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Biomedical subjects

J Rudolf

Publications and source records attributed to J Rudolf.

At least 37 records · Page 2Linked to original sources
PubMed2000

Early [(11)C]Flumazenil/H(2)O positron emission tomography predicts irreversible ischemic cortical damage in stroke patients receiving acute thrombolytic therapy.

BACKGROUND AND PURPOSE: Central benzodiazepine receptor ligands, such as [(11)C]flumazenil (FMZ), are markers of neuronal integrity and therefore might be useful in the differentiation of functionally and morphologically damaged tissue early in ischemic stroke. We sought to assess the value of a benzodiazepine receptor ligand for the early identification of irreversible ischemic damage to cortical areas that cannot benefit from reperfusion. METHODS: Eleven patients (7 male, 4 female, aged 52 to 75 years) with acute, hemispheric ischemic stroke were treated with alteplase (recombinant tissue plasminogen activator; 0.9 mg/kg according to National Institute of Neurological Disorders and Stroke protocol) within 3 hours of onset of symptoms. At the beginning of thrombolysis, cortical cerebral blood flow ([(15)O]H(2)O) and FMZ binding were assessed by positron emission tomography (PET). Those early PET findings were related to the change in neurological deficit (National Institutes of Health Stroke Scale) and to the extent of cortical damage on MRI or CT 3 weeks after the stroke. RESULTS: Hypoperfusion was observed in all cases, and in 8 patients the values were below critical thresholds estimated at 12 mL/100 g per minute, comprising 1 to 174 cm(3) of cortical tissue. Substantial reperfusion was seen in most of these regions 24 hours after thrombolysis. In 4 cases, distinct areas of decreased FMZ binding were detected. Those patients suffered permanent lesions in cortical areas corresponding to their FMZ defects (112 versus 146, 3 versus 3, 2 versus 1, and 128 versus 136 cm(3)). In the other patients no morphological defects were detected on MRI or CT, although blood flow was critically decreased in areas ranging in size up to 78 cm(3) before thrombolysis. CONCLUSIONS: These findings suggest that imaging of benzodiazepine receptors by FMZ PET distinguishes between irreversibly damaged and viable penumbra tissue early after acute stroke.

Aged↗
PubMed2000

One-year follow-Up in acute stroke patients treated with rtPA in clinical routine.

BACKGROUND AND PURPOSE: A recent placebo-controlled study provided evidence of a sustained benefit at 1 year from systemic thrombolysis in patients with acute ischemic stroke. The scope of the present study is to determine whether comparable results may be attained in everyday practice if current management guidelines are closely met. METHODS: Between March 1996 and July 1998, 150 consecutive patients with acute ischemic stroke were treated with systemic thrombolysis using alteplase, strictly in accordance with American Heart Association (AHA) guidelines. The patients were followed up for 12 months after treatment. RESULTS: Baseline characteristics and complication rates were comparable to those of the National Institute of Neurological Disorders and Stroke (NINDS) study, except for a somewhat younger age (mean 63 years) and lower National Institutes of Health Stroke Scale score (median 11). At 1 year, 41% of our patients showed minimal or no disability (Rankin scale score of 0 or 1), comparable to 41% in the NINDS rtPA group. The overall rate of recurrent stroke was 6.6% and the transient ischemic attack rate 3.3% at 1 year. Six patients (4%) died after the first 3 months, none of them due to recurrent stroke, and 5 had already been severely disabled at 3 months. CONCLUSIONS: These observations further encourage the routine use of rtPA for the treatment of acute ischemic stroke in strict accordance with the AHA guidelines.

Acute Disease↗
PubMed2000

Cerebral blood flow and glucose metabolism in multi-infarct-dementia related to primary antiphospholipid antibody syndrome.

The primary antiphospholipid antibody syndrome (PAPS) has been described in patients with a history of fetal loss, thrombocytopenia and arterial or venous thrombosis. In PAPS, a prothrombotic state is mediated by antiphospholipid antibodies (aPLs) leading to disseminated thromboembolic vascular occlusion. Today, the presence of aPLs in the serum is considered as a distinct risk factor for recurrent stroke in young adults. Some PAPS patients develop a multi-infarct-syndrome with a stepwise decline of higher cortical functions. We report on a 55-year-old man suffering from progressive dementia and PAPS, in whom cerebral glucose metabolism and blood flow were examined by positron emission tomography (PET). Cerebral atrophy and moderate signs of leukaraiosis were detected in magnetic resonance imaging (MRI), whereas the PET scans showed a considerable diffuse impairment of cortical glucose metabolism combined with a reduced cerebral perfusion in the arterial border zones. These findings indicate that PAPS-associated vascular dementia is accompanied by a cortical neuronal loss, presumably caused by a small-vessel disease with immune-mediated intravascular thrombosis. This case shows that pathological findings in PAPS are congruent to cerebral changes of metabolism and blood flow in systemic lupus erythematosus (SLE).

Antiphospholipid Syndrome↗
PubMed1999

[Hypokalemic paralysis in furosemide therapy and simultaneous laxative abuse].

BACKGROUND: Clinical signs of hypokalemia are not directly related to the extent of the electrolyte imbalance, and therefore monosymptomatic cases may be observed. CASE REPORT: Following an acute gastroenteritis with considerable diarrhea, a 47-year-old male patient was admitted to hospital for progressive painful paraparesis. Upon admission, the patient complained of painful paresthesias in both legs, and a moderate flaccid paraparesis with widespread fasciculations and loss of leg tendon reflexes was found. Serum potassium level on admission was 1.7 mmol/l. Other signs of hypokalemia were absent, and the ECGs showed a slow sinus rhythm without disturbances of de- or repolarisation or cardiac arrhythmias. Hypokalemic paralysis was diagnosed and was considered to be primarily drug-induced, as the patient had a history of laxative abuse and was on a continuous medication with furosemide (80 mg/d) without regular assessment of serum electrolytes. The additional electrolyte loss following the gastroenteritis precipitated the development of clinical signs of hypokalemia. In parallel to the rise in serum potassium levels, both painful paresthesias and muscle weakness disappeared, and electromyography documented the amelioration of the myopathic syndrome. CONCLUSION: The prominent clinical symptom of hypokalemia was a dyskalemic paralysis in the absence of other sequelae of electrolyte imbalance, such as cardiac arrhythmias or vegetative disturbances.

Cathartics↗
PubMed1999

European brain death codes: a comparison of national guidelines.

The majority of European countries have published recommendations for the diagnosis of brain death as a necessary prerequisite for organ donation. The concept of brain death as defining the death of the individual is accepted in all European countries; however, the guidelines for determining the total and irreversible loss of all brain functions differ somewhat in the various countries. While the clinical examination and documentation of the clinical signs of brain death are very uniform, there are significant differences in the guidelines for using technical confirmatory tests to corroborate the clinical signs. These range from rejecting all technical tests to accepting of multiple neurophysiological tests alone or in combination. The present study examined the similarities and differences in current concepts of brain death in the various European countries and their recommendations for the diagnosis of brain death. The diagnosis of brain death is based on a number of prerequisites, on the clinical diagnosis of deep coma, loss of all brainstem reflexes, and the demonstration of apnea. Neurophysiological tests are recommended by a number of national professional societies as confirmatory tests to confirm the clinical diagnosis of brain death and shorten otherwise necessary waiting periods of 6-12 h. Most brain death codes allow the use of electroencephalography, which must demonstrate electrocortical silence over a certain period. Evoked cerebral potentials can demonstrate the successive loss of activity of various afferent pathways and are accepted in some countries as a confirmatory test. Other neurophysiological tests which demonstrate the loss of cerebral perfusion can be implemented. Brain scintigraphy can confirm the loss of isotope uptake into the brain. Doppler sonography also demonstrates cessation of brain perfusion. Cerebral panangiography may also be used to demonstrate the loss of brain perfusion but is less desirable since it might endanger the patient.

Brain Death↗
PubMed1999

Deterioration of parkinsonian symptoms following treatment of dopaminergic hallucinosis with olanzapine.

The atypical antipsychotic drug olanzapine has been proposed for treatment of dopaminergic psychosis in Parkinson's disease (PD). We report on a 68-year-old patient who developed a severe akinetic-rigid extrapyramidal syndrome, accompanied by additional paranoid symptoms, following olanzapine treatment of optic hallucinosis in PD. Olanzapine may also induce clinically relevant extrapyramidal side effects in PD patients.

Aged↗
PubMed1999

Stroke following internal carotid artery occlusion - a contra-indication for intravenous thrombolysis?

Between March 1996 and December 1997, 15 consecutive patients with carotid artery occlusion diagnosed with duplex sonography were treated with intravenous recombinant tissue plasminogen activator (rt-PA), following a protocol similar to that of the National Institute of Neurological Disorders and Stroke (NINDS) study. On the basis of ultrasound findings, six of the 15 patients had internal carotid artery dissection (ICD), and the remaining nine had atherothrombotic internal carotid artery (ICA) occlusion. No relevant haemorrhagic complications were observed after rt-PA treatment of ICA occlusion. Excellent late functional outcome was observed in three of the 15 patients with ICA occlusion, moderate and poor outcome in four patients. Four patients died, and mortality was related to stroke severity upon admission. A good outcome seemed to be more likely in the small group of patients with ICD, than in the patients suffering atherothrombotic ICA occlusion. As the results of rt-PA treatment in this case series are by no means devastating, our data do not corroborate the hypothesis that patients with acute ischemic stroke following ICA occlusion should a priori be excluded from intravenous thrombolysis. The possible benefit of rt-PA treatment in stroke following acute or chronic ICA occlusion should be assessed in a larger prospective trial, for which this case series might serve as a pilot study.

Adult↗
PubMed1999

Cerebral glucose metabolism in acute and persistent vegetative state.

Regional cerebral glucose metabolism (rCMRglc) was investigated with 18F-2-fluoro-2-deoxy-D-glucose (FDG) and positron emission tomography (PET) in 24 patients with acute (AVS, duration <1 month, n=11) or persistent (PVS, duration >1 month, n=13) vegetative state (VS) following prolonged anoxia due to cardiorespiratory arrest. After a follow-up period of twelve months, 8 patients had died, 13 remained in a permanent vegetative state and three showed moderate improvement of consciousness, without however regaining independence for activities of daily life. As expected, overall glucose utilization (CMRglc) was significantly reduced in VS in comparison to age matched controls. Infratentorial structures showed a less distinct hypometabolism. Differences in metabolic rates between patients who died or remained in a PVS were small and insignificant and probably reflect different age structures of the two groups. A statistically significant correlation between the degree of evoked potential or EEG alterations in VS and the reduction of global or regional cortical metabolic rates for glucose could not be established. Cortical metabolic rates in patients with PVS were significantly reduced when compared to patients studied in AVS (p<0.05 for all cortical regions of interest except the frontal lobe). This phenomenon reflects the progressive loss of residual cortical function following anoxic brain injury that corresponds to the neuropathological findings of progressive Wallerian and transsynaptic degeneration as sequelae of anoxic brain injury in PVS.

Activities of Daily Living↗
PubMed1999

Evidence of anaphylaxy after alteplase infusion.

BACKGROUND AND PURPOSE: Although alteplase, a recombinant tissue plasminogen activator (tPA), is structurally identical to endogenous tPA and therefore should not induce allergy, single cases of acute hypersensitivity reactions have been reported. Until now, specific antibodies against alteplase were not detected in blood samples obtained in these patients. CASE DESCRIPTION: We report an anaphylactic reaction in a 70-year-old white female who was treated with intravenous alteplase for thrombolysis of acute ischemic stroke 160 minutes after onset of a right-sided hemiparesis. Thirty minutes after infusion of alteplase had been started, the patient suffered acute severe sinus tachycardia and hypotension, followed by cyanosis and loss of consciousness. The alteplase infusion was stopped, and following antiallergic therapy, tachycardia and hypotension resolved within 1 hour. The hemiparesis remained unaltered, but additional harm resulting from the hemodynamic complication was not observed. Serum samples analyzed with a radioimmunoprecipitation assay were negative for total antibodies to alteplase, but in a subsequent ELISA, both samples were positive for IgE antibodies to alteplase. CONCLUSIONS: The detection of specific IgE antibodies reactive with alteplase in this patient could provide the first evidence of an anaphylactic-type reaction to alteplase in man. Because previous exposure to alteplase can be excluded, the results suggest that this patient had preexisting antibodies that were cross-reactive with one or more epitopes of alteplase and therefore precipitated the anaphylactic-type reaction.

Aged↗
PubMed1999

Cerebral glucose metabolism in type I alpha-N-acetylgalactosaminidase deficiency: an infantile neuroaxonal dystrophy.

Cerebral glucose metabolism was investigated in a 4.8-year-old boy with alpha-N-acetylgalactosaminidase deficiency using 2-[18F]fluoro-2-deoxy-D-glucose and positron emission tomography (PET). In comparison to normal values for age, the overall cerebral glucose metabolism was reduced and the regional cerebral glucose metabolism was decreased in proportion to the degree of atrophy. In the supratentorial cortical regions, the hypometabolism was asymmetric. However, the level of regional cerebral glucose metabolism in all cortical regions excluded a persistent vegetative state. In the lentiform nucleus and the head of the caudate, comparatively increased regional cerebral glucose metabolism was documented, similar to findings in neurodegenerative disorders with active epilepsy. In contrast, the infratentorial structures (cerebellar hemispheres, brain stem, mesencephalon, and hypothalamus), which are predominantly affected by the atrophic process, showed distinct and symmetric hypometabolism. Thus, the 2-[18F]-fluoro-2-deoxy-D-glucose PET scans provided additional insight into and correlation of the functional and structural disturbances in type I alpha-N-acetylgalactosaminidase deficiency, in addition to documenting the hypometabolism due to brain atrophy.

Blood Glucose↗
PubMed1999

Stereoselectivity of the phase-II-metabolism of the H1 antihistaminic drug dimethindene investigated by capillary electrophoresis.

Two capillary electrophoretic (CE) methods for the determination of conjugated metabolites of the antihistaminic drug dimethindene were developed. These methods allow the determination of the diastereomeric ratios of both Phase II glucuronides, 6-hydroxy dimethindene glucuronide (5) and 6-hydroxy-N-demethyl dimethindene glucuronide (6). Furthermore, after enzymatic deconjugation of both glucuronides, enantiomeric ratios of the hydroxylated Phase I metabolites 3 and 4 were determined. For comparison, glucuronides 5 and 6 were prepared by enzymatic synthesis and identified by MALDI-TOF mass spectrometry and deconjugation with beta-glucuronidase to the corresponding phenols 3 and 4. The assay of the glucuronides in rat urine and serum was performed by a combination of liquid/liquid extraction followed by solid phase extraction. After a high dose treatment with racemic dimethindene the diastereomeric glucuronides 5 and 6 could be directly determined in the urine of a guinea pig by CE without prior extraction or preconcentration of the urine sample. In all cases, stereoselectivities of the formation of Phase I as well as Phase II metabolites were observed.

Animals↗
PubMed1998

Distinct regions of allelic imbalance on chromosome 10q22-q26 in squamous cell carcinomas of the lung.

The genetic mechanisms underlying the progression to the metastatic phenotype of lung cancer are poorly understood. We recently showed that small cell lung cancer (SCLC) and metastasizing squamous cell carcinomas are characterized by an increased incidence of allelic loss on chromosome 10q. In the present study we performed a deletion mapping using 24 polymorphic markers on chromosome 10q22-q26 in 39 squamous cell carcinomas (SCC) of the lung identifying 14 metastatic carcinomas (74%) and three non-metastatic SCC (15%) with allelic imbalance. The allelotype analysis indicated three regions of allelic loss that were clustered at the loci Afm086/D10S541, D10S185 and D10S1782/D10S169. A localized microsatellite instability was observed in two carcinomas for the markers D10S1686 and D10S1782. In addition the PTEN/MMAC1 gene was analysed by direct DNA sequencing and Southern blot analysis in 25 and 28 carcinomas, respectively, without detecting any genomic alterations. Similarly, no altered transcript was detected in 15 tumor cell lines and 20 primary tumors by Northern blot analysis or RT-PCR. In summary, three distinct regions of allelic imbalance were identified suggesting that multiple tumor suppressor genes on chromosome 10q contribute to tumor progression and metastases formation of lung cancer.

Alleles↗
PubMed1998

[Protracted course of bromazepam poisoning in advanced age].

HISTORY AND CLINICAL FINDINGS: A 68-year-old woman was found unconscious and hardly breathing. Artificial ventilation was undertaken by an emergency physician who brought her to hospital. Physical examination provided no evidence of relevant organ abnormalities. Neurological examination of the comatose patient revealed absent brain-stem reflexes and spontaneous respiration. But no other focal neurological abnormalities were found. INVESTIGATIONS: Routine laboratory tests, ECG, chest radiogram, Doppler sonography of arteries to the brain, lumbar cerebrospinal fluid and computed tomography of the skull were unremarkable. Toxicological tests discovered bromazepam intoxication (serum level 6 mg/l; maximal serum level after intake of 6 mg of the active constituent: 0.1 mg/dl). DIAGNOSIS, TREATMENT AND COURSE: When bromazepam poisoning was demonstrated elimination of the drug was no longer feasible; the spontaneous course of the poisoning with slowly falling drug levels could thus be observed over 10 days. In parallel with the fall of bromazepam concentration in blood, restitution of breathing and of brain-stem reflexes was recorded until, 12 days after intake of the drug, normal functions had been restored. CONCLUSION: Central respiratory arrest occurred at a bromazepam serum level of 6 mg/l. Without intensive medical care the patient would not have survived.

Aged↗
PubMed1998

Early intravenous thrombolysis with recombinant tissue-type plasminogen activator in vertebrobasilar ischemic stroke.

BACKGROUND: The optimal therapy of vertebrobasilar ischemic stroke is under debate. In the case of underlying basilar artery occlusion, intra-arterial thrombolysis is recommended. Because this pathologic condition is rarely found and the procedure is time consuming and restricted to specialized centers, the question arises whether early intravenous thrombolysis could also effectively be applied in vertebrobasilar ischemic stroke. OBJECTIVE: To determine if early intravenous thrombolysis could be used effectively in vertebrobasilar ischemic stroke. DESIGN: A case series of 12 consecutive patients with acute vertebrobasilar ischemia were followed up 3 months after thrombolytic treatment at the Department of Neurology of the University Hospital of Cologne, Cologne, Germany, a primary care and referral center. METHODS: Patients with clinically diagnosed moderate to severe vertebrobasilar ischemic stroke with clearly determined symptom onset were treated with intravenous recombinant tissue-type plasminogen activator within 3 hours after symptom onset following a protocol similar to that of the National Institute of Neurological Disorders and Stroke study. RESULTS: On admission, 7 patients exhibited moderate to severe brainstem symptoms without impairment of consciousness and 5 patients had impairment of consciousness, of whom 2 were comatose. Of 12 patients, 10 had a favorable outcome after 3 months defined as full independence (Barthel index score of 100) or return to premorbid condition. One patient had a poor outcome with complete dependency due to reocclusion after primarily successful thrombolysis, and 1 patient died of severe brainstem infarction and additional space occupying parietal hemorrhage. CONCLUSION: Favorable outcome could be achieved in the majority of 12 consecutive patients with moderate to severe vertebrobasilar ischemic stroke treated with intravenous recombinant tissue-type plasminogen activator within 3 hours after symptom onset.

Acute Disease↗
PubMed1998

Potential pitfalls in apnea testing.

To determine the influence of baseline paCO2 on the results of apnea testing in the diagnosis of brain death, we performed an open prospective study on 36 patients fulfilling all other criteria for the diagnosis of brain death according to the criteria proposed by the Advisory Board of the German Federal Chamber of Physicians. For testing of apnea, patients underwent hypoventilation with 100% oxygen supply until a baseline paCO2 of 40 torr (5.3 kPa, n = 24, group 1) or 60 torr (8.0 kPa, n = 12, group 2) was reached. Then, patients were disconnected from the ventilator and apneic oxygenation with insufflation of 61 O2/min into the tracheal cannula was performed for five minutes. Arterial blood gas samples were obtained every minute during the testing period. In parallel, patients were observed for signs of spontaneous breathing. All patients remained apneic during the five minute test period. No relevant hypoxia (paO2 < 80 torr [10.6 kPa]) was observed in either group. In group 1, a mean baseline paCO2 of 45 torr (6.0 kPa) was registered, mean end-paCO2 was 75 torr (10.0 kPa). In group 2, paCO2 values were 66 torr (8.8 kPa) and 90 torr (12 kPa), respectively. Baseline pH in group 1 (7.32) decreased to 7.18 at the end of testing and from 7.23 to 7.13 in group 2. Patients in group 2 were in possible danger of developing a CO2-induced narcosis mimicking apnea. Secondary organ damage due to severe respiratory acidosis could not be excluded in the patients of group 2. As no complications were observed in group 1 and apnea was evident in all these patients, we consider a baseline paCO2 of 40 torr (5.3 kPa) sufficient to establish apnea after five minutes of apneic oxygenation if an increase of baseline paCO2 of at least 20 mmHg is documented by arterial blood gas sampling. A higher baseline paCO2 may endanger patients without yielding more specific testing results.

Apnea↗
PubMed1998

Tissue at risk of infarction rescued by early reperfusion: a positron emission tomography study in systemic recombinant tissue plasminogen activator thrombolysis of acute stroke.

Thrombolytic therapy of acute ischemic stroke can be successful only as long as there is penumbral tissue perfused at rates between the thresholds of normal function and irreversible structural damage, respectively. To determine the proportion of tissue at risk of infarction, cerebral perfusion was studied in 12 patients with acute ischemic stroke who underwent treatment with systemic recombinant tissue plasminogen activator (0.9 mg/kg body weight according to National Institute of Neurological Disorders and Stroke protocol) within 3 hours of onset of symptoms, using [15O]-H2O positron emission tomography (PET) before or during, and repeatedly after thrombolysis. The size of the regions of critically hypoperfused gray matter were identified on the initial PET scans, and changes of perfusion in those areas were related to the clinical course (followed by the National Institutes of Health stroke scale) and to the volume of infarcted gray matter demarcated on magnetic resonance imaging 3 weeks after the stroke. Whereas the initial clinical score was unrelated to the size of the ischemic area, after 3 weeks there was a strong correlation between clinical deficit and volume size of infarcted gray matter (Spearman's rho, 0.96; P < 0.001). All patients with a severely hypoperfused (< 12 mL/100 g/min) gray matter region measuring less than 15 mL on first PET showed full morphologic and clinical recovery (n = 5), whereas those with ischemic areas larger than 20 mL developed infarction and experienced persistent neurologic deficits of varying degree. Infarct sizes, however, were smaller than expected from previous correlative PET and morphologic studies of patients with acute stroke: only 22.7% of the gray matter initially perfused at rates below the conventional threshold of critical ischemia became necrotic. Actually, the percentage of initially ischemic voxels that became reperfused at almost normal levels clearly predicted the degree of clinical improvement achieved within 3 weeks. These sequential blood flow PET studies demonstrate that critically hypoperfused tissue can be preserved by early reperfusion, perhaps related to thrombolytic therapy. The results correspond with experimental findings demonstrating the prevention of large infarcts by early reperfusion to misery perfused but viable tissue.

Acute Disease↗