A myriad of sleep problems have been associated with traumatic brain injury (TBI), including sleep initiating and maintenance insomnia, a lack of restorative sleep, and excessive daytime sleepiness (EDS). There are forms of narcolepsy that can occur due to trauma to the brain, but they are much less common than typical narcolepsy. Mild head trauma may produce sleepiness not associated with REM sleep phenomena such as cataplexy, sleep paralysis, and hypnagogic hallucinations—a condition known as posttraumatic hypersomnia. The following case involving a 14-year-old girl illustrates the relationship between TBI and sleep problems.
Every 21 seconds someone in the United States suffers a TBI. A TBI is caused by a blow or jolt to the head or by a penetrating head injury that disrupts the normal function of the brain. Not all blows or jolts to the head result in TBI. Of the 1.4 million people who sustain a TBI each year in the United States, 50,000 die, 235,000 are hospitalized, and 1.1 million are treated at an emergency department. Among children, TBI results in an estimated 2,685 deaths, 37,000 hospitalizations, and 435,000 emergency visits annually.1 According to the Centers for Disease Control and Prevention, about 5.3 million people (2% of the US population) live with a disability that was caused by TBI. Motor vehicle crashes (20%), falls (28%), struck by/against events (19%), and assaults (11%) are major causes of TBI and a leading cause of death and disability in children and young adults.
Signs and Symptoms
The severity of TBI can range from mild to moderate to severe. A mild case of TBI is called a concussion, and the patient is usually awake following the injury. There is a brief change in mental status or consciousness. Approximately 80% of TBIs fall into this category. In a moderate case, the patient is sleepy following a brief loss of consciousness or disorientation. Approximately 10% of TBIs fall into this category. In severe cases, approximately 10% of TBIs, the patient is comatose and unable to respond. There may also be an extended period of unconsciousness or amnesia after the injury.2
The signs or symptoms of a TBI can be subtle. Symptoms may not appear until days or weeks following the injury or may be missed even though people may act or feel differently. TBI can cause a wide range of functional changes that affect thinking, sensation, language, and/or emotions. The common signs and symptoms include:
- intractable headaches or neck pain;
- difficulty remembering, concentrating, or making decisions;
- slowness in thinking, speaking, acting, or reading;
- getting lost or easily confused;
- feeling tired and fatigued;
- mood changes;
- anger for no reason;
- changes in sleep patterns;
- dizziness or loss of balance;
- increased sensitivity to lights, sounds, or distractions;
- blurred vision;
- loss of sense of smell or taste; and
- ringing in the ears.
Children with a brain injury can have the same symptoms as adults. Emotional changes can include depression, anxiety, personality changes, aggression, acting out, and social inappropriateness. TBI can cause epilepsy and Parkinson’s disease, and other brain disorders that become more prevalent with age. A few cases of posttraumatic hypersomnia and posttraumatic narcolepsy following TBI also have been reported.3
A 14-year-old girl was involved in a motor vehicle accident. After leaving her work at a pizza shop in a small size car, she was hit by another vehicle in a head-on collision and later became comatose. The girl was air-lifted to a regional trauma center with injuries including a sustained head injury with subdural hematoma and with midline shift and blood in the ventricles, which required a ventriculostomy. She also had a chest injury, including lung collapse and lung laceration. The victim experienced fracture of long bones, including the right humerus and left femur, and also required chest tube thoracostomy and mechanical ventilator support. Following the accident, she was in a coma for nearly 2 months but recovered successfully. She underwent rehabilitation and speech therapy for 2 months. At 3 months, she was fully ambulatory, had regained her strength, and was discharged from the rehabilitation center.
The patient’s neurosurgeon referred her to me because of excessive daytime sleepiness and difficulty with concentration. She appeared calm, cooperative, and intelligent. Her Mini-Mental Status and neurological examination were within normal limits. Neurophysiological function testing at another facility confirmed neurocognitive impairment with reduced concentration, short attention span, inability to process information at a normal pace, and memory impairment commonly seen in individuals with TBI and indicative of cerebral dysfunction. Her mother reported that the patient had shown uncontrolled rage, irritability, aggression, and acting out, including crying out obscenities. She fell asleep during her class and required special education. In addition, a CT scan and MRI of the brain showed no organic disturbances like hematomas, posttraumatic hydrocephalus, cerebral vein thrombosis, cerebral hemorrhage, or midline shift.
A diagnostic nocturnal polysomnogram of the patient showed a very short latency of 2.5 minutes, no apnea or hypopneas, and no desaturation events. Her MSLT showed two sleep-onset REM periods (SOREMPs). The mean sleep latency was 2.0 minutes. A diagnosis of posttraumatic narcolepsy was confirmed, and she was treated with modafinil, which later resulted in improvement in daytime sleepiness, fatigue, and alertness.
Persistent sleep difficulties have been reported following TBI in individuals with a history of prolonged coma or diffuse brain injury. The neuroanatomical, neurophysiological, and neurochemical systems responsible for maintaining the normal awake-sleep cycle are disrupted following TBI. Narcolepsy is characterized by the classic tetrad of excessive daytime sleepiness, hypnagogic hallucinations, and sleep paralysis. Abnormality in the hypocretin (orexin) receptor also has been identified in the canine model of narcolepsy. Hypocretins are neuropeptides that have an excitatory effect on the neurons.
Pathophysiology of Acute Brain Injury
Deficiency in hypocretin-1 or orexin A, secreted by a group of neurons situated in the posterolateral hypothalamus, has been reported in acute traumatic brain injury. Hypocretin-1 is involved in the regulation of the sleep-wake cycle. Baumann et al4 prospectively assessed CSF hypocretin-1 levels in 44 consecutive patients with acute TBI. Compared with controls, hypocretin-1 levels were abnormally lower in 95% of patients with moderate to severe TBI and in 97% of patients with posttraumatic brain CT changes. Hypocretin-1 deficiency after TBI may reflect hypothalamic damage and be linked with frequent development of posttraumatic sleep-wake disorders.4 CSF hypocretin-1 deficiency is associated with definite cataplexy in patients with narcolepsy. Hypocretin deficiency identifies a homogenous group of patients with narcolepsy characterized by the presence of definite cataplexy, severe EDS, and frequent SOREMPs. A study showed that lesions of the suprachiasmatic nucleus (SCN) eliminated the daily rhythm of hypocretin-1 release in rats. It was concluded from this study that hypocretin-1 release is under SCN control and that locomotor activity influences the activity of the hypocretin neurons.5
Taj M. Jiva, MD, MPH, DABSM, CBSM, FCCP, is medical director of Phoenix Rising Medical, PC & Behavioral Sleep Laboratories, Buffalo and Silver Creek, NY. He is also medical director of Treasure Coast Sleep Labs, Port St Lucie, Fla. He can be reached at.
- Langlois JA, Rutland-Brown W, Thomas KE. TBI in the United States: emergency department visits, hospitalizations, and deaths. Atlanta: Centers for Disease Control and Prevention, National Center for Injury Prevention and Control; 2004.
- Traumatic Brain Injury. National Center for Injury Prevention and Control. Available at: http://www.cdc.gov/ncipc/tbi/TBI.htm.
- Lankford DA, Wellman JJ, O’Hara C. Posttraumatic narcolepsy in mild to moderate closed head injury. Sleep. 1994;17:S25-S28.
- Baumann CR, Stocker R, Imhof HG, et al. Hypocretin-1 (orexin A) deficiency in acute traumatic brain injury. Neurology. 2005;65:147-149.
- Arnulf I, Lin L, Zhang J, et al. CSF versus serum leptin in narcolepsy: is there an effect of hypocretin deficiency. Sleep. 2006;29:1017-1024. Available at: http://lib.bioinfo.pl/auth:Mignot.