Objectives: To characterize the pathogenesis and clinical features of optic
disc edema associated with obstructive sleep apnea syndrome (SAS).
Methods: A series of 4 patients with SAS and papilledema (PE) underwent com
plete neuro-ophthalmologic evaluation and lumbar puncture. In 1 patient, co
ntinuous 24-hour intracranial pressure (ICF) monitoring was also performed.
Results: All 4 patients had bilateral PE that was asymmetric in 2. Three pa
tients had optic nerve dysfunction, asymmetric in 1, unilateral in 2. Dayti
me cerebrospinal fluid pressure measurements were within normal range. Noct
urnal monitoring performed in one patient, however, demonstrated repeated e
pisodes of marked ICP elevation associated with apnea and arterial oxygen d
esaturation.
Conclusions: We propose that PE: in SAS is due to episodic nocturnal hypoxe
mia and hypercarbia resulting in increased ICP secondary to cerebral vasodi
lation. In these individuals, intermittent ICP elevation is sufficient to c
ause persistent disc edema. These patients may be at increased risk for dev
eloping visual loss secondary to PE compared with patients with obesity-rel
ated pseudotumor cerebri because of associated hypoxemia. The diagnosis of
SAS PE may not be appreciated because daytime cerebrospinal fluid pressure
measurements are normal and because patients tend to present with visual lo
ss rather than with symptoms of increased ICP.