Diffuse axonal injury (DAI) is considered as quantitatively continuous spectrum of traumatic brain injury ranging from prolonged coma state to mild traumatic brain injury. DAI destroys axons and eventually neurons permanently and reduces the bulk of the white matter, thus leaving behind diffuse ventricular enlargement and brain atrophy. In milder DAI such as brain concussion, however, most of the axons temporarily cease functioning only to resume again, thus the victim regains consciousness very soon without obvious neurological deficit nor any noticeable ventriculomegaly. DAI plays the substantial part in the outcome of closed head injury even if associated with local brain injury such as brain contusion. Manifestations of DAI are comprised of mental disorder including neurocognitive dysfunction and emotional or neurobehavioral disorder, and neurological disorder (cerebellar ataxia and spastic hemiparesis) . These disorders are strikingly similar among victims, though varying in severity. One of the characteristic points is lowering or even absence of self-awareness as DAI is more than mild in severity. The victims rarely complain of their own symptoms nor seek medical attentions spontaneously. The outcome of DAI is highly correlated with the duration of the posttraumatic initial unconsciousness and with remaining ventriculomegaly which is compared to the day-of-injury ventricular size as the reference. Another characteristic point is the tendency to clinically improve steadily by months and years. It is faster and more striking in milder DAI and in younger age victims. The neuropsychological scores also improve accordingly. So-called prolonged postconcussive syndrome occasionally observed in selected cases of mild traumatic injury, on the contrary, shows little tendency to improve by time. The neuropsychological test results often decline by time. They visit multiple medical institutions, ardently complain of their subjective symptoms and often create detailed memos of their own symptoms. These are considered as signs of elevated self-awareness or hyperawareness.

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  In order to provide the best care for individuals of cognitive dysfunction caused by head trauma, physicians and caregivers need to understand the pathologic basis of them. This symposium focused on closed (non-missile) head trauma. Epidural hematoma is collection of blood between skull and dura mater. Subdural hematoma is defined the blood collection between the dura mater and subarachnoid membrane, and is caused by tearing bridging veins. Cerebral contusion, parenchymal injury of the cerebral cortex, is usually present at the frontal poles, orbital surfaces, temporal poles and lateral surface of the temporal lobes. Laceration is defined by the parenchymal damage with ruptured pia mater. Traumatic axonal injury is caused by the stretching and tearing of axons. Gross pathology showed small hemorrhages at the corticomedullary junction, corpus callosum, cerebral peduncli and dorsal part of the brainstem. Microscopically, axonal swellings are observed. Chronic traumatic encephalopathy is associated with repeated head trauma due to contact sports. Pathologically, neurofibrillary tangles are usually observed in the upper cortical layers adjacent to the sulcus of the cerebral cortex.

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  Traumatic brain injury (TBI) can cause delayed-onset neurocognitive dysfunctions including such as chronic traumatic encephalopathy (CTE) and psychotic disorder following TBI (PDFTBI) . Initially, CTE was called punch-drunk syndrome since only athletes exposed to recurrent concussions in high-impact sports such as boxing were believed to develop such symptoms. However, it has been revealed that CTE can occur in the wider population including American football players, wrestlers, ice-hockey players and military persons. Pathologically, CTE is characterized by abnormal accumulations of tau proteins and less apparent amyloid-beta proteins, and definitive diagnosis of CTE can be made only at autopsy and no reli able biomarkers of CTE are available. PDFTBI is schizophrenia-like psychosis, which typically occurs several years after single severe TBI. About 3.4-8.9% of single-severe TBI patients develop PDFTBI in later life, and mean onset time after TBI is about 5 years. This temporal interval between onset of psychosis and time of head injury indicates that a neurodegeneration is involved in development of PDFTBI. Al though clinical subtypes associated these post-TBI syndromes are different, evidence suggest that single-severe and mild-repetitive TBI share similar neuropathological features. In this review, we discuss clinical characteristics of CTE and PDFTBI. Next, we describe how novel neuroimaging methods to detect tau and amyloid pathology improve diagnosis and prevention of post-TBI syndromes. Recent development of tau-selective radioligand such as［¹¹C］PBB3 may be a powerful tool to detect tau pathology in the living brain of TBI patients.

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  Disorder of social cognition is one of the important symptoms in the definition of “Kouji-Noukinou-Shougai”. This dysfunction is also thought to be important symptom in the definition of neurocognitive disorder, which is described in DSM-5 recently published. It is suggested that social cognition has its specific neural underpinnings as is in other cognitive function. Therefore even in the case of traumatic brain injury, it would be possible to understand the characteristics of cognitive dysfunction based on the characteristics of brain areas most likely damaged. In this article, brain injury is classified into 2 major types, focal brain injury and diffuse axonal injury. Furthermore cognitive dysfunction caused by the two types of injury is described respectively. Especially, apathy is explained in detail including its definition and underpinning neural circuits.

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  It is essential to investigate communication difficulties in patients with neurodegenerative dementia from a new point of view although the symptomatology of aphasia in cerebrovascular disease is partially useful for understanding their difficulties. To assess psychological symptoms such as anxiety and general cognitive impairments such as attention deficits is important to understand their communication difficulties in addition to understand disease specific symptoms such as relatively preserved social skills in Alzheimerʼs disease, cognitive fluctuation in dementia with Lewy bodies, and stereotypy in frontotemporal lobar degen eration. Maintaining preserved language function should be considering in the care of progressive neuro degenerative dementia.

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  This study aimed to propose the classification of the patients who met the criteria of PNFA/ nfvPPA, which predicts the prognosis. Patients with nfvPPA were included (n＝24) . All patients underwent a standardized clinical assessment, neuropsychological examinations including Western Aphasia Battery, sentence making test and, neuroimaging examinations (MRI and regional cerebral blood flow using SPECT) . Six patients were diagnosed as having aphasia such as Broaʼs aphasia or transcortical motor aphasia which are caused by the frontal lobe lesions. The rest 18 patients showed pure anarthrie/ apraxia of speech were divided into some subgroups: 1) 5 patients developed pseudobulbar symptoms and showed anterior operculum syndrome, 2) 3 patients showed only anarthrie/ apraxia of speech for 5-7 years from the onset, 3) 3 patients were accompanied ataxia in 2-3 years, 4) 7 patients developed parkinsonisms or central gyrus syndromes and diagnosed as having CBS in 2-5 years. The result indicated that the PNFA/ nfvPPA could be divided into at least 3 subtypes, and these clinical symptoms at first consult after 1-3years from the onset could predict the prognosis.

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  In the present study, we investigated the clinical characteristics of verbal semantic memory impairment in Semantic dementia through the comprehension of idiomatic phrase. The subjects were seven SD patients with mild to moderate word meaning (Gogi) aphasia. All subjects showed a severe difficulty in understanding the meaning of idiomatic phrases. Because idiom has a meaning in itself and consists of nothing but language, idiom could be considered as a kind of verbal semantic memory. Therefore, the present result suggested that SD had profound deficit of verbal semantic memory even in the early stage. Secondly, a patient with SD was evaluated his ability to comprehend two types of word meaning, one is the concrete meaning and the other is the figurative meaning which has been derived from the concrete meaning. The patient could comprehend the concrete word meanings but could not comprehend words used as a metaphor at all. Thus we suppose the deteriorated process of language in SD as follows: first, deficits of word meaning as a metaphor, second the loss of concrete word meaning, and development to Gogi aphasia.

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  Language and speech symptoms associated with common type of Alzheimerʼs disease (AD) are reflected by the underlying pathological process, usually presenting as anomic aphasia evolving to transcortical sensory aphasia.
  There are subtypes of AD which show various language symptoms with relatively preserved other cognitive functions. Besides the logopenic progressive aphasia (LPA) that is one of three variants of primary progressive aphasia, there may be other types of aphasic AD, presenting as (1) anomia with agraphia for Kanji, (2) transcortical sensory aphasia, (3) Gogi aphasia-like symptoms which resemble semantic dementia (SD) . Type (1) or (2) is associated with predominant degeneration in the left hemisphere with similar distribution pattern observed in common type of AD. Type (3) is associated with left temporal lobe atrophy, and so possibility of misdiagnosing as SD is high. Careful xamination of language and dementia symptoms, however, would lead to the precise diagnosis of AD.
   Linguistic profiles in the cases with LPA are various in terms of the severity of each symptom that constitute the diagnostic criteria of this syndrome. Therefore, LPA might not be a discrete homogeneous syndrome. Severe disturbance in verbal short-term memory, however, would be the most important symptom in the sense that degenerative aphasia develops a characteristic clinical teature of system degeneration.

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  We conducted consecutive naming tests on aphasic patients to examine how semantic and phonologic relations of words and the response stimulus interval (RSI) influence occurrence of verbal perseveration. We also examined occurrence of perseveration from factors involving relation with the brain lesion areas. The subjects were 14 (right-handed) aphasics attributable to cerebrovascular accident. We created a consecutive naming test using three word lists (semantically related words, phonologically related words, and non-related words) . RSI was set at 1s and 15s. The results indicated that the verbal perseveration occurred more significantly when the patients named semantically related words consecutively with an RSI of 1sec than with any other settings. Concerning the area of brain lesion, the test indicated that when the patients with left frontal lobe lesion named semantically related words with RSI of 15s, verbal perseveration occurred more than in patients with other lesions. These data showed that occurrences of perseveration are related to semantically related target words and the RSI. We concluded that this was caused by dysfunction of the left frontal lobe, which plays a role in selection of suitable information among competing semantic information.

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  Numerous previous studies exist that examine the long-term progress of aphasia from various points of view. However, few well-designed studies have been conducted to investigate long-term assessment of aphasia that includes a period of language therapy interruption. We reported the case of an aphasic patient in which language therapy was interrupted for two years and three months after therapy lasting two years and three months, and then resumed. The present study investigated the progress in this case based on general scores on the Standard Language Test of Aphasia (SLTA) and changes in subordinate items.
  The results revealed functional recovery in language comprehension skills at 7-27 months after onset, recovery in oral reading and other expressive abilities at 28-55 months after onset, and recovery in writing ability at 56-70 months after onset. The progress of treatment administered to this patient suggested: (1) that recovery in language ability may be possible through greater order in language function patterns; (2) that recovery of language function may be possible even when language therapy is interrupted, if the patient receives external stimulation; and (3) that recovery of writing ability may require more external written language stimulation than is present in everyday life.

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