Mechanism of repetition in transcortical sensory aphasia.

A typical case of transcortical sensory aphasia (TSA) is presented, in which the Wada test suggests that it is the right hemisphere which enables the patient to repeat orally. It is supposed that one of the mechanisms of preserved repetition in TSA is linked to an exceptional ability for repetition of the right hemisphere, which may help to explain why cases of TSA are so rare.     

经皮质感觉性失语患者的深部失读

目的分析汉语失读特点并探讨其机制。方法对６例经皮质感觉性失语并深部失读患者做补充阅读检查——９２个词先朗读，后配画或解释。结果６例有８５个错读词。４８个词义错读词中大多可正确配画或解释；１９个近形错读词和１１个近音错读词中大多不能正确配画或解释。７个部分词朗读中３个可正确配画。结论字的视觉传入可激活词义系统，但由于字位－音位转换有缺陷致不能正确选择而出现词义错读。错读的语音可激活语音系统，但从同音异义字中选择有缺陷。未证明汉字朗读有语音途径。     

A case of acquired childhood aphasia with evolution of global aphasia into transcortical sensory aphasia

Abstract

A 11–year-old right-handed boy showed global aphasia after an infarct in the distribution of the left middle cerebral artery involving the whole language area, following an operation for ‘moya-moya disease’. Thus, anatomoclinical correlation between the CT lesion site and the resulting aphasic syndrome in this case was similar to that described in adults. However, he demonstrated rapid recovery of language fluency with poor recovery of language comprehension, in contrast to comparable adult cases. Consequently, his global aphasia resolved into transcortical sensory aphasia. This case seems to support the current view that recovery of fluency in childhood aphasia is quicker and more extensive than in adults.     

Postictal mixed transcortical aphasia.

Postictal aphasia has been described in left temporal lobe seizures. It may be of fluent, non-fluent or global type. We present here a patient who displayed signs of mixed transcortical aphasia (MTCA). The patient was a 67 year old man who underwent excision of a left frontal parasagittal meningioma in 1987. Since then he has been treated with phenytoin for generalized tonic-clonic seizures (GTCS). He was admitted in status epilepticus. On awakening, the patient was non-fluent with palilalia and echolalia. His repetition was relatively preserved but all the other language functions were impaired. This picture faded away within a few hours. Brain CT, performed during this postictal state, was normal except for signs related to frontal craniotomy. SPECT, which was performed after language functions returned to normal, displayed left frontal, cingular and insular hypoperfusion. The postictal language dysfunction of the patient corresponded to MTCA. Although our case has frontal, he had no other structural lesion that could explain either diffuse ischemia of the left hemisphere or watershed areas secondary to the generalized seizures. The uniqueness of this case is the combination of postictal MTCA with good prognosis.     

Anatomic basis of transcortical motor aphasia

Analysis of language profiles and CT anatomy in transcortical motor aphasia (TCMA) suggests that the essential lesion is disruption of connections at sites between the supplementary motor area and the frontal perisylvian speech zone. If the lesion is extended, there may also be poor articulation (lesion deep to motor strip for face), impaired auditory comprehension (lesion in anterior head of caudate, anterior limb internal capsule, anterior putamen, and anterior portion of external capsule, claustrum, extreme capsule, and insula), or stuttering (lesion in pars opercularis and lower third of premotor region). This concept unifies disparate anatomic and psychophysiologic observations about three syndromes: classical TCMA, aphasia after left medial frontal infarction, and TCMA during recovery from Broca's aphasia.     

The use of cueing to alleviate recurrent verbal perseverations: Evidence from transcortical sensory aphasia

Background: Previous studies have demonstrated that stimulus factors, including item frequency, presentation rate, stimulus repetition, and semantic relatedness, can influence the rate of recurrent verbal perseverations. These manipulations alter the balance of activation between current targets and past responses, suggesting that perseverations arise when the activation of a previously presented item overrides the weak processing of a new stimulus. By this view, cues and sentence contexts that bias inter‐item competition towards the target and away from earlier responses should dramatically reduce the frequency of perseverative errors. However, the influence of these factors on perseverations has not been previously investigated.

Aims: To examine the effect on perseverative rate of altering the activational balance between past and present responses using both intrinsic and extrinsic stimulus manipulations.

Methods & Procedures: This study examined repetition, reading, and picture naming in a highly perseverative patient with transcortical sensory aphasia.

Outcomes & Results: The patient's strong perseverative tendencies were impervious to the stimulus factors listed above but he was able to overcome these errors to produce more correct responses when he was provided with phonemic, word, and sentence cues. These environmental constraints had a similar effect on perseverations in reading aloud and picture naming, although active repetition was necessary for a cue to benefit reading, whereas passively hearing the cue was sufficient to improve picture naming.

Conclusions: This task difference is likely to reflect the greater reliance of picture naming on semantic processing, which will benefit from cues regardless of whether they are repeated. We propose that poor internal control of language production allowed perseverations to dominate our patient's output. External constraints in the form of cues/sentence contexts overcame this deficit, dramatically reducing the rate of perseverations.     

An autopsy case of transcortical motor aphasia

An autopsy case of transcortical motor aphasia is presented with a pathology located anterior and superior to the pars opercularis of the left inferior frontal gyrus. Case H. Y. A 60-year-old right-handed man. On Nov. 14, 1978, the patient had surgery to remove cerebral hematoma in the left frontal lobe. In the neuropsychological examination before the operation, he had shown the clinical features of transcortical motor aphasia characterized by good comprehension of language, preserved repetition, and spontaneous speech disorder. In this stage, it was supposed that the underlying disturbance of spontaneous speech was due to the disabilities of contextual constructions of sentences rather than the lack of speech initiation. Following the operation, however, spontaneous speech disappeared completely for several days. At the same time, the patient showed problems in comprehension, reading, writing and confrontation naming as well as symptoms of disorientation, pathological inertia and 'loss of initiation' in the psychomotor domain. During the following three months, however, the patient did show slight improvement, except for contextual sentence constructions and pathological inertia when taking the complex animal drawing test. In his terminal stages, the clinical symptoms could be summarized as transcortical motor aphasia and mild frontal lobe syndrome. On March 1, 1979, the patient died of Hamman-Rich syndrome. Postmortem examination: The brain weighed 1294 gm. The external observation of the brain disclosed the linear tissue defect, about 15 mm in length and 10 mm in width, along the radial sulcus of the pars triangularis of the left inferior frontal gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Mixed transcortical aphasia in nonfamilial dysphasic dementia

The neurolinguistic and cognitive profiles of a patient with mixed transcortical aphasia and non-familial dysphasic dementia associated with progressive, left perisylvian involution are presented. This clinicopathological entity has recently been shown to be an example of a novel class of intrinsic, focal cortical degenerations with sparing of the basal forebrain. The characteristics of the aphasia were unusual. There were occasional literal and verbal paraphasic errors, but no completion phenomenon, embellishment or significant echolalia. Evidence of a generalized lexical disruption was found on detailed analysis of residual abilities in reading, writing and spelling. A newly described form of non-lexical repetition was present, resulting in the patient's inability to correct syntactical and semantic errors. Affective prosodic repetition was intact. A combined paraphasic word-production and semantic anomia was found. These observations combined with evidence of evolving region-specific cognitive impairments suggest that the pathological process resulted in a relative disconnection of integral frontal and parieto-occipital areas from adjacent perisylvian language zones.     

Ataxic hemiparesis associated with transcortical motor aphasia

Two patients, ages 51 and 76 years, suddenly developed transcortical motor aphasia combined with pyramidal signs and ataxia of the right extremities that affected the leg more severely than the arm. Computed tomography revealed nonenhancing lucencies in the distribution territory of the left anterior cerebral artery involving the genu of the corpus callosum, white matter ventral to the left frontal horn, medial primary motor area, supplementary motor area, and superior part of the premotor area. It is postulated that aphasia, ataxia, and weakness resulted from involvement of the supplementary motor area and deep white matter, premotor, and primary motor areas, respectively. Anterior cerebral artery infarctions of the dominant hemisphere may result in transcortical motor aphasia associated with contralateral ataxic hemiparesis.     

Recovery of semantic word processing in transcortical sensory aphasia: a functional magnetic resonance imaging study

In a previous functional magnetic resonance imaging (fMRI) study with normal subjects, we demonstrated regions related to conceptual-semantic word processing around the first frontal sulcus (BA 9) and the posterior parietal lobe (BA 7/40) in agreement with several previous reports. We had the possibility, using the same fMRI paradigm, to study two consecutive cases with left middle cerebral artery (MCA) infarction (RC and HP) and lesions affecting either solely the pre-frontal (HP) or both the pre-frontal and posterior parietal part of the network activated in normal subjects (RC). Both patients showed transcortical sensory aphasia (TSA) on acute assessment. This contradicts classical disconnection accounts of the syndrome stating intact conceptual representations in TSA. Their recovery of language comprehension was associated with activation of a left hemispheric network. Mainly activations of left perilesional pre-frontal regions (RC), left Wernicke's area (RC and HP) or the left posterior middle and inferior temporal cortex (HP) were demonstrated in the TSA patients. The latter findings suggest that in our cases of TSA functional take-over has occurred in regions with related functions ('redundancy recovery') rather than in previously unrelated areas ('vicarious functioning'). Our data support distributed models of conceptual-semantic word processing and multiple left hemispheric representations of closely related functions.     

Repetition of affective prosody in mixed transcortical aphasia

Two patients with mixed transcortical aphasia could repeat propositional speech but not affective prosody. These findings suggest that the intact perisylvian region responsible for propositional speech does not mediate effective prosody. We propose that affective prosody is incorporated into propositional speech by means of an interhemispheric mechanism and that the failure of these patients to repeat affective prosody was caused by a disconnection of the left perisylvian structures from the right hemisphere structures thought to mediate affective prosody.     

A specific pattern of executive dysfunctions in transcortical motor aphasia

Background: Recent studies imply that executive functions (EF) are closely related to our ability to comprehend and produce language. A number of findings suggest that functional communication and language recovery in aphasia depend not only on intact language abilities but on EF as well. Some patients with transcortical motor aphasia (TMA) show language deficits only in tasks in which conflicting representations must be resolved by executive processes. In line with these results, others have proposed that TMA should be referred to as “dysexecutive aphasia”. EF in aphasia have mostly been studied using neuropsychological tests, therefore there is a need for systematic experimental investigations of these skills.

Aims: 1. To investigate EF in TMA, and to test whether executive dysfunctions are specific to TMA. 2. To experimentally measure different components of EF: updating working memory representations and inhibition of prepotent responses.

Methods & Procedures: Five individuals with TMA, five patients with conduction aphasia and ten healthy controls participated. We designed four nonverbal tasks: to measure updating of working memory representations, we used a visual and an auditory n-back task. To assess inhibition of prepotent responses, we designed a Stop-signal and a nonverbal Stroop task. All tasks involved within-subject baseline conditions.

Outcomes & Results: We found certain EF deficits in both groups of individuals with aphasia as compared to healthy controls. Individuals with TMA showed impaired inhibition as indexed by the Stop-signal and the nonverbal Stroop tasks, as well as a deficit of updating of working memory representations as indexed by the auditory n-back task. Participants with conduction aphasia had difficulties in only one of the tasks measuring inhibition, but no clear evidence for impairment of updating of working memory representations was found.

Conclusions: Although the results show different patterns of EF deficits in the groups with aphasia, the findings clearly demonstrate that EF deficits are not specific to participants with TMA. Based on these results, and on earlier data highlighting the role of executive processes in functional communication and language recovery, we suggest that tests of EF should be an inherent part of clinical aphasia assessment.     

Mixed transcortical aphasia without anatomic isolation of the speech area

We report two patients with mixed transcortical aphasia following left frontal lobe infarctions. Although there was no evidence of anatomic isolation of the speech area on computed tomograms or magnetic resonance imaging scans, single-photon emission computed tomography in one case demonstrated diminished blood flow over the left parietal convexity suggestive of "functional isolation" of the posterior perisylvian language zone.     

A case of mixed transcortical aphasia with intact naming.

Altholgh Lichtheim recognized that Wernicke's 'reflex arch' (primary auditory area, to Wernicke's area, to Broca's area, to primary motor area) was important for repetition, he recognized that other areas of the brain (for example, area of concepts or semantic area) must be important in comprehension and voluntary speech. He suggested that Wernicke's area (phonemic area) not only projected to Broca's area (as Wernicke suggested) but that it also projected to the area of concepts. A lesion of this latter pathway or in the area of concepts would produce a syndrome where repetition was intact but comprehension was impaired (e.g. transcortical sensory aphasia). Lichtheim also thought that the area of concepts projected directly to Broca's area and that voluntary speech was mediated by this pathway. Although Lichtheim's model could explain the mechanism underlying transcortical aphasia, his schema could not explain anomic aphasia. Unlike Lichtheim's schema, Kussmaul's schema suggested that the area of concepts projects back to Wernicke's area before projecting to Broca's area. With this schema, a patient with a hypothetical lesion which interrupted the pathway from the area of concepts to Wernicke's area (but did not interrupt the pathway from Wernicke's area to the area of concepts) should be anomic, with normal comprehension and repetition. In order for this latter schema to be plausible there should also be a lesion which interrupts the pathway from Wernicke's area to the area of concepts but does not interrupt the pathway which goes from the area of concepts to Wernicke's area. A patient with this hypothetical lesion should comprehend poorly; however, in spite of poor comprehension, naming and repetition should be intact. We report a patient who demonstrates poor comprehension with intact naming and repetition. This patient could also read aloud but could not comprehend written language. Not only could this patient name objects but he could demonstrate their use. These observations suggest that comprehension of written language is mediated by a different pathway than the recognition of visually presented objects.     

Treatment of verbal akinesia in a case of transcortical motor aphasia

Abstract

Patients with transcortical motor aphasia frequently demonstrate an ‘akinesia of speech’ resulting in decreased word fluency, reduced syntactic complexity, and diminished speech initiative. A treatment protocol targeting verbal generativity in terms of communicative expansion was instituted in this case study to address the patient's deficit area—deficient linguistic planning and goal setting. The patient demonstrated adequate lexical and syntactic skills and improved sentence generation performance as a result of treatment. However, treatment effects were short-lived as the patient returned to pre-treatment levels on the generalization measures three months post-discharge.     

Akinetic mutism and mixed transcortical aphasia following left thalamo-mesencephalic infarction

A 54-year-old man developed somnolent akinetic mutism and acute mixed transcortical aphasia following a left thalamo-mesencephalic infarction. He also exhibited behavioural changes, namely apathy, slowness, lack of spontaneity, disinhibition, perseveration, gait apraxia and incontinence consistent with frontal lobe dysfunction. Presumably the akinetic mutism and language dysfunction were due to the thalamic stroke. All the manifestations could be related to interruption of the frontal-subcortical circuitry.