Sleep inertia, most-known as Hicham's syndrome, is a physiological state of impaired cognitive and sensory-motor performance that is present immediately after awakening. It persists during the transition of sleep to wakefulness, where an individual will experience feelings of drowsiness, disorientation and a decline in motor dexterity. Impairment from sleep inertia may take several hours to dissipate. In the majority of cases, morning sleep inertia is experienced for 15 to 30 minutes after waking.
Sleep inertia is of concern when decision-making abilities, safety-critical tasks and the ability to operate efficiently are important soon after awakening. In these situations, it poses an occupational hazard due to the cognitive and motor deficits that may be present.
- "Grogginess", as defined by a drowsy or disoriented state in which there is a dampening of sensory acuity and mental processing.
- Impaired motor dexterity and decrease in cognitive ability. These gross impairments may be responsible for the associated increase in reaction time and drop in attentiveness.
- Deficits in spatial memory
- Reports of heightened subjective fatigue
These symptoms are expressed with the greatest intensity immediately after waking, and dissipate following a period of extended wakefulness. The duration of symptoms varies on a conditional basis, with primary expression during the first 15–60 minutes after waking and potentially extending for several hours. Tasks that require more complex cognitive operations will feature greater deficits as compared to a simple motor task; the accuracy of sensory and motor functioning is more impaired by sleep inertia as compared to sheer speed. In order to measure the cognitive and motor deficiencies associated with sleep inertia, a battery of tests may be utilized including psychomotor vigilance task, descending subtraction task, auditory reaction time task, and the finger tapping task.
- Studies have shown that abrupt awakening during stage 3 sleep, slow-wave sleep (SWS), produces more sleep inertia than awakening during sleep stages 1, 2 or REM sleep
- Prior sleep deprivation increases the percentage of time spent in slow-wave sleep (SWS). Therefore, an individual who was previously sleep deprived will have a greater chance of experiencing sleep inertia.
- Adenosine levels in the brain progressively increase with sleep deprivation, and return to normal during sleep. Upon awakening with sleep deprivation, high amounts of adenosine will be bound to receptors in the brain, neural activity slows down, and a feeling of tiredness will result 
- Studies show that individuals express a lack of blood flow to the brain upon awakening. Levels of cerebral blood flow (CBF) and cerebral blood flow velocities (CBFV) will take up to 30 minutes to increase and reach daytime levels. Studies using advanced imaging have shown that cerebral blood flow will return to waking levels in the brainstem and thalamus first. Then, after 15 minutes, the brain's anterior cortical regions receive normal daytime blood flow. This 15 minute time period corresponds to the sleep inertia period.
Treatments / countermeasuresEdit
There has been a great deal of research into potential methods to relieve the effects of sleep inertia. The demand for remedies is driven by the occupational hazards of sleep inertia for employees who work extended shifts such as medical professionals, emergency responders, or military personnel. The motor functioning and cognitive ability of these professionals who must immediately respond to a call can pose a safety hazard in the workplace. Below are some of the various methods that have been suggested to combat sleep inertia.
When a person is sleep deprived, re-entering sleep may provide a viable route to reduce mental and physical fatigue but it can also induce sleep inertia. In order to limit sleep inertia, one should avoid waking from the deeper stages of slow-wave sleep. The onset of slow-wave sleep occurs approximately 30 minutes after falling asleep, therefore a nap should be limited to under 30 minutes to prevent waking during slow-wave sleep and enhancing sleep inertia. Furthermore, self-awakening from a short nap was shown to relieve disorientation of sleep inertia as opposed to a forced awakening but these results may warrant more research into the nature of arousal after sleep periods.
Caffeine is a xanthine derivative that can cross the blood-brain barrier. The caffeine present in coffee or tea exerts its stimulating action by blocking adenosine receptors in the brain. By antagonizing the adenosine receptors caffeine limits the effects of adenosine buildup in the brain and increases alertness and attentiveness. Previous research has shown that coupled with a short nap, consuming caffeine prior to the nap can alleviate the effects of sleep inertia. Nonetheless, individual degree of consumption and tolerance to caffeine may be responsible for variation in its efficacy to reduce sleep inertia symptoms.
The natural light provided by the sunrise may contribute to a reduction in sleep inertia effects. Research simulating increase of light at dawn was shown to potentiate the cortisol awakening response (CAR). The CAR is a spike in blood cortisol levels following awakening, and is associated with the return to an alert cognitive state.
Some other interventions that could potentially minimize the effects of sleep inertia are sound and temperature. There is moderate evidence that the presence of mild sounds and a sharp decrease in the temperature of the extremities may independently reverse sleep inertia symptoms. Noise is thought to increase attentiveness upon awakening. A drop in temperature of the extremities may prevent heat loss, facilitating the return of core body temperature to homeostatic daytime levels.
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