SLEEP DISORDER  [ back to Brain Injury 101 ]
Although many people complain of headache, slowed cognitive processing and poor short term memory following a TBI, the one symptom that we see without fail in every survivor of a brain injury is sleep disorder. Why is this important? Lack of sleep causes lost cognitive sharpness with distinct decreases in attention, reaction time and working memory. In the April 2003 Journal of Sleep, Dr. Hans Van Dongen, Assistant Professor of Sleep at the Univ. of Pennsylvania, published a study showing that adults who get 6 continuous hours of sleep per night for two weeks perform as poorly on cognitive testing as people who were up for 48 straight hours. Typical clients of our office average 4-6 hours of highly fragmented sleep per night. You do not need an enormous brain lesion to have problems with concentration, irritability and memory, if your "mild" brain injury is disturbing your sleep-wake cycle.

Although there are some cases of hypersomnia (sleeping too much), it is far more typical to see insomnia with day time sleepiness. Why? Some physicians believe difficulties sleeping are due to depression (which tends to wake people up for the rest of the night around 2 or 3 am.) or anxiety (which makes it very hard to fall asleep in the first place) or both. Either mechanism would create a large sleep debt with oppressive day time fatigue. Other physicians  blame fatigue on cognitive impairments, which force the person with a TBI to expend extra energy to maintain  attention and to perform the mental work involved with retaining information, retrieving memories, making decisions, etc. The theory goes that people with a TBI must work many times harder to perform the same cognitive tasks as people without a TBI, and this extra effort wears the person with TBI down.

While there is some truth to all of these beliefs, if they were the only explanation, we would expect to see better, more refreshing sleep at night and a higher level of energy and alertness during the day in patients receiving appropriate treatment for those sequelae of a a TBI, such as anti-depressant medication, anti-anxiety medication and cognitive therapy. But we do not not. We might also expect correction of the problem from a sleep medication like Ambien (which quiets brain activity and relaxes the skeletal muscles), but we do not. Clinicians know that a planned, temporary period of sleep deprivation may jolt a depressed person out of his depressed mood and help him sleep, at least for a time. Unfortunately this remedy has not worked for persons with a TBI. To the contrary, sleep deprivation makes all their symptoms worse. 

Recent research into sleep disorders has shown that persons with a TBI experience highly disturbed and inefficient night-time sleep, and that (like sufferers of obstructive sleep apnea) they wake up 50 or more times a night. Such highly fragmented sleep accounts for why people with a TBI feel so exhausted and worn down all the time, as if they were suffering from chronic jet lag. While patients with obstructive sleep apnea can be cured with weight loss, laser surgery on the throat, and other methods, there is little help available right now for TBI- induced insomnia.

A consensus as to the cause of the problem has begun to emerge. The sleep-wake cycle in the normal person conforms to the gradual, time sequenced release of pre-set quantities of certain neurotransmitters. The orchestration of neurotransmitter release for initiation and maintenance of sleep is done by the the suprachiasmatic nucleus (SCN) of the hypothalamus (which blocks histamine production and puts us into slow wave sleep), the pineal gland (which produces melatonin to signal the SCN to prepare the brain and body for sleep)and the PGO system (the pontine-lateral geniculate-occipital complex which activates dream or REM sleep in alteration with slow wave sleep). All 3 are affected by changes in light, and activated by the darkening associated with night. The 24 hour cycle of waking, slow wave sleep and REM sleep is controlled by the SCN, which obtains information about light conditions outside the body through the retinohypothalamic tract (RHT) and from intergeniculate leaflet fibers. The darkening of the light associated with the coming of night activates gastrin releasing peptide (GRP) which activates the SCN through BB2 receptors, see J. Neuroscience 7/15/2000. 20(14):5496. The dorsal raphe nuclei in the brainstem also pump serotonin to the SCN to help usher in sleep. During slow wave sleep the mind is calm.

During intervals of dream sleep (known as REM or rapid eye movement sleep) brain secretion of acetylcholine (Ach) peaks and the mind becomes extremely active, but the muscles of the body are paralyzed by nitrous oxide emitted in the brainstem. Ach production peaks in the cholinergic neurons of the basal forebrain in response to release of neurotensin, which provokes burst-like discharges of Ach. Micro-injection of neurotensin into the basal forebrain of rats in slow wave sleep, provokes rapid rise in brain Ach with rapid onset of REM sleep. J. Neuroscience 11/15/00 20(222):8452-8461. Adults generally wake out of REM sleep in the morning. Waking at morning is produced by increases in histamine and cortisol production.

Brain trauma disturbs the normal cascade of neurotransmitter release, which causes frequent night-time awakenings known  as "sleep fragmentation." In a normal sleeper, the levels of norepinephrine, dopamine and serotonin gradually drop during the initial phase of sleep (slow wave) and fall to a virtually zero level during the second phase (rapid eye movement). During REM (the dream stage of sleep) brain levels of acetylcholine rises sharply. It is now believed that secretion of neuropeptides known as orexins (or hypocretins) from the prefornical area of the hypothalamus plays a significant role. People who lack type 2hypocretin (hrct2) are narcoleptic. When the sleeping fit strikes, they move suddenly and instantaneously from a state of wakeful alertness to REM sleep, no matter where they are or what they are doing. This corresponds to a light switch type shut off of neurons in the locus coeruleus of the brainstem which secrete norepinephrine. Injection of type 1 hypocretin (hrct1) activates the locus coeruleus and suppresses REM sleep. J. Neuroscience 10/15/00 20(20)7760-7765. Damage to the hrct producing area of the hypothalamus or the circuits linking it to the locus coeruleus of the brain stem, would appear to play a role in at least some sleep disturbances.

Studies of TBI patients in sleep labs shows them waking up for brief moments as many as 40-50 times a night, interrupting and shortening the periods of SWS (slow wave sleep) and REM (dream) sleep. This robs sleep of its restful, restorative character, leaving TBI people feeling tired, de-energized and out of sync with the rest of the world. Sleep researcher Eve Van Cauter, Phd at the University of Chicago has tracked the sleeping habits of a group of 149 men between the ages of 16 and 83 over a 14 year period. One of her principal discoveries is that HGH (human growth hormone) is secreted at its highest levels during SWS, and that as men age they get less slow wave sleep, secrete less HGH at night and lose muscle mass and muscle tone while gaining fat. Disturbance of SWS due to brain trauma would thus tend to speed up the natural aging of the body. Further, decreases in REM sleep from brain trauma cuts way back on dream time, when people consolidate their memories of newly learned facts and skills. Sleep research has established it is during the  REM phase of sleep that strengthening of new synaptic connections occur, and when REM is obstructed, people show reduced capacity to retain new information. 

College students and grad students who "cram" all night for an exam the next day, may pass the exam yet lose much of what they crammed into their brains. Does lack of sleep somehow prevent long term retention of the material? Yes, says a study in the December 2000 issue of Nature Neuroscience (Vol. 3 No. 12). Researcher Robert Stickgold took 24 Harvard students, had them learn some visual identification skills on computer, let 12 of them sleep the same night and kept the other 12 up. He then let all 24 sleep normally on 2nd and 3rd nights. On the 4th day he retested them. The 12 who got normal sleep the first night did much better and showed greater mastery of the new skill than the sleep deprived group. This is consistent with other studies, and tends to confirm the belief that the structural and chemical changes in the synaptic connections of the hippocampus and other parts of the brain necessary for long term storage of information requires adequate sleep, and that memory consolidation cannot take place without it. Electrical recordings of activity in the brains of songbirds, rats and humans suggests that part of the memory consolidation process involves re-living or replaying the day time event during sleep.

Can anything be done to promote better sleep in TBI patients? Some neurologists prescribe the anti-depressant Trazodone, either alone or with a dose of choral hydrate, to get insomniac patients to sleep at night following a TBI. Literature on effectiveness and safety of treatment is fairly sparse for TBI caused insomnia. Things are just the opposite with insomnia due to simple anxiety, for which Ambien is a great help in many cases. Researchers in England have found that use of lavender as an "aromatherapy" is quite effective in getting hospital patients to fall asleep and remain asleep. So long as one is not allergic to lavender, it might be worth giving it a try. Some persons with insomnia have benefited from an intense dose of light from a sunlamp first thing in the morning upon waking, which appears to affect the SCN and reset the biological clock through "phase advance." If the insomnia is related more to "reactive anxiety" to having a TBI, than to neurotransmitter imbalance, medications such as Ativan or Buspar may help. These are effective anti-anxiety agents. Buspar is less sedating with regard to cognition.

Persons with insomnia and crushing fatigue following a TBI, should consider seeking evaluation and treatment at a sleep disorders clinic, where their disturbed sleep pattern can be documented and interpreted on the basis of night-time EEG tracings (EEB telemetry) and night-time filming of their sleep in a sleep lab. The "gold standard" for diagnosis of sleep disorders is called polysomnography, which combines measurements of brain waves (EEG), muscle tone (EMG) and eye movements (EOG). Such persons should also recognize that at least some of their day time difficulties with mental fuzziness, slowed decision making, poor organization of time, poor memory, slowed movement, apathy, frustration and irritability, have to do with lack of healthy, restorative sleep. Finally, such persons in consultation with their neuropsychologist should reorganize their schedules to promote sleep and avoid activities like driving when they are most likely to be fatigued.

While sleep specialists cannot cure this problem, they can reach good "sleep hygiene" to mitigate the suffering that goes with not sleeping normally. This includes avoiding stimulants like coffee or cola and avoiding stimulating activities like intense exercise or computer games as bedtime nears. It includes having a regular sleep routine and regular bedtime and making sure to use one's bed for sleep and sex but not for eating, reading, etc. Having a chronic sleep disorder from a TBI is like living with permanent jet lag. You are awake while others sleeping, and you are dog tired while others are alert, active and energetic. This is a crucial problem which must be addressed much more vigorously in the diagnosis and care of persons with a TBI.