Delayed Sleep-Wake Phase Disorder: Increased Intrinsic Period Length
The most likely cause of this patient's symptoms is option (d): increased length of the intrinsic period (tau), which is the fundamental pathophysiologic mechanism underlying Delayed Sleep-Wake Phase Disorder (DSWPD). 1
Understanding the Pathophysiology
This patient presents with the classic pattern of DSWPD: inability to fall asleep before 2 AM and inability to wake before 11 AM, persisting for years with functional impairment. 2, 3 The key to understanding the underlying cause lies in the circadian biology:
Patients with DSWPD have a significantly longer intrinsic circadian period (tau) compared to good sleepers (24 hours 54 minutes versus 24 hours 29 minutes), representing a 25-minute difference that causes their biological clock to delay more rapidly than normal individuals. 1
This longer tau explains why DSWPD patients have persistent difficulty phase-advancing to conventional sleep times and why they frequently relapse after treatment—their biological clock naturally runs longer than the 24-hour day. 1
The American Academy of Sleep Medicine confirms that DSWPD is fundamentally a circadian rhythm disorder where the major sleep episode is delayed relative to desired timing, and when allowed to follow their preferred delayed schedule, sleep quality and quantity are normal. 3
Why the Other Options Are Incorrect
Option (a) - Advance in cortisol awakening response: This would cause Advanced Sleep-Wake Phase Disorder (ASWPD), characterized by sleep onset between 6:00-9:00 PM and wake times between 2:00-5:00 AM—the opposite pattern from this patient. 4, 5
Option (b) - Enhanced sensitivity to morning light exposure: This would actually help advance the circadian phase and improve DSWPD symptoms, not cause them. The American Academy of Sleep Medicine recommends bright light therapy in the morning specifically to advance circadian phase in DSWPD patients. 3
Option (c) - Increased amplitude of melatonin secretion: Research shows that the shape of dim light melatonin rhythm does not differ between DSWPD patients and controls; rather, the phase angle between melatonin and sleep propensity rhythms is wider in DSWPD patients. 6 Amplitude is not the primary issue.
Clinical Implications
The longer intrinsic period explains treatment challenges: DSWPD patients show poor compensatory function for sleep loss during their circadian day and early circadian night, making it difficult to reset their sleep phase even after sleep deprivation. 6
Multiple exogenous factors perpetuate the delay: Exposure to indoor lighting during evening hours, delays in weekend wake times, increased autonomy regarding sleep timing, and employment/extracurricular activities all contribute to maintaining the delayed pattern in adolescents and young adults. 2, 3
Conditioned insomnia often develops secondarily: Frustrations at not being able to fall asleep at desired times can lead to concomitant conditioned insomnia, which perpetuates sleep difficulties beyond the primary circadian mechanism. 2, 3
Diagnostic Confirmation
The American Academy of Sleep Medicine recommends sleep diaries and/or actigraphy for at least 7 days to document the characteristic delayed but otherwise normal sleep pattern when unrestricted. 3 Circadian phase assessments such as dim light melatonin onset (DLMO) can confirm the delayed circadian phase if feasible. 3