Hostname: page-component-5c6d5d7d68-7tdvq Total loading time: 0 Render date: 2024-09-02T02:19:33.110Z Has data issue: false hasContentIssue false

Cerebrospinal fluid analysis for diagnosis of noninflammatory, dementive and psychiatric diseases

Published online by Cambridge University Press:  24 June 2014

H. Reiber
Affiliation:
CSF and Complexity Studies, University Goettingen, Germany
M. Otto
Affiliation:
Department of Neurology, Ulm University, Germany
K. Bechter
Affiliation:
Clinic for Psychiatry and Psychotherapy II, Ulm University, Germany

Abstract:

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%).

Type
Crash Course: Cerebrospinal Fluid Diagnostics for Psychiatrists and Neurologists
Copyright
Copyright © 2009 John Wiley & Sons A/S

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

References:

1.Reiber, H & Peter, JB.Cerebrospinal fluid analysis – disease-related data patterns and evaluation programs. J Neurol Sci 2001;184:101122.CrossRefGoogle ScholarPubMed
2.Reiber, H. Basic CSF diagnostic in neuroimmunological diseases. Acta Neuropsychiatrica 2008;20(S1): 910.Google Scholar
3.Reiber, H, Ungefehr, St, Jacobi Chr. The intrathecal, polyspecific and oligoclonal immune response in multiple sclerosis. Multiple Sclerosis 1998;4:111117.CrossRefGoogle Scholar
4.Rostasy, K, Reiber, H.Clinical and neurochemical characteristics of pediatric Multiple sclerosis – CSF analysis as knowledge base for differential diagnosis and pathopysiology. Acta Neuropsychiatrica, 2009; this issue.Google Scholar
5.Bechter, K, Reiber, H, Herzog, S, Fuchs, D, Tumani, H, Maxeiner, HG.Cerebrospinal fluid analysis in affective and schizophrenic spectrum disorders. Recognition of subgroups with immune responses and blood-CSF barrier dysfunction. J Psych Res 2009; submitted.Google Scholar
6.Reiber, H: Dynamics of brain-derived proteins in cerebrospinal fluid. Clin Chim Acta 2001;310:173186CrossRefGoogle ScholarPubMed
7.Reiber, H. Proteins in cerebrospinal fluid and blood: Barriers, CSF flow rate and source-related dynamics. Restorative Neurology and Neuroscience 2003;21:7996.Google ScholarPubMed
8.Reiber, H. Flow rate of cerebrospinal fluid (CSF)- a concept common to normal blood-CSF barrier function and to dysfunction in neurological diseases. J Neurol Sci 1994;122:189203.CrossRefGoogle ScholarPubMed
9.Schaarschmidt, H, Prange, H, Reiber, H.Neuron-specific enolase concentrations in blood as a prognostic parameter in cerebrovascular diseases. Stroke 1994;24:558565.CrossRefGoogle Scholar
10.McKhann, G, Drachman, D, Folstein, M, et al.Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology 1984;34:939944.CrossRefGoogle ScholarPubMed
11.Dubois, B, Feldman, HH, Jacova, C, et al.Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDSADRDA criteria. Lancet Neurol. 2007;6(8):734746.CrossRefGoogle ScholarPubMed
12.Otto, M, Lewczuk, P, Wiltfang, J.Neurochemical approaches of cerebrospinal fluid diagnostics in neurodegenerative diseases. Methods. 2008;44:289298.CrossRefGoogle ScholarPubMed
13.Jesse, S, Steinacker, P, Lehnert, S, Gillardon, F, Hengerer, B, Otto, M.Neurochemical approaches in the laboratory diagnosis of Parkinson's and Parkinson's dementia syndromes: A review. CNS Neuroscience and therapeutics 2009; 126 (online available).Google Scholar
14.Reiber, H, Albaum, W. Statistical evaluation of intrathecal protein synthesis in CSF/Serum quotient diagrams. Acta Neuropsychiatrica 2008;20(S1):4849. Free download of the CSF Statistics Tool from www.COMED-com.de.Google Scholar
15.Reiber, H, Walther, K, Althaus, H.Betra-trace protein as sensitive marker for CSF Rhinorhea and CSF Otorhea. Acta Neurol Scandinavica 2003;108:359362.CrossRefGoogle ScholarPubMed
16.Graef, IT, Henze, T und Reiber, H. Polyspezifische Immunreaktion im ZNS bei Auto-Immunerkrankungen mit ZNS-Beteiligung. Zeitschrift für ärztliche Fortbildung 1994;88: 587591.Google Scholar