Cerebral hypoperfusion precedes nausea during centrifugation.
BACKGROUND
Nausea and motion sickness are important operational concerns for aviators and astronauts. Understanding the underlying mechanisms associated with motion sickness may lead to new treatments. The goal of this work was to determine if changes in cerebral blood flow precede the development of nausea in subjects susceptible to motion sickness.


METHODS
Cerebral flow velocity in the middle cerebral artery (transcranial Doppler), BP, and end-tidal CO2 were measured while subjects were rotated on a centrifuge (250 degrees x s(-1)). Following 5 min of rotation, subjects were translated 51.5 cm off-center, creating a +1 Gx centripetal acceleration in the nasal-occipital plane.


RESULTS
There were 10 subjects who completed the protocol without symptoms while 5 developed nausea (4 while off-center and 1 while rotating on-center). Prior to nausea, subjects had significant increases in BP (+13 +/- 3 mmHg, p < 0.05) and cerebrovascular resistance (+46 +/- 17%, p < 0.05) and decreases in cerebral flow velocity both in the second (-13 +/- 4%) and last minute (-22 +/- 5%) before symptoms (p < 0.05). In comparison, subjects resistant to motion sickness demonstrated no change in BP or cerebrovascular resistance in the last minute of off-center rotation and only a 7 +/- 2% decrease in cerebral flow velocity. All subjects had significant hypocapnia (-3.8 +/- 0.4 mmHg, p < 0.05); however, this hypocapnia could not fully explain the cerebral hypoperfusion associated with the development of nausea.


CONCLUSIONS
These data indicate that reductions in cerebral blood flow precede the development of nausea. Further work is necessary to determine what role cerebral hypoperfusion plays in motion sickness and whether cerebral hypoperfusion can be used to predict the development of nausea in susceptible individuals.
Serrador
Jorge M
JM
Harvard Medical School, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. serrador@hms.harvard.edu
Schlegel
Todd T
TT
Black
F Owen
FO
Wood
Scott J
SJ
D000328:Adult; D000337:Aerospace Medicine; D000704:Analysis of Variance; D001783:Blood Flow Velocity; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D002498:Centrifugation; D002560:Cerebrovascular Circulation / Q000502:physiology*; D005260:Female; D006801:Humans; D018471:Hypergravity / Q000009:adverse effects*; D008297:Male; D020768:Middle Cerebral Artery / Q000502:physiology; D009325:Nausea / Q000503:physiopathology*; D018489:Space Motion Sickness / Q000503:physiopathology*; D014661:Vasoconstriction / Q000502:physiology
D002245:Carbon Dioxide
Stroke. 2000 Jul;31(7):1672-8
10884472
J Vestib Res. 1996 Mar-Apr;6(2):127-34
8925115
Brain Res Bull. 2000 Sep 1;53(1):113-20
11033215
J Appl Physiol (1985). 2001 Jan;90(1):67-82
11133895
J Appl Physiol (1985). 2001 Nov;91(5):1986-94
11641334
Brain Res. 2003 Jan 31;961(2):261-8
12531493
J Neurosurg. 1982 Dec;57(6):769-74
7143059
Cerebrovasc Brain Metab Rev. 1990 Summer;2(2):161-92
2201348
Stroke. 1994 Oct;25(10):1985-8
7916502
Hepatology. 1995 Sep;22(3):730-6
7657276
Ann Otol Rhinol Laryngol. 1963 Jun;72:357-73
13949998
J Appl Physiol (1985). 1996 Sep;81(3):1084-95
8889738
J Cereb Blood Flow Metab. 1996 Nov;16(6):1379-82
8898715
J Vestib Res. 1998 Jan-Feb;8(1):17-25
9416585
Acta Neurol Scand. 1999 Jul;100(1):12-7
10416507