Impact of Acetazolamide and CPAP on Cortical Activity in Obstructive Sleep Apnea Patients

STUDY OBJECTIVES 1) To investigate the impact of acetazolamide, a drug commonly prescribed for altitude sickness, on cortical oscillations in patients with obstructive sleep apnea syndrome (OSAS). 2) To examine alterations in the sleep EEG after short-term discontinuation of continuous positive airway pressure (CPAP) therapy. DESIGN Data from two double-blind, placebo-controlled randomized cross-over design studies were analyzed. SETTING Polysomnographic recordings in sleep laboratory at 490 m and at moderate altitudes in the Swiss Alps: 1630 or 1860 m and 2590 m. PATIENTS Study 1: 39 OSAS patients. Study 2: 41 OSAS patients. INTERVENTIONS Study 1: OSAS patients withdrawn from treatment with CPAP. Study 2: OSAS patients treated with autoCPAP. Treatment with acetazolamide (500-750 mg) or placebo at moderate altitudes. MEASUREMENTS AND RESULTS An evening dose of 500 mg acetazolamide reduced slow-wave activity (SWA; approximately 10%) and increased spindle activity (approximately 10%) during non-REM sleep. In addition, alpha activity during wake after lights out was increased. An evening dose of 250 mg did not affect these cortical oscillations. Discontinuation of CPAP therapy revealed a reduction in SWA (5-10%) and increase in beta activity (approximately 25%). CONCLUSIONS The higher evening dose of 500 mg acetazolamide showed the "spectral fingerprint" of Benzodiazepines, while 250 mg acetazolamide had no impact on cortical oscillations. However, both doses had beneficial effects on oxygen saturation and sleep quality.

Unilateral papilledema after trabeculectomy in a patient with intracranial hypertension

BACKGROUND: Increased intracranial pressure usually leads to bilateral disc swelling. HISTORY AND SIGNS: A patient presented with recurrent visual disturbances following trabeculectomy in the right eye. Intraocular pressure in the right and left eye were 11 and 24 mmHg, respectively. The optic nerve head was swollen in the right, but not in the left eye. Lumbar puncture showed an opening pressure of 32 cmH (2)O. Magnetic resonance imaging, neurological examination and composition of cerebrospinal fluid were normal. According to the modified Dandy criteria, an idiopathic intracranial hypertension was diagnosed. THERAPY AND OUTCOME: Treatment with acetazolamide led to resolution of papilledema in the right eye within six months. CONCLUSION: The intracranial-intraocular pressure gradient in the right eye was markedly higher as compared to that of the left eye. We suggest that this pressure gradient induced the collapse of axoplasmatic transport at the lamina cribrosa with subsequent disc swelling. As no significant pressure gradient was present in the left eye, the optic disc remained normal. Based on analogous calculations in three additional published cases of unilateral papilledema we thus suggest that intraocular pressure should be taken into account when evaluating patients with papilledema.