Major or Minor Neurocognitive Disorder Due to Traumatic Brain Injury DSM-5 294.11 (F02.8)
DSM-5 Category: Neurocognitive Disorders
Introduction
The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (American Psychiatric Association, 2013) has made extensive changes in the classification of cognitive disorders such as dementia, delirium and amnesia. Because of the stigma associated with categorization of cognitive deficits from neurological disease or injury in younger patients as “dementia”, and because some clinicians had questioned the diagnostic use of a term literally meaning “loss of mind”, the various acquired cognitive disorders are now grouped together in a separate category, differentiated as to acquired cause and categorized as mild or severe.
The variously-named types of “age-related cognitive decline” that appear “in other conditions that may be a focus of clinical attention” are now categorized together and not listed individually as possible precursors of dementia. The new classification replaces several imprecise terms, such as mild cognitive impairment (MCI) with and without amnesia or cognitive impairment not dementia, with the single term “minor neurocognitive disorder”, which is similar to “minor depression” . The previous entities of MCI and subsyndromal depression in DSM-4 (American Psychiatric Association, 2000) often predicted progression to dementia or major depression but many people with MCI or subsyndromal depression did not go on to develop a major mental illness. The distinction between “major” and “minor” disorders reflects the growing consensus that minor cognitive problems and minor depression are often but not always the prodromal manifestations of dementia and depression.
The criteria for the diagnosis of dementia in earlier editions of DSM included impairment of memory and learning plus aphasia, apraxia, agnosia or impairment of executive functions, all severe enough to cause social difficulty. The new edition includes domains for social cognition, visuoconstructional perceptual ability (the ability to ability to recognize or reproduce a design), language, learning and memory, executive ability, and complex attention, in which loss of previous abilities can cause functional impairment.
Symptoms of Major or Minor Neurocognitive Disorder Due to Traumatic Brain Injury
Efforts to rehabilitate individuals with neurological deficit after head trauma can be dated back to the Greeks and Romans. Traumatic brain injury (TBI) was usually fatal, but heat, cold, massage and exposure to electrical currents generated by eels and fish were sometimes used to promote recovery. Among the first studies of gunshot wounds to the head were those done in the American Civil War by Confederate surgeon J. John Chisholm, who described diffuse axonal injury from rotation or severe deceleration of the head and outlined the first protocols for head trauma care in his Manual of Military Surgery that was consulted by both North and South (Cifu, Cohen, Lew, Jaffee & Sigford, 2010). Most TBI victims died of septic complications of their wounds. One of the few survivors with neuropsychiatric sequelae was the Vermont railroad worker Phineas Gage, who had little neurological deficit but probable aphasia and behavioral disinhibition after an explosion drove an iron bar through his left frontal lobe in 1848 (Macmillan, 2000).
By the time of the First World War, the mortality of head wounds with dural penetration had decreased to 35 per cent, and first the German and then Allied armies came to realize the need for neurological and psychiatric rehabilitation after such wounds. The Institute for Research into the Consequences of Brain Injuries was established in Frankfurt by Kurt Goldstein, who had earlier assisted Karl Wernicke in the study of aphasia and was later assisted by Fritz Perls and Lore Posner, and observations there contributed to Goldstein’s work on brain and mind and the formulation of Gestalt therapy (Teuber, 1966). In the United States, the Hospital for Head Injury at Cape May, New Jersey engaged 3 corrective speech teachers and began the first speech and language rehabilitation for aphasia (Boake, 1989).
Impact
TBI has historically been a military complication, but is now a major civilian problem, on account of vehicular accidents and the increasing recognition of brain concussion in athletic injuries. Approximately 1.7 million traumatic brain injuries are sustained each year, resulting in 1.4 million emergency department evaluations (80 per cent resulting in release after treatment), 275,000 hospitalizations and 52,000 deaths. About 30 per cent of injury-related deaths are related to TBI, but 75 per cent of TBI cases are concussions or other milder injuries. The direct medical costs of TBI and indirect costs such as lost productivity totaled $60 billion in 2000 (Finkelstein, Corso & Miller, 2006). It is likely that these figures were underestimates, as an unknown percentage of TBI cases do not come to medical attention, and between 2002 and 2006 emergency department visits related to TBI increased by 14 per cent and TBI hospitalizations by 19 per cent (Faul, Xu, Wald & Coronado, 2010).
The greatest likelihood of sustaining TBI is in children under 4 years of age, adolescents 15 to 19 years old and adults over age 65. Children up to age 14 required approximately 500,000 emergency department visits for TBI between 2002 and 2006, but the rate of hospitalization and death is highest among those over 75 years old. Males predominate over females in all age groups of TBI patients. Between 2002 and 2006, 35 per cent of recorded TBI was due to falls, 17 per cent each to vehicular accidents and blows to the head, 10 per cent to assault and 21 per cent to other causes or of unknown origin. The incidence of falls causing TBI is rising, with a 62 per cent increase in emergency department visits due to fall and TBI among children under 14 between 2002 and 2006. The elderly had a 46 per cent increase in fall-related emergency department visits, 34 per cent increase in hospitalizations and 27 per cent increase in deaths during this period (Faul et al., 2010).
Assessment of cognition in the mental status examination, measurement of cognitive function by neuropsychological tests and application of cognitive skills in activities of daily living may be influenced by motivation, which is how effectively and efficiently behavior is initiated and maintained. Significant head injury often causes abulia or lack of motivation, particularly with injury to the ventral tegmentum, ventral pallidum and medial frontal and orbitofrontal cortex. In its most severe form, abulia is characterized by akinetic mutism, in which the patient is awake and tracks visually but makes no other response. Less severe abulia manifests poverty of speech and behavior, lack of initiative, diminished emotional response and psychomotor retardation. Most commonly, abulia is quantitative rather than qualitative: the ability to plan action and to react is preserved but reduced in force (Mega & Cummings, 1994).
The degree of post-traumatic cognitive impairment is determined by the presence and severity of focal brain injuries and the extent of diffuse axonal injury, which is the shearing of nerve axons by head rotation or deceleration. Diffuse axonal injury generally causes global cognitive impairment, while localized brain injuries cause focal deficits such as aphasia (Scheid, Walther, Guthke, Preul & von Cramon, 2006). Generalized cognitive disturbance manifests itself in perseveration, inattention and distractibility that interferes with maintaining conversations and train of thought, impairment of selective and divided attention that hampers multitasking and in defects of declarative and, to a lesser extent, implicit memory. Working memory and prospective memory, exemplified by remembering to pay bills, are affected by frontal lobe lesions (Perlstein, Cole & Demery, 2004). Goal-setting, planning, and initiating, sequencing or inhibiting behavior are executive functions that are affected by injury to circuits connecting thalamus, basal ganglia and frontal lobes, and self-monitoring and -regulation are impaired by frontal lobe damage (Cummings, 1993).
The “postconcussion syndrome”, a frequent sequel of mild-to-moderate head trauma in vehicular accidents and sports, is now subsumed under the heading of “minor neurocognitive disorder”. Minor head injury was estimated to have an incidence of 503 per 100,000 and cause about 1.4 million emergency department visits between 1998 and 2000 (Bazarian, McClung, Shah, Cheng, Flesher & Kraus, 2005). Post-concussive symptoms may be present in as many as 50 per cent of minor TBI patients after 1 month, and 15 per cent after 1 year (Kolias, Guilfoyle, Helmy, Allanson & Hutchinson, 2013).The most common symptom is headache of variable type, persistently present in about 15 per cent of emergency department patients with minor head injury versus 2 per cent of other emergency patients department patients with minor injuries. Dizziness is the second most common symptom, along with diplopia, blurred vision, tinnitus, hearing loss, photo- and phonophobia, decreased taste and smell and nausea or vomiting. Depression, anxiety, fatigue, irritability and decreased libido are common neurovegetative symptoms, and decreased attention, concentration, and memory along with slowed reaction time and information processing are cognitive manifestations (Faux & Sheedy, 2008).
Diagnostic Criteria
Major neurocognitive disorder is characterized by a significant decline from a previous level of performance in one or more cognitive domains (complex attention, executive function, learning, memory, language, perceptual-motor or social). The decline should be confirmed by a knowledgeable observer (family member or friend) or by the clinician, or substantiated by standardized neuropsychological testing or qualified psychological assessment. The cognitive deficits must result in a need for assistance with complex instrumental activities of daily life, such as paying bills or managing medications, or otherwise interfere with independence. The deficits must not be the result of delirium or be better explained by another mental disorder.
Minor neurocognitive disorder does not interfere with everyday independence. There should, however, be evidence of a decline from former levels of ability in one or more of the above cognitive domains, either from the concerns of friends, family members or the clinician or from a deterioration in neuropsychological test performance. These problems must likewise not be due to delirium or another more likely mental disorder.
Treatment of Major or Minor Neurocognitive Disorder Due to Traumatic Brain Injury
Multidisciplinary inpatient rehabilitation is the treatment of choice for the sequelae of severe traumatic brain injury, followed by outpatient speech and language therapy and supportive psychotherapy for families and caregivers when possible (National Institute of Neurological Disorders and Stroke, 2002). Pharmacological treatment has often focused on management of comorbid symptoms with antipsychotic agents, anxiolytic drugs and antidepressants (Arciniegas, Anderson, Topkoff & McAllister, 2005). Centrally-acting cholinergic drugs, developed for Alzheimer’s disease and related dementias, have been found effective for post-traumatic cognitive symptoms in some studies and not different from placebo in others (Nicholl & LaFrance, 2009). Stimulant medications have also improved attention and cognition in some studies (Nicholls, Hildenbrand, Aggarwal, McCarthy & Daly, 2012).
References
American Psychiatric Association (2000). Diagnostic and Statistical Manual of Mental Disorders, ed. 4. Washington, DC, APA Press.
American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders, ed. 5. Arlington, VA, APA Press.
Arciniegas, D.B., Anderson, C.A., Topkoff, J. & McAllister, T.W. (2005). Mild traumatic brain injury: a neuropsychiatric approach to diagnosis, evaluation and treatment. Neuropsychiat Dis Treat, 1(4): 311-327.
Bazarian, J.J., McClung, J., Shah, M.N., Cheng, Y.T., Flesher, W. & Kraus, J. (2005). Mild traumatic brain injury in the United States, 1998-2000. Brain Inj, 19(2): 85-91.
Cifu, D.X., Cohen, S.I., Lew, H.L., Jaffee, M. & Sigford B. (2010). The history and evolution of traumatic brain injury rehabilitation in military service members and veterans. Amer J Phys Med Rehab, 89(8): 688-694.
Cummings, J.L. (1993). Frontal-subcortical circuits and human behavior. Arch Neurol, 50(8): 873-880.
Faul, M., Xu, L., Wald, M.M. & Coronado, V.G. (2010). Traumatic Brain Injury in the United States: Emergency Department Visits, Hospitalizations and Deaths 2002-2006. Atlanta, GA, Centers for Disease Control and Prevention, National Center for Injury Prevention and Control.
Faux, S. & Sheedy, J. (2008). A prospective controlled study in the prevalence of post-traumatic headache following mild traumatic brain injury. Pain Med, 9(8): 1001-1011.
Finkelstein, E., Corso, P. & Miller, T. (2006). The Incidence and Economic Burden of Injuries in the United States. New York, Oxford University Press.
Kolias, A.G., Guilfoyle, M.R., Helmy, A., Allanson, J. & Hutchinson, P.J. (2013). Traumatic brain injury in adults. Pract Neurol, 13: 228-235.
MacMillan, M.B. (2000). An Odd Kind of Fame: Stories of Phineas Gage. Cambridge, MA, MIT Press.
Mega, M.S., Cummings, J.L. (1994). Frontal-subcortical circuits and neuropsychiatric disorders. J Neuropsychiat Clin Neurosci, 6(4): 358-370.
National Institute of Neurological Disorders and Stroke (2002). Traumatic Brain Injury: Hope Through Research (publication No, 02-2478). Bethesda, MD, National Institutes of Health, United States Deaprtment of Health and Human Services.
Nicholl, J. & LaFrance, C., Jr. (2009). Neuropsychiatric sequelae of traumatic brain injury. Semin Neurol, 29(3): 247-255.
Nicholls, E., Hildenbrand, A.K., Aggarwal, R., McCarthy, L. and Daly, B. (2012). The use of stimulant medications to treat neurocognitive deficits in patients with pediatric cancer, traumatic brain injury, and sickle cell disease: a review. Postgrad Med, 124(5): 78-90.
Perlstein, W.M., Cole, M.A. & Demery, J.A. (2004). Parametric manipulation of working memory load in traumatic brain injury: behavioral and neural correlates. J Int Neuropsychol Soc, 10(5): 724-741.
Scheid, R., Walther, K., Guthke, T., Preul, C. & von Cramon, D.Y. (2006). Cognitive sequelae of diffuse axonal injury. Arch Neurol, 63(3): 418-424.
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