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Search Results: 1 - 10 of 812 matches for " Erich Schmutzhard "
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Apoptosis of the fibrocytes type 1 in the spiral ligament and blood labyrinth barrier disturbance cause hearing impairment in murine cerebral malaria
Joachim Schmutzhard, Christian H Kositz, Rudolf Glueckert, Erich Schmutzhard, Annelies Schrott-Fischer, Peter Lackner
Malaria Journal , 2012, DOI: 10.1186/1475-2875-11-30
Abstract: The temporal bones of seven mice with cerebral malaria-four with hearing impairment, three without hearing impairment-were evaluated with immunohistochemistry for cleaved caspase 3 to detect apoptosis and connexin 26, a gap junction protein being a cornerstone in the endocochlear potassium recirculation. Furthermore five animals with cerebral malaria were treated with Evans blue prior to sacrification to detect disturbances of the blood labyrinth barrier.Cleaved caspase 3 could clearly be detected by immunohistochemistry in the fibrocytes of the spiral ligament, more intensively in animals with hearing impairment, less intensively in those without. Apoptosis signal was equally distributed in the spiral ligament as was the connexin 26 gap junction protein. The Evans blue testing revealed a strong signal in the malaria animals and no signal in the healthy control animals.Malfunction of the fibrocytes type 1 in the spiral ligament and disruption of the blood labyrinth barrier, resulting in a breakdown of the endocochlear potential, are major causes for hearing impairment in murine cerebral malaria.Malaria still is one of the most frequent infectious diseases worldwide. Especially, Plasmodium falciparum malaria is known for its severe course with multi-organ involvement [1]. Severe neurocognitive and language developmental impairment in sub-Saharan children following a severe course of malaria have been reported [2,3]. Hearing impairment during childhood is known to be one of the fundamental causes of acquired language disorders. A possible association between fever and hearing impairment has been corroborated by the fact that a high percentage of deaf Tanzanian children had a positive medical history of severe fever-mostly due to malaria or pneumonia [4]. Out of 23 children with neurocognitive impairment after cerebral malaria, 14 suffered from a loss of speech and nine from hearing impairment [5]. This clinical data point towards an involvement of the inner ear in cer
Complications of hypothermia: infections
Gregor Broessner, Marlene Fischer, Peter Lackner, Bettina Pfausler, Erich Schmutzhard
Critical Care , 2012, DOI: 10.1186/cc11277
Abstract: Intriguing data derived from animal models showing a potent neuroprotective effect in various disease entities induced by hypothermia gave way to a broader use of this method in humans. Thus, therapeutic hypothermia has become the standard of care after cardiac resuscitation as studies demonstrated its strong neuroprotective effect and neurologic outcome improvement [1,2]. It is now recommended by the European Resuscitation Council and the International Liaison Committee on Resuscitation in cases of comatose adults with spontaneous circulation after out-of-hospital cardiac arrest (OHCA) [3]. However, in indications other than resuscitation, such promising results could not be achieved in prospective trials shifting the scientific focus on possible side effects of TH [4-6]. Rewarming injury, shivering, electrolyte dysbalance, pharmacological and pharmacodynamic alterations, cardiovascular effects including arrhythmia, insulin resistance and infections have recently been attributed as limitations occurring in a dose-dependent fashion under TH [7]. Taken together, maximal reduction of these side effects should be a treatment goal if dealing with temperature control measures irrespective of the target temperature. Today, infectious complications are thought to be one of the major contributors limiting the effects of hypothermia [7-12]. Thus advancing diagnostic approach, prevention and treatment of these infectious complications is a great concern of the scientific critical care community and need to be addressed in future prospective trials. In various studies enrolling patient populations suffering from such different diseases as traumatic brain injury, ischaemic stroke or resuscitation post cardiac arrest, an increased rate of infections under TH was observed [4,6,11]. Whether this negative effect has to be attributed to a specific cooling measure remains under debate; however, this hypothesis is unlikely as increased infections are found under both endovascular and
Update on therapeutic temperature management
Gregor Broessner, Marlene Fischer, Gerrit Schubert, Bernhard Metzler, Erich Schmutzhard
Critical Care , 2012, DOI: 10.1186/cc11259
Abstract: The aim of this symposium is to enhance the knowledge on temperature management, increase the readiness and stimulate the preparedness to institute therapeutic hypothermia and/or prophylactic controlled normothermia, respectively, in patients in need of tissue and organ protection, uncontrolled body temperatures possibly adding - per se - to neuronal damage. Knowing the medical literature and knowing the issue of potentially life-threatening side effects and complications incurred by this invasive therapeutic manoeuvre, it is the foremost aim of this symposium and this supplementary issue of Critical Care to discuss all these aspects of targeted temperature management in emergency, critical care and, in particular, neurocritical patients and conditions. For this reason the organisers have agreed that the discussion of these various issues, being so important for general critical care, neurocritical care and emergency medicine, must be distributed as widely as possible, making it available to critical care and neurocritical care specialists all over the world. Therefore we are extremely grateful to the Editors of Critical Care for providing a forum for all of the extended abstracts of all invited speakers, covering the entire field of adult emergency and critical care medicine. We do hope and we are convinced that this supplementary issue will be a source of inspiration and knowledge, hopefully becoming a work of reference for intensivists, neurologists, neurointensivists, cardiologists and all emergency physicians alike. It is the aim of the organisers to establish a series of such symposia within the next years in order to keep up with all the developments in this field and to maintain the highest possible level of knowledge of targeted temperature management in the community of emergency and intensive care physicians.
Therapeutic hypothermia: the rationale
Erich Schmutzhard, Marlene Fischer, Anelia Dietmann, Gregor Br?ssner
Critical Care , 2012, DOI: 10.1186/cc11260
Abstract: In a wide range of diseases, secondary damage to the brain or other organs follows the initial impact and may be responsible for aggravation of disease condition or clinical state, in particular neurological morbidity and/or mortality [4-11]. Therapeutic hypothermia, recently renamed targeted temperature management, including prophylactic normothermia, has been used to improve this secondary impact onto brain and other organ tissue. This holds true, in particular, for neurological and neurosurgical intensive care patients since secondary brain and nervous tissue injury may preclude a potentially benign course of disease. The mechanisms of action of hypothermia are complex, not yet fully understood. Therapeutic hypothermia/targeted temperature management aims to attenuate a cascade of secondary injury mechanisms, which is started immediately after the initial event (primary injury) and may last for hours and even days [4,6,12]. The majority of research has focused, so far, on these secondary injury processes being destructive to brain and nervous tissue. It may be expected that any such protective effect can be replicated in other organs and tissues during therapeutic hypothermia/targeted temperature management. A wide range of side effects may negate and counteract its positive initial effect; this implies side effects of hypothermia per se and side effects of rewarming or inconstant maintenance of temperature levels [13-17].This abstract limits itself to potential pathophysiological mechanisms of actions, the risks of any such mechanism and side effects derived from them [4,5,10,12,16-18].The protective effect of hypothermia may be explained by several pathways. A decreased metabolism with less oxygen and energy consumption and carbon dioxide production may prevent secondary injury when oxygen supply is interrupted or, at least, impaired. However, it needs to be stressed that the reduction in metabolic rate, as seen in hypothermia, requires adjustment in ventilator
Controlled prophylactic normothermia
Gregor Broessner, Marlene Fischer, Bettina Pfausler, Erich Schmutzhard
Critical Care , 2012, DOI: 10.1186/cc11268
Abstract: Preliminary animal data for the beneficial neuroprotective effect of therapeutic hypothermia could not satisfyingly be reproduced in patients raising questions about the possible side effects of hypothermia. Controlled prophylactic normothermia (36.5°C) prevents secondary injury through consequent treatment of fever and limits dose-dependent side effects through therapeutic hypothermia. Novel endovascular and gel-pad surface cooling measures have shown to be feasible and efficacious in inducing and maintaining even long-term controlled normothermia.Fever is one of the most frequent complications of intensive care treatment. Up to 90% of patients develop at least one febrile episode within 7 days after being admitted to an ICU [1]. First of all, fever has always to be interpreted as a sign of an infection. Thus temperature modulation by any means has to include a strict protocol identifying any source of infection followed by a straightforward treatment approach. There is widespread consensus that fever alone is associated with unfavourable outcome. This consensus is a result of animal and human data over the past decades. In a meta-analysis conducted by Greer and colleagues including more than 14,000 patients, fever alone was a significant and independent predictor of morbidity and mortality across such different diseases entities as ischaemic stroke, haemorrhagic stroke and traumatic brain injury [2]. Increasing evidence from animal and human studies suggests that fever, irrespective of its cause, can directly and adversely affect neurological outcome in various types of neurological injury [3].The pathophysiological mechanisms by which fever affects patient outcome are discussed, controversially comprising increase of metabolic demand (under circumstances of reduced supply), production of free radicals, local thermopooling, disruption of the blood-brain barrier, intracranial pressure (ICP) elevation, increased enzymatic inhibition of protein kinases, and worsened
Temperature management in central nervous infection
Erich Schmutzhard, Peter Lackner, Ronny Beer, Marlene Fischer, Anelia Dietmann, Bettina Pfausler
Critical Care , 2012, DOI: 10.1186/cc11276
Abstract: Obviously, Dr Roland Burkitt, the uncle of the legendary Prof. Dr Denis Burkitt, after whom the African lymphoma and its association with Epstein-Barr virus was named, had realized that lowering the body temperature in patients with high fevers, in Kenya highly likely to being due to cerebral malaria, meningitis or encephalitis, might influence positively the course of such potentially - at this time, in many instances, definitely - life-threatening disease [1]. Zdravev stipulated that otogenous brain abscesses not only need to be surgically evacuated but, when causing cerebral herniation, may benefit from lowering body temperature. He was the first to conclude that high body temperature in patients with increased intracranial pressure may be a deleterious association [2].The wide variety of mechanisms of injury that are exaggerated by hyperthermia and may be ameliorated by moderate hypothermia are described elsewhere in this supplement (see abstract A1). They include mechanisms of neuroexcitotoxicity [3], release of free radicals, changes in blood-brain barrier and vascular permeability, the release of proinflammatory mediators, drawing leucocytes across the blood-brain barrier, increasing the number of inflammatory cells in the brain tissue and the passage of neutrophils, phagocytes, monocytes and macrophages into the brain, additionally injuring neuronal cells by stimulating further immune reactions [4]. Whether interfering with these mechanisms by moderate hypothermia may reduce secondary insult onto neuronal cells and brain tissue is still a matter of discussion. What has been known for long time is that increased intracranial pressure, as frequently seen in viral encephalitis, severe bacterial meningitis and/or brain abscesses, may be modified by therapeutic hypothermia/targeted temperature management [5]. In addition, long-term morbidity and mortality in CNS infection may additionally deteriorate if bacterial meningitis is complicated by cerebral infarction,
Case report: severe heat stroke with multiple organ dysfunction – a novel intravascular treatment approach
Gregor Broessner, Ronny Beer, Gerhard Franz, Peter Lackner, Klaus Engelhardt, Christian Brenneis, Bettina Pfausler, Erich Schmutzhard
Critical Care , 2005, DOI: 10.1186/cc3771
Abstract: A 38-year-old male suffering from severe heat stroke with predominant signs and symptoms of encephalopathy requiring acute admission to an intensive care unit, was admitted to a ten-bed neurological intensive care unit of a tertiary care hospital. The patient developed consecutive multiple organ dysfunction with rhabdomyolysis, and hepatic and respiratory failure. Temperature elevation was resistant to conventional treatment measures. Aggressive intensive care treatment included forced diuresis and endovascular cooling to combat hyperthermia and maintain normothermia.Analyses of serum revealed elevation of proinflammatory cytokines (TNF alpha, IL-6), cytokines (IL-2R), anti-inflammatory cytokines (IL-4) and chemokines (IL-8) as well as signs of rhabdomyolysis and hepatic failure. Aggressive intensive care treatment as forced diuresis and endovascular cooling (CoolGard? and CoolLine?) to combat hyperthermia and maintain normothermia were used successfully to treat this severe heat stroke.In this case of severe heat stroke, presenting with multiple organ dysfunction and elevation of cytokines and chemokines, which was resistant to conventional cooling therapies, endovascular cooling may have contributed significantly to the reduction of body temperature and, possibly, avoided a fatal result.Heat stroke is a life-threatening disease characterized by hyperpyrexia (elevated core body temperature exceeding 40°C) and predominant central nervous system dysfunction resulting in delirium, convulsion or coma [1]. In many clinical and pathogenetic aspects, heat stroke resembles sepsis, requiring aggressive intensive care treatments, and there is growing evidence that endotoxemia and cytokines may be implicated in its pathogenesis [1-3]. We report a case of severe heat stroke with secondary multiple organ dysfunction being successfully treated with an intravascular cooling device.A 38-year-old male underwent a hiking tour on a hot, humid day in late July 2003. At the end of this
Cardiovascular autonomic function tests in an African population
Malvin Torsvik, Amanda H?ggblom, Geir Eide, Erich Schmutzhard, Kaare Vetvik, Andrea Winkler
BMC Endocrine Disorders , 2008, DOI: 10.1186/1472-6823-8-19
Abstract: We recruited 276 healthy African individuals, 156 men and 120 women, aged > 20 years. Participants were tested for (1) resting heart rate (HR), (2) HR variation in response to deep breathing, (3) HR response to standing, and (4) postural changes in systolic and diastolic blood pressure (SBP and DBP). Respective cut-off values were calculated according to the 95th or 5th percentile.Taking an association of the autonomic test results with gender and age into consideration, we defined the following cut-off values: resting HR (bpm) ≥ 89 for men and ≥ 97 for women; HR (bpm) in response to deep breathing ≤ 13, ≤ 11, ≤ 9, ≤ 8, and ≤ 7 for age groups 20–29, 30–39, 40–49, 50–59, and 60+ years, respectively; HR (bpm) in response to standing ≤ 14 for 20–29 years, and ≤ 11 for 30+ years; postural decreases in SBP ≥ 17 mmHg for all age groups; and postural decreases in DBP (mmHg) ≥ 2 for men and ≥ 5 for women.The test battery revealed cut-off values different from those measured in Caucasians. Further studies are recommended a) to assess whether these cut off values are generally applicable, and b) to establish population specific reference values for Africans.Diabetes mellitus (DM) is increasingly common worldwide. Estimates indicate that the total number of people with DM will more than double from 171 million in 2000 to 366 million in 2030. By 2030, more than 75% of people with DM will live in developing countries. The greatest relative increase is expected to occur in countries in the Middle East, sub-Saharan Africa, and India [1]. DM in these countries is associated with higher mortality rates because of acute and chronic complications that occur early in the course of the disease [2].Peripheral and autonomic diabetic neuropathy (DPN and DAN, respectively) are common chronic complications of DM that occur in nearly half of diabetic patients [3]. DAN in patients with diabetes is an irreversible complication, but early detection is important, because although the condition ca
IgG-index predicts neurological morbidity in patients with infectious central nervous system diseases
Peter Lackner, Elif Guengoer, Ronny Beer, Gregor Broessner, Raimund Helbok, Florian Deisenhammer, Erich Schmutzhard, Bettina Pfausler
BMC Infectious Diseases , 2010, DOI: 10.1186/1471-2334-10-202
Abstract: White blood cell count, CSF/serum glucose ratio, protein, CSF/serum albumin quotient and Immunoglobulin indices for IgG, IgA and IgM were analyzed in 90 patients with bacterial meningitis, 117 patients with viral meningoencephalitis and 36 patients with leptomeningeal metastases in a total of 480 CSF samples.In the initial spinal tap, the IgG-index was the only independent predictor for unfavorable outcome (GOS < 5) in patients with infectious CNS diseases but not in patients with leptomeningeal metastases. The sensitivity and specificity of an IgG-index of 0.75 and higher for predicting unfavorable outcome was 40.9% and 80.8% in bacterial meningitis and 40% and 94.8% in viral meningoencephalitis, respectively. No significant associations between CSF parameters and outcome could be observed in follow-up CSF samples.The present study suggests that in infectious CNS diseases an elevated IgG-Index might be an additional marker for the early identification of patients at risk for neurological morbidity.The clinical course of infectious and neoplastic disorders of the central nervous system is sometimes difficult to predict. While the diagnosis of bacterial meningitis, viral meningitis/meningoencephalitis and leptomeningeal metastases (LM) mainly relies on the analysis of cerebrospinal fluid (CSF), only limited data on the prognostic value of CSF parameters exist [1]. Yet, initial risk assessment of individual patients is of paramount importance in order to choose the appropriate level of further surveillance (i.e. general ward versus critical care unit) [2]. Of course, clinical presentation is one of the most important issues in this respect [3]. This has been shown by different authors and complex scores have been developed in order to raise the predictive accuracy of clinical signs and symptoms [2,4-7]. In addition, other studies have tried to assess the role of imaging techniques such as computed tomography or transcranial Doppler sonography [8,9]. Despite these impr
Antibodies to myelin oligodendrocyte glycoprotein in HIV-1 associated neurocognitive disorder: a cross-sectional cohort study
Peter Lackner, Bettina Kuenz, Markus Reindl, Maria Morandell, Thomas Berger, Erich Schmutzhard, Christian Eggers
Journal of Neuroinflammation , 2010, DOI: 10.1186/1742-2094-7-79
Abstract: IgG antibodies against MOG were measured by ELISA in sera and cerebrospinal fluid (CSF) of 65 HIV-positive patients with HAND (n = 14), cerebral opportunistic infections (HIVOI, n = 25), primary HIV infection (HIVM, n = 5) and asymptomatic patients (HIVasy, n = 21). As control group HIV-negative patients with bacterial or viral CNS infections (OIND, n = 18) and other neurological diseases (OND, n = 22) were included. In a subset of HAND patients MOG antibodies were determined before and during antiviral therapy.In serum, significantly higher MOG antibody titers were observed in HAND compared to OND patients. In CSF, significantly higher antibody titers were observed in HAND and HIVOI patients compared to HIVasy and OND patients and in OIND compared to OND patients. CSF anti-MOG antibodies showed a high sensitivity and specificity (85.7% and 76.2%) for discriminating patients with active HAND from asymptomatic HIV patients. MOG immunopositive HAND patients performed significantly worse on the HIV dementia scale and showed higher viral load in CSF. In longitudinally studied HAND patients, sustained antibody response was noted despite successful clearance of viral RNA.Persistence of MOG antibodies despite viral clearance in a high percentage of HAND patients suggests ongoing neuroinflammation, possibly preventing recovery from HAND.HIV encephalopathy (HIVE) leads to dementia and motor disorder and is the major direct central nervous system (CNS) manifestation of advanced HIV-1 infection. Since the availability of combination antiretroviral therapy (cART) its incidence has decreased, but to a lesser extent than the incidence of extra-cerebral AIDS-manifestations [1]. With the increasing life expectancy of HIV-infected individuals the prevalence of HIV associated neurocognitive disorder (HAND) has risen to 20-50% [2]. While it is generally accepted that HAND is treatable, the extent and sustainability of the effects of cART on cerebral functioning are still unclear. Ther
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