Published online by Cambridge University Press: 24 June 2014
CSF analysis contributes to differential diagnosis of noninflammatory diseases by: 1) exclusion of a chronic or acute inflammation. 2) detection of particular brain-derived proteins, surrogate markers, corresponding to the suggested diagnosis (tumor, dementia, brain hypoxia, hemorrhage, autoimmune disease, psychiatric disease, metabolic disorder, rhinorhea, Table 1) and 3. differential cell count in CSF.
Interpretation of brain-derived proteins in CSF uses absolute concentrations (in contrast to CSF/serum quotients for blood-derived proteins) and must discriminate between different sources: Neuronal or glial proteins like NSE, or tau protein are evaluated using their absolute concentrations in CSF for maximal sensitivity without reference to QAlb. The leptomeningeal proteins like beta trace or cystatin C are evaluated as absolute concentrations with reference to QAlb.
As application examples we review the group of dementive and psychiatric diseases.
Alzheimer's disease, Parkinson's disease dementia, Lewy-body disease and frontotemporal dementia are the major causes of neurodegenerative memory impairment and dementia. Combined analysis of Tau-Protein and Beta Amyloid 1-42 in CSF represent the classic approach, meanwhile extended with further surrogate markers. In 15% of psychiatric patients with schizophrenic or affective disorders an inflammatory process could be detected which points to a brain-organic involvement. In 24% of these patients with a psychiatric disease a moderately increased albumin quotient was observed as the only unexplained pathological sign. In psychiatric diseases it has to be regarded as a serious deficit not to make at least once a CSF analysis in the patients which could modify the diagnosis (in 6%).