Cognitive functioning and cerebrospinal fluid concentrations of neuropeptides for patients with good neurological outcomes after aneurysmal subarachnoid hemorrhage

Citation
Tk. Uski et al., Cognitive functioning and cerebrospinal fluid concentrations of neuropeptides for patients with good neurological outcomes after aneurysmal subarachnoid hemorrhage, NEUROSURGER, 47(4), 2000, pp. 812-818
Citations number
36
Categorie Soggetti
Neurology,"Neurosciences & Behavoir
Journal title
NEUROSURGERY
ISSN journal
0148396X → ACNP
Volume
47
Issue
4
Year of publication
2000
Pages
812 - 818
Database
ISI
SICI code
0148-396X(200010)47:4<812:CFACFC>2.0.ZU;2-V
Abstract
OBJECTIVE: Many patients exhibit cognitive disturbances after aneurysmal su barachnoid hemorrhage (SAH). Structural and functional neuroimaging has fai led to demonstrate any correlation with these complaints. This study was pe rformed to investigate whether neuropeptide concentrations in cerebrospinal fluid could be related to cognitive disturbances after SAH. METHODS: Lumbar cerebrospinal fluid was obtained, 3 to 6 months after surge ry, from 17 patients who experienced good outcomes after aneurysmal SAH. Th e samples were analyzed for various neuropeptides using radioimmunoassays, and the peptide concentrations were evaluated in relation to scores on stan dardized neuropsychological tests. RESULTS: The neuropsychological test results were normal for eight individu als, whereas the remaining nine patients exhibited various degrees of cogni tive impairment. There was no correlation between the concentrations of arg inine vasopressin or neuropeptide Y and test performance. However, signific ant correlations between cognitive impairment and elevated levels of beta-e ndorphins (P = 0.02), corticotropin-releasing factor (P = 0.004), and delta sleep-inducing peptide (P = 0.045) were noted. CONCLUSION: Patients with cognitive impairments after aneurysmal SAH exhibi ted higher cerebrospinal fluid concentrations of endorphins, corticotropin- releasing factor, and delta sleep-inducing peptide than did those with norm al capacity. This is probably attributable to diffuse derangement of transm itter release in the brain, resulting from the insult or ensuing complicati ons, although a secondary increase in corticotropin-releasing factor concen trations caused by increased stress during the testing because of reduced c ognitive capacity cannot be excluded.