Guest blog by Deborah Wardly, MD
It seems to be a little known fact that obstructive sleep apnea (OSA) can cause an increase in intracranial pressure (ICP). In 1989 Jennum and Borgeson showed that individual apneas lead to an increase in ICP in addition to an increase in arterial pressure, but also that in patients with OSA, more than half of them have elevated ICP while awake in the morning, and the ICP in the morning is higher than it is in the evening. Since that time there have been a few papers addressing this phenomenon, but surprisingly less than one might expect, and probably as a result most doctors do not seem to be aware of the connection.
There is more information in the ophthalmology literature and this specialty seems to be knowledgable about the relationship between OSA and papilledema (swelling of the optic nerve head) as seen in pseudotumor cerebri. There are reports of patients with OSA and intracranial hypertension with papilledema showing improvement in disc edema and visual fields with the use of CPAP.
However there is less awareness of the condition of IIHWOP: idiopathic intracranial hypertension without papilledema. In IIHWOP the headache pattern may be identical to that of migraine, and in the absence of papilledema it may not be possible to diagnose it without a lumbar puncture for opening pressure. The diagnosis of this subset of IIH must be considered in order to detect it.
In IIH the symptoms include most prominently headache, which is worse in the morning, and can be increased by anything which increases ICP, like coughing or sneezing (a Valsalva). The pain can go into the neck and upper back, and may be felt behind the eyes. There can also be nausea and vomiting, as well as dizziness. Many patients have a symptom called pulsatile tinnitus, which is a whooshing sound in the ears synchronous with the pulse. Less frequently there can be numbness of the extremities, generalized weakness, and balance problems. The ICP can affect the cranial nerves, notably the sixth nerve, and as above can lead to swelling of the optic disc which may cause visual changes. IIH can even present with psychiatric symptoms: depression, anxiety, and rarely self injurious behavior and psychosis.
The classic presentation of a person with IIH is an obese woman in her 40s, prior to menopause. The IIH is found to improve if the woman loses weight.
However there is a recent association noted in men with IIH: they are more likely to have OSA and testosterone deficiency. Therefore in addition to OSA, hormones seem to play a role in whether a person develops IIH. There is also a suggestion in the literature that IIH may in some cases be related to a hypercoagulable state. This may explain its prominence in people with higher estrogen levels. We know that OSA promotes hypercoagulability, is made worse by obesity, and may cause morning headache. OSA also will improve with weight loss.
I hope the reader can see the correlation and overlap between the symptoms of intracranial hypertension and those of OSA. It is my impression that there is likely a significant amount of IIH that is unrecognized among patients with OSA, because the relationship between apnea and ICP is not well known. Could it be that the severe fatigue and other debilitating symptoms in UARS are actually a result of unrecognized intracranial hypertension? I also suspect that problems in making the diagnosis of OSA may lead to underdiagnosis of OSA as the cause of many recognized cases of IIH.
What is your experience? As physicians were you aware that OSA may cause ICP? Do you have patients with both OSA and IIH? Do you have OSA patients with many of the IIH symptoms who might need further evaluation? As a patient with OSA, do you see yourself in the description of IIH?