thiazide-sensitive sodium chloride cotransporter have been
found to be responsible for this syndrome.
4
Patients may have
seizures, episodes of tetany, muscular weakness, or paresthesia
attributable to hypokalemic alkalosis. Often, patients are
asymptomatic or have slight symptoms. Some may exhibit
arthralgias consecutive with calcium pyrophosphate dihy-
drate deposition disease and “chondrocalcinosis.” A case of
chondrocalcinosis associated with sclerochoroidal calcifica-
tions was recently described.
2
However, we are unaware of
previous reports of Gitelman syndrome or severe hypomag-
nesemia associated with sclerochoroidal calcification and
could find no reference to this association in a computerized
search using MEDLINE.
Much biologic evidence suggests a relationship between
hypomagnesemia, calcium pyrophosphate dihydrate depo-
sition, and sclerochoroidal calcification. Pyrophosphatases,
including alkaline phosphatase, are magnesium dependent.
Moreover, magnesium ions increase the solubility of cal-
cium pyrophosphate crystals.
5
Hypomagnesemia might
therefore promote calcium pyrophosphate dihydrate for-
mation in joints and sclera by means of the inhibition of
pyrophosphate hydrolysis and reduction of crystal solubil-
ity. Consequently, the ocular lesions present in our patient
are probably caused by the sclerochoroidal deposition of
calcium pyrophosphate dihydrate crystals. However, in this
case, sclerochoroidal calcification displayed all the features
of idiopathic senile calcification, even though the patient
was only 58 years old, and we cannot rule out a fortuitous
association with Gitelman syndrome. Conversely, these
calcified sclerochoroidal lesions have a characteristic clin-
ical presentation and are easy to distinguish from other
calcified lesions of the choroid and sclera.
In conclusion, sclerochoroidal calcifications were iden-
tified in a patient with Gitelman syndrome and might be
caused by magnesium deficiency.
REFERENCES
1. Cohen SY, Guyot-Sionnest M, Puech M. Choroidal neovas-
cularisation as a late complication of hyperparathyroidism.
Am J Ophthalmol 1998;126:320 –322.
2. Shields JA. Sclerochoroidal calcification in calcium pyrophos-
phate dihydrate deposition disease. Arch Ophthalmol 1997;
115:1077–1079.
3. Gitelman HJ, Graham JB, Welt LG. A new familial disorder
characterized by hypokalemia and hypomagnesemia. Trans
Assoc Am Physicians 1966;79:231–235.
4. Simon DB, Lifton RP. The molecular basis of inherited
hypokalemic alkalosis: Bartter’s and Gitelman’s syndromes.
Am J Physiol 1996;271:F961–F966.
5. Al-Ghamdi SM, Cameron EC, Sutton RA. Magnesium defi-
ciency: pathophysiologic and clinical overview. Am J Kidney
Dis 1994;24:737–752.
Oscillopsia and Pseudonystagmus
in Kidney Transplant Patients
Michael T. Yen, MD,
Susan J. Herdman, PT, PhD,
and Ronald J. Tusa, MD, PhD
PURPOSE
: Modern immunosuppressants have improved
the success of kidney transplantation for renal failure
patients. They also may induce neurotoxic effects includ-
ing tremor. We report two cases of pseudonystagmus and
oscillopsia in transplant patients caused by immunosup-
pressant-induced head tremor and gentamicin-induced
vestibulotoxicity.
METHODS
: Case reports. Head tremor, static visual acu-
ity, and dynamic visual acuity were measured. Vestibular
function was evaluated with ice water calorics.
RESULTS
: Both patients had significant head tremor and
pseudonystagmus. Head stabilization improved static vi-
sual acuity. Dynamic visual acuity revealed a 4-line and
10-line loss of visual acuity, respectively.
CONCLUSIONS
: These findings of pseudonystagmus and
oscillopsia are likely to become more prevalent as more
renal failure patients receive transplants. Improvement
may be seen with reduction of immunosuppressant,
reduction of stimulant intake, use of medications to
reduce head tremor, and vestibular rehabilitation. (Am
J Ophthalmol 1999;128:768 –770. © 1999 by Elsevier
Science Inc. All rights reserved.)
T
HE VESTIBULO-OCULAR REFLEX PLAYS A CENTRAL ROLE
in maintaining visual fixation during head movements.
With vestibulo-ocular reflex impairment, blurred vision
and oscillopsia occur during head movements. A common
cause of vestibulo-ocular reflex impairment is bilateral
Accepted for publication July 7, 1999.
From the Department of Ophthalmology, Bascom Palmer Eye Institute,
University of Miami School of Medicine (M.T.Y., R.J.T); Department of
Orthopedics and Rehabilitation, Division of Physical Therapy, Univer-
sity of Miami School of Medicine (S.J.H.); and Departments of Neurol-
ogy, and Otolaryngology, University of Miami School of Medicine,
Miami, Florida (R.J.T.). This work was supported in part by grant DC
03196 from the National Institutes of Health, Bethesda, Maryland.
Inquiries to Ronald J. Tusa, MD, PhD, Bascom Palmer Eye Institute,
900 NW 17 St, Miami, FL 33136; fax: (305) 326-6474; e-mail: rtusa@med.
miami.edu
FIGURE 2. Computed tomography of the orbits shows dense
sclerochoroidal plaques compatible with calcium deposition.
A
MERICAN
J
OURNAL OF
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PHTHALMOLOGY
768 D
ECEMBER 1999