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H Reiber

Publications and source records attributed to H Reiber.

At least 37 records · Page 2Linked to original sources
PubMed1997

Intrathecal IgA synthesis in X-linked cerebral adrenoleukodystrophy.

Cerebrospinal fluid data on 25 patients suffering from various phenotypes of X-linked adrenoleukodystrophy have been evaluated neurochemically including cerebrospinal fluid/serum quotient diagrams. Intrathecal IgA production in 13 of 14 patients with cerebral adrenoleukodystrophy was the most sensitive parameter in cerebrospinal fluid and was not seen in any of the neurologically asymptomatic patients or in the patients with adrenomyeloneuropathy. A blood-cerebrospinal fluid barrier dysfunction was found in 9 of these 14 patients. Additional intrathecal IgG or IgM synthesis was observed in 3 patients each. In 1 patient with lumbar punctures before and after onset of neurologic symptoms intrathecal IgA synthesis was seen only after the appearance of neurologic symptoms. Repetition of lumbar punctures in 5 neurologically symptomatic patients with cerebral adrenoleukodystrophy revealed a similar pattern of intrathecal IgA synthesis with a tendency of decreasing IgA concentration. The pathophysiologic aspects of intrathecal IgA synthesis are discussed in relation to other demyelinating and inflammatory neurologic diseases.

Adolescent↗
PubMed1995

Relevance of cerebrospinal fluid variables for early diagnosis of neuroborreliosis.

We describe the specificity and sensitivity of measuring a combination of basic CSF variables and Borrelia burgdorferi (Bb)-specific IgG and IgM antibody index (AI) values for the diagnosis of early neuroborreliosis. Basic CSF variables included total cell count, quantitation of activated B cells (IgG, IgA, and IgM classes), CSF/serum quotient diagrams for IgG, IgA, and IgM (to quantitate brain-derived immunoglobulin fractions in CSF), and CSF/serum albumin ratio as a measure of blood-CSF barrier function. The Bb-specific component of immunoglobulins in CSF and serum was quantitated by ELISA. Results are based on data from CSF and serum of 24 patients with definite neuroborreliosis, 45 patients with other neurologic diseases, and 28 control individuals. Combined evidence of an elevated CSF cell count, IgM-class dominance in both the cellular and intrathecal humoral immune response, and blood-CSF barrier dysfunction yielded 70% diagnostic sensitivity and 98% diagnostic specificity for detection of neuroborreliosis. Intrathecal production of Bb-specific IgM, evaluated as Bb-specific IgM antibody index (Bb-IgM-AI; pathologic value > 1.4) showed 79% diagnostic sensitivity and 96% diagnostic specificity. Correspondingly, elevated Bb-specific IgG antibody index (Bb-IgG-AI; pathologic value > 1.4) displayed 63% diagnostic sensitivity and 89% diagnostic specificity. Combined analysis of Bb-specific AI values and basic CSF variables gave the highest sensitivity (80%) and specificity (98%). Analysis of CSF variables over a disease course showed that acute versus past disease could be discriminated by a combination of basic CSF variables and Bb-specific AI.(ABSTRACT TRUNCATED AT 250 WORDS)

Albumins↗
PubMed1995

The value of CSF analysis for the differential diagnosis of HTLV-I associated myelopathy and multiple sclerosis.

Cerebrospinal fluid (CSF) and serum of 17 patients with HAM/TSP (HTLV-I associated myelopathy/tropical spastic paraparesis), six with multiple sclerosis and six with idiopathic epilepsy (non inflammatory control) from Brazil were analysed for the presence of intrathecal synthesis of virus-specific antibodies against measles, rubella, varicella zoster virus and herpes simplex virus by enzyme-linked immunosorbent assay (ELISA). All HAM/TSP and multiple sclerosis cases had an intrathecal immune response (oligoclonal IgG). In HAM/TSP, only 1/17 case showed a polyspecific intrathecal immune response against measles and rubella virus. In multiple sclerosis, specific antibodies against measles and rubella (MRZ response) were observed in all patients but not in the control with idiopathic epilepsy. The diagnostic and theoretical relevance of mono- and polyspecific immune responses is discussed for these chronic neurological diseases.

Brazil↗
PubMed1995

External quality assessment in clinical neurochemistry: survey of analysis for cerebrospinal fluid (CSF) proteins based on CSF/serum quotients.

Participants (230) from Germany and 20 laboratories in 11 European countries took part in a newly designed cerebrospinal fluid (CSF) survey distributed by INSTAND. Conventional proficiency testing for albumin, IgG, IgA, and IgM in CSF and serum, for total protein in CSF, and for oligoclonal IgG in CSF and serum was combined with evaluation and interpretation of CSF/serum quotients in quotient diagrams. The correct detection of a blood-CSF barrier dysfunction and the pattern of intrathecal immunoglobulin synthesis was judged. The accuracy of CSF/serum quotients and their clinically relevant interpretation was given first priority as a new concept in quality assessment. The main result of the surveys was to confirm that CSF/serum quotients of proteins represent method-independent values approaching the quality of reference values. This finding has consequences for internal quality control of CSF analysis and for accreditation bodies. The sensitivity of the methods for quantifying IgA and IgM in CSF and for detecting oligoclonal IgG fractions is discussed.

Albumins↗
PubMed1994

Flow rate of cerebrospinal fluid (CSF)--a concept common to normal blood-CSF barrier function and to dysfunction in neurological diseases.

Many neurological diseases are accompanied by increased protein concentrations in the cerebrospinal fluid (CSF), described as a blood-CSF barrier dysfunction. The earlier interpretation as a "leakage" of the blood-CSF barrier for serum proteins could be revised by introduction of a "population variation coefficient" of the CSF/serum quotients for IgG, IgA and IgM (delta Q/Q) which is evaluated as a function of increasing albumin quotients (QAlb). The data presented here are based on specimens from 4380 neurological patients. These population variation coefficients were found to be constant over two orders of magnitude of normal and pathological CSF protein concentrations (QAlb = 1.6.10(-3)-150.10(-3)). This constancy indicates that there was no change in blood-CSF barrier related structures with respect to diffusion controlled protein transfer from blood into CSF and hence no change in molecular size dependent selectivity. The pathological increase of plasma protein concentrations in CSF in neurological diseases could also be explained quantitatively by a decrease of CSF flow rate due to its bifunctional influence on CSF protein concentration: reduced volume exchange, and as newly stated, increased molecular net flux into CSF without change of permeability coefficients. Again, on the basis of a changing CSF flow rate, the hyperbolic functions, which describe empirically the changing quotient ratios between proteins of different size (e.g. QIgG:QAlb) with increasing CSF protein content (QAlb) can likewise be derived from the laws of diffusion as the physiologically relevant description. The hyperbolic discrimination line between brain-derived and blood-derived protein fractions in CSF in the quotient diagrams for CSF diagnosis can be further improved on the basis of the large number of cases investigated. Other physiological and pathological aspects, such as high CSF protein values in the normal newborn, in spinal blockade, in meningeal inflammatory processes, CNS leukemia or polyradiculitis as well as animal species dependent variations can each be interpreted as due to a difference or change in the CSF flow rate.

Adolescent↗
PubMed1994

Relevance of endogenous ascorbate and tocopherol for brain cell vitality indicated by photon emission.

In vitro lipid peroxidation of brain cell membranes was recorded directly by monitoring the concomitant photon emission. Chemiluminescence appeared spontaneously after disintegration of vital brain cells (pig brain cell homogenate, isolated oligodendrocytes), decreasing the high intracellular ascorbate concentration in the vital glial cell (1 mmol/L) to a lower overall concentration (< 100 mumol/L). This had a prooxidant effect in the homogenate. Intracellular high antioxidant ascorbate concentrations were also efficient at protecting membrane lipids of vital oligodendrocytes against extracellular low prooxidant ascorbate concentrations (50 mumol/L). The intramembranous alpha-tocopherol content limited the antioxidant efficiency of ascorbate. With physiological concentrations (0.4 nmol of iron to 0.1 nmol of tocopherol per milliter of membrane suspension), a 50% inhibition of lipid peroxidation was obtained with 410 nmol/ml ascorbate; this was reduced to 90 nmol/ml in the case of fivefold increased tocopherol content. So in vivo ascorbate concentrations were sufficient to protect against lipid peroxidation. Only when endogenous tocopherol was decreased to 20% was the in vivo intracellular ascorbate concentration too small for antioxidative protection of lipids. The product of tocopherol concentration and ascorbate concentration, effective for 50% inhibition of lipid peroxidation, remained constant. When iron concentrations were increased 10(4)-fold, maximal chemiluminescence and malondialdehyde formation were increased twofold and less than 50%, respectively. This quantitative description of the interactions between vitamin E, vitamin C, and iron are relevant to the modification of interpretations of pathological conditions in parkinsonian brains.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases.

BACKGROUND AND PURPOSE: To investigate the clinical relevance of plasma concentrations of neuron-specific enolase (NSE) in patients with severe cerebrovascular diseases, serial analyses were performed during the first 10 days after the acute event. METHODS: Plasma samples taken from 61 patients (30 with brain infarction, 13 with intracerebral hemorrhage, 11 with cardiogenic hypoxia-ischemia, and 7 with myocardial infarction [as control group]) were analyzed for NSE concentration using an enzyme immunoassay. The time course of plasma NSE was correlated with clinical findings, clinical outcome, cranial computed tomography, intracranial pressure, and other laboratory data. RESULTS: In cases of hypoxia-ischemia there was close correlation between plasma NSE values during the first 72 hours and the clinical outcome. In brain infarction and intracerebral hemorrhage, high plasma NSE mostly indicated an unfavorable outcome, but low values did not permit a reliable prognostic estimation. In cases of cerebral infarction and intracerebral hemorrhage with secondary neuronal destruction (for example, due to malignant edema), increasing NSE concentrations in plasma preceded the change of clinical or other diagnostic parameters. CONCLUSIONS: The course of plasma NSE levels is seen as a relevant parameter for assessing the prognosis of cerebral hypoxia-ischemia. Additionally, it may prove to be a useful tool for monitoring space-occupying brain infarctions and intracerebral hemorrhages and therefore may contribute to improved therapeutic management of severe cerebrovascular diseases.

Adult↗
PubMed1993

Ascorbate concentration in human cerebrospinal fluid (CSF) and serum. Intrathecal accumulation and CSF flow rate.

Concentrations of ascorbate (vitamin C) in cerebrospinal fluid (CSF) from human controls (median 163 mumol/l, n = 63) were found to be in the same range as CSF samples from patients (n = 56) with various neurological diseases, but excluding those with blood-CSF barrier dysfunction. The CSF/serum concentration ratio in the former group is non-linear, decreasing with increasing serum concentration. Surprisingly, ascorbate concentration in blood (median 41 mumol/l, n = 119) was decreased significantly in cases of neurological diseases with a blood-CSF barrier dysfunction (median 26 mumol/l, n = 30). In this latter group a linear CSF to serum ratio with a mean of 5.7:1 (with CSF/serum albumin quotients QAlb = 7.8-70.8 x 10(-3), median 10.0 x 10(-3)) was observed, approaching a value > 12.5:1 in the case of complete stop of CSF flow. Serum ascorbate concentrations decreased with decreasing CSF flow rate (1 square root of QAlb), indicating a CSF flow-dependent constant contribution from high intrathecal ascorbate concentration to the varying diet-dependent concentrations in blood. In the control group the biological coefficient of variation for CSF ascorbate concentrations (C.V. = 21.1%) was smaller than for serum concentrations (C.V. = 42.6%), confirming an efficient ascorbate homeostasis in human brain. This was different from uric acid which was used as a reference molecule with an inversed gradient in the same group of control patients. Similar variations in CSF(y) and serum(x) for urate concentrations are observed due to the strong correlation y = 0.1x +/- 10 mumol/l, including 99% of the cases with an urate serum concentration range from 80 mumol/l to 460 mumol/l.

Ascorbic Acid↗
PubMed1992

The diagnostic significance of antibody specificity indices in multiple sclerosis and herpes virus induced diseases of the nervous system.

The antibody specificity index (ASI) indicates the cerebrospinal fluid (CSF)/serum difference of antibody amounts per weight unit IgG (normal less than 1.5). It has proven to be the most sensitive inflammation parameter in CSF analysis so far, more sensitive than the Western blot, the "oligoclonal" response, and the empirical differentiation of CSF immunoglobulins. By this diagnostic criterion, several benign viral meningitis cases were found to be caused by the varicella/zoster virus. The diagnostic relevance of local zoster antibody synthesis was greatest in ganglionitis cases, e.g., in zoster oticus sine herpete (facial paresis) and acute radicular syndromes of the elderly. The diagnostic significance of the local immune response against measles, rubella, and zoster antigens (MRZ response) was ascertained further. Together with oligoclonal gamma-globulin fractionation, there is now only 1 out of 100 multiple sclerosis (MS) patients left who has been found to have a normal CSF.

Adult↗
PubMed1991

Clinical relevance of the quantification of apolipoprotein E in cerebrospinal fluid.

Apolipoprotein E was measured in paired sera and cerebrospinal fluid samples from 483 neurological patients. The average apolipoprotein E concentration was 7.5 (+/- 3.1) mg/l in cerebrospinal fluid and 93.5 (+/- 29.7) mg/l in serum. Mean apolipoprotein B concentrations in 88 patients were 0.77 +/- 3.4 mg/l in cerebrospinal fluid and 1.06 +/- 0.31 g/l in serum. The apolipoprotein E concentration in cerebrospinal fluid was much greater than expected for passive diffusion from serum. By contrast to apolipoprotein B, there was no correlation between the apolipoprotein E cerebrospinal fluid/serum concentration quotient and the albumin concentration quotient. This suggests that apolipoprotein E in cerebrospinal fluid, unlike apolipoprotein B, is locally synthesized and that the use of a cerebrospinal fluid/serum concentration quotient is unnecessary. In a control group (n = 64) the mean cerebrospinal fluid apolipoprotein E value (+/- SD) was 5.9 (1.6) mg/l. Elevated cerebrospinal fluid apolipoprotein E concentrations were observed in acute (n = 22, 12.5 +/- 6.2 mg/l) and chronic inflammatory central nervous system diseases (n = 15, 10.4 +/- 2.4 mg/l).

Adult↗
PubMed1991

Quantification of virus-specific antibodies in cerebrospinal fluid and serum: sensitive and specific detection of antibody synthesis in brain.

Specific antibody synthesis in brain could be detected with maximal sensitivity by combining an advanced enzyme immunoassay with a sophisticated evaluation method that involves calculating the ratio between the cerebrospinal fluid (CSF)/serum quotients for specific antibodies (Qspec) and total IgG (QIgG). This Antibody Index (AI = Qspec/QIgG) discriminates between a blood-derived and a pathological, brain-derived specific antibody fraction in CSF and takes into account individual changes in blood/CSF barrier function. For local synthesis of polyclonal IgG in the central nervous system (QIgG greater than QLim), we propose the correction AI = Qspec/QLim (QLim represents that IgG fraction in CSF originating only from blood, calculated from the individual albumin quotient of a single patient). The normal reference range for the AI was between 0.7 and 1.3 (n = 250 control patients for each antibody species). Values of AI greater than or equal to 1.5 indicated a local specific antibody synthesis in the central nervous system. Sensitivity and precision were greatest if we analyzed the virus-specific antibodies in CSF and serum simultaneously with an enzyme immunoassay in continuous concentrations (arbitrary units) instead of titer steps. We have applied the method successfully to antibodies to measles, rubella, herpes simplex, varicella-zoster, human immunodeficiency virus (HIV), and cytomegalovirus, and to anti-Toxoplasma or -Borrelia antibodies. Clinical relevance is demonstrated for an acute zoster virus infection (monospecific response), chronic diseases such as HIV encephalitis with acute opportunistic Toxoplasma infection, and multiple sclerosis (secondary polyspecific response).

Antibodies, Viral↗
PubMed1989

Discrimination between different types of low-level luminescence in mammalian cells: the biophysical radiation.

Cellular low-level luminescence was measured after various disintegrative processes in brain cell preparations. In addition to known origins of low-level luminescence, e.g. oxygen radical reactions or enzymatic and non-enzymatic redox systems, a further source of photon emission is reported which is independent of external oxygen, oxygen radicals and enzyme activities. Vital cells from rat brain homogenates or pig oligodendrocytes could be kept for hours at 37 degrees C without any photon emission. Only after disintegrative processes a cellular photon emission could be induced. The maximal intensity of about 400 impulses/s/mg protein and a total radiation of about 6 X 10(6) l/mg depended on the type of cells. The signal could be retained completely at 4 degrees C or in frozen samples. Heating (10 min, 90 degrees C) did not suppress the photon emission. Luminol and lucigenin did not amplify the signal as is usually observed in oxygen radical-producing cells. Non-specific radical scavengers as well as detergents suppressed the cellular photon emission completely. It is suggested that this cellular luminescence represents a biophysical radiation which originates from the interruption of an intermolecular radiationless energy transfer.

Animals↗
PubMed1988

Clinical relevance of increased neuron-specific enolase concentration in cerebrospinal fluid.

Neuron-specific enolase (NSE) concentrations in cerebrospinal fluid (CSF) and serum have been studied by an EIA-method using monoclonal antibodies against human NSE. In a control group (n = 24) the mean NSE value (+/- SD) in CSF was 10.8 (+/- 4.5) ng/ml. Increased NSE values in CSF (greater than or equal to 20 ng/ml, ie greater than or equal to means + 2s) have been detected in 33/172 patients with the following neurological diseases: CNS tumors (6/30), infarctions (6/36), cerebral ischemias (5/25), inflammatory diseases (7/33), epilepsias (3/10) and miscellaneous neurological diseases (6/38). The NSE assay in CSF was not specific for a single neurological disease. In 9% of all patients with an organic neurological disease the increased NSE concentration was the only abnormal result in the CNS out of variables routinely determined in CSF. The discrimination between an organic and psychogenic origin of epilepsy may be possible by an NSE analysis in CSF. The NSE assay in CSF can be recommended as an unspecific screening parameter for pathological organic CNS processes.

Antibodies, Monoclonal↗
PubMed1988

Cellular immune reactions and blood cerebrospinal fluid barrier dysfunction in guinea pigs.

Both young and adult strain 13 guinea pigs have been treated with complete Freund's adjuvant (CFA). In young animals CFA induced an increase in the lymphocyte cell count in blood and a reversible blood CSF barrier impairment. Both these effects could be suppressed by the immunosuppressant drug Cyclosporin A. In contrast to the young animals treatment with CFA in adult strain 13 guinea pigs influenced neither the lymphocyte cell count nor blood CSF barrier function. In young and adult CFA-treated animals the number of polymorphonuclear cells in blood were increased and this increase was not reversed by Cyclosporin A. We discuss the influence of a systemic immune stimulation and suppression on blood CSF barrier function for proteins and its relevance to the pathogenesis of inflammatory diseases of the central nervous system.

Animals↗
PubMed1987

Protein transfer at the blood cerebrospinal fluid barrier and the quantitation of the humoral immune response within the central nervous system.

The cerebrospinal fluid (CSF)/serum concentration quotients of albumin and the immunoglobulins G, A and M have been determined for 396 patients with a normal blood CSF barrier function or a pure barrier impairment without a humoral immune response within the central nervous system. The ratios between the concentration quotients of the three immunoglobulins and that of albumin increase in a nonlinear fashion with progressive impairments of the blood CSF barrier, i.e. the molecular size dependent discrimination of the protein transfer ('selectivity') decreases. The upper reference values of the concentration quotients for the whole range of passive transfer comply with the hyperbolic function: Q(IgX) = a/b square root Q(Alb)2 + b2 - c with different constants a/b, b2, c for IgG (0.8, 15 X 10(-6), 1.8 X 10(-3), IgA (0.72, 80 X 10(-6), 5.1 X 10(-3) and IgM (0.65, 150 X 10(-6), 7.5 X 10(-3). With these discriminatory functions the locally synthesized fractions IgX(loc) of IgG, IgA and IgM in CSF can be calculated by the general formula: IgX(loc) = [Q(IgX) - a/b square root Q(Alb)2 + b2 + c] X IgX(Ser).

Albumins↗