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Volume 07 No. 04
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Case Reports

Resolution of Papilledema Associated with OSA Treatment

http://dx.doi.org/10.5664/jcsm.1202

Shahrokh Javaheri, M.D., F.A.A.S.M.1; Zeeshan Qureshi, M.D.2; Karl Golnik, M.D., M.Ed.3
1Sleepcare Diagnostics, Cincinnati, OH; 2Baylor College of Medicine, Houston, TX; 3Cincinnati Eye Institute and the University of Cincinnati, Cincinnati, OH

ABSTRACT

Obstructive sleep apnea (OSA) is a common disorder and is associated with brain functional and morphological alterations. The association between OSA and papilledema, however, is not well known. We describe a 53-year-old morbidly obese female who presented with impaired vision due to bilateral papilledema. Polysomnography revealed severe OSA. She was treated with continuous positive airway pressure, and within a few weeks her papilledema and vision improved. This case report is consistent with association of OSA with papilledema but does not prove causality.

Citation:

Javaheri S; Qureshi Z; Golnik K. Resolution of papilledema associated with OSA treatment. J Clin Sleep Med 2011;7(4):399-400.


Idiopathic intracranial hypertension (IIH), also known as pseudotumor cerebri, classically affects young obese women.1 The most reliable clinical sign is papilledema, which occurs because elevated intracranial pressure (ICP) leads to blockage of retrograde axoplasmic transport along the optic nerve.2 This leads to swelling of the optic disc (i.e., papilledema). Computerized visual field analysis is mandatory, as up to 92% of individuals may have an abnormal automated Humphrey Visual Field.1

Although OSA is associated with increased ICP, little is known about OSA and papilledema.25 Our case report should heighten the awareness of this association as early recognition of OSA and appropriate therapy should prevent potentially irreversible optic nerve damage.

REPORT OF CASE

A 53-year-old obese white female with well-controlled hypertension presented for neuro-ophthlamic evaluation in April 2008. Her chief complaint was fluctuating bilateral “blobs” in her visual field since March 2008, as well as associated tinnitus. The patient denied headache, changes in central visual acuity, weight changes, or a medical history of taking vitamin A preparation or tetracycline derivatives. She also denied a history of diabetes or prior ocular surgery. Upon examination, the patient's visual acuity was 20/20 in each eye at distant and near. Pupils constricted from 5 mm to 3 mm bilaterally without relative afferent pupillary defect. Fields were full to confrontation. Eye movements were normal. Dilated funduscopic exam revealed moderate bilateral optic disc swelling consistent with papilledema (Figure 1).

The photo shows the right optic nerve head of our patient. It is markedly swollen. Note the lack of distinct nerve head margins.

jcsm.7.4.399.jpg

jcsm.7.4.399.jpg
Figure 1

The photo shows the right optic nerve head of our patient. It is markedly swollen. Note the lack of distinct nerve head margins.

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The patient had magnetic resonance imaging in May 2008 which was normal, specifically showing no hydrocephalus or venous sinus thrombosis. Lumbar puncture showed elevated intracranial pressure at 37 cm H2O (normal less than 25 cm H2O) with normal CSF fluid composition.

The patient was referred for evaluation for obstructive sleep apnea. She had history of habitual snoring and witnessed apnea and had woken herself up gasping for breath. She denied morning headaches but had unrefreshing sleep. She complained of excessive daytime sleepiness, taking 3 naps a week, becoming drowsy driving a car and falling asleep while watching television. These symptoms were present for at least a year.

Past medical history was significant for systemic hypertension and gout. She was taking olmesartan and allopurinol.

She weighed 134 kg, and body mass index was 46 kg/m2. Her SpO2 while breathing room air in the sitting position was normal at 95%. Her blood pressure at rest was taken 3 times; the last 2 readings were normal at 114/72 and 118/75 mm Hg. Tongue was moderately enlarged and elongated. She had an elongated soft palate. Uvula and tonsils were normal. Neck was 17.3 inches in circumference. Thyroid gland was not palpable. Cardiac examination revealed normal heart sounds. There were no murmurs. Chest examination revealed no crackles or wheezes. There was no peripheral edema. She scored 12 on the Epworth Sleepiness Scale, with 10 being the upper normal limit, consistent with mild subjective daytime sleepiness.

Full-night polysomnography was performed6 as detailed previously. Total recording time was 7 hours with a total sleep time of 5 hours; sleep efficiency was 71%. There were 159 episodes of obstructive apneas and 334 hypopneas for a total of 493 events. The obstructive apnea-hypopnea index was about 100 per hour. This resulted in significant drop in oxygen saturation with a minimum SpO2 of 54%. She spent approximately 200 minutes below SpO2 of 90%.

The next night she underwent CPAP titration, which began at CPAP 5 cm H2O and ended 16 cm H2O. At pressure of 16 cm H2O, her index was 1 per hour with a lowest SpO2 of 92%.

She was seen a few weeks later. Papilledema had improved, and she reported her vision had gotten better. The average nightly use of CPAP based on therapeutic hours was 7.34 hours. She was sleeping well throughout the night, waking up refreshed. She denied being sleepy during daytime and scored 7 on the Epworth Sleepiness Scale, which is considered normal.

Five months after treatment with CPAP, eye examination showed residual papilledema. To eliminate papilledema more quickly, acetazolamide 500 mg twice daily was recommended. She developed paresthesias shortly after beginning this regimen, and the dose was reduced to 500 mg daily. Seven months later, she reported further improvement in vision; examination showed that papilledema had resolved. Acetazolamide was stopped.

Her last visit was June 2009. Her medications were unchanged. She weighed 131 kg. Average nightly use of CPAP based on therapeutic hours was 7.6 hours. The software of the device read an index of about 4 per hour.

DISCUSSION

The true prevalence and pathogenesis (proposed in Figure 1) of papilledema and ICH in OSA are not known. A retrospective review of patients presenting with IIH revealed 22 of 23 patients were female, and those with visual symptoms were likely obese and hypertensive.4 Because obesity and hypertension are major risk factors for OSA, it is conceivable that a number of these patients suffered from OSA. It is well known that weight loss improves papilledema.5 Since weight loss also improves OSA, improvement in OSA might be contributory to improvement of papilledema.

Our patient had severe OSA and treatment with CPAP was associated with improvement in her vision and papilledema within a few weeks, consistent with a previous report of 3 patients who received CPAP alone and had resolution of the optic disc edema.3 These findings along with the proposed mechanisms (see below) and the observation that weight loss improves papilledema suggest that OSA might be a potential cause or contribute to worsening of ICH (pseudotumor cerebri) and papilledema.

We speculate that pathophysiological consequences of sleep apnea create a milieu vulnerable to physiology of intracranial structures (Figure 1). Cycles of apnea result in repetitive episodes of intermittent hypoxemia and hypercapnia (which result in cerebral vasodilatation), and surges in arterial blood pressure. Normally, under steady state conditions, because of the operation of autoregulation, cerebral vasculatures are spared from the rise in arterial blood pressure. However, under unsteady state conditions, such as intermittent cycles of apnea and recovery, cerebral autoregulation remains inoperative; consequently, cerebral vasculature is vulnerable to intermittent rises in arterial blood pressure. In addition, it has been shown that OSA further impairs cerebral autoregulation. Therefore, with surges in blood pressure, hypoxia- and hypercapnia-induced cerebral vasodilatation and loss of autoregulation, cerebral blood flow and volume increase, resulting in periodic and eventually sustained rises in intracranial pressure. In addition to the hemodynamic alterations, OSA is also associated with activation of reactive oxygen species, oxidative stress, and inflammation, which have been associated with neuronal damage and apoptosis, potentially contributing to optic nerve pathology.

In our patient, acetazolamide was used to hasten recovery. However, the therapeutic effect of acetazolamide is questionable, as no randomized clinical trials are available. In one study in which acetazolamide was used, ICH improved only in those with weight loss.5

In conclusion, our case report should heighten early recognition of the association of OSA with papilledema with the hope that treatment of OSA should prevent permanent optic nerve damage. We emphasize, however, that amelioration of the papilledema might not have been attributed to CPAP therapy alone.

DISCLOSURE STATEMENT

This was not an industry supported study. The authors have indicated no financial conflicts of interest.

ACKNOWLEDGMENTS

The authors sincerely thank Mr. K. Byrd for his artwork (Figure 1), and Mr. N. Harris for his editorial assistance.

REFERENCES

1 

Ball AK, Clarke CE, authors. Idiopathic intracranial hypertension. Lancet Neurol. 2006;5:433–42. [PubMed]

2 

Purvin VA, Kawasaki A, Yee RD, authors. Papilledema and obstructive sleep apnea syndrome. Arch Ophthalmol. 2000;118:1626–30. [PubMed]

3 

Lee AG, Golnik KC, Kardon R, Wall M, et al., authors. Sleep Apnea and intracranial hypertension in men. Ophthalmol. 2002;109:482–5

4 

Zayit-Soudry S, Leibovitch I, Kesler A, authors. Idiopathic intracranial hypertension after 40 years of age: Clinical features in 23 patients. Euro J Ophthalmol. 2008;18:989–93

5 

Johnson L, Krohel G, Madsen R, March A Jr., authors. The role of weight loss and acetazolamide in the treatment of idiopathic intracranial hypertension (pseudotumor cerebri). Ophthalmology. 1998;105:2313–7. [PubMed]

6 

Javaheri S, Malik A, Smith J, Chung J, authors. Adaptive pressure support servo-ventilation: a novel treatment for sleep apnea associated with use of opioids. J Clin Sleep Med. 2008;4:305–10. [PubMed Central][PubMed]