Global aphasia due to left thalamic hemorrhage

Acta Neurologica Scandinavica, 2001

Objectives ± The independent predictors of aphasia outcome for patients with left basal ganglia hemorrhage were evaluated. Patients and methods ± We included 140 patients of 1036 patients with spontaneous intracerebral hemorrhage admitted to our hospital from January 1993 through December 1997. Aphasia was assessed using the aphasia scale of the Scandinavian stroke scale. Univariate and step-wise logistic regression analyses were performed to assess the relationships between the initial aphasia score, age, gender, blood volume, locations of hematoma and aphasia outcome. Results ± Step-wise logistic regression analysis revealed that the following two factors were independently associated with the ®nal aphasia outcome: initial aphasia score (P<0.0001) and location of hematoma involving the posterior limb of the internal capsule (P=0.004). Conclusions ± A particularly high likelihood of poor aphasia outcomes of patients with left basal ganglia hemorrhage are predicted in those who have poor initial aphasia score and whose brain computed tomography shows the hematoma involves the posterior limb of the internal capsule.

Annals of neurosciences, 2012

Vascular lesion of the subcortical structures leads to aphasia. Cortical hypoperfusion has been proposed to be the etiological mechanism in aphasia following subcortical vascular lesion. Subcortical aphasia shows considerable variability in its clinical profile. Such variability has been attributed to the variable sites of cortical hypoperfusion following ischemic lesion of the subcortical structures. This study investigated the variability in clinical aphasic profile following subcortical hemorrhagic lesion. We retrospectively investigated the clinical aphasic profiles of twelve patients who reported to our hospital during a period of one year with subcortical hemorrhagic lesions. All patients underwent routine neurological examination, neuroimaging (CT/MRI) investigations and linguistic assessment. Eight patients exhibited lesion to the basal ganglia and four showed thalamic lesion. All of them showed considerable variability in their aphasic profile. Subcortical hemorrhagic lesio...

Ischemic Stroke [Working Title]

Aphasia represents an acquired central disorder of language that impairs a person's ability to understand and/or produce spoken and written language, caused by lesions situated usually in the dominant (left) cerebral hemisphere, in right-handed persons. Aphasia has a prevalence of 25-30% in acute ischemic stroke (vascular aphasia). It is considered as an important stroke severity marker, being associated with a higher risk of mortality, poor functional prognosis, and augmented risk of vascular dementia. The assessment of aphasias in clinical practice is based on classical analysis of oral production and comprehension. The language disturbances are frequently combined into aphasic syndromes which are components of different vascular syndromes that may evolve/involve rapidly at the acute stage of ischemic stroke. The main determinant of the type of vascular aphasia is the infarct location (especially left middle cerebral artery territory). Recent studies at the hyperacute stage of ischemic stroke have observed features of aphasia, have reanalyzed its neuroanatomy using new imaging techniques, and have shown that aphasias have a parallel course to that of cortico-subcortical hypoperfusion. Thus, the reversal of hypoperfusion, following recanalization (spontaneous or secondary to thrombolysis or thrombectomy), is associated with resolution of aphasia. Speech therapy is needed as soon as permitted by clinical condition.

Behavioural Neurology, 2008

Crossed aphasia in dextrals (CAD) following pure subcortical lesions is rare. This study describes a right-handed patient with an ischemic lesion in the right thalamus. In the post-acute phase of the stroke, a unique combination of ‘crossed thalamic aphasia’ was found with left visuo-spatial neglect and constructional apraxia. On the basis of the criteria used in Mariën et al. [67], this case-report is the first reliable representative of vascular CAD following an isolated lesion in the right thalamus. Furthermore, this paper presents a detailed analysis of linguistic and cognitive impairments of ‘possible’ and &#39;reliable&#39; subcortical CAD-cases published since 1975. Out of 25 patients with a pure subcortical lesion, nine cases were considered as ‘possibly reliable or reliable’. A review of these cases reveals that: (1) demographic data are consistent with the general findings for the entire group of vascular CAD, (2) the neurolinguistic findings do not support the data in the...

Brain and Language, 1998

Stroke is the most frequent serious neurological disorder in the world and the third leading cause of death in many countries. Among the diverse cognitive deficits caused by stroke, aphasia is the one of the most devastating. Among aphasia types, Wernicke's aphasia (as described by Wernicke) consists of the loss of comprehension, loss of ability to read and write, and distortion of oral speech. Hearing is intact. Within the Geschwind-Lichtheim model, the disorder is due to cortical lesions: Brodmann's areas 22 and 39 (namely, Wernicke's area). Diaschisis is a functional impairment at a site in the brain remote from the lesion causing it. Cerebellar diaschisis after cortical insult is detailed in the literature; however, cortical diaschisis after cerebellar insult remains a rarely reported occurrence. In the chronic stage of stroke, contralateral cerebellar blood flow and metabolism are depressed, which is known as crossed cerebellar diaschisis (CCD). We reported a Wernicke's aphasia caused by CCD following cerebellar hemorrhage. The patient was a 56 years old, right-handed male. He lived in Beijing and was a businessman. He was admitted by the department of Neurology, Beijing Tiantan Hospital on 10th Aug, 2007. His wife's major complaint was deterioration of his language skills for one month, and she recalled that the patient suffered from cerebellar hemorrhage two months ago and was given some treatment at hospital. When he went home after one month, she found that the patient had difficulty with word-finding. Specifically, when the patient needed words to express his needs, he could not accurately say the correct word but could express his needs with gestures. On the other hand, he had significant impairment in auditory comprehension and he could not perform sentence completion tasks. However, he could perform well in reading comprehension at the sentence level (sentence comprehension, reading instructions and reading the test). His performance in writing names of objects and pictures matching were poor, and could not write down some words during writing and dictation tasks. He was diagnosed as Wernicke's aphasia by using the Western Aphasia Battery. His aphasia severity gradation was level four. Why did cerebellar hemorrhage produce his aphasia? Using positron emission tomography (PET), we found decreased perfusion of the bilateral frontal and temporal lobes, consistent with regional loss of neural activity. As shown in Figure 1, the result of PET showed that bilateral frontal and temporal lobes, especially the right frontal and temporal lobes were in a state of glucose hypometabolism. We gave him language training twice a day, and we observed his language ability improved quickly. We proposed that the patient's aphasia resulted from both anterograde disconnection of the corticopontocerebellar tracts and retrograde deafferentation of dentatothalamocortical projections. This patient provides a case of CCD elicited by cerebellar hemorrhage.

Frontiers in Neurology, 2014

Although aphasia and hemispatial neglect are classically labeled as cortical deficits, language deficits or hemispatial neglect following lesions to subcortical regions have been reported in many studies. However, whether or not aphasia and hemispatial neglect can be caused by subcortical lesions alone has been a matter of controversy. It has been previously shown that most cases of aphasia or hemispatial neglect due to acute non-thalamic subcortical infarcts can be accounted for by concurrent cortical hypoperfusion due to arterial stenosis or occlusion, reversible by restoring blood flow to the cortex. In this study, we evaluated whether aphasia or neglect occur after acute thalamic infarct without cortical hypoperfusion due to arterial stenosis or occlusion. Twenty patients with isolated acute thalamic infarcts (10 right and 10 left) underwent MRI scanning and detailed cognitive testing. Results revealed that 5/10 patients with left thalamic infarcts had aphasia and only 1 had cortical hypoperfusion, whereas 2/10 patients with right thalamic infarcts had hemispatial neglect and both had cortical hypoperfusion.These findings indicate that aphasia was observed in some cases of isolated left thalamic infarcts without cortical hypoerfusion due to arterial stenosis or occlusion (measured with time-to-peak delays), but neglect occurred after isolated right thalamic infarcts only when there was cortical hypoperfusion due to arterial stenosis or occlusion. Therefore, neglect after acute right thalamic infarct should trigger evaluation for cortical hypoperfusion that might improve with restoration of blood flow. Further investigation in a larger group of patients and with other imaging modalities is warranted to confirm these findings.

Neurorehabilitation and Neural Repair, 2010

Background. Current knowledge regarding the time course of aphasia recovery is based on observations limited to the first years after stroke. Objective. The authors studied long-term outcome (25 years) of language in a patient with global aphasia. Methods. A 37-year-old man with global aphasia from a large ischemic lesion in the left middle cerebral artery territory was tested 9 times between 3 weeks and 25 years poststroke by means of the Milan Language Examination, Token Test, Raven Test, and apraxia tests. Results. Three main periods of recovery were identified. The first year after stroke was characterized by recovery of verbal comprehension and word repetition. From 1 to 3 years, naming and reading improved. From 3 to 25 years, progressive improvement of previously emerged functions was found, as well as the appearance of spontaneous speech. Conclusions. This unique long-term follow-up shows that the time span for recovery of language functions in global aphasia after stroke may be much longer than previously documented.

Journal of the Neurological Sciences, 2004

Background: Global aphasia without hemiparesis (GAWH) is a rare stroke syndrome. This study localized the lesion and examined the pathogenic mechanism in Korean patients with GAWH, and investigated whether areas of extensive hypoperfusion existed outside the diffusion-weighted imaging (DWI) lesions seen in these patients. Material and methods: Eleven patients were diagnosed with aphasia using the Western Aphasia Battery. To identify decreased perfusion, which might be functionally relevant to aphasia but not detected by DWI, single photon emission tomography (SPECT) was performed in five patients. To uncover the possible pathogenic mechanisms of ischemic stroke, vascular and cardiologic work-ups were performed in all of the patients. Results: The lesions seen on DWI varied, and included both inferior frontal and superior temporal (three), isolated inferior frontal (four) or superior temporal (one), subcortical (two), and even parietooccipital (one) lesions. Brain SPECT did not reveal an extensive lesion of the peri-sylvian area outside the DWI lesion in any of the patients, except one with the subcortical lesions. Conclusion: Our results indicate that a single lesion in different locations may be sufficient to produce GAWH, and the lesion profile and stroke mechanism in GAWH are heterogeneous, suggesting that lesions to an area of complex functional anatomy result in aphasia. D

Journal of Clinical Neuroscience, 2017

Global aphasia without hemiparesis is a rare condition often associated with embolic stroke. Posttraumatic causes have not been reported, in the literature, to our knowledge. We report a 15-year old boy with transient global aphasia without hemiparesis due to blunt head trauma. In our case, clinical findings occurred 1 week later following head trauma. Emergence of the symptoms after a period of the first mechanical head trauma, draws attention to the importance of secondary process in traumatic brain injury.

Developmental Medicine & Child Neurology, 2007

Five children (three males, two females; four right-, one lefthanded; age range 6 to 14 years) who developed aphasia after gross-total excision of left predominantly thalamic tumors are reported. Three patients had Broca aphasia, one had mixed transcortical aphasia, and one patient had conduction aphasia. In the months after surgery, three children improved while receiving radiation and/or chemotherapy, although none recovered completely. Two patients with malignant tumors developed worsening aphasia when the tumor recurred, and later died. Two of three patients tested had visuospatial difficulties in addition to language deficits. Attention and executive functioning were affected in three of three patients tested. Memory, verbal and/or visual functioning, were affected in four of four patients tested. Both patients who were tested showed transient right hemineglect. Two of two patients tested were probably apraxic. The wide range of deficits in these children highlights the importance of the thalamus and other subcortical structures in developing cognition.