Denise Scalercio Ribeiro Fall 1999 NEURO-REHABILITATION Every year over 3 million people sustain a traumatic brain injury (TBI). It is estimated that per 100,00 people, 14-30 of them will die of a brain injury. This estimate has a wide range, due to the vagueness of the cause of death annotated on the death certificate (Silver, Yudofsky, Hales, 1994). Patients may experience a variety of disabilities including psychological stress, physical impairments, personality changes, and difficulties with relationships and employment. However all hope is not loss. With new technology and assessment tools, neuroscientists are working to create several procedures, which may restore brain function, thereby allowing clients to live normal lives. Assessment is a vital aspect of neuropsychology. One essential variable in assessing a patient with a TBI is looking at their level of functioning before the injury. Unfortunately very few patients undergo extensive neuropsychological testing prior to the brain injury, therefore, it is very difficult to obtain an exact comparison. However there are methods of evaluating the pre-injury functioning. Except when the brain injury has occurred in the posterior left-hemisphere, basic vocabulary and reading skills tend to be less affected by TBI, (Lovell & Franzen, 1994). Reading tests are suppose to estimate the individual's functioning prior to the injury, (Wilshire & Kinsella, 1991). Neuropsychological assessment is necessary in that it guides the process of designing a rehabilitation program. One type of test is called the Category Test. It tests the ability to identify the concept or principle that governs a series of geometric, verbal or numerical object. This very complex test measures the capability of the individual to abstract. In theory, performance on this test would predict a person's capacity to organize, plan, and the ability to solve complex problems. Individuals with poor scores on this test usually suffer from extensive brain dysfunction that often has a recent onset or is rapidly progressive in nature. An individual with a brain lesion who scores relatively well usually does not have a rapidly progressive condition (Goldstein & Ruthven, 1983). Levin, High, & Goethe developed the Neurobehavioral Rating Scale, (1987). This scale is based on a 7 point Likert scale in which the rating ranges from not present to severe. The scale measures disturbances in behavior, cognition, emotion, thought content and language functioning during the long-term recovery from a brain injury. They found that the items that assessed conceptual disorganization, inaccurate self-appraisal, decreased initiative/motivation and poor planning were correlated with the severity of injury. Patients with mild TBI demonstrated greater somatic concern and anxiety (1987). Cognitive functioning is an essential component of assessment. The Neurobehavioral Cognitive Status Examination (NCSE) developed by Kiernan and colleagues can be completed in 5-20 minutes. This test measures the levels of consciousness, attention, orientation, language, visuoconstructional skills, memory, calculations and abstract reasoning, (Kiernan, Muller, & Langston, 1987; Schwamm, Van Dyke, & Kiernan, 1987). Brain imaging and electrophysiological studies have recently been employed as an important diagnostic tool. These noninvasive tools provide accurate pictures of patients' brains without the need to engage in costly and potentially traumatic exploratory surgery. The functional magnetic resonance imaging (fMRI) was developed in 1980. The technique is based on the changes in the magnetic properties of atoms. The MRI scanner is a magnet that measures the direct changes in brain tissue, (Martin, 1999). The positron emission tomography (PET) measures brain function by measuring the brain oxygen consumption, blood flow and glucose metabolism. In order to measure the glucose metabolism, radioactive glucose (2-deoxyglucose is most commonly use) is injected to the patient. The radioactive glucose is taken up by metabolically active cells, which emit positrons. When positrons are emitted and collide with electrons they form gamma rays, which are detected, when they exit the person's skull. The areas that are high in metabolic activity produce more gamma rays because they take up more glucose. Computers then convert the gamma radiation into a 3 dimensional color-coded image on the computer screen. The blood flow is measured by injecting radioactively labeled water (hydrogen and oxygen 15). When the water decays the positrons are emitted. Once the water reaches the brain, the neurons increase their blood flow (Martin, 1999). Data suggests that the PET is more sensitive than the MRI to detect brain abnormalities in TBI patients (Alavi, 1989; Langfitt et al., 1986; Ruff et al., 1989). The electroencephalogram (EEG) reflects the inhibitions and excitations of thousands of neurons. It has been useful in recognizing posttraumatic seizures of comatose patients. Up to 7% of patients with head injuries develop posttraumatic epilepsy (Schaffer et al., 1985). When a person experiences a TBI, the symptoms seen are generally due to two physiological responses, cell death or inhibition. When a neuron dies, it can not be regenerated. Several traumatic brain injuries result in injury to axons, which lead to complex and widespread effects. When an axon is cut, the two ends close, swell and retract from each other. In the area where the trauma occurred as the axon and myelin sheath degenerate, the macrophages, which is a large cell that ingests microorganisms, cells or other foreign particles, absorbs and destroys the axonal debris. Glia cells, which are, cell that support, protect and nourish neurons of the central nervous system along with astrocytes; a form of glia cells form scar tissue. Then one of two things happen, either the cell dies or the Nissl bodies degenerate. The Nissl bodies are grain like bodies formed in the cytoplasm of the cell bodies of neurons and glia cells (Reber, 1985). The severity is contingent on how close the to the cell body the axon was severed and if any connections were restored. It has been found that scar tissues do not provide an adequate environment for the regenerative sprouts to grow, (Cohen, 1993). Several different types of symptomologies are associated with TBI. Personality changes have been seen as the most significant problem, (Livingston et al., 1985; Tomsen et al., 1984; Weddell et al., 1980). Patients with frontal lobe dysfunction may exhibit Borderline personality traits such as impulsively, lack of empathy, lack of a sense of self, and inability to self-monitor. The individual may display a retardation of the maturation process, so that they seem childish. Individuals may also have a "Chameleon" quality, the person assumes behavioral characteristics based on the individuals in the immediate environment (O'Shanick & O'Shanick, 1994). In 1978, Lezak described several differences in personality following a TBI; difficulty in perceiving social situation, difficulty with self-control and monitoring, stimulus bound, emotional changes, and an incapacity to learn from social experiences. Frontal lobe injuries may result in difficulties with abstract though and a loss of a sense of humor. This may be due to a difficulty to maintain one set of information and perform a simultaneous comparison of another set of data (O'Shanick & O'Shanick, 1994). Patients may also experience intellectual changes. Arousal may range from a state of heightened anxiety or impaired arousal. It has been found that the later usually mean a poor prognosis (Clifton et al., 1981 & Woolf et al., 1987). The lower vigilance state are usually related to a reduction in dopaminergic activity (Feeney & Sutton, 1988; Lat et al., 1988; Neppl, 1988) or increases in cholinergic activity in the central nervous system, (Nissen et al., 1987; Rusted & Warburton, 1989). Usually TBI is associated with disturbances in concentration. This is believed to be due to the damage to the pathways the inhibit transmission of afferent impulses (Gualtier & Evans, 1988; Gualtier et al., 1989). Memory usually suffers when a person experiences a TBI. Specifically, the impairment in capacity to encode incoming data, this capacity resides in the hippocampus. This may be due to the location of the hippocampus, which resides in the anterior temporal lobe when upon impact may force tissue into the sphenodial ridge (O'Shanick & O'Shanick, 1994). Language disturbances are observed in 8%-85% of individuals following a TBI, (Grohen, 1977). Patients usually experience problems with verbal memory, auditory processing, integration and synthesis of linguistic information, word retrieval and spelling. Individuals may also experience a difficulty in the spontaneity of speech (O'Shanick & O'Shanick, 1994). Emotional difficulties may also plague individuals with TBI. Patients may suffer from depression, however it may be difficult to distinguish between reactive depression or depression as a consequence of TBI. For example a person with pseudobulbar palsy may display spontaneous crying and laughing that is not related to the patient's mood. Studying depression in TBI patients is important in that cognitive, perceptual and motor deficits may not be related to TBI but to depression, (Goldstein & Ruthven, 1983). Patients with TBI may also develop obsessive compulsive disorder, delirium, mood disorders, psychotic disorder, anxiety disorder, aggressive disorders, sexual dysfunction and/or auditory and visual hallucinations (Silver et al., 1994; Goldstein & Ruthven, 1983). It is easy to see why patients may have difficulties with interpersonal relationships and integrating into a social environment. There are several factors that influence how well a patient will recover. The nature of damage is an important factor. For instance, the anatomical distribution of the lesion may be widespread if the TBI is severe or if the person is suffering from a degenerative disease such as Alzheimer's. Whereas a more focused injury such as a localized tumor may cause less damage (Miller, 1984). In general the smaller the lesion, the less the damage, contingent upon where the lesion is. For instance lesions in the motor system can cause widespread impairment, (Silver et al., 1994). Age is also a very important factor in predicting recovery. Effects of comparable lesions in young children are not as drastic as those in adults. Infants are born with a brain that weighs 350 grams, but the time they reach young adulthood, the brain weighs 1200-1400 grams due to the proliferation of neurons, interconnections, myelination of axons and development of glial cells, (Miller, 1984; Martin, 1999). Therefore, if a young child receives a brain injury, their natural developmental cycles will be able to aid in recovery. Every day there are more and more treatments for individuals with TBI. In terms of drugs, it has been found that Acetycholine (AcH) improves motor function following a TBI in rats, cats, monkeys, and humans with Alzheimer's. Dopamine facilities dopamine receptors by enhancing recovery after septal, basal ganglia and substantia nigra lesions (Cohen, 1993). The last fifteen years fetal neural transplantation in animals has been used in research. Most extensively used in rats with Parkinson disease with varied success. In humans, transplants from patient's adrenal cortex are injected in the caudate nucleus. The patients reported a significant ability in movement. However due to the side effects and complications, the procedure is rare, (Olsen, 1990). Transplantation of human fetal substantia nigra tissue has been done to a limited degree. Patients report that behavioral deficit improved along with performance, (Cohen, 1993). Another form of treatment is physical therapy. Usually when the therapy is mediated by an interdisciplinary team the results are most favorable. An interdisciplinary team usually consists of a psychiatrist, neuropsychologist, speech pathologist and so forth. In that a TBI may effect a myriad of functions it is important that for the patient to get the best care available that all aspects of the dysfunctionality are attended to. Damage to the brain is unlike any other damaged organ. As previously mentioned personality and emotional changes are likely to occur resulting in difficulty in understanding illness and difficulty to establish social relationship (Cohen, 1993). In conclusion, as research and technology continues to expand and explore TBI, it is the hope that more effective treatment and stronger assessment tools will be devised. From a humanistic point of view, patients with TBI usually suffer from several related psychological and social dysfunction, therefore there is a need for these people to be recognized as individuals who may be able to contribute to society under proper care and supervision. References Alavi, A. Functional and anatomic studies of head injury. Journal of Neuropsychiatry Clinical Neuroscience 1 (Suppl 1). S45-S50. Clifton, G.L., Ziegler, M.G., Grossman, R.G. (1981). Circulating catecholamines and sympathetic activity after head injury. Neurosurgery, 8:10-14. Cohen, Helen ed. (1993). Neuroscience for Rehabilitation. Philadelphia: J.B. Lippincott Company. Feeny,D.M., Sutton, R.L. (1988). Catecholamines and recovery of function after brain damage, in Pharmacological Approaches to the Treatment of Brain and Spinal Cord Injury. Edited by Stein, DG, Sabel, B.A. New York, Plenum, pp. 121-412. Goldstein, G., Ruthven, L. (1983). Rehabilitation of the Brain- Damaged Adults. New York: Plenum Press. Groher, M. (1977). Language and memory disorder following closed head trauma. Journal of Speech and Hearing Res., 20:212-223. Gualtieri C.T., Chandler M., Coons, T.B. (1989). Amantadine: a new clinical profile for traumatic brain injury. Clinical Neuropharmacology, 12:258-270. Gualtieri, C.T., Evans, R.W. (1988). Stimulant treatment for the neurobehavioual sequelae of traumatic brain injury. Brain Injury, 2:273-290. Kiernan, R.J., Mueller, J., Langston, J.W. (1987). The neurobehavioral cognitive status examination: a brief but differentiated approach cognitive assessment. Ann Intern Med., 107:481-482. Lal, S., Merbitz, C.P., Grip, J.C. (1988). Modification of function in head-injury patients with Sinement. Brain Injury, 2:225-233. Langfitt T.W., Obrist, W.D., Alavi, A. (1990). Computerized tomography, magnetic resonance imaging and positron emission tomography in the study of brain trauma. Journal of Neurosurgery. 64:760-767. Levin H.S., High, H.M., Goethe, K.M. (1987). The neurobehavioral rating scale: assessment of the behavioral sequelae of head injury by the clinician. Journal of Neurological Neurosurgery Psychiatry, 50:183-193. Lezak, M.D. (1978). Living with the characterologically altered brain injured patient. Journal of Clinical Psychiatry, 39:592-598. Livingston, M., Brooks, N., Bond, M. (1985). Patient outcome in the year following severe head injury and relatives' psychiatric and social functioning. Journal of Neurology Neurosurgery Psychiatry,48:876-881. Martin, G.N. (1999). Human Neuropsychology. London: Prentice Hall. Miller, Edgar. (1984). Recovery and Management of Neuropsychological Impairments. New York: John Wiley & Sons. Neppe, V.M. (1988). Management of catatonic stupor with L-DOPA. Clinical Neuropharmacology, 11:30-31. Nissen, M.J., Knopman, D.S., Schacter, D.L. Neurochemical dissociation of memory systems. Neurology, 34:789-794. O'Shanick, G.J., O'Shanick, A.M. (1994). In Neuropsychiatry of Traumatic Brain Injury, eds. Silver, J.M., Yudofsky, S.C., Hale, R.E., 163-188. Washington, D.C.: American Psychiatric Press, Inc. Olsen, L. (1990). Grafts and growth factors in CNS: Basic surgery with clinical promise. Stereotactic Functional Neurosurgery, 54,55, 250-267. Reber, A.S. (1985). Dictionary of Psychology. London: Penguin Books. Ruff R.M., Buchsbaum, M.S., Troster, A.I. (1989). Computerized tomography, neuropsychology, and positron emission tomography in the evaluation of head injury. Neuropsychiatry, Neuropsychology, and Behavioral Neurology. 2:103-123. Rusted J.M., Warburton, D.M. Cognitive models and cholinergic drugs. Neuropsychobiology, 21:31-36. Schaffer, L., Kranzler, L.I., Siqueria, E.B. (1985). Aspects of evaluation and treatment of head injury. Neurol Clinical, 9:259- 273. Schwamm, L.H., Van Dyke, C., Kiernan, R.J. (1987). The neurobehavioral cognitive status examination: comparison with the cognitive capacity screening examination and the mini-mental state. Ann Intern Med., 107:486-491. Silver, J.M., Yudofsky, S.C., Hale, R.E., eds. (1994). Neuropsychiatry of Traumatic Brain Injury. Washington, D.C.: American Psychiatric Press, Inc. Tomsen, I. (1984). Late outcome of very severe blunt head trauma: a 10-15 year second follow-up. Journal of Neurlogical Neurosurgery Psychiatry, 47:260-268. Weddell, R., Oddy, M., Jenkins, D. (1980). Social adjustment after rehabilitation: a two year follow-up of patients with severe head injury. Psychological Medicine, 10:257-263. Wilshire, D., Kinsella, G., Prior, M. (1979). The problem of premorbid intelligence in neuropsychological assessment. Journal of Clinical Neuropsychology 1:49-54. Woolf P.D. Hamill, R.W.,Lee,L.A. (1987). The predictive value of catecholamines in assessing outcome in traumatic brain injury. Journal of Neurosurgery, 66:875-882.Return to the Project Table of Contents
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