We reviewed the recent findings on aphasia based on a consideration for the clinical utility of Ardila's new classification of aphasias. Regarding the classification of aphasias, we highlight that a multidimensional approach that is focused on multiple components of the language system, such as motor speech, phonologic, and semantic levels is more useful than a categorical approach. We introduce the Mini Linguistic State Examination (MLSE) as a new method of assessment that analyzes impairment patterns based on "error types" rather than the percentage of correct answers to tasks. Finally, we note that the importance of symptomatology continues to grow in aphasia research in the era of open science and artificial intelligence.

Ten years ago, the international consensus criteria for primary progressive aphasia (PPA) were proposed by Gorno-Tempini et al. (2011), establishing both diagnosis and classification criteria for nonfluent and agrammatic variant (nfvPPA), semantic variant PPA (svPPA), and logopenic variant PPA (lvPPA). These guidelines boosted interest in the PPA field, and over 1,200 studies have been published in English language during the past decade. Some problems of the current diagnostic criteria include lvPPA being defined as neither svPPA nor nfvPPA, and PPA patients not matching the classification criteria of any variant. The diagnostic features of each PPA variant do not fully reflect the complexity of language alterations, resulting in PPA patients with either unclassifiable or mixed PPA type.

We suggest three new advancements on PPA variant classification. First, primary progressive apraxia of speech (PPAOS) is differentiated from nfvPPA, when only apraxia of speech manifests as an isolated symptom for several years (Josephs et al. 2012). Second, progressive word deafness with speech disorders (Matsuda 2019) is a new variant of PPA, which is characterized by word deafness and speech disorders including anarthria, dysprosody, and foreign accent syndrome. Finally, we outline subtypes of lvPPA based on language features or etiology, thereby reducing the ambiguity of lvPPA diagnosis.

Research on PPA pathology and genetics has significantly advanced during the past decade. Etiologies of the three variants have been associated with different pathological processes. There are strong relationships between svPPA and the transactive-response DNA binding protein 43 kDa (TDP-43) Type C and between lvPPA and Alzheimer's disease (AD) pathology; however the neuropathological profile of nfvPPA is heterogeneous. More than 50% of nfvPPA patients have tauopathy. PPA is usually sporadic, but it may have an underlying genetic basis in some cases. Long-term follow-up studies will provide valuable insights into the etiology and prognosis of PPA progression.

Depending on the lesion site and age at onset, recovery of aphasia symptoms varies in course greatly; however, many aphasic cases show recovery over long terms of at least six months or more. Functional restoration of language by therapy is not stable but rather fragile. However, the types of therapy that are suitable for the improvement of any given language function remains inconclusive. Recently, constraint-induced (CI) therapy and repetitive transcranial magnetic stimulation (rTMS) have been utilized in the treatment of aphasia. As for speech therapy, direct language stimulation has been found to be universally important. Therefore, if the quality and quantity of language stimulation are improved and if combined therapies with CI therapy and/or rTMS become possible, further improvement of language function may be expected.

Changes in everyday life in recent years have affected brain localization, for example changes in writing from handwriting to typing on a keyboard. Regarding writing, a new term 'dsytypia' first coined by Otsuki et al. (2002) refers a symptoms of typing impairment which cannot be attributed to aphasia, agraphia, apraxia. The following reports of dystypia have indicated at least two causative lesions; one is frontal lobe involving the foot of the middle frontal gyrus and frontal opereculum, and the other is the parietal lobe. We speculate that dystypia with frontal lobe (frontal dystypia) is caused by the impairment of intermediate process from linguistic information to motor reaction such as typing, and dystypia with parietal lesion (parietal type) by the visuo-spatial impairment. Moreover, a term 'dystextia' which refers to an impairment of texting on a cell phone has appeared. Although dystexia is not well established as a pure neurological symptoms because the reports of dystextia include not only the patients with pure dystexia but also texting impairment due to severe aphasia or apraxia or weakness. However, it would be very important to focus on this symptom in future.

The Wernicke-Geschwind model, comprising the Broca's area, the Wernicke's area, the angular gyrus, and the arcuate fasciculus, is widely known as a brain language model. However, with the accumulation of case studies with detailed neuroimaging and advances in neuroscience such as functional brain imaging, it has become clear that various brain regions other than Broca's and Wernicke's area are involved in human language functions. Furthermore, physical models using diffusion MRI have enabled us to evaluate the detailed anatomical properties of human white matter. Accordingly, the brain is now considered a network consisting of many functional areas and complex white matter fibers that bridge each other. In this chapter, we outline new language models and their perspectives.

We investigated a patient with a characteristic impairment in auditory pointing tasks involving pointing to an illustration of a target word. The patient was a 67-year-old right-handed male native Japanese speaker who was employed as a cleaning staff. Brain MRI and single-photon emission computed tomography (SPECT) demonstrated restricted lesions in the left frontal lobe, basal ganglia, and insula. Standardized intelligence examinations revealed that the patient's performance was within the normal range. Furthermore, the results of the auditory verbal comprehension tasks in which the patient used "yes" or "no" responses in Western Aphasia Battery (WAB) were preserved, and there were almost no difficulties in listening to daily conversations. However, the performance declines in auditory pointing tasks were severe, contrary to expectations based on the clinical assessment of his daily activities. Most notably, this patient showed improved results in pointing tasks when the illustrations used for pointing were presented after an auditory presentation of the target word. The results of the modified auditory pointing tasks revealed that the patient tended to show difficulties when he was not only visually but also auditorily exposed to the information regarding non-target words that are semantically related to the target word before the introduction of the target word. We conclude that the patient cannot simultaneously suppress the information related to non-target words and activate the information regarding the target word.

We report on a right-handed man in his 40's who developed amnesia, confabulation, and defective route finding after a hematoma in the splenium of the corpus callosum accompanied by intraventricular hemorrhage. Magnetic resonance imaging in the chronic phase revealed atrophy of the splenium of the corpus callosum, as well as right-dominant damage to the retrosplenial cortex and the crus of the fornix. While he presented transient delirium, amnesia, and prominent spontaneous confabulation in the acute phase, persistent amnesia, provoked confabulation, and defective route finding were the major neuropsychiatric manifestations in the chronic phase. We suspected that the combination of the lesions in the retrosplenial cortex as well as in the crus of the fornix would be responsible for the amnesia and provoked confabulation in the chronic phase. On the other hand, spontaneous confabulation in the acute phase might have occurred in the context of disturbed consciousness, which in part was caused by intraventricular hemorrhage.

Here we report the case of a patient showed meaningless movements with dysesthesia following cerebral infarction. Magnetic resonance imaging revealed lesions on the right in the postcentral gyrus, anterior interparietal sulcus, parietal operculum, and posterior part of the insula. The patient showed no motor paralysis but severe sensory disturbance, including superficial and deep sensations. In addition, she experienced meaningless movements of the left upper limb. She disclosed neither diagnostic apraxia nor compulsive use of tools. The touch by another person or passive movements induced dysesthesia in the left hand, followed by meaningless movements. By contrast, she showed no dysesthesia when touching an object with her left hand or when touching her left hand with the right one. In conclusion, passive somatosensory inputs may be associated with the pathogenesis of dysesthesia and subsequent meaningless movements.