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Chapter 9. Delirium and Posttraumatic Confusion

Paula T. Trzepacz, M.D.; Jacob Kean, Ph.D.; Richard E. Kennedy, M.D., Ph.D.
DOI: 10.1176/appi.books.9781585624201.674873

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Excerpt

Posttraumatic amnesia (PTA) is a term coined by British neurologists William Ritchie Russell and Charles Symonds in the early 20th century to describe the period of impaired consciousness following traumatic brain injury (TBI). Symonds (1937) and Russell (1932) described a broad range of cognitive and neurobehavioral symptoms in TBI survivors during early recovery and acknowledged that the outstanding feature of this period was impairment of consciousness, but they argued that consciousness could not be practically defined and measured and that the return of consciousness following TBI coincided with return of memory. Therefore, PTA was proposed as a proxy measure for the duration of impaired consciousness and operationalized by them as the time when the patient "was fully oriented and able to answer questions intelligently" (Russell 1932, p. 553). Although Symonds and Russell suggested PTA as a proxy measure for a broader syndrome, the influence of their work has led medical and allied health professionals working in the TBI care continuum to focus solely on the duration of orientation and memory impairments and ignore the range and depth of the syndrome, and in so doing lose the essence of PTA as a proxy measure for a broader construct. PTA is a relatively robust predictor of injury severity and outcome (Brown 2005; Ellenberg et al. 1996; Katz and Alexander 1994; Nakase-Richardson et al. 2009), and the mistaken elevation of PTA from proxy measure to construct in the brain injury literature is perhaps attributable to lack of progress in developing better measures of injury severity and indicators of prognosis. Recent investigation in neurorehabilitation demonstrates that valuing only the duration of acute orientation and memory impairments represents a significant oversight. Stuss et al. (1999) found an ordered pattern of recovery of cognitive functions following TBI such that inattention, disorientation, or both cleared before memory deficits, suggesting that the representative symptoms extended beyond orientation and amnesia and that amnesia can be a persistent symptom beyond the confusional period. Similarly, Nakase-Thompson et al. (2004) studied patients after TBI during acute rehabilitation, using a broad set of measures, including the Delirium Rating Scale (DRS), the Galveston Orientation and Amnesia Test (GOAT), the Agitated Behavior Scale (ABS), and the Cognitive Test for Delirium (CTD), and found a broad range of impairments. These authors noted that "traditional measures of PTA do not fully capture the wide array of symptoms defining this early stage of recovery" (p. 140) and that "acute confusion is common and has a complex neurobehavioral presentation that is not adequately captured with traditional PTA measures alone" (p. 140). Kalmar et al. (2008) used a brief formal neuropsychological battery to assess patients in PTA and documented abnormalities in a wide range of cognitive domains, including attention, processing speed, cognitive flexibility, verbal fluency, executive functioning, naming, perceptual-motor ability, reading, verbal recall, and orientation. Sherer et al. (2009) found that psychotic-type symptoms, decreased daytime arousal, and nighttime sleep disturbance were the earliest resolving symptoms, whereas fluctuation and cognitive impairment were the most persistent. Together, these studies show the construct to be broader than orientation and amnesia, consistent with the clinical descriptions and definitions throughout the study of TBI and suggest a temporal pattern of recovery.

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Figure 9–1. Comparing rehabilitation and neuropsychiatric terminology for post–traumatic brain injury (TBI) changes in consciousness and cognition.Posttraumatic amnesia (PTA) is a commonly used term that may overlap with delirium depending on the use by researchers and clinicians, whereas posttraumatic confusion is comparable to delirium. Posttraumatic agitation is not synonymous with delirium and can occur at different stages of TBI recovery; many patients have motor retardation, and not agitation, that can be inadequately recognized. aSome older studies included coma and stupor in PTA. Posttraumatic amnesia is defined as duration of return of new memory and not by broad symptom severity.

Figure 9–2. Terminology for post–traumatic brain injury (TBI) impaired consciousness over time.The terms posttraumatic amnesia, posttraumatic confusion, and delirium have been applied to patients in acute recovery following TBI. All three terms continue to be used, but a growing number of rehabilitation specialists are recognizing the value of capturing the breadth of symptoms as defined in delirium.

Figure 9–3. Schematic representation of the interrelationships among posttraumatic delirium, posttraumatic amnesia, posttraumatic confusion, and posttraumatic agitation.The circles are representational of the overlap across disorders. Delirium is essentially synonymous with posttraumatic confusional state (PTCS), a recently applied term to replace posttraumatic amnesia. Minor differences between delirium and PTCS reflect small differences in incidence as detected by different instruments. Delirium is the recommended term because of its use across specialties of medicine and to enhance awareness that multiple etiologies besides trauma can contribute to delirium in patients with traumatic brain injury.

Figure 9–4. Traumatic brain injury pathology and confusion.Three types of brain injury can each result in delirium (confusion), which commonly occurs following emergence from coma or minimal conscious state. Diffuse axonal injury alone or in combination with focal injuries can lead to delirium; when these are combined with hypoxic/ischemic damage, the resultant delirium can be especially prolonged.Source. Adapted from Katz 1992; Katz and Alexander 1994; Povlishock and Katz 2005.

Figure 9–5. Neurobiological phases of acute recovery following traumatic brain injury.Numerous alterations of brain function and structure, especially at the cellular level, occur immediately at the time of brain injury. The severity of these alterations depends on whether the injury is mild, moderate, or severe. Within hours to days these changes evolve and also induce consequences that impair the normal electrochemical and neural network functioning of the brain. Cortical and thalamic impaired function result in delirium. Ach = acetylcholine; APP = amyloid precursor protein; ATP = adenosine triphosphate; A = amyloid beta; EEG = electroencephalogram.
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Table 9–1. Comparison of DSM-IV-TR criteria for delirium with Lipowski's and Stuss's descriptions
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Table 9–2. Delirium symptoms and characteristics
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Table 9–3. Frequency of positive symptoms on the Delirium Rating Scale–Revised-98 (DRS-R98) and percentage still with posttraumatic amnesia for the study sample (N = 171)
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Table 9–4. Etiologies for delirium in any population that indirectly or directly affect the brain
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Table 9–5. Common causes of delirium in patients with traumatic brain injury
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Table 9–6. Risk factors predisposing to delirium
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Table 9–7. Instruments and scale content used to assess acute recovery period in patients with traumatic brain injury
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Table 9–8. Environmental manipulations in the treatment of delirium

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