Defining Delirium in Traumatic Brain Injury
Delirium is a neuropsychiatric disorder composed of dif-fuse cognitive deficits, language and thought abnormali-ties, psychomotor and affective changes, and sleep-wake cycle disturbances. It is caused by a wide variety of medi-cal, pharmacologimedi-cal, and postoperative conditions.
Approximately 18% of general hospital patients are delir-ious (Trzepacz et al. 2002), and delirium point prevalence ranges from 10%–30% in general hospital patients (Fann 2000). Some surgical populations have an even higher incidence of delirium—approximately 30% in postcar-diotomy patients (Smith and Dimsdale 1989) and as much as 50% in elderly hip surgery patients (Williams et al.
1985). The incidence of delirium after traumatic brain injury (TBI) is uncertain because of classification issues in the TBI literature, but appears to be high, especially with severe injuries and loss of consciousness (LOC). How-ever, brief confusional periods occur after minor concus-sions (Lipowski 1990; Teasdale and Jennett 1974) and
“disturbed consciousness is a feature found in most cases of head injury” (Russell and Smith 1961).
The term delirium is not commonly used in TBI liter-ature, although there is a growing appreciation that a con-fusional state occurs and includes more than just memory and orientation deficits (Sandel et al. 1995; Yuen and Benzing 1996). Terms such as states of impaired conscious-ness, posttraumatic amnesia (PTA), posttraumatic agitation, posttraumatic disorientation, posttraumatic confusional state,
altered consciousness, and loss of consciousness (coma) are used, often without clear definitions of signs and symptoms or, when defined, without a clear consensus regarding usage or practical assessment (Fortuny et al. 1980; Gronwall and Wrightson 1980; Sandel et al. 1995; Stuss et al. 1999;
Tate et al. 2000). The varying definitions and criteria make a review of delirium after TBI difficult and interpre-tation of research on PTA confusing. In psychiatric nosol-ogy, delirium and amnesia are not the same, the former being made up of impairment of attention, memory, ori-entation, and visuoconstructional ability in addition to many other noncognitive symptoms, whereas the latter involves only memory impairment. However, the term posttraumatic amnesia is not used by nonpsychiatrists solely to denote memory impairment after a TBI event.
The closest term to delirium that is widely used in the TBI literature is posttraumatic amnesia; however, this is loosely used and may encompass coma at one extreme or only focal memory deficits at the other and overlaps with a number of neuropsychiatric terms applied to those dif-ferent clinical stages (Figure 9–1). However, definitions of PTA found in most of the TBI literature overlap signif-icantly with what psychiatrists would call delirium followed by an amnestic disorder. Posttraumatic amnesia was defined as the “time elapsed from injury until recovery of full con-sciousness and the return of ongoing memory” (Grant and Alves 1987). Posttraumatic amnesia also has been de-fined as “a period of clouded consciousness which pre-cedes the attainment of full orientation and continuous awareness in persons recovering from head injuries” and as “characterized primarily by a failure of amnestic pro-cesses” (Mandleberg 1975). Thus, PTA overlaps with
coma, stupor, delirium, and amnestic syndrome. How-ever, Ommaya and Gennarelli (1974) defined delirium (“confusion”) as a separate state from either coma or am-nesia in patients with TBI and specified the expected tem-poral relationship between them (Figure 9–2). This para-digm has not been well integrated into the TBI literature, however. Katz (1992) also recognized the confusional state embedded in PTA. Thus, posttraumatic confusional state would be a more accurate term to denote delirium (Stuss et al. 1999).
Delirium resulting from any cause is an abnormal state of consciousness that exists on a continuum between stupor or coma and normal consciousness (Figure 9–3).
However, patients often progress directly from coma into delirium without a clearly defined stupor stage. The placement of a particular delirious episode along this con-tinuum depends on the severity of that delirium. Subclin-ical delirium describes a phase before or during the reso-lution of an episode of diagnosable delirium that is less severe and detectable only by more subtle examination of F I G U R E 9 – 1 . Comparing physiatric and neuropsychiatric terminology for post–traumatic brain injury (TBI) changes in level of consciousness and cognition.
Posttraumatic amnesia (PTA) is a term used in the TBI literature. PTA overlaps with many of the symptoms of delirium, although the term also is used to denote the phase after the resolution of delirium (confusion) when more isolated cognitive impairment (usually memory deficits) persists without other behavioral symptoms. At times, stupor is included in the definition of PTA, whereas stupor is distinct from delirium in neuropsychiatric terminology. When agitation is accompanied by other neuropsychiatric symptoms, posttraumatic agitation overlaps with the hyperactive variant of delirium, but agitation can also occur as an isolated symptom.
*Some older studies included coma and stupor in PTA.
F I G U R E 9 – 2 . Temporal relationships of coma, confusion, and posttraumatic amnesia (PTA) after traumatic brain injury.
Coma and levels of confusion (delirium) after traumatic brain injury, with PTA occurring after resolution of delirium and in the context of normal consciousness, according to Ommaya and Gennarelli (1974). This model differentiates PTA from delirium states.
Source. Reprinted from Ommaya AK, Gennarelli TA: “Cerebral Concussion and Traumatic Unconsciousness.” Brain 97:633–654, 1974. Used with permission of Oxford University Press.
Confusion Confusion
Confusion + amnesia Coma (paralytic)
Coma
Death
Persistent vegetative state Impact
or impulse
Shear strains
Confusion amnesia+
Normal consciousness without amnesia
Confusion amnesia+
Normal consciousness with PTA only
Normal consciousness with PTA plus RGA
I II
III IV
V VI
the patient. This is an important concept in TBI because of the need to distinguish lingering amnestic deficits after a resolved delirium from a subclinical delirium that in-volves more diffuse cognitive deficits accompanied by other behavioral symptoms. Often, these other psychiat-ric symptoms are not evaluated in patients with TBI in whom clinicians and researchers focus more on cogni-tion—especially orientation, attention, and memory (see the section Rating Scales).
Additionally, delirium can have hypoactive, hyperac-tive, or mixed motoric presentations that may be subtypes of delirium (Meagher and Trzepacz 2000). These differ-ing motor presentations are often accompanied by other behavioral symptoms, such as yelling, punching, and mood lability in hyperactive delirious patients. The term posttraumatic agitation overlaps with the hyperactive sub-type of delirium, but because agitation can be either an isolated symptom or associated with other psychiatric and medical conditions besides delirium, delirium and agita-tion are not synonymous in patients with TBI. Fugate et al. (1997a, 1997b) surveyed by telephone 157 United States physiatrists for their understanding of symptoms of agitation and delirium during the acute recovery phase af-ter TBI. Although there was some overlap in symptoms, they did not appreciate use of the term delirium from DSM-III-R symptoms (American Psychiatric Association 1987), although they did associate disorientation, amne-sia, and memory impairment with agitation during acute recovery. Symptoms of disorganized thinking, perceptual disturbance, disorientation and disturbed sleep-wake cy-cle were associated with “delirium.”
There are few studies of the relationships between various signs and symptoms common to delirium and other posttraumatic sequelae. Tate et al. (2000), in a study of severely brain-injured patients, found that disorienta-tion resolved before amnesia in 94% of TBI cases, which supports the idea that a confusional (delirium) phase pre-cedes an amnestic phase. Both disorientation and amnesia occur in delirium, so as TBI delirium resolves, disorienta-tion would be expected to improve, whereas some form of memory impairment could persist depending on the
trauma-related lesion locations (often frontotemporal).
Similar results can occur after mild injury; one study showed only 38% of patients to be well oriented during PTA (Gronwall and Wrightson 1980). A study of behav-ioral disturbances after TBI showed that restlessness and agitation resolved in all patients before the resolution of PTA (van der Naalt et al. 2000), which suggests that the delirium phase includes motoric disturbance. Corrigan et al. (1992) reported that agitation and cognition showed 50% shared variance, with most of this shared variance accounted for by attention. Attentional disturbance is the cardinal feature of delirium and a required criterion for diagnosis. However, all of the variance explained by cog-nition could not be accounted for by agitation, or vice versa, suggesting that not all delirium patients are hyper-active and not all agitated TBI patients have confusional states. Ewert et al. (1989) studied types of memory im-pairment during PTA and found that during the confu-sional phase both procedural and declarative memory were impaired, but as confusion resolved the procedural memory deficits resolved before the declarative ones.
Our own findings from our prospective TBI delirium study at the Traumatic Brain Injury Model Systems in Mississippi are consistent with previous studies (Nakase-Thompson et al. 2004). Forty consecutive patients rated as Rancho Los Amigos Cognitive Scale level IV or better during inpatient rehabilitation hospitalization were pro-spectively evaluated using both neuropsychiatric and re-habilitation rating instruments. All subjects were rated on the Delirium Rating Scale (DRS) and independently us-ing the Agitated Behavior Scale (ABS) and Galveston Ori-entation and Amnesia Test (GOAT). Twenty-four sub-jects met DSM-IV delirium diagnostic criteria (American Psychiatric Association 1994), whereas 26 did not. Using GOAT and ABS in a logistic regression model, the two groups were classified with 77.5% accuracy. Inspection of individual scores revealed that some subjects in the delir-ium group had scores meeting the cutoff for “normal” on the ABS (22.5%) and GOAT (7.5%), whereas some sub-jects in the nondelirious group had scores in the impaired range on the ABS (7.5%) and GOAT (27.5%). This sug-F I G U R E 9 – 3 . Delirium and continuum of levels of consciousness.
Delirium occurs on a continuum between normal consciousness and stupor and/or coma. Delirium often has a prodrome of milder symptoms, called subclinical delirium, as an intermediate state between full-blown delirium and normal consciousness; subclinical delirium also occurs during the resolution of an episode of delirium.
gests that there is significant but incomplete overlap be-tween these clinical syndromes.
Signs and Symptoms of Delirium
Delirium involves a range of cognitive deficits, differenti-ating it from other psychiatric disorders, except for advanced dementias. Attentional deficits are a hallmark to diagnose delirium in contrast to memory impairment being cardinal in dementia. Delirium cognitive impair-ments include disorientation to time, place, and person (usually impaired in that order); deficits in attention and concentration; impaired short-term memory with an inability to learn and retain new information; long-term memory impairment; impaired executive functions (e.g., abstraction, conceptualization, temporal ordering, sequencing, and mental flexibility); and impaired visuo-constructional ability (including wandering and getting lost). Such a breadth of cognitive impairment can occur after TBI depending on the severity of injury. Concussion seems to be a brief, transient mild delirium.
In addition to these cognitive deficits, delirium in-volves many other neuropsychiatric symptoms (Table 9–1). These include an alteration in mood (anxious, de-pressed, irritable, hostile), affective lability (sometimes to the proportions of pseudobulbar palsy), and mood incon-gruency. Thinking is disorganized and may be rambling, tangential, circumstantial, or even loosely associated.
Language abnormalities are variable, but can include
word-finding difficulty, paraphasias, dysnomia, dys-graphia, impaired repetition, impaired articulation, im-paired comprehension, and perseveration of words or phrases. In the most severe cases, speech resembles a flu-ent or a global aphasia. However, deficits in semantics of communication are the most characteristic language dis-turbance of delirium and serve to distinguish it from the language abnormalities associated with other psychiatric disorders. Psychomotor behavior may evidence retarda-tion or agitaretarda-tion, often mixed together (related concepts are the motor subtypes of delirium, called hypoactive or hy-peractive); patients may appear depressed and withdrawn, or may be agitated and remove intravenous lines, or may wander or pace around. Hypoactive delirium is com-monly misdiagnosed as depression. Perceptual distur-bances are common and may take the form of either illu-sions or hallucinations; visual (and occasionally tactile) hallucinations strongly suggest delirium, though auditory hallucinations or illusions also occur in delirium. Suspi-ciousness and persecutory delusions are common, but the latter usually are poorly formed and not well system-atized, often incorporating many of the caregivers into the delusional ideation. Patients may refuse tests because of suspiciousness, thus interfering with their own medical care. The sleep-wake cycle is disrupted and fragmented throughout the 24-hour period, with napping and noc-turnal arousals that are often accompanied by nocnoc-turnal confusion and an inability to distinguish nightmares or dreams from reality. In the extreme, delirious patients may have severe sleeplessness.
These symptoms of delirium typically wax and wane in severity to some degree during a 24-hour period, with phases of increased lucidity alternating with more severe impairment. This waxing and waning makes it more dif-ficult to assess the severity of delirium for short time frames and complicates determining exactly when the ep-isode has ended. DSM-IV-TR criteria (American Psychi-atric Association 2000) for diagnosing delirium require disturbance of consciousness and/or attentional deficits, as well as a change in memory, language, orientation, or perceptual disturbances with a fairly abrupt onset and a fluctuating course, and physical factors that can be impli-cated as causative (Table 9–2).
Descriptions of the clinical symptoms of PTA covering the period after emergence from coma until the later phase of focal memory deficits are essentially descriptions of de-lirium. This is a period of “confusion, restlessness, perplex-ity, irritabilperplex-ity, aggression, withdrawal, and frank psycho-sis” (Grant and Alves 1987) and of “restlessness, agitation, combativeness, confusion, hallucinations and other dis-turbed perceptions, disorientation, depression, paranoid ideation, hypomania, and confabulation” (Fisher 1985).
T A B L E 9 – 1 . Delirium symptoms and characteristics
Disorientation (time, place, person) Attentional deficits
Memory impairment (short and long term) Deficits in higher-order thinking
Visuoconstructional dysfunction Change in mood/affective lability Disorganized thinking
Delusions (distinguish from confabulation) Perceptual disturbances
Language impairments Psychomotor behavior changes Sleep-wake cycle disturbances Abrupt onset
Fluctuating course Usually reversible