Several intriguing features of speech outputs observed in the patients with cerebrovascular disease presenting various types of recurring utterances, and in the patients with advanced Alzheimerʼs disease presenting jargon speech are described. The pathogenesis of recurring utterances is discussed with special references to severe apraxia of speech, serious deficits in word finding and sentence construction, and the monitoring failure for own utterances. I would like to insist that recurring utterances are not merely non-propositional emotional language but at least substitutes for propositonal one, and offer some suspicion about the hypothesis that recurring utterances are produced in the right hemisphere.
  Jargon-like speech in advanced Alzheimerʼs disease is generated based on the disorders in both of pre-linguistic and purely language domains. Attention and monitoring disorders, blurring of boundaries for various concepts or lexical items, serious deficits in word finding and sentence construction, and the repetitive tendency observed in logoclonia, are all relevant to the generation of conspicuous empty speech. In rare cases, recurring utterances or neologistic jargons are also observed, but their characteristics are different from those occurring in the context of cerebrovascular disease.

  In the debate on whether a case study or a mass study is preferable in the field of neuropsychology, I argue in favor of the mass study. If it is a proposition that we are closer to the truth, it is undoubtedly a mass study. Moreover, firm evidence for the treatment of the patients can undoubtedly be obtained from a mass study. However, a case study is a good opportunity to start a research or to generate a hypothesis. I would like to encourage you to use the finding of a case study as an opportunity to explore future research, explore the future research, and sublimate it as a mass study rather than dwell on it.

  The central part of the theory of natural science is the universal proposition. Therefore, no matter how many events fit into it, the theory cannot be proven correct. However, if there is one event that does not fit the theory, we can disprove it. One of the important roles of case reports is to disprove existing theories, to shake them up, and to start the work of producing clearer and more comprehensive theories. I described examples of such case reports by reference to somatoparaphrenia, akinetopsia, and apperceptive visual agnosia.

  I have introduced the paper entitled ʻWord Category Aphasiaʼ (Cortex 9: 112-125, 1973) written by Professor Yamadori, which had been selected among his various achievements. I have traced the peculiar impairments of language of the patient described in this paper from three viewpoints: modality specific impairment (word meaning deafness) , category specific impairment, and impairment of categorical function. Furthermore, I have discussed todayʼs significance of this paper considering how to approach the symptoms, integrate three aspects of impairments, and reveal brain systems for language.

  “Palpatory apraxia” is the first well-documented case report with active touch impairment by Dr. Yamadori. A 68-year-old man with traumatic cerebral hemorrhage around the right central sulcus was admitted to a hospital because of clumsiness of his left hand. There was no weakness in the left hand, and the superficial sensation and graphesthesia were preserved. On the other hand, the operation of putting on gloves, buttoning, etc. was poorly performed, especially with his eyes closed. In the detailed examination, the clumsiness of his left hand became remarkable when actively touching objects without visual input. Two-point discrimination, stereognosis, and texture perception of the left hand were impaired, and movement / sensation of the III-IV fingers with eyes closed was also disturbed. These findings suggested that ʻthe adexterity and the particular sensory defect seen in the present case reflect the defect of a fundamental system supporting palpatory exploration of the external world, i.e., active touchʼ. Active touch refers to the perception of the objects by exploratory movement and touching. ʻWithout the sense of active movement it is difficult to control the actual movement of fingersʼ, which could explain the clumsy hand in the present case. This report is a good example that clarify the mechanism of a “common” limb kinetic apraxia by detailed clinical observation based on the neurophysiological findings. This excellent paper indicates that case reports are still of significant value to neuropsychology.

  Alzheimerʼs disease is the most common cause of dementia. Among people with Alzheimerʼs disease, some do not primarily present with memory impairment. Logopenic progressive aphasia (LPA) is characterized by word-finding difficulty and decreased verbal short-term memory, which results in impaired repetition of sentences and phrases. These symptoms reflect dysfunctions in the left temporoparietal regions. Posterior cortical atrophy (PCA) is characterized by visuospatial and other symptoms related to the dysfunction of the occipitoparietal or occipitotemporal regions.
  We discussed the mechanism of symptoms in LPA and PCA, focusing on two points. First, compared to mostly unilateral lesions in strokes, distribution of pathological changes in neurodegenerative diseases is basically bilateral, even though they often show marked asymmetry, resulting in different symptomatology from those in strokes. Second, degree of lateralization varies among different cognitive functions. Language functions are clearly lateralized to the left cerebral hemisphere in most of right-handed subjects, while visuospatial functions are less lateralized to the right cerebral hemisphere. That is why aphasia occurs with a unilateral left-sided lesion but some of visuospatial symptoms, such as simultanagnosia, are related to bilateral lesions. These features make the symptoms in LPA and PCA different from those in strokes. Examining symptoms in neurodegenerative disorders provides good opportunity to clarify lateralization of human cognitive functions.

  Frontotemporal lobar degeneration is a neurodegenerative disorder mainly damaged in the frontal and the anterior temporal lobe. Cerebral lateralization is often described in the context of the posterior functions such as symbolic or visuospatial manipulation, but there is also a lateralization in frontotemporal lobar degeneration. Progressive semantic memory impairment is characteristics in semantic dementia, that has damage in the anterior temporal lobe. In the left predominant cases, hearing comprehension impairment, naming impairment, and surface dyslexia are prominent from their early stage. In the right predominant cases, prosopagnosia often appears but not in all cases, behavioral changes like frontal symptoms are also exhibited. It is necessary to clarify the disease concept of right temporal dominant cases. Symptoms such as disinhibition, apathy, lack of empathy, stereotypy, changes in eating behavior, and executive dysfunction appear in behavioral variant frontotemporal dementia that have damage mainly in frontal lobe. Previous studies have proposed “right hemisphere hypothesis”, in which behavioral changes are associated with damages in the right hemisphere ventral side. However, hemispheres communication is also seemed to be important. Further neuropathological and network research are expected to elucidate the neural basis of semantic memory and behavioral changes beyond simple localization hypothesis.

  We report a case of DLB with remarkable asymmetry showing a decrease in right hemisphere dominance. In this case, it is assumed that the patient inferred the whole drawing from looking at a part of it since response time to recognize multiple items was delayed. Therefore, this case showed ventral simultanagnosia. The visual cognitive impairment seen in this case was also thought to be due to right hemisphere impairment. It was suggested that if one of the occipital lobes was not disturbed by the remarkable asymmetry, it was suggested that basic visual impairment was mild, whereas various visual cognitive dysfunctions were observed.
  We compared a large number of DLB and AD patients using IMP-SPECT to clarify the degree of left-right difference (LRD) and where in the brain LRD existed. LRD in DLB was less frequent than in AD. In DLB, there was a difference between left and right in occipita (ltongue gyrus, cuneus) and posterior temporal lobe.

  Aphasia is a syndrome of disturbances of speech and language due to brain damage, and aphasics have difficulties in communication because of symptoms of not only oral and written language but also internal language. Therefore, it is necessary to support them neuropsychologically and speech-therapeutically, and to provide information about means to communicate with them to people concerned. Furthermore, since aphasics might preserve emotional aspects, non-verbal aspects should be considered in communication with them.

  Apraxia is a disorder of motor control by a loss of the motor program, not explicable by more elemental motor, sensory, coordination, or language impairments. It is most obvious when the action is performed under commands or in dissociated situation. This feature is called automatico-voluntary dissociation. Hugo Liepmann established its clinical manifestations and explained its complexities. There are four types of apraxia. Ideomotor apraxia is a simple gesture disorder that appears in both verbal commands of imitations due to a lesion in posterior parietal lobes, especially white matter under supramarginal gyrus. Ideational apraxia is a disorder to carry out a series of tasks using multiple objects for an intended purpose due to a lesion in posterior parietal lobes around angular gyrus. When a patient lost manipulating even in one tool, Morlass thought ideotioal apraxia is a type of an agnosia specialized in tool of use. Limb kinetic apraxia is loss of hands and fingers dexterity significantly affecting manipulative movements due to a lesion in pre and post central gyri. These apraxia are due to disconnection between parietal and premotor areas and a lesion in dominant cerebral hemisphere. Unilateral apraxia (apraxia of the left hand) is a limb kinetic apraxia in a left hand due to a lesion in corpus callosum. The motor engram preserved in the left hemisphere was impaired to transfer to the other by disconnection in corpus callosum.

  The agnosia is defined as ʻimpaired recognition of previously meaningful stimuli which is restricted to special sensory modalityʼ. Most of the reported literatures about agnosia is those of visual agnosia, followed by auditory agnosia. Patients complain ʻI cannot see.ʼ or ʻI cannot hear.ʼ, so they are easily misdiagnosed as the disturbance of visual or hearing acuity, dementia, and psychiatric disorders. The naming task is useful to know whether the patient can understand the object correctly. The name and the meaning or concept are the two sides of one coin, and, if one side is recalled, another is automatically recalled. The perception of the object, the recollection of the meaning and concept, the integration of both, and the retrieval of its name function regularly, if the patient can name it correctly. The agnosia is interpreted as the dysfunction of the integration between perceived image and the meaning and concept in special sensory modality. The nomenclature of the visual and auditory agnosia is confused. The dichotomy of the apperceptive and associative agnosia can be easily understood, but, in the real clinical situations, there are many cases which cannot be categorized to either. It is important to describe the symptom correctly and elaborately.

  Patients with right hemisphere damage may show impaired awareness of the contralateral space and/or body. This impaired awareness includes several symptoms, and it is not uncommon that some symptoms appear at the same time after a stroke with a large lesion. By only observing behavior of daily life and rehabilitation, it might be difficult to fully understand what neuropsychological symptoms each patient shows. Therefore, this paper introduces the assessments for typical symptoms such as unilateral spatial neglect, personal neglect, anosognosia for hemiplegia/hemiparesis, hemiasomatognosia and somatoparaphrenia, as well as the lesion site involved in the appearance of each symptom. Based on each patientʼs brain damaged area, carrying out the above-mentioned assessments enables us to understand the severity and characteristics of the symptoms he or she shows as well as the presence or absence of each symptom. In addition, integration of the results from the assessments will lead to a comprehensive understanding of the impairment of awareness of the contralesional space and/or body in each patient.

  It is not easy for learners to identify exact location of lesions demonstrated on imaging modalities, even though they have enough knowledge of both diseases and neuroanatomy. Here, we described, especially for the beginners, how to identify anatomical locations of them, focusing on relevant gyri and sulci for evaluation of patients with aphasia/language symptoms. In order to read the location accurately, we emphasize that it is of tremendous benefit to use 3D-acquisition protocols for MRI, choose appropriate image plains from the axial, coronal, and sagittal plains, depending on sulci and gyri of interests, and evaluate continuous and multiple images of each plain. Reading process of the central sulcus is usually the first and pivotal step, followed by identification of surrounding structures based on the information of it. We believe that it is of great value not only for better understanding of the patient, but also for contributing to advancements of neuroscience, to perform thorough investigations upon each and every patient, evaluating both neuropsychological findings and the exact anatomical location of lesions.

  We report a patient who developed Bálintʼs syndrome following brain tumor excision, whose symptoms were elucidated by a subsequent eye-tracking assessment. The case was a right-handed male in his 40s who underwent surgery to remove a recurrent ventricular meningioma. Neurological features included right homonymous hemianopsia and diplopia ; neuropsychological features included Bálintʼs syndrome, visuospatial deficits, and amnesia. Several symptoms that compromised activities of daily living (ADL) were observed, including skipping over text when reading and an inability to find objects pointed to by others ; his self-awareness of his visual impairment was also poor. Using a Gazefinder eye-tracking system, we measured the patientʼs gaze while he performed a visual task. Data obtained suggested that the majority of his ADL-related problems originated in a failure to acquire compensatory strategies for his visual impairment, in addition to fixation instability, reduced eye velocity, and difficulties in shifting attention within the bilateral visual field. We conclude that rehabilitation strategies to remedy Bálintʼs syndrome should include not only interventions targeting eye movement and visual attention, but also disease education using assessment system that are easy for the patient to understand visual impairment.