Recent publications

Abstract

The case is presented of a 65-year-old man who developed a significant and persistent aphasia subsequent to a cerebrovascular accident involving the straito-capsular region. The findings of a neuroradiological examination and a series of language tests are described. Both computed tomography and magnetic resonance imaging demonstrated the presence of a large subcortical infarct centred on the region of the left basal ganglia and internal capsule and involving the white matter adjacent to the body of the left lateral ventricle. Neither imaging technique showed extension of the lesion to involve the cerebral cortex. Possible mechanisms whereby subcortical infarcts can cause language problems are discussed.     

Aphasia owing to subcortical brain infarcts in childhood

The aim of this study was to further define the clinical features of subcortical aphasia in children with deep brain infarcts and to define the sequelae associated with childhood strokes. We retrospectively studied nine children with left subcortical brain infarcts who presented with acquired language disorder and underwent language investigations based on standardized tests. Stroke in these patients involved the left internal capsule, lenticular or thalamic nuclei, or a combination of these. Early aphasic manifestations following the deep cerebral infarcts affected language expression. These included mutism, nonfluent speech, word finding difficulties, and phonemic and semantic paraphasia. Speech comprehension was generally more preserved. All patients subsequently improved, although variably; sequelae such as dysfluency, word finding difficulties, and written language learning impairment could be detected through standardized tests in six of them (all younger than 6 years at the time of the infarct). Two of the three remaining patients (both older than 6 years at the time of the infarct) had a full recovery. Our study confirms the concept of childhood subcortical aphasia, depicts the linguistic profile in these patients, and sustains the indication of systematic formal language assessment during the follow-up of all children with subcortical infarct involving the dominant hemisphere.     

Regional metabolic correlates of Token test results in cortical and subcortical left hemispheric infarction

We investigated 26 right-handed patients who had aphasia caused by a single infarct in the territory of the left middle cerebral artery (MCA) with cranial CT, positron emission tomography, and a standard language test battery including the Token test. The patients represented an unselected sample of various infarct locations within the left MCA territory and showed a wide range of aphasia types and severity. Stepwise regression analysis revealed that Token test performance mainly depended on parietotemporal metabolism, irrespective of infarct location. Frontal and basal ganglia metabolism did not contribute significantly to Token test performance. These results suggest that disturbance of language comprehension is due to parietotemporal cortical dysfunction in all types of left MCA infarction. Infarcts restricted to basal ganglia or the anterior part of the MCA territory apparently do not disturb language comprehension directly, but via their remote effects on parietotemporal metabolism.     

Ideomotor apraxia without aphasia and aphasia without apraxia: the anatomical support for a double dissociation.

This study aimed to verify the existence of a double aphasia/apraxia dissociation. Apraxic patients without aphasia and aphasic patients without apraxia were included in a consecutive series of patients with cortical or subcortical CT documented vascular lesions in the left hemisphere. Of 699 patients, 10 were found to be apraxic but not aphasic and 149 aphasic but not apraxic. These findings indicate an aphasia/apraxia double dissociation. This suggests that praxis and language make use of two different, partly overlapping networks.     

Singing can improve speech function in aphasics associated with intact right basal ganglia and preserve right temporal glucose metabolism: Implications for singing therapy indication

Clinically, we know that some aphasic patients can sing well despite their speech disturbances. Herein, we report 10 patients with non-fluent aphasia, of which half of the patients improved their speech function after singing training. We studied ten patients with non-fluent aphasia complaining of difficulty finding words. All had lesions in the left basal ganglia or temporal lobe. They selected the melodies they knew well, but which they could not sing. We made a new lyric with a familiar melody using words they could not name. The singing training using these new lyrics was performed for 30 minutes once a week for 10 weeks. Before and after the training, their speech functions were assessed by language tests. At baseline, 6 of them received positron emission tomography to evaluate glucose metabolism. Five patients exhibited improvements after intervention; all but one exhibited intact right basal ganglia and left temporal lobes, but all exhibited left basal ganglia lesions. Among them, three subjects exhibited preserved glucose metabolism in the right temporal lobe. We considered that patients who exhibit intact right basal ganglia and left temporal lobes, together with preserved right hemispheric glucose metabolism, might be an indication of the effectiveness of singing therapy.     

Characteristics of basal ganglia aphasia after stroke and the rehabilitative interventions

To introduce the characteristics of basal ganglia aphasia after stroke and the rehabilitative interventions.DATA SOURCES: Articles related to stroke, subcortical aphasia, basal ganglia aphasia and language rehabilitation published in Chinese from January 1988 to December 2005 were searched in Chinese journal full-text database (CJFD) using the keywords of“stroke, basal ganglia aphasia, language rehabilitation“ in Chinese. Meanwhile, English articles about aphasia published from January 1982 to December 2005 were searched in and Pubmed database. Besides, several books associated with the contents were looked through manually.STUDY SELECTION: The data were checked primarily, the articles about the pathomechanism and neurolinguistic characteristics of basal ganglia aphasia, diagnostic methods of aphasia and language rehabilitation were selected, and those had no obvious relation with the above contents were excluded.Inclusive criteria: literatures explain the clinical characteristics of basal ganglia aphasia, neurolinguistic pathogenesis and methods of rehabilitation therapy in details. The repetitive studies were excluded.DATA EXTRACTION: Totally 95 literatures about basal ganglia aphasia were collected, including 31 about the clinical characteristics of basal ganglia aphasia, 45 about its neurolinguistic pathogenesis, 5 about the evaluation and classification of aphasia, and 14 about its rehabilitation therapy. Thirty accorded with the inclusive criteria were used for review, and the other 65 were excluded.DATA SYNTHESIS: Concisely introduced the definition, past investigation of basal ganglia aphasia after stroke, then dwelled on the multiplicity neurolinguistics characteristics. Aphasia evaluation was dependent upon clinical aphasic symptoms. The relationship between symptom and focus of infection was explored, and the mechanism of pathosis language behavior on basal ganglia aphasia patients was understood to provide consequence data that could authenticate the processing of language in brain. On the other hand, the method of rehabilitation on basal ganglia aphasia after stroke was explained.CONCLUSION: Basal ganglia aphasia is manifested as atypical aphasic symptom, the mechanism for the structure of basal ganglia in the speech formation should be further confirmed. It is effective to select pertinent language rehabilitation for basal ganglia aphasia after stroke.     

Subcortical dementia. Review of an emerging concept

Subcortical dementia is a clinical syndrome characterized by slowness of mental processing, forgetfulness, impaired cognition, apathy, and depression. First recognized in progressive supranuclear palsy and Huntington's disease, the concept has been extended to account for the intellectual impairment of Parkinson's disease, Wilson's disease, spinocerebellar degenerations, idiopathic basal ganglia calcification, the lacunar state, and the dementia syndrome of depression. Disorders manifesting subcortical dementia have pathologic changes that involve primarily the thalamus, basal ganglia, and related brain-stem nuclei with relative sparing of the cerebral cortex. Recent studies of neuropsychologic deficits following focal subcortical lesions also support a role for these structures in arousal, attention, mood, motivation, language, memory, abstraction, and visuospatial skills. The clinical characteristics of subcortical dementia differ from those of dementia of Alzheimer's type where prominent cerebral cortical involvement produces aphasia, amnesia, agnosia, and apraxia.     

Wernicke's aphasia after putaminal hemorrhage: Unusual clinical and SPECT findings

We present a case of a man with a putaminal hemorrhage who presented in the acute stage with a 'classic' Wernicke's aphasia. CT and MRI scans showed a large left basal ganglia hemorrhage involving the posteriorputamen. A SPECT scan performed acutely demonstrated decreased perfusion in the left temporal cortex, frontal cortex and white matter and to the left basal ganglia from the hemorrhage itself. Within five days his language abilities improved dramatically, with complete resolution of his aphasia over the course of six weeks. Repeat SPECT scans continued to show the structural changes to the left putamen and left hemisphere hypoperfusion, suggesting that the resolution of the language symptoms did not correlate with the structural and perfusion changes. Various theories advanced in the literature regarding the pathophysiological mechanisms causing aphasia due to subcortical lesions cannot completely explain the findings of our case. These hypotheses are reviewed and discussed.     

A case of aphasia with speech disorders by infarction of the left caudate nucleus and putamen

An infarction involving the left putamen, caudate nucleus and the anterior limb of the internal capsule, resulted in aphasia with semantic paraphasias, verbal incoherence and verbal memory impairment. Cerebral blood flow (CBF) studies with 133Xe inhalation at 20 days post onset showed, on one hand, a bilateral lowering of cortical blood flow and on the other hand a left frontal-parietal hypoperfusion area. Spontaneous recovery occurred within 2 months. While the mean CBF became normal at 14 months post onset, a relative hypoperfusion area persisted on the anterior left hemispheric cortex. On the basis of these findings and current CBF and metabolic studies carried out in patients with subcortical lesions, the authors discuss the role of cortical and subcortical structures in subcortical aphasic syndromes. The importance of reciprocal connections between cortex, striatum and thalamus is stressed.     

Speech and language disorders subsequent to subcortical vascular lesions

Abstract

The speech and language abilities of four cases with subcortical brain lesions of vascular origin centred on either the thalamus or basal ganglia were investigated at least six months post-onset of their neurological disorder. The results of standardized language assessments indicated that long-lasting, atypical, fluent aphasia was present in all subjects. Considerable variation existed between the language abilities of each subject assessed and a single, invariable ‘subcortical aphasia’ syndrome was not found. In no case could the language disturbance be classified into one of the traditional cortical aphasia syndromes. The language assessment results were used to evaluate a recently proposed model of subcortical participation in language based on the assumption that pre-verbal semantic monitoring is subserved by subcortical structures. Although all subjects examined had deficits in the semantic level of language, the presence of other aphasic characteristics (e.g., agrammatism, verbal dyspraxia and comprehension deficits) indicated that the proposed model may be inadequate to describe the role of various subcortical structures in language.

All subjects exhibited an atypical dysarthria that could not be classified into any of the classical types. In two cases the dysarthria was similar to that reported to follow unilateral upper motor neurone lesions. A mixed spastic-hypokinetic dysarthria was also observed in one case while the remaining case exhibited an atypical spastic dysarthria. The dysarthria observed in each case is discussed in relation to the subcortical lesion site identified by CT scan.     

Cerebral blood flow in thalamic aphasia

Summary A 59-year-old man is reported, who became aphasic after left thalamic infarction, shown by CT. His speech was fluent, with reduced voice volume, impaired auditory and reading comprehension, verbal paraphasias but intact repetition skills. A single photon emission computed tomography (SPECT) scan to measure regional cerebral flow (rCBF) showed a reduction of flow in the parietotemporal areas of the left hemisphere. It is suggested that thalamic aphasia could result from structural subcortical damage with a homolateral functional cortical deficit leading to the specific aphasic disturbance.     

The validity of a simple clinical classification of acute ischaemic stroke

The aim of the study reported here was to test the validity of a simple clinical classification of acute ischaemic stroke (Oxfordshire Community Stroke Project, OCSP) in predicting the site and size of cerebral infarction on computed tomography (CT). Consecutive patients admitted to hospital with acute ischaemic stroke were prospectively identified and classified into one of four clinical syndromes according to the OCSP classification, blind to the result of CT. The CT brain scans were classified blind to the clinical features into those demonstrating: small, medium or large cortical infarcts; small or large subcortical infarcts in the anterior circulation territory; and posterior cerebral circulation territory infarcts. A total of 108 patients were included. A recent infarct was seen. on the CT scan in 91 patients (84%), and the clinical classification correctly predicted the site and size of the cerebral infarct in 80 of these (88%; 95% confidence interval 77–92%). The positive predictive value was best for large cortical infarcts (0.94) and worst for small subcortical infarcts (0.63). The OCSP clinical classification is a reasonably valid way of predicting the site and size of cerebral infarction on CT and can, therefore, be used very early after stroke onset before the infarct appears on the scan.     

Changes of blood flow in the cerebral cortex after subcortical ischemic infarction

The two-dimensional xenon-133 inhalation method was used to measure cortical blood flow in 16 patients with small subcortical ischemic infarcts and in 10 patients with larger cortical infarcts in the chronic phase of stroke. An abnormal hemispheric asymmetry of blood flow was seen, not only in patients with cortical infarcts, but also in those with subcortical infarcts. In the patients with subcortical infarcts, focal areas of reduced cortical blood flow were seen in the symptomatic hemisphere remote from the tissue destruction, usually including part of the noninfarcted frontoparietal cortex. The cortical dysfunction may have contributed to the clinical manifestations including aphasia, which was present in 14 of the 16 patients with subcortical lesions.     

多梗塞性痴呆和Alzheimer型痴呆的SPECT和MRI比较研究

对２２例多梗塞性痴呆，１５例Ａｌｚｈｅｉｍｅｒ型痴呆病人和２４例同龄，同利手健康对照组作了单光子发射计算机断层显角和磁共振成象检查。结果发现ＳＰＥＣＴ在ＭＩＤ病人主要表现为多发性，局灶性脑放射性减低，两侧不对称，以额皮质，皮质下明显；ＤＡＴ病人主要表现为大脑皮质放射性对称性降低，以颞顶枕明显。     

Recovery from aphasia and neglect after subcortical stroke: neuropsychological and cerebral perfusion study.

Cortical regional cerebral perfusion was assessed by N, N, N1-trimethyl-N1-(2)-hydroxy-3-methyl-5-(I-123) iodobenzyl-1, 3-propanediamine 2 HCl I-123 (HIPDM) and single photon emission computerised tomography (SPECT) in six aphasic and two neglect patients with unilateral subcortical vascular lesions. Assessments were carried out both in the acute phase and after a period ranging from 1 to 6 months after stroke onset. In all patients an almost complete spontaneous recovery occurred and was associated with a significant improvement of cortical perfusion. A relationship between severity of aphasia and degree of cortical hypoperfusion was found, in both the acute and the follow up assessments, in the aphasic subgroup.     

脑小血管病

目的探讨伴皮质下梗死和白质脑病的常染色体显性遗传性脑动脉病(cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy,CADASIL)患者脑微出血(cerebral microbleeds,CMBs)的分布特征及临床意义。方法回顾性纳入2017年6月-2019年12月北京协和医院基因确诊的连续CADASIL患者21例(CADASIL组),以及性别匹配的高血压动脉硬化性脑小血管病患者21例(高血压脑小血管病组)。所有患者均行头MRI检查(含T2^*/SWI序列),盲法读片并记录CMBs的数量和部位,分析两组CMBs分布的差异。结果CADASIL组年龄和常见血管病危险因素比例均低于高血压脑小血管病组。CADASIL组47.6%患者检出CMBs(共计115个),而高血压脑小血管病组高达95.2%(共计218个)。CADASIL组CMBs分布以丘脑最常受累(45.2%),其次是脑叶(皮层/皮层下,35.7%)、基底节(11.3%)。高血压脑小血管病组则以丘脑以外的基底节CMBs最多见(35.3%),其次是脑叶(26.6%)、丘脑(19.2%)、脑干(16.1%)。CADASIL患者丘脑CMBs/总CMBs比例、丘脑CMBs/(基底节CMBs+脑干CMBs)比例均高于高血压脑小血管病组(均P<0.001)。结论CADASIL患者CMBs分布以丘脑最常见,其次是皮层/皮层下区域,而高血压脑小血管病患者则以丘脑以外的基底节、脑干更常见。     

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.     

Clinical lacunar syndromes as predictors of lacunar infarcts. A comparison of acute clinical lacunar syndromes and findings on diffusion-weighted MRI

OBJECTIVES: To evaluate if patients with acute lacunar syndromes have acute lacunar infarcts or other types of cerebral lesions on diffusion-weighted MRI. METHODS: Patients with acute lacunar syndromes underwent echo-planar diffusion MRI of the brain within 3 days after stroke onset. Localization and size of lesions with hyperintense signal were determined, compared with clinical characteristics and with findings on follow-up T2-weighted MRI. RESULTS: Twenty-three patients participated in the study. Thirteen patients had pure motor stroke, 1 pure sensory stroke, 8 sensorimotor stroke, and 1 ataxic hemiparesis. Twenty-two patients had at least one lesion with increased signal on diffusion-weighted MR images. These acute lesions were in the internal capsule/ basal ganglia/thalamus in 13 patients, subcortical white matter in 5 patients, brainstem in 2 patients, cortex (multiple small lesions) in 1 patient, and cortex + basal ganglia in 1 patient. The median volume of the lesions was 0.6 ml on the initial examination and on follow-up, of 17 patients after 1 to 5 months, 0.5 ml. CONCLUSIONS: Almost all patients with acute ischemic lacunar syndromes have acute lesions on echo-planar diffusion-weighted MRI within 3 days after stroke onset. These lesions are mostly small and subcortical, compatible with lacunar infarcts caused by single penetrating artery occlusion, but in a minor proportion of patients (2 of 23 in our study) a cortical involvement is found.     

Subcortical infarction resulting in acquired stuttering

Stuttering is an uncommon presentation of acute stroke. Reported cases have often been associated with left sided cortical lesions, aphasia, and difficulties with other non-linguistic tests of rhythmic motor control. Three patients with subcortical lesions resulting in stuttering are discussed. In one patient the ability to perform time estimations with a computerised repetitive time estimation task was characterised.One patient had a pontine infarct with clinical evidence of cerebellar dysfunction. A second patient had a left basal ganglionic infarct and a disruption of timing estimation. A third patient had a left subcortical infarct and a mild aphasia.These findings expand the reported distribution of infarction that can result in acquired stuttering. Subcortical mechanisms of speech control and timing may contribute to the pathophysiology of acquired stuttering.     

The contribution of the left and right hemispheres to early recovery from aphasia: A SPECT prospective study

This prospective study examined the relationship between post-stroke recovery of aphasia and changes in cerebral blood flow (CBF). To address the question of right hemisphere (RH) involvement in restitution of language, we tested the hypothesis that the increase in perfusion of the RH is crucial for early recovery from aphasia. Twenty-four right-handed patients with acute aphasia following left hemisphere (LH) ischaemic stroke were examined twice with a six-month interval. At each session CBF and language scores were measured on the same stroke patients. Language was measured by selected tasks derived from the Boston Diagnostic Aphasia Examination (BDAE). The SPECT scans were obtained using ^99mTc-ECD on a triple-head gamma camera Multispect-3. Although initial CBF measured for the whole group of aphasic patients was not a predictor for future language recovery for either hemisphere, increased perfusion of the RH during a six-month interval was found to parallel the recovery of aphasic disorders. There was a correlation between the change in the right parietal CBF (but not the left) and a change in numerous language abilities. Nevertheless, only CBF values on the left predicted performance on the language tests at initial and follow-up examinations. When the area damaged on structural imaging was excluded from perfusion analysis, only subcortical CBF change on the left showed a positive correlation with language improvement. Thus, the cerebral mechanism associated with early recovery from aphasia is a dynamic and complex process that may involve both hemispheres. Probably this mechanism involves functional reorganisation in the speech-dominant (damaged) hemisphere and regression of haemodynamic disturbances in the non-dominant (structurally intact) hemisphere.