The communication disorder in dialysis dementia: A case report

BRAIN

AND

LANGUAGE%,

378-389 (1980)

The Communication

Disorder in Dialysis Dementia: A Case Report ROBIN BARATZ Beth Israel Hospital

AND

ANDREW G. HERZOG Beth Israel Hospital

and Harvard

University

Medical

School

The communication disorder in dialysis dementia is an integral feature of the syndrome. This report describes the communication disorder in a 67-year-old man over a period of 4 months from his admission to the hospital to his death. In the early stage of the syndrome, the most prominent feature was a speech problem, the characteristics of which may vary among cases. In the middle stage, it was difficult to distinguish among aphemia, aphasia, or a combination of dysarthria and confusional state. The severity of the problems in these stages was temporally related to the dialysis treatments. The final stage was characterized by constant mutism and was unrelated to the dialysis treatments. Death occurred 10 months after the communication problems emerged. Communication studies of dialysis dementia patients may offer a systematic method to monitor the course of the syndrome, its response to therapeutic trials, and a clinical model for the study of communication disorders in general.

Dialysis dementia is generally an irreversible syndrome leading to death, characterized by progressive deterioration in mentation and communication abilities, as well as a number of less constantly occurring neurological features such as myoclonus, seizures, and gait disorder (Alfrey, Mishell, Burks, Contiguglia, Rudolph, Lewin, & Holmes, 1972; Mahurkar, Salta, Smith, Dhar, Meyers, & Dunea, 1973). The associated We are grateful to Dr. Norman Geschwind for his continuous encouragement and review of the manuscript. We thank Dr. Robert S. Brown for allowing us to study his patient, Andrea G. Shindler for sharing early data, and Drs. Robert S. Baratz and Sandra Weintraub for their suggestions on the manuscript. Address reprint requests to Robin Baratz, Behavioral Neurology Unit, Beth Israel Hospital, 330 Brookline Avenue, Boston, MA 02215. 378 0093-934X/80/040378-12$02.00/O Copyright AU rights

@ 1980 by Academic Press, Inc. of reproduction in any form reserved.

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communication disorder is usually the first and most prominent clinical sign in the syndrome. Only two prior accounts (Rosenbek, McNeil, Lemme, Prescott, & Alfrey, 1975; Madison, Baehr, Bazell, Hartman, Mahurkar, & Dunea, 1977), however, detail this aspect of the syndrome. The present report describes the communication problems observed in a 67-year-old man over a period of 4 months from his admission to the hospital to his death. CASE HISTORY

A 67-year-old white male was admitted to the Beth Israel Hospital in April 1977 for an evaluation of progressive changes in speech, gait, and mentation. A review of his medical history revealed that the patient had “kidney trouble” with transient edema at 4 years of age. This problem gradually resolved without treatment. He remained asymptomatic until age 55 when he was diagnosed as having systemic hypertension and chronic renal insufficiency. Treatment with a-methyldopa brought his hypertension under control. Renal failure developed late in 1973. An arteriovenous fistula was placed in January 1974 and triweekly, 4-hr sessions of hemodialysis were begun in March 1974. On this regimen and a restricted diet, his renal failure was controlled for over 2 years without complications. The patient began to have speech difficulty in October 1976-31 months after hemodialysis was begun. The attending neurologist at the time reported that the problem was episodic, starting in the middle or toward the end of dialysis, and lasting 6 to 8 hr thereafter. During these episodes, the patient would sound as if he were “drunk.” At times, he would be “unable to get [a] word out readily.” His tongue would become “tangled,” and he occasionally bit it. Language was judged to be normal. In December, the patient’s wife noted that, following dialysis, he would walk slowly, reeling from side to side and at times, almost fall. She was particularly disturbed by progressive changes in his behavior. He was becoming more anxious and depressed and unjustifiably accused her of infidelity. He was forgetful and, at times, somewhat disoriented and confused. The dialysis-related episodes of disturbed communication gradually worsened in severity and in duration. At the time of his admission to this hospital, the difficulty was present constantly. The patient was admitted to the hospital in April 1977, 37 months after hemodialysis was begun and 6 months after the communication disorders were first noticed. On general examination, the patient’s pulse was 80 and regular. His blood pressure was 160/90 in the right arm in the seated posture. There were no other general physical findings of significance except for a mild increase in skin pigmentation. On neurological examination, he exhibited problems in mental status, coordination, and reflexes. Recent memory fluctuated between normal and mildly impaired. Proverb interpretation and similarities test results were strikingly concrete. Writ-

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ing and constructions were normal (Fig. 1A). The patient was depressed and anxious, perhaps appropriately so. His gait was wide based with a mild tendency to reel from side to side. The Romberg sign was negative. Rapid alternating movements were done well with all extremities and there was no definite ataxia of limbs or trunk. Generalized hyperreflexia was present below the neck. The laboratory data revealed a marked anemia with hematocrit in the 20% range. Urine specific gravity was 1.005 with 4+ albumin in the urine. Electrolytes, including calcium and magnesium, were within normal range. The BUN was 80 mg%. Sedimentation rate was 100 mm/hr. The EEG displayed generalized bursts and runs of sharp delta waves, which became considerably more prominent and frequent after dialysis. Lumbar punctures before dialysis showed opening pressures of 115, 150, and 130 mm water, respectively, on three different occasions, while measurements during and following dialysis were elevated between 245 and 275 mm. Seven red blood cells and no white blood cells were seen in the fluid. The protein was elevated to 98 mg%, but glucose was normal at 57 mg%. The CT scan showed mildly enlarged lateral ventricles without evidence of cerebral atrophy. An indium cisternogram was abnormal showing ventricular uptake of the isotope and no passage over the hemispheres even at 72 hr. A CSF infusion (Katzman) test was abnormal reaching a pressure of 300 mm after a half-hour of saline infusion at the rate of 0.67 cc/min. SPEECH PATHOLOGY

FINDINGS

Portions of the Boston Diagnostic Aphasia Examination (Goodglass 8z Kaplan, 1972b), the Fisher-Logemann Test of Articulation Competence (Fisher and Logemann, 1971), an oral-motor examination, and informal speech and language tasks were done. Language modalities, including auditory comprehension, oral expression, reading comprehension, and written expression, were intact. Speech ability, however, was impaired. While oral-motor functioning was normal for nonspeech tasks (i.e., individual and rapidly sequenced movements of the lips, tongue, velopharynx, vocal folds), movements during speech were aberrant. Articulation consisted of unpredictable, irregular, multiple distinctive feature errors. Some examples are: (1) lltF (glide/stop, reduced precision of tongue tip, voiced/voiceless); by substituting the phoneme “1” for “t” in the final position of a word, our patient emitted a continuous air stream instead of an “explosion” of built-up air pressure. He made a slightly different place of contact between the tip of the tongue and the alveolar ridge of the hard palate. He adducted the vocal cords producing a vibration of the cords as air pulsated through the points of adduction, instead of abducting the cords to allow air to pass through the larynx without an voiceless/ obstruction. (2) tMM (stop/fricative, tip-alveolar/tip-dental,

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voiced): By substituting the phoneme “t” for “th” (as in “father”) in the medial position of a word, our patient emitted an “explosion” of built-up air pressure instead of a continuous air stream. He placed the tip of his tongue at his alveolar ridge instead of at his upper central incisors. He abducted his vocal cords instead of adducting them. (3) ZY:/ae (excessive nasalized assimilation with the contiguous nasal consonant): One’s production of a sound in a word is influenced to a degree by the adjacent sounds. “A” (as in “hat”) is a sound emitted through the oral cavity. “M,” “&” or “ng” are nasal sounds in that they are emitted primarily through the nasal cavity. In words such as “mat” and “tan” the “a” becomes influenced by the adjacent nasal sound. When articulating the “ a,” a small amount of air is emitted through the nasal cavity. The “a” became primarily, if not totally, emitted through the nasal cavity. (4) o/postvocalic consonant (regardless of manner, place, and voicing, and with a high frequency rate): Our patient frequently omitted sounds that occurred in the final position of words, regardless of the skill required of the musculature to produce the sounds. These errors were attributed to impaired coordination and timing of the articulators. The patient was aware of virtually all errors, and made attempts to correct many of them, but was seldom successful. Articulation was improved with repetition and oral reading. Prosody was marked by syllable-by-syllable utterances, produced, as Walshe (1973) has aptly described, “deliberately and slowly as if (each syllable) were a separate word and . . . not run together with its fellow syllables. . . .” This pattern is commonly called “scanning” or “measured” speech. Additionally, prosody had a staccato quality in that each syllable had pronounced loudness and stress, severed at the completion of the syllable. Despite alterations in the continuity of the syllables, intonation patterning was virtually intact. Overall intelligibility was impaired to a mild degree, and did not interfere with the patient’s success in communicating his intentions. COURSE

The opportunities for making the follow-up observations were limited by our schedules and the patient’s tolerance for testing. What appears below is a representative sample of our findings. Three Days after Admission,

during Dialysis

Test results revealed a remarkable deterioration in speech beginning 2 hr after the onset of dialysis. Articulation presented the error pattern described above, but at a higher rate of frequency. Prosody remained measured and staccato to the same degree but additionally was marked by aberrant intonation patterning reminiscent of inebriated speech. Stressed syllables and words were occasionally perseverated. Overall intelligibility

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was impaired to a mild to moderate degree, interfering significantly with the communication of intentions. Three Days after Admission,

2 hr Postdialysis

Deterioration was evident in mental status, reading, writing, speech, and laboratory data. The patient was less attentive. Digit span was decreased to four numbers forward. He read at a slower rate and had difficulty following written commands. His writing was somewhat illegible and contained word omissions, repetitions, and transpositions (Fig. 1B). Misarticulations and dysprosody were increasingly frequent. A breakdown in transitionalization between sounds had emerged, including an inappropriate interval (e.g., glae*s/glass) and a reversed sequence (e.g., va/of). Overall intelligibility was impaired to a moderate degree. The symptoms gradually regressed in severity until they approximated the baseline levels of 24 hr postdialysis. One Month after Admission, 38 Months after Hemodialysis Begun, and 7 Months after the Disorder Emerged

Was

The examination was remarkable in that deterioration was evident in nonverbal oral-motor function, speech, writing, and in the elementary neurological status. Nonverbal oral-motor dysfunction had emerged with slight reduction of strength, range of motion, and speed of the lips and tongue, and by inaccurate “undershooting” and “overshooting” of the tongue. The speech disorder was moderately severe with almost constant misarticulations and dysprosody. Newly observed features were a harsh, strained/strangled phonation quality, hypernasality, a lower pitch, and occasional uncontrollable alternately rising and falling or “reeling” pitch variations. Speaking intelligibly had become so difficult that the patient chose to rely, for the most part, on writing to communicate. Spontaneous writing, however, had frequent errors, including omissions and substitutions of words and misspellings. Hand gestures and facial expressions were also employed. A coarse tremor, asterixis in the right hand, and a left facial nerve palsy had emerged. Two Months Postadmission, 39 Months after Hemodialysis and 8 Months after the Disorders Emerged

Was Begun,

Predialysis. Examination revealed remarkable changes in the patient’s mental status and speech problems. The patient’s affect was marked by inappropriate and uncontrollable smiling and laughing. The patient tended to ramble on effortlessly with a variety of unintelligible phonemes, and he did not halt until the listener interrupted him. Spontaneous writing remained poor as before. Writing to copy, however, was still carried out quite well with only occasional errors in transposition and grammar (Fig. 1C).

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D

E

FIG. 1. Writing samples representative of the progressive long-term and dialysisassociated short-term deteriorations in this case of dialysis dementia. (A) Early stage, spontaneous, predialysis; (B) early stage, spontaneous, postdialysis; (C) middle stage, to copy, predialysis (note: “the” should be “its”); (D) middle stage, to copy, postdialysis; (E) middle stage, spontaneous, postdialysis.

Postdialysis. Problems in mental status, auditory comprehension, speech, and writing were prominent. The patient was not alert to his surroundings or attentive to people trying to communicate with him. He inconsistently responded to his name. He would begin to follow a few commands to perform axial body movements; then he would perseverate one response. He needed verbal cueing in order to shift to listening to conversational input, and responding correctly to only a few statements. His output was primarily a perseveration of ah, prolonged at one pitch or uncontrollably reeling in pitch. The patient had to be coaxed to write, doing so slowly and tediously. Writing to copy (Fig. 1D) and spontaneously (Fig. 1E) was illegible with “scratchy” markings and “work-

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oven.” Content included restarts, word repetitions, substitutions, omissions , and incompletions. Two and One-Half Treatment

Months Postadmission,

1 Day after a Dialysis

Pre-post dialysis comparisons were no longer made, because the patient was experiencing extreme exhaustion on treatment days. Slight improvement since the previous session was observed in mental status, auditory comprehension, and speech. The patient could follow somewhat more than half of statements of one to two sentences in length and questions about himself and the environment. He made several requests for repetition of input and followed conversation more reliably when it was at a slower-than-normal rate. His speech had increased to a phonemic repertoire of about 80%, but accurate sound productions were inconsistent. Content was, at times, either repetitive or rambling in nature. Two Months and 3 Weeks Postadmission, 40 Months after Dialysis Was Begun, 9 Months after Problems Emerged, and 5 Days after a Dialysis Session

Changes in speech and nonverbal oral-motor function were noted. The patient had trouble initiating phonation and articulation postures. He produced primarily one to two word utterances, with an exceedingly low pitch, a hoarse, breathy phonation quality, and occasional uncontrollable changes in pitch and loudness. Nonverbal oral-motor function exhibited a return of normal strength but a slower rate of movement and less coordination than were previously noted. Two Months,

3 Weeks, and 1 Day Postadmission

A lumbar CSF shunt was implanted in an attempt to correct the features suggestive of obstructive hydrocephalus. In the subsequent days, deterioration in elementary neurological status and communication were observed. The patient had seizures and myoclonus. There was slow twitching (l/set) on the right side of the body. He could answer some questions about his health by nodding or shaking his head. He expressed only moaning and snoring sounds. He refused to write. Two Months,

3 Weeks, and 4 Days Postadmission

He was found to be obtunded. His moaning and snoring sounds were rhythmic and unrelenting. Hemodialysis was then discountinued. He was tried instead on peritoneal dialysis but without benefit. Three Months Postadmission

No sounds were made spontaneously or on elicitation. The patient produced ongoing facial contortions, lip smacking, and hand squeezing.

DIALYSIS

Forty-One Months after Dialysis Disorders Emerged

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Was Begun and 10 Months after the

He died of respiratory arrest. POSTMORTEM

DATA

The brain weight was 1240 g. The convexity of the cerebral hemispheres appeared grossly normal. The cerebral cortex was well preserved. The lateral ventricles were, however, moderately enlarged. The basal ganglia were atrophic and, along with the white matter of the cerebral and cerebellar hemispheres, contained multiple old lacunar infarcts and small hemorrhages. The basal penetrating blood vessels showed extensive degenerative hyalinotic changes associated with thromboses and minute perivascular hemorrhages. The concentration of aluminum in the cerebral cortex was 28 mg/kg, which is 20 times higher than normal control values. DISCUSSION

The communication disorder in dialysis dementia is an integral feature of the syndrome. It has been found in all reported cases and is usually the patient’s initial complaint (Lederman & Henry, 1978). In all reports that detail the communication problem (Rosenbek et al., 1975; Madison et al., 1977; and this report) multiple features have been described. In the early stage of the syndrome, the most prominent feature was a speech problem, i.e., incorrect production of sounds. In the middle stage, the clinical symptoms were suggestive of aphasia and aphemia. The severity of problems in these stages was temporally related to the dialysis treatments. The final stage was characterized by constant mutism and was unrelated to the dialysis treatments. Death occurred within a period ranging from 5 to 10 months after the communication problems emerged. The major difference among cases was the manifestation of the speech problem. At its onset, Rosenbek et al. (1975) and Madison et al. (1977) identified stuttering, while we observed ataxic dysarthria. In Rosenbek et al.‘s case, the stuttering was accompanied, at one time or another, by an ataxic-spastic-hypotonic dysarthria. In the present case, the ataxic dysarthria was, at one time or another, accompanied by spastic or flaccid dysarthrias. Madison et al.‘s cases reportedly demonstrated stuttering as the only problem in sound production. Dysarthria, confusional state, and mutism were the prominent features of our patient’s communication problem during the course of his illness. It is possible too that he had aphemia and/or aphasia. Each of these will be discussed below.

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Dysarthria Dysarthria was the most prominent deficit observed in the early part of this patient’s hospitalization. Symptoms included (1) unpredictable, irregular, multiple distinctive feature misarticulations, (2) measured staccato, uncontrollably pitched, uncontrollably loud prosody, and (3) inaccurate, uncoordinated nonverbal oral-motor function. This cluster of symptoms closely resembles ataxic dysarthria as described by Darley, Aronson, and Brown (1975). It is important to note that they associated the cluster of symptoms with a “midportion” cerebellar lesion. Additional symptoms in our patient evolved during the middle period of his hospitalization. At times, harsh and strained/strangled phonation qualities and hypernasality, similar to those seen by Darley et al. in spastic dysarthria, were observed. This cluster has been associated with a lesion in the upper motor neuron system. At other times, hoarse and breathy phonation qualities were noted. These other clinical signs are associated by Darley et al. with flaccid dysarthria and a lesion of the lower motor neuron system. The postmortem data in this case do not specifically confirm or rule out the above suggested lesions. The motor strip of the cerebral cortex bilaterally showed no lesions or atrophy. The cortical neurons were abundant and normal in appearance, although mild gliosis was present. Lacunes in the genu of the internal capsule, however, could account for spastic dysarthria. Similarly, the cerebellar cortex, in particular the simple lobule in the midportion of the cerebellum, appeared to be intact. However, subjacent white matter lesions which could damage cerebellar connections were present. Despite the presence of a flaccid dysarthria, no other clinical or structural correlate of a cranial nerve X lower motor neuron lesion was evident. The course of the dysarthria, including dialysis-related and progressive long-term deteriorations, instead corresponded more closely with certain physiological changes, particularly the EEG and CSF pressure changes. This finding, along with the lack of either consistent pathology or evidence of transmissibility in reported cases, may argue for a toxic, metabolic, or nutritional etiology for this syndrome. The recent isolation of foamy virus from the brain of a patient with dialysis dementia (Cameron, Birchall, & Moses, 1978)and the tendency of the syndrome to cluster in certain dialysis centers, however, raise the possibility of infection as another important consideration. Confusional State Decreased and fluctuating attention (shortened digit span on formal testing, difficulty in maintaining a trend of thought, increased distractibility) and communication disorders (dysprosody, misarticulation, dys-

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graphia) are among the most commonly associated features of a confusional state (Chedru & Geschwind, 1972a). The severity of these features was parallel to each other, showed a temporal relationship with dialysis, and became progressively worse over the course of our patient’s illness. The postmortem findings did not reveal structural lesions in sites in which damage may cause a confusional state, such as the brainstem reticular formation, limbic system, prefrontal cortex, or right parietal lobe (Chedru et al., 1972a, 1972b; Mesulam, Waxman, Geschwind, & Sabin, 1976). The course of the confusional state, like the dysarthria, corresponded more closely to physiological changes. Attempts to minimize the physical influences of dialysis on CSF pressure and osmolarity by the use of higher concentrations of glucose in the dialysate and intravenous mannitol lessened the dialysis-associated decline in attention and communication, but did not eliminate them or reverse the course of the syndrome. Increasing or decreasing the frequency and length of dialysis sessions and a change to peritoneal dialysis late in the patient’s course had no clear beneficial effect. Mutism Toward the end of this hospitalization, our patient was mute. Geschwind (1964) has reviewed the psychiatric and neurological causes of mutism. Among the neurological causes, he discussed metabolic disturbances, damage to Broca’s area, pseudobulbar palsy, multiple lacunar infarcts in the basal ganglia, thalamotomies, and upper brainstem and frontal lobe damage as found in akinetic mutism. Damage to the supplementary motor area may also produce transient mutism (Masdeu, Schoene, & Funkenstein, 1978). In our patient, abnormalities of metabolism as well as bilateral lesions in the basal ganglia and internal capsule were present and provide potential etiologies for his mutism. Effortful

Speech

Regardless of the type of dysarthria before a dialysis treatment, speech became effortful by the end of a treatment. At these times, our patient showed difficulty in initiating phonation and articulation, blocked on phonemes, and failed to transitionalize between sounds. Several disorders might account for this effortful speech. Aphemia is one consideration. It refers to markedly effortful speech like that observed in Broca’s aphasia, but without agrammatism or other disturbance in language (Bastian, 1897). Some authors have used the term “apraxia of speech” (Johns & Darley, 1970; Darley et al., 1975) to refer to this disorder. Broca’s area is generally considered to be the site of the lesion (Mohr, Pessin, Finkelstein, Funkenstein, Duncan, & Davis, 1978). Broca’s aphasia is another consideration. It is characterized by a deficit in spoken expression, in particular, effortful speech, word finding difficulty, and agrammatisms.

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This syndrome is generally associated with damage not only to Broca’s area but also to surrounding frontal lobe regions as well (Mohr et al., 1978). It was not possible to determine with certainty the existence of either aphemia or aphasia in our patient. The impaired speech intelligibility precluded a precise analysis of semantics and syntax. Writing disturbances and comprehension difficulties were consistent with aphasia but, in the presence of inattention, could not readily be differentiated from confusional state. Neither, of course, is a feature of aphemia. Moreover, no lesion was identified in Broca’s region or other language areas. Therefore, we cannot rule out the possibility that dysarthria and confusional state were the basis of our patient’s effortful speech. In summary, the communication disorder in dialysis dementia represents an early, characteristic, and integral feature of the syndrome. It is usually the presenting symptom and has been found to occur in all reported cases (Lederman & Henry, 1978). While its nature, setting, and course are distinctive, variations in the communication disorder exist. The varying characteristics may represent a range of presentations of a single entity or suggest subtypes of the syndrome. These may have implications on its course and treatment and could be correlated with possible differences in physiological and postmortem findings in an effort to better understand the nature and etiology of this entity. Communication studies of dialysis dementia patients offer a systematic method to monitor the course of the syndrome, its response to therapeutic trials, and a clinical model for the study of speech disorders in general. REFERENCES Alfrey, A. C., Mishell, J. M., Burks, J., Contiguglia, S. R., Rudolph, H., Lewin, E., & Holmes, J. H. 1972. Syndrome of dyspraxia and multifocal seizures associated with chronic hemodialysis. Transactions; American Society for Artificial Internal Organs, 18, 257-261. Bastian, H. C. 1897. Some problems in connection with aphasia and other speech defects. Lancer, 1, 1005-1017. Cameron, K. R., Birchall, S. M., & Moses, M. A. 1978. Isolation of foamy virus from patient with dialysis encephalopathy. Lancer, 2, 7%. Chedru, F., & Geschwind, N. 1972. Disorders of higher cortical functions in acute confusional states. Cortex, 8, 395-411.(a) Chedru, F., & Geschwind, N. 1972. Writing disturbances in acute confusional states. Neuropsychologia, 10, 343-353.(b) Darley, F. L., Aronson, A. E., & Brown, J. R. 1975.Motor speech disorders. Philadelphia: Saunders. Fisher, H. B., & Logemann, J. 1971.The Fisher-Logemann test of articulation competence. Boston: Houghton Mifflin. Geschwind, N. (Ed.) 1964. Non-aphasic disorders of speech. In Selected papers on language and the brain. Dordrecht, Holland: Reidel. Pp, 73-85. Goodglass, H., & Kaplan, E. 1972. The assessment of aphasia and related disorders. Philadelphia: Lea & Febiger.(a)

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Goodglass, H., & Kaplan, E. 1972. The Boston diagnostic aphasia examination. Philadelphia: Lea & Febiger.(b) Johns, D. F., & Darley, F. L. 1970. Phonemic variability in apraxia of speech. Journal of Speech and Hearing

Research,

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Lederman, R. J., & Henry, C. E. 1978. Progressive dialysis encephalopathy. Annals of Neurology, 4, 199-204. Madison, D. P., Baehr, E. T., Bazell, M., Hartman, R. W., Mahurkar, S. D., & Dunea, G. 1977. Communicative and cognitive deterioration in dialysis dementia: Two case studies. Journal of Speech and Hearing Disorders, 42, 238-246. Mahurkar, D. D., Salta, R., Smith, E., Dhar, S., Meyers, L., & Dunea, G. 1973. Dialysis dementia. Lancer, 1, 1412-1415. Masdeu, J. C., Schoene, W. C., & Funkenstein, H. 1978.Aphasia following infarction of the supplementary motor area. Neurology, 28, 1220-1223. Mesulam, M-M., Waxman, S. G., Geschwind, N., & Sabin, T. D. 1976. Acute confusional states with right middle cerebral artery infarctions. Journal of Neurology, Neurosurgery

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Mohr, J. P., Pessin, M. S., Finkelstein, S., Funkenstein, H. H., Duncan, G. W., & Davis, K. R. 1978. Broca aphasia: Pathologic and clinical. Neurology, 28, 311-324. Rosenbek, J. C., McNeil, M. R., Lemme, M. L., Prescott, T. E., & Alfrey, A. C. 1975. Speech and language findings in a chronic hemodialysis patient: A case report. Journal

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Walshe, F. 1973. Diseases of the nervous system. New York: Longman. P. 30.