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No Correlation between
Intraocular Pressure and
Intracranial Pressure
Ying Han, MD, PhD,1 Timothy J. McCulley, MD,1
and Jonathan C. Horton, MD, PhD1,2
A recent study has reported an excellent correlation between
intraocular pressure (IOP) and intracranial pressure (ICP),
suggesting that measurement of IOP may serve as a nonin-
vasive means to determine ICP. To reexamine the relation
between IOP and ICP, we reviewed the medical records of
all patients who underwent lumbar puncture between 1991
and 2007 in the neuro-ophthalmology clinic at the Univer-
sity of California San Francisco. Data for IOP and ICP were
available for 55 patients. There was no correlation between
IOP and ICP (Pearson correlation coefficient, r ⫽ 0.07; p ⫽
0.59). IOP measurement is not a useful substitute for ICP
measurement.
Ann Neurol 2008;64:221–224
An accurate noninvasive way to measure intracranial
pressure (ICP) has long been sought, with little success.
If intraocular pressure (IOP) were a faithful reflection
of ICP, it would offer an easy solution. In rhesus mon-
keys, an increase in IOP has been reported after exper-
imental increase of ICP.1 In this study, however, IOP
rarely increased to more than the reference range, lead-
ing the authors to predict that the value of isolated
IOP measurements would be limited, if applied to the
evaluation of patients with intracranial hypertension.
In another macaque study, IOP and ICP were varied
by manipulation of PaCO2.2 Again, IOP remained
within the reference range, even at the maximum re-
corded ICP. In a human study, a correlation was found
between ICP and IOP with repeated measurements in
single patients, but no consistent relation prevailed
from patient to patient.3 Another study found a corre-
lation across patients, but concluded that “enough vari-
ability. . . exists to preclude using IOP to precisely de-
From the 1Department of Ophthalmology, Beckman Vision Center;
and 2Departments of Neurology and Physiology, University of Cal-
ifornia San Francisco, San Francisco, CA.
Received Feb 5, 2008, and in revised form Mar 25. Accepted for
publication Apr 4, 2008.
Published online June 20, 2008, in Wiley InterScience
(www.interscience.wiley.com). DOI: 10.1002/ana.21416
Address correspondence to Dr Horton, Department of Ophthalmol-
ogy, 10 Koret Way, Box 0730, San Francisco, CA 94143.
E-mail: hortonj@vision.ucsf.edu
Han et al: IOP and ICP are uncorrelated 221
termine ICP.”4 Finally, one study found no correlation
between IOP and ICP.5
In contrast, Sajjadi and colleagues6 reported a tight
correlation (r ⫽ 0.955) between IOP and ICP. They
proposed that IOP may be used instead of frequent
lumbar punctures in follow-up of patients with benign
intracranial hypertension and in patients with impaired
consciousness after head trauma. Puzzled by the dis-
crepancy between Sajjadi and colleagues’ study6 and
most prior reports in the literature,1–5 we examined the
correlation between ICP and IOP in our patients to
determine whether IOP can be used as a reliable sur-
rogate for ICP.
Subjects and Methods
This retrospective study was approved by the Institutional Re-
view Board at the University of California San Francisco.
Cases were identified by searching the entire patient database
of a single neuro-ophthalmologist (J.C.H.), who has main-
tained electronic medical records since 1991. The search term
lumbar puncture yielded records of 77 patients older than 18
years who had undergone a spinal tap in the neuro-
ophthalmology clinic between 1991 and 2007, usually for the
evaluation of bilateral optic disc edema. Data from 22 patients
were excluded for the following reasons: IOP was not recorded
(n ⫽ 13), the IOP was not measured the same day (n ⫽ 7),
or the patient was being treated with acetazolamide (n ⫽ 2).
No patient had a history of glaucoma, use of topical medica-
tions to reduce IOP, or recent prior lumbar puncture.
The IOP was measured in each eye by Goldmann contact
tonometry, usually by a resident or fellow. The accuracy of the
tonometer in our clinic is calibrated every 3 months, requiring
an adjustment of less than 1mm Hg. The subarachnoid open-
ing pressure was measured in the left lateral decubitus position
using a manometer after a spinal puncture at L3-4 or L4-5
under local anesthesia. The procedure was performed by the
same physician (J.C.H.) in every patient. The lumbar punc-
ture was always done after measurement of the IOP. Typically,
the IOP was measured by an ophthalmology resident during
the course of a neuro-ophthalmological examination in an af-
ternoon clinic. The patient then waited until the end of the
clinic, when the lumbar puncture was performed. The maxi-
mum time between Goldmann tonometry and lumbar punc-
ture was 5 hours. The exact time between IOP measurement
and ICP measurement was not documented in each patient
but averaged 2 to 3 hours for the cohort.
The main objective of this study was to examine the cor-
relation between mean IOP and ICP. Statistical significance
was assessed by calculating the Pearson’s product-moment
correlation coefficient, using Igor Pro statistics software
(WaveMetrics, Lake Oswego, OR).
Results
After the above-mentioned exclusions, there were 55
patients in whom IOP and ICP were recorded within a
5-hour time window. There were 42 female and 13
male patients, with a mean age of 37.6 years. The fe-
male predominance reflected the fact that the majority
of patients had pseudotumor cerebri (Table).
222 Annals of Neurology Vol 64 No 2 August 2008
Table. Clinical Diagnoses of the Study Group
Diagnosis Cases, n
(%)
Pseudotumor cerebri 38 (69%)
Anterior ischemic optic neuropathy 5 (9%)
Headache 4 (7%)
Idiopathic optic disc swelling 2 (4%)
Optic neuritis 2 (4%)
Acute disseminated encephalomyelitis 1 (2%)
Posterior uveitis 1 (2%)
Dural sinus occlusion 1 (2%)
Unknown 1 (2%)
The average of the IOP in the two eyes for each
patient ranged from 10 to 21 mmHg, with a mean of
14.4 ⫾ 2.7mm Hg. No patient showed a pressure dif-
ference between the two eyes of more than 2mm Hg.
ICP ranged from 70 to 550mm H2O, with a mean of
274.2 ⫾ 102.4mm H2O (Fig). There was no signifi-
cant correlation between the ICP and the average IOP
(Pearson’s product-moment correlation coefficient, r ⫽
0.07, p ⫽ 0.59).
We also broke the comparison down by eye, testing
the correlation between ICP/left eye pressure and ICP/
right eye pressure. Neither eye pressure showed a signif-
icant correlation with ICP. Finally, we selected which-
ever eye pressure yielded the best correlation with ICP.
However, this comparison still did not produce a statis-
tically significant correlation between IOP and ICP.
Discussion
Numerous studies have assessed the relation between
IOP and ICP, in the hope of finding a noninvasive
method of determining ICP. Although a few studies,
both animal and human, have found a slight effect of
ICP on IOP, they have concluded uniformly that IOP
provides no clinically useful estimate of ICP.1–5
The findings of Sajjadi and colleagues6 are inconsis-
tent with previous reports, as well as our data, and are
difficult to explain. They reported a close correlation
(r ⫽ 0.955), with a nearly 1:1 relation between IOP
and ICP. Their IOP measurements were performed
with a Schiotz tonometer, which is a notoriously inac-
curate instrument. In a comparison of five portable
tonometers, the Schiotz tonometer was found to have
the poorest correlation (r ⫽ 0.66) with the gold stan-
dard, the Goldmann tonometer.7 Therefore, even if an
excellent correlation did exist between IOP and ICP, it
would be hard to demonstrate with a Schiotz tonom-
eter. Moreover, Sajjadi and colleagues6 used the
Schiotz tonometer incorrectly, by averaging values ob-
tained with the 5.5 and 10.0 gm weights. The instru-

Fig. Graph showing mean intraocular pressure (IOP) plotted
against intracranial pressure (ICP) for our subjects and for
Sajjadi and colleagues’ 6 report. Our data show no correlation
between IOP and ICP (r ⫽ 0.07), whereas Sajjadi and col-
leagues found a strong correlation (r ⫽ 0.955). The fits are
linear regressions through the data points.
ment performs most accurately when the plunger
makes a minimal impression on the cornea. Instruc-
tions provided with the Shiotz tonometer specify that
the appropriate weight should be chosen to give a scale
reading of 2 to 5 units. It is not recommended to av-
erage two readings, one obtained with the correct
weight and the other with weight that gives a reading
outside 2 to 5 scale units. Such a technique would fur-
ther reduce the accuracy of the Shiotz tonometer.
There are several potential weakness of our study. Up
to 5 hours elapsed between IOP and ICP measurement,
with an average of about 2.5 hours. IOP is known to
fluctuate diurnally, with a peak in the morning followed
by a plateau in the afternoon.8,9 Between 1:00 and 5:30
PM, the mean decline in IOP is less than 2mm Hg. In-
dividual subjects show little short-term pressure variation
on repeated measurements during this time interval.
Therefore, it is doubtful that the time lag between the
two pressure measurements we made could have ob-
scured any correlation between IOP and ICP in our pa-
tients. Another point is that the IOP was measured by a
different physician in each patient. It would have been
ideal had the same person checked the IOP in every pa-
tient, but Goldmann tonometry readings show little in-
terobserver variation, with 95% limits of agreement
of ⫾ 2.6 mm Hg.10 Therefore, the fact that tonometry
data were obtained by different observers introduced
only a minor source of error.
Sajjadi and colleagues6 attribute the correlation be-
tween ICP and IOP that they found to “the anatomical
and physiological connections between the intracranial
fossa and orbit,” noting that compression of the poste-
rior globe is seen by neuroimaging in some patients with
increased ICP.11,12 It is true that globe compression, by
any means, can cause a transient increase in IOP. How-
ever, IOP is dependent on numerous factors, including
aqueous production, episcleral venous pressure, and flow
resistance through the trabecular meshwork. The eye
eventually compensates for external pressure by adjusting
these parameters to restore IOP to its baseline level. This
compensation explains why glaucoma is not a frequent
finding in patients with an orbital neoplasm that com-
presses the globe.
Sajjadi and colleagues6 also state, “other possible
mechanisms include the increase in ophthalmic venous
pressure. . ., which would be transmitted directly to the
ocular fluid. . .” Although episcleral venous pressure
does influence aqueous outflow, it does not have a di-
rect connection with ocular fluid. The trabecular mesh-
work and Schlemm’s canal are interposed between the
intraocular fluid and the episcleral veins, buffering any
effect caused by a change in episcleral venous pressure.
Moreover, the orbit is richly anastomotic with venous
outflow through the inferior orbital fissure (via the in-
ferior ophthalmic vein to the venous plexus of the
pterygopalatine fossa) and through the eyelids both
medially (via the angular vein) and laterally (via the
superficial temporal vessels). We agree that pressure
within the cavernous sinus would result in an increased
superior ophthalmic vein pressure, as evidenced by
ophthalmodynamometry readings.13 However, this
would not necessarily produce an increase in IOP.
In summary, no correlation was present between
IOP and ICP in our patients. IOP should not be relied
on as a means to infer ICP.
This work was supported by Research to Prevent Blindness.
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Abnormal Vestibular
Responses to Vertical Head
Motion in Cerebellar Ataxia
Ke Liao, MS,1–3 Mark F. Walker, MD,1,2
and R. John Leigh, MD1–3
Falls pose an important problem to neurologists caring for pa-
tients with cerebellar disorders. Normal human gait is charac-
terized by prominent up-and-down linear head movements
(vertical translations). Thus, we asked whether patients with
cerebellar gait ataxia showed abnormal responses of otolithic
vestibuloocular reflexes to this motion. Compared with
healthy subjects, all cerebellar patients showed impaired
otolith-ocular responses. Neurologists often test the rotational
vestibuloocular reflexes in cerebellar patients, but our results
indicate that vestibular responses to vertical linear motion are
severely affected. Impairment of the corresponding otolith-
spinal reflexes may contribute substantially to falls.
Ann Neurol 2008;64:224 –227
From the 1Neurology Service and Daroff-Dell’Osso Laboratory,
Veterans Affairs Medical Center; and Departments of 2Neurology
and 3Biomedical Engineering, Case Western Reserve University,
Cleveland, OH.
Received Jan 10, 2008, and in revised form Mar 6, 2008. Accepted
for publication Mar 28, 2008.
Published online in Wiley InterScience (www.interscience.wiley.com).
DOI: 10.1002/ana.21407
Address correspondence to Dr Walker, Department of Neurology,
Case Western Reserve University, Cleveland VAMC, 10701
East Boulevard, 127-W, Cleveland, OH 44106.
E-mail: mark.walker@case.edu
224 Annals of Neurology Vol 64 No 2 August 2008
Imbalance and gait ataxia are major causes of func-
tional disability and falls in patients with cerebellar
ataxia. The mechanisms underlying these deficits re-
main uncertain, but impaired vestibular reflexes are
likely to play an important role, because the vestibular
system provides the brain with essential information re-
garding motion and the body’s orientation relative to
gravity.
Most prior studies of vestibular function in patients
with cerebellar disease have focused on the rotational
vestibuloocular reflex (rVOR). Occasionally, the rVOR
is absent1; most often it is present, although it may
have an abnormal amplitude or direction.2,3 Responses
to linear motion (translation) and gravity, which are
mediated by the otolith organs, are likely to be of par-
ticular importance to balance and walking. In fact, it
has been shown that the horizontal (side-to-side) trans-
lational VOR (tVOR) is commonly impaired by cere-
bellar disease.4,5 The response to vertical head motion
(bob), however, has not previously been studied in
ataxic individuals, although this motion is prominent
during natural human locomotion.6 In a prior study,7
we found that the vertical tVOR is impaired in pa-
tients with progressive supranuclear palsy, another neu-
rodegenerative disease, in which gait and balance defi-
cits are prominent and occur early. Here, we
investigated the vertical tVOR in patients with cerebel-
lar ataxia.
Subjects and Methods
We studied vestibuloocular reflexes in a group of eight pa-
tients (age range, 27–79 years; median age, 57 years; Table)
who presented with gait ataxia as a component of one of a
range of cerebellar disorders. Twenty healthy subjects (8
women; age range, 25–72 years; median age, 55 years) served
as the comparison group.8 Experiments were performed in
ambient light, so that natural visual cues were available, and
the safety of the subject on the platform could be monitored
by one of the investigators who stood by the platform with
an emergency stop switch. All subjects gave informed, writ-
ten consent, in accordance with the Declaration of Helsinki,
under a protocol approved by the Institutional Review Board
of the Cleveland Veterans Affairs Medical Center.
Stimuli
Experimental methods have been described in detail in a
prior report.8 Subjects sat in a chair on a Moog
6DOF2000E electric motion platform (Moog, East Aurora,
NY). Belts were used to secure the subject’s torso, and a
snugly fitting skate-board helmet, inlaid with foam, stabilized
the subject’s head. Any head movements that were decoupled
from chair or platform motion were measured, as described
later. The tVOR stimulus consisted of 2Hz bob (typical am-
plitude ⫾ 2.3cm), and the rVOR stimulus was 1Hz yaw
(typical amplitude ⫾ 6 degrees), each for a duration of 12
seconds. In one patient (P8), only bob stimuli were applied.
Data from two visual conditions, each used for one exper-
imental run, are presented here: (1) subjects binocularly