title: Biochemical markers of cerebrovascular injury in sleep apnoea syndrome.
abstract: Sleep apnoea syndrome (SAS) is a known risk factor for vascular diseases and stroke. Structural brain damage, manifesting as an overt neurological deficit or more subtly as cognitive dysfunction, is a frequent symptom in SAS. The presence of a biochemical marker of cerebral injury would be of great benefit in SAS to screen for even small brain damage and to monitor efficiacy of therapy. Therefore, in 10 patients with mild SAS (age 50.8+/-9.9 yrs, respiratory disturbance index (RDI) 18+/-3.6, lowest arterial oxygen saturation (min Sa,O2) 80.5+/-4.06%) and nine patients with severe SAS (age 50.3+/-11.5 yrs, RDI 75.4+/-21.7, min Sa,O2 56.56+/-14.58%), serum concentrations of neuron-specific enolase (NSE), S-100beta protein, and beta-trace were measured just before and after sleep using commercially available assays. Only serum levels in the normal range could be found, independent of when the blood was taken or the degree of SAS. Structural cerebral injury caused by sleep apnoea syndrome in patients without neurological symptoms or previous cerebrovascular events may be too small to produce a measurable increase in S-100beta, neuron-specific enolase and beta-trace serum concentrations or subclinical cerebral damage may be outside the lower detection limits of the analytical methods which were used. There is a need for biochemical markers and more sensitive methods for detecting small cerebral injury in sleep apnoea syndrome.
authors.affiliation: Dept of Psychiatry and Psychotherapy, University Göttingen, Germany. wjordan@gwg.de
authors.forename: W
authors.initials: W
authors.lastname: Jordan
authors.forename: J
authors.initials: J
authors.lastname: Hagedohm
authors.forename: J
authors.initials: J
authors.lastname: Wiltfang
authors.forename: G
authors.initials: G
authors.lastname: Laier-Groeneveld
authors.forename: H
authors.initials: H
authors.lastname: Tumani
authors.forename: A
authors.initials: A
authors.lastname: Rodenbeck
authors.forename: E
authors.initials: E
authors.lastname: Rüther
authors.forename: G
authors.initials: G
authors.lastname: Hajak
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood*; D001784:Blood Gas Analysis; D001930:Brain Injuries / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D019746:Intramolecular Oxidoreductases / Q000097:blood*; D054834:Lipocalins; D008297:Male; D008875:Middle Aged; D009414:Nerve Growth Factors; D010100:Oxygen / Q000097:blood; D010751:Phosphopyruvate Hydratase / Q000097:blood*; D017286:Polysomnography; D011237:Predictive Value of Tests; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins / Q000097:blood*; D012720:Severity of Illness Index; D020181:Sleep Apnea, Obstructive / Q000097:blood* / Q000150:complications* / Q000503:physiopathology
chemical_list: D015415:Biomarkers; D054834:Lipocalins; D009414:Nerve Growth Factors; D064568:S100 Calcium Binding Protein beta Subunit; D009418:S100 Proteins; D010751:Phosphopyruvate Hydratase; D019746:Intramolecular Oxidoreductases; C022466:prostaglandin R2 D-isomerase; D010100:Oxygen