Commentary: Assessment and Identification of Concomitant Cognitive Impairments in Persons with Traumatic Spinal Cord Injury: Considerations for Rehabilitation Professionals
Ann Marie Warren, PhD, and Timothy R. Elliott, PhD
Individuals who incur a spinal cord injury (SCI) face immediate, profound, and often permanent life changes. The enormity of the SCI, however, often dominates the clinical picture, and when concomitant impairments such as traumatic brain injury (TBI) occur they are often overlooked. This can create less than optimal outcomes for individuals as they move through the continuum of care. Pioneering research of these issues suggested that 25% to 57% of persons with acute SCI might have a concomitant traumatic brain injury (Roth et al., 1989; Scheuman & Morris, 1982), and some cognitive impairment may be present in 67% of individuals in SCI rehabilitation (Wilmot, Cope, Hall, & Acker, 1985). Most studies indicate that cognitive impairment affects between 40% and 50% of persons with SCI (Davidoff, Roth & Richards, 1992). Consequently, individuals who sustain co-morbid TBI or have pre-morbid cognitive deficits can have poorer outcomes, especially during inpatient rehabilitation.
Co-morbid traumatic brain injury is often not identified, or is misinterpreted as a behavioral or psychological effect of the SCI. According to Davidoff and colleagues (1992), the sequelae of even mild cognitive impairment include “…difficulties with attention, concentration, memory, problem solving, abstract reasoning, new learning, and high-level cognitive skills” (p. 275). Macciocchi, Bowman, Coker, Apple and Leslie (2004) suggest the presence of any brain injury may be sufficient to delay or offset skill acquisition in rehabilitation. Their data indicate that during acute rehabilitation, dual diagnosis of TBI and SCI may be associated with fewer functional gains in comparison to patients with SCI, but the association between TBI and overall response to SCI rehabilitation may be more complex than clinically assumed.
One of the most challenging aspects to the issues of concomitant SCI and TBI is the accurate identification and assessment of cognitive deficit. Unfortunately, due to the severity of problems associated with primary SCI, mild or moderate head injuries may be overlooked during initial assessment (Narayan, Gokaslan, Bontke & Berrol, 1990; Ricker & Regan, 1999). A thorough assessment of cognitive deficits requires an examination of any pre-injury cognitive deficits and acquired cognitive deficits due to trauma. Pre-injury sources of cognitive impairment can include past TBI, alcohol and substance use, poor pre-injury academic, intellectual or occupational functioning, age-related cognitive decline, and other medical conditions and psychiatric disorders. Pre-injury cognitive deficits can contribute to poorer rehabilitation outcomes, even without the presence of an acute TBI at the time of injury. For example, the general cognitive deficits associated with chronic alcohol consumption can include decreased motor coordination, difficulty with abstract thought, deficits in attention and concentration, and loss of visual and verbal memory (Ryan & Butters, 1986). Chronic alcoholism also negatively affects higher-order cognitive processes, such as planning, organizing, and behavior regulation (Arria & Van Thiel, 1992), all of which can affect the inpatient rehabilitation process.
Pre-injury sources of cognitive impairment can also be a factor in the development of secondary complications. A history of alcohol abuse also contributes to secondary medical complications at a predictable rate. For example, Elliott, Kurylo, Chen, and Hicken (2002) found rates of diagnosed pressure sores among persons in acute SCI rehabilitation were 2.5 times higher over the first three years of SCI among those with severe alcohol abuse histories prior to SCI onset when compared to their peers without alcohol use problems.
A thorough assessment of the individual with a traumatic SCI must examine both pre-morbid and acutely sustained TBI. The assessment of acute TBI is challenging and often not done due to the more obvious presentation of the SCI. The following methods of assessment should be included to help identify the presence of traumatic brain injury:
Documented Loss of Consciousness
Loss of Consciousness (LOC) may occur at the time of a spinal cord injury. Loss of Consciousness is routinely documented by emergency personnel at the scene of an accident; additionally, this documentation is usually found in the admitting History and Physical from the emergency room physician. Clinicians cannot take the lack of this documentation at face value, however, since victims or witnesses may not report LOC at the time of the accident. The clinician is therefore advised to include a specific question about LOC in rehabilitation assessment protocols.
Glasgow Coma Scale
The Glasgow Coma Scale (GCS) was designed in to objectively measure the degree of unconsciousness following a TBI. It is the most widely used severity scale in United States emergency rooms and hospitals (Sorenson & Kraus, 1991). The GCS was developed in 1974 to standardize the clinical assessment of unconsciousness by examination of three primary areas: motor response, verbal response and eye opening (Sternbach, 2000). In its current use, the GCS allows clinicians to determine severity, predict outcome and direct clinical management. A GCS score of 13 to 15 is considered a mild head injury, 9-12 is considered moderate and 8 or less is considered to be severe (Teasdale, Pettigrew, Wilson, Murray, & Jennett, 1998).
Post-traumatic Amnesia
Posttraumatic amnesia (PTA) is a severity measure for traumatic brain injury. PTA has been described as the transient stage of confusion and disorientation characterized by intellectual and behavioral disturbances (Ahmed, Bierley, Shekh, & Date, 2000). Posttraumatic amnesia is considered to begin at the moment of injury and last until the time when a patient can provide a clear and consistent account of present events. It also provides some predictive utility in that longer duration of PTA is associated with increased cognitive, neurological and functional outcome deficits.
One of the most widely used measures of PTA is the Galveston Orientation and Amnesia Test (GOAT). The GOAT was developed by Levin (1979) to provide clinicians with a brief, quantitative measure of disorientation and amnesia in a closed head injury. The GOAT is easily used with patients in the acute hospital setting and has been determined to be very beneficial for making a diagnosis of PTA in the SCI population (Davidoff et al., 1988) The GOAT allows clinicians to identify the patient’s current orientation as well as estimate the period of PTA. Additionally, the GOAT may be used as a repeated measure in order to evaluate a patient’s progress from PTA onset to PTA resolution.
Medical Assessments
Medical assessments, such as routine skull films, computed tomography (CT) scans and magnetic resonance imaging (MRI) are frequently used to identify TBI. Skull films are also utilized in the emergency room to detect the existence of TBI. These diagnostic tools will also provide valuable clinical information about the likelihood and severity of cognitive impairment associated with SCI. The clinician must be aware, however, that a negative result in these types of measures does not mean that a traumatic brain injury has not occurred. For example, the changes from a mild traumatic brain injury resulting in a LOC may not be detected in an MRI yet still result in cognitive deficits.
The general literature concerning SCI and concomitant TBI has been plagued by inconsistent means for diagnosing mild to moderate brain injury. There has also been a general failure to account for possible brain injuries or cognitive deficits that occurred prior to SCI onset, and behaviors attributed to suspected mild TBI may instead be related to other long-standing behavioral patterns that predate the SCI. Longitudinal research has yet to find meaningful empirical differences over time between persons with and without LOC at injury onset, or by level of injury or completeness of lesion (Richards, Brown, Hagglund, Bua, & Reeder, 1988). Consequently, the empirical scrutiny of concomitant TBI and SCI should be a recognized priority in rehabilitation psychology. Further, education of rehabilitation professionals on the issues related to identification and assessment of possible co-morbid TBI is critical for all clinicians working with traumatic SCI in order to enhance rehabilitation outcome.
References
Ahmed, S., Bierley, R., Sheikh, J. I., & Date, E. S. (2000). Post traumatic amnesia after closed head injury: A review of the literature and some suggestions for future research. Brain Injury, 14, 765-780.
Arria, A., & Van Thiel, D. (1992). The epidemiology of alcohol-related chronic diseases. Alcohol Health and Research World, 16, 209-216.
Davidoff, G., Thomas, P., Johnson, M., Brent, S., Dyker, M, & Doljanac, R. (1988). Closed head injury in acute traumatic spinal cord injury: Incidence and risk factors. Archives of Physical Medicine and Rehabilitation, 69, 869-872.
Davidoff, G. N., Roth, E. J., & Richards, J. S. (1992). Cognitive deficits in spinal cord injury: Epidemiology and outcome. Archives of Physical Medicine and Rehabilitation, 73, 275-284.
Elliott, T. R., Kurylo, M., Chen, Y., & Hicken, B. (2002). Alcohol abuse history and adjustment following spinal cord injury. Rehabilitation Psychology, 47, 278-290.
Levin, H. S., O’Donnell, V. M., & Grossman, R. G. (1979). The Galveston Orientation and Amnesia Test. A practical scale to assess cognition after head injury. The Journal of Nervous and Mental Disease, 167, 675-684.
Macciocchi, S., Bowman, B., Coker, J., Apple, D., & Leslie, D. (2004). Effects of co-morbid traumatic brain injury on functional outcome of persons with spinal cord injuries. American Journal of Physical Medicine and Rehabilitation, 83, 22-26.
Narayan, R. K., Gokaslan, Z. L., Bontke, C. F., & Berrol, S. (1990). Neuropsychologic sequelae of head injury. In M. Rosenthal, E. R. Griffith, M. R. Bond, & J. D. Miller (Eds.), Rehabilitation of the adult and child with traumatic brain injury (2nd ed., pp. 94-106). Philadelphia: F. A. Davis.
Richards, J. S., Brown, L., Hagglund, K., Bua, G. & Reeder, K. (1988). Spinal cord injury and concomitant traumatic brain injury: Results of a longitudinal investigation. American Journal of Physical Medicine and Rehabilitation, 67, 211-216.
Ricker, J. H., & Regan,T. (1999). Neuropsychological and psychological factors in acute rehabilitation of individuals with both spinal cord injury and traumatic brain injury. Topics in Spinal Cord Injury Rehabilitation, 5, 76-82.
Roth, E., Davidoff, G., Thomas, P. Doljanac, R., Dijkers, M., Berent, S., et al. (1989). A controlled study of neuropsychological deficits in acute spinal cord injury patients. Paraplegia, 27, 480-489.
Ryan, C., & Butters, N. (1986). The neuropsychology of alcoholism. In D. Wedding, A. Horton, & J. Webster (Eds.), The neuropsychology handbook: Behavioral and clinical perspectives (pp. 376-409). New York: Springer.
Schueneman, A. L., & Morris, J. (1982). Neuropsychological deficits associated with spinal cord injury. Science Digest, 64, 35-36.
Sorenson, S. B., & Kraus, J. F. (1991). Occurrence, severity, and outcomes of brain injury. Journal of Head Trauma Rehabilitation, 6, 1-10.
Sternbach, G. L. (2000). The Glasgow Coma Scale. The Journal of Emergency Medicine, 19, 67-71.
Teasdale, G. M., Pettigrew, L. E., Wilson, J. T., Murray, G., & Jennett, B. (1998). Analyzing outcome of treatment of severe head injury: A review and update on advancing the use of the Glasgow Coma Scale. Journal of Neurotrauma, 15, 587-597.
Wilmot, C., Cope, D., Hall, K., & Acker, M. (1985). Occult head injury: Its incidence in spinal cord injury. Archives of Physical Medicine and Rehabilitation, 66, 227-329.
Ann Marie Warren, PhD, is a licensed psychologist with the Spinal Cord Injury Team at Baylor Institute for Rehabilitation in Dallas, Texas where she also serves as the Administrative Coordinator of Rehabilitation Research.
Timothy R. Elliott, PhD, is a professor at Texas A&M University in the Department of Educational Psychology and is the current Editor of Rehabilitation Psychology.
Sam Gontkovsky, PsyD, editor of the Commentary section of SCI Psychosocial Process, is an associate professor in the Department of Psychology, Jackson State University. He is also a scientist at the Center for Neuroscience and Neurological Recovery, Methodist Rehabilitation Center, also in Jackson. Comments or suggestions are welcome and Dr. Gontkovsky may be reached at sgontkovsky@hotmail.com.
