should compare the patient’s performance on neuropsy-chological measures to his or her ability to function in ev-eryday activities. For example, a patient who performs in the severely impaired range on neuropsychological test-ing yet continues to perform well in graduate-level coursework is demonstrating an inconsistency between his test performance and academic functioning. Obvi-ously, this disparity suggests suboptimal effort on testing.
Last, when assessing for malingering it is important to keep in mind that some patients may appear to be malin-gering but are not. A variety of factors can influence neu-ropsychological test performance (e.g., psychiatric disor-ders such as depression, poor rapport with the evaluator, uncooperativeness, and the context in which the evalua-tion is conducted) (Franzen and Iverson 1997). Franzen and Iverson (1997) stated that when assessing for malin-gering “It is important to remember that these test instru-ments evaluate the likelihood of nonoptimal perfor-mance, not malingering itself. As such, the specific assessment instruments provide information about biased responding, that is, information about the probability that variables other than skill level have adversely affected the level of effort” (p. 396).
Neuropsychological Screening Instruments
Time constraints, patient fatigue or noncompliance, and lack of health insurance and financial restrictions may necessitate the administration of a screening battery rather than a full neuropsychological evaluation. How-ever, although the advantages of neuropsychological screening are cost-effectiveness and short administration time, this approach has limited value in making differen-tial diagnoses. For example, the Mini-Mental State Examination (MMSE) is useful in determining the pres-ence or abspres-ence of dementia, but it is not useful for dif-ferentiating Alzheimer’s disease from other types of dementia. Additionally, screening devices are limited in their ability to discriminate mild head injury, and they do not provide specific information about rehabilitation needs (e.g., memory retraining) and individual strengths and weaknesses (e.g., impaired auditory memory but intact visual memory). Some examples of screening instruments are
• Mini-Mental State Examination (Folstein et al. 1975)
• Repeatable Battery for the Assessment of Neuropsy-chological Status (Randolph 1998)
• Neurobehavioral Cognitive Status Examination (Kier-nan et al. 2001)
• Shipley Institute of Living Scale (Revised Manual) (Zachary 1986)
• BNI Screen for Higher Cerebral Functions (Priga-tano 1991)
The MMSE is a well-known screening instrument that is brief and easy to administer. The MMSE is most useful for moderate to severe impairment in dementia pa-tients. However, its sensitivity and specificity decline with other patient populations, particularly those with mild cognitive impairment, focal neurological deficits, and psychiatric disorders (Spreen and Strauss 1998).
The Repeatable Battery for the Assessment of Neu-ropsychological Status (Randolph 1998) is a relatively new cognitive screening instrument that takes less than 30 minutes to administer and provides a total scale score and five specific cognitive ability index scores. It was de-signed for the dual purpose of identifying and character-izing abnormal cognitive decline in the older adult and as a neuropsychological screening battery for younger pa-tients (Randolph et al. 1998). It has also been found to be particularly useful in evaluating neuropsychological change in patients with schizophrenia (Wilk et al. 2002).
Differential Diagnosis of TBI From
pat-tern of neuropsychological test scores. This method is based on the assumption that cognitive processes such as basic reading skills and vocabulary tend to be less affected by TBI than other skill areas. A few tests that are consid-ered to be relatively resistant to neurological impairment are the Vocabulary, Information, Picture Completion, and Object Assembly subtests from the WAIS—Revised (Vanderploeg 1994a; Wechsler 1981) and WAIS-III (Wechsler 1997a). These have traditionally been known as “hold” tests and have been considered to be relatively unaffected by TBI. However, caution is advised when im-plementing this method because the traditional “hold”
tests can indeed be influenced by different types of brain injury, particularly if it is of a focal nature. For example, patients with aphasia would obviously perform poorly on the Vocabulary and Information subtests. Reading skill, as mentioned previously, is also considered to be resistant to TBI, and, as a result, basic word reading tests, such as the North American Adult Reading Test, are frequently used for premorbid estimates. Another common method for estimating premorbid functioning is the use of demo-graphic variable methods. This is based on the premise that certain demographic variables such as social class and education are correlated with scores on intelligence tests (Franzen 2000). In general, most clinicians use a combi-nation of methods and measures to predict premorbid functioning.
Depression
Depression can interfere with the normal expression of cognitive abilities and can also cloud the diagnostic picture in an individual who has had a TBI. Depressed patients who have not had a TBI may demonstrate cognitive diffi-culties such as slowed mental processing, psychomotor retardation, mild attentional deficits, decreased drive and initiation, and impairments in short-term recall and learn-ing for verbal and visuospatial material. Cognitive impair-ment is most frequently encountered in the areas of atten-tion, specific aspects of memory, and psychomotor speed.
Impairment in language, perception, and spatial abilities tends to be secondary to poor attention, motivation, or organizational abilities (Mayberg et al. 1997).
A large body of research on depressed patients has fo-cused on memory processes. In attempting to differenti-ate the neurocognitive effects of depression from TBI, there are certain key factors that should be considered.
Neuropsychological testing of patients diagnosed with depression reveals that the “memory deficit” is often ex-pressed in free-recall retrieval errors rather than as a def-icit in actually learning the information. As a result, the patient requires a cue or recognition stimulus for the
memory to become available for recall (Lezak 1995).
This can be evaluated by tests such as the CVLT (Delis et al. 1987) that assess the ability to learn across trials as well as the patient’s ability to benefit from semantic cues and recognition.
Differential diagnosis of the cognitive consequences of depression versus TBI is often clouded by the comor-bidity of depressed mood with TBI. A review by Busch and Alpern (1998) suggests that the prevalence of depres-sion after mild TBI is at least 35%. A careful and thor-ough history addressing the patient’s premorbid cognitive and emotional functioning is essential in attempting to understand the contribution of both disorders. Examin-ing the pattern of the patient’s performance on neuropsy-chological testing (e.g., learning vs. retrieval) is helpful, as well as qualitatively looking at individual subtest scores and performance. For example, if given extra time and en-couragement, many depressed patients perform ade-quately. Memory disturbances in depressed patients are likely the result of attention and concentration difficulties typically associated with depression, whereas patients with TBI may have a more consistent pattern across the tests designed to assess memory. Assessing the rate of for-getting of information from immediate recall to a delayed recall is one method that can contribute to the differential diagnosis.
Anxiety
Anxiety can interfere with the patient’s ability to attend to, learn, and remember new information and therefore can be similar to the pattern of deficits seen after mild TBI. The experience of anxiety is also common during the neuropsychological evaluation process and may relate to performance anxiety or general frustration on the part of the patient. It is therefore important for the clinician to create an atmosphere that reduces the normal anxiety that a patient might feel when undergoing the evaluation pro-cess. Patients with a history of anxiety disorders can have particular difficulty in participating in formal neuropsy-chological assessment and may manifest mental efficiency problems such as slowing, scrambled or blocked thoughts and words, memory failure, and increased distractibility (Lezak 1995). Additionally, patients who are anxious about appearing “stupid” may respond with “I don’t know” rather than providing their best response to a par-ticular question. Encouraging patients to make their best guess and trying to optimize their effort is essential to obtaining a valid neuropsychological profile. In addition to performance-related anxieties that can occur during the evaluation, there are specific anxiety disorders that are likely to be more prevalent among the TBI population.
Posttraumatic Stress Disorder
Posttraumatic stress disorder (PTSD) is common after TBI, and many patients with mild TBI vividly recall and are distressed by the details of their injury. Additionally, there is symptom overlap between postconcussion syn-drome and PTSD (Cummings et al. 1995). In general, postconcussive symptoms tend to decrease or remit within 3–6 months, whereas the course and duration of PTSD may be much longer (Evans 2000; Silver et al.
1997). Similar symptoms include, but are not limited to, amnesia for certain aspects of the traumatic event, diffi-culty concentrating, somatic complaints (headache, dizzi-ness, fatigue, insomnia), perceptual symptoms (sensitivity to noise and light), and irritability (American Psychiatric Association 2000; Silver et al. 1997). Although much of the research on TBI and PTSD focuses on mild head injury, there is evidence to suggest that PTSD can develop after severe TBI even with impaired conscious-ness during the trauma and a relative absence of traumatic memories of the event (Bryant et al. 2000; Harvey et al.
2003).
Turnbull et al. (2001) investigated whether memory loss of the injury event and whether the type of memory (e.g., traumatic or nontraumatic) influence the develop-ment of PTSD symptoms. Subjects were divided into three groups on the basis of memory of the injury event:
those with no memory of the injury event, those who re-membered the injury but had nontraumatic memory of the event, and those who had a traumatic memory of the injury event. The results of this research indicated that patients with no memory of the injury and patients with memories that are traumatic reported higher levels of psychological distress than the group without traumatic memories. However, ratings of PTSD symptoms were less severe in the “no memory” group as compared to those with traumatic memories of the event. Thus, they found that amnesia did not protect against PTSD but does protect against the severity and presence of specific intrusive symptoms. Feinstein et al. (2002) addressed the relationship between the length of posttraumatic amnesia and symptoms of PTSD after TBI. They found that pa-tients with brief posttraumatic amnesia (<1 hour) are more likely to experience a PTSD reaction than those with longer posttraumatic amnesia (>1 hour). Mayou et al. (2000) examined the relationship between uncon-sciousness, amnesia, and psychiatric symptoms after road traffic accidents. In general, their results suggested that PTSD, anxiety, and depression were more common at 3 months in those patients who had documented uncon-sciousness than in patients who had no loss of conscious-ness. However, at 1-year follow-up there were no
differ-ences between the two groups. They found clear evidence that PTSD is at least as common in those who experience brief unconsciousness as in those who were not uncon-scious. Explanations for the onset of PTSD in patients with posttraumatic amnesia are that the intrusive memo-ries may relate to events before or after the period of am-nesia, and there may be islands of preserved memory (Parker 1996). It has also been suggested that there are implicit memories that result in “intensive psychological distress on exposure to internal or external cues that sym-bolize or resemble an aspect of the traumatic event” (Bry-ant et al. 2000).
In terms of treatment for PTSD symptoms, Bryant et al. (2003) found that brief cognitive behavioral therapy provided early (2 weeks postinjury) to patients with mild brain injury was more effective than supportive counsel-ing for treatment of acute stress disorder as well as for prevention of PTSD symptoms at 6-month follow-up.
Obsessive-Compulsive Disorder
Obsessive-compulsive–like behaviors can occur after TBI. These behaviors frequently evolve when mental inefficiency, such as the attentional deficits that are typi-cally associated with slowed processing and diffuse dam-age, is the prominent feature (Lezak et al. 1990). Rigidity in thinking and perseverative tendencies can be evidenced on some of the tests typically used to assess executive functioning such as the WCST. Perseveration can also be detected across different subtests (e.g., carrying aspects of one subtest into the next subtest). Socially, these patients may act inappropriately and be disruptive due to failing to respond to social cues (Stringer 1996). Patients who are perseverative may repeat a task in a stereotyped manner or may have difficulty switching topics during a conversa-tion and appear to repeat themselves. They can also appear hypervigilant (Stern and Prohaska 1996).
Schizophrenia
Using neuropsychological testing to differentiate the cognitive sequelae of schizophrenia from TBI is difficult, given that patients with schizophrenia often demonstrate impairment on formal neuropsychological testing (Cros-son 1994). It has been suggested that at least in some cases of schizophrenia the disorder may be the result of earlier cerebral insult rather than being merely an expression of the disease entity. This hypothesis is based on the high incidence of premorbid neurological disorders such as head injury, perinatal complications, and childhood ill-nesses in patients with schizophrenia (Lezak 1995; McAl-lister 1998).
Neuropsychological studies indicate that persons with schizophrenia demonstrate difficulties in attention, mo-tor behavior, speed of processing, abstraction, learning, and memory (Sackeim and Stern 1997). However, reviews of the research suggest that the deficits seen in schizo-phrenia can be broad, and no cognitive domain is entirely spared. It has also been suggested that cognitive deficits are not present in every individual at all times, and the pattern of deficits can change over time within an individ-ual (Tamminga 1997). Malloy and Duffy (1994) reviewed literature on the frontal lobes in neuropsychiatric disor-ders and found that frontal dysfunction has been linked to the negative subtype of schizophrenia on the basis of neu-ropsychological, structural and functional imaging, and electrophysiological studies. However, they state that there is controversy as to whether the results indicate dis-tinct subtypes of schizophrenic patients or predominant symptoms that occur at different stages of the schizo-phrenic process in the same patient. A study by Sachdev et al. (2001) compared patients with TBI who developed schizophrenia-like psychosis (SLP) after their injury and patients with TBI who did not develop SLP. Their results indicated that the patients with TBI who developed SLP had a mean age at onset of 26.3 years, a mean latency of 54.7 months after the head injury, and usually a gradual onset and a subacute or chronic course. They also found that prodromal symptoms were common as well as the presence of depression at the onset of SLP. The predom-inant features were paranoid delusions and auditory hal-lucinations. However, formal thought disorder, catatonic features, and negative symptoms were uncommon. Addi-tionally, the SLP group had more widespread brain dam-age on neuroimaging, particularly in the left temporal and right parietal regions, and was more cognitively impaired than the TBI group without SLP. Last, they found that a positive family history of psychosis and duration of loss of consciousness were the best predictors of SLP. The re-sults from the Sachdev et al. study (2001) are inconsistent with past studies (Bond 1984; Kwentus et al. 1985), which indicate that schizophrenia-like symptoms after TBI are more likely to be of the negative subtype, with flat affect, suspiciousness, and social withdrawal as opposed to posi-tive symptoms of delusions and hallucinations. The vari-ability in research findings points to the need for further research into possible subtypes of schizophrenia and course of cognitive deficits.
Attention-Deficit/Hyperactivity Disorder
Attention-deficit/hyperactivity disorder (ADHD) is a dis-order involving disturbances in attention span (e.g., poor attention to task), self-regulation (e.g., inability to
con-sider consequences of behavior), activity level (e.g., motoric overactivity), and impulse control (e.g., impul-sive behaviors) (Teeter and Semrud-Clikeman 1997).
As mentioned throughout this chapter, deficits in atten-tion are common after TBI. The diagnosis ADHD not otherwise specified can technically be used to diagnose adults with attentional deficits resulting from brain dam-age. However, this diagnosis is misleading given that ADHD is considered a developmental disorder, and some of the symptoms must be present before age 7 (Stringer 1996). During the clinical interview, it is important to as-sess for premorbid diagnosed and undiagnosed ADHD symptoms. It is useful to ask developmentally oriented questions and to seek information collaterally. This is par-ticularly important because there are commonalities in be-havioral and cognitive sequelae of TBI and ADHD, partic-ularly in response inhibition (Konrad et al. 2000). Konrad et al. (2000) compared children with TBI and children with developmental ADHD during two inhibition tasks. Addi-tionally, they divided the children with TBI, according to Actigraph data, into hypo-, hyper-, and normokinetic sub-groups. They concluded that slowing of information pro-cessing speed is a general consequence of TBI in childhood and that inhibitory deficits are associated with postinjury hypo- and hyperactivity. Specifically, hyperactive children with TBI had the same inhibitory deficit patterns as chil-dren with developmental ADHD.
Neuropsychological testing can contribute to the diag-nosis of persons with ADHD without TBI and TBI patients with a history of ADHD that predates their injury by high-lighting the cognitive strengths and weaknesses and helping to distinguish attentional disturbances from an underlying memory disorder. Because there is a high comorbidity of ADHD with learning disorders, neuropsychological testing can also diagnose the presence of learning disabilities or other deficits that may be contributing to the clinical presen-tation of the patient (Cohen and Salloway 1997).
Learning Disorders
A learning disorder involves a deficit in the acquisition and performance of certain academic skills (Popper and Steingard 1996). DSM-IV-TR (American Psychiatric Association 2000) addresses four classifications of learn-ing disorders: readlearn-ing disorder, mathematics disorder, disorder of written expression, and learning disorders not otherwise specified. Although learning disorders are usu-ally first evident in childhood, they can have major conse-quences for lifetime functioning. The cognitive effects of learning disorders can be mistaken for those of head injury (Crosson 1994), and a careful neuropsychological evaluation can assist in differentiating these two
condi-tions. This process should involve a careful education and social history as well as the review of school transcripts.
Summary
This chapter provides a summary of the role of neuropsy-chological assessment strategies in the evaluation of trau-matically brain-injured individuals. Neuropsychological testing can be a useful adjunctive tool within the neuropsy-chiatric context and can help to separate TBI from other disorders, thus guiding the treatment planning and reha-bilitation process. Neuropsychological assessment is help-ful in identifying psychosocial and neurological compo-nents of TBI and is particularly helpful with regard to differential diagnosis.
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