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At least 343 records · Page 19Linked to original sources
PubMed2002

[Pathophysiology of migraine: models to explain the generation of migraine headache].

Migraine attacks can be elicited by many different trigger situations such as light, food and the menstruation cycle. However, patients share a common pathophysiology, and a number of theories have been proposed as to how migraine can be generated. After a brief introduction of the trigeminal nociceptive system, 4 attempts to explain the generation of migraine attacks are described and discussed: One deals with the "cortical spreading depression (CSD) theory" which favors a cortical dysfunction. The second provides some evidence that a genetic mutation of calcium channels might be the cause. The third is based on a pathophysiological role of endogenous serotonin because serotonin agonists are effective drugs in the treatment of migraine and the last one postulates a migraine generator in the brainstem.

Chromosomes, Human, Pair 19↗
PubMed2003

[Pathophysiological and therapeutic aspects of amniotic fluid embolism (anaphylactoid syndrome of pregnancy): case report with lethal outcome and overview].

A 35-years old gravida IV and para II underwent caesarean section because of fetal distress following induction of labour. During operation the patient developed disseminated intravascular coagulation (DIC), severe haemorrhage and shock necessitating massive blood transfusion,hysterectomy with pelvic packing, and high-dose catecholamines. Ultimately, recombinant factor VIIa was given to control bleeding. During the first 24 hours after operation, both clinical and laboratory findings showed that the severe DIC was on the course to recovery.However, the patient subsequently developed multiple organ dysfunction syndrome with respiratory and renal failure requiring mechanical ventilation and haemodialysis.All therapeutical efforts could not help that the patient passed away due to an inevitable multiple organ failure on the 12th day after the operation. Given the constellation of diagnostic and clinical findings, the most likely diagnosis was amniotic fluid embolism (AFE), a rare complication of pregnancy. The following differential diagnoses were less likely or excluded in this reported patient: pre-eclampsia/pregnancy-induced hypertension,HELLP syndrome,anaphylaxis,uterine rupture, transfusion reactions,pulmonary embolism. AFE occurs rarely, and because studies in animal models cannot reproduce accurately the pathophysiological and clinical alterations seen in humans, its pathogenesis remains unclear. It has been proposed that the clinical syndrome of AFE occurs when fetal antigens pass the maternal immunological barrier in susceptible mothers. The recognition of fetal antigens by maternal immune system subsequently triggers the release of endogenous mediators that are responsible for dramatic pathophysiological disturbances.Furthermore, the components of amniotic fluid initiate the DIC. These events are more consistent with septic shock and anaphylactic shock than with an embolic process and it was proposed that the term "amniotic fluid embolism" be changed to "anaphylactoid syndrome of pregnancy". At present, no therapy has been found to consistently improve outcomes in women with AFE.Patients who survive the initial insult are at high risk for multiple organ failure. The mortality of AFE remains high.

Adult↗
PubMed2000

[Detection of nitric oxide synthases in physiological and pathophysiological processes of the nasal mucosa].

Nitric oxide (NO) can play an important role in the regulation of vascular tone and neurotransmission, as well as in non-specific immunoreactions and inflammation in a variety of tissues. Increased quantities of nitric oxide in respired air can be measured during inflammatory processes. However, the exact role and precise sources of NO under physiological and pathophysiological conditions within the airways remain to be defined. Three isoforms of NO-synthases can be distinguished: two constitutive (neuronal and endothelial) Ca(2+)-dependent cNOS and one inducible Ca(2+)-independent iNOS (NOS II). Constitutive NOS (NOS I and III) release a basal amount of NO under physiological conditions. The inducible form once expressed can catalyse the generation of large quantities of NO. Many kinds of cells, such as macrophages, neutrophils, endothelium and smooth muscle cells, are capable of expressing NOS II. Since all isoforms of NO-synthase seem to be present in nasal tissues and the expression of iNOS under inflammatory conditions seems to be responsible for excessive production of NO, the distribution of NOS-isoforms (especially NOS II) in normal and inflammatory nasal tissue, as well as the exact requirements for expression of iNOS remain to be proven. Non-inflamed fresh human nasal mucosa from the middle turbinate was compared immuno-histologically with nasal mucosa having the typical findings of chronic polypoid rhinosinusitis (i.e., polypoid middle turbinates and polyps of the middle nasal duct). In order to gain more information about the mechanisms of acute inflammation, non-inflamed vital turbinates were incubated in vitro with the proinflammatory substances bacterial lipopolysaccharides (LPS) and tumor necrosis-factor (TNF) for 30, 60, 90, 120, 180 and 240 min. Subsequent to exposure to NADPH-diaphorase and immunostaining with specific antibodies to each NOS-isoform, clearly increased or initiated expressions of inducible NOS (iNOS) in blood vessels, glands, macrophages and epithelium of chronically inflamed and LPS-incubated nasal tissue became apparent in comparison to the non-inflamed controls. In contrast, NOS III/NOS I seemed to be not affected. The onset of immunohistochemically recognizable NOS II expression was observed after 90 min incubation with of LPS/TNF-alpha. Polypoid tissue showed a strong increase in submucosal thickness and a high infiltration of iNOS-positive leukocytes (granulocytes and macrophages) compared to the LPS-incubated non-inflamed specimens. These findings implicate NOS II generated nitric oxide as a key agent for causing swelling, secretion and obstruction in patients with acute and chronic polypoid or allergic rhinitis. These findings also suggest that molecular NO has to be considered in the pathophysiology of chronic polypoid rhinosinusitis.

Chronic Disease↗
PubMed2005

The endocannabinoid system in the physiology and pathophysiology of the gastrointestinal tract.

Numerous investigations have recently demonstrated the important roles of the endocannabinoid system in the gastrointestinal (GI) tract under physiological and pathophysiological conditions. In the GI tract, cannabinoid type 1 (CB1) receptors are present in neurons of the enteric nervous system and in sensory terminals of vagal and spinal neurons, while cannabinoid type 2 receptors are located in immune cells. Activation of CB1 receptors was shown to modulate several functions in the GI tract, including gastric secretion, gastric emptying and intestinal motility. Under pathophysiological conditions induced experimentally in rodents, the endocannabinoid system conveys protection to the GI tract (e.g. from inflammation and abnormally high gastric and enteric secretions). Such protective activities are largely in agreement with anecdotal reports from folk medicine on the use of Cannabis sativa extracts by subjects suffering from various GI disorders. Thus, the endocannabinoid system may serve as a potentially promising therapeutic target against different GI disorders, including frankly inflammatory bowel diseases (e.g. Crohn's disease), functional bowel diseases (e.g. irritable bowel syndrome) and secretion- and motility-related disorders. As stimulation of this modulatory system by CB1 receptor agonists can lead to unwanted psychotropic side effects, an alternative and promising avenue for therapeutic applications resides in the treatment with CB1 receptor agonists that are unable to cross the blood-brain barrier, or with compounds that inhibit the degradation of endogenous ligands (endocannabinoids) of CB1 receptors, hence prolonging the activity of the endocannabinoid system.

Animals↗
PubMed2004

[Pathophysiology of posttraumatic osteitis].

Over the last few decades, significant reduction of post-traumatic infections could be attained by establishing novel surgical techniques and tactics, by adapting surgical decisions to the risk of infection, by employing chemotherapeutic agents, and by developing new implants. Here a novel understanding of the pathophysiologic mechanisms of post-traumatic and postoperative osteomyelitis were directive. Nevertheless, post-traumatic infections later cause significant physical and economic sequelae. This article sums up the fundamental pathophysiological mechanisms of post-traumatic infection. New ideas about post-traumatic prevention and therapy of osteomyelitis are discussed.

Foreign-Body Reaction↗
PubMed2004

Standardized lung recruitment during high frequency and conventional ventilation: similar pathophysiologic and inflammatory responses in an animal model of respiratory distress syndrome.

OBJECTIVE: To evaluate standardized lung recruitment strategy during both high frequency oscillation (HFO) and volume-targeted conventional ventilation (CV+V) in spontaneously breathing piglets with surfactant washout on pathophysiologic and inflammatory responses. DESIGN: Prospective animal study. SETTING: Research laboratory. SUBJECTS: Twenty-four newborn piglets. INTERVENTIONS: We compared pressure support and synchronized intermittent mandatory ventilation, both with targeted tidal volumes, (PSV+V, SIMV+V) to HFO. Animals underwent saline lavage to produce lung injury, received artificial surfactant and were randomized to one of the three treatment groups (each n=8). After injury and surfactant replacement, lung volumes were recruited in all groups using a standard protocol. Ventilation continued for 6 h. MEASUREMENTS AND MAIN RESULTS: Arterial and central venous pressures, heart rates, blood pressure and arterial blood gases were continuously monitored. At baseline, post lung injury and 6 h we collected serum and bronchoalveolar lavage samples for proinflammatory cytokines: IL 6, IL 8 and TNF-alpha, and performed static pressure-volume (P/V) curves. Lungs were fixed for morphometrics and histopathologic analysis. No physiologic differences were found. Analysis of P/V curves showed higher opening pressures after lung injury in the HFO group compared to the SIMV+V group ( p<0.05); no differences persisted after treatment. We saw no differences in change in proinflammatory cytokine levels. Histopathology and morphometrics were similar. Mean airway pressure (P(aw)) was highest in the HFO group compared to SIMV+V ( p<0.002). CONCLUSIONS: Using a standardized lung recruitment strategy in spontaneously breathing animals, CV+V produced equivalent pathophysiologic outcomes without an increase in proinflammatory cytokines when compared to HFO.

Animals↗
PubMed2006

Clozapine-induced sialorrhea: pathophysiology and management strategies.

RATIONALE: Clozapine is an atypical antipsychotic agent with proven efficacy in refractory schizophrenia, but its widespread use is limited by adverse effects such as agranulocytosis, seizures, sedation, weight gain, and sialorrhea. Clozapine-induced sialorrhea (CIS) is bothersome and has socially stigmatizing adverse effects, which result in poor treatment compliance. The pathophysiology of this condition is poorly understood and the treatment options available are based mostly on case reports and open-label studies. OBJECTIVE: To review the available studies on CIS. METHOD: All relevant studies available through PUBMED search supplemented with manual search were undertaken. RESULT: The clinical features, complications, assessment, pathophysiology, and management of CIS are discussed. CONCLUSION: Although the studies evaluating the therapeutic options has limitations and no drug has been found to be superior, judicious use of pharmacological agents along with behavioral methods will reduce this troublesome side effect and enhance compliance.

Adrenergic alpha-Agonists↗
PubMed2003

Pathophysiologic patterns influencing fetal surgery.

There are a growing number and variety of fetal disorders that may benefit from intervention prior to birth. Despite the diversity, there are common pathophysiologic denominators or patterns that tie together many seemingly disparate disorders. The purpose of this article was not to review disorders presented in other, accompanying articles but, rather, to present pathophysiologic patterns that common influence fetal surgery within a cohesive framework.

Airway Obstruction↗
PubMed2002

Pharmacokinetics of ecteinascidin 743 administered as a 24-h continuous intravenous infusion to adult patients with soft tissue sarcomas: associations with clinical characteristics, pathophysiological variables and toxicity.

PURPOSE: Ecteinascidin 743 (ET-743) is a potent cytotoxic alkaloid of marine origin that has shown promising evidence of antitumor activity during phase I clinical trials. In the study reported here, the influence of clinical characteristics and pretreatment pathophysiological variables on the pharmacokinetics of ET-743 and their associations with drug-related toxicity was examined in sarcoma patients treated in three phase II clinical trials. METHODS: Adult patients with various histological subtypes of soft tissue sarcoma received 1.5 mg/m(2) of ET-743 by 24-h continuous i.v. infusion once every 3 weeks. Eligibility criteria were similar for each study, except for the histological subtype of the tumor or the extent of prior treatment with other anticancer agents, and all patients had normal or near-normal liver and renal function. The maximum plasma concentration (C(max)) and area under the plasma profile from time zero to infinity (AUC) of the drug were determined during the first cycle of therapy. Patients were evaluated for toxicity every week. RESULTS: Geometric mean +/- SD values of the pharmacokinetic parameters in 69 patients were: C(max) 1.14 +/- 0.52 ng/ml, AUC 39.9 +/- 16.6 ng.h/ml, and total body clearance (CL) 36.7 +/- 16.4 l/h per m(2). The only significant correlation involving physical characteristics of the patients or pretreatment pathophysiological variables was a very weak relationship between alkaline phosphatase and AUC (r=0.39, P<0.01). The 15 patients with any baseline liver function test exceeding the upper limit of the normal ranges had a significantly greater (P=0.02) incidence of severe toxicity (80% vs 44%). Although the mean AUC of ET-743 in patients with elevated serum levels of hepatic enzymes was 17% greater than that in patients with normal pretreatment liver function tests, the difference was not significant ( P=0.22). In addition, there was no distinct relationship between the grade of the most severe drug-related toxicity that occurred during the first cycle of therapy and the AUC for the entire cohort. The CL of ET-743 was found to be 27% greater in patients concurrently receiving dexamethasone as a preventative antiemetic than in those who were not, but the difference did not achieve statistical significance (P=0.08). There were no significant associations between CL (liters per hour) and body surface area or any other variable related to body size. CONCLUSIONS: The risk of developing severe toxicity was substantially enhanced in patients with relatively moderate indications of hepatic dysfunction without a coincident effect on the CL of ET-743. Dexamethasone cotreatment appeared to decrease the incidence of severe toxicity as well as the AUC of the drug. Delivering a fixed amount of drug without adjustment for the height or weight of the patient may be more appropriate than dose normalization due to the absence of an association between CL and body surface area. Optimizing dosing strategies to further enhance the therapeutic index of ET-743 may depend upon obtaining a better understanding of the metabolic fate of the drug in humans.

Adult↗
PubMed1998

To what extent has the pathophysiology of normal-pressure hydrocephalus been clarified?

The causes and pathophysiology of idiopathic normal-pressure hydrocephalus (NPH) still remain poorly understood. We reviewed the recent pertinent literature on NPH from the past 3 years (1994- 1996) in this journal [Crit Rev Neurosurg (1997) 7:263-275] and here review further manuscripts that appeared mainly in 1997. Recent investigations suggest that idiopathic NPH may be a primary cerebral parenchymal disease rather than a disorder of cerebrospinal fluid (CSF) absorption. The pathophysiology of idiopathic NPH has a wide spectrum ranging from purely hydrodynamic problems owing to a CSF absorption defect to parenchymal changes caused by hemodynamic problems owing to ischemic vascular risk factors. Magnetic resonance imaging (MRI) of NPH frequently shows ischemic vas-cular encephalopathy. NPH may coexist with subcortical white matter vascular encephalopathy, because Binswanger's encephalopathy and idiopathic NPH share common clinical symptoms. Most patients with suspected NPH may suffer from both problems. Because of MRI findings of suspected NPH, ischemic parenchymal changes caused by vasculopathy have been receiving attention. Brain biopsy findings of suspected NPH suggest the presence of parenchymal changes caused by vasculopathy such as arteriosclerosis. Patients with brain biopsy findings of Alzheimer's disease may benefit from shunting. Pathological changes seen by brain biopsy are not specific for NPH. The information accumulated so far about NPH shows a wide clinical spectrum and multifactorial etiology. Therefore, patients with NPH are inhomogeneous, and this makes it difficult to diagnose and select patients for shunting.

Journal Article↗
PubMed2005

Current understanding of coronary in-stent restenosis. Pathophysiology, clinical presentation, diagnostic work-up, and management.

In-stent restenosis is the limiting entity following coronary stent implantation. It is associated with significant morbidity and cost and thus represents a major clinical and economical problem. Worldwide, approximately 250 000 in-stent restenotic lesions per year have to be dealt with. The pathophysiology of instent restenosis is multifactorial and comprises inflammation, smooth muscle cell migration and proliferation and extracellular matrix formation, all mediated by distinct molecular pathways. Instent restenosis has been recognised as very difficult to manage, with a repeat restenosis rate of 50% regardless of the mechanical angioplasty device used. Much more favourable results were reported for the adjunctive irradiation of the in-stent restenotic lesion, with a consistent reduction of the incidence of repeat in-stent restenosis by 50%. Data from the first clinical trials on drug-eluting stents for the treatment of in-stent restenosis have shown very much promise yielding this strategy likely to become the treatment of choice. This review outlines the histological and molecular findings of the pathophysiology, the epidemiology, the predictors and the diagnostic work-up of in-stent restenosis and puts emphasis on the various treatment options for its prevention and therapy.

Animals↗
PubMed2003

Recent advances in the study of the pathophysiology of pemphigus.

Recent rapid advances in the basic research into pemphigus have provided many insights into its pathophysiology. In particular, a recently developed enzyme-linked immunosorbent assay (ELISA) for desmogleins 1 and 3 (Dsg1 and Dsg3), antigens for pemphigus foliaceus (PF) and pemphigus vulgaris (PV), respectively, has led to great progress in the diagnosis and classification of pemphigus, as well as in understanding its pathomechanisms. Studies with the anti-Dsg1 and anti-Dsg3 antibodies have indicated that there are two types of PV, the mucosal dominant type and the mucocutaneous type. The same ELISA has identified the antigens in pemphigus herpetiformis. The autoantigens detected by this ELISA correlate well with the clinical features in pemphigus patients in showing the shift between PV and PF. In addition, the Dsg compensation theory proposed by Stanley and Amagai can reasonably explain the different depths of skin lesions and the different occurrences of skin and oral mucosal lesions between PV and PF. Furthermore, a complicated profile of autoantigens in paraneoplastic pemphigus (PNP) has been indicated in various biochemical studies, and IgG anti-Dsg1 and anti-Dsg3 antibodies have been detected in serum from all the PNP patients by the above ELISA. On the other hand, serum from subcorneal pustular dermatosis type IgA pemphigus patients have been shown to react with Dsc1, another type of desmosomal cadherin, by a novel cDNA transfection method. In addition, IgA anti-Dsg1 and anti-Dsg3 antibodies have been detected in a few patients with IgA pemphigus by an ELISA for IgA antibodies. Various autoimmune bullous diseases, including several types of pemphigus, are the only diseases in which the pathogenic role of circulating autoantibodies has been confirmed using the newborn mouse animal model. Therefore, studies of the pathophysiology of pemphigus are extremely important as a paradigm for research into various types of autoimmune diseases in other fields.

Animals↗
PubMed2002

Three-dimensional analysis of nystagmus in benign paroxysmal positional vertigo. New insights into its pathophysiology.

Nystagmus is a rhythmical rotation of the eyeball. Its characteristics can be defined mathematically by the axis of rotation and the angular velocity around this axis. We analysed the axis of rotation for the nystagmus in benign paroxysmal positional vertigo (BPPV) to elucidate its pathophysiology. Thirteen patients with typical unilateral BPPV participated in the present study. The axis of rotation for the nystagmus was calculated from images recorded on digital videotape with an infrared CCD camera, using an algorithm that we developed. The patients' responsiveness to Semont's liberatory maneuver was also assessed.The results showed that patients could be assigned to one of two groups based on the rotation axis of the nystagmus. In one group of patients (n = 7; Group A), the axis of rotation was almost vertical to the plane containing the posterior semicircular canal (PSC) on the presumed affected side. In the other group of patients (n = 6; Group B), it was clustered around the naso-occipital axis. These results suggest that in the patients in Group A the responsible lesion is confined to the PSC, whereas the pathogenesis underlying the conditions in those in Group B is considered to be more complicated. This speculation was reinforced by the difference in responsiveness to Semont's liveratory maneuver. All of the patients in Group A showed remission of vertigo within 10 days (mean, 2.4 days) after onset of treatment using Semont's liberatory maneuver, whereas the patients in Group B required much longer periods of time for remission to occur (mean, 25.7 days). Our findings lead to the conclusion that by considering the spatial orientation of individual semicircular canals, in the patients in Group B the pathophysiology is not confined to the PSC, but most probably all three semicircular canals are involved.

Adult↗
PubMed1998

Clinical and pathophysiological significance of severe neurotrauma in polytraumatized patients.

INTRODUCTION: Traumatic brain injury (TBI) is present in up to two-thirds of multiply injured patients. The degree of TBI influenced the mortality and morbidity of multiple trauma significantly. RESULTS: Important prognostic predictors are: injury severity score (ISS); Glasgow coma score [(GCS), motor score]; pupil size and reactivity; coma grade and duration; age; morphological primary brain lesion; and pathophysiological changes leading to secondary brain damage. The time course of brain edema, raised intracranial pressure and, especially, pathophysiology of disturbed cerebral blood flow and metabolism characterizes early and late periods of ischemic vulnerability. CONCLUSION: These should be taken into consideration when planning operative procedures in multiple-trauma patients. Avoidance of secondary ischemic brain damage by reducing the number of systemic insults (hypovolemia, hypotension, hypoxia) will improve prognosis of critically ill polytraumatized patients with head injury.

Brain Edema↗
PubMed1997

Pathophysiological and clinical aspects of the CO2 pneumoperitoneum (CO2-PP).

Experimental studies demonstrated a severe cardiac load of the CO2 pneumoperitoneum caused by an accelerated after- and a decreased preload. Patients displaying cardiovascular risks are therefore often rejected from laparoscopic surgery. Hence, the pathophysiological changes and the intraoperative risk of the CO2 pneumoperitoneum in high-risk cardiopulmonary patients (NYHA II-III, n = 15) undergoing laparoscopic cholecystectomy are described. The changes in cardiac after- and preload seem to be due to the elevated intraabdominal pressure rather than transperitoneally resorbed CO2 and are reversible by desufflation. In one patient conversion to open operation had to be performed because of a severe drop in cardiac output and right ventricle ejection fraction. Mixed oxygen saturation was predicting intraoperative worsening in this case. The described pathophysiological changes may seem to be well tolerated even in high-risk cardiac patients. Monitoring of hemodynamics should include an arterial catheter line and blood gas analyses. Pharmacologic interventions or pressureless laparoscopic procedures might not be necessary as long as laparoscopic cholecystectomy is performed.

Aged↗
PubMed2004

Pathophysiology, diagnosis, and treatment of methylmalonic aciduria-recent advances and new challenges.

Classical methylmalonic aciduria is a relatively rare inborn error of branched-chain amino acid metabolism, occurring in 1:50,000 to 1:80,000 newborns. Three decades after its recognition, major progress has been made in survival and prevention of neurological sequelae in affected children, if the diagnosis is made early and treatment and follow-up care are meticulous. Therapy consists of a specially formulated protein diet, carnitine supplementation, and vigorous emergency treatment during intercurrent illnesses aimed at preventing the development of catabolism. Recently the clinician has been challenged by partially unexpected long-term complications. These include chronic neurological symptoms, specifically an extrapyramidal movement disorder caused by progressive destruction of the basal ganglia, which are similar to those observed in other organic acid disorders, such as propionic aciduria or glutaric aciduria type I. Unexpected and unique is the development of chronic renal failure in a major subset of patients. As the pathophysiological basis of renal failure is still obscure, no causative treatment is available and hemodialysis may become necessary. Experience with transplantation of liver, kidney, or kidney and liver is very limited and allows as yet no conclusions. Interdisciplinary research efforts in this field should reveal new pathophysiological links and hopefully provide additional therapeutic approaches.

Amino Acid Metabolism, Inborn Errors↗
PubMed2002

Pathophysiology and treatment for cervical flexion myelopathy.

Previous studies have suggested that spinal cord compression by the vertebral bodies and intervertebral discs during neck flexion cause cervical flexion myelopathy (CFM). However, the exact pathophysiology of CFM is still unknown, and surgical treatment for CFM remains controversial. We examined retrospectively patients with CFM based on studies of the clinical features, neuroradiological findings, and neurophysiological assessments. The objectives of this paper are to investigate the pathophysiology of CFM, and to examine an optimal surgical treatment. Twenty-three patients (20 male, three female) with age of onset ranging from 11 to 23 years (mean 15.7 years) were examined for the study. All patients were inspected by magnetic resonance imaging (MRI), myelogram, or computed tomographic myelogram (CTM) of the cervical spine. In eight patients, dynamic motor evoked potentials (MEP) studies were performed. Five patients underwent surgical treatment; two patients had cervical duraplasty with laminoplasty, two patients had musculotendinous transfer, one patient had both of these procedures, and the remaining 18 patients were treated conservatively. Amyotrophy of the hand intrinsic and flexor muscle group of the forearm except the brachioradial muscle was observed hemilaterally in 20 patients and bilaterally in three patients. In three patients, T1-weighted MRI with neck flexion showed linear high intensity regions in the epidural space. In all patients, axial MRI/CTM demonstrated flattening of the spinal cord with the posterior surface of the dura mater shifting anteriorly. The amplitude of MEPs decreased after cervical flexion in two patients with progressive muscular atrophy. In three patients, dysesthesia of the upper extremities disappeared following cervical duraplasty. Musculotendinous transfer for three patients significantly improved the performance of their upper extremity. The findings of this study suggest that degenerative changes of the dura mater may be a characteristic pathology of CFM. Cervical duraplasty with laminoplasty is effective for cases at an early stage, and musculotendinous transfer should be selected in patients at a late stage.

Adolescent↗
PubMed2002

The pathophysiology of syringomyelia - historical overview and current concept.

Various ideas and hypotheses have been brought forward to explain the development of syringomyelia in the past two centuries. None of them offers a sufficient basis to serve as a concept for the treatment of all affected patients. Apart from a discussion of the different hypotheses this paper proposes a new pathophysiological concept based on clinical, experimental and literature studies. Syringomyelia is understood as a state of chronic interstitial edema of the spinal cord due to accumulation of extracellular fluid (ECF). This accumulation is caused by a cascade of events starting with obstruction of cerebrospinal fluid (CSF) flow and/or spinal cord tethering which ultimately alter ECF flow and increase ECF volume. Treatment should be targeted against the pathological process which causes CSF flow obstruction and cord tethering to inhibit this pathophysiological process at a decisive point.

Animals↗