[ON THE SYMPTOMATOLOGY OF THE PARIETAL BRAIN SYNDROME OF THE DOMINANT HEMISPHERE. APROPOS OF PARIETAL DYSLEXIA AND CONDUCTION APHASIA].
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This study describes the linguistic and neuropsychological findings in three right-handed patients with crossed conduction aphasia. Despite the location of the lesion in the right hemisphere, all patients displayed a combination of linguistic deficits typically found in conduction aphasia following analogous damage to the left hemisphere. Associated cognitive deficits varied across the three patients. In addition, all cases showed deficits classically attributed to non-dominant hemisphere damage (visuoperceptual deficits and reduced figural memory). As a result, lesion-behaviour relationships in our study sample indicate both dominant and non-dominant qualities of the right hemisphere.
To evaluate the role of the sub-cortical white matter and cortical areas of the supramarginal gyrus in short-term memory impairment (shortened digit or letter span) and repetition difficulty, four patients with conduction aphasia and impaired short-term memory and two patients with only short-term memory impairment were given digit span, letter span, speech audiometry and dichotic listening tests. The results showed that in most of the patients letter span was inferior to digit span and that bilateral ear suppression in the dichotic listening test was observed in two patients with a lesion in the inferior part of the supramarginal gyrus, suggesting that what was affected was phonological information and that the supramarginal gyrus was the storage site. The overlapped lesion of conduction aphasia patients with short-term memory impairment was the periventricular white matter at the upper to middle part of the trigone, while patients with only short-term memory impairment had a lesion in the inferior supramarginal gyrus in common. Thus, damage to the periventricular white matter at the trigone may yield the phonemic paraphasia characteristic of conduction aphasia, while damage to the inferior part of the supramarginal gyrus may result in the impairment of short-term memory. We believe that as a part of the mechanisms of short-term memory and repetition, phonological information is processed in the primary auditory cortex and goes through the periventricular white matter to the inferior part of the supramarginal gyrus and is temporarily stored there.
An 11-year old girl is described who acquired conduction aphasia after head trauma. Detailed study of her repetition defect showed that it was because of impaired short-term verbal memory. CT scan showed two hypodense areas in the left hemisphere, which included the supramarginal gyrus and Wernicke's area. This case is similar to adults with conduction aphasia, indicating the early intrahemispheric specialisation for verbal functions, in this case auditory verbal short-term memory.
In this study, the linguistic performance of 20 patients with acute conduction aphasia (CA) is described. CA presented as a relatively homogeneous aphasic syndrome characterized by a severe impairment of repetition and fluent expressive language functions with frequent phonemic paraphasias, repetitive self-corrections, word-finding difficulties, and paraphrasing. Language comprehension as assessed by tests of auditory and reading comprehension was only mildly impaired, whereas most patients performed poorly on the Token Test. Verbal-auditory short-term memory was reduced in all patients except one and seems to play a role in associated cognitive deficits, such as impaired syntactic comprehension or reduced mental arithmetics. A follow-up examination of 12 patients showed that CA often resulted in a chronic language deficit. Lesion locations were the posterior temporal and inferior parietal lobe.
Assessment of eloquent functions during brain mapping usually relies on testing reading, speech, and comprehension to uncover transient deficits during electrical stimulation. These tests stem from findings predicted by the Geschwind-Wernicke hypothesis of receptive and expressive cortices connected by white matter tracts. Later work, however, has emphasized cortical mechanisms of language function. The authors report two cases that demonstrate that conduction aphasia is cortically mediated and can be inadequately assessed if not specifically evaluated during brain mapping. To determine the distribution of language on the dominant cortex, electrical cortical stimulation was performed in two cases by using implanted subdural electrodes during brain mapping before epilepsy surgery. A transient isolated deficit in repetition of language was reported during stimulation of the posterior portion of the dominant superior temporal gyrus in one patient and during stimulation of the supramarginal gyrus in the other patient. These cases demonstrate a localization of language repetition to the posterior perisylvian cortex. Brain mapping of this region should include assessment of verbal repetition to avoid potential deficits resembling conduction aphasia.
A unique infarction limited to the posterior insula and intrasylvian parietal opercular cortex produced a subtype of conduction aphasia, characterized by a predominance of semantic paraphasias. Temporal lobe hypoperfusion seen on hexamethylpropyleneamineoxime single-photon emission computed tomography in the absence of any signs of ischemia suggested that cortical diaschisis played a role in the emergence of this syndrome.
Aphasia is an uncommon manifestation of MS, which is somewhat surprising because various disconnection syndromes, such as conduction aphasia, would be expected to occur with some regularity in this white matter disease. We present a case study of an MS patient with conduction aphasia associated with a large white matter lesion underlying the left supramarginal gyrus.
OBJECTIVE: Disruption of fascicular tracts that connect Wernicke's to Broca's areas is the classic mechanism of conduction aphasia. Later work has emphasised cortical mechanisms. METHODS: To determine the distribution of language on dominant cortex, electrical cortical stimulation was performed using implanted subdural electrodes during brain mapping before epilepsy surgery. RESULTS: A transient, isolated deficit in repetition was elicited with stimulation of the posterior portion of the dominant superior temporal gyrus. CONCLUSION: This finding suggests that cortical dysfunction, not just white matter disruption, can induce conduction aphasia.
The classical view of conduction aphasia and the isolation syndrome holds that there is, respectively, preferential damage to, or sparing of, a (repetition) pathway between the posterior and anterior speech areas. This concept is deeply entrenched in neurological thinking, but is supported neither by clinical nor pathological evidence. These two disorders are explained from the standpoint of a more dynamic theory of language organization. This new approach has implications for our understanding of anatomical relationships "between" the speech areas.
Sequences of attempts to name pictured objects were used to examine phonological dysfunction in three diagnostic subgroups of aphasia. A prevalence of "phonologically-oriented sequences" (i.e., those sequences that contained only attempts with a phonological resemblance to the target word) was found to be a diagnostic criterion for conduction aphasia. When compared to a group of Broca's (n = 7) and Wernicke's (n = 5) aphasics, all the conduction aphasics (n = 6) produced proportionately more of such phonologically-oriented sequences on a picture naming test. An examination of the phonologically-oriented sequences produced by the conduction aphasics indicates that speech production in conduction aphasia involves dysfunction at an early stage of sound-encoding. The theoretical implications of this view are discussed.
A case of relatively pure conduction aphasia in a 66 year old woman is reported. A detailed linguistic analysis was performed and the patient's handling of the phonogrammic and ideogrammic aspects of the Japanese language was analysed. The patient showed a comparable pattern of difficultly in the following four operations: (1) naming of pictures (2) reading aloud of Kanji and Kana characters, (3) repetition of words and (4) transcription of heard words into Kanji and Kana characters. Of special note was the patient's superior written transcription of the ideographic symbols and the superior oral reading of the phonogrammic symbols. These results indicate that the patient had a basic defect in expressing the predetermined target word in verbal or writter form. From the analysis of Kana writings it is hypothesized that the in ability to establish a stable and distinct acoustic word image is responsible for this basic expressive difficulty leading to both paraphasic and paragraphic errors.
In order to investigate functional cortical reorganization during recovery from conduction aphasia, regional cerebral blood flows (rCBF) were measured by the two-dimensional 133 Xenon inhalation method in ten stroke patients. rCBF measurements were performed at rest and during the performance of a linguistic task, one month and three months after onset. The analysis of flow changes from rest to test condition indicates an increasing contribution of the right hemisphere as time goes on. The absence of flow increase in Broca's region suggests that this region is definitively disconnected from posterior language "centers" by the arcuate fasciculus lesion.
A 3-year-old, right-handed girl developed a conduction-type aphasia following a second generalized seizure in the setting of a developing abscess involving left subcortical and cortical angular gyrus and arcuate fasciculus, and the posterior corpus callosum. The language disorder was fluent, characterized by age appropriate mean length of utterance and syntax, but with markedly reduced spontaneity of output, rapid rate of speech and mild dysarthria. Comprehension was relatively, but not completely spared. Naming, repetition, and reading (letters) were initially markedly impaired. Improvements in naming and repetition were associated with both literal and semantic paraphasias. Writing skills in the form of drawing were spared, but a mild apraxia to verbal command and imitation was initially present. Despite her young age, this child's fluent conduction aphasia and lesion localization were adult-like. Multimodal memory difficulties appeared to underlie what is best described as conduction aphasia.
Cerebral glucose metabolism was evaluated in patients with either Wernicke's (N = 7), Broca's (N = 11), or conduction (N = 10) aphasia using 18F-2-fluoro-2-deoxy-D-glucose with positron emission tomography. The three aphasic syndromes differed in the degree of left-to-right frontal metabolic asymmetry, with Broca's aphasia showing severe asymmetry and Wernicke's aphasia mild-to-moderate metabolic asymmetry, while patients with conduction aphasia were metabolically symmetric. On the other hand, the three syndromes showed the same degree of metabolic decline in the left temporal region. The parietal region appeared to separate conduction aphasia from both Broca's and Wernicke's aphasias. Common aphasic features in the three syndromes appear to be due to common changes in the temporal region, while unique features were associated with frontal and parietal metabolic differences.
A 10-year-old right-handed boy showed conduction aphasia with left-ear verbal extinction (paradoxical ipsilateral ear extinction) after removal of a arteriovenous malformation in the left parietal lobe. Buccofacial and ideomotor apraxia were not observed. Recovery from aphasia was dramatic. Postoperative computed tomography (CT) and magnetic resonance imaging scans demonstrated damage confined to the left supramarginal gyrus invading the arcuate fasciculus. Together with recently reported cases of acquired fluent aphasia in children with CT-verified left posterior lesions, this case seems to support the current view that both fluent and nonfluent aphasia that share many similarities with the symptoms and lesion localization associated with adult cases may exist in children.
Repetition is viewed typically as a primary deficit in conduction aphasia. Consequently, repetition is considered to be a target of treatment, as opposed to an approach to treatment for this syndrome. However, our experience with a conduction aphasic who had greater speech fluency in repetition than in conversation encouraged us to develop a treatment programme based on sentence repetition. The treatment programme has three components: (1) a pre-/post-test of sentence repetition; (2) the treatment component, in which a new set of sentences is introduced each week in outpatient therapy for daily repetition; (3) analysis of verbal picture description prior to and following treatment as an independent language measure. The patient CM participated in 2 months of sentence repetition treatment, after which he displayed improvement in both sentence repetition and picture description. The reasons for such improvement and the general utility of the treatment programme are discussed.