Guest blog by Deborah Wardly, MD
Previously I blogged about the relationship between intracranial hypertension and obstructive sleep apnea, and pointed out the similarity between the signs and symptoms of upper airway resistance syndrome (UARS), obstructive sleep apnea (OSA) and those of intracranial hypertension. Intracranial hypertension is characterized by headaches, fatigue, dizziness/vertigo, ringing in the ears (which can be pulsatile), and visual disturbances to include papilledema (swelling of the optic disc). It can be present without papilledema (idiopathic intracranial hypertension without papilledema, or IIHWOP), which many doctors don’t seem to realize, and in these scenarios a lumbar puncture (spinal tap) is the only way to diagnose it. It is associated with obesity in many cases, as is OSA.
Recently a study was published showing that in a group of patients with chronic fatigue syndrome (CFS), 20% of them met criteria for idiopathic intracranial hypertension (IIH), and 85% of them had improvement in their chronic fatigue syndrome symptoms after reduction of their intracranial pressure after lumbar puncture. The only thing missing from this study was the sleep study results on these patients! But we know how closely UARS can appear to resemble CFS, and this study begs further evaluation of UARS patients’ intracranial pressures, especially given the knowledge that apneas increase intracranial pressure.
My recent published paper discusses what is currently known about how OSA can increase intracranial pressure (ICP), and then further discusses other possibilities for this phenomenon that could be investigated. We know that individual apneas can increase ICP, and that an increase in carbon dioxide effecting an increase in cerebral blood flow may be causal, as well as perhaps an increase in intrathoracic pressure at the termination of the apnea. In my paper I discuss how OSA can increase glutamate excito-toxicity in the brain, and the evidence for glutamate being able to cause brain edema. I discuss how OSA may open the blood-brain barrier, which would also cause brain swelling.
Alperin, et al. has demonstrated that in obese women with idiopathic intracranial hypertension, they have evidence of both brain swelling and poor jugular venous drainage. I suggest in my paper how the anatomical relationship of the recessed jaw to the narrowed airway, something we recognize is present in many cases of OSA, may also be involved in a compression of the internal jugular veins. This would contribute to the poor jugular venous flow observed in IIH by Alperin, and would increase resistance to CSF outflow. We know that obesity increases the risk of OSA in part by fat compression of the airway in the neck. Perhaps obesity increases the risk of IIH by fat compression of the jugular veins in the neck? Such that it is not entirely a direct causal relationship between OSA and IIH, but that they are conditions which go hand in hand when there is a recession of the mandible or increased fat content of the neck.
An important point that I discuss in my paper is the fact that a Valsalva maneuver will increase ICP. A Valsalva maneuver is created upon “bearing down”, something we do when coughing, sneezing, grunting, crying or shouting, yet even upon laughing, singing or talking. Many people with intracranial hypertension do not tolerate any Valsalva activity, as it will increase their headaches. Think about what it feels like to exhale with your CPAP on—it is a Valsalva as well. Could this be the reason that some people with OSA/UARS do not tolerate CPAP, but must use BiPAP, or cannot use PAP at all? Do these individuals have undiagnosed IIH?
If you do not tolerate CPAP, or even BiPAP, do you have headaches or any of the other symptoms of IIH?
Do you find you must have perfect control of your airway problem in sleep, in order to prevent or reduce the headaches, dizziness, and fatigue?
If you have CFS symptoms or IIH symptoms in conjunction with your OSA/UARS, would you consider a spinal tap to further elucidate your symptoms?