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S Schwab

Publications and source records attributed to S Schwab.

At least 109 records · Page 6Linked to original sources
PubMed1997

[Infection: impaired consciousness as the initial symptom. Clinical and pathophysiologic aspects of septic encephalopathy].

Septic encephalopathy (SE) is present in up to 70% of all patients with sepsis. In some cases, SE may proceed other parameters of sepsis. Loss of consciousness to a various extent is the leading symptom. CSF findings and CCT are usually unremarkable. EEG is a sensitive parameter to monitor SE. EEG-changes deteriorate in correspondence to the degree of SE. If sepsis can be treated successfully, clinical and electrophysiological signs are completely reversible. SE has a complex etiology. Bacterial endotoxins and other microbial products trigger the release of a multitude of mediators of sepsis. Due to liver dysfunction in sepsis, the brain neurotransmitter profile may be deranged. Other etiological factors include bacteriemia, liver or renal dysfunction, fluid and electrolyte imbalance, hypoglycemia and drug effects. Due to the prognostic significance of early adequate treatment, recognition of SE as a possible initial sign may be crucial for patients with sepsis.

Aged↗
PubMed1997

[Neurogenic disorders of heart and lung function in acute cerebral lesions].

Incidence and clinical significance of cardiopulmonary complications of acute cerebral lesions are still unclear. Neurogenic pulmonary edema (NPE) is characterized as an acute, protein-rich lung edema occurring shortly after cerebral lesions associated with an acute rise of intracranial pressure. NPE is infrequently diagnosed, usually in association with head trauma. Pathophysiological mechanisms include a rise of the pulmonary vascular hydrostatic pressure either due to sympathetic innervation with pulmonary vasoconstriction or increased left-atrial pressure following systemic arterial hypertension or an increase in pulmonary capillary permeability. In contrast to NPE, cardiac complications are frequently observed, most consistently in patients with subarachnoid hemorrhage. Typical ECG changes are repolarization abnormalities, similar to those observed in coronary heart disease, and cardiac arrhythmias. The CK-MB may be slightly elevated; echocardiographic findings show a depressed left-ventricular function. Pathological examination reveals myofibrillar necrosis. Cardiac complications are explained with overactivity of the sympathetic innervation and high levels of circulating catecholamines. For adequate treatment, close cardiac monitoring is required in all patients with acute cerebral lesions.

Arrhythmias, Cardiac↗
PubMed1997

Intraventricular brain-derived neurotrophic factor reduces infarct size after focal cerebral ischemia in rats.

Brain-derived neurotrophic factor (BDNF), acting through the high-affinity receptor tyrosine kinase (TrkB), is widely distributed throughout the central nervous system and displays in vitro trophic effects on a wide range of neuronal cells, including hippocampal, cerebellar, and cortical neurons. In vivo, BDNF rescues motorneurons, hippocampal, and substantia nigral dopaminergic cells from traumatic and toxic brain injury. After transient middle cerebral artery occlusion (MCAO), upregulation of BDNF-mRNA in cortical neurons suggests that BDNF potentially plays a neuroprotective role in focal cerebral ischemia. In the current study, BDNF (2.1 micrograms/d) in vehicle or vehicle alone (controls) was delivered intraventricularly for 8 days, beginning 24 hours before permanent middle cerebral artery occlusion by intraluminal suture in Wistar rats (n = 13 per group). There were no differences in physiological variables recorded during surgery for the two groups. Neurological deficit (0 to 4 scale), which was assessed on a daily basis, improved in BDNF-treated animals compared with controls (P < 0.05; analysis of variance and Scheffe's test). There were no significant differences in weight in BDNF-treated animals and controls during the experiment. After elective killing on day 7 after MCAO, brains underwent 2,3,5-triphenyltetrazolium chloride staining for calculation of the infarct volume and for histology (hematoxylin and eosin and glial fibrillary acid protein). The mean total infarct volume was 83.1 +/- 27.1 mm3 in BDNF-treated animals and 139.2 +/- 56.4 mm3 in controls (mean +/- SD; P < 0.01, unpaired, two-tailed t-test). The cortical infarct volume was 10.8 +/- 7.1 mm3 in BDNF-treated animals and 37.9 +/- 19.8 mm3 in controls (mean +/- SD; P < 0.05; unpaired, two-tailed t-test), whereas ischemic lesion volume in caudoputaminal infarction was not significantly different. These results show that pretreatment with intraventricular BDNF reduces infarct size after focal cerebral ischemia in rats and support the hypothesis of a neuroprotective role for BDNF in stoke.

Animals↗
PubMed1997

The htpG gene of Bacillus subtilis belongs to class III heat shock genes and is under negative control.

We show that the htpG gene of Bacillus subtilis is induced by heat, as has been reported for the Escherichia coli homolog. Analysis of different mutants revealed that the htpG gene belongs to class III heat shock genes in B. subtilis. An about 10-fold induction after thermal upshock was found at the levels of both transcription and translation, and this induction resulted from enhanced synthesis of mRNA. By primer extension, we identified one potential transcription start site immediately downstream of a putative sigmaA-dependent promoter which became activated after thermal upshift. Northern blot analysis revealed that htpG is part of a monocistronic transcriptional unit. An operon fusion where the complete region between htpG and its upstream gene was fused to the bgaB reporter gene accurately reflected htpG expression. Analysis of this fusion revealed that, in contrast to other class III heat shock genes, htpG was not induced by osmotic upshock, by ethanol, or by oxygen limitation, suggesting that it belongs to a subgroup within class III. Deletion of the region upstream of the putative promoter resulted in an enhanced basal level of htpG expression, but the 10-fold induction was retained, suggesting that the upstream sequences are involved in the regulation of expression in the absence of heat shock.

Bacillus subtilis↗
PubMed1997

Superoxide dismutase activity in serum of patients with acute cerebral ischemic injury. Correlation with clinical course and infarct size.

BACKGROUND AND PURPOSE: Superoxide dismutase (SOD) is one of the major free radical scavenging systems that might play a role in both degenerative and acute diseases of the central nervous system. METHODS: We measured SOD activity in the serum of 41 patients with acute ischemic stroke with a chemiluminometric assay based on the generation of oxygen free radicals by xanthine and xanthine oxidase. RESULTS: SOD activity was significantly lower in patients with ischemic stroke than in age-matched control patients with nonvascular, neurological illnesses (n = 24; P < .034, Wilcoxon rank test). The activity was inversely correlated with the size of infarction on CT (P = .01, Spearman correlation) and the severity of neurological deficits (P < .001, Spearman correlation). The decreased SOD activity recovered within 5 days after stroke to values found in serum of control patients. CONCLUSIONS: Our data suggest that the SOD activity in serum is reduced in stroke patients, and replacement of antioxidative activity could be beneficial in the acute treatment of cerebral ischemia.

Acute Disease↗
PubMed1997

Plasma insulin-like growth factor I and IGF binding protein 3 levels in patients with acute cerebral ischemic injury.

BACKGROUND AND PURPOSE: The insulin-like growth factors (IGF) are synthesized in the brain and are involved in fetal brain development. An increased expression of IGF-I and IGF-II occurs in cerebral regions with neuronal damage after experimental hypoxic injury. Furthermore, the expression of mRNAs coding for IGF-I and the binding proteins IGFBP-2 and IGFBP-3 is augmented in response to unilateral ischemia in animal models. The secretory dynamics of IGF-I in human cerebral ischemia have not yet been investigated. METHODS: Plasma IGF-I and IGFBP-3 were measured sequentially in 20 patients with acute ischemic stroke (within 24 hours and 3, 5, and 10 days thereafter). For analysis the patients were assigned to three groups according to the diameter of the infarct area as measured on CT scan: small (< 1.5 cm), moderate (> or = 1.5 cm and < or = 5 cm), and large (> 5 cm). Eight age-matched patients with nonvascular, neurological illnesses served as controls. RESULTS: Plasma IGF-I and IGFBP-3 plasma concentrations after acute cerebral ischemia were strikingly lower than those in control subjects and healthy individuals reported in the literature. Plasma IGF-I levels in patients with large infarcts were significantly statistically lower than those in control subjects (P < .05), and plasma IGFBP-3 levels were significantly lower than those in control subjects on days 5 and 10. CONCLUSIONS: IGF-I and IGFBP-3 plasma levels are decreased in patients after cerebral ischemia. After acute ischemic stroke, increased demand for growth factors, altered tissue distribution, and accelerated metabolic clearance rate or central inhibition of the somatotrophic axis may contribute to these low plasma concentrations. Growth factors such as IGF-I and IGFBP-3 may play an important role in the pathophysiology of acute cerebral ischemia, and growth factors may have a considerable effect on future therapeutic regimens.

Acute Disease↗
PubMed1997

Meningeal involvement in Wegener's granulomatosis confirmed and monitored by positive circulating antineutrophil cytoplasm in cerebrospinal fluid.

MRI and CSF investigations revealed meningeal involvement in a 29-year-old patient with biopsy-confirmed Wegener's granulomatosis. The intracranial manifestation of Wegener's granulomatosis was supported by the detection of pathologic circulating antineutrophil cytoplasm (c-ANCA) in the CSF. We monitored disease activity by c-ANCA measurement in the CSF. After repeated cycles of intrathecal administration of methotrexate and corticoids, progression of meningeal infiltration stopped, and CSF c-ANCA titers became negative.

Adult↗
PubMed1997

Craniectomy: an aggressive treatment approach in severe encephalitis.

BACKGROUND AND OBJECTIVE: Focal encephalitis may be associated with brain edema, which is often fatal. The control of intracranial pressure (ICP) is therefore crucial for further therapeutic strategies in space-occupying edema following encephalitis. However, aggressive treatment strategies such as hemicraniectomy have not been described in a larger series of patients. PATIENTS AND METHODS: We describe the clinical course and outcome in six patients who developed severe brain edema associated with acute encephalitis. All received maximum medical treatment for elevated ICP, but with signs of brainstem compression emerging, hemicraniectomy was performed to control ICP. RESULTS: All patients had a very severe encephalitic syndrome and were treated over the course of weeks in the neurocritical care unit (NCCU). However, all patients recovered almost completely and showed only mild or no neurologic deficit when reexamined after 4 months to 3 years. CONCLUSIONS: Hemicraniectomy should be considered in patients with severe brain edema following encephalitis as a potentially lifesaving therapeutic measure. Moreover, the initial neurologic deficit seems to have no impact on the long-term clinical outcome.

Adult↗
PubMed1997

Brain temperature monitoring and modulation in patients with severe MCA infarction.

BACKGROUND: Brain temperature has been measured only occasionally in humans. After head trauma, a temperature gradient in brain temperature compared with body temperature of up to 3 degrees C degrees higher in the brain has been reported. Elevated temperature facilitates neuronal injury after ischemia. At present, no information concerning changes in brain temperature after acute stroke is available. METHODS: In 15 patients who had suffered severe ischemic stroke in the MCA territory, intracerebral temperature was recorded with use of two different thermocouples, with intraventricular, epidural, and parenchymatous measurements. Body-core temperature (Foley catheter temperature) and jugular bulb temperature (n = 5) were recorded simultaneously. Measures for reducing brain temperature were compared. RESULTS: In all patients, brain temperature exceeded body-core temperature by at least up to 1 degrees C (range, 1.0 to 2.1 degrees C). Temperature in the ventricles exceeded epidural temperature by up to 2.0 degrees C. Brain temperature modulation was independent of single pharmacologic (paracetamol, metamizol) treatments. Only systemic cooling was effective and sustained hypothermic (33 to 34 degrees C) brain temperatures. CONCLUSION: After MCA stroke, human intracerebral temperature is higher than central body-core temperature. There is also a temperature gradient within the brain, with the ventricles warmer than the surface. Mild hypothermia in the treatment of severe cerebral ischemia with use of cooling blankets is both easy to perform and effective in the therapy of severe hemispheric infarction.

Adult↗
PubMed1997

Barbiturate coma in severe hemispheric stroke: useful or obsolete?

Barbiturates are administered in a variety of clinical conditions to control elevated intracranial pressure (ICP). However, their routine use to treat elevated ICP has been questioned because it may cause severe side effects. We therefore investigated the effect of high-dose barbiturate therapy on ICP and outcome in patients with severe brain edema after severe middle cerebral artery (MCA) or hemispheric infarction. Barbiturate coma was induced with thiopental infusion in 60 patients with critically increased ICP due to large hemispheric or MCA territory infarction, defined by CT. ICP was monitored in all patients during barbiturate therapy. Barbiturate coma was induced after a standardized treatment protocol for increased ICP after failure of osmotherapy and mild hyperventilation. During barbiturate administration, cerebral perfusion pressure (CPP) and mean arterial pressure were recorded. Clinical outcome of these patients and the individual effect on ICP were analyzed. Only five of 60 patients who were treated with barbiturate coma survived (8%). All other patients died after transtentorial herniation with subsequent brain death. Barbiturate infusion was followed by a drop in ICP in 50 patients and showed no effect on ICP values in 10 patients. CPP decreased with a mean of 9 mm Hg (range, 5 to 20 mm Hg). Although barbiturates were initially effective, only in some patients was ICP control sustained. Severe side effects of barbiturate therapy, besides arterial hypotension, were seen in 15 patients (25%). Barbiturate coma in the therapy of increased ICP after severe ischemic hemispheric stroke can lower critically elevated ICP levels. However, it seems to have no positive effect on neurologic outcome.

Adult↗
PubMed1997

Basilar artery embolism. Clinical syndrome and neuroradiologic patterns in patients without permanent occlusion of the basilar artery.

The objective of this study was to clarify the clinical and radiologic features, risk factors, and prognosis of basilar embolism without permanent basilar artery occlusion. Forty-five patients (mean age, 59 years) with basilar artery embolism participated in the study. Patients with basilar artery occlusion were excluded. The Glasgow Coma Scale (GCS) score on admission was < 7 in five patients, 7 to 12 in 11 patients, and > 12 in 29 patients. Etiologic factors were cardiac arrhythmia (17 patients), vertebral artery occlusion (12 patients), cervical spine trauma (4 patients), embolism following angiography (2 patients), and surgery (1 patient). MRI was performed in 17 patients and CT in 39 patients. Radiologic examinations were initially normal in 14 patients and remained normal in three patients. Final infarct localization was the thalamus (36 patients), cerebellum (20 patients), posterior cerebral artery territory (21 patients), midbrain (12 patients), and pons (8 patients). Eight to 12 weeks after stroke 12 patients were without clinical signs (Glasgow Outcome Scale [GOS] 1), 15 patients had minor neurologic deficits (GOS 2), 10 were severely disabled (GOS 3), and eight patients had died (GOS 5). Outcome correlated with GCS on admission (p < 0.0001) and with the number of ischemic lesions (p = 0.0001). The typical syndrome is an acute loss of consciousness followed by multiple brainstem symptoms. Usually, clinical symptoms improve rapidly and, in some patients, completely. Compared with basilar occlusion, basilar embolism has a relatively low mortality and outcome is frequently excellent.

Adult↗
PubMed1996

'Malignant' middle cerebral artery territory infarction: clinical course and prognostic signs.

BACKGROUND: Although the clinical features of space-occupying ischemic stroke are well known, there are limited prospective data on the clinical course of complete middle cerebral artery territory infarction and on the predisposing factors leading to subsequent herniation and brain death. METHODS: The clinical course of patients with complete middle cerebral artery territory infarction, defined by computed tomography and vascular imaging, was evaluated. Initial clinical presentation was assessed by the Scandinavian Stroke Scale and the Glasgow Coma Scale. Serial computed tomography with measurement of midline and septum pellucidum shift and data on the presence and location of vascular occlusion by angiography or Doppler ultrasound were obtained directly after admission. Time course and outcome were analyzed with regard to the clinical findings on admission and at follow-up. The functional status of surviving patients was assessed using the Barthel Index. RESULTS: Fifty-five patients with complete middle cerebral artery territory infarction caused by occlusion of either the distal intracranial carotid artery or the proximal middle cerebral artery trunk were studied. In all patients, embolic infarction was presumed. The mean Scandinavian Stroke Scale score on admission was 20, and the time course of deterioration varied between 2 and 5 days. Forty-nine patients required ventilator assistance during the acute stage of disease. Only 12 patients (22%) survived the infarct. The cause of death was transtentorial herniation with subsequent brain death in 43 patients. Survivors had a mean Barthel Index score of 60 (range, 45 to 70). CONCLUSIONS: The prognosis of complete middle cerebral artery territory stroke is very poor and can be estimated by early clinical and neuroradiological data within the first few hours after the onset of symptoms. A space-occupying mass effect develops rapidly and predictably over the initial 5 days after presentation. Herniation occurred as an end point in 43 (78%) of these patients.

Adult↗
PubMed1996

Excess glutamate levels in the cerebrospinal fluid predict clinical outcome of bacterial meningitis.

BACKGROUND: The clinical course of bacterial meningitis still is characterized by a high mortality and frequent neurological deficits in survivors. In addition to other potentially neurotoxic mediators of inflammation, the excitatory amino acid glutamate, which has been implicated in neuronal death in a variety of other neurological diseases, may also be involved in the pathological process of bacterial meningitis. OBJECTIVES: To investigate the prognostic value of the glutamate concentration in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. PATIENTS AND METHODS: Thirty consecutive patients with bacterial meningitis were included in a prospective study. The clinical severity of the disease was assessed on admission and 14 days after the beginning of antibiotic treatment by means of the Glasgow Coma Scale. Studies of CSF were performed on admission and after 3 to 6 days. In addition to standard CSF investigations, including cell count, cytologic findings, protein analysis, glucose and lactate levels, and microbiological tests, the concentration of glutamate in the CSF was measured by an enzymatic assay. RESULTS: At admission, both CSF cell count and concentration of glutamate correlated well with the severity of the disease. After treatment, glutamate concentrations decreased significantly to normal or only slightly elevated levels in 23 patients. However, in 7 patients glutamate levels remained markedly increased. In this group, clinical outcome was significantly worse than in the group of patients with low glutamate levels in the second CSF analysis. CONCLUSIONS: A prolonged increase of glutamate levels in the CSF may predict poor clinical outcome in patients with bacterial meningitis, possibly because of the sustained neurotoxic effects of this excitatory neurotransmitter.

Adolescent↗
PubMed1996

[Epidural cerebrospinal fluid pressure measurement and therapy of intracranial hypertension in "malignant" middle cerebral artery infarct].

BACKGROUND AND PURPOSE: A permanent elevation of ICP after severe brain injury for instance in subarachnoid or intracerebral hemorrhage or neurotrauma is associated with a poor clinical outcome. Although increasingly being used in the intensive care of patients with elevated ICP, continuous epidural ICP monitoring in ischemic stroke has not been firmly established yet. PATIENTS AND METHODS: We prospectively evaluated the clinical course and outcome of patients with raised ICP due to space occupying ischemic middle cerebral artery (MCA) infarction as seen in CT, who underwent continuous ICP monitoring. Epidural ICPprobes were inserted ipsilaterally (all patients) and contralaterally (additional in 7 patients) to the side of infarctation. Glasgow Coma and Scandinavian Stroke Scales (GCS and SSS) were obtained initially and in the further clinical course. All patients were subjected to a standardized treatment protocol for raised ICP. ICP values were correlated with clinical presentation at the time point of deterioration, with outcome and CT findings. Effectiveness of different treatment modalities to lower ICP were analyzed and discussed. RESULTS: 9 of 48 patients survived the MCA infarct (19%), with the cause of death being transtentorial herniation with subsequent brain death in all 39 patients. Mean SSS at admission was 20.6 (survivors 21.5 +/- 5.6, nonsurvivers 19.8 +/- 6.5). All patients showed clinical signs of herniation before the increase of ICP. All 39 patients who died developed ICP values higher than 35 mmHg and no patient with ICP values of more than 35 mmHg survived. CCT changes dit not necessarily reflect the absolute measured ICP values. All treatment modalities for raised ICP including osmotherapy, controlled hyperventilation, tromethamol and barbiturates were initially effective, but only in a minority of patients ICP control could be sustained. CONCLUSIONS: We conclude that ICP monitoring in large hemispheric infarction may predict clinical outcome. ICP monitoring was not helpful in guiding long term treatment of ICP. It remains doubtful, whether ICP monitoring has a positive influence on clinical outcome of acute severe ischemic stroke.

Adult↗
PubMed1996

Excess glutamate in the cerebrospinal fluid in bacterial meningitis.

We investigated possible neurotoxic components in the cerebrospinal fluid (CSF) of patients with bacterial meningitis. On murine cerebellar neuronal cell cultures, CSF exerted a dose-dependent toxic effect, which was attenuated by the NMDA receptor antagonist MK-801. Glutamate concentrations in the CSF of patients with bacterial meningitis were measured by an enzymatic assay and found to be significantly elevated (p < 0.001) as compared to viral meningitis and non-inflammatory neurological diseases. The concentration of glutamate in the CSF of patients with bacterial meningitis varied considerably and correlated with the severity of the disease as scored by the Glasgow Coma Scale. Cells in the CSF, mainly comprising polymorphonuclear granulocytes, did not release any glutamate into the culture medium, whereas blood monocytes produced remarkable amounts. These findings implicate an important role of monocytic inflammatory cells in bacterial meningitis by the release of glutamate, which may contribute to neuronal cell death.

Adult↗
PubMed1996

Emollients and photo(chemo)therapy: a call for caution.

BACKGROUND: Emollients used for skin care, treatment of a disease or lubrication, before irradiation during the course of phototherapy or photochemotherapy, may significantly interfere with the transmission of UV light and may influence the outcome of the therapy. OBJECTIVE: These experiments should characterize and quantify the possible interactions of usual emollients with UV light transmission. METHOD: The method was an in vitro technique similar to the one already used for the determination of sun protection factors of topical sunscreen preparations. RESULTS: Among the products tested, two showed a significant photoprotection capable of interfering with the course of therapy. Oils enhanced UV light transmission significantly. CONCLUSIONS: Emollients may show significant interference with UV light transmission during phototherapy or photochemotherapy. The outcome and course of the therapy could thus be significantly modified.

Contraindications↗