Azusa Sugimoto

Correlation between motor and cognitive functions in the progressive course of Parkinson's disease

Correlations between motor function and frontal‐executive function in Parkinsons disease (PD) have been examined previously, but correlations with other cognitive domains remain unknown. We examined the correlation between motor dysfunction and cognitive impairment with regard to their precise domains.

Picture agnosia as a characteristic of posterior cortical atrophy.

Background: Posterior cortical atrophy (PCA) is a degenerative disease characterized by progressive visual agnosia with posterior cerebral atrophy. We examine the role of the picture naming test and make a number of suggestions with regard to diagnosing PCA as atypical dementia. Methods: We investigated 3 cases of early-stage PCA with 7 control cases of Alzheimer disease (AD). The patients and controls underwent a naming test with real objects and colored photographs of familiar objects. We then compared rates of correct answers. Results: Patients with early-stage PCA showed significant inability to recognize photographs compared to real objects (F = 196.284, p = 0.0000) as measured by analysis of variants. This difficulty was also significant to AD controls (F = 58.717, p = 0.0000). Conclusion: Picture agnosia is a characteristic symptom of early-stage PCA, and the picture naming test is useful for the diagnosis of PCA as atypical dementia at an early stage.

perceiving "ghost" images: a unique case of visual allesthesia with hemianopsia in mitochondrial disease

A 49-year-old man with mitochondrial disease presented with visual allesthesia, a rare and puzzling phenomenon. He was admitted for treatment because of convulsions. After the convulsions ceased, he exhibited left homonymous hemianopsia. Brain diffusion-weighted magnetic resonance imaging (MRI) showed a high-intensity area in the right occipital lobe. Both the hemianopsia and the MRI activation in this area disappeared by day 36 of hospitalization. On the morning of day 57, right homonymous hemianopsia emerged in a singular manner. The patient perceived an illusory object (a bottle placed by the bedside) in his left visual field, while the real object was in his blind right field. This case of visual allesthesia was accompanied by palinopsia, ie, perseveration of the image of the bottle. Diffusion-weighted MRI showed a new, high-intensity area in the left occipital lobe. We believe the visual allesthesia resulted from transfer of cortical information obtained by blindsight between hemispheres as a result of epileptic excitation.

The Montreal Cognitive Assessment and Neurobehavioral Cognitive Status Examination are useful for screening mild cognitive impairment in Japanese patients with Parkinson's disease

Diagnosis of mild cognitive impairment (MCI) in Parkinsons disease (PD; PD‐MCI) can be difficult. We examined whether the Japanese version of the Montreal Cognitive Assessment (MoCA‐J) and the Neurobehavioral Cognitive Status Examination (COGNISTAT‐J) were suitable to screen PD‐MCI.

Brodmann area 12 An historical puzzle relevant to FTLD

Background: Brodmann brain maps, assembled in 1909, are still in use, but understanding of their animal–human homology is uncertain. Furthermore, in 1909, Brodmann did not identify human area 12 (BA12), a location now important to understanding of frontotemporal lobar degeneration (FTLD). Methods: We re-examined Brodmanns areas, both animal and human, in his 1909 monograph and other literature, both historical and contemporary, and projected BA12 onto the medial surface of a fixed human brain to show its location. Results: We found Brodmann did identify human BA12 in later maps (1910 and 1914), but that his brain areas, contrary to his own aims as a comparative anatomist, are now used as physiologic loci in human brain. Conclusion: Because of its current link with frontotemporal dementia, BA12s transition from animal (1909) to human (1910 and 1914) is not only an historical puzzle. It impacts how Brodmanns areas, based on comparative animal–human cytoarchitecture, are widely used in current research as functional loci in human brain.

Another piece in the jigsaw: a case report of prosopagnosia with symptomatological, imaging and post mortem anatomical evidence.

This study was supported by a grant from the Tamagawa University Center of Excellence under the Ministry of Education, Culture, Sports, Science and Technology (MEXT), a Grant-in-Aid for Scientific Research on Innovative Areas, “Face perception and recognition” from MEXT (No. 21119518), a Showa University Grant-in-Aid for Innovative Collaborative Research Projects and a Special Research Grant-in-Aid for the Development of Characteristic Education from MEXT.

Successful use of anti-epileptic drugs in three cases of epilepsy with higher brain dysfunction

To clarify the diagnosis and treatment of epilepsy with higher brain dysfunction (E‐HBD).

A new disorder of praxis in neurodegenerative disease that may be part of Alzheimer's disease

Apraxia is a well-known disorder of praxis and is caused mainly by damage to the left parietal lobe. We presented two cases of neurodegenerative disease with a distinct disorder of praxis, predominantly involving left parietal lobe. While both patients could understand what they should do, they were not able to initiate action and often stopped during execution of actions. They had no apraxia and no temporal and spatial errors on praxis. Magnetic resonance imaging of both patients showed atrophy of the left parieto-occipital and temporo-occipital lobes, and single photon emission computed tomography showed hypoperfusion in the same lobes. Moreover, one of our cases, using [11C] PIB PET, demonstrated increased uptake in the cerebral cortices, suggesting Alzheimers disease. The symptoms described are different from other disorders of praxis and similar to bradyphrenia or freezing.

Is this a new type of primary prosopagnosia, both progressive and apperceptive?

Prosopagnosia, the inability to recognize faces, has a history going back to Charcot and Hughlings-Jackson, but was first named by Bodamer in 1947. Its anatomical loci are still unclear. However, progressive prosopagnosia is normally linked to right dominant temporal lobe atrophy, and diagnosed as part of frontotemporal lobar degeneration. Here we report a case of prosopagnosia linked to posterior cortical atrophy. Although case reports of posterior cortical atrophy-prosopagnosia do already exist, it is normally described as an accessory symptom. The interest of our own posterior cortical atrophy patient, possibly the first such case, is that he had a rare apperceptive type of prosopagnosia unrelated to the associative, frontotemporal lobar degeneration-type.

[Mental time dysfunction in Parkinson's and Alzheimer's diseases].

Mental time is altered by a number of factors and the underlying neural processing involved is highly complicated. Recent research suggests that mental time in patients with particular neurological diseases is perceptually shorter than in normal individuals. This review introduces mental time dysfunction and a model for processing of mental time in Parkinsons and Alzheimers disease. Although the two diseases show the same dysfunction of mental time in behavior, we expect the underlying neural mechanism to vary in each disease. It is possible that the dysfunction of mental time in Parkinsons disease is caused by the abnormal striatum acting as a pacemaker, while that in Alzheimers disease is caused by abnormal hippocampal memory.