Aneurysmal subarachnoid hemorrhage (aSAH) results in low prevalence of neuro-endocrine dysfunction and NOT deficiency.
Neuro-endocrine deficiencies have been argued to be common sequelae after aneurysmal subarachnoid hemorrhage (aSAH). As this, however, does not resemble our clinical experience, we studied the incidence of neuro-endocrine and neuropsychological deficits after aSAH. Twenty-six patients (20 females) were prospectively screened for neuro-endocrine and neuropsychological deficits 3, 6 and 12 months after aSAH. GH, IGF-1, prolactin, LH, FSH, estradiol, testosterone, ACTH as well as cortisol during ACTH-stimulation were assessed. Neuropsychological analysis covered verbal comprehension, short term and working memory, visuospatial construction, figural memory, psychomotor speed, attention, and concentration. During the study period 5 individuals demonstrated neuro-endocrine dysfunction. Hypogonadotrophic hypogonadism resolved spontaneously in 2 patients and central hypothyroidism in one of these patients during the study. After 12 months three patients presented low IGF-1 levels. 73.9% of our cohort was affected by neuropsychological deficits during follow-up. At 3, 6 and 12 months the prevalences were 56.5, 52.6 and 42.1%, respectively. Interestingly, all patients with neuro-endocrine dysfunction presented impaired clinical outcome with a GOS 4 at some time point of the study (GOS 4 vs. 5, 45.5% vs. 0, P = 0.007). We found a low prevalence of neuro-endocrine and a high prevalence of neuropsychological deficits in patients 3, 6 and 12 months after aSAH without significant interrelation. Spontaneous recovery of neuro-endocrine alterations most likely presents an adaption to or dysfunction after severe illness. This hypothesis is strengthened by the fact that only patients with inferior clinical outcome after aSAH as assessed by GOS demonstrated neuro-endocrine dysfunction.
Fifth Department of Medicine, University Medical Center Mannheim, Mannheim, Germany.
Alexander
A
Lammert
Hinrich
H
Bode
Hans-Peter
HP
Hammes
Rainer
R
Birck
Marc
M
Fatar
Katrin
K
Zohsel
Kirsten
K
Schmieder
Gerrit Alexander
GA
Schubert
Claudius
C
Thomé
Marcel
M
Seiz
D000324:Adrenocorticotropic Hormone / Q000378:metabolism; D000328:Adult; D004958:Estradiol / Q000378:metabolism; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D019382:Human Growth Hormone / Q000378:metabolism; D006801:Humans; D007037:Hypothyroidism / Q000378:metabolism / Q000503:physiopathology; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D007986:Luteinizing Hormone / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009483:Neuropsychological Tests; D011388:Prolactin / Q000378:metabolism; D011446:Prospective Studies; D013345:Subarachnoid Hemorrhage / Q000378:metabolism* / Q000503:physiopathology*; D013739:Testosterone / Q000378:metabolism
D019382:Human Growth Hormone; D013739:Testosterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone