Awareness Gaps Drive Narcolepsy, IH Delays: Logan Schneider, MD

Diagnostic delays in narcolepsy and idiopathic hypersomnia (IH) persist largely because of low awareness among patients, families, and clinicians, and patients often pass through other diagnoses, including mental health conditions, before reaching a sleep specialist, said Logan Schneider, MD, a sleep medicine specialist and adjunct clinical associate professor of psychiatry and behavioral sciences at Stanford Health Care.

In an interview with The American Journal of Managed Care^® (AJMC^®), Schneider described what patients typically look like when they arrive at a sleep center and why the diagnostic journey is so long. He also outlined how primary care clinicians and psychiatrists can use a sleepiness score and a sleep health framework to prompt earlier referral, how he rules out other explanations before diagnosing a central disorder of hypersomnolence, and how narcolepsy type 1 differs from type 2.

This interview has been edited for clarity.

AJMC: Idiopathic hypersomnia (IH) and narcolepsy are both frequently missed or misattributed. In your sleep center, what do these patients typically look like when they first walk in, and who have they already seen before they come to the sleep center?

Schneider: Patients with chronic disorders of hypersomnolence typically arrive as part of a long diagnostic journey. Many times, they’re coming in because of unresolved issues with their daytime sleepiness and the impact that it’s having on their life. Clearly, it’s such a severe degree of excessive sleepiness and/or need for sleep. That can be that they’re drowsy at inappropriate times or needing to take naps in order to get through the day. Or that sleep is eating away at their day, for example, in folks with idiopathic hypersomnia. It has now caused a dysfunction in their life or maybe has been causing [it] for quite some time, and yet, despite the treatments and diagnoses that they’ve gotten, they haven’t resolved it. They’re still searching for that answer. That’s typically what brings patients to the center and what their lives look like.

They may have come through many different paths because sleepiness is sometimes hard to articulate as distinct from tired, fatigued, exhausted, and so they’ll often take many different routes that are completely appropriate. In fact, many of these central disorders of hypersomnolence, you have to have ruled out those other conditions and/or managed them before you can actually treat these folks. The common culprits are things like metabolic conditions, thyroid dysfunction, blood abnormalities like anemias, and certainly mental health issues are ones that crop up quite frequently. It’s challenging, particularly in those cases, because treatments for those mental health conditions sometimes can improve the symptoms themselves. But also, it’s completely understandable to have an emotional or mental health reaction to the burden that this places on their lives. So that’s typically what we see: folks coming in with a number of different diagnoses and/or attempts at improving their symptoms.

AJMC: Diagnostic delay in narcolepsy has long been reported to exceed 10 years.¹ Why does this gap persist, and what is happening to these patients in their everyday lives during those years?

Schneider: We feel as a community that potentially the reason is lack of awareness, and that awareness can come from any point in their lives. That can be from a self-awareness of what’s normal vs abnormal. We only live our own life and don’t have many external frames of reference. [It also could be] the family members of these individuals and/or caregivers. And then the providers, or health care professionals, that they’ve seen along the journey, not necessarily recognizing what is unique and abnormal about this, because when you hear hoofbeats, you have to think about horses, not necessarily zebras, and these are rare conditions.

The longest delays are occurring in the younger populations, and I would imagine the reason for that is we look at young populations as sleepy in general. They have higher sleep needs. They have all these impositions on their schedule from school and extracurricular requirements that justify, “Oh, they’re expectedly sleepy. No wonder they’re drowsy, no wonder they’re sleeping in on weekends, no wonder it’s hard to get them up. They’re not getting enough sleep.” Or the societal perception, I think we’re starting to rectify, which is that sleepiness is laziness in some sense. I think that has been a reason for the diagnostic delays: “Well, everybody needs sleep, and you’re just not getting enough. You just need to get more rest.”

In a similar way that we look at other mental health issues, it’s like, “Oh, this is your fault,” rather than, “This might actually be an indication of something underlying that we need to address.” So, I think that’s the main issue: awareness of what is abnormal and pathologic across the spectrum.

AJMC: What are two to three questions that you would want a primary care clinician or a psychiatrist to ask patients that would prompt a sleep referral sooner?

Schneider: What I would want frontline providers who are seeing these patients to consider is, one, add this as a vital sign. In the sleep medicine community, it has its pros and its cons, [but] we have the Epworth Sleepiness Scale score,² which is a good indication of excessive sleepiness. It’s been used for decades, been validated in different populations, and so treat this just like you would any other vital sign, because if you’re not able to stay awake during the day, it’s a good indication that something is wrong. So, step 1, just assess it at the most superficial level; it’s a vital sign.

The other aspect is not really a question but actually a framework for thinking that I like to champion, and it was pioneered by Dr Buysse, one of the luminaries in the sleep and psychiatry field. It’s the RU-SATED framework³ for thinking about sleep health. This gives you 6 sleep health dimensions, extensively validated since its inception in 2014, to demonstrate meaningful impacts on health outcomes. Just use this to check off the boxes and say, “Is this healthy, or is this not healthy?” And if not healthy, maybe I can probe more or refer on.

The RU-SATED paradigm has RU for regularity or routine; S for sleep quality or satisfaction, that can be objective or subjectively reported; A for alertness, how are you functioning during the day, in addition to are you sleepy or not; T for timing, the alignment between your circadian rhythm and your actual sleep schedule; E for efficiency, of the time you spend trying to sleep, how much of it are you actually getting in sleep, with the denominator being time in bed and the numerator being how much sleep you got; and then last but not least, D is duration. Are you getting what seems to be an adequate amount for somebody your age? Putting all of that together, just check those six boxes with a quick screener, and you can suss out if somebody might need more investigation or even a referral.

AJMC: Psychiatric comorbidities are common in narcolepsy. What clinical clues help you tell a primary hypersomnolence disorder from depression or anxiety, and when are both true at once?

Schneider: That’s quite challenging, and I think there are several clues. One is typically the time course. If the sleepiness, which tends to onset in early life, adolescence, and what have you, precedes the mental health issues, that typically suggests that the mental health issues cropped up as a result of the impact it was having on their life. That’s often a clue. If they come concomitantly, like you’re depressed and suddenly sleeping excessively, that would be more in favor of a psychiatric condition.

Another is sometimes the descriptions of the symptoms. Instead of clinophilia, where somebody’s just lying around in bed, [these patients] are actually falling asleep. Typically, mental health disorders don’t make you sleepy excessively, so you’re not just dozing off at inappropriate times, despite maybe having depleted energy or just not having the motivation to go around.

And then finally, your ability to respond to treatments. Treatments that treat mental health issues don’t improve sleepiness as robustly as you would hope. So fundamentally, it’s just those three things: time course, the description of the symptoms and true pathologic sleepiness, and what symptoms respond to the treatments.

AJMC: In a survey from the Hypersomnia Foundation, 57% of providers acknowledged having misdiagnosed IH, and 86% of patients were often labeled as depressed or anxious.⁴ Does this match what you’re seeing in referrals, and why is the overlap with mood disorders so persistent?

Schneider: I see a number of individuals being misdiagnosed. But again, as we mentioned before, hindsight is 20/20. Once you arrive at the correct diagnosis, it’s very easy to say that that was a misdiagnosis. In some sense, people are doing what is familiar and correct according to the symptoms that patients are reporting, and sometimes they may not know to probe or how to probe to find out that this is abnormal. Sometimes they get that spidey sense: “Oh, right, this person has refractory symptoms to a treatment that is very commonplace,” or now when we’ve delved a little bit deeper, and the story unravels a little bit more, now I am alerted to the fact that I need to refer on. So sometimes it takes a failure of therapy to be an indication of what’s going on.

The other aspect is that not only are these individuals able to be treated for symptoms that look very similar to mental health issues and responsive to treatments in some regards, so many of the medications that are used can also improve the symptoms of sleepiness; even though they’re not primary sleep medications, they work on similar chemicals in the brain. But also, it’s completely understandable that they would have higher rates of mental health issues because of the impact that this has on their lives. The excessive sleepiness, excessive need for sleep not only eat away at your ability to do things and satisfaction with life but also result in this stigmatization. Again, as mentioned, society looks at sleepiness as laziness, and that’s not the case at all. If you need to fall asleep, that’s not because you’re lazy; it’s because you have a physiologic need for more sleep.

These individuals often internalize their condition or the societal perception of them as lazy individuals or unable to perform, and sometimes that can result in mental health issues themselves, which are worthy of treatment and, when treated, can improve. So, it’s a very challenging set of conditions to separate.

AJMC: Before you diagnose a central disorder of hypersomnolence, you have to rule out other explanations, including insufficient sleep and sleep apnea. What does that workup look like in your practice, and how do you decide that patients have had enough tests to determine their diagnosis?

Schneider: To be able to make a diagnosis of these central disorders of hypersomnolence, even though they’re not strictly disorders of exclusion, you’ve ruled out other conditions. In all of the diagnostic criteria for them, it can’t be attributable to another sleep disorder, another mental health disorder, another medical disorder, or the treatments of those disorders, because those are common reasons to have the symptoms that these individuals will experience, including the excessive daytime sleepiness, including the excessive need for sleep as well. Lots of medications that we use are sedating. So, part of the standard evaluation is, can I find a different explanation that would say this isn’t a primary condition? Because the primary conditions are treated differently than maybe we just change your medication regimen or get that condition under control.

That pertains to sleep disorders as well. As part of that investigation, we have to make sure that if you’re sleepy during the day, you’re offering enough sleep to not be sleepy during the day. That’s certainly an important thing, so that you’re not behaviorally inducing this and we’re treating your bad behavior, so to speak. The other aspect is, obviously, there are sleep disorders that are primary causes for having sleepiness during the day, and so we certainly don’t want to be treating a symptom and not addressing the underlying problem. For example, sleep apnea, a very common cause of sleepiness. If I give you something that sedates you, or if I give you a stimulant, but I haven’t treated the underlying cause of that, you still are at risk for the consequences of that underlying condition, for which the symptom was the red flag that we should be hunting it down and treating it.

I think that pertains to any sleep disorder as part of the standard course: assess for and treat any conditions that can cause us to have the symptom, and if we’ve treated everything and you still have these symptoms, well, then now we need to start considering [that] maybe there’s a primary concern that we actually have to now treat specifically. Now, again, it’s still symptom-based treatments for most of these conditions. Granted, that’s all changed with type 1 narcolepsy and the recent approval of orexin 2 agonists,⁵ where it’s actually targeting the disease state or the deficiency of the hypocretin or orexin molecule in those folks. But otherwise, it’s symptom management.

AJMC: How do you distinguish narcolepsy type 1 from type 2 in practice, and why does that distinction matter for counseling, treatment selection, and overall patient expectations?

Schneider: This is wonderful; we actually have very good diagnostics for this. Type 1 narcolepsy is fundamentally defined by the deficiency of a peptide or a molecule in the brain. It’s variably known as either orexin or hypocretin. Finding that is easy if you do a lumbar puncture, basically collect cerebrospinal fluid by a standard diagnostic procedure and demonstrate the absence of that molecule. That’s a very clear indication that that disorder is present.

If that’s not something that you can avail yourself of, even though [there is] a clinical laboratory to do that investigation, you can also rely upon a very characteristic symptom in type 1 narcolepsy called cataplexy, where muscle paralysis sets in in the setting of an emotional surge, particularly a surprising one, along with the demonstration of excessive sleepiness and REM [rapid eye movement] dysregulation on our standard diagnostic testing. If you found the very clear phenotype of type 1 narcolepsy, it’s an imperative to treat this individual. The reason being because they won’t get hypocretin back. It’s often because the cells in their brain have been destroyed by some mechanism. We believe infection kicks the immune system into overdrive and kills all of these cells off, or most of them, such that you basically can’t produce this molecule anymore. And thus, you are at high risk for dangerous and hazardous consequences: the onset of the muscle paralysis of cataplexy, like when you’re driving, or sleepiness that’s excessive and you can’t control and might happen at inopportune times. Those folks really have a strong imperative: we need to treat this, and you’re never going to get these cells to grow back, so we have to provide lifelong care for that. It’s certainly a much more severe phenotype than all the other central disorders of hypersomnolence.

That being said, type 2 narcolepsy doesn’t have cataplexy, and in fact, having cataplexy would make you type 1 narcolepsy. Also, we don’t know what’s going on with their levels of that orexin/hypocretin molecule. It could be that it’s normal but has signaling pathway problems. It could be something completely different. We don’t actually know what’s going on in them. So, they’re characterized just by the presence of a positive napping study; basically, they’ve demonstrated that they have irregular sleep-wake control by having REM dysregulation, meaning their dream sleep happens at abnormal times when it shouldn’t, as well as they’re demonstrating excessive sleepiness despite adequate amounts of sleep preceding that. So, they look like narcolepsy based on the REM dysregulation and sleepiness, but they don’t have the cataplexy or hypocretin deficiency that we can demonstrate.

For those individuals, it’s a much more challenging thing because we don’t know what is causing these symptoms. Typically, it’s solely focused on symptom-based management. In those folks, I tend to be a bit more cautious just because I don’t know what the correct treatment is necessarily, so we go through the menu of options, there’s shared decision-making, and I step in a little bit less aggressively to see if I can get larger improvements in their symptoms through less risky medications, because these are a lot of risky medications. They’re medications that are heavily sedating sometimes, or have addictive potential, or just can cause consequences for blood pressure and headaches and things like that, because they’re trying to be stimulant or wake-promoting.

References

Zhang Z, Dauvilliers Y, Plazzi G, et al. Idling for Decades: A European Study on Risk Factors Associated with the Delay Before a Narcolepsy Diagnosis. Nat Sci Sleep. 2022;14:1031-1047. Published 2022 May 31. doi:10.2147/NSS.S359980

Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;14(6):540-545. doi:10.1093/sleep/14.6.540

Buysse DJ. Sleep health: can we define it? Does it matter?. Sleep. 2014;37(1):9-17. Published 2014 Jan 1. doi:10.5665/sleep.3298

Gavidia M. Idiopathic Hypersomnia Campaign Seeks to Spread Awareness, Empower Patients. AJMC. April 6, 2021. Accessed October 13, 2026. https://www.ajmc.com/view/idiopathic-hypersomnia-campaign-seeks-to-spread-awareness-empower-patients

Grossi G. FDA Approves First Orexin Agonist for Narcolepsy Type 1. AJMC. August 21, 2026. Accessed October 13, 2026. https://www.ajmc.com/view/fda-approves-first-orexin-agonist-narcolepsy-type-1