1/22. Subcortical mechanisms in language: lexical-semantic mechanisms and the thalamus.Four previously published cases of dominant thalamic lesion in which the author has participated are reviewed to gain a better understanding of thalamic participation in lexical-semantic functions. Naming deficits in two cases support Nadeau and Crosson's (1997) hypothesis of a selective engagement mechanism involving the frontal lobes, inferior thalamic peduncle, nucleus reticularis, and other thalamic nuclei, possibly the centromedian nucleus. This mechanism selectively engages those cortical areas required to perform a cognitive task, while maintaining other areas in a state of relative disengagement. Deficits in selective engagement disproportionately affect lexical retrieval based on semantic input, as opposed to lexical and sublexical processes, because the former is more dependent upon this attentional system. The concept of selective engagement is also useful in understanding thalamic participation in working memory, as supported by data from one recent functional neuroimaging study. Other processes also may be compromised in more posterior thalamic lesions which damage the pulvinar but not other components of this selective engagement system. A third case with aphasia after a more superior and posterior thalamic lesion also had oral reading errors similar to those in neglect dyslexia. The pattern of deficits suggested a visual processing problem in the early stages of reading. The fourth case had a category-specific naming deficit after posterior thalamic lesion. Taken together, the latter two cases indicate that the nature of language functions in more posterior regions of the dominant thalamus depends upon the cortical connectivity of the thalamic region. Together, findings from the four cases suggest that thalamic nuclei and systems are involved in multiple processes which directly or indirectly support cortical language functions.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
2/22. Transient crossed aphasia and persistent amnesia after right thalamic haemorrhage.A 45-year-old right-handed woman suffered transient aphasia and persistent amnesia after a right thalamic haemorrhage. This patient appeared to have crossed aphasia, although it disappeared within 8 weeks. It is noteworthy that the patient had a unilateral right thalamic lesion but exhibited both verbal and non-verbal memory impairment. Computed tomography and magnetic resonance imaging revealed cerebral haemorrhage in the right thalamus involving the ventral anterior nucleus, medioventral nucleus, mamillothalamic tract, internal medullary lamina, and mediodorsal nucleus. An amytal test was performed and suggested that the right hemisphere was dominant for language functions and the left hemisphere was dominant for visuospatial functions. Single photon emission CT revealed a low perfusion area only in the right thalamus. These findings suggest that the right hemisphere might be dominant for both verbal and non-verbal memory function in this patient, although visuospatial function was lateralized in the left hemisphere.- - - - - - - - - - ranking = 1.5keywords = nucleus (Clic here for more details about this article) |
3/22. Multimodal functional imaging of prolonged neurological deficits in a patient suffering from familial hemiplegic migraine.The case of a patient with familial hemiplegic migraine (FHM) suffering from prolonged right sided hemiparesis and aphasia that persisted for more than 10 days is reported. The symptoms were accompanied by slowing of the magnetoencephalogram over the left hemisphere, which normalized parallel to the clinical improvement. Positron emission tomography obtained on the 6th day revealed glucose-hypometabolism (hemispheric difference > or =10%) in left hemisphere's fronto-basal cortex, caudate nucleus, and thalamus. In contrast, magnetic resonance imaging including perfusion and diffusion weighted imaging was normal and did not show significant alterations of cortical perfusion or water mobility during the episode. We hypothesize that this finding provides evidence for a primary neuronal dysfunction causing the prolonged neurological deficits in FHM.- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
4/22. Rapidly progressive aphasic dementia with motor neuron disease: a distinctive clinical entity.The association of motor neuron disease (MND) with rapidly progressive aphasic dementia has been recognized as a distinct clinical syndrome within the group of frontotemporal dementias (FTDs). Although the clinical and neuropsychological features of this syndrome have been defined, a small number of post-mortem studies have been published with heterogeneous neuropathological findings. We performed cognitive, neuro-imaging and neuropathological studies on a 71-year-old male with rapidly progressive aphasic dementia and MND. We initially found a selective non-fluent aphasia associated with hypoperfusion of the left frontotemporal cortex. Proton magnetic resonance spectroscopy revealed an asymmetric change of brain metabolites, with greater changes in the left temporal lobe. The bulbar manifestations of MND occurred over the following 6 months, and the patient died of bronchopneumonia. The neuropathological examination revealed loss of neurons in the hypoglossal nucleus and anterior horns of the cervical spinal cord with microvacuolation and dot-like ubiquitin-positive deposits in the frontoparietotemporal cortex, but no changes suggestive of Alzheimer's, Pick's or lewy body disease. These findings support the conclusion that MND with rapidly progressive aphasic dementia is a distinctive clinical entity within the group of FTD-MND.- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
5/22. Tau and alpha-synuclein inclusions in a case of familial frontotemporal dementia and progressive aphasia.Recent studies have shown that neurofibrillary tangles are frequently accompanied by alpha-synuclein inclusions in sporadic and familial alzheimer disease, in down syndrome, in progressive supranuclear palsy, and Parkinsonism dementia complex of guam. Here we report the cases of 2 brothers with familial progressive aphasia who developed features of frontotemporal dementia with predominant tau pathology but also alpha-synuclein pathology. The 2 patients' brains revealed abundant tau pathology in the hippocampus and basal ganglia, whereas tau and alpha-synuclein aggregates coexisted only in the nucleus basalis of Meynert, the only region where alpha-synuclein was present. In this brain region, abundant lewy bodies, Lewy neurites, and tau inclusions were found; the pathology was more abundant in the older than in the younger brother. Sarkosyl-insoluble tau extracted from brains of the 2 patients showed the presence of tau filaments that contained 3 major tau bands of 60, 64, and 68 kDa on Western blot analysis. These bands contained mainly tau with 3 and 4 repeats and no amino-terminal inserts and tau with 4 repeats and one amino-terminal insert. No mutations were identified in the tau, alpha-synuclein, beta-synuclein, or parkin genes. We think that this is the first report showing a specific colocalization of neurofibrillary tangles and lewy bodies in a family with progressive aphasia.- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
6/22. Progressive dysphasic dementia with localized cerebral atrophy: report of an autopsy.A 64-year-old Japanese woman showed an initially aphasic disturbance followed by complete mutism, progressive dementia, parkinsonism and muscular atrophy. autopsy revealed localized cortical atrophy confined to the pars triangularis, pars opercularis of the inferior frontal gyrus, supramarginal and angular gyri of the inferior parietal lobe, precuneus and posterior half of the middle and inferior temporal gyrus predominantly on the left hemisphere. The right cerebellar hemisphere showed crossed cerebellar atrophy with shrinkage of the right middle cerebellar peduncle. In the atrophied cerebral areas there were diffuse outfall of neuronal cells in all cortical layers and remaining neurons generally showed simple atrophy, and there were a few swollen neurons. gliosis of the subcortical white matter was confined to the affected gyri and GFAP positive astrocytes were observed in the 1st, 2nd, 5th and 6th layers of the cortex. In addition, the degenerative changes of the substantia nigra, gliosis of the amygdaloid complex and inferior olivary nucleus were bilaterally observed. The distribution and characteristics of the cortical and white matter degeneration are different from those of Pick's disease, and it is likely that this case belongs to a group of so-called degenerative dysphasic dementias.- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
7/22. ubiquitin-positive frontotemporal lobar degeneration presenting with progressive Gogi (word-meaning) aphasia. A neuropsychological, radiological and pathological evaluation of a Japanese semantic dementia patient.A patient with progressive anomia and alexia with agraphia for kanji (Japanese morphograms) is described. The patient showed a deficit in single-word comprehension and on-reading (a type of reading that conveys phonetic value) dominance in kanji reading, i.e. on-preceding (pronouncing first with on-reading, irrespective of its preferred reading) and kun-deletion (inability to recall and recognize kun-reading [another type of reading that conveys meaning]) when reading a single-character kanji. These features were due to loss of lexico-semantic information and thus the patient was regarded as having progressive Gogi (word-meaning) aphasia by Imura, a Japanese manifestation of semantic dementia. Macroscopically, neuropathological examination disclosed atrophy of the left frontotemporal lobe with accentuation in the anterior portion of the temporal lobe. Histologically, there was neuronal loss in the cerebral cortex, hippocampus, parahippocampal gyrus, amygdala, caudate nucleus, and putamen. ubiquitin-immunoreactive neuronal inclusions were present in the hippocampal dentate granular cells. This case demonstrates that progressive Gogi aphasia is semiologically identical to semantic dementia, and our patient clinicopathologically resembled those of Rossor et al. [Rossor, M.N., Revesz, T., Lantos, P.L., Warrington, E.K. Semantic dementia with ubiquitin-positive tau-negative inclusion bodies. brain 2000; 123: 267-76.] and Hodges et al. [Hodges, J.R., Davies, R.R., Xuereb, J.H., Casey, B., Broe, M., Bak, T.H., et al. Clinicopathological correlates in frontotemporal dementia. Ann Neurol 2004; 56: 399-406.].- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
8/22. language disturbances from mesencephalo-thalamic infarcts. Identification of thalamic nuclei by CT-reconstructions.The authors report the cases of two patients with CT-documented paramedian mesencephalo-thalamic infarcts, showing language disturbances. The first patient showed a non fluent, transcortical motor-like aphasia, the other had a fluent but severely paraphasic language disorder. The CT study disclosed that it was the dorso-median thalamic nucleus that was mostly involved in both cases. These findings agree with a few previous pathological studies suggesting that the paramedian thalamic nuclei, particularly the dorso-median nucleus may play some role in language disturbances. However the anatomical basis for thalamic aphasia remains speculative, taking into account the importance of cortical connections in the origin of subcortical neuropsychological disturbances.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
9/22. language disturbances from paramedian thalamic infarcts: a CT method for lesion location.The authors describe the case of three patients suffering from language disorder secondary to mesencephalo-thalamic infarcts. One of them showed the clinical features of transcortical motor aphasia, while the other two presented the typical pattern of the so-called "thalamic aphasia". The CT-stereotaxic method for lesion localization disclosed that the dorso-medial was the mostly involved thalamic nucleus in each case. Since this nucleus is connected both with Broca's and Wernike's areas, the authors suggest that the more or less extensive involvement of the fibres connecting these structures may be responsible for the different aphasic features presented in these cases.- - - - - - - - - - ranking = 1keywords = nucleus (Clic here for more details about this article) |
10/22. Focal capsular vascular lesions can selectively deafferent the prerolandic or the parietal cortex: somatosensory evoked potentials evidence.Four patients with a unilateral focal vascular accident involving the internal capsule (but not the cortex) were studied electrophysiologically. Averaged somatosensory evoked potentials (SEPs) to electrical stimulation of the median nerve on the left or the right side were analyzed. In the 3 patients with hemiparesis and normal somatic sensation, the precentral P22 and N30 SEP components were lost, whereas the parietal components were preserved. In another patient with clinical somatosensory loss unaccompanied by any central motor impairment, the precentral SEP components were preserved, whereas the parietal SEP components were lost. Thus, a small capsular lesion can eliminate distinct cortical SEP components by selectively involving either the axons of the thalamic VPLc nucleus going to parietal receiving cortex or the axons of thalamic VPLo going to motor area 4. These findings extend to subcortical lesions the diagnostic value of SEPs in patients with dissociated clinical motor and sensory signs.- - - - - - - - - - ranking = 0.5keywords = nucleus (Clic here for more details about this article) |
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