[Improved instrumental activities of daily living in acquired savant syndrome patient after developing interest in drawing].

We performed examinations of a 73-year-old, right-handed man who developed herpes simplex encephalitis, with cognitive dysfunction including severe Wernicke's aphasia. Although he had never previously been interested in arts, use of a coloring book, recommended by his wife, led him to start drawing. A few years after the onset of brain disease, the patient began to copy pictures of landscapes. The lesion was in the left hemisphere and his work showed a strongly realistic tendency, thus we think that this case demonstrated characteristics of acquired savant syndrome. Along with the increase in drawing ability, instrumental activities of daily living (IADL), such as shopping and use of public transport, were also considerably improved in this patient. On the other hand, results of neuropsychological tests, such as the Standard Language Test of Aphasia, were not improved. We concluded that a sense of accomplishment from the drawing activity and communication with supporters might have led to improvement of IADL in this case.

Stroke rehabilitation using noninvasive cortical stimulation: aphasia.

Poststroke aphasia results from the lesion of cortical areas involved in the motor production of speech (Broca's aphasia) or in the semantic aspects of language comprehension (Wernicke's aphasia). Such lesions produce an important reorganization of speech/language-specific brain networks due to an imbalance between cortical facilitation and inhibition. In fact, functional recovery is associated with changes in the excitability of the damaged neural structures and their connections. Two main mechanisms are involved in poststroke aphasia recovery: the recruitment of perilesional regions of the left hemisphere in case of small lesion and the acquisition of language processing ability in homotopic areas of the nondominant right hemisphere when left hemispheric language abilities are permanently lost. There is some evidence that noninvasive cortical stimulation, especially when combined with language therapy or other therapeutic approaches, can promote aphasia recovery. Cortical stimulation was mainly used to either increase perilesional excitability or reduce contralesional activity based on the concept of reciprocal inhibition and maladaptive plasticity. However, recent studies also showed some positive effects of the reinforcement of neural activities in the contralateral right hemisphere, based on the potential compensatory role of the nondominant hemisphere in stroke recovery.

Transcranial direct current stimulation improves naming reaction time in fluent aphasia: a double-blind, sham-controlled study.

BACKGROUND AND PURPOSE: Previous evidence suggests that anodal transcranial direct current stimulation (A-tDCS) applied to the left hemisphere can improve aphasic participants' ability to name common objects. The current study further examined this issue in a more tightly controlled experiment in participants with fluent aphasia. METHODS: We examined the effect of A-tDCS on reaction time during overt picture naming in 8 chronic stroke participants. Anode electrode placement targeted perilesional brain regions that showed the greatest activation on a pretreatment functional MRI scan administered during overt picture naming with the reference cathode electrode placed on the contralateral forehead. A-tDCS (1 mA; 20-minute) was compared with sham tDCS (S-tDCS) in a crossover design. Participants received 10 sessions of computerized anomia treatment; 5 sessions included A-tDCS and 5 included S-tDCS. RESULTS: Coupling A-tDCS with behavioral language treatment reduced reaction time during naming of trained items immediately posttreatment (Z=1.96, P=0.025) and at subsequent testing 3 weeks later (Z=2.52, P=0.006). CONCLUSIONS: A-tDCS administered during language treatment decreased processing time during picture naming by fluent aphasic participants. Additional studies combining A-tDCS, an inexpensive method with no reported serious side effects, with behavioral language therapy are recommended.

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.

Ambient sensory conditions: modification of receptive speech deficits in left-side stroke patients using bright light.

Previous research has demonstrated the potential for the use of ambient sensory conditions to improve cognitive functioning. Both light and sound have been shown to improve task performance in various populations including children, younger adults, and elderly participants; however, these cognitive gains may possibly be offset by detrimental cardiovascular reactivity in elderly persons. We now have some evidence for ambient sensory conditions affecting cognitive function following left- or right-side cerebrovascular accidents.

Subcortical aphasia.

We critically review the literature on subcortical aphasia, suggest that a number of traditional concepts regarding mechanisms of aphasia are inconsistent with now abundant data, and propose several new hypotheses. The absence of aphasia in 17 reported cases of dominant hemisphere striatocapsular infarction and the finding of nearly every conceivable pattern of language impairment in 33 different reported cases of striatocapsular infarction provide strong evidence against a major direct role of the basal ganglia in language and against disconnection or diaschisis as mechanisms of nonthalamic subcortical aphasia. However, detailed consideration of the vascular events leading to striatocapsular infarction strongly suggests that associated linguistic deficits are predominantly related to sustained cortical hypoperfusion and infarction not visible on structural imaging studies. Thalamic disconnection, as may occur with striatocapsular infarcts with extension to the temporal stem and putamenal hemorrhages, may also contribute to the language deficits in some patients. Review of the literature on thalamic infarction, in conjunction with previously unreported anatomic details of four cases, suggests that what infarcts in the tuberothalamic artery territory and the occasional infarcts in the paramedian artery territory associated with aphasia have in common is damage to the frontal lobe-inferior thalamic peduncle-nucleus reticularis-center median system that may be involved in regulating the thalamic gate in attentional processes. Disruption of attentional gating in the pulvinar and lateral posterior nuclei resulting from such lesions may impair selection of specific neuronal networks in the projection field of these nuclei that serve as the substrate for lexical-semantic function, which is in effect a disruption of a type of working memory, as defined by Goldman-Rakic. We define this as a defect of selective engagement.

Subcortical aphasia and the problem of attributing functional responsibility to parts of distributed brain processes.

N&C's discussion is, in places, an exemplar of the sort of rigor and attention to detail that will bring us closer to an understanding of the functional organization of the brain. Indeed, it is this level of work that pushes us to reflect on the assumptions that undergird our research efforts. Our criticisms have developed four main points. First, the level of rigor applied to the consideration of basal ganglionic aphasia should extend to each application of the CPC method (thalamic aphasia included). Second, in our haste to identify specific brain systems with distinct cognitive functions we should not neglect the more basic question of the causal mechanisms by which the brain organizes behavior. Questions of "direct" versus "indirect" involvement of a particular organ in a cognitive function are only likely to distract our attention from this more basic and less inferentially perilous issue. Third, pure cases should no longer be considered touchstones against which all behavioral disturbances are measured. Reifying such ideals is more likely to shroud than reveal the brain's true complexity. Finally, the functions that we enshrine in particular brain regions should explain the particular character of the symptoms observed when they are damaged and should admit of independent verification.

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 affected. 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.

Auditory middle-latency responses in patients with localized and non-localized lesions of the central nervous system.

Auditory middle-latency responses were recorded in 45 neurological patients. In 4 patients with localized lesions in the thalamus, or subcortical white matter, the component Na was attenuated or delayed at T3, Cz and T4, exclusively on stimulation of the ear contralateral to the lesion. In 5 patients with temporal lobe lesions with receptive aphasia, the amplitude of component Pa was decreased on the lesion side (T3), regardless of the side of stimulation. These findings suggest that Na is generated from a subcortical structure and Pa is generated from the temporal cortex. In 25 patients with diffuse CNS lesions, V-Na interpeak latency was prolonged in 2 cases.

[On a case of aphasia with thalamic lesion (author's transl)]. / Su un caso di afasia da lesione talamica.

The possibility of aphasic disorder caused by thalamic lesions has been supported by anatomo-clinical findings, stereotaxic surgery and more recently by radiological investigations with new techniques, i.e. ct and brain scan. A case of thalamic aphasia investigated with these techniques and the Luria's neuropsychological test is reported in this paper. The case concerns a 50 years old woman who developed a sudden right hemiplegia with marked motor aphasia. C.T. and radioisotope brain scan revealed a left capsular haemorrhage with involvement of thalamic structures. Later, when this patient's aphasia decreased, Luria's test showed reduction of spontaneous speech, anomia, paraphasic and disarthric disorder, distractibility without impairment of comprehension and repitition. These findings are similar to those reported by some AA. in left thalamic lesions and similar to aphasic syndromes caused by cortical lesions. Another important observation was the presence of widespread cortical functional disorder involving the left fronto-temporo-parietal region without evidence of cortical anatomical alteration. The above data and those reported in the literature suggest a very close relationship between thalamic structures, other central nuclei and cortical areas particularly in the control of speech.