It is widely recognized that neuropsychiatric disturbances contribute substantially to disability among persons with traumatic brain injury (TBI). This issue of Psychiatric Clinics addresses the most common and the most clinically challenging neuropsychiatric sequelae of TBI. The overarching aim of this publication is to provide clinicians with information about the clinical characteristics, diagnostic assessment, neurobiology and treatment of these conditions that will be useful in their work with individuals and families affected by TBI. Topics include: Posttraumatic Encephalopathy; Cognitive Disorders after TBI; Emotional and Behavioral Dyscontrol after TBI; Mood Disorders following TBI; Apathy following TBI; Psychotic Disorders following TBI; Sleep and Fatigue following TBI; TBI and Posttraumatic Stress Disorder; Neuropsychiatry of Persistent Post-concussive Symptoms; Psychiatric Disorders following Pediatric TBI.
Front Cover 1
Neuropsychiatry ofTraumatic Brain Injury 2
copyright
3
Contributors 4
Contents 8
Psychiatric Clinics Of North America 11
Preface 12
References 14
Cognitive Sequelae of Traumatic Brain Injury 18
Key points 18
Introduction 18
Epidemiology of cognitive dysfunction following TBI 19
Short-Term Cognitive Impairment 19
Long-Term Cognitive Impairment 20
Deficits of executive function and everyday thinking skills 20
Pathophysiology of cognitive deficits following TBI 23
Neuropsychological assessment 24
Treatment 24
Summary 25
References 26
Mood Disorders After TBI 30
Key points 30
Introduction 30
Depressive disorders 31
Epidemiology 31
Risk Factors 32
Diagnostic Assessment 33
Differential Diagnosis 34
Ancillary Studies 35
Psychotherapy 35
Pharmacotherapy 36
Electroconvulsive Therapy and Brain Stimulation Techniques 37
Manic, hypomanic, and mixed disorders 37
Epidemiology 37
Risk Factors 38
Diagnostic Assessment 38
Differential Diagnosis 39
Ancillary Studies 39
Pharmacotherapy 40
Psychotherapy 41
ECT and Brain-Stimulation Techniques 41
Summary and future directions 41
Acknowledgments 41
References 42
Emotional and Behavioral Dyscontrol After Traumatic Brain Injury 48
Key points 48
Emotional dyscontrol 50
Pathological Laughing and Crying 50
Affective Lability 52
Irritability 53
Behavioral dyscontrol 55
Disinhibition 56
Aggression 57
Summary 60
References 60
Traumatic Brain Injury and Posttraumatic Stress Disorder 72
Key points 72
Introduction 73
Epidemiology 74
Definitions of TBI and PTSD 74
Frequency of PTSD Among TBI Survivors 75
The Influence of TBI on the Development and Course of PTSD 77
Neurobiology of co-occurring TBI and PTSD 77
Imaging and Lesion-Behavioral Correlates 79
Evaluation 80
Neuroimaging and Neuropsychological Assessment 82
Treatment implications 82
Symptom Management 84
Pharmacological Treatments for PTSD and TBI 84
Psychotherapy for PTSD and TBI 85
Combined Interventions for PTSD and TBI 85
Summary 85
References 86
Sleep and Fatigue Following Traumatic Brain Injury 94
Key points 94
Sleep disturbances after TBI—their nature and assessment 95
Causes of sleep disturbance after TBI 96
Fatigue after TBI—its nature and assessment 97
Causes of fatigue after TBI 98
Consequences of fatigue and sleep disturbances 100
Current treatment approaches 100
Summary 102
References 102
Neuropsychiatry of Persistent Symptoms After Concussion 108
Key points 108
Introduction 108
Did a mild TBI occur? 109
Self-report 110
Medical Records 110
Brain Imaging 110
Neuropsychological Testing 111
What is causing the symptoms? 111
Psychiatric Factors 111
Physical Factors 112
Psychological Factors 112
Legal Factors, Insurance Factors, and Effort 112
Treatment 113
References 116
Apathy Following Traumatic Brain Injury 120
Key points 120
Introduction 120
Apathy: definition and phenomenology 120
Diagnosis of apathy 121
Apathy in TBI: differential diagnosis 123
Frequency of apathy in TBI 124
Apathy, depression, and cognitive impairment 124
Correlates of apathy after TBI 124
Mechanism of apathy in TBI 125
Treatment of apathy in TBI 126
Summary 126
References 126
Psychotic Disorder Caused by Traumatic Brain Injury 130
Key points 130
Diagnosis of psychosis caused by TBI 131
Psychotic Symptoms 131
Relationship of Psychosis to TBI 132
Differential Diagnosis 133
Functional Consequences of PDDTBI 135
Treatment 136
Pharmacotherapy 136
Nonpharmacologic Treatment 136
Theoretic model of the proposed relationships between TBI and psychosis 137
Summary and future directions 138
References 139
Neuropsychiatry of Pediatric Traumatic Brain Injury 142
Key points 142
Introduction 142
Epidemiology 142
Pathophysiology 143
Evaluation 143
Methodological Concerns 144
Preinjury Psychiatric Status 144
Postinjury Psychiatric Status 144
NPD 145
Specific Psychiatric Disorders/Symptom Clusters 145
Personality Change due to TBI 145
Secondary ADHD 147
ODD/Conduct Disorder 147
PTSD 148
Other Anxiety Disorders 148
Mania/Hypomania 149
Depressive Disorders 149
Psychosis and Autism 149
Treatment 149
Nonpharmacologic Treatment Strategies 149
School 149
Family-based treatment 150
Pharmacotherapies 150
PC due to TBI: Labile and Aggressive Subtypes 150
PC due to TBI: Disinhibited, Paranoid, Apathetic Subtypes 151
ADHD 151
Depression 151
Emerging Treatment Approaches 151
Summary 152
References 152
Index 158
Cognitive Sequelae of Traumatic Brain Injury
Amanda R. Rabinowitz, PhDa∗ rabinowitz.a@gmail.com and Harvey S. Levin, PhDb, aDepartment of Neurosurgery, University of Pennsylvania School of Medicine, 370 Stemmler Hall, Philadelphia, PA 19104, USA; bMichael E. DeBakey Veterans Affairs Medical Center, 2002 Holcombe Boulevard, Houston, TX 77030, USA; and Departments of Psychiatry and Behavioral Sciences, Physical Medicine and Rehabilitation, Pediatrics, and Neurosurgery, Baylor College of Medicine, 6560 Fannin #1144, Houston, TX 77030, USA
∗Corresponding author.
Cognitive dysfunction is the leading cause of disability following traumatic brain injury (TBI). This article provides a review of the cognitive sequelae of TBI, with a focus on deficits of executive functioning and everyday thinking skills. The pathophysiology, assessment, and treatment of TBI-related cognitive problems are also discussed.
Keywords
Traumatic brain injury
mTBI
Concussion
Executive functioning
Neuropsychological assessment
Key points
• Cognitive deficits are a common consequence of acute traumatic brain injury (TBI), even at the lowest level of injury severity: concussion and mild TBI (mTBI). Approximately 65% of patients with moderate to severe TBI report long-term problems with cognitive functioning, and as many as 15% of patients with mTBI have persistent problems, which often include cognitive deficits.
• Deficit leads to disability when it interferes with patients’ functional status (ie, their ability to perform their usual preinjury activities). Cognitive dysfunction is the leading cause of TBI-related disability, which affects approximately 43% of moderate to severe patients.
• Frontal lobe regions and their related circuitry are particularly vulnerable to TBI pathophysiology; and hence, executive deficits are common.
• Evaluation of cognitive functions should be routine in the assessment and treatment of postacute TBI. Referral to a neuropsychologist can provide a thorough profile of an individual patient’s cognitive strengths and weaknesses, which may aid in setting goals for treatment, career and education planning, or provide information about independent functioning.
• Cognitive rehabilitation therapy (CRT) is a safe treatment option for patients with TBI with cognitive deficits; however, more methodologically rigorous research is needed to demonstrate its efficacy and identify which patients are most likely to respond.
Introduction
Traumatic brain injury (TBI) has a profound effect on injured individuals and their families. Cognitive deficits caused by TBI interfere with work, relationships, leisure, and activities of daily living, exacting a personal and economic cost that is difficult to quantify.
Abbreviations
| TBI | Traumatic brain injury |
| PTA | Posttraumatic amnesia |
| mTBI | Mild traumatic brain injury |
| DAI | Diffuse axonal injury |
| DLPFC | Dorsolateral prefrontal cortex |
| DTI | Diffusion tensor imaging |
| FITBIR | Federal Interagency Traumatic Brain Injury Research |
| NIH | National Institutes of Health |
| CDEs | Common data elements |
| CRT | Cognitive rehabilitation therapy |
| GMT | Goal Management Training |
| IOM | Institute of Medicine |
The cognitive sequelae of TBI are determined by a number of injury-related variables, including TBI severity, complications, concomitant injuries to other body regions, and chronicity of the injury. Patient characteristics, such as age, preinjury neuropsychiatric status, and genotype also play a role. In addition, cognitive recovery from TBI also can be moderated by the quality of the postacute environment.
In this article, we review the cognitive sequelae of closed head injury in adults, with a focus on deficits of executive function and everyday decision making. Although animal models have made valuable contributions to knowledge of TBI, we focus on human studies for the sake of clinical relevance. First, we review the epidemiology and nature of cognitive changes following TBI. We also discuss the pathophysiology of TBI-related cognitive deficits, and review clinical assessment and treatment options.
Epidemiology of cognitive dysfunction following TBI
Short-Term Cognitive Impairment
Impaired consciousness and posttraumatic amnesia (PTA) are neurobehavioral hallmarks of acute TBI. According to consensus definitions, moderate and severe TBI are characterized by loss of consciousness for longer than 30 minutes and/or PTA persisting for at least 24 hours. PTA is the transitory period of disorientation, confusion, and amnesia following TBI which leaves a gap in memory. Patients in PTA also commonly experience disturbed sleep-wake cycle, decreased daytime arousal, agitation, affective lability, and perceptual disturbance.1 In PTA, gross fluctuations in the severity of cognitive and behavioral symptoms are common. During this acute confusional state, patients require supervision at the mild end of the spectrum and hospitalization at the moderate to severe end of the spectrum. Contrastingly, mild TBI (mTBI) may occur with or without loss of consciousness and PTA.
Recovery on clinical outcome measures typically occurs within several days after uncomplicated sports-related mTBI in young adults, but the clinical course can be longer in patients with other injury etiologies (eg, motor vehicle crashes), preinjury risk factors, concomitant injuries to other body regions, or age older than 50 years.
In general, cognitive deficits associated with mTBI resolve fully within 3 to 6 months in approximately 80% to 85% of patients who sustain their first mTBI without the presence of a brain lesion on computed tomography or other intracranial complication.2 Although there appears to be a subgroup of patients with mTBI with persistent cognitive complaints,3,4 the precise prevalence and etiology of these sequelae remain unclear. Data from a recent, prospective cohort study suggest that approximately one-third of patients with mTBI continue to experience functional impairment (Glasgow Outcome Scale-Extended score ≤6) 3 months postinjury.5
Moderate and severe TBI are associated with more severe and persistent cognitive deficits, which can involve cognitive domains typically preserved in mild TBI, such as awareness, reasoning, language, visuospatial processing, and general intelligence.
Long-Term Cognitive Impairment
As many as 65% of patients with moderate to severe TBI report long-term problems with cognitive functioning.6 Cognitive deficits cause disability when they interfere with a patient’s ability to perform their usual roles at work or home. Epidemiologic research indicates that about 43% of moderate and severe TBI patients experience disability over periods of 6 months or longer, characterized by functional limitations, postinjury symptoms that limit activities, cognitive complaints, and/or mental health problems.7 Nearly a quarter of patients with moderate to severe TBI fail to return to work in the year following their injury.6 At their most extreme, TBI-related cognitive deficits can impair a patient’s ability to perform activities of daily living, such as driving, meal preparation, and handling money. Although TBI can cause sensory and motor deficits, cognitive and behavioral changes are more closely associated with long-term disability.8
In general, the relationship between acute TBI severity and cognitive sequelae is approximately linear, with longer duration of impaired consciousness predicting greater extent of cognitive dysfunction.9 However, heterogeneity in TBI pathology and patient characteristics also influence cognitive outcomes, complicating prediction of recovery. The cognitive domains that are most often affected by mild to moderate TBI include memory, attention, processing speed, and executive functioning and are mostly resolved within 3 to 6 months of injury.2,10–12 However, it is possible that cognitive dysfunction in a subgroup of individuals is poorly characterized by effect-size estimates based on aggregate data.13 Moderate to severe TBI is also associated with deficits in memory, attention, processing speed, and executive functioning, and additionally involves functions such as communication, visuospatial processing, intellectual ability, and awareness of deficit.14–16
Cognitive recovery after moderate to severe TBI has a steep trajectory in the first year followed by...
| Erscheint lt. Verlag | 28.3.2014 |
|---|---|
| Sprache | englisch |
| Themenwelt | Medizin / Pharmazie ► Gesundheitsfachberufe |
| Medizin / Pharmazie ► Medizinische Fachgebiete ► Neurologie | |
| Medizin / Pharmazie ► Medizinische Fachgebiete ► Psychiatrie / Psychotherapie | |
| ISBN-10 | 0-323-28719-0 / 0323287190 |
| ISBN-13 | 978-0-323-28719-7 / 9780323287197 |
| Haben Sie eine Frage zum Produkt? |
PDF (Adobe DRM)Größe: 2,1 MB
Kopierschutz: Adobe-DRM
Adobe-DRM ist ein Kopierschutz, der das eBook vor Mißbrauch schützen soll. Dabei wird das eBook bereits beim Download auf Ihre persönliche Adobe-ID autorisiert. Lesen können Sie das eBook dann nur auf den Geräten, welche ebenfalls auf Ihre Adobe-ID registriert sind.
Details zum Adobe-DRM
Dateiformat: PDF (Portable Document Format)
Mit einem festen Seitenlayout eignet sich die PDF besonders für Fachbücher mit Spalten, Tabellen und Abbildungen. Eine PDF kann auf fast allen Geräten angezeigt werden, ist aber für kleine Displays (Smartphone, eReader) nur eingeschränkt geeignet.
Systemvoraussetzungen:
PC/Mac: Mit einem PC oder Mac können Sie dieses eBook lesen. Sie benötigen eine
eReader: Dieses eBook kann mit (fast) allen eBook-Readern gelesen werden. Mit dem amazon-Kindle ist es aber nicht kompatibel.
Smartphone/Tablet: Egal ob Apple oder Android, dieses eBook können Sie lesen. Sie benötigen eine
Geräteliste und zusätzliche Hinweise
Buying eBooks from abroad
For tax law reasons we can sell eBooks just within Germany and Switzerland. Regrettably we cannot fulfill eBook-orders from other countries.
EPUB (Adobe DRM)Kopierschutz: Adobe-DRM
Adobe-DRM ist ein Kopierschutz, der das eBook vor Mißbrauch schützen soll. Dabei wird das eBook bereits beim Download auf Ihre persönliche Adobe-ID autorisiert. Lesen können Sie das eBook dann nur auf den Geräten, welche ebenfalls auf Ihre Adobe-ID registriert sind.
Details zum Adobe-DRM
Dateiformat: EPUB (Electronic Publication)
EPUB ist ein offener Standard für eBooks und eignet sich besonders zur Darstellung von Belletristik und Sachbüchern. Der Fließtext wird dynamisch an die Display- und Schriftgröße angepasst. Auch für mobile Lesegeräte ist EPUB daher gut geeignet.
Systemvoraussetzungen:
PC/Mac: Mit einem PC oder Mac können Sie dieses eBook lesen. Sie benötigen eine
eReader: Dieses eBook kann mit (fast) allen eBook-Readern gelesen werden. Mit dem amazon-Kindle ist es aber nicht kompatibel.
Smartphone/Tablet: Egal ob Apple oder Android, dieses eBook können Sie lesen. Sie benötigen eine
Geräteliste und zusätzliche Hinweise
Buying eBooks from abroad
For tax law reasons we can sell eBooks just within Germany and Switzerland. Regrettably we cannot fulfill eBook-orders from other countries.
aus dem Bereich
