SUBSTANCE ABUSE   [ back to Brain Injury 101 ]
The anxiety, depression, social isolation, loneliness and tedium of rehab, which accompany a TBI, can push some survivors into excessive consumption of alcohol, prescription drugs or street drugs. So can chronic somatic pain from spinal or other injuries incurred from the traumatic event which caused the TBI. Substance abuse is an obstacle to full and meaningful participation in rehabilitation and can preclude reaping the benefits of rehab. It is crucial to identify the persons at highest risk of substance abuse post-TBI, to counsel them, monitor them and work with them to control the urge to use alcohol or drugs. The persons at highest risk are those persons who have a pre-injury history of addiction or abuse of substances. These same persons tend to have a genetic propensity to "crave" alcohol or drugs and a family history of abuse. The common denominator appears to be low serotonin production. Some people are born with a serotonin deficiency which produces a chronic, low level dissatisfaction with life known as dysthymia. While this condition can be effectively treated with drugs like Prozac or Zoloft, many people with the condition go undiagnosed and end up using alcohol to make themselves feel better. Alcohol abuse causes insomnia which further depletes serotonin. Other people actually create their own neurotransmitter deficiency. One brand new example is the use of the drug Ecstasy. A study in Neurology published on 7/25/00 indicates that autopsy of young ecstasy abusers shows a 50-80% reduction in expected levels of serotonin for age matched controls. We also know that heroin addicts who are tricked into buying a certain form of synthetic heroin destroy the part of the brain which produces dopamine, and they develop Parkinson's Disease. Persons who become euphoric with speed or cocaine, get extra secretion of dopamine, because there is an absence of serotonin to blunt excitatory glutamate transmission from the pre-frontal lobes to the dopamine producing area of the midbrain.

One tip off or red flag to the clinician should be the role of alcohol in the occurrence of the injury or presence of high blood alcohol content at the time of injury. Astute clinicians who are on the look out for a history of substance abuse can then gauge the potential for relapse under the stresses of the TBI, and guard against it. Statistics show that relapse can be prevented and that substance abuse can be eliminated or controlled in rehab, and after, when the treaters are aggressive in dealing with it. Ignoring a pre-injury history of addiction, and failing to be pro-active, are the surest ways of promoting a return to substance abuse during the rehab process. Since excessive consumption of alcohol sedates and slows the activity of brain cells, impairs new learning (skill acquisition) and blunts regeneration of damaged neural circuitry in the brain, it is imperative to use the rehab process to stop such abuse. Preventing relapse will maximize the survivor's chances of good recovery of brain function. Treatments include 12 step groups, individual psychotherapy, drugs like buspar or sinequan which decrease anxiety by activating the GABA circuits in the amygdala, drugs like Prozac or Zoloft which eliminate the craving for euphoria by increasing serotonin and drugs like Naltexone which block activation of the reward center (and resultant euphoria) that accompanies drinking. Heavy alcohol intake is bad for anyone, because it burns up glucose needed for mental activity and leads to a protein deficient diet with undersupply of important neurotransmitters. Hypoglycemia and neurotransmitter deficiency hit TBI patients harder, because they are working with less. Further, alcohol can trigger epileptic seizures.