gene-related peptide and neurokinin A, that may promote, when released, plasma protein leakage and vasodilation within dura mater, characteristic of neurogenic inflammation. Thus, it has been hypothesized that a sterile neurogenic inflammation in the meninges may be involved in generating or sustaining, via occurrence of a vicious cycle, the pain accompanying the migraine attacks. We here review the evidence in support of this hypothesis as well as its potential significance in better tailoring therapies in migraine or other types of primary headaches.
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PMID:Neurogenic inflammation in primary headaches. 1281 94

We report a case of refractory tuberculous meningitis which was markedly improved by intrathecal administration of isoniazid (INH). The patient was a 35-year-old woman diagnosed with systemic lupus erythematosus (SLE) at age 25, who was being managed with steroid therapy. She was admitted to another hospital due to miliary tuberculosis at age 34, and after discharge continued with a regimen of 2 anti-tuberculosis drugs (INH. Rifampicin (RFP)). She was admitted to our hospital with severe headache and fever on June 18, 2001. She showed severe meningeal irritation, and cerebrospinal fluid (CSF) examination revealed cell counts of 207/microliter (72% polynuclear cells), protein level of 300 mg/dl, glucose level of 13 mg/dl, chloride (Cl) level of 104 mEq/l, adenosine deaminase (ADA) level of 10.0 IU/l. The CSF culture was negative for Mycobacterium tuberculosis (M. tuberculosis) and direct polymerase chain reaction (PCR) for M. tuberculosis DNA was negative, but nested PCR was positive in preserved CSF samples. Marked leptomeningeal enhancement at the basilar meninges was noted by cranial MRI on gadolinium (Gd)-DTPA enhanced T1-weighted images. We diagnosed her condition as tuberculous meningitis and administered a total of 5 anti-tuberculosis drugs over about 2 months. However, during this period, both her clinical and CSF findings worsened, and she developed severe consciousness disturbance showing marked hydrocephalus on cranial MRI in August 2001. Therefore, we initiated intrathecal administration of INH 100 mg 3 times a week for progressive tuberculous meningitis. After the initiation of intrathecal therapy, both her consciousness disturbance and CSF findings were improved almost immediately. Ventriculo-peritoneal shunt operation was performed for hydrocephalus on September 26, 2001, and her clinical symptoms were further improved. To our knowledge, this is the first reported case of refractory tuberculous meningitis markedly improved by intrathecal administration of INH. Our findings suggested that intrathecal administration of INH was useful for refractory tuberculous meningitis.
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PMID:[A case of refractory tuberculous meningitis markedly improved by intrathecal administration of isoniazid (INH)]. 1282 May 46

A 56-year-old woman presented with severe orthostatic headache in association with nausea and vomiting. Lumbar puncture for the patient revealed significantly low cerebrospinal fluid pressure (CSF) and the clinical diagnosis of intracranial hypotension syndrome was made. An initial gadolinium-enhanced brain magnetic resonance imaging (MRI) disclosed diffuse meningeal enhancement as well as brain sagging. No definite CSF leakage was found using radionuclide cisternography. Her headaches abated with proper usage of analgesics, strict bed rest, and intravenous hydration. Follow-up neuroimaging studies showed partially resolved meningeal enhancement 2 months after treatment and complete resolution 6 months after treatment. The temporal changes found on MRI suggest that the pachymeningeal enhancement is reversible in patients with spontaneous intracranial hypotension. Moreover, proliferation of meninges is likely to be responsible for this type of delayed resolution phenomenon.
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PMID:Spontaneous intracranial hypotension in a patient with reversible pachymeningeal enhancement and brain descent. 1284 30

Neurones in the trigeminocervical complex are the major relay neurones for nociceptive afferent input from the meninges and cervical structures; therefore, they are the neural substrates of head pain. This review highlights the importance of two basic mechanisms in headache physiology: convergence of nociceptive afferents and sensitization of trigeminocervical neurones. These physiologic findings have clinical correlates such as hypersensitivity and spread and referral of pain frequently seen in patients with primary headache, such as migraine. Special reference is made to the influence of structures from the upper cervical spine in generating and contributing to migraine headaches. The pathophysiology and functional relevance of these basic mechanisms to headaches is discussed in the context of recent experimental findings with regard to pain processing.
Curr Pain Headache Rep 2003 Oct
PMID:The trigeminocervical complex and migraine: current concepts and synthesis. 1294 90

Cluster headache is characterized by typical autonomic dysfunctions including facial and intracranial vascular disturbances. Both the trigeminal and the cranial parasympathetic systems may be involved in mediating these dysfunctions. An experimental model was developed in the rat to measure changes in lacrimation and intracranial blood flow following noxious chemical stimulation of facial mucosa. Blood flow was monitored in arteries of the exposed cranial dura mater and the parietal cortex using laser Doppler flowmetry. Capsaicin (0.01-1 mm) applied to oral or nasal mucosa induced increases in dural and cortical blood flow and provoked lacrimation. These responses were blocked by systemic pre-administration of hexamethonium chloride (20 mg/kg). The evoked increases in dural blood flow were also abolished by topical pre-administration of atropine (1 mm) and [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (0.1 mm), a vasoactive intestinal polypeptide (VIP) antagonist, onto the exposed dura mater. We conclude that noxious stimulation of facial mucosa increases intracranial blood flow and lacrimation via a trigemino-parasympathetic reflex. The blood flow responses seem to be mediated by the release of acetylcholine and VIP within the meninges. Similar mechanisms may be involved in the pathogenesis of cluster headache.
Cephalalgia 2004 Mar
PMID:Noxious chemical stimulation of rat facial mucosa increases intracranial blood flow through a trigemino-parasympathetic reflex--an experimental model for vascular dysfunctions in cluster headache. 1500 14

The activation of the trigeminal nociceptive system is the neural substrate of pain in primary headache syndromes such as migraine and cluster headache. The nociceptive inflow from the meninges to the spinal cord is relayed in brainstem neurones of the trigemino-cervical complex (TCC). Two important mechanisms of pain transmission are reviewed: convergence of nociceptive trigeminal and cervical afferents and sensitization of trigemino-cervical neurones. These mechanisms have clinical correlates such as hyperalgesia, allodynia, spread and referral of pain to trigeminal or cervical dermatomes. Neurones in the TCC are subject to a modulation of pain-modulatory circuits in the brainstem such as the periaqueductal grey (PAG). Recent experimental and clinical findings of a modulation of these pain processes are discussed. The review focuses on TCC neurones as integrative relay neurones between peripheral and central pain mechanisms. The understanding of these mechanisms has implications for the understanding of the clinical phenomenology in primary headache syndromes and the development of therapeutical options.
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PMID:[The trigemino-cervical complex. Integration of peripheral and central pain mechanisms in primary headache syndromes]. 1525 26

The shared anatomical and physiological substrate for headache syndromes is the neural innervation of the cranial circulation. Evidence suggests, that the observed dilatation of vessels in trigeminal pain is not inherent to a specific headache syndrome but rather a feature of the physiology of the trigeminal neural innervation of the cranial circulation. Moreover, the impact of vascular changes for the generation of headaches remains elusive. The trigeminal nerve innervates blood vessels within ipsilateral meninges. Upon activation neuropeptides such as CGRP are released. Blockade of both the trigeminal nerve system and neuropeptides are crucial targets for headache alleviating drugs. While these mechanisms are well known the events within and outside the CNS which initiate headaches are poorly understood. This article will review the anatomy and physiology of the trigeminovascular system which demand renewed consideration of the neural influences in many primary headaches.
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PMID:[What is needed to develop a headache? Anatomical and pathophysiological implications]. 1525 41

Hyperostosis is a volume-unit osseous increase of very diverse etiology. We present the case of a 68-year woman with a cranial hyperostosis debuting with frontal protrusion, headache and neurologic symptoms. Image proves demonstrated a hyperostosis in the calotte and meningeal enhancement, without intracerebral lesions nor malignant cells in the cerebrospinal fluid. Analytic data were unspecific. Cranial biopsy showed huge neoplastic infiltration in bone and meninges. Primary site remained unknown after a CAT and a mammography.
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PMID:[Cranial hyperostosis as a metastasic adenocarcinoma presentation form]. 1553 5

Solitary fibrous tumor (SFT) is a mesenchymal neoplasm that has been recognized to occur almost all along the organism. Since its description in 1996 at the meninges, a total of 59 cases of meningeal SFT have been reported. Different authors have emphasized the difficulties in the differential diagnosis with other more frequent meningeal neoplasms such as meningioma or hemangiopericytoma, as the clinico-radiological characteristics of this lesion seem to be non specific and the morphological features on pathological study may resemble other spindle cell neoplasms. The diffuse and strong reactivity for CD34 and the negativity for EMA and S-100 are data allowing the diagnosis of SFT. We report the case of a 50-year-old woman suffering from headache, in whom MRI study showed a tentorial lesion initially thought to be a meningioma. In spite of morphological similarities with a fibrous meningioma, inmunohistochemical study finally led to the diagnosis of SFT. As occurred in previous cases, the findings in our patient reflect the similarities in clinico-radiological and pathological characteristics between meningeal SFT and other spindle cell meningeal neoplasms, mainly fibrous meningioma. When a clear diagnosis cannot be done based on typical findings on conventional hematoxylin-eosin study, inmunohistochemical study should be performed in meningeal spindle cell lesions to exclude SFT.
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PMID:Solitary fibrous tumor of the tentorium cerebelli. Case report. 1555 Aug 99

The vascular hypothesis of migraine has now been superseded by a more integrated theory that involves both vascular and neuronal components. It has been demonstrated that the visual aura experienced by some migraineurs arises from cortical spreading depression, and that this neuronal event may also activate perivascular nerve afferents, leading to vasodilation and neurogenic inflammation of the meningeal blood vessels and, thus, throbbing pain. The involvement of the parasympathetic system supplying the meninges also causes increased vasodilation and pain. As an acute attack progresses, sensory neurones in the trigeminal nucleus caudalis become sensitized, resulting in the phenomenon of cutaneous allodynia. Triptans may act at several points during the progression of a migraine attack. However, the development of central sensitization impacts upon the effectiveness of triptan therapy.
Cephalalgia 2004
PMID:Migraine pathophysiology and its clinical implications. 1559 88


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