Search PubMed⌕ Search

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.

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

At least 73 records · Page 4Linked to original sources
PubMed2000

Evidence for the involvement of the hippocampus in the pathophysiology of schizophrenia.

The hippocampus, a medial temporal lobe structure, is often considered to play an important role in the pathophysiology of schizophrenia. Recent developments of neuroimaging and molecular postmortem techniques have significantly increased our ability to study the role of discrete brain regions in the pathophysiology of schizophrenia. This article describes animal models, structural, histological, molecular biology, and neuropsychological evidence for the involvement of the hippocampus in the pathophysiology of schizophrenia. The major findings in schizophrenic patients are decreased volumes, hypometabolism, and cytoarchitectural abnormalities which are more robust on the left hippocampus, as well as verbal memory impairment. It is yet to be determined whether these changes are neurodevelopmental or neurodegenerative in nature. Overall, these findings indicate that there are subtle changes in the hippocampus of schizophrenic patients. More comprehensive and focused hippocampal research in schizophrenia is required to elucidate the contribution of this intriguing brain structure to the pathophysiology of schizophrenia.

Animals↗
PubMed2000

Pathophysiology of erectile dysfunction: the contributions of trabecular structure to function and the role of functional antagonism.

Erectile dysfunction (ED) is estimated to impact more than 150 million men this year worldwide. An understanding of the pathophysiology of ED both furthers the basic scientific knowledge of disease processes and provides a rational design of pharmacotherapy. At present, there are two major views regarding the pathophysiology of ED. In the first hypothesis, the oxygen tension-dependent changes in the penis during erection are proposed to impact corpus cavernosum structure by inducing various cytokines, vasoactive factors and growth factors at the two different oxygen tensions (flaccidity and erection) which, in turn, alter smooth muscle metabolism and connective tissue synthesis. Decreases in the corpus cavernosum smooth muscle/connective tissue ratio have been correlated with an increased likelihood of diffuse venous leak and a failure of the veno-occlusive mechanism in prospective patient studies. Evidence for such a hypothesis incorporates nocturnal penile tumescence and circadian changes in oxygenation as important in maintaining erectile health. The alternate hypothesis proposes that ED is the result of a metabolic imbalance between relaxatory and contractile processes within the trabecular smooth muscle such that contractile processes predominate. Based on this hypothesis, therapy can be accomplished via drugs which shift this balance towards vasodilatation, or by gene therapy approaches to supplement the deficient components favoring smooth muscle relaxation. Both of these hypotheses predict a management strategy for ED that impacts pharmacotherapeutics. In this review of the pathophysiology of ED, each hypothesis will be examined and a synthesis devised incorporating both views. The future of research in this area as well as pharmacotherapy in ED in terms of pathophysiology is discussed including the merits and drawbacks of prophylaxis and prevention of ED. International Journal of Impotence Research (2000) 12, Suppl 4, S39-S46.

Animals↗
PubMed1986

Cholinergic-monoaminergic interaction in the pathophysiology of the affective disorders?

Cholinergic and monoaminergic hypotheses have dominated affective disorders research. The propriety of an hypothesis is determined by the point of a field in its development. Both categories of hypotheses have encouraged important research but their utility can be limited by the assumption that the pathophysiology of depression and mania is due to cholinergic or monoaminergic pathology. In actuality, neurotransmitter networks interact and are mutually regulating. The cholinergic-monoaminergic interaction theory (CMIT) is a dynamic account of the mutual inter- and intra-regulation of cholinergic, noradrenergic, dopaminergic and serotonergic systems in the pathophysiology of affective disorders. This model maintains that virtually every variable related to the neurobiology of bipolar disorder is regulated by mechanisms internal and external to those neurotransmitter systems involved in its pathophysiology. In principle, these variables include receptor density and sensitivity, membrane properties, cytosolic calcium, magnesium and sodium ion concentrations, activities of ATPases and calcium channel gating and cascade mechanisms. This array of variables stems from the assumption that the brain is a complex, unified dynanism. The CMIT posits homeostatic mechanisms preserving the direction of this dynanism. In this article, the theme of neurotransmitter-neurotransmitter system interaction is developed and the CMIT is offered as a paradigm useful in addressing the pathophysiology of affective disease from within the conceptual framework of a neurotransmitter system interaction theory.

Humans↗
PubMed1993

Chronic pathophysiologic circulating endothelin levels produce hypertension in conscious dogs.

Although recent studies have reported endogenous plasma endothelin (ET) levels to be elevated two- to fivefold in chronic pathophysiologic states, whether such an increase in circulating ET levels alone can lead to significant long-term alterations in cardiovascular function is not known. The purpose of this study was to examine the long-term systemic hemodynamic effects of a pathophysiologic increase in circulating ET concentration in chronically instrumented, conscious dogs (n = 4). Infusion of endothelin (2.5 ng/kg/min) for 8 days increased plasma concentration of endothelin two- to threefold. ET increased mean arterial pressure from 85 +/- 3 to 103 +/- 3 mm Hg, which was sustained throughout the period of infusion. Total peripheral resistance was increased by approximately 70%. Cardiac output decreased transiently by 25% and remained below control levels at the termination of ET infusion. These data indicate the importance of pathophysiologic levels of ET in controlling systemic hemodynamics in chronic conditions. Furthermore, ET may play a role as a mediator of chronic hypertension in pathophysiologic states associated with endothelial dysfunction.

Animals↗
PubMedDate not supplied

Transforming pathophysiology instruction through narrative pedagogy and Socratic questioning.

Pathophysiology, heavily content driven, has typically been taught through the use of traditional behavioral pedagogy and a reliance on the formal lecture. The author describes the limitations of this approach to teaching pathophysiology and describes the use of narrative pedagogy and Socratic questioning as alternative methods of instruction to augment lecture methods. Specific strategies for transforming traditional classroom teaching by using Socratic questions in a pathophysiology course for nurse practitioners are described. Student and faculty reactions to the initial efforts to transform pathophysiology instruction are also described.

Education, Nursing, Graduate↗
PubMedDate not supplied

Pathophysiology of the rheumatoid joint.

The precise cause of rheumatoid arthritis (RA) is, as yet, unknown. But with more sophisticated techniques in the fields of immunogenetics and molecular biology, there is increasing knowledge of the pathophysiology of the rheumatoid joint. Pathophysiologic knowledge should be part of the orthopaedic nurse's repertoire when dealing with the "whole" patient; therefore orthopaedic nurses who care for patients with rheumatoid disease should understand certain pathophysiologic concepts. This article reviews the pathophysiology of the rheumatoid joint and describes the changes that take place in the joint with specific reference to the cells of the immune system, the synovium, and articular cartilage.

Arthritis, Rheumatoid↗
PubMed1985

A specific antigen-antibody interaction triggers the cellular pathophysiology of bullous pemphigoid.

Autoantibodies found in both the skin and sera of patients with bullous pemphigoid (BP) are capable of initiating the pathophysiology of blister formation that occurs in this disease. Current concepts of the pathophysiology of BP suggest that antibody alone cannot cause blister formation, but that antibody acts through complement-fixation, degranulation of mast cells and subsequent recruitment of leukocytes to the epidermal basement membrane. These leukocytes then release proteolytic enzymes which result in dermal-epidermal separation. This paper addresses the question of whether a specific molecule in the basement membrane zone is involved in the antigen-antibody reaction which triggers the cellular pathophysiology of BP. Immunoprecipitates of extracts of cultured human or mouse epidermal cells, radiolabelled with either [35S]methionine or 14C-labelled amino acids, indicated that sera from 25 of 26 BP patients precipitated the same molecule, as determined by co-migration on sodium dodecyl sulphate (SDS) polyacrylamide gel electrophoresis (PAGE). This molecule is a protein with a mol. wt. of approximately 230 kd. A similar protein was identified in SDS extracts of normal human epidermis, as determined by immunoperoxidase staining of proteins separated by SDS-PAGE, then electrophoretically transferred to nitrocellulose sheets. Thus, in almost all cases of BP, one specific molecule of the epidermal basement membrane is involved in the antigen-antibody interaction that triggers the cellular pathophysiology of blister formation.

Antigen-Antibody Reactions↗
PubMed1994

Late pathophysiologic sequelae after utilization of an intravenacaval oxygenator in experimental animals.

The intravenacaval hollow fiber oxygenator (IVOX) has been shown to be remarkably free from acute adverse effects on the venae cavae, right heart, and lungs when indwelling experimentally in sheep and in human clinical trial patients. However, all pathophysiologic assessments reported to date have been carried out during or immediately after IVOX utilization. It is recognized that IVOX indwelling in the venae cavae for up to 3 weeks could produce minor or unrecognized acute injury that could become more evident or more harmful after several weeks had elapsed following removal of the device. Therefore, this current study was designed and carried out to assess any pathophysiologic sequelae that could be recognized on follow-up examination 4 months after removal of an IVOX device that had been indwelling in the venae cavae for from 7 to 13 days. Extensive clinical and physiologic assessments of the blood, hemodynamics, and pulmonary functional status of 8 sheep were carried out 4 months after removal of IVOX devices that had been indwelling for 7 to 13 days. Each animal was then euthanized and complete necropsy examination was conducted looking especially for gross or histologic lesions in the venae cavae, access veins, right heart, and lungs. Findings indicated that all animals were normal, without clinically or pathologically significant pathophysiologic abnormalities or adverse effects from the IVOX utilization. Detailed hematologic, hemodynamic, blood chemistry, pulmonary function, and gross and histopathologic findings, presented in graphic, tabular, and photographic form, document the conclusion that utilization of an IVOX device in normal sheep for from 7 to 13 days produces no significant adverse late pathophysiologic sequelae.

Animals↗
PubMedDate not supplied

Hiatal hernia controversies--a review of pathophysiology and treatment options.

OBJECTIVE: To provide a detailed discussion of the aetiology and pathophysiology of hiatal hernia in both humans and small animals, and review current medical and surgical treatments. DESIGN: Review article. SUMMARY: Hiatal hernia is not completely understood in humans or animals. It has a complex multifactorial aetiology and pathophysiology. A primary disturbance of the lower oesophageal sphincter has not been shown in humans or animals. Knowledge of pathophysiology is necessary to institute appropriate treatment. Medical and/or surgical therapy is not indicated in asymptomatic cases. Medical treatment should be used for up to 1 month in stable cases of sliding hiatal hernia. Paraoesophageal hiatal hernias and any large sliding hiatal hernia should be considered for prompt surgical treatment. Surgical techniques used depend on the type of hiatal hernia present. Surgical treatment of hiatal hernia cases should be performed by experienced surgeons, and must include hiatal closure and gastropexy. The Nissen fundoplication procedure has been discontinued in the veterinary field due to poor success rates, coupled with the published view that there is a marked difference in pathophysiology between humans and dogs. Reported complications associated with the original Nissen fundoplication technique are identical in the human and veterinary literature. There have been no complications reported with use of the modified or 'floppy' Nissen fundoplication in dogs. Both oesophagopexy and Nissen fundoplication require further evaluation in small animals.

Animals↗
PubMed2003

How do learning issues relate with content in a problem-based learning pathophysiology course?

The relation between learning process and content coverage is becoming increasingly important for the understanding of the effects of problem-based learning (PBL) on students' learning. In our medical school, PBL is used as a major educational strategy in the discipline of pathophysiology. A computer program was developed allowing students to register learning issues identified as needed during tutorial sessions and learning issues stated as covered during the individual study periods. In our study, we compared "planned" (learning issues identified during PBL sessions) and "accomplished" learning issues (covered after the independent study periods) identified by pathophysiology students from three consecutive years. We found that the planned learning issues raised during tutorial sessions related to the issues effectively accomplished during the independent study and that their number grew stepwise from basic to preclinical to clinical sciences. Pathophysiology was, globally, the most mentioned discipline. Moreover, the most mentioned disciplines from the basic, preclinical, and clinical areas were physiology, histopathology, and internal medicine, respectively. The single-discipline approach did not limit the student's capacity to identify and cover learning issues beyond the objectives of pathophysiology.

Education, Medical↗
PubMed1995

Systemic hemodynamics and renal function during long-term pathophysiological increases in circulating endothelin.

Although recent studies have reported endogenous plasma endothelin levels to be elevated two- to fivefold in chronic pathophysiological states, whether such an increase in circulating endothelin levels alone can lead to significant long-term alterations in cardiovascular and renal function is not known. The purpose of this study was to examine the long-term systemic hemodynamic and renal effects of a pathophysiological increase in plasma endothelin concentration in chronically instrumented, conscious dogs (n = 7). Infusion of endothelin-1 (2.5 ng.kg-1.min-1) for 8 days increased plasma concentration of immunoreactive endothelin approximately two- to threefold from 6.7 +/- 0.4 to 16.0 +/- 2.2 pg/ml. Mean arterial pressure increased 21% from a control value of 86.7 +/- 2.1 to 105.0 +/- 2.5 mmHg during the endothelin infusion period. Cardiac output averaged 2,200 +/- 205 ml/min during control and fell by 33% on day 4 of endothelin infusion (1,484 +/- 146 ml/min) and was still 14% below control after day 8 of endothelin infusion (1,885 +/- 154 ml/min). Endothelin increased total peripheral resistance from 42.0 +/- 3.1 to 80.3 +/- 9.1 mmHg.l-1.min. Increasing plasma endothelin two- to threefold was associated with an increase in renal vascular resistance and decreases in glomerular filtration rate and renal plasma flow. Endothelin-1 had no long-term effect on plasma renin activity or aldosterone concentration. These data indicate the importance of pathophysiological levels of endothelin in controlling renal and cardiovascular function in chronic conditions. Furthermore, the results indicate that endothelin may play a role as a mediator of chronic hypertension in pathophysiological states associated with endothelial dysfunction.

Animals↗
PubMed1991

Cardiovascular and endocrine effects of endothelin-1 at pathophysiological and pharmacological plasma concentrations in conscious dogs.

BACKGROUND: Increased plasma concentrations of endothelin-1, a potent vasoconstrictor produced by the endothelium, have been reported in various pathological conditions. This study was conducted to evaluate effects of endothelin-1 at pathophysiological and pharmacological plasma concentrations. METHODS AND RESULTS: Endothelin-1 was infused at increasing doses (2.5, 5, 10, and 20 ng/kg.min for 1 hour each) in nine conscious dogs. During endothelin-1 infusion, plasma endothelin-1 rose from a basal value of 1.8 +/- 0.4 pmol/l to 5.8 +/- 1.1 (pathophysiological), 20.8 +/- 3.9 (pathophysiological), 85.4 +/- 18.9 (pharmacological), and 311.4 +/- 55.7 (pharmacological) pmol/l at each dose, respectively. Heart rate increased at 2.5 ng/kg.min (from 129 +/- 7 to 146 +/- 12 beats/min) but decreased at 20 ng/kg.min (97 +/- 7 beats/min) (p less than 0.001). Such a biphasic response was also observed for peak (+)dP/dt and (dP/dt)/DP40 (p less than 0.005). Left ventricular systolic pressures, mean aortic pressure, and left atrial pressure increased over time (p less than 0.05, p less than 0.005, and p less than 0.001, respectively). The time constant of early isovolumic relaxation rose progressively (p less than 0.001). The percent systolic shortening decreased at 10 and 20 ng/kg.min (p less than 0.005). Pressure-segment length loops showed a reduction in systolic shortening associated with an increase in left ventricular systolic pressure at 20 ng/kg.min. Atrial natriuretic factor rose after 5 ng/kg.min from 28.5 +/- 6.5 to 92.0 +/- 18.2 pmol/l (p less than 0.005). Angiotensin II and catecholamines did not change significantly. Serum urea and creatinine rose progressively (p less than 0.05), whereas glucose decreased (p less than 0.05). The above results differed significantly from measurements obtained in a time-control group of six dogs. CONCLUSIONS: A fourfold increase of plasma endothelin-1 obtained after doubling the infusion rate suggests a reduction in endothelin-1 clearance or endothelin-1 endogenous production. The biphasic response of heart rate is consistent with baroreflex-mediated effects resulting from vasodilation at the pathophysiological level and vasoconstriction at the pharmacological level. Hemodynamic data suggest an increase followed by a decrease in contractility at both levels, respectively. Finally, endothelin-1 is a stimulator of atrial natriuretic factor.

Animals↗
PubMed1999

Pathophysiology of secondary depressions in the elderly.

Although the pathophysiology of depression is not fully understood in either primary depression (i.e., no known neuropathology related to depression) or secondary depression (i.e., neuropathologic disorder that leads to depression), a number of studies have begun to identify aspects of the pathophysiology of both primary and secondary depression. This article reviews the findings of studies examining the pathophysiology of depression following stroke, Parkinson's disease, or Huntington's disease and compares them to findings in primary depression. Studies examining glucose metabolic rates or blood flow changes in regional brain areas found that stroke, Parkinson's disease, and Huntington's disease, as well as primary depression, were all associated with decreased activity or brain lesions in the orbital frontal cortex and basal ganglia. There were also abnormalities noted in the basal temporal lobes, cingulate cortex, and thalamus in some but not all disorders. Studies in stroke have also noted depletions of serotonin receptors in left temporal cortex associated with depression. These findings are consistent with the hypothesis that the pathophysiology of secondary and primary depression involves the dysfunction of one or more of the cortical-basal ganglia-thalamic neuronal loops. This dysfunction may be mediated by decreased serotonin release. These studies may ultimately lead to more focused and specific treatments.

Aged↗
PubMed1999

Photosensitive epilepsies and pathophysiologic mechanisms of the photoparoxysmal response.

OBJECTIVE: To identify the pathophysiologic mechanisms of the photoparoxysmal response (PPR) in various photosensitive epilepsy syndromes, and to discuss the relation between these pathophysiologic mechanisms and the classification of epilepsies and epileptic syndromes. BACKGROUND: The authors found two types of pathophysiologic mechanisms of PPRs (wavelength-dependent PPRs and quantity-of-light-dependent PPRs) in patients with idiopathic generalized epilepsy and hereditary dentatorubral-pallidoluysian atrophy. METHODS: Intermittent photic stimulation with wavelength-specific optical filters was performed in photosensitive epileptic patients: six patients had severe myoclonic epilepsy in infancy (SMEI), eight had localization-related epilepsy (LRE), and seven had symptomatic generalized epilepsy (SGE). RESULTS: Four of the six photosensitive SMEI patients had quantity-of-light-dependent PPRs. Five of the eight photosensitive LRE patients had wavelength-dependent PPRs. Four of the seven photosensitive SGE patients had wavelength-dependent PPRs, and two had quantity-of-light-dependent PPRs. CONCLUSIONS: The type of pathophysiologic mechanism for eliciting PPRs by low-luminance photic stimulation was closely related to the classification of the epilepsy syndrome.

Adolescent↗
PubMed2005

Effects of ADMA upon gene expression: an insight into the pathophysiological significance of raised plasma ADMA.

BACKGROUND: Asymmetric dimethylarginine (ADMA) is a naturally occurring inhibitor of nitric oxide synthesis that accumulates in a wide range of diseases associated with endothelial dysfunction and enhanced atherosclerosis. Clinical studies implicate plasma ADMA as a major novel cardiovascular risk factor, but the mechanisms by which low concentrations of ADMA produce adverse effects on the cardiovascular system are unclear. METHODS AND FINDINGS: We treated human coronary artery endothelial cells with pathophysiological concentrations of ADMA and assessed the effects on gene expression using U133A GeneChips (Affymetrix). Changes in several genes, including bone morphogenetic protein 2 inducible kinase (BMP2K), SMA-related protein 5 (Smad5), bone morphogenetic protein receptor 1A, and protein arginine methyltransferase 3 (PRMT3; also known as HRMT1L3), were confirmed by Northern blotting, quantitative PCR, and in some instances Western blotting analysis to detect changes in protein expression. To determine whether these changes also occurred in vivo, tissue from gene deletion mice with raised ADMA levels was examined. More than 50 genes were significantly altered in endothelial cells after treatment with pathophysiological concentrations of ADMA (2 microM). We detected specific patterns of changes that identify pathways involved in processes relevant to cardiovascular risk and pulmonary hypertension. Changes in BMP2K and PRMT3 were confirmed at mRNA and protein levels, in vitro and in vivo. CONCLUSION: Pathophysiological concentrations of ADMA are sufficient to elicit significant changes in coronary artery endothelial cell gene expression. Changes in bone morphogenetic protein signalling, and in enzymes involved in arginine methylation, may be particularly relevant to understanding the pathophysiological significance of raised ADMA levels. This study identifies the mechanisms by which increased ADMA may contribute to common cardiovascular diseases and thereby indicates possible targets for therapies.

Arginine↗
PubMed2003

Pathophysiological aspects of cellular pyridine nucleotide metabolism: focus on the vascular endothelium. Review.

In recent years, pyridine nucleotides NAD(H) and NADP(H) have been established as an important molecules in physiological and pathophysiological signaling and cell injury pathways. Protein modification is catalyzed by ADP-ribosyl transferases that attach the ADP-ribose moiety of NAD+ to specific aminoacid residues of the acceptor proteins, with significant changes in the function of these acceptors. Mono(ADP-ribosyl)ation reactions have been implicated to play a role both in physiological responses and in cellular responses to bacterial toxins. Cyclic ADP-ribose formation also utilizes NAD+ and primarily serves as physiological, signal transduction mechanisms regulating intracellular calcium homeostasis. In pathophysiological conditions associated with oxidative stress (such as various forms of inflammation and reperfusion injury), activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) occurs, with subsequent, substantial fall in cellular NAD+ and ATP levels, which can determine the viability and function of the affected cells. In addition, NADPH oxidases can significantly affect the balance and fate of NAD+ and NADP in oxidatively stressed cells and can facilitate the generation of various positive feedback cycles of injury. Under severe oxidant conditions, direct oxidative damage to NAD+ has also been reported. The current review focuses on PARP and on NADPH oxidases, as pathophysiologically relevant factors in creating disturbances in the cellular pyridine nucleotide balance. A separate section describes how these mechanisms apply to the pathogenesis of endothelial cell injury in selected cardiovascular pathophysiological conditions.

ADP Ribose Transferases↗
PubMed2000

Pathophysiology of long-standing overt ventriculomegaly in adults.

OBJECT: Long-standing overt ventriculomegaly in adults (LOVA) is a unique form of hydrocephalus that develops during childhood and manifests symptoms during adulthood. The aim of the present study was to analyze the specific pathophysiological characteristics of LOVA. METHODS: The specific diagnostic criteria for LOVA include severe ventriculomegaly in adults that is associated with macrocephalus measuring more than two standard deviations in head circumference and/or neuroradiological evidence of a significantly expanded or destroyed sella turcica. Twenty patients who fulfilled these criteria, 14 males and six females, were retrospectively studied. These patients' ages at diagnosis ranged from 15 to 61 years (mean 39.4 years). All had symptoms and/or signs indicating that hydrocephalus first occurred at birth or during infancy in the absence of any known underlying disease. The authors performed a pathophysiological study that included specific variations of magnetic resonance (MR) imaging, such as fluid-attenuated inversion recovery and cardiac-gated cine-mode imaging; intracranial pressure (ICP) monitoring; three-dimensional computerized tomography (CT) scanning; and other techniques. Hydrocephalus was caused by aqueductal stenosis in all patients. Severe ventriculomegaly involving the lateral and third ventricles was associated with a marked expansion or destruction of the sella turcica in 17 cases. Cardiac-gated cine-MR imaging did not reveal any significant movements of cerebrospinal fluid in the aqueduct. Three-dimensional CT ventriculography confirmed that the expanded third ventricle protruded into the sella and, sometimes, extended a diverticulum. Fourteen patients revealed symptoms and signs that indicated increased ICP with prominent pressure waves. Dementia or mental retardation was seen in 11 patients, gait disturbance in 12, and urinary incontinence in eight; all three of these symptoms were observed in seven patients. Thirteen patients experienced visual disturbance. Nine patients underwent ventriculoperitoneal shunt implantation as the initial treatment, leading to postoperative subdural hematoma in all seven cases in which a differential pressure valve was used. Nine patients, three of whom were initially treated by shunt placement, underwent a neuroendoscopic procedure, mainly for third ventriculostomy. Postoperatively, ICP returned to normal, and marked to-and-fro pulsatile movements at the site of ventriculostomy were recognized on cine-MR imaging in patients treated endoscopically. However, the ventriculomegaly was little improved. Consequently, all patients eventually demonstrated improvement in response to either a shunt equipped with a pressure-programmable valve or an endoscopic procedure; however, depression appeared in six patients, who required psychiatric consultation or medication. CONCLUSIONS: Such remarkably decreased intracranial compliance but relatively high ICP dynamics are the pathophysiological characteristics of LOVA. The therapeutic regimen should be determined based on the individual's specific pathophysiological makeup.

Adolescent↗
PubMed2000

Pathophysiology of epilepsy.

This work reviews the current knowledge on epileptogenesis and pathophysiology of epilepsy. Recently, gene defects underlying four monogenic epilepsies (generalized epilepsy with febrile seizures, autosomal dominant nocturnal frontal lobe epilepsy, benign familial neonatal convulsions and episodic ataxia type 1 with partial seizures) have been identified, shedding new light on the pathophysiology of epilepsy as these diseases are caused by ion channel mutations. Although epileptic syndromes differ pathophysiologically, common ictogenesis-related characteristics as increased neuronal excitability and synchronicity are shared as well as mechanisms involved in interictal-ictal transition. Emerging insights point to alterations of synaptic functions and intrinsic properties of neurons as common mechanisms underlying hyperexcitability. This work also reviews the neurochemical mechanisms of epilepsy. An imbalance between glutamate and gamma-aminobutyric acid neurotransmitter systems can lead to hyperexcitability but catecholaminergic neurotransmitter systems and opioid peptides were shown to play a role in epileptogenesis as well. An overview of currently available anti-epileptic drugs and their presumed mechanisms of action is given as an illustration of the neurochemistry of epileptogenesis. Most anti-epileptic drugs exert their anti-epileptic properties through only a few neurochemical mechanisms that are meanwhile basic pathophysiological mechanisms thought to cause seizures.

Adult↗