Numbsense is a phenomenon, wherein patients can correctly respond to somatosensory stimuli at a higher rate than expected by chance, but cannot perceive the same stimuli consciously. Previously, numbsense has been reported in tactile localization of stimuli on the patientʼs own body. Recently we reported a patient with numbsense that involved touched objects. The patient could not recognize the majority of somatosensory stimuli after left parietal infarction, but could correctly select shape, texture, and object stimuli more frequently than expected by chance. For both types of numbsense, the characteristics and possible pathophysiological mechanisms are described.

  Somatotopagnosia is a disorder in which a person is able to name body parts but has difficulty in spatially localizing them. A variety of tests were performed on a case exhibiting such disorder to self and others. As a result, his somatotopagnosia occurred not only in humans but also in animals in general. It could not be explained by the problems in body-specific language or semantic information, relating ability between whole and partial, or visual memory of body parts. There was no problem in pointing to oneʼs own body part based on the somatosensory stimulation given to himself. However, there were impairments in pointing to other's body parts based on the somatosensory stimulation given to himself and in applying semantic information to the otherʼs body. Thus, it was thought that there is a possibility that body parts cannot be recognized when the viewpoint of looking at the body from the outside is required.

  Delusions are defined as judgments and beliefs that are difficult to modify. It has been reported that delusions occur during the progression of mental disorders such as dementia, schizophrenia, and depression. In particular, delusional misidentification syndrome (DMS) is a delusion that exhibits identity disorders, such as Capgras syndrome and the Fregoli illusion. It is often observed in right hemisphere injuries and bilateral frontal lobe injuries. It is thought that this is caused by excessive activity of the left frontal lobe and disruption of the reality-monitoring function due to the dysfunction of the right frontal lobe.
  In this paper, I reported a case of subarachnoid hemorrhage after clipping surgery for subarachnoid hemorrhage due to rupture of an anterior communicating artery aneurysm with delusions that deceased relatives were still alive and delusions of pregnancy mistaking interoceptive sensations such as anorexia for pregnancy, and considered the mechanism of DMS.

  In nurturing syndrome and Fregoli delusion, the patient believes that the deceased loved one exists in the real world. Hirayama et al. hypothesized that both of these two delusional misidentifications are caused by excessive emotional arousal and assumed a common neural basis. Based on Hirayama's hypothesis, we discussed the mechanism of “feeling” the presence of the deceased, and then the mechanism of “believing” in the presence of the deceased. The “feeling” of the presence of the deceased was thought to be derived from an emotional reaction to recalling autobiographical memories of the deceased, while the “believing” of the presence of the deceased was thought to be related to a disturbance in belief evaluation system due to a dysfunction of the right prefrontal cortex. Our case in which the nurturing syndrome was converted to the Fregoli delusion seemed to be evidence of the close relationship between the two syndromes.

  Parkinson's disease (PD) is a neurodegenerative disease that occurs predominantly in the elderly, and the number of patients with PD is exploding with the aging population. One important factor that interferes with the quality of life of patients with PD is dysphagia. Dysphagia in PD is highly prevalent and does not necessarily correlate with severity of the disease. Dysphagia causes weight loss, aspiration pneumonia, and drooling. Dysphagia in PD can occur in all swallowing stages (anticipatory, preparatory, oral, pharyngeal, and esophageal) due to various lesion sites outside of the basal ganglia circuit and medullary swallowing centers. Because patients with PD are often unaware of their dysphagia and have subclinical aspiration, PD patients without dysphagia should be interviewed, and if dysphagia is suspected, aggressive evaluation of dysphagia should be done by videofluorography or videoendoscopy. It is important to estimate the site of the lesion based on the pattern of dysphagia and determine a treatment plan.

  Patients with Parkinsonʼs disease (PD) show a variety of non-motor symptoms including olfactory dysfunction, abnormal REM sleep behavior, autonomic dysfunction, cognitive dysfunction, and psychiatric symptoms in addition to motor symptoms such as bradykinesia, rigidity, and rest tremor. Since cognitive dysfunction is a clinically important symptom that can lead to dementia in severe cases, and has a significant impact on the quality of life of patients and care givers and prognosis, appropriate early evaluation and therapeutic intervention are required. However, it is currently difficult to accurately predict cognitive decline in PD from an early stage because the degree and pattern of cognitive dysfunction and the rate of cognitive decline vary greatly from patient to patient. In this article, how olfactory dysfunction, a typical non-motor symptom of PD, can be linked to early detection of cognitive dysfunction and therapeutic intervention will be discussed.

  Pareidolia is a visual illusion in which meaningful figures (faces, humans, or animals, etc.) are found in ambiguous objects. While pareidolia is experienced by healthy persons, it is frequently observed in patients with Parkinsonʼs disease (PD) and is associated with subsequent cognitive dysfunction. Our resting-state functional MRI study revealed that PD patients with face pareidolia show decreased functional connectivity between the medial prefrontal cortex and fusiform gyrus compared with those without pareidolia. By using simultaneous eye-tracking and electroencephalography recording, we also found that PD patients with face pareidolia show increased activation in frontal electrodes during the pareidolia task, and the frontal brain network was altered immediately before the pareidolic reactions. Taken together, the alteration of the frontal-temporal network is suggested to play an important role in the pathological face pareidolia in PD. On the other hand, previous SPECT studies have indicated the reduced occipital blood flow in PD patients with pareidolia. We suggest that face pareidolia in PD might be related to two major mechanisms: frontal “top-down” attentional regulation and occipital “bottom-up” visual information. Visual illusions and hallucinations in PD are complex phenomena involving widespread brain activities, and further studies, including functional brain imaging, are expected to elucidate the functional and pathological background.

  In Parkinsonʼs disease (PD) , it has become increasingly evident that a wider range of visual perceptional abnormalities are observed than previously assumed. These visual abnormalities can reduce the quality of life. Diplopia, visual illusion, false sense of presence, and passage hallucinations are crucial risk factors for the emergence of dementia. Additionally, tasks involving such as incomplete letters and bistable perceptions, which require completion and attention, may exhibit abnormalities from the early stages of PD. Through optical coherence tomography and network analysis using brain MRI, it is suggested that in PD, changes in the retina, pupils, and other peripheral levels related to visual processing, as well as the higher networks, which include visual network, ventral and dorsal attention networks, default mode network, and the limbic network are involved in the pathophysiology. Visual perceptual impairments in PD are frequent and diverse, with the possibility that various pathologies and extensive lesions are involved depending on the stage of the disease.

  Case 1 involved a patient with the left posterior temporal variant of Alzheimerʼs disease. The patient initially developed amnestic aphasia and progressed to transcortical sensory aphasia, which ultimately resulted in jargon aphasia. Magnetic resonance imaging (MRI) and single-photon emission computed tomography (SPECT) showed left-predominant atrophy and hypoperfusion in the posterior temporal and parietal cortices. Neuronal loss with spongiform changes, abundant neurofibrillary tangles (NFTs) , neuropil threads, and neuritic plaques were observed in the temporal cortex with a left-sided predominant distribution. Case 2 involved a patient with semantic dementia, typical gogi-aphasia, and behavioral disturbances. The patient had no apparent left anterior temporal atrophy on MRI during the early stage of the illness. Neuronal loss with spongiform changes was observed in the left temporal cortex. The presence of phosphorylated TAR-binding DNA protein of 43 kDa (TDP-43) positive long dystrophic neurites (DNs) , which was consistent with TDP type C pathology, was observed in the frontal and parietal cortices, instead of the temporal cortex. The regions with TDP type C pathology were spared. Conversely, lesions with severe degeneration had few long DNs. Moderate amyloid pathology and mild NFTs (A2B1C2) were also observed ; however, these lesions were considered unrelated to the patientʼs symptoms. Since neuronal loss and spongiform changes corresponded to the focal neuropsychological symptoms in neurodegenerative diseases, these pathological findings serve as neuroimaging marker for establishing the diagnosis and treatment this disease.

  We describe a rare case of crossed aphasia due to right frontal lobe infarction concomitant with moyamoya disease (MMD) , a chronic occlusive cerebrovascular disorder characterized by bilateral stenosis of the supraclinoid portion of the internal carotid arteries with the formation of an abnormal vascular network at the base of the brain. According to our literature search, to date, only two other studies have been reported this condition. A 58-year-old, completely right-handed woman was admitted to our hospital for recovery rehabilitation after cerebral infarction. She was diagnosed with MMD at the age of 44 years. On admission, she had left hemiparesis and speech disorder. Her speech was slow and lacked intonation, with phonological errors and agrammatism. She omitted kana letters when writing, and the aphasia syntax test revealed grammatical errors. She was diagnosed with aphasia characterized by prosodic disorder and agrammatism. Moreover, she exhibited hypergraphia ; however, neither left unilateral spatial neglect nor constructional disorder was observed. Magnetic resonance images of the head revealed infarction in the right frontal lobe including the precentral gyrus. Single-photon emission computed tomography revealed decreased blood flow in the right frontal lobe and left cerebellar hemisphere, suggesting crossed cerebellar diaschisis. Clinical features of aphasia and accompanying symptoms vary among patients with crossed aphasia concomitant with MMD. We speculate that in our case prosody and grammatical functions were located in the right frontal lobe.