SEARCH · Search PubMed

Results for “pathophysiology”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources

PubMed1985

Pathophysiological mechanisms underlying tardive dyskinesia.

Movement abnormalities in neuroleptic-treated, psychiatric patients are classified as (a) initial syndromes, including dystonia, parkinsonism, and hyperkinetic abnormalities such as initial dyskinesia (ID) and akathisia, all of which are related to the neuroleptic dose and can be considered as overdose phenomena; (b) tardive syndromes, mainly the classic tardive dyskinesia (TD) syndrome, more seldom tardive akathisia and tardive dystonia, which may all develop or aggravate after withdrawal of neuroleptic treatment; and (c) age-related, spontaneous dyskinesia, akathisia, and dystonia, and schizophrenia-related, hyperkinetic, often stereotyped, movements and restlessness. ID and TD can occur simultaneously, and may depend, at least partially, on identical mechanisms. The pathophysiology of TD is still not clear, and the traditional dopamine (DA) hypersensitivity model seems inadequate. Animal experiments suggest that blockade of some DA receptors in the brain (e.g., in ventromedian striatum) may counteract hyperkinesia and produce parkinsonism, while a concomitant blockade of other similar receptors in other brain regions (e.g., in anterodorsal striatum) may aggravate movements. This offers an explanation for the concomitant occurrence of parkinsonism and hyperkinetic movement abnormalities (ID and akathisia) relatively early in a neuroleptic treatment, and may also contribute to the understanding of the pathophysiology of TD. It is concluded that pathophysiologically TD is a heterogeneous syndrome depending on a subtle balance between several neurotransmitters in the brain, including DA receptor blockade and hypersensitivity of DA and GABA receptors.

Antipsychotic Agents↗

PubMed1994

Role of hypoxic pulmonary vasoconstriction in pulmonary gas exchange and blood flow distribution. 2. Pathophysiology.

In this review, the second of a two part series, the analytic techniques introduced in the first part are applied to a broad range of pulmonary pathophysiologic conditions. The contributions of hypoxic pulmonary vasoconstriction to both homeostasis and pathophysiology are quantitated for atelectasis, pneumonia, sepsis, pulmonary embolism, chronic obstructive pulmonary disease and adult respiratory distress syndrome. For each disease state the influence of principle variables, including inspired oxygen concentration, cardiac output and severity of pathology are explored and the actions of selected drugs including inhaled nitric oxide and infused vasodilators are illustrated. It is concluded that hypoxic pulmonary vasoconstriction is often a critical determinant of hypoxemia and/or pulmonary hypertension. Furthermore this analysis demonstrates the value of computer simulation to reveal which of the many variables are most responsible for pathophysiologic results.

Humans↗

PubMed1986

[Etiology and pathophysiology of post-traumatic bone infection].

The present study deals with etiology and pathophysiology of posttraumatic bone infections. Great importance is attached to the description of intracortical transformations. The authors underline that the chronic infection originates in disturbances of blood flow caused primarily in the corticalis by trauma or osteosynthesis. All further pathophysiologic processes have to be considered as an effort made by the organism to heal the damage. The pathophysiologic processes resulting in the different end stages (recovery, persisting necrosis, sequester) are described.

Bone Regeneration↗

PubMed2002

Pathophysiological changes after traumatic brain injury: comparison of two experimental animal models by means of MRI.

In an experimental study MRI was used to compare the pathophysiological changes of brain tissue after lateral fluid percussion injury (FPI) versus cold injury (CI) as models of traumatic brain injury (TBI). Two groups of Sprague-Dawley rats (n=23) were subjected to mild FPI, respectively, CI localized over the right parietal cortex. MRI was performed at different time points including T1w, T2w and T1w-CE (Gd-DTPA 0.2 mmol/kg BW) sequences as well as perfusion-weighted imaging with calculation of regional cerebral blood volume (rCBV) and regional cerebral blood flow (rCBF). T2w and T1w-CE images showed hyperintense areas in the traumatised cortex demonstrating brain edema and blood-brain barrier (BBB)-breakdown increasing up to 12 h. Perfusion-weighted imaging demonstrated a significant decrease of rCBV and rCBF in the ipsilateral cortex of CI animals compared with the contralateral hemisphere. In contrast, rats of the FPI group showed only slight differences in rCBF and rCBV comparing the left and right cortex. The results of our study confirm that both mild FPI and CI produced focal brain edema with concomitant breakdown of the BBB as a model of TBI. Since differences regarding perfusion are much more pronounced in CI our results suggest that, this model more likely seems to reflect pathophysiological changes of brain ischemia, whereas FPI seems to be better suited to model the pathophysiological characteristics of TBI.

Animals↗

PubMed2002

The incidence, pathophysiology, treatment and prognosis of Cheyne-Stokes breathing disorder in patients with congestive heart failure.

DEFINITION: Cheyne-Stokes respiration is a breathing disorder characterized by recurrent central sleep apneas, mainly during sleep, alternating with a crescendo-decrescendo pattern of tidal volume. PATHOPHYSIOLOGY AND PROGNOSIS: The pathophysiology of Cheyne-Stokes respiration, involving the cardiovascular, pulmonary and sympathetic nervous systems, is still not well understood. Although 50% of moderate to severe congestive heart failure patients suffer from significant Cheyne-Stokes respiration, studies been undertaken to determine the prevalence of this phenomenon and its implications regarding patients' life expectancy and quality of life were conducted only in recent years. Other studies suggest that Cheyne-Stokes respiration has a negative prognostic value upon congestive heart failure patients. TREATMENT: Novel therapeutic approaches have been attempted in order to treat Cheyne-Stokes respiration; they include oxygen delivery, various pharmaceutical treatments aimed to stabilize the ventilatory system and other pharmaceutical treatments aimed to improve the left ventricular ejection fraction. However, none of them was effective. OBJECTIVES: This review summarizes some of the current knowledge regarding Cheyne-Stokes respiration pathophysiology, prevalence, prognostic implication and available treatments.

Cardiotonic Agents↗

PubMed2006

[Pathophysiology of hypertension: what's new?].

The pathophysiology of primary hypertension is still unresolved and appears more complex than ever. It is beyond the scope of this article to review all new scientific developments in this field. On clinical grounds, hypertension is divided into primary and secondary forms. Here, the authors discuss the pathophysiology of hypertension associated with three common disease entities showing a large overlap with primary hypertension: chronic kidney disease (CKD), obstructive sleep apnea (OSA), and hyperaldosteronism. Especially in CKD and OSA, the activation of the sympathetic nervous system plays a crucial role. It is the authors' belief that hypertension due to these three diseases is more common than previously appreciated and may account for about 20% of the hypertensive population. The knowledge of the underlying pathophysiology allows early diagnosis and guides optimal treatment of these hypertensive patients.

Adipocytes↗

PubMed2004

[Cytokine network in patients with schizophrenia and its significance for the pathophysiology of the illness].

Experimental findings from psychoimmunologic research in humans and epidemiological data suggest that alterations in cytokine networks may induce acute psychopathologic symptoms and may be involved in the pathogenesis and pathophysiology of schizophrenia by influencing brain development. However, there is insufficient evidence from genetic, post-mortem, and cerebrospinal fluid studies to demonstrate this in the CNS of schizophrenic patients. In contrast, there are quite robust findings from peripheral blood that interleukin (IL)-2, IL-6, tumor necrosis factor-alpha, and interferon cytokine systems in patients are regulated differently than in controls. However, these findings are not specific to schizophrenia, they are confounded by numerous intervening variables such as stress, smoking, and medication, and their pathophysiologic relevance for processes in the CNS is undetermined. Therefore, future research on the involvement of cytokines in the pathogenetics, pathophysiology, and treatment of schizophrenia is needed.

Brain↗

PubMed2004

Prevalence, impact on the quality of life and pathophysiological determinants of nocturia in urinary incontinent women.

The objective of this study was to estimate the prevalence of nocturia in incontinent women in a urogynaecologic practice and its association with the quality of life and to estimate the prevalences of the pathophysiological categories among nocturics. From 1 January 2002, all patients with complaints of urinary incontinence were analysed according to a specific protocol: multichannel urodynamic testing, a 1-h International Incontinence Society (ICS) pad test and a 3-day frequency-volume (FV) chart. From 1 June 2002, subjects had to fill in a standardised quality of life questionnaire as well. Nocturia was defined as two or more micturitions per night calculated from the FV chart. Evaluable FV charts were received from 111 patients, and 72 patients completed the questionnaires correctly. The overall prevalence of nocturia was 48.6% (confidence interval: 43.9-53.3%). Nocturia had a negative impact on several aspects of the quality of life. The maximum voided volume was significantly (p=0.005) less in nocturics. The 24-h frequency was higher in nocturics (p=0.001). Nocturics lost more urine during the pad test (p=0.039). The multivariate logistic regression analysis showed that the greater the proportion of 24-h urine excreted at night, the greater the odds of having nocturia and that the lesser the maximum voided volume, the greater the odds of having nocturia. The majority (92.7%) of the nocturics can be classified into one of the responsible pathophysiologic categories: nocturnal polyuria in 51.2%, a low functional bladder capacity in 14.6%, a combination of both in 9.8%, polyuria in 4.9% and a combination of polyuria and nocturnal polyuria in 12.2% of the cases. Nocturia is a frequent symptom among urinary incontinent patients, with a negative impact on several aspects of the quality of life. With a FV chart, nocturics can be classified into one of the responsible pathophysiologic categories in the majority (92.7%) of the cases.

Adolescent↗

PubMed2016

Gene co-expression analysis identifies brain regions and cell types involved in migraine pathophysiology: a GWAS-based study using the Allen Human Brain Atlas.

Migraine is a common disabling neurovascular brain disorder typically characterised by attacks of severe headache and associated with autonomic and neurological symptoms. Migraine is caused by an interplay of genetic and environmental factors. Genome-wide association studies (GWAS) have identified over a dozen genetic loci associated with migraine. Here, we integrated migraine GWAS data with high-resolution spatial gene expression data of normal adult brains from the Allen Human Brain Atlas to identify specific brain regions and molecular pathways that are possibly involved in migraine pathophysiology. To this end, we used two complementary methods. In GWAS data from 23,285 migraine cases and 95,425 controls, we first studied modules of co-expressed genes that were calculated based on human brain expression data for enrichment of genes that showed association with migraine. Enrichment of a migraine GWAS signal was found for five modules that suggest involvement in migraine pathophysiology of: (i) neurotransmission, protein catabolism and mitochondria in the cortex; (ii) transcription regulation in the cortex and cerebellum; and (iii) oligodendrocytes and mitochondria in subcortical areas. Second, we used the high-confidence genes from the migraine GWAS as a basis to construct local migraine-related co-expression gene networks. Signatures of all brain regions and pathways that were prominent in the first method also surfaced in the second method, thus providing support that these brain regions and pathways are indeed involved in migraine pathophysiology.

Atlases as Topic↗

PubMed2005

Rickettsial infections around the world, part 1: pathophysiology and the spotted fever group.

BACKGROUND: The rickettsial diseases are an important group of infectious agents that have dermatological manifestations. These diseases are important to consider in endemic areas, but in certain suspicious cases, possible acts of bioterrorism should warrant prompt notification of the appropriate authorities. OBJECTIVE: In this two part review article, we review these diverse diseases by examining established and up-to-date information about the pathophysiology, epidemiology, clinical manifestations, and treatment of the ricksettsiae. METHODS: Using PubMed to search for relevant articles, we browsed over 500 articles to compose a clinically based review article. RESULTS: Part one focuses on pathophysiology of the rickettsial diseases and the clinical aspects of the spotted fever group. CONCLUSIONS: At the completion of part one of this learning activity, participants should be able to discuss all of the clinical manifestations and treatments of the sported fever group. Participants should also be familiar with the pathophysiology of the rickettsial diseases.

Animals↗

PubMed2005

Pathophysiology of tension-type headache.

Tension-type headache is one of the most common primary headache disorders. Advances in basic pain and clinical research have improved our understanding of pathophysiologic mechanisms of tension-type headache. Increased excitability of the central nervous system generated by repetitive and sustained pericranial myofascial input may be responsible for the transformation of episodic tension-type headache into the chronic form. Studies of nitric oxide (NO) mechanisms suggest that NO may play a key role in the pathophysiology of tension-type headache and that the antinociceptive effect of nitric oxide synthase inhibitors may become a novel principle in the future treatment of chronic headache. Future studies should focus on investigation of the source of peripheral nociception, the role of descending pain modulation, and the development of an animal model of tension-type headache to support the pathophysiologic importance of central sensitization in tension-type headache.

Humans↗

PubMed2002

The pathophysiologic background for current treatments of premenstrual syndromes.

Multiple hypotheses on the etiology of premenstrual syndromes (PMS) that have been proposed during the past 70 years have led to a multitude of treatment modalities. During the past two decades, the following two classes of pharmacologic interventions have emerged: hormonal interventions--mostly suppression of ovulation; and neurotransmitter's activity stimulation--mostly by specific serotonin reuptake inhibitors. These treatment modalities are based on the hypothesis that the etiology and pathophysiology of PMS are related to ovulation-related luteal activity of gonadal hormones, and their interaction with serotonin and other neurotransmitters. Two other components of the pathophysiology of PMS--the genetic propensity and the dynamically evolving-vulnerability--have not yet been addressed for treatment. Environmental inputs to pathophysiology, which are not discussed here, have been addressed by attempts at changes of lifestyle, coping style, and environment.

Adult↗

PubMed1993

Differentiating systolic from diastolic heart failure: pathophysiologic and therapeutic considerations.

PURPOSE: To compare and contrast the pathophysiology and therapy of heart failure with normal and abnormal systolic ventricular function. METHODS: Review of basic pathophysiologic mechanisms, clinical data, and therapeutic trials. CONCLUSIONS: The clinical features of heart failure may be similar regardless of whether ventricular function is normal or abnormal. However, the pathophysiologic mechanisms leading to heart failure with normal ventricular function differ considerably from those producing heart failure with abnormal systolic function. The key problems in heart failure with abnormal systolic function involve impaired contractility, neuroendocrine activation, increased intracardiac volume and pressure, and enhanced sensitivity to change in afterload. With normal systolic function, the key problem is an abnormal diastolic pressure/volume relationship, which may be due to a variety of active and passive processes affecting diastole. Assessing left ventricular systolic function is crucial before initiating therapy in a patient with heart failure, since treatment for systolic dysfunction may be ineffective or even counterproductive if symptoms are due to abnormal diastolic properties with preserved systolic function.

Clinical Trials as Topic↗

PubMed1987

Obsessive-compulsive disorder: psychobiological approaches to diagnosis, treatment, and pathophysiology.

The diagnosis, treatment, and pathophysiology of obsessive-compulsive disorder (OCD) were examined in a series of studies utilizing psychobiological approaches. Putative biological markers previously reported in depression were studied in this disorder and revealed that on some measures [Dexamethasone Suppression Test and rapid eye movement (REM) latency on sleep electroencephalogram (EEG)], OCD patients resemble those with major depressive disorder (MDD), whereas on others [REM density, platelet serotonin uptake, probably platelet 3H-imipramine binding, and 5-hydroxy-indoleacetic acid (5-HIAA) in cerebral spinal fluid (CSF)] they do not. The relationship between OCD and MDD was further explored in a double-blind, randomized crossover study designed to compare the antiobsessional effects of two tricyclic antidepressants, clomipramine (CMI) and desipramine (DMI), in a nondepressed cohort of OCD patients. CMI was found to have significant antiobsessional effects in this group, whereas in the same patients, DMI lacked therapeutic effects. These results suggest that not all antidepressants are antiobsessive and that some property of CMI, such as its potent serotonergic effects, may be of pathophysiological relevance for OCD. The role of serotonin in this disorder was then tested using the pharmacological challenge strategy. A novel serotonin postsynaptic receptor (5HT-1) agonist, m-chlorophenylpiperazine (m-CPP), was administered orally (0.5 mg/kg) under double-blind, placebo-controlled conditions to OCD patients and controls. In addition, a serotonergic receptor antagonist, metergoline (4 mg), was given to a subset of OCD patients. Relative to healthy volunteers, the OCD patients became significantly more anxious, depressed, and dysphoric after m-CPP administration. Moreover, in the OCD patients, obsessive-compulsive symptoms increased markedly after m-CPP and decreased significantly following metergoline administration. These results demonstrate that agents that bind to the 5HT-1 receptor can acutely affect the symptoms of OCD patients. The striking behavioral effects of these direct postsynaptic receptor ligands and the relative specificity of clomipramine as an antiobsessional agent suggest that serotonergic neurons may play a role in the pathophysiology, as well as mediating the pharmacological reduction, of obsessional symptoms.

Adult↗

PubMed1991

Effect of sustained release and pulse release anthelmintic intraruminal devices on development of pathophysiological changes and parasite populations in calves infected with Ostertagia ostertagi and Cooperia oncophora.

An experiment was conducted in calves to investigate the effect of sustained release and pulse release anthelmintic intraruminal boli on the development of pathophysiological changes following daily infection with Ostertagia ostertagi and Cooperia oncophora for six weeks. After infection various pathophysiological changes were detected including increases in serum pepsinogen concentration, enteric plasma protein losses and in the catabolic rate of albumin. Such changes developed rapidly in the unprotected calves following patency after 17 days and persisted until the termination of the study. There were indications that the sustained anthelmintic release device was more efficacious than the pulse anthelmintic release device in reducing the worm burdens and early pathophysiological changes associated with infection. It was found at necropsy that the release of anthelmintic by the oxfendazole pulse release bolus had been delayed in several calves.

Animals↗

PubMed1990

Pathophysiology of aplastic anaemia.

It is the conventional opinion that acquired aplastic anaemia is a heterogenous disease including basically different conditions, such as idiopathic or virus induced pancytopenia, toxic-allergic marrow damage or autoimmunity. Here, an alternative concept is proposed, according to which aplastic anaemia is one disease, but multifactorial in all patients, apparent differences being due to the relative prevalence of one or the other pathophysiological component in individual patients. Bone marrow from patients in the severe phase of aplastic anaemia does not grow in culture and is therefore not suitable for experimentation. Alternatively, bone marrow from patients who have resumed some degree of autologous bone marrow function, but still have residual signs of the disease after non-invasive therapy, offers the possibility to study pathophysiological mechanisms in vitro. The majority of experiments presented in this chapter have been done in such patients, assuming that their status of disease in some way reflects the original, more serious pretreatment condition. Three major pathophysiological components will be discussed, and it will be proposed how these factors act in concert to cause or aggravate aplasia.

Anemia, Aplastic↗

PubMed1986

The effect of dietary protein on the pathophysiology of acute ovine haemonchosis.

An experiment was conducted to examine the effect of dietary protein on the pathophysiology of acute haemonchosis in Finn Dorset/Dorset Horn lambs. Erythrokinetic and metabolic studies using 51Cr-red cells, 59Fe-transferrin and 125I-albumin and digestive efficiency and nitrogen balance measurements were conducted between 19 and 39 days after infection. Identical radioisotopic and nutritional studies were conducted later on pair-fed control lambs. The results demonstrated that lambs on a low protein diet (88 g crude protein (CP) kg-1 dry matter (DM)) were less able to withstand the pathophysiological consequences of infection with 350 Haemonchus contortus larvae kg-1 body weight than lambs given a high protein (170 g CP kg-1 DM) diet, despite similar worm burdens. Erythrokinetic studies indicated that abomasal blood loss was similar in both groups of infected lambs, and circulating red cell volumes were reduced and plasma volumes were expanded to a similar degree in both groups. The majority of infected lambs in both dietary groups responded equally well to the gastric haemorrhage by increasing the rate of red cell production and their absorption of dietary iron was greater than in the control lambs. Albumin catabolism was increased in both groups of infected lambs, particularly in those given the low protein diet. Within each dietary group there were no differences in the digestibilities of the various proximate fractions of the experimental diets and no differences in the urinary or faecal nitrogen losses between infected lambs and their pair-fed controls. However, loss of appetite was a major feature of the disease, particularly in the lambs given the low protein diet and this feature appeared to be crucial in determining the ability of the infected sheep to withstand the pathophysiological effects of the parasite.

Acute Disease↗

PubMed1981

Pathophysiology of the alcohol withdrawal syndrome.

A characteristic withdrawal syndrome appears following the interruption of chronic heavy consumption of alcoholic beverages. The pathophysiological elaborations of the various withdrawal signs and symptoms are considered. Among the unlikely, although plausible, pathophysiologic mechanisms of the tremulousness and skeletal muscle hyperreactivity of withdrawal is the accumulation or the sustained production of one or more circulating "toxic substances." Evidence consistent with such a mechanism includes the reported alleviation by dialysis of an impending withdrawal syndrome in alcoholic patients, the appearance of reflex hyperreactivity in withdrawing animals below the level of a chronic section of the spinal cord, and the time course of the appearance and disappearance of withdrawal syndromes. The various potential pathophysiological and neurochemical manifestations of the withdrawal illness are discussed--alterations in neural inhibition, in alpha-aminobutyric acid, catecholamines, acetylcholine, dopamine, prostaglandin, and in peptides. Experimental tests whereby a "toxic substance hypothesis" of withdrawal can be ruled in or out are proposed.

Animals↗