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. 2019 May 29;19(7):39. doi: 10.1007/s11910-019-0952-9

Table 1.

Early studies on the effects of obstructive sleep apnea on intracranial pressure, SaO2, and PaCO2

Author/year Findings
Meyer et al., 1961 [47] Pickwickian patient with papilledema, excessive sleepiness, hypoxemia, and hypercapnia; lumbar puncture showed elevation of CSF pressure to 480 mm H2O.

Lugaresi et al.,

1978 [48]

45 OSA subjects: Arterial hypertension in 1/3 cases; all had transient hypoxemia and elevated PaCO2 with sleep apnea episodes; values worsened during REM sleep.
Iijima et al., 1979 [49] OSA: Arterial blood gases showed transient hypoxemia and hypercapnia with apnea episodes.

Kaneda et al., 1983 [50]; Kuchiwaki et al.,

1983 [51]

First described the association of OSA and NPH. ICP recording in patients with NPH showed increased ICP with presence of Lundberg B-waves with each apnea episode.

Kuchiwaki et al.,

1984 [52]; 1988 [53]

17 patients with NPH and OSA showed elevation of CSF pressure during sleep apnea events. CSF shunting in 13 cases failed to improve the hypoxemia and hypercapnia observed with OSA. Authors suggested that OSA contributes to progression and worsening of hydrocephalus.
Sugita et al., 1985 [54] 3 patients with OSA: Marked increase of CSF pressure (50–750 mm H2O) measured at lumbar level following each episode of OSA/hypopnea. Longer apneas during REM sleep resulted in worse SaO2 decreases and higher increases of CSF pressure.
Jennum and Børgesen, 1989 [55] 6 OSA patients (none with NPH): Each apnea event increased ICP. ICP at rest was high (> 15 mmHg) and also in the morning (20·7 mmHg). While asleep, all patients developed apnea-associated elevated ICP.
Pasterkamp et al., 1989 [56] 1 patient with hydrocephalus treated with CSF shunt developed OSA years later: Rising intraventricular ICP up to 50 cm H2O occurred with each episode of apnea probably contributing to worsening syringomyelia.
McNamara et al., 1992 [57] NPH symptoms worsened with nasal CPAP in 1 patient with NPH; treatment of NPH with VPS allowed use of CPAP with clinical improvement. CPAP and PEEP increase central venous pressure decreasing venous and CSF outflow, causing increased ICP.
Krauss et al., 1995 [58] In 13 NPH patients, sleep apneas caused elevation of intraventricular ICP with Lundberg B-waves. Frequency of B-waves was higher during REM sleep and sleep stage 2.
Kristensen et al., 1998 [59] Sleep-disordered breathing is very common in NPH: OSA was documented in 65% or 11/17 NPH patients. VPS failed to ameliorate sleep-disordered breathing in patients with NPH. OSA causes additional cognitive dysfunction in NPH patients.
Tsunoda et al., 2002 [60] Using MRI, ventricular volume and intracranial CSF volume were increased in 17 patients with NPH; compared with controls, brain atrophy was also present in NPH patients.

Abbreviations: CPAP, continuous positive airway pressure; CSF, cerebrospinal fluid; ICP, intracranial pressure; MRI, magnetic resonance imaging; NPH, normal-pressure hydrocephalus; OSA, obstructive sleep apneas; PaCO2, arterial partial pressure of carbon dioxide; PEEP, positive end-expiratory pressure; REM, rapid eye movement; SaO2, arterial oxygen saturation; VPS, ventriculoperitoneal shunt