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

Chronic fatigue syndrome (CFS) is a specific clinical condition that characterises unexplained disabling fatigue and a combination of non-specific accompanying symptoms for at least 6 months, in the absence of a medical diagnosis that would otherwise explain the clinical presentation. Other common symptoms include headaches, myalgia, arthralgia, and post-exertional malaise; cognitive difficulties, with impaired memory and concentration; unrefreshing sleep; and mood changes. Similar disorders have been described for at least two centuries and have been differently named neurasthenia, post-viral fatigue, myalgic encephalomyelitis and chronic mononucleosis. Recent longitudinal studies suggest that some people affected by chronic fatigue syndrome improve with time but that most remain functionally impaired for several years. The estimated worldwide prevalence of CFS is 0.4-1% and it affects over 800,000 people in the United States and approximately 240,000 patients in the UK. No physical examination signs are specific to CFS and no diagnostic tests identify this syndrome. The pathophysiological mechanism of CFS is unclear. The main hypotheses include altered central nervous system functioning resulting from an abnormal immune response against a common antigen; a neuroendocrine disturbance; cognitive impairment caused by response to infection or other stimuli in sentient people. The current concept is that CFS pathogenesis is a multifactorial condition. Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported. The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects of CFS and offers an immunological hypothesis for the disease processes.
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PMID:Immunological aspects of chronic fatigue syndrome. 1880 65

Nitric oxide (NO) is a marker of pulmonary inflammation. In asthma, the levels of exhaled NO are elevated and the source of this increased NO is inducible nitric oxide synthase (iNOS) within airway epithelial cells. Epimagnolin and fargesin are compounds isolated from the ethanol extract of Magnoliae flos, the seed of the Magnolia plant and are used to treat nasal congestion, headache and sinusitis in Asian countries. This study investigated whether epimagnolin and fargesin inhibit extracellular signal-regulated kinase (ERK) activation and decrease iNOS expression and NO production in stimulated human respiratory epithelial cells. An immortal Type II alveolar cell line of human origin (A549) was stimulated by cytomix (CM), composed of IL-1beta, TNF-alpha and IFN-gamma, with or without concurrent exposure to M. flos extract (epimagnolin or fargesin). CM-induced levels of NO production, iNOS expression and ERK activation were evaluated. A549 cells stimulated with CM showed increases in iNOS mRNA and protein expression, and NO synthesis. However, treatment with epimagnolin or fargesin decreased levels of iNOS mRNA and protein expression, and NO synthesis. CM stimulated a rapid increase in the activity of ERK, whereas epimagnolin and fargesin inhibited ERK phosphorylation. Epimagnolin and fargesin inhibit iNOS expression and decrease production of NO via ERK pathway in cytokine-stimulated human respiratory epithelial cells.
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PMID:Extracts of Magnoliae flos inhibit inducible nitric oxide synthase via ERK in human respiratory epithelial cells. 1897 18

Cytokines have been measured in cerebrospinal fluid (CSF) from headache patients [infrequent episodic tension-type headache (TTH) and migraine with or without aura, all during attack, and cervicogenic headache] and compared with levels in pain-free individuals. Both proinflammatory [interleukin (IL)-1beta, tumour necrosis factor-alpha and monocyte chemoattractant protein-1 (MCP-1)] and anti-inflammatory cytokines [IL-1 receptor antagonist (IL-1ra), IL-4, IL-10 and transforming growth factor-beta1 (TGF-beta1)] were included. There were significant group differences in IL-1ra, TGF-beta1 and MCP-1 in episodic TTH and migraine compared with controls, and a significant difference in MCP-1 between cervicogenic headache and migraine with aura. Intrathecal MCP-1 correlated with IL-1ra, IL-10 and TGF-beta1 in episodic TTH, and MCP-1 with IL-10 in migraine with aura. Cytokine increases were modest compared with those often accompanying serious neurological conditions, and may represent a mild response to pain. We believe this to be the first comparative study of CSF cytokine levels in connection with headache.
Cephalalgia 2009 Mar
PMID:Cerebrospinal fluid cytokine levels in migraine, tension-type headache and cervicogenic headache. 1917 74

Scrub typhus is a zoonotic disease that is caused by Orientia tsutsugamushi. Although hepatic dysfunction occurred in 77-96.7% of the scrub typhus patients, its mechanism is unknown. IL-17 is a potent proinflammatory cytokine known for its role in several chronic disease conditions. Abundant IL-17 was found in conditions affected by microbial pathogens, including the synovial fluid of patients with Lyme arthritis or Chlamydia-induced reactive arthritis, Helicobacter pylori-infected gastric mucosa, and listeria infection. It is also suggested as a marker of acute hepatic injury. In our study, we postulated that IL-17 might be a cytokine with a role in hepatic dysfunction in scrub typhus. In September-November 2006, our study involved 43 patients with Boryong-type scrub typhus patients and 40 age- and sex-matched control healthy people. Scrub typhus was confirmed on the basis of immunofluorescence and a nested polymerase chain reaction assay. IL-17 was measured using human IL-17 immunoassay. We gathered the clinical and laboratory data by chart reviews. We used an independent t-test, Kolmogorov-Smirnov test, and correlation analysis. The IL-17 levels were significantly higher in scrub typhus patients than in the healthy group. Also, the patients with scrub typhus showed significantly higher aspartate aminotransferase and alanine aminotransferase levels, and lower hemoglobin levels than the healthy group. However, in our correlation analysis, we did not find any correlation between IL-17 and hepatic, kidney, and hemogram panels. The IL-17 level in patients with headaches was higher than in patients without headaches, showing a borderline significance. This suggests that IL-17 level might be a cause of a vasculitis-associated headache. More prospective, large-scale studies are needed about the mechanism of hepatic dysfunction and headaches in scrub typhus patients.
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PMID:Does IL-17 play a role in hepatic dysfunction of scrub typhus patients? 1948 73

Toward understanding the role of cytokines in migraine, this study focused on selected proinflammatory cytokines. The study group consisted of 21 children who had migraine with and without aura; the control group was 24 children with episodic tension-type headache. Plasma interleukin-1 alpha was undetectable in 19 control subjects with tension-type headache, but was detectable in 16 patients with migraine, which suggests that interleukin-1 alpha level might be higher in migraine. Soluble tumor necrosis factor receptor 1 in the migraine group was significantly higher than in the control group (P < 0.0005). Migraine patients tended to have increased tumor necrosis factor alpha level, compared with the control group. The interleukin-1 alpha level was significantly higher in migraine with aura than in migraine without aura (P < 0.05). Tumor necrosis factor alpha and soluble tumor necrosis factor receptor 1 levels tended to be increased in the migraine with aura subgroup. The results suggest that proinflammatory cytokines may be involved in the pathogenesis of migraine attacks, although fluctuations in cytokine levels could be different in children than in adults. Such difference could be due to long medical history of migraine in adult patients and frequent intake of analgesic drugs or prophylactic treatment.
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PMID:Proinflammatory plasma cytokines in children with migraine. 1952 Feb 68

Malaria is an important tropical mosquito-borne infectious disease. In this article, the author briefly reviewed headache profile in patients with malaria focusing on its mechanism. Headache is an important presentation in malaria, either cerebral type or not. The cytokine is believed to be an important factor leading to headache in acute malaria. Some antimalarial drugs can cause headaches. In addition, headache is one of the symptoms of postmalaria neurologic syndrome.
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PMID:Headache and malaria: a brief review. 1953 76

Matrix metalloproteinases (MMP) are proteolytic enzymes involved in the remodelling of almost all protein components of the extracellular matrix (ECM), characterized in 1960's during the metamorphosis process in tadpole tails. Ever growing research has identified MMP expression in a variety of physiological processes. Uncontrolled or inappropriate expression/activity of MMPs contributes to different pathologic conditions, including inflammation, tumour growth, cancer cell invasion and infection diseases. Under physiological conditions, MMP activity is precisely controlled by TIMPs and may have beneficial actions in the mature nervous system. However, an alteration of the MMP/TIMP balance is thought to be a key feature of the pathology of many inflammatory, degenerative and malignant neurological diseases; their pathogenesis is correlated to the detrimental effects of altered MMP/TIMP expression, leading to breakdown of the blood-brain barrier (BBB), demyelination, cytokine production and propagation of inflammatory response, deposition of amyloid proteins, tumor invasion and metastasis). Migraine is a complex, disabling disorder of the brain that manifests itself as attacks of often severe, throbbing head pain with sensory sensitivity to light, sound, smell and head movement (migraine without aura), and in a third of patients, with neurological symptoms (migraine with aura). In this issue of Clinica Chimica Acta, Martins-Oliveira et al. examine the different circulating MMP and TIMP profiles in women with migraine with and without aura. They confirm and expand the observation of increased MMP-9 plasma levels in migrainous patients, also describing for the first time that MMP-2, TIMP-1 and TIMP-2 show a different expression profile in migraine. Their findings are critically evaluated and reviewed. The knowledge of MMP- and TIMP-dependent pathways in migraine headache, the new proteolytic pathophysiological mechanisms, and the beneficial and detrimental effects of MMP inhibitory drugs may represent pieces of the complex migraine jigsaw puzzle, which is finalized to optimize cost-effectiveness of treatment and patient outcomes.
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PMID:New implications of the proteolytic balance between matrix metalloproteinases and their tissue inhibitors in migraine with and without aura. 1963 13

The study objective was to evaluate levels of the cytokines tumor necrosis factor alpha, interleukin-1beta, and interleukin-6 and of leptin, and then to determine the relationship between these levels and clinical responses in children with migraine after prophylactic therapy with one of four drugs. In all, 77 children who needed prophylactic drugs were treated with cyproheptadine, amitriptyline, propranolol, or flunarizine. Serum levels of the cytokines and leptin were measured before and 4 months after the treatment. Results were compared by drug for headache frequency, severity, and duration, the PedMIDAS score, and levels of each cytokine and of leptin. Each of the four drugs not only decreased the frequency and duration but also the severity of headache, and the PedMIDAS score. None of the drugs was found to be superior to others in terms of reduction in cytokine levels (P > 0.05). Both cyproheptadine and flunarizine (but not amitriptyline and propranolol) caused an increase in leptin levels (P < 0.05). These data suggest that cytokine levels are related to clinical responses, and might help in objective evaluation of clinical response in migraine. To our knowledge, the present study is the first trial to compare the effects of prophylactic drugs, cytokine levels, and leptin levels in children with migraine.
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PMID:Prophylactic drugs and cytokine and leptin levels in children with migraine. 1974 48

Enhanced pain perception is common among patients with rheumatoid arthritis (RA). Given the putative role of proinflammatory cytokines in the development of hyperalgesia, a greater understanding of factors that facilitate increased cytokine expression in RA stands to increase understanding of the sources of enhanced pain perception. Patients with RA have significantly greater stress-induced proinflammatory cytokine release. Although absolute deficiencies in cortisol have not been demonstrated, functional abnormalities have been described, including "abnormally normal" cortisol levels in the face of increased inflammation and deficient responses to stressful challenges. Parasympathetic insufficiency has also been demonstrated, which may enhance pain perception indirectly through disinhibited cytokine expression. Several psychological variables have also been demonstrated to affect pain perception in patients with RA. Identification of factors that contribute to enhanced pain perception in RA may aid in the development of novel analgesic strategies that, in turn, may decrease disease activity and improve general clinical outcomes.
Curr Pain Headache Rep 2009 Dec
PMID:Enhanced pain perception in rheumatoid arthritis: novel considerations. 1988 84

Mollaret meningitis (MM) occurs mainly in females and is characterized by recurrent episodes of headache, transient neurological abnormalities, and the cerebrospinal fluid containing mononuclear cells. HSV-2 was usually identified as the causative agent. Recently, we found that recurrent headaches in non-HIV-infected subjects were due to acquired cerebral toxoplasmosis (CT). The aim of the study was therefore to focus on molecular pathomechanisms that may lead to reactivation of latent CT and manifest as MM. Literature data cited in this work were selected to illustrate that various factors may affect latent CNS Toxoplasma gondii infection/inflammation intensity and/or host defense mechanisms, i.e., the production of NO, cytokines, tryptophan degradation by indoleamine 2,3-dioxygenase, mechanisms mediated by an IFN-gamma responsive gene family, limiting the availability of intracellular iron to T. gondii, and production of reactive oxygen/nitrogen species, finally inducing choroid plexitis and/or vasculitis. Examples of triggers revealing MM and accompanying disturbances of IFN-gamma-mediated immune responses that control HSV-2 and T. gondii include: female predominance (female mice are more susceptible to T. gondii infection than males); HSV-2 infection (increased IFN-gamma, IL-12); metaraminol (increased plasma catecholamine levels, changes in cytokine expression favoring T(H)2 cells responses); probably cholesterol contained in debris from ruptured epidermoid cysts (decreased NO; increased TNF-alpha, IL-6, IL-8). These irregularities induced by the triggers may be responsible for reactivation of latent CT and development of MM. Thus, subjects with MM should have test(s) for T. gondii infection performed obligatorily.
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PMID:Mollaret meningitis may be caused by reactivation of latent cerebral toxoplasmosis. 1992 80


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