Pure topographical disorientation in novel environments without anterograde amnesia: a case study.

Topographical disorientation (TD) in novel environments is considered to be a part of anterograde amnesia. A 56-year-old woman presented with pure TD only in novel environments following limbic encephalitis. She could not remember directions inside the hospital on weekly outpatient visits; however, her verbal and visual anterograde memories were normal. In the test of learning photographs of scenes, faces, and objects, only her scores for landscapes were worse than those in healthy controls. These findings suggested that her TD specific to landscapes and directions in novel environments was caused by category-specific memory impairment related to bilateral hippocampal and parahippocampal dysfunction.

Transient Lesion of the Splenium of the Corpus Callosum after Acute Ischemic Stroke.

Two patients who showed transient lesions in the splenium of the corpus callosum (SCC) secondary to acute ischemic stroke are reported. Both patients had embolic strokes and showed an isolated lesion in the SCC on magnetic resonance imaging (MRI) 1-2 weeks after the onset of stroke, with a hyperintense lesion on diffusion-weighted imaging and decreased apparent diffusion coefficient values, with no symptoms related to the lesion. In both cases, the lesion disappeared on MRI approximately 1 week later. Clinicians should note that transient SCC lesions can occur following acute ischemic stroke and avoid misdiagnosing them and performing unnecessary examinations or treatment.

Parechovirus A3 (PeV-A3)-associated myalgia/myositis occurs irrespective of its genetic cluster: a longitudinal molecular epidemiology of PeV-A3 in Yamagata, Japan between 2003 and 2016.

No longitudinal molecular epidemiology of parechovirus A3 (PeV-A3) over a decade is available and PeV-A3-associated myalgia/myositis has been reported only in Japan. Thus, we aimed to clarify the longitudinal molecular epidemiology of PeV-A3 with a major focus on the strains detected from PeV-A3-associated myalgia/myositis cases. We performed sequence and phylogenetic analysis for the VP1 region of PeV-A3 strains in Yamagata, Japan, between 2003 and 2016. The phylogenetic analysis indicated that PeV-A3 strains caused PeV-A3-associated myalgia/myositis as well as a variety of infectious diseases, ranging from mild to severe, in subjects ranging from neonates to adults, irrespective of genetic cluster or variations. PeV-A3 strains are causative agents of a variety of human diseases, irrespective of their genetic cluster. Furthermore, we consider that PeV-A3-associated myalgia/myositis may occur, not only in Japan, but also in other countries, as closely related PeV-A3 strains have been circulating around the world.

Clinical characteristics of 17 adult patients with epidemic myalgia associated with human parechovirus type 3 infection.

We investigated 17 adult cases (14 males and 3 females) of myalgia induced by human parechovirus type 3 (HPeV3) infection, treated during the summers of 2008, 2011, 2014, and 2016. The patients were aged between 21 and 50 years. The limbs and trunk of all patients were affected, and severe myalgia, muscle weakness, and decreased grip strength were observed. In addition to myalgia and muscle weakness, symptoms included fever in 14 (82%), upper respiratory inflammation in 8 (47%), gastroenteritis in 4 (24%), and scrotal pain in 4 (29% of males) patients. Tendon reflexes were preserved, and serum creatine kinase level increased in all but 1 patient. Spinal MRI was performed for 3 patients, with normal results. Musculoskeletal MRI scans showed abnormal signals in the femoral muscles in 2 of 5 patients. In a nerve conduction test, the frequency of F wave appearance in the median nerve was 40% or less in 5 of 9 patients, and repeater F waves were seen in 2 patients. Of these, 7 patients had infants in their families, and developed fever around the same time; they may have been infected by these infants. All patients recovered within 1-2 weeks. HPeV3 infection is characterized by severe myalgia, and is frequently observed in summer every 2-3 years.

[Case of cardiac tamponade during the treatment of acute cerebral infarction].

A 59-year-old man was admitted to our hospital because of sudden weakness in his left foot. He had been treated for lung cancer by chemotherapy and irradiation 3 years earlier. Brain magnetic resonance (MR) imaging revealed multiple acute cerebral infarctions in the area of the right anterior cerebral artery. MR angiography (MRA) revealed that the right anterior cerebral artery was patent, with slight irregularity in the A3 portion. He was treated by administration of aspirin (200 mg/day) and a continuous intravenous unfragmented heparin infusion (10,000 IU/day). Four days after admission, he developed dyspnea. Chest computed tomography (CT) performed 5 days after admission revealed both a marked pericardial effusion and a pleural effusion. Emergency pericardiocentesis was therefore performed. While 1,000 ml of bloody pericardial effusion were aspirated, his dyspnea ameliorated dramatically. Histological examination of the pericardial effusion revealed infiltration of lung adenocarcinoma cells in the pericardium. Intracranial 3D-CT angiography revealed the pearl and string sign in the right anterior cerebral artery 6 days after admission. Anterior cerebral artery dissection was diagnosed as the cause of his cerebral infarction. It is important to recognize the possibility of cardiac tamponade as an uncommon complication of the treatment for acute cerebral infarction.

Epidemic myalgia associated with human parechovirus type 3 infection among adults occurs during an outbreak among children: findings from Yamagata, Japan, in 2011.

BACKGROUND: Based on our findings in Yamagata, Japan, in 2008, we reported that human parechovirus type 3 (HPeV3) could be associated with epidemic myalgia among adults, although HPeV3 is generally associated with infectious diseases in children. OBJECTIVES: To clarify the relationship between community outbreaks among children and myalgia through the continued surveillance of HPeV3 infections. STUDY DESIGN: In the summer season (June-August) of 2011, we collected 586 specimens from children with infectious diseases, and throat swabs, and stool and serum specimens from 5 patients with myalgia. We detected HPeV3 using virus isolation and reverse-transcription PCR, and carried out phylogenetic analysis. We also performed screening for HPeV3 using 309 stocked frozen specimens collected in 2008 for a comparison between 2008 and 2011 strains. RESULTS: We detected HPeV3 in 59 children and isolated HPeV3 from all myalgia patients. Phylogenetic analysis indicated that the HPeV3 strains circulating in 2008 and 2011 could be clearly distinguished, apart from two strains. Further, we detected HPeV3 strains with identical nucleotide sequences from children and adults in 2008 and 2011, respectively. Two children belonging to one myalgia patient had upper respiratory infections prior to the onset of their father's illness, and the HPeV3 isolates from these three patients had identical nucleotide sequences. CONCLUSIONS: These findings suggest that HPeV3, circulating among children in the community, infects their household, including parents, a portion of whom may subsequently show symptoms of myalgia. Our observations in 2008 and 2011 strongly suggest that clinical consideration should be given to HPeV3 in children as well as in adults during summer seasons in which an HPeV3 outbreak occurs among the children in the community.

Bow hunter's syndrome after contralateral vertebral artery dissection.

Bow hunter's syndrome is characterized by transient vertebrobasilar insufficiency that is elicited by neck rotation. This syndrome is has various causes, such as osteophytes, tumors, fibrous bands, infection, and trauma. We report a unique case of bow hunter's syndrome. The patient visited our hospital because of left nuchal pain. A magnetic resonance imaging scan revealed left vertebral artery (VA) dissection, which was the cause of his nuchal pain. He began to feel faintness upon turning his neck to the left after left VA dissection. Digital subtraction angiography revealed that the right VA was fully patent in a neutral neck position, but focal stenosis appeared at the C2 vertebral level upon turning his head 60° to the left. This stenosis became complete occlusion at turning his head to the end of his range of motion. From these findings, a diagnosis of bow hunter's syndrome was made. Dissection of the contralateral (left) VA caused a failure in compensatory blood flow, resulting in bow hunter's syndrome. This represents the first report of bow hunter's syndrome occurring after onset of the contralateral VA dissection.