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The role of P300 in the recovery of post-stroke global aphasia.

Seventeen right-handed patients suffering from global aphasia caused by a recent stroke in the left-hemisphere were studied. Passive P300 auditory event related potential paradigm was applied every months for 6 months. Aachen subtests were used for evaluating comprehension. Only a minority of the patients displayed the P300 at the baseline. Those patients had the best outcome at the Aachen comprehension subtest. Latency and amplitude changed over time in an unpredictable way. The number of patients presenting with the P300 also fluctuated, since some patients could regain the potential, whereas some other patients could lose that from month to month. Passive P300 is a monitor of recovery following global aphasia. A single passive P300 recording is useful for prognostic purposes. Repairing mechanisms in the first 6 months have a non-linear trend.

Aphasia↗

Aphasia following right striato-insular infarction in a left-handed child: a clinico-radiological study.

The case of six-year-old girl with non-fluent aphasia following a subcortical right-hemispheric cerebrovascular accident is reported. Examination by computerised tomographic scan revealed a right paraventricular area of diminished density involving the internal capsule, lenticular nucleus and the insula. The speech disturbance was followed by typical right-hemispheric signs and by left-channel extinction in dichotic listening tests. The aphasia cleared in two weeks, paralleled by an improvement in left-channel performance, suggesting that language recovery was dependent on right-hemispheric structures.

Aphasia↗

Acquired conduction aphasia in a child.

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.

Aphasia↗

Crossed aphasia in early childhood.

A four-year-old child was admitted to hospital with an infarct of the right middle cerebral artery involving the frontoparietal area. His symptoms included left hemiplegia and aphasia. After two weeks, he had hemiparesis, word-finding and naming problems and enuresis. A year later he demonstrated elective mutism at school, had attention and short-term memory impairments, occasional enuresis and an average IQ. He was shy and withdrawn; this is interesting, since depression is usually associated with left-hemispheric lesions. It is suggested that an early period of mutism should be included among the criteria for the study of crossed aphasia in children, as this is a common occurrence in such cases. Even after recovery of speech, impairments in attention and academic skills may persist.

Aphasia↗

Acquired aphasia, dementia, and behavior disorder with epilepsy and continuous spike and waves during sleep in a child.

Severe persistent neuropsychological disorders sometimes develop in the course of a focal epilepsy of unknown origin in previously normal children. Very frequent bilateral focal or generalized discharges are often noted on the sleep EEG records of these patients with no evidence of clinical seizures. The relation between these paroxysms and the observed deterioration remains unclear. We report a child with a partial complex epilepsy and severe disturbances of language, cognition, and behavior acquired in the early years of development who was followed for 15 years. A correlation between the evolution of the striking EEG abnormalities during sleep and the neuropsychological disorders could be established retrospectively. The observed sequence of onset and recovery of the aphasia, the dementia, and the "psychotic" behavior makes a direct causal relation between the deficits quite unlikely. Rather it suggests an association of independent symptoms with a specific language disorder becoming manifest in the course of the evolution. This child shows many of the main characteristics of the syndromes of "acquired aphasia with convulsive disorder" (Landau-Kleffner syndrome) and "epilepsy with continuous spike waves during sleep." Both syndromes describe probably different facets of a similar underlying, still unexplained cerebral dysfunction.

Adolescent↗

Global aphasia with seizure onset in the dominant basal temporal region.

A 33-year-old right-handed woman had intractable simple and complex partial seizures (SPS, CPS) that began with global aphasia. EEG closed-circuit TV (EEG-CCTV) monitoring with sphenoidal electrodes showed left inferomesial temporal ictal onset of CPS. Subdural electrodes were implanted over the left frontotemporal convexity, subtemporally and subfrontally. Stimulation of the basotemporal cortex produced global aphasia. A posterolaterotemporal language area was also identified. Spontaneous SPS had focal onset in the basal temporal language area (BTLA). Ictal discharges did not involve the posterotemporal region. This case shows that aphasic speech arrest at seizure onset may be due to seizure discharge in the basotemporal region and that the BTLA is clinically relevant in seizure semiology.

Adult↗

Aphasia and epilepsy in childhood.

The syndrome of progressive aphasia and epilepsy in childhood is delineated. Four cases are presented, three of which show the typical gradual onset, fluctuating course and EEG changes with bilateral foci of spike and spike-wave activity, and, finally, normalization after some years of the EEG. Also the aphasia tends to subside, but often with considerable delay in relation to the other features. Neuropsychological assessment showed varying residual defects mainly on language functions. The aetiology is unknown. No pathoanatomical data on this disorder has hitherto been published. In one of the present cases a cortical biopsy was performed on suspicion of a left temporal tumour. The biopsy showed changes indicative of a slow virus infection. It is therefore suggested that the newly established language function in children particularly is vulnerable to a subchronic viral encephalitis affecting both hemispheres.

Adolescent↗

A case of slowly progressive aphasia without generalized dementia in a Japanese patient.

A Japanese patient with a 4-year history of slowly progressive aphasia without generalized dementia is described. From 1985 on, this 61-yr-old right-handed dentist showed insidiously progressive deterioration in his speech and auditory comprehension, but has no memory disturbance, disorientation of space, time or persons, acalculia or other impairments in his behavior. His personality changes are unremarkable. He still treats patients at his clinic. General physical and neurological examinations were normal. CT and MRI (1.5T) scans showed widening of the left sylvian fissure and lateral ventricle without any vascular lesions. A PET scan demonstrated focal hypometabolism restricted to the left temporal lobe. The clinical course and picture of our patient corresponds, well to those of slowly progressive aphasia without generalized dementia, described by Mesulam.

Aphasia↗

Review of research on the clinical presentation of acquired childhood aphasia.

AIMS: The traditional description of the clinical picture of acquired childhood aphasia (ACA) claims that ACA is invariably nonfluent, that recovery of language disorder is rapid and complete, and that ACA commonly occurs after right hemisphere damage. However, since the late 1970s the publication of several case studies has led to reject this longstanding standard doctrine. This review, which concerns the revised insights into ACA, aims at making an inventory of the recently described aphasic symptomatologies and neuroradiological data. MATERIAL: The literature on ACA with emphasis on the studies published since 1978. RESULTS: Recent case studies show a great variety of aphasic symptomatologies including auditory comprehension disorders, paraphasias, neologisms, logorrhoea, jargon, impaired repetition abilities, and a host of linguistic deficits in reading and writing. Not only the typology of the aphasias but also the recently established clinicoradiological correlations appear to resemble those found in adults. Also, recovery from ACA shows to be less complete than previously thought. CONCLUSION: These findings bear consequences as to theories on cerebral organization of language in childhood. It appears that already in infancy the two cerebral hemispheres are no equal substrate for language representation. Therefore, prognosis and final outcome of ACA are not uniformly favourable.

Aphasia↗

Quantitative electroencephalography and anatomoclinical principles of aphasia. A validation study.

No single technology in isolation can provide a full view of the anatomoclinical principles evident in the clinical populations we study. The dynamic nature of quantitative electrophysiology makes it an ideal complement to anatomic and metabolic imaging. The statistical conundrum it has presented may be resolved by the approach incorporated in CART. The intent of this study was to examine QEEG and CART in the evaluation of the neurologic bases of a well-defined behavioral disorder like aphasia. The combined power of QEEG and CART yielded objective electrophysiologic methods to predict aphasia that rival the reliability of the language examination. Such success is unprecedented. This success allows us to incorporate QEEG and CART into our technological armamentarium and to return to the evaluation of less well-understood disorders with confidence in both our findings and anatomoclinical principles we derive from them.

Adolescent↗

Brain-behavior relationships in aphasia studied by positron emission tomography.

Positron emission tomography allows for the study of human brain physiology and chemistry including cerebral blood flow, oxygen or glucose metabolism. We applied PET to study glucose metabolism using aphasia as a model of neurobehavior. The most striking observation was that the extent of cerebral glucose metabolic changes in aphasic patients consistently involve brain regions that are not structurally damaged. The remote metabolic effects can be predicted depending on the location and extent of structural damage. Two observations were made: (1) In our experience, all right-handed aphasic patients with left hemisphere structural lesions have metabolic abnormalities in the left temporoparietal region, and (2) metabolic abnormalities are variably found in undamaged, left prefrontal lobe, basal ganglia, and thalamus. Variations in clinical aphasic syndromes were found to relate to these frontal metabolic changes, suggesting that aspects of the aphasia result from differences in prefrontal function rather than directly from structural damage to perisylvian or deep structures.

Aphasia↗

How to improve repetition ability in patients with Wernicke's aphasia: the effect of a disguised task.

Dissociation "automatico-voluntaire" is a symptom observed in aphasic patients. We elucidated the difference between voluntary and involuntary speech output in a quantitative manner using the same task materials in nine patients with Wernicke's aphasia. All the patients exhibited better ability and less paraphasias in a repetition task elicited in a disguised condition than in an ordinary repetition condition. This result indicates that the output difficulty in Wernicke's aphasia might be a disability of volitional control over the language system.

Aged↗

Spared musical abilities in a conductor with global aphasia and ideomotor apraxia.

A conductor suddenly developed global aphasia and severe ideomotor apraxia as a result of an infarct in the territory of the left middle cerebral artery. Although aphasia and apraxia remained unchanged during the following six years, his musical capacities were largely spared and he was still able to conduct. This case provides some evidence in favour of right hemisphere dominance for music.

Aged↗

Dementia presenting with aphasia: clinical characteristics.

Dementia, a disorder of multiple cognitive functions, may atypically present as an aphasia. The clinical characteristics are reported of 13 patients with up to 14 years of progressive language impairment before developing dementia. In reviewing the literature, it was found that these patients were similar to those reported with progressive aphasia. It is concluded that dementia may present with an anomic, dysfluent language disorder due to the focal left sylvian onset of several dementing illnesses.

Aged↗

Subcortical aphasia from a thalamic abscess.

A patient is reported who was treated successfully for a left thalamic abscess that resulted in subcortical aphasia. A SPECT scan showed large areas of hypoperfusion in the cortex of the left hemisphere. At follow up after seven months there was marked improvement in the language disorder and the cortical hypoperfusion. It is suggested that aphasia in patients with subcortical lesions results from secondary cortical dysfunctions. The evidence is confined to patients with stroke lesions. The possible implications of this case on current theories of pathophysiological mechanisms, in particular the ischaemic penumbra theory and the cortical diaschisis theory, are briefly discussed. Cortical diaschisis may be the appropriate explanation in this patient.

Adult↗

Familial progressive aphasia: its relationship to other forms of lobar atrophy.

Two brothers presented with slowly progressive aphasia. One brother, who became behaviourally disturbed only at the end of his illness, was found at necropsy to have predominant left frontotemporal atrophy. The other brother developed severe behavioural disturbances shortly after the onset of language impairment. His brain revealed bilateral frontotemporal atrophy. In both there was non-Alzheimer's disease pathology with the histological features of loss of large cortical nerve cells, spongiform change and mild gliosis. The differential anatomical atrophy supports the view that clinical manifestations of lobar atrophy are dictated by the topographical distribution of a common underlying pathology, linking the syndromes of progressive aphasia to dementia of frontal lobe type (DFT) and DFT with motor neuron disease.

Aphasia↗

Conduction aphasia elicited by stimulation of the left posterior superior temporal 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.

Adult↗

Primary progressive aphasia with glial cytoplasmic inclusions.

We report a 80-year-old woman who suffered from primary progressive aphasia for 3 years. Cranial CT and MRI studies showed moderate cerebral atrophy, more marked in the left frontal and temporal lobes, and SPECT brain scans revealed marked hypometabolism in the left frontal and temporal lobes. Neuropathologic examination of a temporal lobe biopsy demonstrated Gallyas-positive intracytoplasmic inclusions looking like fibrillary tangles and of Gallyas-positive cell processes, probably from glial cells. Glial intracytoplasmic inclusions were immunolabelled with antibodies to ubiquitin and with phosphorylion-dependent antitau antibodies, indicating the presence of hyperphosphorylated tau in the inclusions. There was only mild pathology of cortical neurons consisting in rare perikarya diffusely stained with antitau antibodies. There were no senile plaques, neurofibrillary tangles, 'achromatic' neurons, ballooned cells, Pick or Lewy bodies, nor microvacuoles or spongiform changes of the neuropil. The glial intracytoplasmic inclusions found in this case were similar to those found in multiple system atrophy, and differ from the cortical changes hitherto reported in primary progressive aphasia.

Aged↗