Neuropsychiatric Disease and Treatment - Annotated Bibliography Example

Annotated Bibliography Affiliation HISTORY OF MTBI Arciniegas, D. B., Anderson, C. A., Topkoff, J., & McAllister, T. W. (2005). Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatric disease and treatment, 1(4), 311. Every year, about 235,000 people experience traumatic brain injury that requires them to be hospitalized for treatment and monitoring. In addition to that, about 1.1 million people experience Traumatic Brain Injury for which they are evaluated and released without hospitalization. Traumatic Brain is bimodally distributed by age with the highest rate of injury being experience in the 15-24 age bracket and those older than 65 .Majority of these injuries result from motor vehicle accidents, fall or assault. Those cases resulting from motor vehicle accidents and assault are common among urban youths. A study on the case that requires hospitalization reveals that about 50,000 of the patients die. The study further reveals that about 5.4 million Americans are currently living with chronic disabilities that result from Traumatic Brain Injury. This has resulted in annual cost of above $48 million in treating these cases. Even though many physicians are familiar with management of mild TBI, it still results in 70% o such injuries. This is because the deficits from mild TBI are subtle and not easily recognized. Majority of these people still end up recovering within the first year of the accident. Differential diagnosis of Mild Truamatic Brain Damage Giza, C. C., & Hovda, D. A. (2001). The neurometabolic cascade of concussion. Journal of Athletic Training, 36(3), 228. Differential diagnosis of mild traumatic brain injury involves use of a methodology that attempts to identify the internal disease that produces the patient’s symptoms. It rarely deals with the external causes of the mild Traumatic injury. Traumatic Injury is transient neurologic dysfunction that results from biomechanical force. Loss of consciousness is clinical hallmark of mild Traumatic Brain Injury or concussion but it is not needed to make diagnosis. The symptoms that are likely to be considered in the differential diagnosis may include confusion, dizziness, disorientation, headache and visual disturbance. The neurologic dysfunction occurs as a result of ionic shifts, changes in neurotransmissions, impaired connectivity and altered metabolism. Henry, L. C., Tremblay, S., Boulanger, Y., Ellemberg, D., &Lassonde, M. (2010). Neurometabolic changes in the acute phase after sports concussions correlate with symptom severity. Journal of neurotrauma, 27(1), 65-76. Diagnosis carried out on athletes show that these athletes display neurophysiological alterations as well as post concussion symptoms like headache and sensitivity to light and noise. The authors carried out a study to investigate the effect of concussion on athletes .The study explored the effect of concussion on the athlete’s verbal memory, information processing speed, reaction time, verbal memory and visual memory. No group difference was detected in the study relative to controls. The paper therefore concluded that the neurophysiological alterations that are normally experienced by athletes are as a result of neurometabolic changes. Henry, L. C., Tremblay, S., Leclerc, S., Khiat, A., Boulanger, Y., Ellemberg, D., &Lassonde, M. (2011). Metabolic changes in concussed American football players during the acute and chronic post-injury phases. BMC neurology, 11(1), 105. Understanding differential diagnosis requires understanding of effect of concussion on brain metabolism to fully understand the effect of mild traumatic brain injury. To explore the effect of concussion on brain metabolism the authors investigated the effect of sport concussion on brain metabolism in a sample group of ten athletes that had experienced concussion and 10 others that had not experienced concussion. The athletes that had experienced concussion showed nuerometabolic impairment in the prefrontal as well as the motor cortices. The outcome demonstrated that there is usually the occurrence of cortical neurometabolic change after concussion has taken place POST CONCUSSION SYNDROME Chen, J. K., Johnston, K. M., Collie, A., McCrory, P., & Ptito, A. (2007). A validation of the post concussion symptom scale in the assessment of complex concussion using cognitive testing and functional MRI. Journal of Neurology, Neurosurgery & Psychiatry, 78(11), 1231-1238. Clinical assessment of mild traumatic brain injury relies heavily on the presence of post concussion symptoms as well as the duration of these symptoms .The post concussion symptoms are always subjective in nature and are not always specific to concussions resulting in the need to validate their usefulness. Typically acute post concussion symptoms may include physical problems such as dizziness, headache and visual impairment. Other symptoms include cognitive impairment like attention and memory dysfunction. Behavioral problems like irritability, anxiety and depression are also some of the post concussion symptoms. The development of these symptoms according to the journal is predicted on complex set of factors like neural injury resulting from mild TBI or pre existing psychiatric disorder. The response accuracy and speed of cognitive tests of moderate PSC group is slower than that of a low PCS group. Clarke, L. A., Genat, R. C., & Anderson, J. F. (2012). Long-term cognitive complaint and postconcussive symptoms following mild traumatic brain injury: The role of cognitive and affective factors. Brain Injury, 26(3), 298-307. Neuropsychological test performance factors can be effectively used to predict long term post concussive symptoms as well as cognitive complaints that are normally as a result of mild traumatic brain injury. The authors performed a study with a sample of individuals with spinal and brain injuries as well as a control group with no injury .The individuals completed post concussive tests symptoms as well as depression and anxiety tests. It revealed that depression, neuroticism and anxiety are very good signs of post concussive symptoms than neuropsychological test performances. King, N. S., &Kirwilliam, S. (2011). Permanent post-concussion symptoms after mild head injury. Brain injury, 25(5), 462-470. A small group of individuals do experience permanent post concussion symptoms as a result of mild head injury. There is no systematic quantitative research that examines the wide range of variables in a sample comprising of such patients. The authors explored a broad spectrum of demographic, emotional and psychosocial factors to study the patients with permanent post concussion injury. The study revealed that very high levels of post concussion symptoms can be a permanent feature of mild head injury. Quality of one’s life is also directly related to the severity of the post concussion symptoms. POST CONCUSSION SYNDROME: Clarke, L. A., Genat, R. C., & Anderson, J. F. (2012). Long-term cognitive complaint and post concussive symptoms following mild traumatic brain injury: The role of cognitive and affective factors. Brain Injury, 26(3), 298-307. Neuropsychological test performance factors can be effectively used to predict long term post concussive symptoms as well as cognitive complaints that are normally as a result of mild traumatic brain injury. The authors carried out a study involving on individuals with mild traumatic brain injury, spinal injury and those with no brain injuries. The individuals completed post concussive tests symptoms as well as depression and anxiety tests. This shows that depression, neuroticism and anxiety are very good signs of post concussive symptoms than neuropsychological test performances. Psychological test performances are good signs of cognitive complaints .From the findings it was concluded that long term post concussive symptoms are largely a representative of psychological symptoms. King, N. S., &Kirwilliam, S. (2011). Permanent post-concussion symptoms after mild head injury. Brain injury, 25(5), 462-470. A small group of individuals do experience permanent post concussion symptoms as a result of mild head injury. There is no systematic quantitative research that examines the wide range of variables in a sample comprising of such patients. The paper explored a broad spectrum of demographic, emotional and psychosocial factors to study the patients with permanent post concussion injury. The study revealed that very high levels of post concussion symptoms can be a permanent feature of mild head injury. Quality of one’s life is also directly related to the severity of the post concussion symptoms. MTBI AND WHITE MATTER INTEGRITY Gao, X., & Chen, J. (2011). Mild traumatic brain injury results in extensive neuronal degeneration in the cerebral cortex. Journal of neuropathology and experimental neurology, 70(3), 183. It is known that mild traumatic brain injury leads to long term cognitive as well as emotional difficulties and behavioral disturbance. The lack of evidence based correlates of clinical manifestations of the disorder has hugely hampered treatment and diagnosis of mild traumatic brain injury. Unlike the severe traumatic brain injury, mild brain injury does not show significant tissue lesions or cavities in the cortex. In addition to that, neuro-imaging through magnetic resonance has always produced negative results indicating that the damage is beyond the resolution of the current scanning technologies. Investigation of the morphologies of spared neurons in the cortex after mild traumatic brain injury reveals that mild TBI it leads to limited tissue lesions and cell death. Mild traumatic brain injury also causes widespread, significant synapse degeneration in the cortical neurons that were spared. This widespread loss disrupts neural circuitry leading to neurologic dysfunction. Bazarian, J. J., Zhong, J., Blyth, B., Zhu, T., Kavcic, V., & Peterson, D. (2007). Diffusion tensor imaging detects clinically important axonal damage after mild traumatic brain injury: a pilot study. Journal of neurotrauma, 24(9), 1447-1459. It is usually important to detect clinically important axonal damage in cerebral white matter after traumatic brain injury. This is because it helps in understanding, diagnosis and treatment of mild traumatic brain disorder. The authors evaluate a prospective pilot study of six subjects with isolated mild TBI and six matched orthopedic controls. In the study, all the subjects underwent DTI scanning, PCS assessment and neurobehavioral testing. At the end of the study, it was the images revealed significant damage of the cerebral white matter. Cubon, V. A., Putukian, M., Boyer, C., &Dettwiler, A. (2011). A diffusion tensor imaging study on the white matter skeleton in individuals with sports-related concussion. Journal of neurotrauma, 28(2), 189-201. Understanding the effect of TBI on the white matter integrity is critical in managing and recognizing effects of cerebral concussion due to the discrete symptomology. Most sportsmen who experience mild traumatic brain injury experience rapid onset of short lived neurological impairment with no structural changes in the magnetic resonance imaging and computer tomography. Diffusion tensor imaging is an objective tool that can be used to asses severity and recovery functions after a concussion. It involves assessing the white matter fiber tract integrity. The paper states that qualitative comparison of fractional anisotropy and mean diffusivity suggest that with increasing level of injury severity, MD might be more sensitive in detecting mild injury .Fractional anisotropy on the other hand is more effective in capturing more severe injuries. Tract-based spatial statistics (TBSS) analysis can therefore be used to evaluate axonal injury of the white matter skeleton. It effectively detects structural changes in sport related concussions. Inglese, M., Makani, S., Johnson, G., Cohen, B. A., Silver, J. A., Gonen, O., & Grossman, R. I. (2005). Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study. Journal of neurosurgery, 103(2), 298-303. Diffuse axonal injury is a major complication of TBI that results in functional and psychological deficits.DAI is always under diagnosed by the convectional imaging techniques. The study reveals that despite the fact that means diffusivity and fractional anisotropy abnormalities in patients with Traumatic Brain Injury are not easy to detect they are still present in the brain. The diffusion tensor changes are a sign of subsequent brain damage. Kraus, M. F., Susmaras, T., Caughlin, B. P., Walker, C. J., Sweeney, J. A., & Little, D. M. (2007). White matter integrity and cognition in chronic traumatic brain injury: a diffusion tensor imaging study. Brain analysis of radial and axial diffusivity values suggests that all severities of TBI results in a degree of axonal damage. The analysis also shows that irreversible myelin damage is associated with moderate to severe TBI. Therefore TBI white matter changes are primarily due to axonal damage as opposed to myelin damage. SIMILARITY TO AGING, ALZHEIMERS AND DEMENTIA: Van Den Heuvel, Corinna, Emma Thornton, and Robert Vink. (2007).Traumatic brain injury and Alzheimers disease: a review. Progress in brain research, 161 303-316. Studies have revealed that traumatic brain injury is a possible predisposing factor in Alzheimer disease. There has been extensive research on how exactly it leads to AD .This study shows that despite significant discrepancies in the literature, there appears to be an increasing trend to support the belief that TBI is a potential risk factor for Alzheimer diseases. Furthermore the authors link apolipoprotein genotypes to AD but states that its link to TBI remains inconclusive and ambiguous. Jellinger, K. A. (2004). Head injury and dementia. Current opinion in neurology, 17(6), 719-723. The link between head injury and dementia/ Alzheimer‘s disease remains ambiguous. The paper states that although epidemiological studies as well as retrospective autopsy data have provided evidence that a later cognitive declines occurs after severe traumatic head injury, the relationship is still ambiguous. Both human post-mortem and experimental studies show apolipoprotein beta deposition after head injury support link between traumatic brain injury and dementia. Mielke, M. M., Savica, R., Wiste, H. J., Weigand, S. D., Vemuri, P., Knopman, D. S., & Jack, C. R. (2014). Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study. Neurology, 82(1), 70-76. The authors states that among individuals with MCI, self reported trauma with at least momentary loss of consciousness is associated with greater amyloid deposition. This therefore suggests that trauma may be associated with Alzheimer Disease related neuropathology. Tremblay, S., De Beaumont, L., Henry, L. C., Boulanger, Y., Evans, A. C., Bourgouin, P., & Lassonde, M. (2013). Sports concussions and aging: a neuro imaging investigation. Cerebral Cortex, 23(5), 1159-1166. This paper studies the correlation between cognitive decline in late adulthood and sports concussions sustained in early adulthood. The study unveiled brain anomalies in otherwise healthy former athletes with concussion and associated the manifestations to long term detrimental effect of sport concussions on the cognitive functions. It highlights the patterns of decline that are often associated with abnormal aging. CHRONIC TRAUMATIC ENCEPHALOPATHY: McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., & Stern, R. A. (2009). Chronic traumatic encephalopathy in athletes: progressive tauopathy following repetitive head injury. Journal of neuropathology and experimental neurology, 68(7), 709. Chronic traumatic encephalopathy is a neuropathlogically distinct slowly progressive tauopathy that is known to have environmental etiology .CTE is associated with memory disturbances, behavioral as well as personally changes.CTE is characterized by autophy of the cerebral hemisphere, thalamus and brain stem. Ann C. McKee, MD, Robert C. Cantu, MD, [...], and Robert A. Stern, (2009). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury. Journal of neuropathology and experimental neurology, 68(7), 709–735. CTE is a progressive neuro degeneration that is associated with memory disturbances, behavioral and personality change as well as speech and gait abnormalities. There is overwhelming evidence that the condition is as result of repeated sub lethal brain trauma. It often occurs before development of clinical manifestations of sub lethal brain trauma. Omalu BI, DeKosky ST, Hamilton RL, et al. (2006). Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery. 2006; 59:1086–92. This study recommends the need for further empirical elucidation of pathology and pathological cascades of long term neurogenerative sequel of footballers. It carries out a study on professional footballers. In its conclusion, it is stated that the footballers who had long careers without multiple recorded concussions manifested Major Depressive Disorder in retirement. The athletes exhibited neuro fibrilary tangles, neuropil threads and coronatry atherosclerotic diseases. Webbe FM, Barth JT. Short-term and long-term outcome of athletic closed head injuries. Clinical Sports Med. 2003; 22:577–92. Rapid growth of computerized neuro-cognitive assessment provides an efficient and valid technology that can be used to test the long term and short-term implications of head injuries in athletes. EXERCISE AND WHITE MATTER INTEGRITY Baker, J. G., Freitas, M. S., Leddy, J. J., Kozlowski, K. F., &Willer, B. S. (2012). Return to full functioning after graded exercise assessment and progressive exercise treatment of post concussion syndrome. Rehabilitation research and practice, 2012. Aerobic training as well as exercise assessment is known to reduce physiological symptoms and signs that occur after mild traumatic brain injury. This study has clearly shown that the recovery from the symptoms happens by increasing the flow of blood in the brain of the patients that had suffered concussion. Leddy, J. J., Kozlowski, K., Fung, M., Pendergast, D. R., &Willer, B. (2007). Regulatory and auto regulatory physiological dysfunction as a primary characteristic of post concussion. This study advises that patients with post concussion symptoms are not supposed to be involved in exercise due to concerns from symptoms of flare up. The paper further suggest that extended rest may also lead to the PCS patients experiencing deconditioning and secondary effects like depressive set of symptoms. It further suggests that PCS may be reduced by the patients being put under aerobic exercise. This kind of exercise improves flow of blood in the brain. Mabbot, D, Timmons, B., Bartels, U., Bouffet, E., Laughlin, S., Piscione, J., Scantlebury, N., & Scheinemann, K. (2014). Exercise intervention in children treated with radiation for brain tumors. Canadian Cancer Society Research Institute. It explores neurocognitive outcomes of exercise outcomes in children. It uses DTI to study exercise outcomes in children who have been treated with radiations for brain tumor. When carrying out studies on exercise interventions it is important to understand that neurogenesis takes place within the hippocampus, a structure that is important for learning a memory. References Ann, C., McKee, M. D, Robert C., Cantu, M. D, [...] & Robert A. S. (2009). Chronic Traumatic Encephalopathy in Athletes: Progressive Tauopathy following Repetitive Head Injury. Journal of neuropathology and experimental neurology, 68(7), 709–735. Arciniegas, D. B., Anderson, C. A., Topkoff, J., & McAllister, T. W. (2005). Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation, and treatment. Neuropsychiatric disease and treatment, 1(4), 311. Bazarian, J. J., Zhong, J., Blyth, B., Zhu, T., Kavcic, V., & Peterson, D. (2007). Diffusion tensor imaging detects clinically important axonal damage after mild traumatic brain injury: a pilot study. Journal of neurotrauma, 24(9), 1447-1459. Chen, J. K., Johnston, K. M., Collie, A., McCrory, P., & Ptito, A. (2007). A validation of the postconcussion symptom scale in the assessment of complex concussion using cognitive testing and functional MRI. Journal of Neurology, Neurosurgery & Psychiatry, 78(11), 1231-1238. Clarke, L. A., Genat, R. C., & Anderson, J. F. (2012). Long-term cognitive complaint and post concussive symptoms following mild traumatic brain injury: The role of cognitive and affective factors. Brain Injury, 26(3), 298-307. Cubon, V. A., Putukian, M., Boyer, C., &Dettwiler, A. (2011). A diffusion tensor imaging study on the white matter skeleton in individuals with sports-related concussion. Journal of neurotrauma, 28(2), 189-201. Gao, X., & Chen, J. (2011). Mild traumatic brain injury results in extensive neuronal degeneration in the cerebral cortex. Journal of neuropathology and experimental neurology, 70(3), 183. Giza, C. C., & Hovda, D. A. (2001). The neurometabolic cascade of concussion. Journal of Athletic Training, 36(3), 228. Henry, L. C., Tremblay, S., Leclerc, S., Khiat, A., Boulanger, Y., Ellemberg, D., &Lassonde, M. (2011). Metabolic changes in concussed American football players during the acute and chronic post-injury phases. BMC neurology, 11(1), 105. Inglese, M., Makani, S., Johnson, G., Cohen, B. A., Silver, J. A., Gonen, O., & Grossman, R. I. (2005). Diffuse axonal injury in mild traumatic brain injury: a diffusion tensor imaging study. Journal of neurosurgery, 103(2), 298-303. Jellinger, K. A. (2004). Head injury and dementia. Current opinion in neurology, 17(6), 719-723. King, N. S., &Kirwilliam, S. (2011). Permanent post-concussion symptoms after mild head injury. Brain injury, 25(5), 462-470. Kraus, M. F., Susmaras, T., Caughlin, B. P., Walker, C. J., Sweeney, J. A., & Little, D. M. (2007). White matter integrity and cognition in chronic traumatic brain injury. A diffusion tensor imaging study. Leddy, J. J., Kozlowski, K., Fung, M., Pendergast, D. R., &Willer, B. (2007). Regulatory and auto regulatory physiological dysfunction as a primary characteristic of post concussion Mabbot, D, Timmons, B., Bartels, U., Bouffet, E., Laughlin, S., Piscione, J., Scantlebury, N., & Scheinemann, K. (2014). Exercise intervention in children treated with radiation for brain tumors. Canadian Cancer Society Research Institute. McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., & Stern, R. A. (2009). Chronic traumatic encephalopathy in athletes: progressive tauopathy following repetitive head injury. Journal of neuropathology and experimental neurology, 68(7), 709. Mielke, M. M., Savica, R., Wiste, H. J., Weigand, S. D., Vemuri, P., Knopman, D. S., & Jack, C. R. (2014). Head trauma and in vivo measures of amyloid and neurodegeneration in a population-based study. Neurology, 82(1), 70-76. Omalu BI, DeKosky ST, Hamilton RL, et al. (2006). Chronic traumatic encephalopathy in a national football league player: part II. Neurosurgery. 2006; 59:1086–92. Tremblay, S., De Beaumont, L., Henry, L. C., Boulanger, Y., Evans, A. C., Bourgouin, P., & Lassonde, M. (2013). Sports concussions and aging: a neuro imaging investigation. Cerebral Cortex, 23(5), 1159-1166. Van Den Heuvel, Corinna, Emma Thornton, and Robert Vink.(2007). Traumatic brain injury and Alzheimers disease: a review. Progress in brain research 161 (2007): 303-316. Webbe FM, Barth JT. Short-term and long-term outcome of athletic closed head injuries. Clinical Sports Med. 2003; 22:577–92. Read More