Free fatty acids in human cerebrospinal fluid following subarachnoid hemorrhage and their potential role in vasospasm: a preliminary observation.
OBJECTIVE
The mechanisms leading to vasospasm following subarachnoid hemorrhage (SAH) remain unclear. Accumulation in cerebrospinal fluid (CSF) of free fatty acids (FFAs) may play a role in the development of vasospasm; however, in no previous study have concentrations of FFAs in CSF been examined after SAH.


METHODS
We collected samples of CSF from 20 patients with SAH (18 cases of aneurysmal SAH and two cases of spontaneous cryptogenic SAH) and used a high-performance liquid chromatography assay to determine the FFA concentrations in these samples. We then compared these findings with FFA concentrations in the CSF of control patients. All FFA concentrations measured 24 hours after SAH were significantly greater than control concentrations (p < 0.01 for palmitic acid and < 0.001 for all other FFAs). All measured FFAs remained elevated for the first 48 hours after SAH (p < 0.05 for linoleic acid, p < 0.01 for palmitic acid, and p < 0.001 for the other FFAs). After 7 days, a second elevation in all FFAs was observed (p < 0.05 for linoleic acid, p < 0.01 for palmitic acid, and p < 0.001 for the other FFAs). Samples of CSF collected within 48 hours after SAH from patients in whom angiography and clinical examination confirmed the development of vasospasm after SAH were found to have significantly higher concentrations of arachidonic, linoleic, and palmitic acids than samples collected from patients in whom vasospasm did not develop (p < 0.05).


CONCLUSIONS
Following SAH, all FFAs are initially elevated. A secondary elevation occurs between 8 and 10 days after SAH. This study provides preliminary evidence of FFA elevation following SAH and of a potential role for FFAs in SAH-induced vasospasm. A prospective study is warranted to determine if CSF concentrations of FFAs are predictive of vasospasm.
Department of Neurosurgery, Wayne State University Detroit, Michigan 48201, USA. jpilitsis@neurosurgery.wayne.edu
Julie G
JG
Pilitsis
William M
WM
Coplin
Michael H
MH
O'Regan
Jody M
JM
Wellwood
Fernando G
FG
Diaz
Marilynn R
MR
Fairfax
Daniel B
DB
Michael
John W
JW
Phillis
D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016718:Arachidonic Acid / Q000134:cerebrospinal fluid; D004281:Docosahexaenoic Acids / Q000134:cerebrospinal fluid; D005230:Fatty Acids, Nonesterified / Q000134:cerebrospinal fluid* / Q000502:physiology*; D005260:Female; D006801:Humans; D019787:Linoleic Acid / Q000134:cerebrospinal fluid; D008297:Male; D008875:Middle Aged; D019814:Myristic Acid / Q000134:cerebrospinal fluid; D009829:Oleic Acids / Q000134:cerebrospinal fluid; D010169:Palmitic Acids / Q000134:cerebrospinal fluid; D013345:Subarachnoid Hemorrhage / Q000134:cerebrospinal fluid* / Q000150:complications / Q000503:physiopathology*; D013997:Time Factors; D020301:Vasospasm, Intracranial / Q000134:cerebrospinal fluid* / Q000209:etiology / Q000503:physiopathology*
D005230:Fatty Acids, Nonesterified; D009829:Oleic Acids; D010169:Palmitic Acids; D019814:Myristic Acid; D004281:Docosahexaenoic Acids; D016718:Arachidonic Acid; D019787:Linoleic Acid