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At least 631 records · Page 35Linked to original sources
PubMed2001

Epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Spinal cord injury occurs through various countries throughout the world with an annual incidence of 15 to 40 cases per million, with the causes of these injuries ranging from motor vehicle accidents and community violence to recreational activities and workplace-related injuries. Survival has improved along with a greater appreciation of patterns of presentation, survival, and complications. Despite much work having been done, the only treatment to date known to ameliorate neurologic dysfunction that occurs at or below the level of neurologic injury has been intravenous methylprednisolone therapy. Much research over the past 30 to 40 years has focused on elucidating the mechanisms of spinal cord injury, with the complex pathophysiologic processes slowly being unraveled. With a greater understanding of both primary and secondary mechanisms of injury, the roles of calcium, free radicals, sodium, excitatory amino acids, vascular mediators, and apoptosis have been elucidated. This review examines the epidemiology, demographics, and pathophysiology of acute spinal cord injury.

Age Factors↗
PubMed2004

Examining novel concepts of the pathophysiology of depression in the chronic psychosocial stress paradigm in tree shrews.

Despite decades of research on psychiatric disorders, the aetiology and precise biological mechanisms that underlie depressive diseases are still poorly understood. There is increasing evidence that psychiatric disorders not only have a neurochemical basis but are also associated with morphological alterations in central nervous neurons and/or glial cells. Antidepressants may act by restoring structure as well as function of neural networks, meaning that they may, as a fundamental principle, affect neural plasticity underlying normal brain functioning. To examine these novel concepts of the pathophysiology of depression and antidepressant medication we have carried out a series of experiments using the chronic psychosocial stress paradigm in male tree shrews, an animal model with a high validity for the pathophysiology of depressive disorders, in which the animals were treated with the tricyclic antidepressant compound clomipramine. We found that one month of stress reduced cell proliferation in the dentate gyrus, and decreased the total hippocampal volume. Gene transcription analysis revealed that, under these experimental conditions, expression of genes known to be involved in processes of cell differentiation is suppressed. These effects of social conflict on hippocampal cells, including gene transcription, and on the entire hippocampal volume could be counteracted by chronic treatment with the antidepressant clomipramine. Stress also induced a constant hyperactivity of the hypothalamic-pituitary-adrenal axis, and suppressed both motor and marking behaviour. These neuroendocrine and behavioural stress-induced changes were also re-normalized by clomipramine.

Animals↗
PubMed2001

Angiotensin II type 2 receptors: signalling and pathophysiological role.

The signalling mechanisms and biological significance of the angiotensin II type 2 receptor have long been unknown. In recent years, studies, first in cell culture models but now increasingly also in vivo, have shed some light on the molecular events occurring after a stimulation of the receptor with its ligand as well as on its physiological effects and its significance for pathophysiological processes. There is increasing evidence that the angiotensin II type 2 receptor is involved in different pathophysiological processes, such as myocardial infarction, heart and kidney failure, and stroke.

Animals↗
PubMedDate not supplied

Malignant hyperthermia: pathophysiology, clinical presentation, and treatment.

Malignant hyperthermia (MH) was first described as an inherited highly lethal disorder in 1960. There has since been significant progress in the clinical management, identification of MH susceptible (MHS) persons, and understanding of the underlying pathophysiology. When patients are known to be MHS prior to surgery, an MH episode can easily be avoided by the use of safe nontriggering anesthetic agents. Current MH mortality is <10%, but many experts believe this can be significantly reduced by improved MH preparedness. MH is triggered in humans by an MH triggering anesthetic agent, which causes the release of calcium from the sarcoplastic reticulum of the skeletal muscle cell at an uncontrolled rate resulting in a hypermetabolic state. Recent molecular genetic studies have shown that MH is related to an abnormal ryanodine receptor that controls the release of calcium from the sarcoplastic reticulum. This article reviews the current understanding of the pathophysiology, diagnosis, clinical presentation, and treatment of MH.

Biopsy↗
PubMedDate not supplied

HIV peripheral neuropathy: pathophysiology and clinical implications.

One of the most debilitating neurological complications of human immunodeficiency virus (HIV), affecting nearly one in three patients, is painful peripheral neuropathy. Although HIV infection can cause distal sensory polyneuropathy (DSP), the advent of highly active antiretroviral therapy (HAART) to treat HIV infection has resulted in a significant number of patients developing a clinically indistinguishable form of toxic neuropathy. The predominant symptom, regardless of etiology, is excruciating unremitting pain, resistant to pharmacological treatments, that leads to a reduction in the ability to conduct activities of daily living and, eventually, inability to ambulate. Since withdrawal from nucleoside therapy is not typically recommended, a more thorough understanding of the etiology and pathophysiology underlying nucleoside-induced peripheral neuropathy, through basic and clinical research endeavors, will aid in the development of new therapeutic treatments aimed at alleviating or ameliorating pain. This article provides the latest information regarding the pathophysiology and clinical implications of HIV peripheral neuropathy.

Activities of Daily Living↗
PubMed2000

University of Miami Division of Clinical Pharmacology therapeutic rounds: irritable bowel syndrome-pathophysiology, diagnosis, and treatment.

Irritable bowel syndrome, or IBS, is a common disorder of the bowels that causes significant patient morbidity, work-absenteeism, physician visits, and, frequently, extensive evaluations. The syndrome has been classified as a functional disorder because of the lack of clearly elucidated pathophysiology, although altered visceral sensitivity, intestinal motility, and psychosocial factors all likely play a role. Treatment includes fostering a strong, trusting relationship with the patient, with pharmacotherapy directed at the predominant symptoms. The authors review the pathophysiology, diagnosis, and treatment of this difficult disorder.

Adult↗
PubMed2003

Pulmonary oedema in SCUBA divers: pathophysiology and computed risk analysis.

SCUBA diving has become a popular sport, with an increasing number of people participating in it. Although it is an essentially very safe activity, several specific medical problems are associated with diving. The present paper addresses diving-related pulmonary oedema, which is a rarely reported condition. It has been described mostly in cold water diving, and its occurrence in warm water has not been documented before. We delineate the pathophysiology of this condition and its treatment, and use a novel computational model to analyse further the mechanisms leading to diving-related pulmonary oedema. A better understanding of diving-related pulmonary oedema may lead to earlier recognition and treatment, and, potentially, to its prevention. The physiological mechanisms likely to lead to diving-related pulmonary oedema are well recognized. Consequently, we could design and construct a bio-mechanical computer model of the alveolar septa to explore the pathophysiology of diving-related pulmonary oedema and the vulnerability of individual divers as they relate to some mechanical characteristics of their lung structure. The physiological mechanisms of diving-related pulmonary oedema and the results provided by the computational model successfully delineated the process. The model predicted that the risk of injury is significantly increased in individuals who have a stiffer lung parenchyma or lower lung compliance values.

Biomechanical Phenomena↗
PubMed2003

Pathophysiology of pulmonary hypertension due to lung disease.

Pulmonary hypertension (PH) often complicates the course of patients with advanced lung disease, and it is associated with a worse prognosis. Per the recent classification of pulmonary hypertensive disorders, PH due to lung disease is considered as a separate category within a group of disorders that was previously referred to as "secondary" PH. Among the lung diseases associated with PH, the incidence and clinical course of PH is best known for patients with COPD. Per studies in patients with COPD and other lung disorders, it is evident that the pathophysiology and treatment of these disorders is generally distinct from that of pulmonary arterial hypertensive disorders. Changes in the pulmonary vasculature that accompany elevations in pulmonary vascular pressure are generally referred to as pulmonary vascular remodeling. Chronic hypoxia is well known to cause pulmonary vascular remodeling and PH, and it is the major mechanism implicated for the development of PH in patients with lung disease. Other mediators have also been implicated in the pathogenesis of PH in animal models and patients with PH, including patients with pulmonary diseases. General features of pulmonary vascular remodeling are discussed with particular emphasis on those changes that have been described in patients with lung diseases. Recent discoveries in these areas are also reviewed, and findings in pulmonary arterial hypertensive diseases are contrasted with those found in patients with PH due to lung diseases. Some of these discoveries have already led to new treatment strategies for patients with the most severe forms of PH. PH due to lung diseases shares some common pathophysiologic features with pulmonary arterial hypertension. Therefore, it is likely that these discoveries and new treatments will also be extended to benefit patients with PH due to lung disease.

Animals↗
PubMedDate not supplied

Pathophysiology and current management of burn injury.

PURPOSE: To provide the physician and registered professional nurse with an overview of the pathophysiology and current management of burn injuries. TARGET AUDIENCE: This continuing education activity is intended for physicians and nurses with an interest in learning about evidence-based prevention and management of burn wounds. OBJECTIVES: After reading the article and taking the test, the participant should be able to: (1) Explain the pathophysiology of skin function. (2) Describe the different types of burn injuries. (3) Identify the treatment strategies for burn injuries.

Anti-Bacterial Agents↗
PubMed2006

Retinal nerve fiber layer analysis in the diagnosis of glaucoma.

PURPOSE OF REVIEW: The detection of optic disc and retinal nerve fiber layer damage and change is the cornerstone of glaucoma management. Assessment of the retinal nerve fiber layer for localized and diffuse damage has been traditionally based on clinical examination, with documentation of change primarily qualitative. With the latest improvements in optical imaging instruments, objective and quantitative measurements of the retinal nerve fiber layer are now possible. This review summarizes the results from recent cross-sectional studies evaluating the discriminating ability of automated retinal nerve fiber layer measurements to detect glaucoma, and from longitudinal studies assessing the ability to predict and monitor glaucomatous changes. RECENT FINDINGS: Numerous cross-sectional studies have documented good diagnostic accuracy of a scanning laser polarimeter (GDx VCC), the optical coherence tomograph (Stratus), and the Heidelberg Retina Tomograph retinal nerve fiber layer measurements for differentiating between healthy and glaucoma eyes. There are only limited data available on the ability of these retinal nerve fiber layer measurements to document change over time. SUMMARY: It is essential that the clinician understand the specific strengths and weaknesses of each technique so that only good quality retinal nerve fiber layer information will be used in conjunction with careful clinical examination and visual function testing for glaucoma management decisions. Longitudinal studies are needed to evaluate the ability of these instruments to document retinal nerve fiber layer change over time.

Diagnostic Imaging↗
PubMed2003

Pathophysiology of disseminated intravascular coagulation (DIC) progresses at a different rate in tissue factor-induced and lipopolysaccharide-induced DIC models in rats.

Tissue factor (TF) and lipopolysaccharide (LPS) are frequently used to induce disseminated intravascular coagulation (DIC) in experimental animal models. Although the pathophysiology of DIC may differ depending on which agent is used for induction, previous studies on models of DIC have not distinguished which DIC-inducing agent was used. In the present paper, we evaluate the characteristics of TF-induced and LPS-induced DIC using two types of DIC models, with special reference to selected hemostatic parameters and pathological findings within the kidney. Male Wistar rats were administered TF (3.75 U/kg; sustained infusion for 4 h) or LPS (30 mg/kg; sustained infusion for 4 h) via the tail vein, and blood sampling was performed at 0, 1, 3, 4, 5, 7, 9, 11, and 28 h. Judging from changes in the levels of thrombin-antithrombin complex, fibrinogen levels, and platelet counts, it is reasonable to conclude that the severity of both types of experimental DIC is similar with regard to hemostatic activation and consumption coagulopathy. A marked elevation in the level of D-dimer was noted without any organ dysfunction or much fibrin deposition in the kidney upon administration of TF. However, a markedly prolonged period of elevation in plasminogen activator inhibitor activity, a prolonged depression in antithrombin III activity, severe organ failure, and a markedly prolonged period of fibrin deposition in the kidney was observed following LPS administration. A modest number of the rats from the TF-induced DIC model died during the experimental period, whereas a large number of rats died during LPS-induced DIC, especially after 9 h. Since the time course of the pathophysiology differed remarkably among the TF-induced and LPS-induced DIC models in rats, we recommend that TF-induced and LPS-induced DIC be approached as distinct models in order to determine the implications of their experimental and clinical use.

Animals↗
PubMed2005

Pathophysiology of cholangiopathies.

The diseases of the intrahepatic biliary tree are a large group of potentially evolutive congenital and acquired liver disorders affecting both the adult and pediatric populations. They represent a relevant cause of liver-related morbidity and mortality and an important indication for liver transplantation, particularly in children. While the practical approach to patients affected by biliary tree diseases has not significantly changed yet, the conceptual approach to the pathophysiology of cholangiopathies has witnessed important advances that will be discussed. The primary cell target of the pathogenetic sequence of these disorders is the biliary epithelium. Cholangiocytes have multifaceted functions, not limited to bile production. Their capability to secrete a range of different pro-inflammatory mediators, cytokines, and chemokines indicates a major role of cholangiocytes in the inflammatory reaction. Furthermore, paracrine secretion of growth factors and peptides mediates an extensive cross-talk with other liver cell types, including hepatocytes, stellate, and endothelial and inflammatory cells. Cholangiopathies share a number of pathogenetic mechanisms, including inflammation, cholestasis, fibrosis, apoptosis, altered development, and neoplastic transformation. These basic disease mechanisms will be discussed in detail, along with the distinct features of a number of cholangiopathies. Furthermore, an increase in the biliary cell compartment is a common response to many forms of liver injury, from cholangiopathies to viral and fulminant hepatitis. Elucidation of these pathophysiologic mechanisms will likely provide clues for future therapeutic strategies. Furthermore, understanding the role of cholangiocytes in liver regeneration/repair and the mechanisms of cholangiocyte activation and their relationship with liver progenitor cell will be of further interest.

Adult↗
PubMed2006

Pathophysiology of nonalcoholic steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) affects approximately 30% of adults and 20% of children in the United States. Nonalcoholic steatohepatitis (NASH) is its most severe histologic form and progresses to cirrhosis in 20% of these patients. Once developed, 30% to 40% of patients with NASH cirrhosis will experience a liver-related death. Consequently, it has become extremely important to understand the pathophysiology of NASH to develop sound therapeutic interventions. It is now recognized that nonhepatic mechanisms are largely responsible for the development of insulin resistance, which causes hepatic steatosis. Once developed, oxidative stress and diminished antioxidants within the liver initiate the progression from steatosis alone to NASH and ultimately to cirrhosis. However, not all patients progress to cirrhosis. As is the case for other common complex metabolic diseases, it is the interaction between the environment and genetics that will determine the phenotypic expression of NAFLD and NASH in each individual patient. Which of the pathophysiologic factors (which are discussed in this review), either alone or in combination, will eventually provide the basis for the most effective therapy has yet to be determined.

Animals↗
PubMed2005

Flexible endoscopic evaluation of swallowing with sensory testing in patients with unilateral vocal fold immobility: incidence and pathophysiology of aspiration.

OBJECTIVES/HYPOTHESIS: The objective was to examine the incidence and pathophysiology of aspiration in patients with unilateral vocal fold immobility presenting with dysphagia. STUDY DESIGN: Retrospective review of flexible endoscopic evaluation of swallowing with sensory testing (FEESST) data and medical records in two tertiary medical care centers. METHODS: The data for all patients with unilateral vocal fold immobility who underwent FEESST between 2000 and 2003 were reviewed. RESULTS: Eighty-one patients (45 male and 36 female patients) were included in the study. The mean age was 59 years. The most common causes or origins were iatrogenic (42%), malignancy (23%), and neurological (18%). The immobility was left-sided in 59% of patients. A majority of the patients exhibited laryngeal edema/erythema (90%), difficulty with secretions (60%), and decreased laryngopharyngeal sensation (83%). The laryngeal adductor reflex was absent in 34% of the patients. An aspiration rate of 35% was detected with thin liquids. Trials of purees revealed a 76% rate of pooling, 44% rate of spillage, 32% rate of penetration, 18% rate of aspiration, and 24% rate of regurgitation. Rates of penetration and aspiration with purees were significantly higher in patients who had decreased laryngopharyngeal sensation, absent pharyngeal squeeze, and absent laryngeal adductor reflex. CONCLUSION: Dysphagia in patients with unilateral vocal fold immobility is demonstrated during FEESST by pooling, spillage, penetration, and aspiration. The pathophysiology of dysphagia is multifactorial with decreased sensation and limitation of airway protective mechanisms both acting as contributing factors.

Adolescent↗
PubMed2005

Diabetic neuropathies. Classification, clinical features, and pathophysiological basis.

Diabetes mellitus is associated with a wide spectrum of neuropathy syndromes, ranging from a mild asymptomatic distal sensory neuropathy to a severe disabling radiculoplexus neuropathy. As the pathophysiology of these separate conditions is better understood, classification of the various phenotypes becomes important because of treatment implications. Here we provide a short summary of the history of the classification of diabetic neuropathies and try to describe the most common forms classified according to their presumed pathophysiology. We have tried to include epidemiological data where available, as well as histopathology of nerve in several diabetic neuropathies.

Diabetic Neuropathies↗
PubMed2006

A conceptual model for the pathophysiology of vulvar vestibulitis syndrome.

UNLABELLED: Vulvar vestibulitis syndrome (vestibulitis), the most common type of chronic vulvovaginal pain, impairs the psychologic, physical, and reproductive health of approximately 10% of women at some point in their lives. Research on the pathophysiology of vestibulitis suggests abnormalities in 3 interdependent systems: vestibular mucosa, pelvic floor muscles, and central nervous system pain regulatory pathways. To date, causes and relative contributions of these abnormalities to the development and maintenance of vestibulitis remain poorly understood. Research consistently supports the conceptualization of vestibulitis as a chronic pain disorder-akin to fibromyalgia, irritable bowel disorder, and temporomandibular disorder (TMD)-that is far more complex than vestibular hypersensitivity alone. Nevertheless, the clinical diagnosis of vestibulitis continues to rely on subjective report of pain during intercourse and vestibular sensitivity on clinical examination after exclusion of other gynecologic disorders. We propose that current diagnostic criteria, which are based on highly subjective patient and clinician measures, are not sufficient to describe and properly classify the heterogeneous clinical presentations of this disorder. To inform clinical care or research, we must be able to objectively characterize women with vestibulitis. This narrative review critically appraises current conceptualization of vestibulitis and presents a context for studying vestibulitis as a chronic pain disorder, emphasizing the need for objective assessment of clinical features. TARGET AUDIENCE: Obstetricians & Gynecologists, Family Physicians. LEARNING OBJECTIVES: After completion of this article, the reader should be able to state that vulvar vestibulitis is common; recall that the disorder has three major pathophysiological pathways and that understanding of these pathways is important in selecting treatment options, and explain that the clinician must attempt to properly classify the clinical presentations of the disorder.

Female↗
PubMed2005

Section 3: The nature of pain: pathophysiology.

An understanding of the pathophysiology of pain involves the concepts of neuronal plasticity at the levels of the nociceptor neurons, spinal cord, and brain. Neuroplasticity allows the neurons in the brain to compensate for injury and adjust their activity in response to new situations or changes in their environment. This is an important physiologic event in the development of central sensitization. Other concepts include modulatory effects at the nociceptor, sympathetically mediated pain, the "wind-up" phenomenon, central sensitization, and descending and ascending central modulatory mechanisms for the perception of pain, as well as the related pain motivations and behaviors. Numerous modulatory mechanisms for pain have been postulated that control the degree of pain perceived and the emotional and behavioral phenomena associated with a patient's pain experience. These numerous mechanisms take place at all levels of the nervous system: peripheral nerves, spinal cord, and brain. Despite great advances in unraveling the complexities of the pathophysiology of pain, much remains to be discovered. It is hoped that further research into this critical area will lead to better therapies.

Acute Disease↗
PubMed2004

Pathophysiology of focal cerebral ischemia: a therapeutic perspective.

The pathophysiology of cerebral ischemia is best understood in animal models of stroke. Within minutes of interrupted blood flow, mitochondria are deprived of substrate, which prevents adenosine triphosphate generation and results in membrane depolarization. This leads to increased intracellular calcium and sodium concentration followed by generation of free radicals and initiation of apoptosis. Glutamate release from ischemic neurons contributes to cellular damage. Each step in this complex, interdependent series of events offers a potential point to intervene and prevent neuronal death. Although many human trials in acute stroke therapy have had disappointing results, many promising therapies are in the pipeline, including hypothermia and free-radical inhibitors. Herein, the author discusses the pathophysiology of focal cerebral ischemia as has been revealed in rodent models and reviews the major human trials according to treatment mechanism.

Animals↗