Narcolepsy

Prevalence approximately 1:2000

Women and men equally affected

Prevalence higher in Japan (1:600)

Potential for masking or mimicking periop complications

Potential deleterious interactions between drugs for narcolepsy and drugs administered periop

There is little evidence that pts with narcolepsy actually have an increased periop risk.

Theoretical concerns are:

• Potential drug interactions with anesthetics leading to

  • Hemodynamic changes.

  • Altered anesthetic requirements.

  • Increased risk of serotonin syndrome.

• Periop narcoleptic episodes mimicking or masking other anesthesia complications (e.g., delayed emergence or postop residual curarization).

Chronic neurologic sleep disorder

Onset usually in adolescence

May take years to be diagnosed (polysomnography and multiple sleep latency test)

Classic symptoms: Excessive daytime sleepiness, cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations (nocturnal sleep disruption)

Excessive daytime sleepiness:

• Daytime sleep episodes occurring at inappropriate times

• Difficult to avoid falling asleep

• Frequently rationalized

• Differential Dx: OSA, sleep deprivation

Cataplexy:

• Sudden decrease in muscle tone

• Usually partial (e.g., affecting only facial or neck muscles)

• May be complete, with fall risk; pts are fully conscious

• Both partial/complete can be triggered by emotions (e.g., periop anxiety)

• Can last up to 60 min

Hallucinations:

• Hypnagogic (during transition from waking to sleep) or hypnopompic (during transition from sleep to waking)

• Often visual but may also be auditory, tactile, or multisensory

• May be misdiagnosed as mental illness

Sleep paralysis:

• Inability to move during sleep onset or offset

• Pt fully conscious

• Breathing unaffected

• May occur in conjunction with hallucinations

Other symptoms:

• Automatic behavior (performing routine tasks without conscious awareness)

• Memory lapses

• Secondary psychological symptoms (e.g., depression)

Multiple etiologies, at least partially genetic (HLA-DR and HLA-DQ).

Decreased concentrations of neurotransmitter (hypocretin, also known as orexin) in lateral hypothalamus.

Undetectable levels of hypocretin in CSF of most pts.

Current theory favors an autoimmune process that attacks hypocretin-producing neurons (possibly triggered by upper airway infections).