The Association of Normal-Pressure Hydrocephalus With Obstructive Sleep Apnea M. Eileen McNamara, MD; Richard P. Millman, MD; Me1 H. Epstein, MD; Bany S. Fogel, MD

Abstract This report describes a 70-year-old man with obstructive sleep apnea who deteriorated rapidly when nasal continuous positive airway pressure was begun. The patient was found to have normal-pressure hydrocephalus, which was possibly exacerbated by the nasal continuous positive airway pressure. A review of the literature indicates several significant associations between apnea, normal-pressure hydrocephalus, and increased intracranial pressure and suggests that the association of obstructive sleep apnea and hydrocephalus might not be rare. Implications for diagnosis and treatment are discussed. Geriatr Psychiafy Neirrol 1992;5:238-240).

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0th normal-pressure hydrocephalus (NPH) and obstructive sleep apnea (OSA) can present with changes in personality and cognition, and the distinction of these potentially treatable illnesses from other psychiatric or degenerative neurologic diseases is crucial. Moreover, the literature suggests that NPH and OSA may in some cases be associated disorders, with significant implications for diagnosis and treatment. We report such a case. Case Report A 70-year-old man presented in April 1989 complaining of confusion. For 2 weeks prior to admission, he had had problems with forgetfulness, getting lost while driving, and inappropriate behavior such as exposing himself. Obstructive sleep apnea, which by history had probably been present for Received May 15, 1991. Received revised Nov 4, 1991. Accepted for publication Feb 6, 1992. From the Departments of Psychiatry (Drs McNamara and Fogel), Neurology (Drs McNamara and Fogel), Pulmonary Diseases (Dr Millman), and Neurosurgery (Dr Epstein), Rhode Island Hospital, and the Department of Psychiatry and Human Behavior (Drs McNarnara and Fogel), Brown University, Providence, RI. Presented at Harvard Medical School Education Center, Fourth Annual Meeting, Northeastern Sleep Society, Boston, MA, March 31-April 1, 1990. Address correspondence to Dr M. Eileen McNamara, Department of Psychiatry, APC-608B, Rhode Island Hospital, Providence, RI 02903.

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more than 20 years, had been diagnosed 3 years before admission. Formal polysomnographic study at that time demonstrated obstructive apneas occurring at a rate of two per minute, associated with oxygen desaturation in non-rapid-eye-movement (N-REM) sleep falling to 92% during the apneas. Nasal continuous positive airway pressure (CPAP) had been prescribed but was rarely used by the patient, who found it inconvenient. Ambulatory 24-hour electroencephalogram performed 1 year prior to admission showed marked fragmentation of stage 2 and REM sleep accompanied by significant daytime drowsiness, consistent v i t h significant disruption of nocturnal sleep by apnea. The past medical history included insulin-dependent diabetes mellitus, hypothyroidism with replacement therapy, minor gait instability attributed to diabetic peripheral neuropathy, and urinary frequency and hesitancy attributed to benign prostatic hypertrophy. There was also a lifelong history of prominent anxiety, and claustrophobia that had caused him to refuse further workup, including head computed tomographic (CT scan. He was admitted for management of his psy chiatric condition dnd further diagnostic investiga tion. On physical examination, the patient was ar obese man with a hoarse voice. On mental status ex amination, he was irritable, distractible, unhappy self-blaming, suspicious, and pessimistic. Cogni

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Hydrocephalus and Sleep Apnea

tively, he was oriented in all spheres and generally cooperative. Presidents, serial sevens, similarities, and recall of three items at 5 minutes were all done well, but he had difficulty on bedside tests of verbal fluency (listing words starting with ”s”), more difficult calculations (eg, 7 X 35), and memory for the details of a complex sentence. Gait was slightly wide-based and mildly unstable, with a negative Romberg test. Cranial nerves I1 through XI1 and the motor examination were normal. Position and vibration jerk were diminished in the feet. Reflexes were present and symmetrical in the upper extremities and absent in the lower extremities; the plantar responses were flexor. Because his affective symptoms were limiting his ability to cooperate with medical care, the patient was begun on perphenazine 2 mg bid and nortriptyline 25 mg, with initial improvement in anxiety. Nasal CPAP was advised at the same time, then adjusted to 10 cm H20, but the patient used it only briefly. The morning following theinstitution of this treatment, he appeared calmer and more cooperative’. However, the following night, he refused psychotrobic medications and continued to use his CPAP inconsistently. The next two nights, he agreed to a slightly lower dose of psychotropics (norhiptyline 10 mg, then 20 mg, and perphenazine 2 mg bid) and accepted CPAP most of the night. The fifth night of treatment, in preparation for another attempt at a CT scan the next day, perphenazine was boosted to 4 mg bid. Also, constant observation was provided to ensure that CPAP was kept on all night. The next day, he developed a frank gait apraxia with shuffling and magnetic gait and was markedly somnolent, confused, and disoriented. At no time, however, did the patient show tremor or rigidity suggestive of drug-induced parkinsonism, nor was there any tachycardia or orthostatic hypotension. Emergency CT scan showed enlarged lateral ventricles, open third and fourth ventricles, and obliterated sulci, consistent with hydrocephalus. Isotope cisternography at 48 and 72 hours showed activity within the ventricles without migration over the convexities, consistent with normal-pressure hydrocephalus. The patient’s nasal CPAP, perphenazine, and nortriptyline were discontinued, and his examination returned to his admission baseline within the next 2 days. Later, following a ventriculoperitoneal shunt, the gait instability and incontinence seen on admission remitted, and his memory, attention, and behavior improved. The patient continued to refuse nasal CPAP and further polysomnographic evalua-

tion, but was reported by his wife to have considerable improvement in his cognitive function, as well as his sleep, with less snoring and more daytime alertness. Discussion A 70-year-old patient is described who has both OSA and NPH. The institution of nasal CPAP may have worsened the symptoms of his NPH. Both OSA and NPH are relatively common diseases, particularly in the geriatric population,’ and their concurrence in our patient may have been fortuitous. Casmiro et a1 reported a frequency for NPH of at least 0.5% in the general male population over 65 years of age.’ OSA has been estimated to affect 1% or more of males over age 50 years3 However, there may be physiologic reasons for an association of NPH with sleep apnea. Kuchiwaki et a14 reported results of polysomnographic evaluation and intracranial pressure monitoring in a series of 16 patients with NPH from a variety of causes including idiopathic, subarachnoid hemorrhage, and meningitis. All 16 patients (100%) had some degree of sleep apnea with apneic episodes per night ranging from 30 to 210 apneas per night. These were associated with significantly shallow and fragmented sleep with reductions in stages 3 and 4 and REM sleep. The onset of intracranial pressure waves, which are a feature of NPH,5,6 was associated with apneas and arousals. Conversely, apnea is known to cause increases in intracranial pressure. In 1989, Jennum and Borgesen7 used epidural pressure monitors to study six otherwise normal patients with OSA. During apneas, elevations of intracranial pressure were observed, with steep preasure increases at the termination of apneas. Pressure waves during nonREM sleep met criteria for intracranial B waves, while pressure waves in REM sleep met criteria for intracranial A waves. Moreover, four of the six patients were also found to have pathologically elevated intracranial pressure while awake, 20.7 0.8 mm Hg in the morning and 17.7 f 0.5 mm Hg in the evening (normal intracranial pressure, below 15 mm Hg). These independent studies, showing a high association of apnea with NPH, and showing increased intracranial pressure in OSA, suggest that the association of NPH and OSA in our patient may not have been coincidental. Similarly, Kuchiwaki et a14 and others’ suggest that the transient elevations of intracranial pressure produced by apneas, super-

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imposed on a previously impaired cerebrospinal fluid circulation contained within a rigid intracranial space, could have some relationship to the chronic progression of hydrocephalus. Further, the patient reported here appeared to deteriorate when treated with nasal CPAP, albeit in conjunction with psychotropic drugs. While the psychotropics prescribed may have contributed to his deterioration, they are not likely to be the only cause because the doses were relatively small, and the initial response to them was positive. It is remarkable that the deterioration occurred in the first night of constant observation to ensure full compliance with CPAP. (Unfortunately, that day's increase in perphenazine dosage makes the correlation less clearcut than it would.be otherwise.) To our knowledge, the effects of nasal CPAP on intracranial pressure have not been studied, although our case suggests this may be worthwhile. Positive end expiratory pressure (PEEP) can increase central venous pressure, -decreasing outflow and hence affecting intracranial pressure, particularly if intracranial compliance is reduced." The continuous ' elevation of pressures by nasal CPAP, as opposed to the more intermittent PEEP pressures, might cause even greater elevations of intracranial pressure. There are two clinical inferences. First, if a patient with signs compatible with hydrocephalus also appears to have sleep apnea, this is compatible with the diagnosis, and may even make it more likely. Second, if a patient deteriorates neurologically following initiation of CPAP, a primary central nervous system problem should be considered. NPH is one such problem, although presumably a tumor or other space-occupying lesion could also be aggravated if increased intracranial pressure is exacer-

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bated by CPAP. Further, the case reported here suggests that when sleep apnea and NPH occur together, treatment of the NPH should take precedence. References 1. McNamara ME: Detection of sleep apnea during standard ambulatory cassette EEG recording for seizures: Two case reports . Clin Electroencephulogr 1990;21: 168- 169. 2. Casmiro M, Benassi G, Cacciatore FM. DAlessandro R Frequency of idiopathic normal pressure hydrocephalus, letter. Arch Neurol 1989;46:608. 3. Phillips B, Cook Y, Schmitt F, Berry D: Sleep apnea: Prevalence of risk factors in a general population. Soul11 Med 1989;82:1090- 1092. 4. Kuchiwaki H, Takada S, Ishiguir H, et al: Pressure wave with apnea evaluated by sleep level in patient with ventricular dilatation. Neurol Res 1988;10:105-111. 5. Gucer G, Vierstein L, Walker A E Continuous intracranial pressure recording in adult hydrocephalus. Surg Neurol 1980;13:323-328. 6. Jensen F, Jensen ET: Acquired hydrocephhus 11: Diagnostic and prognostic value of quantitative isotope ventriculography (QIV),lumbar isotope cisternography and continuous intracranial pressure recording (ICP). Actu Neurochir (Wien) 1979;46:243-257. 7. Jennum P, Borgesen SE: Intracranial pressure and obstructive sleep apnea. Chest 1989;95:279-283. 8. Lodrini S, Montolivo M, Pluchino F, Borroni V: Positive endexpiratory pressure in supine and sitting positions: Its effect in intrathoracic and intracranial pressures. Neurosurg 1989; 24m-m. 9. Pasterkamp H, Cardoso ER, Booth F A Obstructive sleep apnea leading 'to increased intracranial pressure in a patient with hydrocephalus and syringomyelia. Chest 1989;95: 1064- 1067. 10. Rockoff MA, Ropper AH: Treatment of intracranial hypertension, in Ropper AH, Kennedy SK, Zervas NT (eds): Neurologi d and Neurosurgical Intensive Cure. Baltimore, University Park Press, 1983, p 21-37.

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The association of normal-pressure hydrocephalus with obstructive sleep apnea.

This report describes a 70-year-old man with obstructive sleep apnea who deteriorated rapidly when nasal continuous positive airway pressure was begun...
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