Psychosomatics 48:258-264, June 2007
doi: 10.1176/appi.psy.48.3.258
© 2007 Academy of Psychosomatic Medicine
Aphasia: Associated Disturbances in Affect, Behavior, and Cognition in the Setting of Speech and Language Difficulties
Szofia S. Bullain, M.D.,
Lyvia S. Chriki, B.A., and
Theodore A. Stern, M.D.
Received March 1, 2006; revised May 26, 2006; accepted June 8, 2006. From the Depts. of Neurosurgery and Psychiatry, and the Psychiatric Consultation Service, Massachusetts General Hospital, and Harvard Medical School. Send correspondence and reprint requests to Szofia S. Bullain, M.D., Massachusetts General Hospital, EDR 410, 70 Blossom St., Boston, MA 02114. e-mail: SBullain{at}Partners.org
© 2007 The Academy of Psychosomatic Medicine
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ABSTRACT
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Patients with disturbances in affect, behavior, and cognition present a variety of challenges to healthcare providers; their evaluation and treatment becomes especially problematic in the setting of speech and language difficulties. The authors present the case of a man who sustained a left-side cerebrovascular accident with aphasia and discuss the approach to his diagnosis and treatment. Moreover, since a variety of speech and language problems can arise after stroke and since patients and their treaters can become frustrated by impaired communication and diagnostic uncertainties, authors review the clinical manifestations, timing, and treatment of such conditions so that treatment can be improved.
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INTRODUCTION
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The ability to express ourselves with spoken words and writing makes us, as humans, unique. Language (which represents the formulation, transmission, and comprehension of thoughts by verbal and nonverbal symbols) and speech (which refers to the actual verbalization) do not only facilitate interpersonal interactions but are also vital for cognition.1 Therefore, when these fundamental brain functions are disrupted or lost, the result is devastating.
Aphasia is a neurological disorder that affects language functioning, most often as a consequence of stroke2 or dementing illnesses (e.g., Alzheimer’s disease) in the areas of the brain responsible for language. Moreover, aphasias may also coexist with speech disorders (e.g., dysarthria or apraxia of speech). Roughly 1 in every 275 adults, accounting for 1 million individuals in the United States, suffers from aphasia; with approximately 80,000 new cases occurring each year,3 representing more than one-third of new stroke patients.4,5 Among these patients, a variety of neuropsychiatric symptoms arise as a complication of cerebrovascular accidents (CVAs),6 but their diagnosis is often delayed by the presence of speech and language problems. Aphasia is also a source of frustration to patients, their family members, and their caregivers.
We present the case of "Mr. A," who is a composite of patients we have seen on the Psychiatric Consultation Service, to highlight the issues involved in the diagnosis and treatment of poststroke patients with speech and language difficulties who develop affective, behavioral, and cognitive disturbances.
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Case Report
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Mr. A, a 57-year-old, right-handed, stand-up comedian, suddenly developed a severe left-sided headache during a performance. He became nauseated and left the stage. Within minutes, he was unable to stand unassisted (as his right side became paretic), and he was unable to speak coherently. An ambulance was called. On arrival at the local Emergency Department, he was awake and alert, but apprehensive and slightly agitated. His vital signs revealed a heart rate of 105 bpm, a respiratory rate of 22 breaths per minute, and a blood pressure of 156/92 mmHg. Physical examination was notable for a dense right-sided hemiplegia with normal muscle tone and sensation, hyperreflexia on the right, and a positive Babinski sign. He could follow simple commands, but he was unable to produce complete sentences (in speech or writing). Even though he retained the proper usage of nouns and verbs, he searched for words and could not produce more than 10 to 15 words per minute. His ability to understand spoken words was impaired, and he expended enormous effort to express himself. Although Mr. A was frustrated, he cooperated with physical and laboratory examinations. The remainder of his physical examination revealed bilateral carotid bruits; it was otherwise unremarkable. A noncontrast CT scan of the head, obtained within 2 hours after the onset of symptoms, revealed an ischemic stroke in the left third frontal convolution, with some extension to the adjacent posterior inferior part of the motor strip.
Mr. A’s medical history included essential hypertension and benign prostatic hypertrophy. There was no history of diabetes mellitus, stroke, transient ischemic attack, coronary artery disease (CAD), affective illness, or substance abuse; however, several members of his family (his father and an older brother) had a history of CAD and hypertension.
After completion of the physical examination and laboratory work-up, Mr. A received recombinant tissue plasminogen activator (t-PA) therapy in a dose of 0.9 mg/kg.
During the first week of his hospital stay, Mr. A appeared both apathetic and emotionally distant, and he had difficulty engaging in physical therapy. Upon transfer to a rehabilitation hospital 8 days after his stroke, both his family members and the hospital staff noted that he had been sleeping poorly, concentrating with difficulty, losing weight, and avoiding family members during their visits with him. A psychiatric consultation was requested; the consultant made a diagnosis of major depression and initiated a selective serotonin reuptake inhibitor (SSRI), citalopram (20 mg/day). Symptoms of depression began to abate within the next 2 weeks. However, Mr. A remained frustrated by his limitations. After 2 months of intensive speech therapy, psychotherapy, physical therapy, and pharmacotherapy (use of an antidepressant), he was discharged from the rehabilitation facility. Six months after his stroke, with continued support from both his family and a variety of health professionals, he returned to work and was entertaining effectively.
What Types of Speech and Language Problems Can Arise After Stroke?
Key language centers of the brain, in most people, are located in the left hemisphere, adjacent to the Sylvian fissure; these centers are supplied by the middle cerebral artery or its branches. From a functional standpoint, language centers can be divided into two groups: 1) receptive, and 2) expressive. Receptive language centers are responsible for understanding and analyzing spoken language (Wernicke’s area or Brodmann’s Area 22 and the primary auditory center, or Brodmann’s Areas 41 and 42) and written language (Brodmann’s Area 39), whereas the executive centers are important in the implementation of speech (Broca’s area or Brodmann’s Areas 44 and 45) and writing (Exner writing area or Brodmann’s Area 6).1
Damage to these brain territories can produce a variety of speech and language disorders. One of the most common nonfluent aphasias is Broca’s aphasia, which was described by a French physician, Pierre Broca, in 1861. As seen in the case of Mr. A, speech with this type of aphasia is greatly impaired; it is nonfluent, agrammatical, and effortful, despite intact understanding. Those afflicted by Broca’s aphasia are typically frustrated; they are aware of their errors and may respond to them with a catastrophic reaction (e.g., with crying, screaming, or yelling). The labored, sparse speech of a person with Broca’s aphasia stands in stark contrast to the fluent speech of an individual who suffers from Wernicke’s aphasia.
Wernicke’s aphasia results from damage to the posterior part of the planum temporale. Affected individuals present with fluent, well-articulated, but meaningless speech; they often create neologisms. Their speech may sound like the "word salad" of a patient with schizophrenia; this makes the evaluation of a patient with a history of a psychiatric illness particularly difficult. The presentation of speech and language problems, especially with the features seen in Wernicke’s aphasia, can be interpreted as an exacerbation of the patient’s preexisting psychotic illness.7 Since those with Wernicke’s aphasia are often unaware of their deficits, they might appear inappropriately ecstatic and joyful or sometimes incensed or doubtful.
If damage to the brain involves both Broca’s and Wernicke’s area and most of the region between them, the deficit will affect all aspects of speech and language and result in a total or global aphasia. A patient who suffers from a global aphasia can usually understand only a few words or phrases and may only be able to say a few words or imitate a few sounds; however, most often, he or she is absolutely unable to read or write. Also, affected individuals are often depressed.
Language and speech problem can also result from damage to the main language centers and/or from the interruption of the pathways that connect them; resulting in "disconnection syndromes" (e.g., conduction aphasia and transcortical aphasia).
Conduction aphasia, caused by a separation of the receptive areas from the expressive language areas, is manifested by more-or-less fluent speech, word-finding difficulties, variable reading and writing abilities, and poor repetition. Transcortical aphasia, caused by a dissociation of the perisylvian language areas from the cerebral cortex, presents with intact repetition but with difficulties in the production of spontaneous speech or understanding of spoken language. A patient with a transcortical motor aphasia will be able to comprehend but will have diminished speech output; a patient with a transcortical sensory aphasia will be able to speak fluently but be unable to fully understand speech.
Other, less frequently seen speech and language disorders include "pure" word-deafness (where patients cannot comprehend spoken language despite intact hearing and ability to understand written language), "pure" word-blindness (where patients fail to read aloud but are still able to write spontaneously despite the inability to read it later), "pure" word-mutism (which causes a failure to speak when all other aspects of language functions are preserved), and, finally, anomic aphasia (an uncommon form of aphasia that presents with naming difficulty).
Who Develops Speech and Language Problems?
In children, it is important to distinguish delayed speech from an acquired aphasia (where language development is initially unaffected). However, anyone can acquire aphasia; speech and language problems can arise from virtually any medical condition that affects the brain, even though it most often occurs as a complication of CVA.2 Aphasia appears to be more frequent in women (37%) after ischemic strokes than it is in men (28.3%); however, there is no evidence of a gender difference among patients suffering from intracerebral hemorrhages.8
A study analyzing 192 adults with aphasia found that although stroke was seen in nearly two-thirds of cases (58%), the second most common cause of aphasia was trauma (10%), which was followed closely by dementia (7%); there was no statistical difference between the prevalence of aphasia in patients with tumors (4%) or Parkinson’s disease (3%).9 This study made no mention of infections or seizure as a cause of aphasia, even though other reports link these disorders with speech and language problems.10,11 Aphasia, as a focal neurological manifestation of HIV infection12 or as a sign of seizures,13 can be particularly important, especially in pediatric populations. In 1957, Landau and Kleffner14 first reported their observations of paroxysmal EEG discharges and language problems in children; this phenomenon was later named Landau-Kleffner syndrome (LKS), or acquired epileptiform aphasia. The etiology of this relatively rare childhood disorder is still unclear. Some reports suggest a genetic predisposition, whereas others have found LKS in patients with various types of tumors, inflammation, or abnormal zinc metabolism.15 The wide spectrum of etiological factors in LKS demonstrates the variety of pathophysiological conditions that can lead to aphasia, both in adults and children.
Delayed speech, manifest by lagging language development in early childhood, is associated with numerous disorders and conditions (e.g., bilingualism, hearing loss, autism, psychosocial deprivation, or receptive aphasia).16 Because some cases can be treated (e.g., by use of hearing aids, cochlear implants, or reconstruction of the external auditory canal), timely recognition of speech delay can prevent further damage to personal, social, academic, and vocational development.16
In adulthood, the most common cause of speech and language disorders is ischemic stroke. After a stroke, a valid prognosis for the aphasia can be made within 1 to 4 weeks. Prognosis depends on the initial severity (i.e., lesion location and size); these are the only clinically relevant predictors of outcome. Gender, handedness, and the side of the lesion are not predictors of outcome; and the influence of age on prognosis is minimal.5 Since the risk of stroke doubles with each passing decade after the age of 55, the risk of aphasia also increases with advancing age;17 however, the course of the various poststroke speech and language problems differs. Many patients with poststroke aphasia improve. Those with smaller temporal lobe lesions (with resultant Wernicke’s aphasias) can improve toward conduction or anomic aphasia, and even patients with global aphasia can evolve toward Broca’s aphasia or, occasionally, toward Wernicke’s or anomic aphasia.18
How Can One Identify or Diagnose Specific Language Disorders?
Identification of an aphasia starts with the recognition of components of a speech and language problem, and then exclusion of other conditions not due to aphasia (e.g., delayed speech development, motor speech disorder, and speech problems due to psychiatric conditions).18
Because aphasia means "language-function impairment," it can only be diagnosed if the patient had already acquired the appropriate language skills and showed normal speech development. Also, verbal communication requires an intact motor apparatus for speech; therefore, its integrity should be scrutinized. Motor speech disorders are not causes of aphasia.
Finally, disorders of language content due to psychiatric illnesses must be investigated. In many psychotic conditions (e.g., schizophrenia), the content of the speech is peculiar or inappropriate (e.g., clanging, neologisms, or thought-blocking); however, grammar and accuracy of the words used may be preserved.19 The psychotic patient’s behavior is also bizarre and out-of-the-ordinary, in contrast to the aphasic patient’s mostly appropriate manner; therefore, the difference lies in the patient’s nonlinguistic behavior.18. A variety of tests (e.g., the Boston Diagnostic Aphasia Examination [BDAE-3] by Goodglass and Kaplan, the Western Aphasia Battery [WAB] by Kertesz, and the Porch Index of Communicative Ability [PICA]) can be used to diagnose aphasia.18 However, administration of these language assessment tools requires a substantial amount of time (35 minutes to 4 hours) or special training (e.g., with the PICA). During a brief evaluation, the examiner should check three aspects of the examinee’s language. These are 1) spontaneous speech; 2) comprehension; and 3) word repetition. Assessment of these components should help to explore the nature of the language problem and distinguish it from psychiatric conditions. Alternatively, tests have been developed that can be used for brief bedside evaluations (e.g., the Sheffield Screening Test for Acquired Language Disorder [SST] and the Frenchay Aphasia Screening Test [FAST]), involving a few short and simple measures. A British study compared these two assessment tools and demonstrated similar predictive value for screening and diagnosis of aphasia; however, the SST had the benefit of not requiring special equipment or stimulus cards and being independent of visual attention.20
Patients with a Broca’s aphasia have difficulties with the formation of words and with word repetition. Comprehension of spoken and written language, however, might be preserved, so an afflicted patient can follow simple commands. In contrast, comprehension in a patient with Wernicke’s aphasia is usually greatly impaired; such an individual cannot follow commands or repeat verbal expressions, even though the fluency of their speech may be intact.
If all three of these aspects are impaired, the patient most likely suffers from a global aphasia. If only one aspect is impaired, the patient has either a conduction or transcortical (sensory or motor) aphasia. If repetition is damaged, but speech and comprehension are relatively preserved, then a conduction aphasia is present. If either fluency or comprehension is affected, but repetition is spared, the most likely diagnosis is a motor or sensory transcortical aphasia.1
How Can Language and Speech Disorders Be Treated?
Speech and language therapies (SLTs) have been studied extensively; they are thought to be efficacious when provided intensely in the first 3 months after stroke. Less intense therapy given over a longer time might not provide statistically significant benefits.21 Methods of speech rehabilitation are complex and specialized. Most therapeutic approaches (including group therapy, constraint-induced aphasia therapy [CIAT], computer-based treatment, and community-based therapy) consist of individualized SLTs designed by speech pathologists. CIAT involves the mass practice of the language over a short period of time (at least 30 hours of training within 2 weeks) and is constrained by compensatory (nonverbal) communication strategies22 that can lead to substantial and lasting improvement of language. Involvement of family members and friends in the training can further increase the efficacy of the rehabilitation.23 Computer-based language therapies can improve specific measures of language functioning in a wide range of chronic aphasias; since most patients have access to a computer outside of their rehabilitation facilities, the application is available to most individuals with an aphasia.24 Community-based programs can also facilitate recovery. Improvements have been seen in both chronic and acute aphasias, independently from the type of aphasia or the severity of the impairment at the start of treatment.25
Aside from the above-mentioned SLTs, there are abundant, but preliminary, efforts to find pharmacologic agents that could facilitate recovery from aphasia. These medications either target the release or the activity of acetylcholine, norepinephrine, and dopamine, or the perfusion of the brain. Daily administration of 300 mg of bifemelane (a cholinergic agent) in combination with SLT, improved naming and comprehension in fluent aphasic patients as compared with untreated patients.26 This correlated with the observation that cholinergic blockade impairs naming ability in healthy individuals.27 Moreover, the use of bromocriptine (a dopamine agonist) as an adjuvant to traditional SLTs was associated with significant improvement in those with nonfluent aphasia.28 Also, dopamine and its agonists not only improved the dopaminergic stimulation-dependent language functions (i.e., verbal latency and reading comprehension), but they also seemed to alter the mood of patients. Some research participants reported an elevated mood, whereas others felt depressed.29 On the basis of animal experiments showing that norepinephrine enhanced behavioral recovery after injury, a double-blind, placebo-controlled trial studied the effect of amphetamine in the treatment of aphasia.30 Administration of 10 mg dextroamphetamine paired with SLT (on a 3-day/4-day cycle for 10 sessions over 5 weeks) helped recovery from aphasia after stroke.
Finally, efforts have been made to improve the functioning of other brain areas that could potentially take over the role of the damaged language centers. Even though the exact mechanism of its action remains unknown, piracetam, a  -aminobutyric acid derivative noötropic agent, has been found to enhance learning and memory and facilitate recovery and rehabilitation in some patients with poststroke aphasias.31
Other alternative treatment approaches (e.g., relaxation therapy and acupuncture) have also been tested in patients with cognitive problems or communication disorders.32 Relaxation therapy is the most commonly used complementary and alternative medicine approach. It results in psychological changes that can increase cerebral blood-flow, especially in the prefrontal area. These alterations can contribute to improvements in speech and language functioning in those with aphasia.33 Acupuncture, a technique that has been used in China for over 3,000 years, reportedly stimulates specific anatomic points in the body to reestablish the smooth flow of qi (body energy), which supposedly restores health and normal body functions. Although several acupuncture studies have shown improvement of verbal fluency in aphasic patients, the benefits of acupuncture remain statistically unproven.32
Currently, there are vast arrays of options to treat aphasia; finding the best therapeutic approach can be complex and challenging. Consequently, consultation with a speech and language specialist is advised before one inaugurates therapy. Initiation of rehabilitation should also be postponed until the severity and course of the illness can be judged. Frustration and depression that often complicate aphasia might require special care and attention, including the assistance of a mental health professional.
Can Other Neuropsychiatric Problems Coexist With Speech and Language Disorders and Complicate Their Care?
Aphasia and depression commonly coexist and develop as a consequence of stroke; moreover, having dysphasia increases the risk of developing depression.34 Other neuropsychiatric conditions (e.g., dementia, anxiety disorders, and psychotic disorders) and symptomatic correlates (e.g., apathy or fatigue), may further obscure the diagnosis and the care of stroke patients.35 These conditions arise, in part, from the size and location of the lesion, as well as the neurological consequences of the CVA. Among these sequelae, poststroke depression (PSD) has been the most widely studied; attention to the signs and symptoms of affective dysregulation after stroke remains a cornerstone of care.
PSD has the same signs and symptoms (i.e., disturbed sleep, lack of interests, guilt or preoccupation of thought, reduced energy, diminished ability to concentrate, disturbed appetite, psychomotor agitation or retardation, and thoughts of death or suicide) as does both minor and major depressive disorder (MDD); four or more of these symptoms, in the presence of depressed mood or anhedonia (loss of pleasure), for a duration of 2 weeks or longer, satisfy criteria for MDD.36
Initiation of somatic therapies (such as an SSRI, a stimulant [e.g., modafinil], or electroconvulsive therapy [ECT]) can contribute to symptomatic relief and help to ensure sufficient cooperation of the patient with both psychiatric and neurological therapy.
In summary, treatment options include use of an antidepressant medication (e.g., an SSRI, a tricyclic antidepressant [TCA] or a monoamine oxidase inhibitor [MAOI]) and a behavioral therapy (such as cognitive-behavior therapy [CBT] or other forms of talk therapy, especially interpersonal therapy [IPT]). Rehabilitation, however, is more effective if the above-mentioned treatments are used in combination with SLTs and other physical therapies. Incorporating family members and caregivers into the treatment plan may also be beneficial.
As was the case with Mr. A, identification of his depression and the initiation of prompt treatment led to clinical improvement. Within 6 months of his CVA and his aphasia, he was able to return to show business and to entertain effectively (through humorous verbal expression) again.
How Can One Diagnose Neuropsychiatric Conditions in the Presence of Speech and Language Problems?
As seen in the case of Mr. A, antidepressants can effectively treat PSD, if it is recognized early. However, the identification of an individual’s emotional state in the presence of a language and speech difficulty can be challenging, even for the most experienced of clinicians.
Most well-known and routinely-administered questionnaires for depression are either self-reports, such as the Beck Depression Inventory (BDI), or integrated parts of the regular clinical interview (like the Hamilton Rating Scale for Depression) conducted by a trained person.37 Even though both of these tests (developed in the 1960s) have been validated several times, there are limited data for their use in the evaluation of aphasic patients, since their reliance upon verbal output alone challenges their validity. That is why the diagnosis of PSD in aphasic patients often relies on nonverbal clues (e.g., crying and overt sadness) or input from family members and caregivers.
Sutcliffe and Lincoln developed a questionnaire that utilizes feedback from caregivers to assist clinicians in this special situation. The Stroke Aphasia Depression Questionnaire, Shortened Version (SADQ-10) was created to foster the recognition of PSD in aphasic patients.38 The SADQ-10 consists of 10 questions regarding various behavioral patterns that are associated with depressed mood and can be observed by family members and caregivers. In the initial study that analyzed the reliability of the SADQ-10, it was found to have a strong correlation with the results of other depression assessment tools, such as the Wakefield Self-Assessment of Depression Inventory (WDI) and the Hospital Anxiety and Depression Scale (HADS) that were filled out by stroke patients.38 Each question or item on the SADQ-10 is scored on a 0–3 scale, giving a maximum score of 30, with a score of 10 as the cutoff point for a suspected mood disorder (i.e., the higher the score, the lower the mood). However, another study that evaluated the clinical use of the SADQ-10 on a special stroke unit found that a cut-point of 14 out of 30 had a sensitivity of 70% and a specificity of 77% for the detection of depression.39 Furthermore, the SADQ-10 outcomes were only moderately correlated with the results of the Geriatric Depression Scale (GDS-15) self-rated depression scale; therefore, researchers suggest that the SADQ-10 not be used as the only measure of depression in stroke patients.
In conclusion, screening of stroke patients for depression is recommended to facilitate patients’ rehabilitation and return to the community, and several screening tests have been developed to facilitate the recognition of disturbances in affect, behavior, and cognition in those with an aphasia.
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ABSTRACT
INTRODUCTION
