[German diagnosis related groups (G-DRG): results of sociomedical expertises in acute cerebrovascular diseases]. / German Diagnosis Related Groups (G-DRG): Sozialmedizinische Begutachtungsergebnisse bei akuten zerebrovaskulären Erkrankungen.

Acute cerebrovascular diseases are the most common cause for permanent disability and the most expensive diseases in industrialised countries. Therefore, all sociomedical DRG expertises (n=7 227, 94.15% initial expertises, 5.85% subsequent expertises) of the Medical Services of the German Statutory Sickness Insurance (MDK) Berlin-Brandenburg in the years 2005-2008 concerning correct G-DRG coding in acute cerebrovascular diseases were evaluated using descriptive statistics. Changes of major diagnostic category (MDC) were done in 4.35% of initial and in 2.84% of subsequent expertises, G-DRG changes without MDC change in 10.41% of initial and 14.42% of subsequent expertises, changes of severity code within one G-DRG in 25.81% of initial and 24.82% of subsequent expertises. No change of cost weight was seen in 59.44% of initial and 57.92% of subsequent expertises. In 1.29% of initial and 1.89% of subsequent expertises, the cost weight given by the hospital was lower than the cost weight determined by MDK. In 39.27% of initial and in 40.19% of subsequent expertises the cost weight given by the hospital was higher than the cost weight determined by MDK. Longitudinal comparisons of the years 2005-2008 showed an increase of changes of severity codes and of the cases with cost weight given by the hospital being higher than the cost weight determined by MDK. A decrease was seen in MDC changes, in G-DRG changes without MDC change and of cases with unchanged cost weights. The results point at learning effects considering the right coding as well as at the existence of further room for improvement concerning the quality of coding after hospital treatment of acute cerebrovascular diseases.

Immunoreactivities of amyloid beta peptide((1-42)) and total tau protein in lumbar cerebrospinal fluid of patients with normal pressure hydrocephalus.

Immunoreactivities of amyloid beta peptide((1-42)) (Abeta42-IR) and total tau protein (TTIR) were measured in lumbar cerebrospinal fluid of 48 patients (12 patients in each group) with normal pressure hydrocephalus (NPH), vascular dementia (VD), Alzheimer's disease (AD), Parkinson's disease without dementia (PD) and 24 controls (CON) using sensitive and specific enzyme immunoassays. TTIR in NPH was not significantly changed compared with VD, PD and CON, while NPH-Abeta42-IR was significantly decreased compared with PD and CON. In AD, significant increases of TTIR and significant decreases of Abeta42-IR were found. Using a TTIR by Abeta42 plot, all NPH, PD, and CON samples were within the non-AD plot region. 92% of AD and VD samples were within the AD and non-AD area, respectively. We conclude that combined measurement of Abeta42-IR and TTIR contributes to the differential diagnosis of NPH vs. AD and of AD vs. VD, respectively.

Clinical significance of neurobiochemical profiles in the lumbar cerebrospinal fluid of Alzheimer's disease patients.

Immunoreactivities of total apolipoprotein E (ApoE-IR), amyloid beta peptide(1-42) (Abeta42-IR), interleukin-6 (IL-6-IR), substance P (SPIR) and total tau protein (TTIR) were measured in lumbar cerebrospinal fluid samples of patients with Alzheimer's disease (AD), non-Alzheimer's dementias (NAD), neurological disorders without cognitive impairment (OND) and controls without central nervous system disease using sensitive and specific enzyme immunoassay methods. TTIR was highly significantly increased (P < 0,001) and Abeta42-IR was significantly decreased (P < 0,001 vs. OND/CO, P < 0,03 vs. NAD) in the AD cohort compared with the other diagnostic groups. Significant increases in AD were also found for ApoE-IR (P < 0,001) and IL-6 (P < 0,03), but there was a considerable overlap between groups. In the total AD cohort, SPIR was not significantly changed, but AD patients with late disease onset (>65 years) showed significantly higher values than both early onset patients (<65 years) and controls (P < 0,05). Discriminant function analysis showed that Abeta42-IR (cut-off value 375pg/ml) and TTIR (cut-off value 440 pg/ml) levels contributed most to the group classification of patients. At 85% sensitivity for AD and 100% specificity for controls, the combined evaluation of Abeta42-IR and TTIR in this cross-sectional study resulted in a graph separating AD from non-AD patients with increased specificity of 91% and 75% for AD versus OND and NAD, respectively.

Intra vitam lumbar and post mortem ventricular cerebrospinal fluid immunoreactive interleukin-6 in Alzheimer's disease patients.

OBJECTIVES: In view of contradictory findings in previous studies, to examine the diagnostic value of interleukin-6 measurements in cerebrospinal fluid (CSF) of Alzheimer's disease patients. MATERIAL AND METHODS: Interleukin-6-immunoreactivity (IL-6-IR) was measured in 169 intra vitam lumbar and 21 post mortem ventricular CSF samples of patients with probable and neuropathologically confirmed Alzheimer's disease (AD), non-AD dementias (NAD), neurological disorders without cognitive impairment (OND) and controls (CON) using a specific sandwich enzyme immunoassay. RESULTS: Intra vitam lumbar samples had significantly elevated (P < 0.03) IL-6-IR not only in the AD, but also in the NAD and OND group compared with controls. AD patients with late onset (> 65 years) had slightly (P > 0.05) higher values than patients with early onset (< 65 years). In post mortem ventricular fluid, differences among groups did not reach significance (P > 0.05). CONCLUSION: We conclude that elevations of CSF IL-6-IR can not serve as a diagnostic marker of the disease, but, hypothetically, could reflect presence or activity of IL-6 mediated immunological phenomena in single AD patients.

Ex vivo lumbar and post mortem ventricular cerebrospinal fluid substance P-immunoreactivity in Alzheimer's disease patients.

The concentration of substance P-immunoreactivity (SPIR) in ex vivo lumbar cerebrospinal fluid (CSF) of patients with probable Alzheimer's disease (AD), non-Alzheimer dementias, neurological patients without dementia and control subjects was determined using a sensitive and specific competitive enzyme-immunoassay. There were no significant differences between AD patients and the other groups, but patients with late onset AD (>65 years) showed significantly higher levels of SPIR than patients with early onset (<65 years) and controls. In post mortem ventricular fluid, SPIR levels of all groups were lower compared with the lumbar compartment, but without significant group differences. It is concluded that CSF SPIR may not serve as a diagnostic marker for AD, but possibly could reflect immunological or neuroprotective processes modulated by substance P in late onset AD patients.

[Dementias--diagnosis, differential diagnosis and therapy]. / Demenzerkrankungen--Diagnose, Differentialdiagnose und Therapie.

The most common cause of primary (degenerative) dementia in old age is Alzheimer's disease, with vascular forms of dementia taking second place. Endocrinopathies, normal pressure hydrocephalus and space-occupying lesions are frequent causes of secondary dementia. A multitude of further, more rare clinical presentations results in a wide differential diagnostic spectrum necessitating a careful diagnostic work-up of the demential syndrome before considering treatment. This work-up must include clinical, laboratory and equipment-based investigations. The multimodal therapeutic approach to dementia covers not only the elimination of treatable underlying causal conditions and the medical treatment of cognitive symptoms and psychiatric accompanying symptoms, but also non-medicamentous aspects.

Intra vitam lumbar cerebrospinal fluid and serum and postmortem ventricular immunoreactive apolipoprotein E in patients with Alzheimer's disease.

Using a specific enzyme linked immunosorbent assay (ELISA) method, total apolipoprotein E immunoreactivity (tApoE-IR) was measured in premortem lumbar CSF and serum of patients with "probable" Alzheimer's disease and in postmortem ventricular CSF of patients with Alzheimer's disease confirmed by necropsy. Concentrations were compared with those from patients with other neurological diseases and controls. The mean serum:lumbar CSF ratio of ApoE-IR was 15.9 suggesting that the main portion of lumbar ApoE-IR is synthesised intrathecally. No significant differences in ApoE-IR between patients with Alzheimer's disease and the other groups were detected in either CSF compartment. In lumbar CSF, there was no correlation between ApoE-IR of patients with Alzheimer's disease and their mini mental state scores. These results suggest that the diagnostic value of ApoE-IR measurements in CSF of patients with Alzheimer's disease as a single determination is less than that of other markers, in particular tau protein. On the other hand, ApoE determinations could be useful as part of a neurochemical profile of Alzheimer's disease.

Tau protein and apolipoprotein E in CSF diagnostics of Alzheimer's disease: impact on non Alzheimer's dementia?

Tau protein and apolipoprotein E are suggested to be biochemically related to neurofibrillary tangles and senile plaques in Alzheimer's disease (AD) brains. They can be detected as immunoreactive material (total tau immunoreactivity [TTIR] and apolipoprotein E-immunoreactivity [ApoEIR]) in the cerebrospinal fluid (CSF). TTIR and ApoE-IR have been measured in ex vivo lumbar and post mortem ventricular CSF in AD, other neurological diseases without cognitive impairment, elderly depressive patients, and young and elderly controls. In lumbar CSF, there was a highly significant increase of TTIR and a minor, insignificant decrease of ApoE-IR in CSF of AD patients. The latter result was also found in ventricular CSF, whereas TTIR showed no significant difference between groups in the rostral CSF compartment. As depressive periods in the elderly may mimick a dementing process, these findings contribute to the differential diagnosis of these disorders by showing a different neurobiochemical CSF profile. Work in progress will include a variety of non-Alzheimer's dementias and possibly will further increase the value of CSF investigation in neurodegenerative disorders.

Cerebrospinal fluid levels of immunoreactive substance P and somatostatin in patients with multiple sclerosis and inflammatory CNS disease.

Cerebrospinal fluid (CSF) levels of substance-P like immunoreactivity (SPLI) and somatostatin-like immunoreactivity (SLI) were measured in 43 patients with multiple sclerosis (MS), differentiated according to course and activity of the disease, in 23 patients with inflammatory disease of known bacterial or viral etiology and in 16 control patients using specific radioimmunoassay. SPLI and SLI levels were not significantly different from controls in MS patients whereas SLI was significantly increased in patients with infectious disease of central nervous system and/or subarachnoidal space. It is assumed that CSF SPLI and SLI cannot serve as a diagnostic or prognostic indicator of disease state in multiple sclerosis. Analysis of immunoreactivity by reverse phase HPLC-RIA revealed marked molecular heterogeneity of both neuropeptides.

Immunoreactive substance P and somatostatin in the cerebrospinal fluid of senile parkinsonian patients.

The concentration of substance-P-like immunoreactivity (SPLI) and somatostatin-like immunoreactivity (SLI) in the lumbar spinal fluid of senile parkinsonian patients (mean age 77.6 +/- 6.7 years) and senile control patients (mean age 83.5 +/- 5.6 years) were determined by specific radioimmunoassays. Mean SPLI and SLI levels in the control group were 8.1 +/- 2.0 (SD) and 32.5 +/- 12.0 fmol/ml, respectively. The mean SPLI levels were not significantly different in the groups. The mean SLI level was significantly lower in the group of patients with Parkinson's disease (19.8 +/- 9.0 fmol/ml). A comparison with results in patients with senile dementia of Alzheimer type (SDAT) shows that, in addition to clinical and pathological correlations, Parkinson's disease of late onset may share a deficit in somatostatinergic neuromodulation with SDAT.

Cerebrospinal fluid immunoreactive substance P and somatostatin in neurological patients with peripheral and spinal cord disease.

We have measured substance P-like (SPLI) and somatostatin-like (SLI) immunoreactivities in cerebrospinal fluid of 49 patients with peripheral (polyneuropathy, lumboischialgia) and spinal cord disease and in 16 control patients. The patient groups showed significantly higher CSF SPLI levels than controls while the mean SLI levels were unchanged. Fractionated sampling of CSF (total volume 30 ml) in 20 patients with various neurological diseases showed no significant differences between early and late fractions for SLI. In contrast, lumbar-cisternal concentration gradients were negative for SPLI, total protein and IgG, and positive for the dopamine metabolite homovanillic acid and the serotonin metabolite 5-hydroxyindolacetic acid. This suggests that SPLI may be released into the lumbar CSF from lower levels of the neuraxis, presumably the spinal cord and spinal ganglia, whereas SLI stems from diffuse CSF secretion without spinal preponderance.