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Severe hyperglycemia often occurs when acute stroke patients receive enteral tube feeding. Hyperglycemia should be managed because it adversely affects stroke outcome. However, it remains unclear how blood glucose level (BGL) changes with enteral nutrition in acute stroke patients. Our purpose was to investigate features of the blood glucose curve in acute stroke patients receiving enteral feeding. We retrospectively evaluated acute stroke patients who developed hyperglycemia during enteral tube feeding and underwent CGM in our institution. We evaluated characteristics of blood glucose curves, fasting and peak BGL, and time to peak of BGL. Six patients were analyzed. The median fasting BGL was 125.5 mg/dL and the median peak BGL was 351.5 mg/dL. The blood glucose curve showed the following characteristics following: 1) BGL elevated slowly reach the peak in 180 to 240 minutes; 2) BGL decreased slowly or very little after its peak; 3) there was a large gap between fasting and peak BGL regardless of presence of diabetes mellitus. We grouped the curves into four types by time to peak and how BGL decreased after peak. (Received August 17, 2017; Accepted February 1, 2018; Published July 1, 2018).

Objective: The aim of this retrospective study was to investigate whether the radial force of a self-expandable stent alone is sufficient to dilate an atherosclerotic carotid artery without the need for post-carotid artery stenting (CAS) balloon dilatation (PCasBD)., Methods: We included in our analysis patients who had undergone (1) elective CAS without PCasBD from January 2012 to March 2014, and (2) follow-up conventional angiography 3 months after CAS. We recorded the patients' baseline characteristics and stent types (open-cell [OP] or closed-cell [CL]). Using the minimum width on the lateral projection, stent diameters (SDs) were measured at the site both post-operatively and 3 months after CAS., Results: Fifty-eight lesions in 55 patients were analyzed. The average age of the patients was 74.4 years;the median SD immediately after CAS was 3.27 mm (interquartile range: 3.09-3.64 mm), while after 3 months it was 3.97 mm (3.58-4.25 mm), a significant increase (p<0.0001). In Regarding OP stents specifically (n=18), the median SD increased from 3.59 to 4.05 mm, while the median diameter of CL stents (n=44) increased from 3.22 to 3.83 mm. The median diameter of OP stents was larger than that of CL stents at both time points (p<0.05), whereas the expansion rate of CL stents was higher., Conclusion: All stents had spontaneously dilated by 10% to 20% without PCasBD. The diameter of OP stents was larger than that of CL stents, both immediately and 3 months after CAS.(Received:April 1, 2015, Accepted:August 3, 2015).

The transfemoral approach is a common technique for carotid artery stenting(CAS)and involves the risk of distal embolism when a high-grade stenosis occurs at the common carotid artery(CCA). In this study, to minimize the risk of thromboembolic complications, we used a guide sheath that was specifically designed for direct cannulation to the CCA without the use of a guidewire or coaxial catheter. This study included 5 patients who underwent CAS of the CCA by using a guide sheath. Of these patients, 2 had right CCA stenosis and the other 3 had left CCA lesions. In all cases, direct cannulation to the target CCA by using the guide sheath was achieved, and CAS was performed safely. The median time from puncture to the end of the procedure was 61 min(interquartile range: 53-63). No periprocedural complications or cardiovascular events occurred within 30 days after CAS. CAS was safely and successfully performed for CCA stenosis by using the transbrachial guide sheath that was specifically designed for direct cannulation to the CCA.

Purpose: The purpose of this study was to investigate the significance of the shunt-effect evaluation of SPECT in idiopathic normal pressure hydrocephalus (iNPH)., Subjects and Methods: The subjects were 15 patients with possible iNPH, aged 62-83 (mean 75.3, the ratio of males to females to 6:9), who were treated at our department during the period from June to September, 2004. All patients received the lumbar tap test (LTT) at the outpatient section before surgery. An L-P shunt was conducted on patients whose the LTT positive or negative with cerebrospinal fluid outflow resistance value (Ro) was 10 mmHg/ml/min. or higher patients. As for SPECT, a 3D-SSP Z-score, as well as an mCBF, was conducted before and after the LTT and within one month after surgery. Comparisons were made for (1) the shunt effect, (2) mCBF before and after the LTT and after surgery, (3) mean cerebral blood flow increase rate (mIR) after the LTT, and (4) 3D-SSP before and after surgery., Results: (1) The shunt was effective for all the patients. (2) The mCBF levels was 30.8 +/- 4.02 ml/100 g/min. before the LTT, 37.1 +/- 100 g/min. after the LTT, and 38.6 +/- 3.4 ml/100 g/min. after surgery. A significant increase in mCBF was observed both after the LTT and after surgery (p < 0.05). (3) The mean mIR after the LTT was 21.2 +/- 8.01%, with all the patients showing 10% or higher. (4) The ischemic patterns in the SD-SSP Z-score before surgery were the frontal type (F: 10 cases, 66.7%), the occipitotemporal type (OT: 3 cases, 20%), and the mixed type (M: 2 cases, 13.3%), but not the parietal localized type. The post-operative course showed no-change in 4 cases, disappearance-reduction in 9 cases, and shift to OT in 2 cases., Conclusion: The evaluation factors in the measurement of the cerebral blood flow for evaluation of the shunt effect were the following two items. (1) The mIR of mCBF after the LIT was 10% or higher. (2) As for the preoperative cerebral ischemic patterns, there were many F cases and no parietial localized types found.

We report a 10-year-old boy with chronic enteroviral meningitis associated with agammaglobulinemia (CEMA) and hydrocephalus. He was treated with a low-dose intravenous administration (100 mg/kg/4 weeks) of gammaglobulin (gamma-gl) since he was diagnosed as having Bruton type agammaglobulinemia at 1 year of age. At this admission, neurological examination revealed meningeal signs, Babinski sign, frontal signs, urinary incontinence, and mental retardation (IQ = 48) which was considered to be a sequela of the enteroviral encephalitis which had occurred in his first year of life. T 1-weighted MR imaging of the brain following gadolinium administration revealed a marked dilatation of the lateral ventricles and dense enhancement of the meninges. Enterovirus was detected in the cerebrospinal fluid (CSF) using tissue culture. Histological examination of a biopsied leptomeningeal specimen revealed inflammatory thickening, which was a likely cause of the obstruction to the flow of CSF. The hydrocephalus in this patient was treated with external drainage of CSF from the lateral ventricle. The CEMA was brought into remission by means of the intraventricular administration of gamma-gl, at a dose of 125-250 mg/week (total dose: 1.5 g/8 weeks), in addition to the high dose intravenous administration (400 mg/kg/4 weeks) of gamma-gl. Because of the poor prognosis of patients with CEMA, the intraventricular administration of gamma-gl should be initiated immediately following a diagnosis of enteroviral meningitis.

We report a patient of posterior cortical atrophy (PCA) with progressive memory disturbance and incomplete Bálint's syndrome consisting of optic ataxie (ataxie optique type) and visual inattention without psychic paralysis of fixation of gaze. The patients is a 58-year-old woman who noticed memory disturbance at 53 years old. Neurological deficit at 54 years old was detected only in the domain of memory, and mild diffuse brain atrophy was revealed on MRI. Memory disturbance progressed gradually, and at the age of 58 she was noticed to have visual disorder. Neuropsychological examination revealed severe memory disorder, incomplete Bálint's syndrome, transcortical sensory aphasia, mild ideational apraxia, and severe constructional apraxia. Visual inattention was too severe to evaluate visual acuity and visual field. MRI showed moderate dilatation of bilateral lateral ventricles, especially in their posterior horns, with atrophy of bilateral temporo-parieto-occipital lobes and hippocampus. IMP-SPECT revealed a diffuse decrease of cerebral blood flow in the bilateral temporo-parieto-occipital region, predominantly in the parietal regions. We believe that she is still in the early phase of PCA, and that psychic paralysis of fixation of gaze, visual agnosia will be noted in several years. Our patient represents an example of early stage PCA from neuropsychological and MRI findings.

We report a 72-year-old man with sporadic amyotrophic lateral sclerosis (ALS) who showed concomitant histopathology of Alzheimer's disease (AD) and incidental Lewy body disease. The patient presented at the age of 70 years with distal upper limb amyotrophy. Thereafter, gait disturbance and respiratory distress progressed. Neuropathological examination showed mild frontal lobe and anterior spinal root atrophy. There was moderate loss of upper and lower motor neurons, and Bunina bodies and skein-like inclusions were present in the spinal anterior horns and facial and hypoglossal nuclei, confirming the pathology of ALS. In addition, however, numerous amyloid plaques were observed throughout the entire cerebral neocortex, nucleus accumbens and amygdaloid body. Many neurofibrillary tangles were also evident in the medial temporal cortex. Moreover, the substantia nigra showed mild degeneration, and Lewy bodies were found in the substantia nigra, locus ceruleus, basal nucleus of Meynert and peripheral autonomic ganglia. Although neither parkinsonism nor dementia was noted during the clinical course, our final neuropathological diagnosis was sporadic ALS, AD and incidental Lewy body disease (or presymptomatic Parkinson's disease). Whether or not the coexistence of these three diseases in the same patient was merely coincidental is of considerable interest.

We report a patient of posterior cortical atrophy with progressive visual agnosia, Bálint's syndrome and dementia in which posterior cortical atrophy with similar characteristics on CT and progressive dementia were found in a sister. The patient was a 75-year-old woman who noted the onset of a progressive visual disorder at the age of 70, and whose family first noticed disoriented behavior at around the same period. Ophthalmologic examinations revealed mild cataract but no evidence of peripheral optic nerve or retinal lesions. Neuropsychological examination showed right homonymous hemianopia, visual agnosia, Bálint's syndrome, mild transcortical sensory aphasia, Gerstmann's syndrome, constructional apraxia, mild ideomotor apraxia and memory disorder. MRI showed marked dilatation of both lateral ventricles, especially the posterior horns, and severe atrophy of the occipital lobes, hippocampus, and the parahippocampal gyrus. Assessment of regional cerebral blood flow by IMP-SPECT revealed a generalized decrease in the temporo-parieto-occipital region bilaterally. The patient's sister began to show evidence of progressive dementia at 80 years of age and CT of the brain revealed marked atrophy, predominantly in the occipital lobes, similar to that of the patient. We believe this to be the first report of posterior cortical atrophy with a positive family history, suggesting the possibility of a hereditary syndrome.

A 16-year old woman with LGL leukemia developed peripheral neuropathy. She showed virus-associated hemophagocytic syndrome (VAHS)-like signs including high fever, liver dysfunction, huge splenomegaly, hepatomegaly and pancytopenia. The presence of chronic active EB virus infection was proved by marked high titers for IgG and IgA antibodies to the Epstein-Barr viral capsid and early antigens and low titers of antibody to Epstein-Barr nuclear antigens. She showed dysesthesia and paresthesia of bilateral lower extremities with marked swelling and tenderness, and later developed muscular weakness and atrophy with areflexia of lower extremities. Findings of the central nervous system dysfunction were not observed except for the acceleration of jaw jerk. Pleocytosis and increased protein levels in the cerebrospinal fluid were found. Pulse therapy of methyl-prednisolone and high dose intravenous immunoglobulin therapy (20 g/day for 3 days) were effective for neurological findings. The increased neopterin in the cerebrospinal fluid suggested that peripheral neuropathy was caused by activated macrophages.