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Biomedical subjects

G Luef

Publications and source records attributed to G Luef.

At least 37 records · Page 2Linked to original sources

Early determination of neurological outcome after prehospital cardiopulmonary resuscitation.

BACKGROUND AND PURPOSE: Although there are various methods of determining neurological prognosis after cardiopulmonary resuscitation, the final outcome of patients often remains unclear for quite a long time. METHODS: We investigated 30 consecutively admitted patients who had been successfully resuscitated by the team of the local mobile intensive care unit after cardiac arrest. Determinations of the period of anoxia and of the cardiopulmonary resuscitation time, clinical investigation, echocardiography, electroencephalography, evoked potentials, magnetic resonance imaging, and magnetic resonance spectroscopy were performed. RESULTS: Demonstration of brain lactate in proton magnetic resonance spectroscopy (P < .01) and absent N20 waves in short-latency somatosensory evoked potentials (P < .01) proved to be significant in terms of a poor prognosis. Correlations between both duration of anoxia and cardiopulmonary resuscitation time and neurological outcome could be shown as well (both P < .05). CONCLUSIONS: Proton magnetic resonance spectroscopy and short-latency evoked potentials are of great benefit in the prognostic evaluation after cardiopulmonary resuscitation.

Adolescent↗

The effects of brain lesions on the course of chronic epilepsies.

The effect of intercurrent brain lesions on the characteristics of chronic epilepsies has not yet been the subject of detailed investigation. We therefore retrospectively examined this issue for idiopathic, cryptogenic as well as symptomatic chronic epilepsies in patients documented in routine investigations at our outpatient seizure unit between the occurrence of epilepsy and commencement of the study. The clinical criteria for inclusion in this study were brain injury by trauma, stroke or intracerebral hemorrhage, documented by CT scan, and the occurrence of this so-called index event in patients with established chronic epilepsy. These requirements were met by 63 patients (40 male, mean age 44.8 years, SD 14.7 a; 23 female, mean age 43.1 years, SD 16.4 a). Seizure characteristics, EEG recordings as well as seizure frequencies before and after the index event were compared. Patients and controls were observed for a mean time of 22.12 years (SD 7.33 a) and 22.01 years (SD 11.31 a), respectively. Two patients presenting with generalized seizures prior to brain injury underwent a change in seizure characteristics. One control (without intercurrent brain lesion; matched for age, sex, age at onset of seizure disorder and classification of seizure disorder) primarily presenting with partial seizures evolving to generalized seizures showed changed seizure characteristics. These changes are statistically insignificant (McNemar test for the significance of changes). Seizure frequencies decreased significantly after brain injury. EEG recordings mirrored clinical findings with additional focal aspects according to brain lesion. These findings are discussed mainly with respect to the cofactorial etiology of epilepsies.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Phenytoin overdosage and cerebellar atrophy in epileptic patients: clinical and MRI findings.

Mild overdosage of phenytoin produces reversible cerebellar symptoms (nystagmus, double vision, dysarthria and ataxia). Several case reports suggest that relatively mild and relatively short intoxication can lead to cerebellar degeneration. We observed 11 patients who had episodes of abnormally increased serum levels, most of which developed clinical signs of cerebellar dysfunction. All of these patients were examined with a 1.5-tesla whole-body system (Magnetom, Siemens). Five patients had normal cerebellar structures, although 3 of them had a history of clinical intoxication and all had at least one episode of increased serum level of diphenylhydantoin. The remaining 5 had moderate to severe cerebellar atrophy. Two of them never experienced signs of clinical intoxication. There was no correlation between degree of atrophy and severity of clinical symptoms and elevation of serum DPH levels. There was no correlation between cerebellar atrophy, duration of epilepsy and frequency of seizures.

Adult↗

[Microbiological diagnosis of tuberculosis].

The increased incidence of tuberculosis as well as the availability of new diagnostic testing methods clearly have various implications for the routine microbiology laboratory: samples must be sent to the microbiology lab for testing immediately after being taken and microscopically investigated the same day. In other countries, difficult to treat, multi-resistant Mycobacterium tuberculosis strains have occurred. Thus decisive hygienic measures must be taken early on in cases of highly infectious patients (i.e. patients with microscopically positive sputum). Liquid media (MB Check Roche, Bactec) as well as Löwenstein Jensen media must be inoculated in the lab. Liquid media allow both faster detection of certain atypical mycobacteria and increased accuracy. Classification of culturally established agents through commercial genetic probes (AccuProbe Mycobacterien) or with high pressure liquid chromatography is possible within hours when acid-fast rods are present. Time consuming identification by determination of biochemical and culture morphological characteristics should be reserved for reference labs. Today, rapid tests like analysis of tuberculostearic acid or polymerase chain reaction are already useful for special questions like ruling out tuberculous meningitis. In most cases, however, these rapid tests cannot replace identification of microbes with culture techniques.

AIDS-Related Opportunistic Infections↗

[Neurologic manifestations of diabetes mellitus: an overview].

Neurological manifestations of diabetes mellitus comprise structural changes in both central and peripheral nervous system, as well as functional cerebral disturbances. Macro- and microangiopathy are responsible for the development of cerebrovascular diseases; microangiopathic and metabolic disturbances are considered in the discussion to be responsible for the development of the various forms of diabetic polyneuropathy. Acute metabolic episodes with progressive impairment of consciousness have to be differentiated from structural neurological disorders. As a further point of interest the association between diabetes mellitus and special neurological diseases is mentioned.

Brain Diseases, Metabolic↗

Association of serum antibodies to heat-shock protein 65 with carotid atherosclerosis.

Arteriosclerotic lesions can be induced in normocholesterolaemic rabbits by immunisation with heat-shock protein (hsp) 65, a stress protein expressed in high concentrations in human atherosclerotic lesions. If an immune reaction to hsp65 also plays a part in human atherogenesis, it should be possible to detect anti-hsp65 antibodies in patients with atherosclerotic lesions. To study the possible relation between immune reaction to hsp65 and atherosclerosis, 867 normal inhabitants of South Tyrol, aged 40-79 years, were selected randomly for determination of serum antibodies against hsp65, simultaneous sonographic assessment of carotid atherosclerotic lesions, and evaluation of established risk factors--ie, blood cholesterol, hypertension, smoking, diabetes mellitus, and obesity. Autoantibodies to nuclear antigens, thyroid antigens, and rheumatoid factors were also measured. Serum anti-hsp65 antibodies were significantly (p < 0.05) increased in subjects aged 60-79 years with carotid atherosclerosis compared with those without lesions, and increased antibody concentration was independent of age, sex, and other established risk factors. On the other hand, the incidence and titres of autoantibodies did not correlate with carotid atherosclerotic lesions. Our data provide the first evidence of a strong correlation between anti-hsp65 antibodies and carotid atherosclerosis, suggesting that hsp65 might be involved in the pathogenesis of atherosclerosis.

Adult↗

Successful treatment of spinal sarcoidosis by high-dose intravenous methylprednisolone.

A man with known pulmonary sarcoidosis presented with paraplegia and a rod-shaped increase in T2 signal intensity in his cervical and upper thoracic spine. Initial treatment efforts using oral doses of 40 mg of methyl-prednisolone were futile, but intravenous bolus therapy (500 mg of methyl-prednisolone daily for 1 week) led to long-lasting improvement of his neurological status and to normalization of MRI findings.

Adult↗

Staining of endothelial cells and macrophages in atherosclerotic lesions with human heat-shock protein-reactive antisera.

Our previous epidemiological studies have shown that levels of serum antibodies against mycobacterial heat-shock protein (hsp) 65 correlate positively with carotid atherosclerosis in subjects aged 40 to 79 years. To determine whether these high-titer sera also react with homologous human hsp60 and/or cell components of atherosclerotic lesions, we selected 15 human sera samples, each with high or low titers to recombinant mycobacterial hsp65, and investigated their reactivity with human arterial lesion components by immunoblotting and immunofluorescence techniques. All five higher-titer sera against hsp65 reacted with a 60-kDa band of atherosclerotic lesion proteins and human recombinant hsp60 on Western blots. Pooled sera with low antibody titers to hsp65 diluted similarly as high-titer sera did not show reactivity with atherosclerotic lesion and media proteins. By immunohistochemistry and immunofluorescence with human immunoglobulin G isolated from different sera, labeled with biotin, and visualized with a streptavidin conjugate, positive staining was observed in sections of fatty streaks and atherosclerotic plaques of carotid arteries, and weak staining was observed in the normal intima. Double immunofluorescence identified the majority of positively stained cells as macrophages, endothelial cells, and a few smooth muscle cells. In summary, serum antibodies against hsp65 cross-react with the human 60-kDa homologue present in high levels in atherosclerotic lesions and are mainly reacting with macrophages and endothelial cells, supporting our concept of a possible involvement of humoral-mediated immune reaction against hsp60 in atherogenesis.

Aged↗

[Course and management of tetanus].

Within a span of 18 months 4 patients (2 men, 2 women) were admitted with generalized tetanus to our neurological intensive care unit. The "period of onset" ranged from 2 to 14 days. All patients needed artificial ventilation over 17 to 38 days. The clinical course was complicated by gram-negative pneumonia in 3 of the 4 patients. Time of hospitalization ranged between 35 and 60 days. One patient had never been immunized against tetanus. The other 3 had not received a booster dose for over 10 years. All 4 patients survived, 3 of them without sequelae.

Adult↗

[Cerebellar atrophy and phenytoin poisoning. An MR study].

Phenytoin has been considered a possible cause of cerebellar degeneration, especially after clinical intoxication. Magnetic resonance provides the diagnosis of anatomical structures in the posterior fossa without the limitation of beam hardening artefacts. The aim of this study was to evaluate the relationship of phenytoin medication and cerebellar atrophy in 11 patients with increased serum levels (21.4 micrograms/ml-95.6 micrograms/ml). Five patients had normal cerebellar structures, although three of them had a history of clinical intoxication and all had at least one episode of increased serum level of DPH. The remaining six patients had moderate severe cerebellar atrophy (n = 4) and atrophy of the vermis cerebelli (n = 5). Two of them had never experienced clinical intoxication. There was no correlation between the degree of atrophy and severity of clinical symptoms and evaluation of serum DPH levels (up to four times normal values). There was also no correlation between cerebellar atrophy, duration of epilepsy and frequency of seizures. We conclude that phenytoin overdosage does not necessarily result in cerebellar atrophy and it is unlikely that phenytoin medication was the only cause of cerebellar atrophy in the remaining patients.

Adult↗

1-H-localized magnetic resonance spectroscopy: preliminary observations in transient ischemic attacks.

Water-suppressed proton magnetic resonance spectroscopy which has recently shown diagnostic potential in human stroke victims was performed in two patients who had suffered a hemispheric transient ischemic attack. Localized spectra were targeted from routine MR images. In one patient lactate could be observed 8 weeks after a transient ischemic attack. Lactate concentration was low compared with that of a patient who had suffered acute stroke. The other TIA patient did not show evidence of lactate production. Although these observations are preliminary, we demonstrated that localized in vivo proton spectroscopy can detect persistent biochemical alterations after transient ischemic attacks. We suggest that non-invasive in vivo proton spectroscopy will become a useful method in diagnosis and management of TIA in the future.

Aged↗

[Snuff aspiration as a cause of recurrent pulmonary infiltrations in a 60-year-old patient with chronic renal failure].

Pulmonary infiltrations associated with renal failure demand several diagnostic procedures to exclude autoimmune disorders affecting both organ systems or to find an infectious cause of the disease. We report the case of a 60 year-old man with chronic renal failure and recurring pulmonary infiltrations. On admission to hospital all diagnostic parameters for systemic vasculitis, infectious or neoplastic disease were negative, including the histological report on transbronchial biopsies. Eventually, follow-up biopsies taken 3 months later showed vegetable fibres and necrosis due to intensive snuff abuse during the previous months. After the patient stopped taking snuff the pulmonary infiltrations improved quickly. Uraemic neuropathy, which may have facilitated aspiration, as well as the reduced pulmonary and systemic defence mechanisms due to chronic renal failure probably contributed to a considerable degree to the development of pulmonary infiltration.

Biopsy↗