the role of the right hemisphere in recovery from aphasia. two case studies

THE ROLE OF THE RIGHT HEMISPHERE IN RECOVERY FROM APHASIA. TWO CASE STUDIES

Anna Basso!, Maurizia GardellP, Maria Pia GrassP, Marita MariottP

(lNeurolo~ical Clinic, Milan University; 2Rehabilitation Service, Cremona; Neurological Department, "L. Sacco" Hospital, Milan)

A century-old question concerns the role of the right hemisphere (RH) in recovery from aphasia. This possibility has been supported since the end of the 19th century by clinical observation. Gowers, in describing an aphasic patient, made the following comment: "Loss of speech due to permanent destruction of the speech region in the left hemisphere (LH) has been recovered from, and that this recovery was due to supplemental action of the corresponding RH is proved by the fact that in some cases, speech has been again lost when a fresh lesion occurred in this part oftheRH" (Gowers, 1887, pp. 131-132).

Some indirect evidence that supports transfer oflanguage dominance comes from studies using tachystoscopic or dichotic presentation of linguistic stimuli. Contrary to what occurred in normal controls, a significant left visual field preference for verbal stimuli was found in a group of 30 aphasic patients (Moore and Weidner, 1974). When they were divided into three groups according to time-post-onset, no significant group difference emerged in the mean scores for the left visual fields, as if the shift in visual field preference had already been completed in the first months of disease.

The same patients also showed a left ear preference on verbal dichotic tests (Moore and Weidner, 1975) when seen more than 6 months post-onset, a finding also confirmed by Johnson, Sommers and Weidner (1977). Results of a subsequent study (Pettit and Noll, 1979) tend to support the hypothesis that as language recovery takes place cerebral dominance becomes more firmly established in the RH. When retested 2 months after the first examination, aphasic patients did show a greater reduction of errors in the left ear than in the right ear.

More direct evidence supporting the hypothesis that the RH has an important role in recovery of language and that this process takes a long time comes from studies using the techniques of carotid barbiturate injection and regional cerebral blood flow. In Czopfs study (1972) an injection on the right caused total arrest of speech in 10 severe aphasics seen 3 weeks to 13 years post-onset; it moderately worsened speech in 8 patients seen 12 days to 2 years post-onset and had no effect in 3 acute patients. Kinsbourne (1971) studies 3 aphasic patients; after none of the 3 left-sides injections was there any speech arrest, which did occur following the 2 right intracarotid amobarbital injections.

Cortex, (1989) 25, 555-566

556 Anna Basso, Maurizia Gardelli, Maria Pia Grassi, Marita Mariotti

Meyer et al. (1980) studied rCBF in 14 patients with LH infarctions and aphasia. Patients were divided into 2 groups according to whether they had or had not regained functional language, irrespective of initial severity. The 8 patients with functional language showed sizable increase in the circulation of the right frontal area but not of the left Broca's area during behavioral activation, while the 6 patients who did not regain functional language had paradoxical decrease of rCBF in the middle cerebral artery territory of both hemispheres. The authors consider this result as evidence of the participation of the RH in language function in patients with good recovery. Results of a second rCBF study (Knopman et al., 1984) are more difficult to interpret. Group 2 patients, who had higer auditory comprehension scores at follow-up, showed a diffuse significant increase in the mean RH CBF when investigated within 100 days after stroke, and a significant increase of the left posterior temporal-inferior parietal CBF at follow-up, approximately 100 days later. In Group 1 patients with lower auditory comprehension scores at follow-up, there was no hemispheric difference in the early study and a significant increase in both inferior frontal areas at follow-up. The authors interpreted this finding as evidence for early participation of the RH in language comprehension recovery with later return of function in the LH.

A contribution of the right hemisphere to recovery of language in aphasic patients has also been suggested by results of studies using an evoked potential (EP) paradigm (Papanicolaou, Levin and Eisenberg, 1984; Papanicolaou et al., 1987). During a language task there was EP amplitude attenuation in the LH of normal subjects and the RH of aphasic patients. Due to disparity of the techniques used and heterogeneity of experimental groups, results of these studies are not directly comparable. Time-post-onset was extremely variable: from 1 month in a patient of Papanicolaou et aI's study (1984) to 93 months in Moore and Weidner's studies (1974, 1975). When shift of cerebral dominance for verbal tasks occurs rapidly, it can point to the removal of the LH inhibition on the RH's intrinsic verbal capacity that can now be utilised; when it takes a longer time to occur, it can be attributed to a real taking over of a new verbal competence by the RH. A second major problem in interpreting these results is that, since the initial severity of aphasia was generally not taken into account, it is not possible to know whether "recovered" patients simply had a more functional language at first examination or whether they really ameliorated. Only in the latter case can the RH be assumed to take over; if amelioration has not occurred, the RH may simply be displaying its preexisting language capacity. Clinical evidence of a shift in cerebral dominance for language in aphasics is much more meager and is based on the worsening of a partially recovered aphasia following a new lesion located in the RH (Gowers, 1887; Nielsen, 1946; Levine and Mohr, case 3, 1979; Lee et al., 1984). Nielsen (1946), for example, observed some patients who recovered partially or completely from aphasia precipitated by LH lesion and were apparently again rendered aphasic by new RH lesions. More compelling proof that the RH participates in recovery after non-infantile focal damage has been obtained only in the setting of hemispherectomy. In the cases reported (Hillier, 1954; Smith, 1966; Gott, 1973; Burklund and Smith, 1977), some language comprehension could be demonstrated, with rather remarkable recovery in a few cases, while expressive language abilities remained much more impaired.

Right hemisphere and recovery from aphasia 557

In this paper we report 2 women who, after having partly recovered from global aphasia consequent to an LH stroke, showed severe worsening of the language disturbances after a second vascular accident affecting the RH which occurred after 3 years and 6 months, respectively. These cas.es are illustrative of the possibilities and limits of RH take over.

CASE REpORTS

Case TC

In December 1984, TC - a 53-years-old right-handed woman without any evidence of familial left-handedness and with 17 years of schooling - manifested a right-sided

Fig. 1 - CT o/patient TC.: after theftrst stroke.

558 Anna Basso. Maurizia Gardelli. Maria Pia Grassi. Marita Mariotti

weakness and inability to speak. Approximately 20 years previously, mitral steno-insufficiency had been diagnosed. She was never treated but recent ECG controls were normal.

On admission, she was comatose with severe right hemiplegia, deficit oflower right VII nerve and right Babinski. An ECG showed atrial fibrillation. A CT scan performed on the following day revealed a large hypodense fronto-temporo-parietal area in the left hemisphere, possible expression of an ischemic lesion. In the following days she gradually regained consciousness. Episodes of possible atrial fibrillation were noted. The right hemiplegia and the language disturbances remained stable. A CT scan performed 3 months post-onset confirmed the presence of a large cortico-subcortical hypodense lesion in the LH affecting the fronto-temporo-parietal region, the head of caudate nucleus, the lenticular nucleus, the internal capsule and corona radiata and revealed dilatation of the left lateral ventricle (see Figure 1). The patient was discharged on April 4, 1985 in relatively good health, with right hemiparesis and global aphasia.

Fig. 2 - CT of patient TC.: after the second stroke.


TABLE I

Test Results of Patient TC at 1st (January, 1985), 2nd (February, 1987) and lrd (December, 1987) Examination after the Left-sided Stroke, and at 1st Examination (February, 1988) after the Right-sided

Stroke

O. Prod. O. Compr. Wr. Prod. R. Compr Token Apraxia

W S W S W S W S Test BF 1M (% correct) (0-36) (0-20) (0-72)

Jan 85 0 0 55 5 0 0 35 0 7 3 50 Feb 87 90 10 90 90 20 0 100 80 13 13 / Dec 87 85 50 100 75 45 0 100 80 17 17 64 Feb 88 0 0 0 0 5 0 95 0 (wr) 0 2 47

o =oral; Wr =written; R =reading; Prod =production; Compr =comprehension; BF =buccofacial; 1M =ideomotor; W =words; S =sentences.

In January, 1988, when she was 56, TC had an epileptic fit for which she was readmitted to the hospital. On admission the neurological examination revealed a mild deficit of the lower right VII nerve, right hemiparesis with the arm and hand most affected and right Babinski. There were no motor disorders of the left arm or leg. The language disturbance had much worsened. A CT scan performed 5 days post-onset revealed, in addition to the old left-sided lesion, a dishomogeneous density area in the right temporoparietal region which was confirmed by a second CT scan carried out in February, 1988. In one slice the lesion on the left appeared slightly more extended anteriorly than after the first stroke. This difference, however, can be explained by the different inclination of the CT sections in the 2 exams (see Figure 2).

Auditory evoked potentials were recorded and showed normal brain stem response, an almost total suppression of cortical response in the RH and abnormal and unclassifiable waves in the LH. First Neuropsychological examination (January, 1985) and follow-up (November, 1985 -December, 1987).

While in hospital in January 1985, the patient was given a first aphasia examination. There was no speech output except for some vocal sounds. She could not speak, repeat or read aloud. Writing was also impossible; the patient could not write to dictation, sign her name or copy. She comprehended isolated words (11 of 20 correct) but not sentences and scored 7/36 on the Token Test (De Renzi and Faglioni, 1978). Severe oral apraxia (OA) was also present (3 of 20; cut-off score: 16/20, according to De Renzi, Pieczuro and Vignolo, 1966) and mild ideomotor apraxia (IMA): 50 of 72 (cut-off score: 53 according to De Renzi, Faglioni and Sorgato, 1982). Test results of this and subsequent examinations are reported in Table I.

Daily language rehabilitation was undertaken. Initially the patient was not very cooperative and only rehabilitation of oral comprehension was undertaken. After approximately one month articulation of simple phonemes was started and soon the patient was asked to name to confrontation.

A first control examination was given in November, 1985. Spontaneous language was possible in disjointed words but not complete sentences. Repetition and reading aloud of words and short sentences were now possible and she could sign her name. She scored 10/36 on the Token Test. Language therapy was continued 4 times a week. Recovery was very slow but gradual and continuous.

In February, 1987, oral confrontation naming was generally correct (18/20) but written confrontation naming was still severely impaired (4/20). Repetition and reading aloud were performed more easily and were generally correct for words and sentences. On the Token Test she only gained 3 points (13/36) but comprehension appeared to be easier and the patient was more self-confident about what she understood. Speech output was still scarce but no longer confined to isolated words. The patient could describe a picture or relate an event, even though she omitted some verbs and mentioned only some of the


indispensable items. At that time she could answer the telephone and have a simple conversation with her family and friends. OA was still present but much less severe than initally (13/20) (see Table I).

A last control before the second stroke was performed in December 1987. Overall amelioration was evident. Spontaneous speech was richer but some main verbs were still omitted. Writing of isolated words was possible (9/20 correct on a written confrontation naming task and 16120 correct in a writing to dictation task). She scored 17/36 on the Token Test which corresponds to the mean score for a group of unselected nonfluent aphasics (De Renzi and Faglioni, 1978). OA and IMA were no longer present. She was classified as Broca aphasic (see Table I).

Second Neuropsychological Examination (February, 1988)

The examination was undertaken on the 18th day after the second stroke and lasted for 8 days. The patient's condition remained stable during this time.

Oral comprehension was completely abolished: The patient behaved like a deaf person, paying no attention to sounds or when spoken to. Written comprehension of single words and some very simple sentences and commands was possible. Speech output was nearly completely absent, except for one word ("again") which she frequently uttered. TC could sign her name and write 1 of 20 words in a confrontation naming task. Repetition, writing to dictation and reading aloud were totally impossible. Only the written version of the Token Test was undertaken but she scored 0/36. OA again was extremely severe (2120) and also IMA was present (47172) (see Table I). She performed only the first 3 items of the constructive apraxia test and refused to continue. In a cancellation task, she cancelled all the lines. After the second stroke, TC was depressed and unwilling to cooperate, but she improved and has now resumed language therapy. Auditory comprehension is still totally abolished but she pays attention to noises (telephone, ringing bell, car, farm tractor) even if inconsistently. She lip-reads some words but it is easier to communicate with her by writing. She makes herself understood by uttering some rare words and, more frequently, by gestures. She is active at home and has resumed some house-work.

CaseAB

AB is a 61-year-old right-handed woman with no familial history ofleft-hendedness and unremarkable medical history except for rare episodes of migraine and epistaxis until the onset of the present disease. She had completed 5 years of schooling and had always worked as a house-wife. On April 21 , 1988 her husband found her lying on the floor, alert but incapable of speaking and with right hemiplegia. She was immediately admitted to hospital, where she arrived alert but with global aphasia.

Neurological examination revealed a deficit of the lower right VII nerve, a complete right hemiplegia and a Babinski sign on the right. Blood pressure was 240/110. An ECG showed sequelae of septal necrosis. A CT scan showed an intracerebral deep left hemorrhage affecting the insula, external capsule, lenticular nucleus, internal capsule, head of caudate nucleus and corona radiata, a mass effect upon left lateral ventricle with shifting of the median line. A CT scan performed a month later demonstrated a low density lesion in the same region still displacing the ventricle (see Figure 3). During her stay in hospital there was good recovery of language (see infra) but much less so of motor disorders: her arm remained totally plegic. She was discharged at the beginning of August, 1988. The motor disorder had not changed and she could only walk with help. She pursued language therapy daily at home with good recovery, while the motor disorder remained unchanged.

On October 17, she suddenly found herself unable to speak and was readmitted to hospital. On admission the patient was alert, speechless, with deficit of the VII right nerve, complete right hemiplegia and Babinski on the right. ECG was unchanged. She also had severe impairment of voluntary movements of the bucco-facial apparatus and difficulty in swallowing foods and liquids. Two days later a CT scan without contrast injection showed a right hemorrhage, mainly temporal with perifocal edema and mass effect on the right lateral ventricle and on the left a deep cystic cavity with dilatation of the left lateral


ventricle (see Figure 4). On the third day AB became stuporous. Neurologically she was unchanged except for bilateral Babinski. After introduction of cortisone she progressively regained normal vigilance. On the 7th day she managed to swallow, and on the 14th day to walk. When discharged, her neurological conditions were the same as in May except for language.

First aphasia examination and follow-up (May, 1988 - October, 1988)

Three weeks after onset, a language examination was administered. AB was uncooperative and most of the times she did not respond to the examiner's requests. Spontaneous language was abolished: she could only repeat some simple bisillabic words and emit some vocalic sounds. Comprehension of some isolated words and very simple sentences was possible. She scored 8/36 on the Token Test (De Renzi and Faglioni, 1978). Reading and writing were impossible. Severe apraxia (oral, ideomotor, of use) was also present but it was not possible to quantify her defect as she did not always attempt to imitate what the examiner showed her.

Fig. 3 - CT of patient AB.: after the first stroke.


Daily language rehabilitation was undertaken and a week later AB could easily repeat simple words and was heard saying her daughter's name. By the end of May, her comprehension had improved and she correctly answered yes or no to personal questions. High frequency objects were correctly named on confrontation. Daily rehabilitation continued at home. In october, AB could easily have a conversation with her family and friends. Reading and writing were also better and she could correctly write simple words, spontaneously or after dictation. A control language examination was planned for the end of the month but it could not be given due to her second stroke.

Second language examination (November 1988)

AB had a second language examination 20 days after her second stroke .. Her aphasia profile was quite similar to that found at first examination but she was now totally speechless and performance of voluntary movements of the facio-bucco-lingual muscles was greatly impaired. Mimicry was normal. Oral and written comprehension were pos-

Fig. 4 - CT of patient AB.: after the second stroke.


siJ>le only for some isolated words and the simplest sentences. She scored 6 on the Token Test. She could sign her name and write some letters to dictation. She scored 15/36 on the Raven's Colored Matrices 47. She was classified as global aphasic with total loss of overt articulation. OA was not tested because of impairment in performance of voluntary movements. In the apraxia-of-use test she used the toothbrush to brush her skirt; the other objects were correctly used. IMA was not present (53/72).

She resumed daily language rehabilitation. At the beginning of January, 1989, a control examination showed marked improvement in all language modalities but AB was still well below the level of proficiency she had attained before her 2nd stroke. Speech output was scarce with frequent phonemic errors and rare word finding difficulty. Oral confrontation naming was correct for 12 of 20 words. Writing was more impaired and the patient managed to correctly write only 2/20 words in a written confrontation task and none in writing to dictation. Comprehension was sufficient for simple sentences and she scored 15/36 on the Token Test. Reading aloud and repetition were possible with many phonemic errors and deletions. IMA (63/72) and apraxia of use were not present and OA had improved (11/20). She scored 23/36 on the Raven's Colored Matrices 47.

DISCUSSION

TC was a global aphasic who gradually regained some functional language to the point of becoming a Broca aphasic with agrammatic output and severely impaired spontaneous writing 3 years post-onset. A second stroke in the RH left her with totally abolished auditory comprehension; written comprehension was still possible but severely impaired and there was no speech output. AB, too, was initially a global aphasic who gradually recovered and regained a language level sufficient for family life six months later.

After the RH stroke, TC had word deafness and a global deterioration of her language functions; AB became speechless and showed a worsening of aphasia. In neither case can the aggravation be attributed to a temporary suppression of activity due to functional shock or diaschisis, because their recovery after the second stroke was not as quick as implied by such an assumption.

Neither is it possible to attribute the whole aphasic picture shown by these patients to word-deafness in TC and to loss of overt articulation. in AB. TC's word-deafness can easily explain the aggravation of the auditory comprehension disorder and the impossibility to repeat and write to dictation, but not the severe aggravation of reading comprehension, speech production and oral confrontation naming. Speechlessness due to damage to cortical areas crucial for realization of speech has indeed been reported (Levine and Mohr, 1979; Villa and Caltagirone, 1984; Vallar and Cappa, 1987) but it cannot account for the worsening of oral and written comprehension and writing observed in AB after the RH hemorrhage.

We can safely conclude that the RH lesion was responsible for the language disruption following the second stroke and, by inference, assume that the RH had taken over language functions after the first stroke. The RH contribution to verbal activity can be attributed to one of the following reasons. (1) In these patients language had always been bilaterally represented, as it happens in a minority of right-handed subjects (Milner, Branch and Rasmussen, 1964). (2) A lesion in the language dominant LH disinhibited the RH. The rapid recovery observed in some cases of childhood aphasia has suggested to some authors that


at an early age the right and left hemispheres do not differ in language competence but that, subsequently, inhibitory processes would progressively develop and cause hindrance to RH linguistic specialization. On this account, damage to the LH would lead to disinhibition or reactivation oflatent language potentialities of the RH (see Lenneberg, 1967). (3) What appeared to be due to recovery was in fact the manifestation of the normal verbal contribution of the RH language processing (Zaidel, 1976, 1977, 1978). (4) Finally, the RH may be able to "take over" language capacity.

The first hypothesis, bilateral representation of language, is ruled out by the fact that it took TC 3 years and AB 6 months to partially recover from global aphasia.

By the same token, the second and third hypotheses can can also be dismissed. If dishinibition of original RH language competence or the manifestation of the normal contribution ofthe RH to language processing were the cause of recovery, its effects would have become manifest quicker.

The third hypothesis of a "normal" participation of the RH in language is also difficult to reconcile with the failure of most global aphasics to recover functional language when their RH is intact. Moreover, at least in AB, the pattern of improvement did not correspond with the features of speech and language competence attributed to the RH, viz. a greater ability to comprehend than to produce speech and.a relatively sophisticated semantics in contrast to poor phonological or syntactic competence. Though not abundant, her speech was fluent and without phonemic errors, and sentences were rather short but correct. Apparently, TC's language was more consistent with putative RH competence, as her speech was non-fluent and she omitted some main verbs in speaking.

The last possibility is that the RH can partially "take over" language. Even if this appears to be the most likely explanation in the present cases, one has to admit that this lateral shift can hardly be considered the rule and differs remarkably from one patient to another since with rare exceptions (Cummings, Benson, Walsh and Levine, 1979), global aphasics, who presumably have large lesions destroying all the classical LH language areas, do not improve substantially. That compensation by the RH is rare is also suggested by Rasmussen and Milner's (1975) findings that only 12 per cent of adult patients with early LH damage had RH speech representation, determined by carotid barbiturate injection. It is conceivable that the percentage would be even less in patients who have incurred in LH lesions at a later stage.

A last point is worth mentioning. A number of data from clinical studies point to a less marked asymmetrical representation of linguistic competence in the female than in the male brain and aphasic females have also been reported to improve more than aphasic males (Basso, Capitani and Moraschini, 1982; Pizzamiglio, Mammucari and Razzano, 1985). On this account it may be relevant that both patients were women.

ABSTRACT

We report two female patients who became global aphasic following a large left hemisphere lesion. With passage of time they recovered to a considerable extent, but three years and six months, respectively, after the former eVA, a new stroke lateralized to the


right hemisphere occurred and they showed a definite worsening of language disturbances.

Possibilities and limits ofthe right hemisphere in "taking over" language functions are discussed.

Acknowledgments. This research has been supported by a grant from CNR. We are grateful to Dr. Villani for permission to investigate the patients and to Dr. S. Della Sala for his helpful comments on a previous draft of the paper.

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Anna Basso, Clinica Neurologica, via F. Sforza 35 - 20122 Milan - Italy.

the role of the right hemisphere in recovery from aphasia. two case studies

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