Aphasia in border‐zone infarcts has a specific initial pattern and good long‐term prognosis

Background: While border‐zone infarcts (BZI) account for about 10% of strokes, studies on related aphasia are infrequent. The aim of this work was to redefine specifically their early clinical pattern and evolution. Methods: We prospectively studied consecutive patients referred to our stroke unit within a 2‐year period. Cases of aphasia in right‐handed patients associated with a MRI confirmed left‐sided hemispheric BZI were included. These patients had a standardized language examination in the first 48 h, at discharge from stroke unit and between 6 and 18 months later. Results: Eight patients were included. Three had anterior (MCA/ACA), two posterior (MCA/PCA), two both anterior and posterior, and one bilateral BZI. All our patients initially presented transcortical mixed aphasia, characterized by comprehension and naming difficulties associated with preserved repetition. In all patients, aphasia rapidly improved. It fully recovered within a few days in three patients. Initial improvement was marked, although incomplete in the five remaining patients: their aphasias specifically evolved according to the stroke location toward transcortical motor aphasia for the three patients with anterior BZI and transcortical sensory aphasia for the two patients with posterior BZI. All patients made a full language recovery within 18 months after stroke. Conclusions: We report a specific aphasic pattern associated with hemispheric BZI, including an excellent long‐term outcome. These findings appear relevant to (i) clinically suspect BZI and (ii) plan rehabilitation and inform the patient and his family of likelihood of full language recovery.     

Distributed anatomy of transcortical sensory aphasia

We examined four patients with transcortical sensory aphasia and eight with milder language disturbances but with similar thalamic and/or temporo-occipital lesions. Specific attention was paid to differentiation of the computed tomographic lesion site of the milder cases from the transcortical sensory aphasia cases. The critical lesion for transcortical sensory aphasia in these patients involved pathways in the posterior periventricular white matter adjacent to the posterior temporal isthmus, pathways that are probably converging on the inferolateral temporo-occipital cortex. Analysis of the language function of these patients, of the influence of sensory modalities on language function, and of the interaction between semantic memory and semantic lexical functions suggests the existence of a specific brain system for semantic functions. This semantic system has a particular distributed anatomy. We propose that damage to this system may have a variety of clinical manifestations in language and in memory, depending on the exact lesion configuration.     

Pathophysiology of language switching and mixing in an early bilingual child with subcortical aphasia

Acquired aphasia after circumscribed vascular subcortical lesions has not been reported in bilingual children. We report clinical and neuroimaging findings in an early bilingual boy who incurred equally severe transcortical sensory aphasia in his first language (L1) and second language (L2) after a posterior left thalamic hemorrhage. Following recurrent bleeding of the lesion the aphasic symptoms substantially aggravated. Spontaneous pathological language switching and mixing were found in both languages. Remission of these phenomena was reflected on brain perfusion SPECT revealing improved perfusion in the left frontal lobe and left caudate nucleus. The parallelism between the evolution of language symptoms and the SPECT findings may demonstrate that a subcortical left frontal lobe circuity is crucially involved in language switching and mixing.     

Pathophysiology of language switching and mixing in an early bilingual child with subcortical aphasia

Acquired aphasia after circumscribed vascular subcortical lesions has not been reported in bilingual children. We report clinical and neuroimaging findings in an early bilingual boy who incurred equally severe transcortical sensory aphasia in his first language (L1) and second language (L2) after a posterior left thalamic hemorrhage. Following recurrent bleeding of the lesion the aphasic symptoms substantially aggravated. Spontaneous pathological language switching and mixing were found in both languages. Remission of these phenomena was reflected on brain perfusion SPECT revealing improved perfusion in the left frontal lobe and left caudate nucleus. The parallelism between the evolution of language symptoms and the SPECT findings may demonstrate that a subcortical left frontal lobe circuity is crucially involved in language switching and mixing.     

Aphasia with a left frontal interhemispheric hematoma

We studied a patient with transcortical motor aphasia resulting from a traumatic interhemispheric left frontal hematoma. The aphasia was caused by compression exerted by the hematoma on the left supplementary motor area, which is known to have a function in speech. This cause of a transcortical motor aphasia has not been described earlier.     

Transcortical sensory aphasia due to extensive infarction of left cerebral hemisphere]

We report a case of transcortical sensory aphasia occurred after extensive infarction of left cerebral hemisphere. A 68-year-old, right-handed man with atrial fibrillation suddenly developed cerebral embolism of left middle cerebral artery. He was treated conservatively, and the right hemiplegia, aphasia, apraxia in a slight degree and right hemispatial neglect in a slight degree consequently existed. MRI showed a large cortical and subcortical infarct lesion including the left Broca's area, central region, perisylvian area with Wernicke's area and temporal lobe. In contrast, neuropsychological evaluation using the Western Aphasia Battery (WAB) demonstrated transcortical sensory aphasia, e.g., fluency 8, auditory comprehension 1. repetition 10 and object naming 2.4. In addition to preserved repetition, both linguistic prosody and affective prosody were well preserved. Most cases with transcortical sensory aphasia are known to occur with the lesion including temporo-parieto-occipital junction of dominant hemisphere. Our patient and a few other reported cases of transcortical sensory aphasia had a lesion in perisylvian area including Wernicke's area. Therefore, it is possible that their minor hemisphere worked selectively for repetition. Furthermore, we suggest that this patient presented dissociative aphasia that all the process of repetition and the function of linguistic and emotional prosody were represented in the right hemisphere and the other functions including comprehension of word meanings were existed in the left hemisphere. We believe that our case of transcortical sensory aphasia with dissociative aphasia gives a suggestion about the mechanism and localization of repetition and prosody in the whole system of language.     

Infarction in the territory of the anterior choroidal artery: A cause of transcortical motor aphasia

Abstract

We report a case of transcortical motor aphasia associated with an infarction in the territory of the left anterior choroidal artery. The same clinical picture has been described in a small number of patients with a similar lesion site. The implications of this finding for theories of subcortical aphasia are discussed.     

Primary progressive aphasia with focal neuronal achromasia

We describe the clinical, radiologic, neuropsychological, and neuropathologic features of a 69-year-old man with a 3-year history of progressive transcortical expressive aphasia. Neuropsychological testing showed progressive dysfunction of expressive language. Neuropathologic examination demonstrated focal cortical degeneration involving the left superior frontal gyrus, with swollen achromasic neurons and no evidence of Alzheimer's disease, Pick's disease, Creutzfeldt-Jakob disease, Lewybody disease, or other dementing disorders. This case adds to the known heterogeneity of the underlying pathology of patients with primary progressive aphasia.     

Crossed optic ataxia: possible role of the dorsal splenium.

An unusual combination of disconnective syndromes is reported: transcortical motor aphasia, left arm apraxia and optic ataxia. Neuropathological examination showed a left parieto-occipital and a subcortical frontal infarct and a lesion of the dorsal part of the posterior two-fifths of the callosum. The frontal lesion caused the transcortical motor aphasia and produced the left arm apraxia. Visuomotor incoordination in the right hemispace was due to the left parieto-occipital infarct, while the crossed optic ataxia in the left hemispace was attributed to the callosal lesion. It is proposed that the pathway that serves crossed visual reaching passes through the dorsal part of the posterior callosum. This case reinforces the growing evidence that fibres in the corpus callosum are arranged in ventro-dorsal functional lamination.     

Agnosic attacks with speech disorders and asymmetric EEG anomalies]

The semantic and semiological limits of aphasia and agnosia are imprecise: in the present paper, aphasia is defined as a disorder of the verbal abstract representation of the world of signified, while agnosia is defined as a semantic disorder of sensorial analysis. Three electro-clinical observations of aphasic-agnosic paroxisms with intricated speech disorders and disorders of sensorial identification are reported here. These paroxisms are associated with bilateral and asymetric EEG discharges. The reported observations raise the problem of the function of speech as regards somatic representation or the concept of body image.     

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.     

Impairments of procedures for implementing complex language are due to disruption of frontal attention processes.

Production of complex discourse-lengthy, open-ended utterances and narratives-requires intact basic language operations, but it also requires a series of learned procedures for construction of complex, goal-directed communications. The progression of clinical disorders from transcortical motor aphasia to dynamic aphasia to discourse impairments represents a progression of procedural deficits from basic morpho-syntax to complex grammatical structures to narrative and a progression of lesions from posterior frontal to polar and/or lateral frontal to medial frontal. Two cases of impaired utilization of language exemplify the range of impairments from clearly aphasic agrammatic, nonfluency to less and less "aphasic" and more and more executive impairments from transcortical motor aphasia to dynamic aphasia to narrative discourse disorder. The clinical phenomenology of these disorders gradually comes to be more accurately defined in the terminology of executive deficits than that of aphasia. The executive deficits are, in turn, based on impairments in various components of attention. Specific impairments in energizing attention and setting response criteria associated, respectively, with lesions in superior medial and left ventrolateral frontal regions may cause defective recruitment of the procedures of complex language assembly.     

Acute aphasia in multiple sclerosis

Acute aphasia is rare in multiple sclerosis. We describe 3 patients with multiple sclerosis who had acute exacerbations presenting as aphasias. One patient had a mixed transcortical aphasia, 1 had a transcortical motor aphasia, and 1 had a Broca aphasia. Magnetic resonance imaging scans of the brain with contrast enhancement revealed new white matter lesions in the left hemisphere in all 3 patients. Two of the 3 patients had a good response to treatment with methylprednisolone sodium succinate. Arch Neurol. 2000;57:1207-1209     

Clinical-anatomical correlation in a selective phonemic speech production impairment

Although phonemic paraphasias are common in aphasic disorders, including Broca's aphasia, conduction aphasia and transcortical motor aphasia, selective phonemic speech production impairment, or phonemic disintegration, is unusual. A patient with a selective phonemic speech production disorder underwent clinical, neuropsychological and structural neuroradiological assessment over a period of 6 years. The disorder was characterised by phonemic paraphasias (phonemic disintegration) with preserved comprehension and naming. Imaging showed a focal lesion in the white matter of the left precentral gyrus and, to a lesser extent, the posterior part of the left middle frontal gyrus, with overlying cortical atrophy. Biopsy of the lesion, after several years of observation, showed a calcified haemangioma. Clinical-anatomical correlation in this case suggests the importance of primary motor cortex of the inferior precentral (pre-Rolandic) gyrus and subjacent white matter in phoneme production, with sparing of the posterior inferior frontal gyrus (Broca's area).     

Recovery of semantic word processing in global aphasia: a functional MRI study

One important issue concerning the recovery of higher cognitive functions-such as word comprehension in aphasia-is to what extent impairments can be compensated for by intact parts of the network of areas normally involved in a closely related function ("redundancy recovery"). In a previous functional MRI investigation, we were able to show that left hemispheric redundancy recovery within a distributed system of related lexical-semantic functions was the most probable basis of recovery of comprehension from transcortical sensory aphasia. The question remained, however, whether redundancy recovery may play a more general role in the recovery of comprehension after large left hemispheric lesions and severe aphasia. We had the possibility, using the same fMRI paradigm, to study seven cases with left middle cerebral artery (MCA) infarction and partial recovery of comprehension > or =6 months after presentation with global aphasia on acute assessment. Lateralization of activation did not differ significantly between patients and controls. The most consistent regions of activation included the left extrasylvian posterior temporal and the right posterior parietal cortex. Recovery of language comprehension was associated predominantly with activations in regions, which were also activated in several normal subjects. We suggest that a redundancy recovery mechanism within multiple representations of closely related functions was more important than take-over of function by previously unrelated areas (vicariation) as the basis of recovery of word comprehension in our patients in spite of extensive left hemispheric damage. We conclude that redundancy within the lexical-semantic system seems to make an important contribution to recovery of comprehension even in severe aphasia.     

Transcortical sensory aphasia following a left frontal lobe infarction probably due to anomalously represented language areas

A 57-year-old right-handed man presented with speech disturbance 1 day prior to his admission. The standardized aphasia test batteries showed transcortical sensory aphasia. MRI revealed a left frontal and insular infarct. Positron emission tomography scans also revealed a glucose hypometabolism in the same region as the infarcted area on MRI. Repeated aphasia testing showed that his aphasia only partially improved.     

交叉性失语

右利手者右大脑半球病变所致的失语称为交叉性失语。交叉性失语少见。我科八年来共诊断八例（占我组失语症患者２５０例的２．８％），均为男性右利手者，头颅ＣＴ扫描均证实右大脑半球单发病灶，其中脑梗塞７例，脑出血１例。均于发病三个月内作失语检查。其中交叉性Ｂｒｏｃａ失语一例，交叉性传导性失语一例，交叉性Ｗｅｒｎｉｃｋｅ失语一例，交叉性经皮质运动性失语一例，交叉性经皮质感觉性失语三例，交叉性丘脑性失语一例。此８例各型交叉性失语之临床表现与右利手左大脑半球病变产生的各相应类型失语无根本不同。产生交叉性失语是患者的大脑半球语言中枢的逆转所致（不在左侧而在右侧大脑半球的对称部位），它与遗传有关。失语症类型与患者年龄和性别的关系有待进一步研究。     

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 and infarction of the posterior cerebral artery territory

Spoken language disorders are rarely mentioned in superficial infarction of the posterior cerebral (PCA) territory. Two clinical types have been reported: transcortical sensory and amnesic aphasia. Between 1979 and 1990, we studied retrospectively 76 patients suffering from an occipitotemporal infarction located in the superficial territory of the posterior cerebral artery, all well documented by CT. Aphasia was one of the first and prominent signs in 18 cases. Middle cerebral artery concomitant infarction could have been the cause of language impairment in 10. In 8 patients aphasia was only explained by a PCA territory infarct. Three patients showed features of transcortical sensory aphasia. CT localization showed internal lobe and thalamic involvement of the dominant hemisphere. Five patients exhibited word finding impairment with various degrees of amnestic syndrome. The dominant internal temporal lobe was always afffected. Dominant thalamus involvement was found in one case only. Some correlations between clinical features and anatomical support (vascular supply and anatomical structure) might be suggested in our 8 cases of aphasic disorders due to PCA infarcts. They are discussed and compared with data in the literature.     

Crossed aphasia: a PET follow up study of two cases.

Two cases of aphasia after right hemispheric stroke in right handed patients are described. The first patient had a severe mixed transcortical aphasia, apraxia and neglect after a lesion involving the right lenticular nucleus and periventricular white matter; aphasia was still present after three months. The second patient had a mild, transient fluent aphasia after a small right hemispheric periventricular lesion. Studies with [18F]FDG and positron emission tomography (PET) showed functional depression extending to the structurally unaffected left hemisphere in both patients in the acute stage. After three months, in the patient with persistent aphasia, metabolism was still reduced in the right hemisphere, with some recovery of hypometabolism on the left, while metabolic values had returned to normal in the patient with full language recovery. A close parallelism between glucose metabolism and clinical course in crossed aphasia is shown, as well as the presence of a functional involvement of the structurally unaffected left hemisphere in the acute stage.