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Biomedical subjects

S Schwab

Publications and source records attributed to S Schwab.

At least 91 records · Page 5Linked to original sources
PubMed1999

Stroke--a medical emergency.

Acute ischaemic stroke as an urgent-to-treat condition has gained a more prominent role in the consciousness of emergency physicians and neurologists over the past decade. This is mainly due to an increasing insight into the pathophysiological mechanism of ischaemia, the definition of therapeutical goals, such as reperfusion or neuroprotection, and the recent application of respective treatment strategies in large multicentre studies. This review article will focus on the emergency assessment of stroke patients, on general treatment strategies, and particularly on specific measures of intensive care therapy of stroke including thrombolysis, decompressive surgery, hypothermia and treatment of brain oedema.

Adult↗
PubMed1999

[Therapy of increased intracranial pressure in space-occupying media infarcts].

Following complete middle cerebral artery (MCA) infarction, up to 10% of all patients develop space-occupying brain edema. Despite intensive care therapy, 80% of these patients die due to transtentorial herniation. Over the past years, two alternative therapeutical options for the therapy of space-occupying MCA infarction have been developed. Decompressive surgery effectively decreases ICP and helps to improve outcome of these patients. Mortality can be reduced from 80% to less than 20%. Moderate hypothermia induced within the first hours after stroke has been shown to decrease ICP as well. However, the routine use of this therapy should not be recommended since further clinical studies are available. Knowledge on indications and limitations of different antiedema therapies will allow an effective therapy of increased ICP.

Brain Edema↗
PubMed1998

Manganese augments nitric oxide synthesis in murine astrocytes: a new pathogenetic mechanism in manganism?

Since manganese (Mn2+) is known to be sequestered in glial cells, we investigated possible neurotoxic mechanisms involving astrocytes in vitro. Low concentrations of Mn2+ were toxic only in astrocyte-neuronal cocultures but not in pure astrocyte or neuronal cultures. As a possible mediator of manganese-derived neurotoxicity, we measured the production of nitric oxide in astrocytes. Manganese, but not other transition metals, dose dependently increased iNOS mRNA and protein levels and the release of nitric oxide in activated astrocytes. This effect was specific for astrocytes, since we observed no stimulation in microglial cells. The observations suggest that besides the known inhibition of mitochondrial function the neurotoxic effect of manganese in low concentrations might be mediated by the increased production of nitric oxide in astrocytes.

Animals↗
PubMed1998

Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction.

Elevated temperature is known to facilitate neuronal injury after ischemia. After head injury a gradient between temperature and body temperature of up to 3 degrees C higher in the brain has been reported. Hypothermia may limit some of the deleterious metabolic consequences of such increased temperature. In 20 patients who had suffered severe ischemic stroke in the middle cerebral artery (MCA) territory, intracerebral temperature combined with ICP monitoring was recorded using two different thermocouples, with epidural, and parenchymatous measurements. Mild hypothermia was induced using cooling blankets. Patients were kept at 33 degrees C core temperature for 48 to 72 hours. In all patients brain temperature exceeded body-core temperature by at least up to 1 degree C (range 1.0-2.1 degrees C). Systemic cooling was effective and sustained hypothermic (33-34 degrees C) brain temperatures. With mild hypothermia critically elevated ICP values could be controlled. 12 patients survived the hemispheric stroke with a mean Barthel index of 70. Severe side effects of hypothermia were not detected. After MCA stroke, human intracerebral temperature is higher than central body-core temperature. Mild hypothermia in the treatment of severe cerebral ischemia using cooling blankets is safe and does not lead to severe side effects. Mild hypothermia can help to control critically elevated ICP values in severe space-occupying stroke and may improve clinical outcome in these patients.

Adult↗
PubMed1998

["Paradoxical" herniation after decompressive trephining].

The intracranial space is divided into two large compartments by the tentorium. The hydrostatic pressure of spinal fluid is responsible for buoyancy of the brain within these compartments. In patients with craniectomy this equilibrium is exposed to atmospheric pressure. We report on four cases of reversible herniation after either bilateral or unilateral decompressive craniectomy performed for increased intracranial pressure (ICP) and failure of conservative ICP treatment. All four patients had survived a severe neurological disease (encephalitis, subdural haematoma, stroke) which required craniectomy to control raised ICP. All were successfully weaned from the ventilator and awake and CT scans showed no space-occupying lesion anymore. The patients showed a typical "sunken pattern" at the trepanation site. All patients developed clinical signs of transtentorial herniation (i.e. unilateral dilated pupils, deteriorated alertness, and extensor posturing) shortly after either diagnostic or presumed therapeutic lumbar puncture. One patient developed herniation a second time while in the typical 30 degrees upright position. After craniectomy, transtentorial herniation is possible even in the absence of increased ICP. It is related to a negative gradient between atmospheric and intracranial pressure, which is enhanced by changes in the CSF compartment following lumbar puncture. Lumbar puncture should be avoided if possible and, when necessary, only be performed in the head-down position. Acute therapy in these cases is quite simple; it requires flat or even head-down positioning and early cranioplasty.

Adult↗
PubMed1998

[Hyperbaric oxygen therapy (HBO) after acute focal cerebral ischemia].

For a large number of patients with stroke no therapeutic option can be offered, even after approval of thrombolytic therapy for treatment of acute ischemic stroke in the US. In cerebral ischemia local anoxia and energy failure lead to further cellular damage and finally to complete stroke. All therapeutic concepts try to salvage structurally intact tissue which is at risk for irreversible damage (so-called penumbra). Hyperbaric oxygen (HBO) treatment has been reported in animal models of cerebral ischemia, and in a few clinical reports. In general, the results of these studies have been promising. This review focuses on the clinical perspective of HBO therapy and summarizes both the clinical and experimental data available on HBO therapy following ischemic stroke.

Acute Disease↗
PubMed1998

Acute ischaemic stroke: revascularizing therapy. Stroke Council of the American Heart Association.

The principal goals of thrombolytic therapy for stroke are early restitution of cerebral blood flow, reduction of ischaemia, and attenuation of neurological disability through lysis of an occluding thrombus and consequent rapid restoration of circulation in the affected territory. Therapy should be initiated as soon as possible, at least within 4-6 h of stroke onset, to prevent major infarction and to salvage the hypoperfused but potentially viable zone adjacent to the central ischaemic area known as the ischaemic penumbra. This survey focuses on the safety and efficacy of thrombolytic therapy in acute ischaemic stroke in clinical trials. The results of two successful major randomized studies using tissue plasminogen activator (t-PA) were recently published. Intravenous thrombolysis seemed to be effective in improving functional and neurological outcome in a clearly defined subgroup of patients meeting the inclusion criteria of the studies. However, the identification of those patients proved to be difficult and depended on expertise in recognizing the early infarction signs on initial computed tomography. Since treating ineligible patients is associated with an unacceptable risk of intracranial bleeding complications and death, intravenous thrombolysis should only be performed at selected centres in selected patients.

Cerebral Revascularization↗
PubMed1998

Reoxygenation increases the release of reactive oxygen intermediates in murine microglia.

Respiratory burst activity of murine microglial cells was investigated in vitro under normoxic and hypoxic conditions with a chemoluminometric assay. Hypoxia for 24 hours reduced the release of extracellular reactive oxygen intermediates (ROIs), whereas reoxygenation increased the chemoluminescence more than sevenfold. Blockade of potassium channels inhibited the increase of oxidative burst after reoxygenation, indicating that potassium ions, which were increased in the supernatant of hypoxic microglial cells, were involved in this activation process. Also, blockade of voltage-gated calcium channels with nifedipine attenuated the increased release of ROIs. With fura-2 analysis, it was shown that the activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase by potassium ions was mediated by calcium influx via voltage-gated calcium channels. Thus, influx of calcium ions through voltage-gated channels activates the NADPH oxidase in microglial cells during reoxygenation. By the increased production of ROIs, microglial cells may add to the reperfusion injury after ischemia in vivo.

Animals↗
PubMed1998

Secondary hemorrhage after intraventricular fibrinolysis: a cautionary note: a report of two cases.

OBJECTIVE AND IMPORTANCE: To hasten the lysis of intraventricular hemorrhages, intraventricular administration of recombinant tissue plasminogen activator (rt-PA) or urokinase has been advocated as an effective and safe treatment for patients with intraventricular hemorrhage. Until now, cases of secondary hemorrhage after intraventricular fibrinolysis, to our knowledge, have not been reported in the literature. We present a report of two patients with clinically significant bleeding complications associated with intraventricular infusion of rt-PA. CLINICAL PRESENTATION: Both patients, a 42-year-old woman (Patient 1) and a 70-year-old man (Patient 2), suffered from hypertensive left-sided thalamic hemorrhage with ventricular extension and ventricular dilatation. INTERVENTION: Both patients required external ventricular drainage and were treated with intraventricular rt-PA. In Patient 1, a secondary intraventricular hemorrhage occurred 20 minutes after the first instillation of 2 mg of rt-PA and was associated with a sudden loss of consciousness. Treatment with rt-PA was stopped, and the patient needed a permanent shunt. In Patient 2, intraventricular subsequent bleeding was noted 4 hours after the second 4-mg dose of rt-PA, clinically apparent as anisocoria. In Patient 2, rt-PA administration was continued without further complications. In both patients, a second external ventricular drainage was required after secondary hemorrhage. CONCLUSION: Intraventricular lysis is a potentially hazardous therapy. To weigh the potential benefits against the potential risks, a controlled study of this promising new treatment is urgently warranted.

Adult↗
PubMed1998

Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Animal research and clinical studies in head trauma patients suggest that moderate hypothermia may improve outcome by attenuating the deleterious metabolic processes in neuronal injury. Clinical studies on moderate hypothermia in the treatment of acute ischemic stroke patients are still lacking. METHODS: Moderate hypothermia was induced in 25 patients with severe ischemic stroke in the middle cerebral artery (MCA) territory for therapy of postischemic brain edema. Hypothermia was induced within 14+/-7 hours after stroke onset and achieved by external cooling with cooling blankets, cold infusions, and cold washing. Patients were kept at 33 degreesC body-core temperature for 48 to 72 hours, and intracranial pressure (ICP), cerebral perfusion pressure, and brain temperature were monitored continuously. Outcome at 4 weeks and 3 months after the stroke was analyzed with the Scandinavian Stroke Scale (SSS) and Barthel index. The side effects of induced moderate hypothermia were analyzed. RESULTS: Fourteen patients survived the hemispheric stroke (56%). Neurological outcome according to the SSS score was 29 (range, 25 to 37) 4 weeks after stroke and 38 (range 28 to 48) 3 months after stroke. During hypothermia, elevated ICP values could be significantly reduced. Herniation caused by a secondary rise in ICP after rewarming was the cause of death in all remaining patients. The most frequent complication of moderate hypothermia was pneumonia in 10 of the 25 patients (40%). Other severe side effects of hypothermia could not be detected. CONCLUSIONS: Moderate hypothermia in the treatment of severe cerebral ischemia is not associated with severe side effects. Moderate hypothermia can help to control critically elevated ICP values in severe space-occupying edema after MCA stroke and may improve clinical outcome in these patients.

Adult↗
PubMed1998

Effects of hypertonic saline hydroxyethyl starch solution and mannitol in patients with increased intracranial pressure after stroke.

BACKGROUND AND PURPOSE: The purpose of this study was to prospectively evaluate a protocol with hypertonic saline hydroxyethyl starch (HS-HES) and mannitol in stroke patients with increased intracranial pressure (ICP). METHODS: We studied 30 episodes of ICP crisis in 9 patients. ICP crisis was defined as (1) a rise of ICP of more than 25 mm Hg (n = 22), or (2) pupillary abnormality (n=3), or (3) a combination of both (n=5). Baseline treatment was performed according to a standardized protocol. For initial treatment, the patients were randomly assigned to either infusion of 100 mL HS-HES or 40 g mannitol over 15 minutes. For repeated treatments the 2 substances were alternated. ICP, blood pressure, and cerebral perfusion pressure (CPP) were monitored over 4 hours. Blood gases, hematocrit, blood osmolarity, and sodium were measured before and 15 and 60 minutes after the start of infusion. Treatment was regarded as effective if ICP decreased >10% below baseline value or if the pupillary reaction had normalized. RESULTS: Treatment was effective in all 16 HS-HES-treated and in 10 of 14 mannitol-treated episodes. ICP decreased from baseline values in both groups, P < 0.01. The maximum ICP decrease was 11.4 mm Hg (after 25 minutes) in the HS-HES-treated group and 6.4 mm Hg (after 45 minutes) in the mannitol-treated group. There was no constant effect on CPP in the HS-HES-treated group, whereas CPP rose significantly in the mannitol-treated group. Blood osmolarity rose by 6.2 mmol/L in the mannitol-treated group and by 10.5 mmol/L in the HS-HES-treated group; sodium fell by 3.2 mmol/L in the mannitol and rose by 4.1 mmol/L in the HS-HES-treated group. CONCLUSIONS: Infusion of 40 g mannitol and 100 mL HS-HES decreases increased ICP after stroke. The maximum effect occurs after the end of infusion and is visible over 4 hours. HS-HES seems to lower ICP more effectively but does not increase CPP as much as does mannitol.

Adult↗
PubMed1998

Early hemicraniectomy in patients with complete middle cerebral artery infarction.

BACKGROUND AND PURPOSE: Malignant, space-occupying supratentorial ischemic stroke is characterized by a mortality rate of up to 80%. Several reports indicate a beneficial effect of hemicraniectomy in this situation. However, whether and when decompressive surgery is indicated in these patients is still a matter of debate. METHODS: In an open, prospective trial we performed hemicraniectomy in 63 patients with acute complete middle cerebral artery infarction. Initial clinical presentation was assessed by the Scandinavian Stroke Scale (SSS) and the Glasgow Coma Scale (GCS). All survivors were reexamined 3 months after surgical decompression, with the clinical evaluation graded according to the Rankin Scale (RS) and Barthel Index (BI). We analyzed the influence of early decompressive surgery (<24 hours after symptom onset, based on clinical status at admission and initial CT findings) versus late surgery (>24 hours after first reversible signs of herniation) on mortality, functional outcome, and the length of time of critical care therapy was needed. RESULTS: In total, 46 patients (73%) survived. Despite complete hemispheric infarction, no survivor suffered from complete hemiplegia or was permanently wheelchair bound. In patients with speech-dominant hemispheric infarction (n=11), only mild to moderate aphasia was present. The mean BI score was 65, and RS score revealed severe handicap in 13% of the patients. In 31 patients with early decompressive surgery, mortality was 16% and BI score 68.8. Early hemicraniectomy led to a significant reduction in the length of time critical care therapy was needed (7.4 versus 13.3 days, P<0.05). CONCLUSIONS: In general, the outcome of patients treated with craniectomy in severe ischemic hemispheric infarction was surprisingly good. In addition, early decompressive surgery may further improve outcome in these patients.

Adult↗
PubMed1998

[Psychosocial impact of the first oncogenetic consultation in a familial context of cancers of the breast and the ovary].

The purpose of the oncogenetic consultation, is to respond to persons who wonder about their risk of developing a tumour and wish to learn about ways of prevention and detection. The object of this investigation is (1) to study the impact of a first consultation in genetics on the quality of life and the psychology of women with a family history of cancer, and women with or without family antecedents but who suffered themselves from breast cancer at an early age (< or = 35 years); (2) to evaluate their risk perception and their comprehension of the information after the consultation. The study was performed on 200 women attending a first consultation at Institut Curie. Fifty-nine of them had no cancer. Among the 141 consultants with cancer, 54 had developed breast cancer at an early age (< or = 35 years). Their quality of life, their psychological state and their knowledge of the risk of breast tumour were evaluated before consulting and 6-8 months afterwards. Before consulting, their quality of life was altered in some (non-relational) fields but their psychic condition was relatively maintained. Six-nine months after consulting, their quality of life had not deteriorated, but tests results on their psychological state were not as good. The initial psychic condition, itself related to the medical status of the consulting women, was the most significant predictor of their quality of life a few months after their first genetics consultation. After consulting, the women expressed satisfaction with the information delivered by the genetician and their appreciation of tumour risks was improved.

Adult↗
PubMed1998

[Follow-up monitoring with magnetic resonance tomography after decompressive trephining in experimental "malignant" hemispheric infarct].

Acute ischemia in the complete territory of the carotid or the middle cerebral artery may lead to cerebral edema with raised intracranial pressure and progression to coma and death. Although clinical data suggest benefit for patients undergoing decompressive surgery for massive space occupying hemispheric stroke, little data about the effects of this procedure on morbidity and outcome is available. The experimental data support an early surgical approach. For early and probably most effective treatment of severe, space-occupying cerebral ischemia, the "malignant" character of the brain edema has to be recognized early after onset of vessel occlusion. Hereby magnetic resonance imaging (MRI) may allow to determine the clinical significance of brain edema early after onset, simultaneously allowing to monitor the evolution of ischemia. We performed serial SE-MRI in rats with acute hemispheric infarctions treated by decompressive craniectomy. Focal cerebral ischemia was induced in 36 rats using an endovascular occlusion technique. Decompressive craniectomy was performed 4 and 24 hours after vessel occlusion in groups of 12 animals each. Twelve animals were not treated by decompressive craniectomy (control group). Four, 24, 48, 72 and 168 hours after MCAO all animals were examined with conventional T1- and T2-weighted SE-MRI. Shift of the midline structures and compression of the ventricles were scored. Changes in weight and neurological performance were measured daily. The infarction volume was calculated by triphenyltetrazolium chloride staining 168 hours after MCAO. While mortality in the untreated group was 33.3%, none of the animals treated by a decompressive craniectomy died (mortality 0%). Neurological behaviour, weight loss and infarction volume were significantly better in the animals treated by early decompressive craniectomy (p < 0.05). Four hours after MCAO all untreated animals showed a massive shift of the midline structures and a massive compression of the ventricles; only 7 of 12 animals treated early by craniectomy showed mild mass effects. Correlation of the histological brain damage with T2-weighted MRI 4 hours after MCAO was poor (r = 0.41); later than 24 hours there was a good correlation (r > 0.7). Our results suggest that decompressive craniectomy in malignant cerebral ischemia reduces mortality and significantly improves outcome. If performed early after vessel occlusion, it also significantly reduces infarction size. In the acute phase of hemispheric infarction conventional SE-MRI is not sensitive in estimation of infarction size. Later than 24 hours, conventinal SE-MRI proved to be useful in monitoring brain edema and infarction size in this rat model of malignant hemispheric stroke.

Animals↗
PubMed1997

[Therapeutic possibilities in acute cerebral ischemia].

Therapy for acute ischemic stroke includes general care of the stroke patient including respiratory and cardiac care, as well as fluid and electrolyte management, blood pressure control and metabolic monitoring. More specific treatment is directed to recanalization of the occluded brain vessel. In this article special emphasis is laid on the indications and use of thrombolytic therapy. Furthermore current concepts in the intensive care of patients with severe brain edema are discussed.

Acute Disease↗
PubMed1997

Hemicraniectomy with dural augmentation in medically uncontrollable hemispheric infarction.

Surgical decompression to alleviate raised intracranial pressure has been reported repeatedly in the past decades in small series of patients. Only recently have there been indications from larger trials that surgical decompression may be beneficial in treating space-occupying hemispheric infarction. However, surgical requirements for the procedure to be effective have not yet been defined. Based on theoretical criteria, the authors operated on 43 patients with medically uncontrollable hemispheric infarctions. The craniectomies were planned to be as large as possible and performed in combination with a subtemporal decompression. Postoperative computerized tomography scans were evaluated for these criteria. The mean survival rate for the group of 43 patients was 72.1% and no surviving patient ended up in a vegetative state. The mean area of craniectomy was found to be 84.3 +/- 16.5 cm2 and the mean distance of the inferior craniectomy margin to the middle fossa was 1.8 +/- 1.3 cm. Comparison of survivors and nonsurvivors failed to show a significant difference in the size of craniectomy or the distance to the floor of the middle fossa. Compared with the reported 80% fatality rate for medically treated stroke patients, in this subgroup the outcome (72.1% survival rate) is remarkably good. The authors conclude that decompressive craniectomy is an effective treatment, able to reduce mortality, and to improve neurological outcome in patients with space-occupying cerebral infarction if the size of craniectomy is large enough. Nevertheless, there is a need for further investigation to identify patients who will benefit from surgery and predictors to optimize the timing of surgical intervention.

Journal Article↗
PubMed1997

Suppression of the oxidative burst in murine microglia by nitric oxide.

The effect of nitric oxide (NO) on the oxidative burst was analyzed in purified murine microglial cells in vitro. The generation of reactive oxygen derivatives was monitored with the use of luminol-dependent chemiluminescence. After inducing the endogenous NO production with interleukin 1beta (IL-1beta) and interferon-gamma (IFN-gamma) the superoxide anion release was significantly reduced, which was reversed by the inhibition of the NO synthase. Additionally, chemical NO-releasing compounds reduced the generation of reactive oxygen derivatives rapidly and independently of the pathway used to trigger the oxidative burst. This effect of NO was not mediated via guanylyl cyclase and cGMP, or due to the scavenging of released superoxide anions. This attenuation of superoxide anion generation by NO may limit deleterious effects of the release of reactive oxygen derivatives in tissue inflammation or injury.

Animals↗