The Prevalence of Pre- and Post-Injury Substance Abuse in Persons with a Traumatic Brain Injury or Spinal Cord Injury
By Tobi Gilbert, Psy.D.
Alcohol abuse is a growing problem within the United States and even more significantly among the brain injured and spinal cord injury population. Approximately one third to one half of persons with brain injury or spinal cord injuries were under the influence of alcohol or other substances at the time of their injury (Kreutzer et al., 1996). Additionally, research on pre- and post- injury substance abuse patterns have demonstrated that a preponderance of people who experienced a traumatic brain injury or spinal cord injury return to or surpass their premorbid substance usage (Kreutzer et al., 1996). This paper will identify physiological and psychological challenges that traumatic brain injury (TBI) and spinal cord injury (SCI) individuals face following their accident. Additionally, understanding how alcohol use impacts the brain physically and neuropsychologically can potentially increase the reader’s knowledge and empathy for this population.
A TBI is generally defined as an injury that occurs to the brain such as a closed head injury, blunt head injury, penetrating injury, open head injury, stroke, or anoxia. In 1993, researchers estimated that approximately 400,000 people experienced a TBI each year, 44,000 of which were in the moderate to severe range (Abrams, Barker, Haffey, & Nelson, 1993). Some of the major causes of such injuries included automobile, bicycle and motorcycle accidents; and violence and recreational activities (Kreutzer, Witol, & Marwitz, 1996). Persons between the ages of 15 and 24, followed by individuals ages 5 to 14, were at highest risk for sustaining injury (Lezak, Howieson, & Loring, 2004). Research conducted by Ragnarsson, Thomas, and Zasler (1993) indicated that persons 16 to 25 constituted more than one third (39%) of persons treated at major trauma centers for brain injury.
Alcohol use has been identified as the most common factor among people with TBI and SCI, relevant to both cause of injury and post-injury adjustment (Kolakowsky-Hayner et al., 2002). A review of literature conducted by Kreutzer, Witol, & Marwitz (1996) suggested that among 78% of 199 consecutive patients admitted to major trauma centers with moderate brain injury, 56% met the legal criteria for intoxication. Of persons who were diagnosed with mild TBI following admission to a major trauma center (538 subjects), 43 % were found to have met the legal criteria for intoxication. These are staggering results lending credibility to the influence of substances among the major causes of TBI and SCI.
Even more alarming were research studies indicating that many patients continue to use alcohol post-injury, with 27-50% of patients reporting post-injury alcohol use (Kolakowsky-Hayner et al. 2002). As a result, research has concluded that TBI patients with prior histories of alcohol abuse tend to have poorer outcomes as measured by performances on neuropsychological tests (Lezak, Howieson, & Loring, 2004).
Common neurobehavioral effects of TBI included physical symptoms of dizziness, balance problems, ataxia, and fatigue. Neuropsychological symptoms included problems with attention, memory, learning, information processing, motor speed and strength, and visuoperceptual difficulties (Lezak, Howieson, & Loring, 2004). Other prominent symptoms included executive dysfunction, mood lability, irritability, low frustration tolerance, and problems with self-awareness. Psychosocial adjustments were noted to include unemployment, academic failure, and family adjustment difficulties. A high prevalence of frustration, depression, and social isolation were found to impact overall psychosocial adjustment following injury (Kreutzer, Witol, & Marwitz, 1996).
Developing a basic understanding of the neuroanatomy and pathophysiology of the impact of alcohol on the brain will highlight the significance and potential problems associated with continued use of alcohol following a TBI or SCI. To begin, abuse of alcohol leads to neuropathic and encephalopic changes in the brain, meaning that actual structures of the brain are changed and subsequently compromised. Most significantly, cerebral atrophy affecting mostly the subcortical white matter of the brain is affected. This eventually causes an overall cortical atrophy that leads to cognitive dysfunction (Lezak, Howieson, & Loring, 2002). Additionally, since alcohol is a central nervous system (CNS) depressant, the metabolites of alcohol initiate chains of biochemical and physiological events involving other bodily systems. Chronic heavy alcohol ingestion reduces the function of dendrites in the brain, mostly in the hippocampus (responsible for memory) and the cerebellum (responsible for fine motor control, coordination, and postural regulation). Furthermore, cerebral blood flow is significantly decreased, mostly in the frontal and parietal regions causing visuospatial and cognitive impairment. Neurocognitively, alcohol use affects executive and cognitive functions, memory, and complex visuospatial abilities and psychomotor speed, while well-structured and familiar functions such as language, academics, and attention remain relatively unimpaired (Lezak, Howieson, & Loring, 2004).
Tears and shearing within the brain are particularly dangerous for individuals who experienced a TBI. Often times these injuries are not visualized by CT or MRI scanning, thus leaving an individual unaware of potential problems and risk for further damage or injury (Lezak, Howieson, & Loring, 2004). For example, alcohol causes a person’s blood to thin for various, complicated reasons. If an individual has a small, undetected tear, the addition of alcohol to the brain could cause that tear to bleed, potentially creating a life threatening condition. Additionally, because of structural changes and deficits of the brain caused by the injury, the propensity for poorer rehabilitation outcomes, decreased life satisfaction, increased depression and increased risk for seizures is substantial (Kolakowsky-Hayner, et al. 2002). Studies evaluating post-injury alcohol and drug use in TBI individuals have indicated that persons who continue to drink exhibit higher rates of psychiatric disorders and more aggressive behavior. Persons with SCI who continue to drink or use drugs post-injury are also at risk for negative outcomes. Specifically, alcohol use after a SCI is a leading cause of death and has been associated with increased risk for medical complications and adverse rehabilitation outcomes (Kolakowsky-Hayner, et al. 2002).
Pre-and post-injury alcohol use patterns have been investigated in the recent years. A longitudinal study conducted by Kreutzer et al. (1996) found that the proportion of persons classified as moderate or heavy drinkers was generally comparable to that in the general population. They also found that a pattern of increasing consumption of alcohol among those with TBI was indicated. Furthermore, relationships were observed between injury severity and consumption levels. Higher levels of disability were associated with lower consumption rates, while in contrast, lower levels of disability were associated with higher consumption rates.
Interestingly, Kolakowsky-Hayner (2002) found that there were higher rates of abstinence in the TBI sample compared to those in the SCI population. Importantly, these abstinence rates are also much higher than rates described in pre-injury TBI (19%) and SCI (4%). Thus, it would appear that a large proportion of patients follow their physician’s advice and abstain from alcohol use post-injury.
Despite these high abstinence rates, Kolakowsky-Hayner’s (2002) results show that per4sons with TBI and person with SCI are at a high risk for alcohol abuse. The rates of moderate and heavy drinking in both populations exceed the 25% of persons in the general population considered moderate or heavy drinkers. Higher rates of moderate or heavy drinking are reported in pre-injury SCI and TBI populations as well.
Without a doubt, these statistics are alarming and worrisome. Despite high abstinent rates reported in both groups, the proportion of persons abusing alcohol after injury continues to exceed rates found in the general population. Thus, it seems reasonable to conclude that early identification of per-injury substance abusers in the rehabilitation process is important so that appropriate, adaptive coping strategies can be taught and highlighted. The research shows that people with a TBI or SCI either abstain from the use of alcohol or use it frequently to deal with increased stress, anxiety and depression. Efforts toward intensive education early in the rehabilitation process may prove beneficial in assisting an individual with TBI or SCI to obtain optimal recovery and an improved quality of life.
In conclusion, traumatic brain injuries, spinal cord injuries and substance abuse have long had an intimate relationship, and the link between them is well documented. It is often difficult to determine if the substance abuse existed prior to the brain injury or if the abuse was exacerbated by the injury. Research on the topic demonstrated that it is likely that the abuse of substances existed prior to the person sustaining the traumatic brain injury and that although there is typically an immediate decrease in substance usage, users frequently return to premorbid usage and often times surpass their pre-injury intake. Research also demonstrated that some individuals with TBI and SCI follow medical advice and fully abstain from alcohol use and illegal substances. Early identification and intervention by professionals has the potential to help maximize recovery and increase an individual’s quality of life. Understanding the prevalence of alcohol abuse in this population is a first step towards developing programs and increasing research to support funding for rehabilitation programs focused on TBI, SCI, and substance abuse.
REFERENCES
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Kolakowsky-Hayner, S., Gourley, E., Kreutzer, J., Marwitz, J., Meade, M., & Cifu, D. (2002). Brain Injury, 16(7), 583-592.
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Ragnaarsson, J., Thomas, J., & Zasler, N. (1993). Model systems of care for individuals with traumatic brain injury. Journal of Head Trauma Rehabilitation, 8(2), 1-11.
