J Neurosurg 76:207-211, 1992

Effect of head elevation on intracranial pressure, cerebral

perfusion pressure, and cerebral blood flow in headinjured patients
ZEEV FELDMAN,M.D., MALCOLMJ. KANTER,M.D., CLAUDIAS. ROBERTSON,M.D.,
CHARLES F. CONTANT, PH.D., CHRISTOPHER HAYES, P.A.-C, MICHAEL A. SHEINaERG, B.S.,
CYNTHIA A. VILLAREAL,M.D., RAJ K. NARAYAN,M.D., AND ROBERT G. GROSSMAN,M.D.
Department of Neurological Surgery, Baylor Collegeof Medicine, Houston, Texas
v- The traditional practice of elevating the head in order to lower intracranial pressure (ICP) in head-injured
patients has been challenged in recent years. Some investigators argue that patients with intracranial hypertension should be placed in a horizontal position, the rationale being that this will increase the cerebral perfusion
pressure (CPP) and thereby improve cerebral blood flow (CBF). However, ICP is generally significantly higher
when the patient is in the horizontal position. This study was undertaken to clarify the issue of optimal head
position in the care of head-injured patients. The effect of 13"and 30* head elevation on ICP, CPP, CBF, mean
carotid pressure, and other cerebral and systemic physiological parameters was studied in 22 head-injured
patients. The mean carotid pressure was significantly lower when the patient's head was elevated at 30~ than
at 0* (84.3 _+ 14.5 rata Hg vs. 895 _ 14.6 ram Hg), as was the mean ICP ( 14.1 _ 6.7 rata Hg vs~ 19.7 -+ 8.3
mm Hg). There was no statistically significant change in CPP, CBF, cerebral metabolic rate of oxygen,
arteriovenous difference of lactate, or cerebrovascular resistance associated with the change in head position.
The data indicate that head elevation to 30~significantly reduced ICP in the majority of the 22 patients without
reducing CPP or CBF.
KEY WORDS
head injury 9 head elevation
cerebral blood flow 9 intracranial pressure
"

LEVATED intracranial pressure (ICP) or inadequate cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) are common causes of
secondary brain damage in head-injured patients. In
patients with raised ICP, it is a common practice to
position the patient in bed with the head elevated above
the level of the heart. Kenning, et a[., 4 reported that
elevating the head to 45* or 90* significantly reduced
ICP. However, some studies suggest that head elevation
may also lower the CPP. Durward, et al.,2 studied the
effect of head elevation at 0 ~ (horizontal), 15", 30*, or
60 ~ on ICP, systemic and pulmonary pressure, and CPP
in patients with intracranial hypertension. They concluded that 15" or 30* of head elevation significantly
reduced ICP while maintaining CPP and cardiac output. However, further elevation of the head to 60*
caused an increase in ICP and a significant decrease in
CPP and cardiac output. More recently, Rosner, et
a/., 16-19have emphasized the importance of adequate
CPP and have provided physiological and clinical evi-

J. Neurosurg. / Volume 76 /February, 1992

9 cerebral perfusion pressure

dence suggesting that CPP is maximum when patients

are in the horizontal position, even though ICP is
usually higher in this position. Davenport, etal.,' assessed the role of head elevation at 20", 40", or 60 ~ in
eight patients suffering from hepatic coma. They found
inconsistent effects of head elevation on ICP but a
significant decrease in mean arterial blood pressure
(MABP) and CPP at 40* and 60*. No study has yet
measured CBF when evaluating the effects of postural
changes on cerebral perfusion. As maintenance of adequate CBF is the primary rationale for maintaining
adequate CPP in patients with increased ICP, we have
studied the changes in CBF, as well as changes in ICP,
CPP, and other cerebral and systemic physiological
parameters induced by changes in head position in
patients with head injury.
Clinical Material and Methods

Twenty-two head-injured patients admitted to the

neurosurgical intensive care unit at Ben Taub General
907

Z. Feldman, et al.
TABLE 1
Characteristics qf 22 head-injured patients*
CharacteristicCategory
No.
sex (M:F)
19:3
mean age (yrs)
35
age range
18-75
pathology
subdural hematoma
8
cerebral contusion
5
intracerebralhematoma
2
epidural hematoma
2
diffuse axonalinjury
2
gunshot woundto head
2
traumatic subarachnoidhemorrhage
1
initialGCS score
3-5
3
6-8
14
9-12
5
CBF (ml/100 gm/min)
low (< 35)
7
normal (35-60)
9
high (> 60)
6
outcome
good recovery
6
moderatelydisabled
7
severelydisabled
5
vegetativestate
1
dead
3
* GCS = GlasgowComa Scale;CBF = cerebralblood flow.
Hospital between January, 1990, and January, 1991,
were studied. The demographic characteristics of the
patients are given in Table 1. The mean age of the
patients was 35 years (range 18 to 75 years). The primary diagnosis was subdural hematoma in eight patients, cerebral contusion in five, intracerebral hematoma in two, epidural hematoma in two, diffuse axonal
injury in two, gunshot wound to the head in two, and
traumatic subarachnoid hemorrhage in one. Postresuscitation Glasgow Coma Scale scores were 3 to 5 in three
patients, 6 to 8 in 14, and 9 to 12 in five. At 3 months
after injury, six patients bad a good recovery, seven
were moderately disabled, five were severely disabled,
one was in a permanent vegetative state, and three had
died (Table 1).

All patients were treated according to a protocol that

emphasized early intubation and respiratory support,
prompt evacuation of intracranial hematomas, and prevention of secondary insults to the brain. 13The patients
were initially ventilated to maintain a PaO2 of 100 m m
Hg or above and a PaCO2 of 30 to 35 m m Hg. Intracranial pressure greater than 20 m m Hg was treated by
cerebrospinal fluid (CSF) drainage, hyperventilation
(PaCO2 25 to 30 m m Hg), sedation, paralysis, and
administration of mannitol. Barbiturate coma was induced only if ICP was refractory to the above treatment. 3 Medications included morphine for sedation,
pancuronium for paralysis, and phenytoin for seizure
prophylaxis. The treatment protocols were approved by
the Institutional Review Board of Baylor College of
Medicine, and informed consent for each patient was
obtained from the next of kin.
Within 72 hours after injury, two consecutive sets of
physiological measurements were performed. In the
first 13 patients, the initial set of measurements was
performed with the head elevated to 300; in the subsequent nine patients, the initial set was taken at 0* head
elevation. The patient's head elevation was changed
after the initial set of measurements and a second set
of measurements was taken 45 minutes later. Measurements were made of CBF (using the Kety-Schmidt
N20 techniqueS-7), ICP (measured with the transducer
zeroed at the level of the foramen of Monro), arteriovenous oxygen difference, cerebral metabolic rate of
oxygen (CMRO2), oxygen saturation in the jugular bulb,
cerebrovascular resistance (CVR), PaCO2, PaO2, arteriovenous difference of lactate, and MABP. The MABP
was measured with the transducer zeroed at the level of
the foramen of Monro, giving an estimate of the mean
carotid pressure (MCP), which was then used for calculation of the CPP.
Differences were computed by subtracting the value
obtained when the patient was lying flat from the value
obtained when the head was elevated to 30 ~. These
differences were evaluated using the paired t-test. Comparisons among subgroups of patients were made using
analysis of variance of the individual differences.

TABLE 2
Effects of head elevation on cerebral and systemic pkysiologicat parameters in 22 patients*
Parameter
mean carotid pressure (mm Hg)
intracranialpressure(ram Hg)
cerebral perfusionpressure(CPP) (mm Hg)
cerebral blood flow(CBF)(ml/100gm/min)
cerebrovascularresistance(CPP/CBF)
cerebral metabolicrate of oxygen(zmol/100gm/min)
arteriovenousoxygendifference(umol/ml)
PaCO2(mm Hg)
arteriovenousdifferenceof lactate (umol/ml)
oxygensaturationin jugularbulb (%)
* Values representmean _+standarddeviation.
208

30~Head Elevation
84.3 _+14.5
14.1 + 6.7
70.2 +__18.1
47.8 _+ 16.9
1.72 _ 0.8
1.35 "- 0.59
1.81 _+0.63
32.34 _+5.89
-0.05 + 0.05
69.9 _+9

0~Head Elevation
89.5 -+ 14.6
19.7 __.8.3
69.7 _+ 18.7
48.9 ---20.4
1.72 + 0.9
1.28 + 0.53
1.72 _+0.73
32.46 -+ 6.4
-0.05 _+0.06
70.3 + 10.2

MeanDifference
-5.2 --. 8.1
-5.7 _-X5.6
0.45 - 8.8
-1.03 + 10.8
-0.0014 ---0.356
0.075 _+0.23
0.093 + 0.35
-0.1 + 1.9
-0.0002+ 0.06
-0.0043_+0.042

P Value
0.0062
0.0001
0.8
0,657
0.9844
0.14
0.23
0.77
0.18
0.63

J. Neurosurg. / Volume 76 / February, 1992

Effects of head elevation in head-injured patients

FIG. 1. Graph showing cerebral and systemic physiological parameters at head elevations of 0~ and 30~ in
22 patients with head injury. At 30", the intracranial pressure (ICP) was lower in 77% of patients, higher in
14%, and the same in 9%; mean carotid pressure (MCP) was lower in 59%, higher in 23%, and the same in
18%; cerebral perfusion pressure (CPP) was lower in 55% and higher in 45%; and cerebral blood flow (CBF)
was lower in 36%, higher in 36%, and the same in 14%. See text for analysis of the significance of the
differences.

Results
The effects of head elevation on ICP, MCP, CPP,
and CBF are illustrated in Fig. 1 and are given in Table
2 for all parameters measured. The mean values (+
standard deviation) for the MCP and ICP were significantly lower at 30 ~ head elevation than at 0": 84.3 +
14.5 m m Hg versus 89.5 + 14.6 m m Hg for MCP, and
14.1 + 6.7 mm Hg versus 19.7 + 8.3 m m Hg for ICP.
The mean values for CPP and CBF were unaffected by
head elevation: 70.2 ___ 18.1 m m Hg at 30 ~ and 69.7 +
18.7 m m Hg at 0 ~ for CPP, and 47.8 _+ 16.9 ml/100
gm/min at 30* and 48.9 _+ 20.4 ml/100 gm/min at 0 ~
for CBF. None of the other parameters showed a statistically significant difference between head elevations at
30* and at 0 ~ The results were not affected by whether
the head was at 30* or at 0* for the initial measurements.
Correlation analysis revealed a significant relationship between the ICP level at 0* head elevation and the
amount of change in ICP after 30* head elevation (r =
-0.5890). The higher the ICP with the patient in the
horizontal position (0*), the greater the reduction in
ICP at head elevation of 30* (Fig. 2). The effect of head

J. Neurosurg. / Volume 76/February', 1992

FIG. 2. Correlation between the level of intracranial pressure (ICP) at 0 ~ head elevation and the amount of change in
ICP after head elevation to 30~ The higher the ICP level in
the horizontal position (0~ the greater was the reduction in
ICP at 30~ of head elevation (r = -0.5890).
909

Z. Feldman, et al.
TABLE

Effects of head elevation on cerebra! and systemic physiological parameters" in six patients with ICP greater than 25 mm Hg*
Parameter
mean carotid pressure (ram Hg)
intracraniaI pressure (ICP) (ram Hg)
cerebral perfusion pressure (CPP) ( m m Hg)
cerebral blood flow (CBF) (ml/100 g m / m i n )
cerebrovascular resistance (CPP/CBF)

30 ~ Head Elevation
74.7
20.3
54.3
55.9
0.992

_+ 14.5
+ 3.9
_+ 12.8
+ 9.6
+ 0.226

0 ~ Head Elevation
83.7
30.7
53
59.8
0.976

+ 15.1
_+ 3.3
+ 17.1
_+ 26.4
_+ 0.398

Mean Difference

P Value

-9
-10.33
1.3
-3.9
0.016

0.085
0.0079
0.5301
0.6042
0.8639

_+ 5.3
+ 5.9
+ 4.8
-+ 17.26
_+ 0.219

* Values represent mean + standard deviation of the mean.

elevation on ICP in the six patients who had an ICP

greater than 25 mm Hg compared with the effect observed in the other 16 patients revealed that the decrease
in ICP observed was significant in the patients with
raised ICP. The mean reduction in ICP with head
elevation was - 10.33 _+ 5.9 mm Hg in these six patients,
compared with -3.9 _+ 8.6 mm Hg for the remaining
16 patients (p < 0.05) (Table 3). In these six patients,
the ICP fell from a mean of 30.7 mm Hg at 0* to 20.3
mm Hg at 30*.
Although CBF was unchanged with head elevation
to 30 ~ when the data for all 22 patients were averaged,
in five patients the CBF fell by more than 5 ml/100
gm/min with head elevation. In these five, CBF fell
from a mean of 67.2 + 26 ml/100 gm/min at 0 ~to 50.7
_+ 16.5 ml/100 gin/rain at 30 ~ (p < 0.05). Therefore,
we tried to identify physiological parameters that would
predict such a fall. The CMRO2 was also lower after
head elevation in these five patients, falling from 1.09
+ 0.5 #mol/100 gm/min at 0* to 0.9 _ 0.5 ~mol/100
gm/min at 30*. As in the entire group, MCP and ICP
were lower with the head elevated: 83.2 _ 13.2 mm Hg
versus 90.8 _ 11.9 mm Hg for MCP, and 18 +_ 3.7 mm
Hg versus 22.4 _+ 7 mm Hg for ICP. The CVR was
higher at 30* elevation than at 0": 1.51 _+ 0.56 versus
1.22 _+ 0.49, respectively. Comparison of the changes
in these five patients to those occurring in the other 17
patients revealed that the changes in CBF, CMRO2,
and CVR were significant (p = 0.0001 for CBF, p =
0.01 for CMRO2, and p = 0.0221 for CVR). Although
the decrease in CPP in these five patients was not
significantly different from that observed in the other
patients (p = 0.119), the combination of increased CVR
and decreased CPP resulted in a decrease in CBF.
Further analysis revealed that in four of these patients,
the CBF, although lower at 30 ~ head elevation, was still
within the normal range (> 35 ml/100 gm/min). In
only one of the five patients did the CBF drop below
35 ml/100 gin/rain (from 37 to 25 ml/100 gin/rain). In
this patient, the CPP was low: 59 mm Hg at 0 ~and 50
mm Hg at 30 ~ Interestingly, the ICP rose marginally
in this patient from 12 mm Hg at 0 ~ head elevation to
14 mm Hg at 30 ~ Other than the suggestion that a low
CPP may be associated with a fall in CBF with head
elevation, the five patients in whom head elevation
produced a decrease in CBF of more than 5 ml/100
gm/min had no distinguishing features.

910

Discussion
The ideal head position for patients with head injury
has been disputed in recent years. Rosner 16 provided
evidence that plateau waves are triggered by a fall in
CPP and that maintaining CPP above 70 to 80 mm Hg
prevented plateau waves. In patients with intracranial
hypertension, Rosner and c o w o r k e r s ls'19 advocated
keeping the patient's head at 0 ~ elevation and using
fluid expansion or pharmacological means to maintain
CPP. Our data indicate that, although the MCP is lower
at 30 ~ head elevation than at 0", CPP and CBF are not
significantly altered in most patients by head elevation
to 30*.
Because the MCP could not be obtained by direct
measurement of the internal carotid artery pressure in
the patients we studied, we used the MABP recorded
with the transducer placed at the level of the foramen
of Monro as an estimate of the MCP, a technique
commonly used to compute CPP? 8 However, the results of a study by Woischneck, et al.,22 suggest that the
fall in MCP that we observed at 30* head elevation may
be largely an artifact of this measurement technique.
In their study addressing the accuracy of CPP measurements, they found the pressure in the superficial temporal artery to be almost identical to the pressure in the
internal carotid artery. When evaluating the effect of
head elevation on CPP, computed using the pressure of
the superficial temporal artery, they found the CPP to
be constant when the head was elevated from 0* to 30*.
If our measurement technique implied a fall in MCP
that did not actually occur, it would suggest that the
CPP might actually increase at 30 ~ of head elevation
and explain the lack of change in CBF seen in our
patients with head elevation.
We have also demonstrated a direct relationship between the ICP level and the change in ICP after head
elevation. Our data suggest that in head-injured patients
with normal ICP, head position does not greatly affect
ICP and that these patients can be positioned either
horizontally or with the head elevated to 30 ~. However,
when the ICP is increased, elevation of the head is very
effective in reducing the ICP. This is apparently due to:
1) hydrostatic displacement of the CSF from the cranial
cavity to the spinal subarachnoid space;4 and 2) facilitated venous outflow from the brain.S-10'14'ls'2LThe contributions of CSF displacement and changes in venous
volume to the reduction in ICP in head-injured patients

J. Neurosurg. / Volume 76/February, 1992

Effects of head elevation in head-injured patients

after head elevation may depend upon the relative size
of each intracranial compartment at the time of head
elevation, m.~vIn patients with raised ICP, the intracranial compliance decreases, t~ 12,20 and smaller changes
in intracranial volume, such as those produced by CSF
displacement, will produce greater changes in ICP.
Although the overall results of the present study show
no effect of head elevation on CBF, one must bear in
mind that our measurements are of global CBF and
that regional areas of decreased CBF may exist in the
presence of normal global blood flow measurements.
Only in one patient did the CBF fall to ischemic levels
after head elevation, and the vasodilatory cascade suggested by Rosner t<~7 seemed to be demonstrable. In
this patient, the low CPP (59 m m Hg) emphasizes once
more the importance of maintaining adequate levels of
CPP. The results of the present study suggest that, in
general, head-injured patients with raised ICP should
be maintained with the head elevated to 30 ~ which will
produce a fall in ICP without a significant decrease in
CBF in the majority of these patients.
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Manuscript received May 19, 1991.

This study was supported in part by National Institutes of
Health Grant PO 1-NS27616.
Some portions of this paper were presented at the Eighth
International Symposium on Intracranial Pressure, in Rotterdam, The Netherlands, in June, 1991.
Address reprint requests to: Robert G. Grossman, M.D.,
Department of Neurosurgery, Baylor College of Medicine,
One Baylor Plaza, Houston, Texas 77030.

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