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[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)

Aphasia↗

[Transcortical sensory aphasia produced by lesions of the anterior basal ganglia area].

We reported three cases of an aphasic syndrome caused by unusual lesion distribution. Our patients, language disorders could be summarized as transcortical sensory aphasia and showed following symptoms; (1) fluent paraphasic verbal output, (2) anomia which was not facilitated by cueing, (3) impaired comprehension of spoken language, (4) preserved capacity of repetition, (5) preserved ability of reading aloud with impaired comprehension of the written material and (6) agraphia. In addition, all had no associated physical neurological signs such as hemiparesis or hemianopsia. All were right handed. All three cases showed the similar lesion distribution by computed tomographic scanning of the brain. All had low density areas in the anterior portion of the left basal ganglia including the head of the caudate nucleus, the anterior portion of the putamen, the anterior portion of the anterior limb of the internal capsule and the nearby white matter. Case 2 also had the small right hemisphere lesion in the white matter near the anterior portion of the lateral ventricle. Transcortical sensory aphasia with this lesion distribution has not been reported. We attributed the causative damage to lesions of the white matter and not to lesions of the basal ganglia per se. It was also speculated that fluent aphasia can be produced by the anteriorly situated white matter lesion if issuing fibers from the Broca's area were spared. Finally a possible anatomoclinical correlation for "transcortical alexia" (preserved oral reading and impaired reading comprehension) was attempted. The symptom is probably a reflection of the fact that the posterior speech area including the angular gyrus was left intact.

Aged↗

[Broca's aphasia and apraxia of speech (author's transl)].

The paper shows that the aphasic syndrome originally described by Paul Broca corresponds to what is now called anarthria or apraxia of speech rather than to the nosological entity which nowadays goes by the name of Broca's aphasia. The paper further endeavours to demonstrate that the output difficulties of anarthric patients are different from those of patients with Broca's aphasia, and it suggests a number of criteria to discriminate between anarthria and Broca's aphasia (Acta neurol belg., 1982, 82, 80-90).

Aphasia↗

Crossed aphasia in a right-handed bilingual Chinese man: a second case.

A persistent nonfluent aphasia following a right cerebral infarction developed in a 74-year-old right-handed Chinese man. Computerized axial tomography localized the lesion in the right frontal lobe. This case is similar to a previously reported one, also with crossed aphasia in a bilingual and dextral Chinese person. Despite these two independent observations and in spite of the fact that unusual cerebral organization might be related to early learning of a nonalphabetic (ideographic) language, preliminary sampling has failed to demonstrate a greater incidence of crossed aphasia in two separate Chinese populations.

Aged↗

Atypical conduction aphasia. A disconnection syndrome.

Conduction aphasia was originally proposed to result from separation of the posterior language comprehension area and the anterior motor speech area of the left hemisphere. The arcuate fasciculus has been the most frequently suggested site of such a disconnection, but the syndrome has been reported in cases in which the abnormality involved the dominant Wernicke's area. This challenges the arcuate fasciculus theory, and it has been suggested that a cortical lesion, not a disconnection, is the crucial factor. Three new cases in which the lesion does not lie in the arcuate fasciculus are reported, two in left-handed patients with left temporoparietal lesions and one in a right-handed patient with a right temporoparietal infarct, a "crossed" aphasia. While atypical, these cases offer evidence that disconnection of the circuit linking language comprehension to motor speech output, not damage to a specific cortical region, underlies the syndrome of conduction aphasia.

Adult↗

'Inner speech' in conduction aphasia.

It has been suggested by Kurt Goldstein, MD, that conduction aphasia is a disturbance of "inner speech." We tested this hypothesis in five patients who had conduction aphasia with similar speech disturbances. The patients were presented with pictures and were required to perform, without overt vocalization, comparisons of word length and homophonic and rhyming matches. Four patients successfully performed such judgments on words they could not vocalize, but one patient could not. These findings suggest that the hypothesis may have been correct for only a subgroup of conduction aphasics. The findings also provide evidence for heterogeneity within the class of conduction aphasia.

Aged↗

Paul Broca's less heralded contributions to aphasia research. Historical perspective and contemporary relevance.

In addition to discovering the dominant role of the left hemisphere for language and describing what is now known as Broca's aphasia, Paul Broca made other insightful, but less well-recalled, aphasiologic observations. He distinguished symptoms of Wernicke's aphasia five years before Carl Wernicke's famous monograph, and he was the first to exploit the surgical relevance of language localization. Broca investigated the anatomic substrate of language laterality by comparing the relative weights of the two hemispheres and the two frontal lobes. He considered language lateralization from a developmental point of view and in relation to handedness. A relatively small portion of Broca's prodigious scientific career was devoted to the study of aphasia, but his seminal work encompasses a number of issues of contemporary concern.

Aphasia↗

Disconnection and cerebral metabolism. The case of conduction aphasia.

Ten patients with conduction aphasia were studied with computed tomography and 18-F-fluorodeoxyglucose positron emission tomography to examine glucose metabolism. Computed tomographic results identified a postrolandic structural locus for conduction aphasia. All patients demonstrated resting glucose hypometabolism throughout the parietal and temporal regions, and half of the patients also demonstrated reduced metabolic rates in the posterior, inferior, frontal (Broca's) regions. These data suggest that disconnection between posterior and anterior language areas may not be the best anatomical explanation for conduction aphasia.

Adult↗

A longitudinal examination of crossed aphasia.

OBJECTIVE: To longitudinally examine neuropsychological performance in an adult dextral man with crossed aphasia after cerebrovascular accident. DESIGN: Case report using longitudinal neuropsychological, neurological, and radiological examinations performed in close temporal proximity to one another. SETTING: The patient was seen on both an inpatient and an outpatient basis by members of the Department of Neurology and Radiology of the University of Miami (Fla) School of Medicine. PATIENT: Thirty-four-year-old right-handed monolingual Hispanic man without family history of left-handedness. RESULTS: Initial neuropsychological testing revealed classic Broca's dysphasia, visual neglect, and visuospatial disturbances. The visuospatial disturbance resolved within 6 months whereas expressive language remained severely impaired. There was a dissociation between praxis and language. Mood was jovial with indifference toward his neurologic and cognitive limitations. Serial magnetic resonance imaging studies unequivocally localized the lesions to the right hemisphere, involving the right frontal, anterior parietal, and subcortical white matter. CONCLUSIONS: The clinicoanatomic correlation is compatible with the view that crossed aphasia is a "mirror" representation of that seen in cases of uncrossed aphasia. The course of recovery suggests complete lateralization of language to the right hemisphere with bilateral or crossed representation of nonverbal skills.

Adult↗

Alzheimer disease and nonfluent progressive aphasia.

OBJECTIVE: To describe a patient with pathologically proven Alzheimer disease (AD) who presented with a non-fluent progressive aphasic syndrome. DESIGN: Longitudinal neuropsychological assessment, structural (magnetic resonance imaging) and functional (single photon emission computed tomography) imaging, and postmortem brain examination. SETTING: Memory and cognitive disorders clinic in a tertiary referral hospital. PATIENT: A 66-year-old man presented with a 5-year history of progressive nonfluent aphasia characterized by marked deficits in phonology and syntax with preservation of everyday abilities. His condition deteriorated rapidly and he died suddenly of a myocardial infarction 12 months later. RESULTS: Neuropsychological testing revealed mild global intellectual impairment with marked impairment of auditory verbal short-term memory, syntactic, and phonological abilities. His naming errors were predominantly phonological paraphasias. Magnetic resonance imaging scans showed left perisylvian atrophy and results of a Tc 99m hexamethyl-propyleneamine-oxime single photon emission computed tomographic scan were normal. Postmortem pathological examination revealed typical AD pathological features with atypical distribution, involving predominantly perisylvian language areas, but sparing the medial temporal lobe. CONCLUSIONS: The language deficits in AD, which have received considerable attention, are thought to involve predominantly lexicosemantic processes. When AD presents as a relatively isolated language disturbance, the aphasia is usually of the fluent anomic type. To our knowledge, our patient represents the first fully documented case of progressive nonfluent aphasia with pathologically verified AD.

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Aphasia in hyperacute stroke: language follows brain penumbra dynamics.

During the first few hours after onset, stroke symptoms may evolve rapidly. We studied the correlation between brain perfusion and aphasia changes during the hyperacute phase of stroke using a new technique of perfusion computed tomography (P-CT). Using an aphasia score developed for each language modality, language was evaluated within 6 hours after onset, then sequentially during the first week. Maps of the penumbra and infarct obtained from P-CT images and definite infarct size evaluated using T2 and diffusion-weighted MRI (DWI) on day 3 were rated by a neuroradiologist, blinded to the clinical deficit. Within 6 hours, deficits in all language modalities were present in 13 out of 24 consecutive patients, corresponding to large anterior-posterior perfusion deficits of the left middle cerebral artery (MCA) territory. The aphasia score correlated with a corresponding perfusion deficit in specific areas of the MCA territory, and showed significantly less improvement when the penumbra evolved toward infarction than when at least part of the penumbra was rescued. Our findings suggest a particularly good correlation between the evolution of aphasic symptoms and penumbra dynamics. Further studies on the relevance of penumbra dynamics in function-specific brain areas to decision taking in hyperacute stroke management are required.

Adult↗

Slowly progressive aphasia without generalized dementia.

Six right-handed patients experienced a slowly progressing aphasic disorder without the additional intellectual and behavioral disturbances of dementia. The symptoms almost universally started in the presenium. The initial difficulty was an anomic aphasia in five of the patients and pure word deafness in the sixth. Continuous and gradual deterioration occurred in the five patients who presented with an anomic aphasia. They eventually experienced additional impairment of reading, writing, and comprehension. In four patients, other areas of comportment were not involved within the 5 to 11 years of follow-up. A more generalized state of dementia may have emerged in the other two patients, but only after 7 years of progressive debilitating aphasia. Neurodiagnostic procedures were consistent with preferential involvement of the left perisylvian region. In one patient, cortical biopsy did not show any pathognomonic change; specifically, no neurofibrillary tangles, amyloid plaques, neuronal inclusions, or gliosis were seen. This condition may constitute a syndrome of relatively focal cerebral degeneration with a predilection for the left perisylvian region.

Adolescent↗

Caregiver strain and caregiver burden of primary caregivers of stroke survivors with and without aphasia.

Little is known about how the burden and strain of caring for stroke patients with or without aphasia affects primary caregivers. This article (a) critically examines the literature on the burden and strain of care experienced by caregivers of stroke patients and (b) examines the relationship between aphasia and caregiver burden and strain. Two literature reviews of three databases were conducted. Fourteen articles (12 quantitative articles, 1 mixed-design article, and 1 qualitative article) were found to comply with the study criteria for the first literature search. A second literature search focused on the effects of stroke survivors' aphasia on caregiving; none of the articles retrieved met the inclusion criteria. This article suggests that there is a lack of research in this area and that several key initiatives are needed, including the development of an instrument with psychometric properties appropriate for assessing the burden and strain on caregivers of stroke patients. Implications for future nursing practice and research are highlighted.

Adaptation, Psychological↗

The structural determinants of recovery in Wernicke's aphasia.

Recovery of comprehension and total language in 22 Wernicke's aphasics was correlated with lesion size and extent of involvement of certain structures on CT. Recovery rates and outcomes were separately examined using 0-3 months and 0-12 months poststroke language data. Quantitative measures of structural damage were regressed on total aphasia and comprehension outcome measures. Supramarginal and angular gyri appeared to be the most significant structures in recovery in addition to initial severity and lesion size. This was confirmed by using ANOVA to compare the extent of involvement in each postcentral structure among the poor, moderate, and good recovery groups. The superior temporal and middle temporal gyri are less involved in the good recovery group. Structures posteriorly adjacent to Wernicke's area are important for compensation in Wernicke's aphasia and in the accompanying comprehension deficit. Persisting Wernicke's aphasia usually involves the supramarginal and angular gyri in addition to the superior temporal area.

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Theodor Meynert's contribution to classical 19th century aphasia studies.

Carl Wernicke (1848-1905) is traditionally considered the first to have described the features of, and the brain pathology underlying, impaired auditory comprehension and related symptoms. Although Wernicke (1874) clearly and repeatedly indicates his indebtedness to Theodor von Meynert (1833-1892), this is usually understood as an acknowledgment that Meynert taught Wernicke neuroanatomy (Eggert, 1977); Wernicke's own words in part support this interpretation. A more sophisticated historical analysis notes that, prior to Wernicke, both Johann Schmidt in 1871 and Charlton Bastian in 1869 had described the concept of receptive aphasia, but neither had supported their analyses with autopsy evidence as did Wernicke, thus not dislodging Wernicke's claim of priority. However, a virtually unknown work by Theodor von Meynert, published in 1866, has recently been rediscovered by us ["Ein Fall von Sprachstörung, anatomisch begründet." Medizinische Jahrbücher. XII Band der Zeitschrift der K. K. Gesellleschaft der Arzte in Wien, 22. Jahr. Pp. 152-189]. In this paper Meynert analyzes the anatomical basis for localizing the comprehension of language in the superior temporal gyrus, he argues that lesions in this area should (by analogy to Broca's earlier observations on language expression) cause impairments in language comprehension, and he presents a case of receptive aphasia with autopsy evidence of destruction of the superior temporal gyrus in the left hemisphere. The patient's aphasia was classic; impaired auditory comprehension, and fluent speech with paraphasias. It is clear that Meynert should be given historical credit for his work.

Aphasia↗

On the notion of a "subtle phonetic deficit" in fluent/posterior aphasia.

Phonetic investigations in the past decade or so have reported instances of a "subtle phonetic deficit" in the fluent aphasias, thereby challenging the traditional dichotomy of a motoric deficit characterizing the nonfluent aphasias and a selection deficit characterizing the fluent aphasias. This paper critically reviews the acoustic, physiological, and perceptual studies which have attempted to examine this phenomenon. These investigations have been evaluated in terms of differences in subject populations, task demands, subjects' performance, and problematic interpretations. Suggestions are offered for an experimental design which can help us operationalize this term and help us to better understand the speech production deficit in fluent aphasic patients.

Aphasia, Wernicke↗

Crossed aphasia and related anomalies of cerebral organization: case reports and a genetic hypothesis.

Anomalous lateralization of cognitive functions is observed in a small percentage of right-handed patients with unilateral brain damage, either crossed aphasia (aphasia after right brain damage) or "crossed nonaphasia" (left brain damage without aphasia but with visuospatial and other deficits typical of right brain damage). No comprehensive theory of these anomalous cases has been proposed. Nine new right-handed cases (plus one left-handed case) were analyzed and the literature was reviewed. The dramatically anomalous organization of cognitive functions is best explained by random lateralization of all cognitive functions in a small subset of the population. The RS theory of cerebral dominance can account for this pattern of anomalies in right-handers and may account for the most common patterns of dominance observed in left-handers.

Adult↗

On the status of object concepts in aphasia.

While verbal comprehension is often impaired in aphasia due to left hemispheric damage, the status of nonverbal conceptual knowledge of objects remains controversial. We tested 16 aphasic subjects for their comprehension of concrete single words. Eight showed significant impairment on word-to-picture matching, when distractors were semantically and not just perceptually confusable. These 8 also made errors in answering verbal probe questions concerning the same items. When tested on a nonverbal pictorial version of the same probe questions, however, 3 of these 8 improved their performance to the level of normal controls. The other 5 showed continuing impairment in indicating responses to pictorial probes. These 5 showed no evidence of generalized intellectual impairment, and it is concluded that they demonstrated a comprehension deficit not limited to the verbal domain. Unlike the other aphasic patients, these latter 5 also had CT scan lesions extending into the posterior left temporal lobe (involving Brodmann's areas 22, 21, and 37). They were also more impaired in terms of general aphasia severity. It is suggested that a nonverbal (as well as verbal) semantic memory deficit occurs in a subgroup of patients with single word comprehension disturbance due to aphasia, and this may reflect general severity of language impairment as well as damage to certain localized brain regions.

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