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Background: Aphasia often appears in persons living with dementia; however, aphasia and the mirror phenomenon are rarely present at the same time., Case Presentation: Here, we report a case of fluent conversation with a person in a mirror or a magazine, and examine the underlying mechanism using brain imaging and neuropsychological findings. We found that the appearance of the mirror phenomenon may be associated with a visuospatial dysfunction caused by a decreased function of the posterior region of the right temporal and parietal lobe. Moreover, active talking to a person in a mirror or a person in a magazine could be associated with disinhibition caused by a decline in bilateral frontal lobe function., Conclusions: This case represents a very valuable and interesting presentation because it is the first report of a long-term follow-up of the course of dementia using neurological imaging, and of the neuropsychological analysis of the mechanism of conversation with a mirror image combined with aphasia.

Introduction: Successful riddle solving requires recognition of the meaning of words, attention, concentration, memory, connectivity and analysis of riddle content, and sufficiently developed associative thinking., Objective: The aim of the study was to determine the ability to solve riddles in stroke patients who do or do not have speech and language disorders (SLDs), to determine the presence of SLDs in relation to the lesion localization, as well as to define the relationship between riddle-solving and functional impairment of a body side., Methods: The sample consisted of 88 patients. The data used included age, sex, educational level, time of stroke onset, presence of an SLD, lesion localization, and functional damage of the body side. The patients were presented with a task of solving 10 riddles., Results: A significant SLD was present in 38.60% of the patients. Brain lesions were found distributed at 46 different brain sites. Patients with different lesion localization had different success in solving riddles. Patients with perisylvian cortex brain lesions, or patients with Wernicke and global aphasia, had the poorest results. The group with SLDs had an average success of solved riddles of 26.76% (p = 0.000). The group with right-sided functional impairments had average success of 37.14%, and the group with functional impairments of the left side of the body 56.88% (p = 0.002)., Conclusion: Most patients with SLDs had a low ability of solving riddles. Most of the patients with left brain lesions and perisylvian cortex damage demonstrated lower ability in solving riddles in relation to patients with right hemisphere lesions.

Alzheimer's disease (AD) is a clinically heterogeneous disease that may have atypical presentations with focal cortical syndromes and relatively preserved episodic memory. The posterior variant of AD has two subtypes: occipitotemporal, presenting with visuoperceptive impairment, and biparietal, presenting with visuospatial dysfunction and apraxia. We report a case of a 51-year-old woman with progressive limb apraxia and choreiform movements. Her neuropsychological evaluation was compatible with dementia, and revealed ideomotor and ideational limb apraxia, severe visuoconstructive ability impairment, dyscalculia and posterior aphasia. Workup excluded metabolic, infectious, inflammatory or neoplastic causes, and hereditary conditions as Huntington's disease and familial AD. Cerebrospinal fluid biomarkers revealed β-amyloid reduction and τ protein increase. Brain imaging showed marked biparietal atrophy and hypoperfusion, and widespread cortical β-amyloid deposition. Biparietal variant of AD was diagnosed and acetylcholinesterase inhibitor treatment induced clinical stabilisation. AD may present with atypical features and a high clinical suspicion is necessary for an early diagnosis., (2015 BMJ Publishing Group Ltd.)

Following a stroke, a patient may present with varying degrees of neurological impairment, depending on the area of the brain which is damaged. Specifically, damage to the left cortical hemisphere may result in aphasia. The characteristic speech in a patient with an aphasia caused by a stroke can be similar to the speech in some patients with schizophrenia or other psychotic disorders. In a new patient without a reliable history who presents with suspected aphasia, it is important to include psychotic disorders as part of the differential diagnosis. Failure to differentiate psychotic disorders from aphasia could result in either a lack of treatment that would improve the patient's thought process, thought content, or language, or in a delayed treatment for a stroke, respectively. While a number of psychotic disorders exist and must be differentiated from one another in accordance with DSM-IV guidelines, speech abnormalities in patients with schizophrenia are well described in the literature. For this reason, schizophrenia is the psychotic disorder of focus in this paper. This case report illustrates a clinical situation where a patient required both a psychiatric and neurological consultation in order to determine the etiology of his language disorder. The purpose of this paper is to emphasize the need to consider both psychiatric disorders and aphasia in patients with unknown histories who present with language abnormalities, and to help the clinician critically examine the patient's speech so that, in conjunction with other clinical data, the correct diagnosis can be made and appropriate treatment initiated.

Background and Purpose: Stroke is the leading cause of disability in many countries. Aphasia is a common sign of stroke that is observed in about one-third of stroke patients and contributes to disease morbidity. However, the relationship between anatomy and different forms of aphasia remains poorly understood. We intend to study the characteristics of aphasia in the acute stage of stroke and to identify neuroanatomical correlates using MRI., Methods: Lesion sites were selected from 1198 patients with cerebral infarction, who were hospitalized in the stroke unit of our hospital between March 2002 and March 2006. We enrolled 325 patients who fulfilled our criteria. All patients received an MRI examination within 1 week after admission and were evaluated with the Western battery aphasia (WAB) test, in order to determine what type of aphasia they had. The severity of their language deficit was further classified using the Boston diagnostic aphasia examination (BDAE) severity grading standard., Results: Among 1198 cases, five cases with Broca's areas and four cases with Wernicke's areas lesions on MRI works were free of language deficits. Within the 325 patients who demonstrated clinical signs of aphasia, the results of WAB showed that there were 83 Broca' aphasia cases, 48 Wernicke's aphasia cases, 12 conduction aphasia cases, 36 transcortical motor aphasia cases, 17 transcortical sensory aphasia cases, 19 transcortical mixed aphasia cases, 58 global aphasia cases and 52 anomic aphasia cases. Two hundred and eighty-eight cases were located within classical language centers while 37 cases were located at other sites. In 325 aphasia patients with grade criteria of BDAE of grades 0, 1, 2, 3 or 4, there were 84, 79, 77, 63 and 22 cases respectively. Many of cases with grades 0 and 1 were distributed within classical language centers., Conclusion: This study showed that it is possible to draw a neuroanatomical map of aphasia that encompasses the 95% of aphasia cases. It also demonstrates that the main determinant of aphasic disorders is the neuroanatomical location of the lesion. Furthermore, this study shows that most lesion locations associated with specific aphasic disorders fit classical data associated with previous aphasia research. More importantly, the language disorders of patients whose lesions were located at classical language centers were more serious. Consequently, this paper demonstrates the power of MRI in prognosticating the potential for a patient to recover from aphasia due to stroke.

Background: The relationship between functional recovery after brain injury and concomitant neuroplastic changes is emphasized in recent research. In the present study we aimed to delineate brain regions essential for language performance in aphasia using functional magnetic resonance imaging and acquisition in a temporal sparse sampling procedure, which allows monitoring of overt verbal responses during scanning., Case Presentation: An 80-year old patient with chronic aphasia (2 years post-onset) was investigated before and after intensive language training using an overt picture naming task. Differential brain activation in the right inferior frontal gyrus for correct word retrieval and errors was found. Improved language performance following therapy was mirrored by increased fronto-thalamic activation while stability in more general measures of attention/concentration and working memory was assured. Three healthy age-matched control subjects did not show behavioral changes or increased activation when tested repeatedly within the same 2-week time interval., Conclusion: The results bear significance in that the changes in brain activation reported can unequivocally be attributed to the short-term training program and a language domain-specific plasticity process. Moreover, it further challenges the claim of a limited recovery potential in chronic aphasia, even at very old age. Delineation of brain regions essential for performance on a single case basis might have major implications for treatment using transcranial magnetic stimulation.

Well-documented cases of crossed (transcortical sensory) aphasia, especially those with longitudinal evaluation, are rare. We report a case of crossed transcortical sensory aphasia following watershed infarcts in the right hemisphere, from the moment of the accident until 15 months afterward. The aphasia type, and the course of recovery, is a "mirror" representation of that seen in cases of uncrossed aphasia. Unfortunately, the data do not permit strong conclusions regarding the lateralization of language in association with praxis and visuospatial abilities. This underlines the need for more well-documented (case) studies to come to a better understanding of the mechanisms through which lateralization occurs., (Copyright 1999 Academic Press.)

Many aspects of subcortical aphasias are not accounted for by a unique pathophysiological mechanism; rather the diversity of the observed symptoms suggests that many functional ensembles, more or less related, to language functions may be disturbed by subcortical lesions. However, such disorders are only moderate in intensity and subcortical aphasias certainly constitute an interesting model for studying the dynamics of recovery of language functions and related neural systems, combining neurolinguistic concepts with advanced functional imaging techniques.

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.

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.

A right-handed Japanese crossed Wernicke's aphasic showed complete neologistic jargonagraphia in kanji and kana with anosognosia of his writing deficits. Prominent jargonagraphia in kanji is quite rare and has not been previously described in the literature. Marked dissociation between speaking and writing during the course suggested that his jargonagraphia might be unique to crossed aphasia. His condition was interpreted for the main part by Yokoyama, Okubo, Doseki, and Yamadori's hypothesis (1981) that free-running on of motor engrams of characters stored in the left hemisphere caused jargonagraphia in crossed aphasia. This case of jargonagraphia in kanji suggests that this hypothesis should be supplemented by the following points: (1) in kanji, not necessarily a character as a whole, but radicals or parts of radicals, function as motor units, which may be released to produce jargonagraphia in kanji; (2) free-running on of visual images as well as of kinesthetic images should be considered especially in written jargon in kanji.

Recovery of comprehension and total language in 22 Wernicke's aphasics was correlated with lesion size and extent of involvement of certain structures on CT. Recovery rates and outcomes were separately examined using 0-3 months and 0-12 months poststroke language data. Quantitative measures of structural damage were regressed on total aphasia and comprehension outcome measures. Supramarginal and angular gyri appeared to be the most significant structures in recovery in addition to initial severity and lesion size. This was confirmed by using ANOVA to compare the extent of involvement in each postcentral structure among the poor, moderate, and good recovery groups. The superior temporal and middle temporal gyri are less involved in the good recovery group. Structures posteriorly adjacent to Wernicke's area are important for compensation in Wernicke's aphasia and in the accompanying comprehension deficit. Persisting Wernicke's aphasia usually involves the supramarginal and angular gyri in addition to the superior temporal area.

This study was concerned with the relationship between defects in sound recognition and intrahemispheric locus of lesion. Previous studies have shown that defects in sound recognition are common in association with left hemisphere lesions resulting in aphasias with comprehension deficits and are uncommon in association with other unilateral lesions. Current findings indicate that defects in sound recognition, occurring within the first month post onset of aphasia, may be associated with lesions of basal ganglia, the auditory cortex (both primary and association cortices), supramarginal gyrus, angular gyrus, and area 37. At the same time, however, a number of patients with lesions in these areas failed to show sound recognition defects.

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.

We report the clinical and pathological study of a patient with vascular leucoencephalopathy almost restricted to the left posterior hemisphere. A 65 year--old right handed hypertensive woman has presented with a neuropsychological symptomatology of transcortical sensorial aphasia. We discuss the following points: 1) the patient's disease must be considered as Binswanger's subcortical encephalopathy despite the asymetric topography of the lesions ; 2) particular hemodynamic cerebral factors has possibly determined the asymetric nature of the disease ; 3) a lesion of the left temporo-parieto-occipital area that was strictly sub-cortical, with complete destruction of the posterior part of the arcuate fasciculus has presented with the clinical picture of a transcortical sensorial aphasia.

Severe Wernicke's aphasia occurred suddenly in a right-handed man and persisted with little improvement until he died 54 days later. Postmortem examination showed an infarct in the posterior temporoparietal region of the right hemisphere. This case demonstrates two new features of crossed dextral aphasia. First, language skills may be fully lateralized to the right hemisphere in right-handed patients. Second, when crossed lateralization occurs, the usual localization of aphasic syndromes is common, suggesting that the intrahemispheric organization mediating language activities is the same in the right hemisphere of the crossed dextral and the left hemisphere of the typical right-handed individual.