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INSOMNIA
Insomnia is a scourge of people with a TBI. While it may result in part from anxiety (which makes it hard to fall asleep) or depression (which tends to wake people up for good around 3 a.m.), it appears to be caused frequently by trauma-induced imbalance of neurotransmitters. It has recently been established that cells in the basal forebrain (the undersurface of the frontal lobes) suppress production of histamines (a waking agent) in the posterior hypothalamus. If these cells become damaged, histamine production increases and so does night time wakings. TBI patients observed over night in sleep labs have been seen waking up 40-50 times a night. What can help? There is no magic bullet. Many of my clients were prescribed Ambien by their family physician or internist with little benefit. A number have benefited temporarily from the anti-depressants Trazodone or Elavil, but discontinued them due to side effects. Chicago neurologist James Kelly who care for sports concussions in professional football players has reported that his TBI patients show good relief from insomnia while taking a combination of Trazodone and chloral hydrate. One paper on treatment of insomnia reported some success with combined administration of melatonin extract and Luvox (another anti-depressant). See, Archives of General Psych. 2000; 57:812.

There are different types of insomnia. Primary insomnia is "learned" in the sense of being psychologically conditioned by repeated failures to sleep well in a particular environment. People with primary insomnia may sleep soundly away from home in a hotel or sleep lab. Other insomnias are hereditary (confined to families), medical (associated with physical injury, disease or illness) or psychiatric (associated with mental disorders such as anxiety or depression).

As a historical matter, different sleep remedies were devised for different types of insomnia. For acute, transitory insomnia (the kind "normal" people suffer when under big pressures at work or home), there are over the counter benzodiazepine pills that activate all the receptors for GABA , the main inhibitory neurotransmitter in the brain. These include Valium, Xanax and Restoril. While effective in the short term, they cannot be used for long because of "hangover" grogginess and drowsiness the next day. For people with chronic but mild anxiety that makes it difficult to fall asleep, there is Ambien and Sonata. These benzodiazepines are specially crafted to activate selected GABA receptors, so they relax the person for a short time so he can get to sleep, but do not produce a carry-over lethargy the next day.

The increased recognition of a strong relationship between depression and insomnia has led many physicians to opt for anti-depressants when medicating insomnia. Unfortunately, most anti-depressants activate the receptors for serotonin (the mood boosting brain chemical), which suppresses REM (dream) sleep. Although effective in producing non-REM (slow wave) sleep, many anti-depressants cause daytime drowsiness and fatigue. Trazodone (Desyrel) and nefazodone (Serzone) are becoming more popular among physicians, because they less carry over "sedation" the next day. While helpful, anti-depressants are not the solution for everyone. A full one-third of depressed patients do not respond to them. For everyone with insomnia, but especially for this group of "non-responders" sleep hygiene is important. This involves avoidance of coffee, cola or alcohol and avoidance of intense exercise or upsetting TV shows close to bedtime. It involves preparation for sleep including such things as warm bath, gentle stretching, meditation, slow rhythmic breathing or a warm glass of milk. It means no stimulation once in bed - no reading, no TV and no conversation. These and other methods have proven helpful for patients suffering insomnia who have not had a TBI.

Physicians treating TBI patients have no special remedy tailored just for them at this time, and tend to fall back on what works for their other patients. A recent article in the Journal of Neuropsychiatry 11:504-506 Nov. 1999 entitled "Persisting Insomnia Following Traumatic Brain Injury" chronicle the struggles of a man with with recalcitrant insomnia following a TBI, marked by frequent night time awakenings. The patient sustained a TBI at age 35 in 1991 by being beaten on the head with a blunt object. The TBI was confirmed by PET scan. Over the next 8 years he was treated with desipramine, divalproex, carbamazepine, buspirone, zolpidem, choral hydrate, haloperiodol, risperiodone, diazepam, melatonin and combinations of these drugs; yet he never began to sleep normally. The medications were all discontinued due to side effects including nausea, vomiting and tremor from the anti-seizure and neuroleptic drugs. Clearly the desperation generated by such terrible insomnia can lead one to become a human guinea pig for drug remedies, but just as clearly, this is not the solution. There is a critical need for medical research on relieving the insomnia generated by TBI, and until we get this research, there will be more stories like this one.