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At least 253 records · Page 14Linked to original sources
PubMed1999

[Effects of Helicobacter pylori(Hp) eradication on gastric mucosal pathophysiology in Hp-positive, NSAIDs-induced gastric ulcer].

It has been suggested that the mechanisms of NSAIDs-induced peptic ulcer disease are totally different from those induced by Hp. Although a number of studies have examined the effects of Hp eradication on pathophysiology of NSAIDs-induced ulcer diseases, the results have been controversial. At present, therefore, we do not know whether Hp should be eradicated in Hp-positive NSAIDs-induced ulcer patients. Recent studies have shown that both Hp eradication and NSAIDs treatment increases gastric acid secretion, and often causes mucosal lesions in upper GI tract. Based on this back ground, we have decided to review pathophysiology of the Hp-dependent ulcer, and the NSAIDs-induced ulcer. We also discussed the merit and demerit of Hp eradication on gastric mucosal pathophysiology in Hp-positive, NSAIDs-induced ulcer.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1999

The epidemiology and pathophysiology of erectile dysfunction.

PURPOSE: Published studies on the epidemiology of erectile dysfunction and the physiology/ pathophysiology of erectile function are reviewed. MATERIALS AND METHODS: A literature search of more than 400 studies of the epidemiology and pathophysiology of impotence and erectile dysfunction published during the last 3 decades was conducted and the most pertinent articles are discussed. RESULTS: It has been estimated that the prevalence of erectile dysfunction of all degrees is 52% in men 40 to 70 years old, with higher rates in those older than 70 years. Erectile dysfunction has a significant negative impact on quality of life. Risk factors for erectile dysfunction include aging, chronic illnesses, various medications and cigarette smoking. A nitric oxide/cyclic guanosine monophosphate mechanism has an important role in mediating the corporal smooth muscle relaxation necessary for erectile function. Other mechanisms involving neuropeptides, gap junctions and ion channels also may modulate corporal smooth muscle tone. Erectile dysfunction can be due to vasculogenic, neurogenic, hormonal and/or psychogenic factors as well as alterations in the nitric oxide/cyclic guanosine monophosphate pathway or other regulatory mechanisms, resulting in an imbalance in corporal smooth muscle contraction and relaxation. CONCLUSIONS: Erectile dysfunction is a common condition associated with aging, chronic illnesses and various modifiable risk factors. Normal penile erection is a hemodynamic process that is dependent on corporal smooth muscle relaxation mediated by parasympathetic neurotransmission, nitric oxide, and possibly other regulatory factors and electrophysiological events. As more knowledge is gained of the physiology and regulatory factors that mediate normal erectile function, the mechanisms involved in the pathophysiology of erectile dysfunction should be further elucidated.

Erectile Dysfunction↗
PubMed1999

No pathophysiologic relationship of soluble biliary proteins to cholesterol crystallization in human bile.

This study explores the pathophysiologic effects of soluble biliary glycoproteins in comparison to mucin gel and cholesterol content on microscopic crystal and liquid crystal detection times as well as crystallization sequences in lithogenic human biles incubated at 37 degrees C. Gallbladder biles from 13 cholesterol gallstone patients were ultracentrifuged and microfiltered (samples I). Total biliary lipids were extracted from portions of samples I, and reconstituted with 0.15 m NaCl (pH 7.0) (samples II). Portions of samples II were supplemented with purified concanavalin A-binding biliary glycoproteins (final concentration = 1 mg/mL) (samples III), or mucin gel (samples IV), respectively, isolated from the same cholesterol gallstone biles. Samples V consisted of extracted biliary lipids from uncentrifuged and unfiltered bile samples reconstituted with 0.15 m NaCl (pH 7.0). Analytic lipid compositions of samples I through IV were identical for individual biles but, as anticipated, samples V displayed significantly higher cholesterol saturation indexes. Detection times of cholesterol crystals and liquid crystals were accelerated in the rank order of samples: IV > V > I = II = III, indicating that total soluble biliary glycoproteins in pathophysiologic concentration had no appreciable effect. Crystallization sequences (D. Q-H. Wang and M. C. Carey. J. Lipid Res. 1996. 37: 606-630; and 2539-2549) were similar among samples I through V. Crystal detection times and numbers of solid cholesterol crystals were accelerated in proportion to added mucin gel and the cholesterol saturation of bile only. For pathophysiologically relevant conditions, our results clarify that mucin gel and cholesterol content, but not soluble biliary glycoproteins, promote cholesterol crystallization in human gallbladder bile.

Bile↗
PubMed1999

Selectins in the HIT syndrome: pathophysiologic role and therapeutic modulation.

The pathophysiology of heparin-induced thrombocytopenia (HIT) is now known to be a complex process which involves platelets, vascular endothelium, and leukocytes. The activation products from these sites also contribute to the activation of coagulation and to the fibrinolytic deficit. While many of the markers of hemostatic activation processes have been found to be at increased levels during acute phases of the HIT syndromes, the circulating levels of soluble P-, E-, and L- selectins have not been reported. Since the pathophysiology of HIT involves the activation of platelets, endothelium, and leukocytes, it is expected that activation products related to these hemostatic systems, including soluble selectins, will also be increased in circulating blood. These alterations may provide an index of the pathophysiologic process. With the availability of highly sensitive ELISAs for soluble P-, E-, and L-selectins, it is now possible to measure these adhesion molecules in biological fluids. This study reports on the circulating levels of P-, E-, and L-selectins in HIT patients and their modulation after therapeutic intervention. With the availability of recombinant hirudin, it is now possible to provide alternate anticoagulants to HIT patients. However, the immunoactivation of platelets and other cells may require additional adjunct therapeutic approaches.

Anticoagulants↗
PubMed1999

Success in using non-invasive mechanical ventilation is predicted by patient pathophysiology. A retrospective review of 199 patients.

BACKGROUND: To determine the effect of patient pathophysiology on the success or failure of noninvasive mechanical ventilation as determined by the need for subsequent endotracheal intubation. METHODS: Center-based, retrospective case analysis of all patients placed on non-invasive mechanical ventilation for acute respiratory distress. MEASUREMENTS AND RESULTS: Retrospective chart review was performed on patients who were treated with non-invasive mechanical ventilation from 1/94-6/97. Patients were divided into those with rapidly reversible disease processes (RRDP), and those with non rapidly reversible disease processes (NRRP). The proportion of patients requiring subsequent intubation in each group was compared. There were 116 patients with RRDP and 83 patients with NRRD. In the RRDP group, 85.8 percent (95 percent confidence interval 80.9-90.7 percent) of patients did not require intubation. In the NRRP group, 35.7 percent (95 percent C.I. 29.0-42.4 percent) did not require intubation (X2 analysis, p < .001). Multivariate analysis identified patient pathophysiology as the only variable associated with subsequent intubation. CONCLUSIONS: Patient pathophysiology based upon their expected clinical course can be used to predict the success of non-invasive mechanical ventilation (NIMV). Patients with NRRD, such as pneumonia, myocardial infarct and sepsis, are much more likely to fail non-invasive mechanical ventilation and require subsequent endotracheal intubation.

Adolescent↗
PubMed1999

Vascular compression of cranial nerves: II: pathophysiology.

The pathophysiology of trigeminal neuralgia, hemifacial spasm and other disorders that can be cured by microvascular decompression of cranial nerves, is reviewed and different hypotheses about its pathophysiology are discussed. It is found that the pathophysiology of these disorders is complex and other factors than vascular compression are necessary to cause symptoms. While the efficacy of the microvascular decompression (MVD) operation is indisputable, it is questionable if the symptoms and signs of these disorders are caused by abnormal neural activity in the respective cranial nerves that result from the compression from a blood vessel. Instead, studies point to hyperactivity and hyperexcitability of the respective nuclei as a cause of the symptoms and signs of these disorders. Results of several studies indicate that irritation of the cranial nerve in question from close contact with a blood vessel may promote such development, and it seems necessary that other factors in addition to the vascular contact must be present in order that such a condition develops.

Cerebellopontine Angle↗
PubMed1999

[The pathophysiology of acute cerebral ischemia: clinical approach using physiologic imaging].

Physiologic imaging has recently allowed major new insights into the pathophysiology of acute ischemic stroke in man. The main observation concerns the major heterogeneity in pathophysiological patterns, with three situations being encountered: 1) cortical ischemic penumbra persisting up till 16 hrs post onset, which would represent an ideal therapeutic target; 2) early spontaneous reperfusion, predictive of favourable clinical and tissular outcome, and a priori requiring no specific therapy; and 3) early extensive necrosis, predictive of malignant hemispheric infarction. Physiologic imaging should soon become a fundamental tool in the evaluation of the individual pathophysiologic situation before a therapeutic decision about entry into trials is made.

Humans↗
PubMed2000

Pathophysiology of seasonal affective disorder: a review.

The study of the pathophysiology of seasonal affective disorder (SAD, also known as winter depression) has historically been intimately linked to investigations into the mechanisms of action of light therapy. This paper reviews the studies on the pathophysiology of SAD with emphasis on circadian, neurotransmitter, and genetic hypotheses. There is substantial evidence for circadian phase shift and serotonergic hypotheses, but conflicting results may indicate that SAD is a biologically heterogeneous condition. Recent progress in defining the molecular mechanisms of the human circadian clock and retinal phototransduction of light will provide important new directions for future studies of the etiology and pathophysiology of SAD.

Circadian Rhythm↗
PubMed2000

Do anxiety and depression have a common pathophysiological mechanism?

OBJECTIVE: To review, examine and propose a common mechanism for anxiety and depression based on modifications observed in neurotransmitter systems (mainly noradrenergic and serotonergic) and dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis. METHOD: The relevant papers were identified by searches in Medline, Excerpta Medica, PsychLIT and other databases. The primary reports were reviewed and classified into animal and human data concerning: modifications of the monoamine receptors in anxiety and depression, pathophysiology of endocrine factors in anxiety and depression, pathophysiology of the hypothalamic-pituitary-adrenal (HPA) axis and the pathophysiology of the HPA dysregulation in anxiety and in depression. In addition, a proposed model of a neuroendocrine continuum for anxiety and depression, in which anxiety occurs first during the life course and major depressive episodes occur later, was examined. RESULTS: Based on the available literature, increased concentrations of corticotropin-releasing factor (CRF) in the cerebrospinal fluid has been reported in both anxiety and depression. However, release of other peptides or hormones of the HPA axis is regulated differently in the two disorders. Anxiety is characterized by hypocortisolemia, supersuppression after dexamethasone and increased numbers of glucocorticoid receptors, whereas depression is characterized by hypercortisolemia, nonsuppression after dexamethasone and decreased numbers of glucocorticoid receptors. A 'neuroendocrine continuum' model is proposed to explain these differences. A general desensitization of CRF receptors at pituitary, limbic (amygdala) and cortical as well as hippocampal levels could be secondary to the loss of hippocampal inhibition resulting from hippocampal damage linked to repeated stressing events. CONCLUSION: The proposed hypothesis remains to be tested by examination of either the changes in receptors and neurotransmission or the mechanisms underlying the dysregulation of endocrine factors.

Anxiety Disorders↗
PubMedDate not supplied

Ascites fluid in severe acute pancreatitis: from pathophysiology to therapy.

Several pathophysiological mechanisms are involved in the development of the inflammatory necrotizing process that takes place in the retroperitoneal area during the early phase of acute pancreatitis. They include premature intraglandular activation of pancreatic proenzymes (zymogens) and in particular trypsin, early microcirculatory impairment with subsequent ischaemia/reperfusion and overstimulation of immune effector cells. Although intra-acinar or interstitial activation of trypsinogen is most probably the trigger of acute pancreatitis, in recent years much emphasis has been put on the role of leukocytes. Based on numerous experimental and human data several pro-inflammatory mediators including cytokines, arachidonic acid derivatives, activated oxygen species and proteases are released locally by overactivated neutrophils and monocytes/macrophages among other cells. They are now believed to play a central role in the development of pancreatic necrosis and, once they gain access to the systemic circulation, in the emergence of early multisystem organ failure. However the sequential and relative contribution of each of these 3 pathophysiological mechanisms remain controversial and the precise identification of the mediators incriminated in local and remote tissue injury is still awaited. Severe acute pancreatitis still carries a mortality of 20% to 30%. With advances in intensive care management 80% of the deaths occur somewhat late in the attack due to infected pancreatic necrosis. Nevertheless early remote organ failures still remain a lifethreatening condition for most of these patients. A peritoneal exudate rich in activated lipolytic and proteolytic enzymes, vasoactive substances and several other pro-inflammatory mediators collect in over 60% of the patients with severe acute pancreatitis. On the basis of favourable animal experiments early percutaneous or surgical peritoneal lavage with or without the addition of antiproteases has been carried out in human acute pancreatitis. The rationale behind this procedure was the washout of potential toxic mediators from the peritoneal cavity before they gain access to the systemic circulation. Contrary to animal and uncontrolled human data no prospective randomized study could ever demonstrated a significant effect of peritoneal lavage neither in the prevention and control of remote organ failures or in early mortality and ultimate survival after severe acute pancreatitis in humans. Differences between experimentally-induced pancreatitis, difference in the timing of the initiation of lavage and a type II error in controlled human studies may account for the discrepancy in the outcome between these studies. Anyway, this disparity should raise the question as whether the peritoneal cavity acts simply as a reservoir or as a route of transfer of toxic mediators to the systemic circulation. Although data are scarce, conflicting and limited to animal experiments and to a few molecules, peripancreatic veins and lymphatics seem to be the major routes of transfer whereas transperitoneal absorption is trivial. Nevertheless early peritoneal aspiration of ascitic fluid in acute pancreatitis and measurement of trypsinogen activation peptides may be used as a means of severity assessment and identification of pancreatic necrosis. This implies that even if not taking part actively in the emergence of remote organ failures ascitic fluid may reflect the peripancreatic necrotizing process. So careful comparative analysis of peritoneal exudate, plasma and lymph with regards to putative mediators of local and remote injury may provide essential pathophysiological clues. At the time of trials of antimediator therapy early in the attack this kind of insight is essential.

Acute Disease↗
PubMed2001

Mycobacterium avium subspecies paratuberculosis triggers intestinal pathophysiologic changes in beige/scid mice.

We investigated whether infection of beige/scid mice with Mycobacterium avium subspecies paratuberculosis can induce intestinal pathophysiologic changes. Six-week-old beige/scid mice were inoculated intraperitoneally with M. paratuberculosis, then were killed 32 weeks after inoculation when the small intestine was evaluated for physiologic and morphologic abnormalities. All infected mice developed clinical disease. The lamina propria of the intestine from infected mice was mildly infiltrated with mononuclear cells containing acid-fast bacteria, and had significantly increased villus width. In vitro physiologic studies in Ussing chambers indicated that M. paratuberculosis infection caused significant abnormalities in intestinal transport parameters. Baseline short circuit current and potential difference were abnormally high in tissues from infected, compared with control mice, indicative of increased ion secretion. Baseline conductance was significantly decreased in infected mice, suggesting that intestinal tissue from infected mice was less permeable to ions. The change in short circuit current following transmural electrical and glucose stimulation was significantly reduced in intestines from infected mice, suggesting that inflamed intestine had neural and/or epithelial cell damage. We conclude that infection of beige/scid mice with M. paratuberculosis triggers significant intestinal pathophysiologic changes consistent with chronic inflammation. These functional abnormalities may contribute to the pathogenesis of the wasting syndrome seen in bovids with paratuberculosis. This animal model provides evidence that T cell-independent mechanisms are sufficient to cause mucosal pathophysiologic changes and inflammation in response to a specific pathogen, and may be of relevance to inflammatory bowel disease in humans.

Animals↗
PubMed2002

Pathophysiological aspects of hypertensive disease in women.

Although during the past two decades there has been considerable progress in the understanding of the pathophysiology of human essential hypertension, the basic mechanisms responsible for the development and progression of the disease still remain largely undefined. This also applies to the pathophysiology of hypertension in women, although a number of haemodynamic, vascular, metabolic and neurohumoral factors have been identified throughout the years as being characterized by a gender-specific relation. This paper will examine the main differences in the haemodynamic, vascular, metabolic and neurohumoral profile characterizing normotensive as well as hypertensive females as compared with age-matched males. Although in some instances clearcut differences between genders can be found, overall the pathophysiological picture of the hypertensive state does not seem to have significant differences in men and women, at least up to the years when the menopausal-related hormonal changes take place.

Evidence-Based Medicine↗
PubMed2003

Unfolding the pathophysiological role of bioactive lysophospholipids.

Lysophospholipids (LPLs), including glycerol- and sphingoid-based lipids, stimulate cell signaling and play important pathophysiological roles in humans and other animals. These LPLs include lysophosphatidic acid (LPA), lysophosphatidylinositol (LPI), lysophosphatidylcholine (LPC), lysophosphatidylserine (LPS), sphingosine-1-phosphate (S1P), and sphingosylphosphorylcholine (SPC). Analyses of LPLs in human body fluids from subjects with different pathophysiological conditions reveal not only the relevance of LPLs in human diseases, but also their potential application as biomarkers and/or therapeutic targets. In recent years, the identification and/or characterization of the plasma membrane receptors for LPLs and enzymes regulating the metabolism of LPLs have greatly facilitated our understanding of their role and signaling properties. In vitro and in vivo functional and signaling studies have revealed the broad and potent biological effects of LPLs and the mechanisms of LPL actions in different cellular systems. Development of specific antagonists for each of the LPL receptors will provide powerful tools for dissecting signaling pathways mediated by receptor subtypes. More importantly, these antagonists may serve as therapeutics for relevant diseases. Genetic depletion of LPL receptors in mice has provided and will continue to provide critical information on the pathophysiological roles of LPL receptors. It is important to further evaluate the significance of targeting these bioactive LPL receptors, their downstream signaling molecules, and/or metabolic enzymes in the treatment of cancers and other diseases.

Animals↗
PubMed2003

[Sensory sensitization, part II: Pathophysiology in dysfunctional disorders. Understanding the inner life of the nerve pathways may explain hitherto unexplainable symptoms].

This article is based on a vast clinical experience from patients presenting with widespread pain syndromes as well as dysfunctional symptoms from inner organs. A literature survey has been performed. Allodynia and hyperalgesia that partly explain the fibromyalgia and local myalgia syndromes seem to arise from a pathophysiological process of nociceptive sensitisation. It is proposed that the concept of "sensory sensitisation dysfunctional disorders" be applied to conditions like bronchial hyperreactivity, Da Costas syndrome, Dercum's disease (Adipositas dolorosa), dry eyes and mouth syndrome, fibromyalgia, gastralgia, globus hystericus, interstitial cystitis, chronic prostatitis, irritable bowel syndrome, photo- and phonosensitivity, rhinitis, tension headache, tinnitus, vestibulitis syndrome. These dysfunctional disorders cannot be satisfactorily explained by presently known pathophysiological models like ongoing inflammatory process, tissue degeneration, fibrosis, blood vessel diseases, tumours, immune reactions, toxic or deficiency conditions, metabolic disturbances. Neurogenic mechanisms also seem to play an important role in the pathophysiology of arthritic conditions, and might be worthwhile to include in forthcoming discussions concerning the aetiology of chronic inflammatory disease.

Chronic Disease↗
PubMed2002

Functional Anatomy, Pathomechanics, and Pathophysiology of Lateral Ankle Instability.

OBJECTIVE: To describe the functional anatomy of the ankle complex as it relates to lateral ankle instability and to describe the pathomechanics and pathophysiology of acute lateral ankle sprains and chronic ankle instability. DATA SOURCES: I searched MEDLINE (1985-2001) and CINAHL (1982-2001) using the key words ankle sprain and ankle instability. DATA SYNTHESIS: Lateral ankle sprains are among the most common injuries incurred during sports participation. The ankle functions as a complex with contributions from the talocrural, subtalar, and inferior tibiofibular joints. Each of these joints must be considered in the pathomechanics and pathophysiology of lateral ankle sprains and chronic ankle instability. Lateral ankle sprains typically occur when the rearfoot undergoes excessive supination on an externally rotated lower leg. Recurrent ankle sprain is extremely common; in fact, the most common predisposition to suffering a sprain is the history of having suffered a previous ankle sprain. Chronic ankle instability may be due to mechanical instability, functional instability, or most likely, a combination of these 2 phenomena. Mechanical instability may be due to specific insufficiencies such as pathologic laxity, arthrokinematic changes, synovial irritation, or degenerative changes. Functional instability is caused by insufficiencies in proprioception and neuromuscular control. CONCLUSIONS/RECOMMENDATIONS: Lateral ankle sprains are often inadequately treated, resulting in frequent recurrence of ankle sprains. Appreciation of the complex anatomy and mechanics of the ankle joint and the pathomechanics and pathophysiology related to acute and chronic ankle instability is integral to the process of effectively evaluating and treating ankle injuries.

Journal Article↗
PubMed1992

Physiology and pathophysiology of atrial natriuretic factor in lungs.

UNLABELLED: OBJECTIVE AND DATA SOURCE: Experimental and clinical data reported in the international literature have been collected and critically reviewed to summarize knowledge of the role of atrial natriuretic factor (ANF) in lung physiology and pathophysiology. DATA SYNTHESIS: Lung contribution to circulating ANF concentration is modest, whereas its capability of degrading ANF is very high, the lung being one of the major sites of ANF catabolism. The impairment of ANF protease activity in lung tissue by hypoxia and pulmonary hypertension could be responsible for the increase in ANF plasma levels observed in several pulmonary pathological conditions. ANF-specific binding sites in lung are reportedly greater than in any other tissue. ANF induces a cGMP-mediated relaxation of central (rather than peripheral) bronchi. ANF bronchodilating effect has also been clinically demonstrated; eg, asthmatic patients show increased plasma ANF levels and exogenous ANF infusion provokes bronchial relaxation comparable with the salbutamol-induced effect. Moreover, ANF determines pulmonary artery vasodilation, thus contributing to improved pulmonary circulation. When pathophysiological levels are present in plasma, ANF influences pulmonary fluid regulation provoking protein mobilization from arteries to the alveolar space whereas ANF pharmacological concentrations re-equilibrate the transwall gradient. A remarkable enhancement of guanylate cyclase activity in lung tissue before hemodynamic modifications by both endogenous end exogenous ANF has been reported in pneumocytes of cardiomyopathic hamsters. On the other hand, ANF infusion provokes a reduction of pulmonary edema induced by pneumotoxic chemicals through a mechanism independent of the natriuretic/hypotensive action of the peptide and not mediated by cGMP. CONCLUSIONS: The modest amount of specific research on ANF effects on lung does not permit a final assessment of natriuretic peptides in pulmonary physiology and pathophysiology. In particular, further investigations are needed to determine the potential clinical relevance of ANF in asthma and pulmonary edema.

Animals↗
PubMed2004

[Possible involvement of protein kinase C in the pathophysiology and treatment of bipolar disorder].

Over the past decade, the focus of research into the pathophysiology of bipolar disorder has shifted from an interest in the biogenic amines to an emphasis on second messenger systems within cells. Emerging evidence implicates protein kinase C (PKC) intracellular signaling cascade in the pathophysiology and treatment of bipolar disorder. This review explores the possible involvement of PKC in bipolar disorder summarizing results from laboratory and clinical studies. Bipolar patients were demonstrated to have altered PKC levels, activity or distribution in platelets and in the brain. Chronic administration of lithium and valproate produced a striking reduction in protein kinase C (PKC) human cells and in rats. PKC inhibition in animals resulted in altered affective-like behavior and in a small study, tamoxifen (a PKC inhibitor) had marked antimanic efficacy. The results of studies at the molecular, cellular, animal and clinical levels all suggest that regulation of PKC signaling pathways may play a major part in the pathophysiology and treatment of bipolar disorder. Therefore, this pathway may be a promising candidate for the development of new, more specific drugs for the disease.

Antimanic Agents↗
PubMedDate not supplied

[Chronic daily headache: I. Diagnosis and pathophysiology].

INTRODUCTION: Chronic daily headache (CDH), or headache more than 15 days/month or over 180 days/year, is one of the main reasons for visits to specialised headache centres and accounts for up to 5% of primary headaches. AIMS: Our objective was to determine the classification, epidemiology, risk factors and pathophysiology of CDH by reviewing the literature. DEVELOPMENT: CDH has a prevalence of 2 to 3% in the general population and is subdivided into two groups according to the headache duration. The first group (more than four hours) represents over 90% patients; includes chronic migraine (60 to 87.4%), chronic tension-type headache (0.9 to 28.8%), new daily persistent headache (0.8 to 20%) and hemicrania continua (2.2%), which represents over 90% of patients. The second group (less than four hours) is made up of cluster, chronic paroxysmal hemicranial, idiopathic stabbing-type headache and cranial neuralgias. The pathophysiology of CDH is multifactorial; it has been suggested that genetic factors, peripheral and central neuronal dysfunction derived from the alteration of protein and receptor synthesis, inadequate release of inhibitory and excitatory neuropeptides, imbalance, excitatory and inhibitory neuropeptides concentration imbalance, in association with abuse of analgesics, high comorbidity with psychiatric disorders (anxiety, depression and panic) and sleep disorders may all be involved. CONCLUSIONS: CDH is a frequent cause of headache and chronic migraine is the main presenting symptom. Pathophysiology is multifactorial; there is a strong association with analgesic abuse, high comorbidity with psychiatric disorders and sleep disorders.

Analgesics↗