Case Report Stroke-RelatedAphasias Mistaken for Psychotic Speech: Two Case Reports Angelo Sambunaris, MD, and Thomas M. Hyde, MD, PhD ~~~ ~ ABSTRACT A large portion of the human central nervous system is dedicated to and specialized for language function. Aphasias, disorders of language, can be seen in many psychiatric and neurologic conditions. On occasion, it is difficult to differentiate between language abnormalities secondary to a patient’s psychiatric illness and those secondary to a superimposed neurologic condition. In particular, in the evaluation of a patient with a history of a psychotic illness, it is easy to misinterpret the presentation of “abnormal” speech as a n exacerbation of the patient’s pre-existing psychiatric illness. To show this psychoneurologic comorbidity, two case reports are presented. ( J Geriatr Psychiatry Neurol 1994; 7:144-147). “Psychotic speech” can range from a poverty of speech or mutism to a copious jargon-laden word salad. In an acute psychotic episode, or an episode that superficially appears to be an exacerbation of a psychotic illness, the psychiatrist should not automatically attribute disordered speech to the psychiatric illness. Instead, neurologic comorbidity should always be considered, especially in the geriatric patient. This is especially true if the abnormal speech is accompanied by anxious or agitated behavior, confusion, or focal neurologic signs or symptoms. A screen of language function during the mental status examination (MSE) is indicated in all psychiatric patients, especially during the initial evaluation. Even in patients well known to the physician, a major change in condition requires a re-evaluation and comparison to previous baselines. One cannot automatically attribute a change in speech pattern to an exacerbation of the patient’s psychotic disorder. During the MSE, a formal evaluation of speech should be completed to exclude the possibility of a diagnosis of aphasia, as the following two cases will serve to illustrate. Case 1 A Lig-year-old, right-handed, black female with a 30-year history of schizophrenia, paranoid type, was seen at the Neurol~~ ~~ Received September 16,1992. Received revised November 4,1992.A~cepted for publication hlarch 3,1993. From the Neuropsychiatry Branch (Dr. Sambunaris) and the Clinical Brain Disorders Branch (Dr. Hyde), N.1.hI.H. Neuropsychiatric Research Hospital, Washington, District of Columbia. Reprint requests: Dr. Angel0 Sarnbunaris, Neuropsychiatry Branch, N.1.hl.H. Neuropsychiatric Research Hospital, 2700 Martin Luther King Jr. Ave., S.E., Washington, DC 20032. ogy Clinic of the N.I.M.H. Neuropsychiatric Research Hospi- tal. One month prior to her clinic visit, she had a n acute onset of mild weakness and clumsiness of her right hand and arm, mild imbalance when standing, and peri-oral numbness. She was taken to the local emergency room, evaluated, and discharged several hours later. Her case manager reported that there was no residual disability or any speech problems. Several days later, her speech became slurred, and the case manager noted a change in the patient’s ability to communicate verbally. She was taken to the same emergency room and evaluated by a physician who recorded no focal neurologic deficits. Records of that visit noted her previous psychiatric history and treatment, as well as hr: current difficulty in expressing herselfverbally. She was also noted to be alert but disoriented and confused. While awaiting a CT scan in the emergency room, she became quite agitated, screaming continuously, and talking to herself incoherently. Physical restraints were applied, and she was subsequently admitted for psychiatric hospitalization. Neurologic evaluation one month later in our clinic revealed the following. The patient was alert, awake, attentive, and cooperative. Her speech was slightly dysarthric, and she had difficulty naming objects. In conversation, she would search for words, although overall, she was quite fluent. When agitated or excited, her speech would degenerate into word salad and be full of jargon. She was able to read the alphabet but had difficulty pronouncing words. She was able to write her name. She had difficulty following two- and three-step commands. When talking in full sentences, her speech content was disorganized and difficult to follow. On neurologic examination, cranial nerves II-XI were normal. On motor testing, she showed a right pronator drift. Her gait was notable for a decreased arm swing on the right. Downloaded from jgp.sagepub.com at CARLETON UNIV on June 24, 2015 Stroke-RelatedAphasias 1Sumbunaris and Hyde Reflexes on the right upper extremity were slightly brisk, along l i t h 3+ knee and anklejerks on the right. Her sensory examination was intact. The rest of the neurologic examination was within normal limits. She was diagnosed as suffering from a ivernicke’s aphasia with acalculia along with a concurrent exacerbation of her underlying psychiatric disorder. A magnetic resonance imaging (MRI) scan revealed a large left parietal lobe infarct. Case 2 A 67-year-old, right-handed, black male with a history of chronic schizophrenia, undifferentiated type, presented to the Neurology Clinic for evaluation and treatment of his recent psychotic exacerbation and increasingly disorganized behavior. The patient first presented with symptoms of a psychiatric illness 27 years earlier with a n acute onset of auditory hallucinations, bizarre behavior, and somatic delusions that hlartians had replaced his nerves with “electric cords.” He was chronically institutionalized until 53 years of age, when he was placed in a residential treatment facility, His outpatient chart revealed chronic complaints of persistent auditory hallucinations of male voices, as well as of God, offering commentary on his behavior and directing his actions. He was receiving perphenazine, and his medication regimen had remained stable during the previous 7 years. There was a history of mild systolic hypertension treated with diuretics, and a history of osteoarthritis. There was no history of alcohol or drug abuse. Three months prior to his evaluation in the Neurology Clinic, his behavior changed. He became uncommunicative, had difficulty following commands, and only grunted when addressed. The only sound h e would make was “Hi” and he seemed genuinely frustrated that he could not make his wishes known. He became increasingly agitated and combative, which lead to hospitalization due to a n “exacerbation of his schizophrenia.” He was treated with increasing doses of haloperidol, which caused him to become progressively somnolent and rigid. There was no other change noted in his condition. For the most part, he remained mute. Due to this clinical course, he was referred to the Neurology Clinic for evaluation. When seen in the clinic, he was awake, alert, and attentive. He followed simple commands, such as “openyour mouth,” but perseverated in his response to other commands and often appeared t o be following visual cuing. The only spontaneous Table 1. Impaired Speech Aspect Relative to Anterior and Posterior Aphasia and Psychosis Speech Aspect Naming Comprehension Fluency Repetition Neologisms/ paraphasic errors Neurologic signs Anterior Aphasia (Broca‘s) Posterior Aphasia (Wernicke‘sl Psychosis* Impaired Preserved Impaired Impaired Fluent Impaired Preserved Impaired Yes Visual Field cut Yes No Non-fluent Impaired Yes Hemiparesis affecting face and arm *On occasion, some psychotic exacerbations present as mutism. Fluent Preserved 14f sound uttered was ”Hi.” The rest of the mental status exami nation was untestable. Cranial nerves 11-XI1 were symmetric and intact bilaterally, except for mild flattening of the righi nasolabial fold. His fundi were normal. Motor examination wa: normal, except for a mild right pronator drift and slightly in creased deep tendon reflexes in the right arm at the biceps triceps, and brachioradialis. His gait was normal except fol decreased right arm swing. He had cogcvheel rigidity in thc left arm. He grimaced and withdrew all four limbs in responsc to noxious stimuli. General physical examination was normal with no heart murmurs or carotid bruits detected. An hlRI scan revealed a cerebral infarct, of indetermi nate age, in the distribution of a branch of the left, middle cerebral artery, involving a small wedge-shaped area of thc left, inferolateral, frontal cortex. An echocardiogram was nega tive, while a carotid Doppler ultrasound revealed a 60%stenosi: at the bifurcation of the right common carotid artery. DISCUSSION Verbal interchange during the evaluation, especiallj during the mental status examination, is a major com. ponent of the initial diagnostic assessment. The char. acter of a patient’s verbal output is often diagnostic il analyzed properly by the trained clinician.As Gerson el all point out, it is not surprising that errors in diagno. sis are made. Psychiatrists, by habit and by training learn to generate their diagnostic impression after pay ing careful attention to the content of the patient’s ver. bal utterances rather than to the quality of their speech. This quality includes the repetition, fluency, comprehension, syntax, verbal substitutions, patterns of pauses agrammaticisms, and coherence of verbalizations, among others. The term “thought disorder” is not used to describc a disturbance in the content of a person’s speech, bui rather to describe the disturbance in the form of thought. As McGrath2 states: We describe someone as thought disordered when we, thc listener, become confused attempting to follow the speak. er’s discourse. . . .The crucial distinction between disor. ders in the form of thought and disorders of the content 01 thought needs to be kept clear in the researcher’s mind when attempting to tease out the underlying neurology oj these symptoms. In patients with a history of a chronic psychiatric disorder, there is a tendency to regard any change in their mental status as an exaterbation of the underlying psychiatric disorder. In any patient, but particularly the geriatric psychiatric patient, such a perspective can lead one astray. In this report, we present two cases in which the patients’ language abnormalities were inappropriately attributed to their pre-existing formal thought disorder rather than a proper diagnosis of a stroke-induced aphasia. Put simply, aphasia is the difficulty in the production, use, or comprehension of language. As Damasio? Downloaded from jgp.sagepub.com at CARLETON UNIV on June 24, 2015 146 Journal of Geriatric Psychiafryand Neurology I Vol. 7 ,July-September 1994 presents in his review of aphasia: “The essence of aphasia is a disorder of linguistic processing, a disruption of the mechanism for translating thought to language.” Aphasia is not a disorder of perception, a disorder of movement, nor a disorder of the basic thought processes. It is not a disorder of the organization of thoughts into a coherent form. Aphasia represents an alteration in the basic perception and organization of language, whether spoken or written. While patients with aphasia can vary in their clinical presentation, formal, yet simple, language testing will usually uncover primary deficits in this sphere of cognitive functioning. To evaluate a patient for the major types of aphasia, we test for the fluency of spontaneous speech, the ability to repeat, the ability to comprehend, and the ability to respond to visual confrontation naming. Written as well as spoken language should be assessed, and this, as a matter of course, should be included in the mental status examination of all patients whenever possible. Case 1 presents a patient with a Wernicke’s, or posterior fluent, aphasia which is noted for a fluent speech that is effortless, melodic, woven together well, and produced a t normal to faster rates. The content of this speech is often unintelligible due to frequent errors in both word choice as well as the choice of individual speech sounds or phonemes. Patients with this problem often have difficulty comprehending the speech of others and usually have impaired repetition. Due to the absence of major neurologic signs such as weakness or reflex asymmetries, these patients can be difficult to differentiate from the patient presenting with “psychotic Figure 1. A proton-weighed MRI of the patient identified in case 1 revealing a hyperintensity in the left temporal parietal region. speech.” This form of aphasia can be associated with a visual field defect. Case 2 presents a patient with a Broca’s, or anterior nonfluent, aphasia. In this type of aphasia, verbal output is sparse, comprehension is relatively intact, speech is effortful and choppy. There are marked, wordfinding dificulties and difficulty in repetition. In addition, there are paraphasic errors, such as calling a pen a “Ben,” and not infrequently, neologisms. Anterior aphasias ’are often associated with a contralateral hemiparesis (usually of the right face and arm). If an error in diagnosis is made due to confusion from the similarities in speech abnormalities, the patient with an aphasia may be confined inadvertently to a psychiatric facility. Such a patient would not receive the proper treatment for stroke,’such as anticoagulation or speech therapy. Moreover, the patient may be subject to the unnecessary use of neuroleptics. The information from the MSE that can help the clinician differentiate aphasic from psychotic speech can also be used. to detect the presence of cerebral involvement in chronically institutionalized patients, who are quite often isolative and relatively uncommunicative. These patients, especially the geriatric population, may suffer a mild stroke that may go undetected. Numerous studies have been undertaken in an attempt to elucidate the differences between %.chizophrenic” or “psychotic” speech from that of an aphasic patient. All of these studies?.4-9 conclude that uschizophrenic” speech can be differentiated from aphasia by applying rigorous testing methods. Gerson et all evaluated the speech of 8 patients with a posterior aphasia and 10 patients with schizophrenia. This study noted six major differences between the speech of schizophrenic patients and those with posterior aphasia. In the posterior aphasia, they noted shorter length of response, a self-awareness of communication problems, paraphasic errors (unintended substitutions in language), and efforts to enlist the assistance of the examiner to aid in communication. In the schizophrenic patient, the speech content carried a bizarre theme, absent in the aphasic group. One category was present in both groups, vagueness of responses, attributed to wordfinding problems in the posterior aphasic, and to attentional disturbances in the schizophrenic, patient. They concluded that the characteristics of the speech of the posterior aphasic represents a disorder of language, whereas the speech of a schizophrenic patient derives from a thought disorder. Contrasting this study, Faber and Reichstein4were able to identify a subset of schizophrenia patients who displayed a formal thought disorder with significant language dysfunction. These patients demonstrated significantly more aphasic abnormalities than did those without a formal thought disorder. Their difficultyboth with the Token Test and in the repetition of phrases test suggested that deficits in language comprehension and repetition may be Present in a small group ofschizo- Downloaded from jgp.sagepub.com at CARLETON UNIV on June 24, 2015 Stroke-Related Aphasias I Sambunaris and Hyde phrenia patients. A significant body of evidence has correlated pathology in the mesial temporal lobes with s~hizophrenia.~ Extension of this pathology into adjacent temporal lobe structures subserving language may explain why a small subset of schizophrenia patients have profound language disturbances. However, the majority of schizophrenia subjects do not display this degree of language dysfunction. Therefore, the speech of psychotic patients can usually be accurately differentiated from aphasic patients through standard language tests. DiSimoni et a16 have also presented evidence that “schizophrenic speech” is distinct from aphasic speech. They found that the communicationdifficultiesof schizophrenia patients are unlike those of patients with aphasia. Schizophrenia subjects were considered deviant regarding the relevance of their responses and reading comprehension; while the rest of their speech, such as syntax, naming, and adequacy (substitution, deletion, or addition of substantive words) of their responses, were essentially normal. The aphasic subjects have less difficulty with reading comprehension and relevance, but have far more difficulty with adequacy. Halpern and McCartin-Clark7 found that six language categories seemed to differentiate aphasic from schizophrenic language. These categories include (1)writing from dictation, (2) naming, (3) syntax, (4) relevance, and to a lesser extent (5) auditory retention span and fluency. Rausch et als demonstrated distinct differences between an aphasic group and a schizophrenia group on a word-ordering task. All the patients with aphasia carried a neurologic diagnosis of left, cerebral hemisphere damage. These two groups could be distinguished by the amount of time taken to complete a word-ordering task and also by the number and types of errors. In fact, the performance of schizophrenia subjects was indistinguishable from normal controls in all areas, except that schizophrenic subjects had a higher number of errors in rearranging sentences involving both direct and indirect objects. The long-term effects of schizophrenia and the effects of institutionalization on language were studied by Silverberg-Shalev et a19 and Halpern.’ SilverbergShalev and associates found that chronic schizophrenia patients that were tested for neuropsychological function demonstrated a selective deterioration of language. The data revealed that progressive cognitive dysfunction in the area of language is part of the symptom complex of chronic schizophrenia, but that no other abnormalities or decline in other areas of cognitive functioning (memory, attention, and rate of processing) were noted. Along these lines, Halpern found that length of institutionalization and speaking errors were positively correlated, indicating that the longer a patient is institutionalized, the more speech errors (especially adequacy and naming) the patient will produce. I n the majority of studies on schizophrenia and aphasia, the authors comment on the need to test a large 147 sample of subjects in order to find significant differences between these two disorders. The goal of these studies was to determine which elements of language dysfunction distinguish psychotic from aphasic speech. Cummingslo offers clinical guidelines that, in general, can be used to differentiate aphasia from schizophrenic speech. A diagnosis of schizophrenia is favored if the onset is before 30 years of age, there is a history of psychosis, and in the absence of a known medical illness. On the other hand, onset after 50 years of age; the presence of a predisposing medical condition, such as hypertension, diabetes mellitus, hyperlipidemia atrial fibrillation, or valvular heart disease; the absence of previous psychiatric illness; and the presence of focal neurologic findings all suggest a hemispheric insult and support the diagnosis of aphasia. If during the course of the mental status examination, the psychiatrist finds changes from previous speech patterns, additional testing must be performed. A consultation with a neurologist familiar with psychiatric patients is often indicated for such a patient.An MRI or CT scan can be an invaluable tool in the evaluation of a patient with disordered language. As CummingsIo points out, one must remember, “Schizophrenics are at the same risk as the general population for the development of cerebrovascular or neoplastic disease.” Acknowledgment This research is supported by funding from the Intramural Research Program of the National Institute of hIental Health. We also thank Drs. R.J. Wyatt and ME.Egan for their contributions to this paper. References 1. Gerson SN, Benson F, Frazier SH. Diagnosis: schizophrenia versus posterior aphasia. Am JPsychiatry 1977;134(9):966969. 2. McGrath J. Ordering thoughSs on thought disorder. Br J Psychiatry 1991;158~307-316. 3. DamasioAR.Aphasia. New Engl JMed 1992;326(8):531-539. 4. Faber R, Reichstein MB. Language dysfunction in schizophrenia. Br JPsychiatry 1981;139:519-522. 5. Hyde Thl, Casanova hlF, Kleinman JE, Weinberger DR. Neuroanatomical and neurochemical pathology in schizophrenia. In: Tasman A, Goldfinger SM, eds. Review ofpsychiatry, Vol. 10.Washington, DC: American Psychiatric Press Inc, 723. 6. DiSimoni FG, Darley FL, Aronson AE.Patterns of dysfunction in schizophrenic patients on an aphasia test battery. J Speech Hear Disord 1977;42:498-513. 7. Halpern H, Mecartin-Clark hl. Differential language charaeteristics in adult aphasic and schizophrenic subjects. J Commun Dis 1984;17:289-307. 8. Rausch hfA, Prescott TE, DeWolfe AS. Schizophrenic and aphasic language: discriminable or not? J Consul Clin Psych 1980;48(1):63-70. 9. Silverberg-Shalev R, Gordon HW, Bentin S , Aranson A. Selective language deterioration in chronic schizophrenia. J Neurol Neurosurg Psychiatry 1981;44:547-551. 10. Cummings J.Clinical neuropsychiatry. Orlando, F L Harcourt Brace Jovanovich, 1985:1735. Downloaded from jgp.sagepub.com at CARLETON UNIV on June 24, 2015