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)     

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.     

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.     

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     

Frontal lobe hematoma associated with transcortical motor aphasia: case report]

An 81-year-old woman with left medial frontal lobe hematoma, which involved the supplementary motor area, is reported. She was right-handed and was initially mute for several hours after the onset. On admission, she exhibited mild paresis of the right lower extremity. Her spontaneous speech was sparse and not fluent, but her articulation and auditory comprehension were normal and repetition was good. She exhibited excellent performance in the confrontation naming task, but showed difficulty in recalling words from a given category during the word fluency task. On the basis of these clinical features, she was diagnosed as having transcortical motor aphasia. Our case may corroborate previous findings that the left medial frontal lobe is important in word fluency but not in confrontation naming.     

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。     

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.     

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.     

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.     

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).     

Acute mixed transcortical aphasia with bihemispheric neurological deficits following diffuse cerebral dysfunction

A 78 year old man presented with acute mixed transcortical aphasia with intact naming and bilateral involvement of the motor systems following a left internal carotid artery stenosis. The CT scan showed hypodense areas in the border zones of the left hemisphere together with diffuse areas of ischaemia. Intact repetition the hallmark of transcortical aphasias and the exceptional preserved naming in this patient support the earlier findings that the contralateral hemisphere could mediate some aspects of language function. The patient also had bilateral motor abnormalities which could be explained on the occipito-parietal lesion. It is suggested that widespread hypofunction of the left hemisphere following cerebral ischaemia could give rise to bihemispheric neurological deficits which could be short lived and could possibly be attributed to bilateral cerebral blood flow changes that may occur with the hemispheric lesion.     

Aphasia after stroke: type, severity and prognosis. The Copenhagen aphasia study

AIM: To determine the types, severity and evolution of aphasia in unselected, acute stroke patients and evaluate potential predictors for language outcome 1 year after stroke. METHODS: 270 acute stroke patients with aphasia (203 with first-ever strokes) were included consecutively and prospectively from three hospitals in Copenhagen, Denmark, and assessed with the Western Aphasia Battery. The assessment was repeated 1 year after stroke. RESULTS: The frequencies of the different types of aphasia in acute first-ever stroke were: global 32%, Broca's 12%, isolation 2%, transcortical motor 2%, Wernicke's 16%, transcortical sensory 7%, conduction 5% and anomic 25%. These figures are not substantially different from what has been found in previous studies of more or less selected populations. The type of aphasia always changed to a less severe form during the first year. Nonfluent aphasia could evolve into fluent aphasia (e.g., global to Wernicke's and Broca's to anomic), whereas a fluent aphasia never evolved into a nonfluent aphasia. One year after stroke, the following frequencies were found: global 7%, Broca's 13%, isolation 0%, transcortical motor 1%, Wernicke's 5%, transcortical sensory 0%, conduction 6% and anomic 29%. The distribution of aphasia types in acute and chronic aphasia is, thus, quite different. The outcome for language function was predicted by initial severity of the aphasia and by the initial stroke severity (assessed by the Scandinavian Stroke Scale), but not by age, sex or type of aphasia. Thus, a scoring of general stroke severity helps to improve the accuracy of the prognosis for the language function. One year after stroke, fluent aphasics were older than nonfluent aphasics, whereas such a difference was not found in the acute phase.     

Aphemia-like syndrome from a right supplementary motor area lesion

Lesions in the left supplementary motor area (SMA) can result in a transcortical motor aphasia with nonfluent spontaneous verbal output and relatively preserved repetition. Reading and writing are proportionally affected. We report a patient with an ischemic lesion in the right SMA. He had impaired articulation and normal repetition plus preserved reading and writing, consistent with an aphemia. This patient supports the dissociation of articulatory fluency and linguistic fluency and suggests that both SMAs affect the initiating of articulatory movements required to produce words whereas the left SMA also affects linguistic aspects of speech.     

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.     

Transcortical motor aphasia due to a right hemisphere lesion in a right-handed man

Abstract

A 67-year-old, right-handed male became aphasic following a right hemispheric infarction involving the frontal and parietal regions. The patient was evaluated by means of neurological, behavioural, and neuroradiological examinations. Behavioural investigations included Ianguage and nonverbal visuospatial and constructive evaluations. Language evaluation demonstrated transcortical motor aphasia and nonverbal tests showed left-sided visual neglect, left hemiakinesia, and constructional apraxia. Besides the information concerning crossed aphasia in a right-handed person, this case also supports the hypothesis that right-sided language representation does not affect right hemisphere dominance for visuospatial abilities.     

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.     

Aphasia caused by paramedian lesion of the dominant hemisphere: report of a case

A 41 year old woman with a ruptured left pericalosal artery aneurysm and hematoma in the inter-hemispheric fissure and paramedian region of the left hemisphere presented with mutism which turned to aphasia characterized by absent spontaneous speech, lack of paraphasias, relative preservation of repetition and evident preservation of comprehension. This picture conforms to the so called "trans-cortical motor aphasia". The fact that lesions of the paramedian region of the dominant hemisphere, in and around the secondary motor area, can produce aphasia is unknown to many neurologists and several such cases are probably misdiagnosed due to the transience of the major symptoms and to confusion with non-specific dementia.     

"Alien hand" and loss of bimanual coordination after dominant anterior cerebral artery territory infarction.

Three patients with dominant anterior cerebral artery territory infarction demonstrated a severe disturbance of upper limb motor control with impaired bimanual coordination, the "alien hand" sign, and intermanual conflict, in addition to signs of callosal interruption and a transcortical motor aphasia. Recordings of movement-related potentials in one patient showed an attenuated Bereitschaftspotential and a greater asymmetry of the NS' component of the premotor negativity with left finger than with right finger movement. The impairment of bimanual motor control and associated abnormal motor behaviour of the right hand in these cases are postulated to be due to involvement of the supplementary motor area and related areas of the medial frontal cortex.     

卒中后失语症类型及其影响因素分析

目的 通过探讨性别、年龄、病变部位及卒中病因等与失语症类型之间的关系,探索影响卒中后失 语类型的因素。 方法 回顾性分析2004年1月-2018年12月于首都医科大学附属北京天坛医院就诊、因语言障碍进行 西部失语成套测验（western aphasia battery,WAB）的卒中后失语症患者临床资料。分析失语症类型与 性别、年龄、卒中类型、卒中病因及发病机制之间的关系。 结果 共纳入失语症患者681例,按照失语症类型分为完全性失语（global aphasia,GA）（n =185）、 运动性失语（broca’s aphasia,BA）（n =148）、经皮质混合性失语（mixed transcortical aphasia,MTCA） （n =30）、经皮质运动性失语（transcortical motor aphasia,TCMA）（n =67）、感觉性失语（werni cke’s aphasia,WA）（n =69）、经皮质感觉性失语（transcortical sensor aphasia,TCSA）（n =21）、传导性失 语（conduction aphasia,CA）（n =32）和命名性失语（anomic aphasia,NA）（n =129）。将患者分为青年组 （18～44岁）、中年组（45～59岁）、老年组（≥60岁）,校正其他因素影响后,三组人群间失语症类型 无统计学差异。男性和女性患者的失语症类型也无统计学差异。各类型失语症患者的病变部位具有 异质性,除合并经典语言区损伤外,还可合并左侧基底节及丘脑损伤。在脑出血所致的各类型失语 症患者中,最常见的病因均为高血压（77.8%～100.0%）。脑梗死后GA患者中,最常见的卒中发病机制 是混合型（42.4%）和动脉-动脉栓塞（27.3%）,而BA、WA及CA患者以动脉-动脉栓塞（分别占51.5%, 71.4%和40.0%）最常见,TCMA、TCSA及NA以低灌注/栓子清除能力下降（分别占65.9%,58.3%和 38.4%）最常见。 结论 年龄及性别对失语症类型均无明显影响。男性和女性患者均以GA、BA和NA最为常见。病变 部位对失语症类型具有重要影响,卒中病因及发病机制对失语症类型的影响可能与特定血管及血管 供血区损伤有关。     

Global aphasia without hemiparesis: language profiles and lesion distribution

OBJECTIVES: Global aphasia without hemiparesis (GAWH) is an uncommon stroke syndrome involving receptive and expressive language impairment, without the hemiparesis typically manifested by patients with global aphasia after large left perisylvian lesions. A few cases of GAWH have been reported with conflicting conclusions regarding pathogenesis, lesion localisation, and recovery. The current study was conducted to attempt to clarify these issues. METHODS: Ten cases of GAWH were prospectively studied with language profiles and lesion analysis; five patients had multiple lesions, four patients had a single lesion, and one had a subarachnoid haemorrhage. Eight patients met criteria for cardioembolic ischaemic stroke. RESULTS: Cluster analysis based on acute language profiles disclosed three subtypes of patients with GAWH; these clusters persisted on follow up language assessment. Each cluster evolved into a different aphasia subtype: persistent GAWH, Wernicke's aphasia, or transcortical motor aphasia (TCM). Composite lesion analysis showed that persistent GAWH was related to lesioning of the left superior temporal gyrus. Patients with acute GAWH who evolved into TCM type aphasia had common lesioning of the left inferior frontal gyrus and adjacent subcortical white matter. Patients with acute GAWH who evolved into Wernicke's type aphasia were characterised by lesioning of the left precentral and postcentral gyri. Recovery of language was poor in all but one patient. CONCLUSIONS: Although patients with acute GAWH are similar on neurological examination, they are heterogeneous with respect to early aphasia profile, language recovery, and lesion profile.