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Aims Elevated serum alkaline phosphatase (ALP) levels are associated with an increased risk of cerebrocardiovascular diseases. However, the associations of ALP with peripheral arterial disease (PAD) and outcomes in patients with acute ischemic stroke (AIS) are not well-known. Methods We examined the association between ALP levels and the ankle-brachial index (ABI) in 2111 consecutive patients with AIS. A poor functional outcome was defined as a modified Rankin Scale (mRS) score of 3-6 at 3 months after stroke. A low ABI was defined as a value of ≤ 0.9. Results Of the total cohort, 482 patients (22.8%) had a low ABI. ALP levels were higher in patients with a low ABI than in those without (p＜0.001). The multivariable logistic analysis revealed that quartiles of ALP levels were significantly associated with a low ABI (odds ratio [OR]: 1.20, 95% confidence interval [CI]: 1.08-1.33). Of the 1322 patients with a premorbid mRS score of 0-2, 434 patients (32.8%) had a poor outcome. The multivariable analysis revealed that elevated serum ALP levels and a low ABI were independently associated with poor stroke outcomes after adjustment for baseline characteristics (OR: 1.21, 95% CI: 1.07-1.38, and OR: 2.00, 95% CI: 1.40-2.84, respectively). Conclusions Increased serum ALP levels are significantly associated with a low ABI. These indicators are independent prognostic factors for poor stroke outcomes at 3 months.

Although the assessment of nutrition is essential for stroke patients, detailed associations between nutritional status at admission, subsequent complications, and clinical outcomes in patients with acute intracerebral hemorrhage (ICH) are unclear. We aimed to elucidate these associations using the Controlling Nutritional Status (CONUT) score. Consecutive patients with acute ICH were investigated. Nutritional status was evaluated using the CONUT score, calculated from the serum albumin level, lymphocyte count, and total cholesterol level. Subsequent complications, such as hemorrhage expansion (HE) during the acute stage and aspiration pneumonia during hospitalization, were evaluated. Poor outcome was defined as a modified Rankin Scale score of ≥ 3 at 3 months. Of the 721 patients, 49 had HE, 111 had aspiration pneumonia, and 409 had poor outcomes. Patients with HE had significantly lower total cholesterol levels than those without HE. Patients with aspiration pneumonia had significantly lower albumin levels, lower lymphocyte counts, and higher CONUT scores than those without aspiration pneumonia. Patients with poor outcomes had significantly lower albumin levels, lower lymphocyte counts, lower total cholesterol levels, and higher CONUT scores than those with good outcomes. Multivariable logistic analysis showed that higher CONUT scores were independently associated with poor outcome (odds ratio, 1.28; 95% confidence interval, 1.09-1.49; P = 0.002) after adjusting for baseline characteristics, HE, and aspiration pneumonia. Each component of CONUT was a useful predictor of subsequent complications. Malnutrition, determined using the CONUT score, was independently associated with poor outcomes in patients with ICH after adjusting for these complications.

Cancer-associated ischemic stroke (CAS) refers to a hypercoagulation disorder related to malignant tumors, especially adenocarcinoma. Carbohydrate antigen (CA) 125 is a mucinous serum marker that might reflect hypercoagulation status, but the association between CA 125 and CAS is unclear across various types of cancer. The aim of this study was to investigate the associations among tumor markers, coagulation markers, and clinical factors in acute ischemic stroke (AIS) patients with active cancer. Consecutive AIS patients with active cancer (a diagnosis or ongoing active therapy for cancer within 6 months) were prospectively enrolled at four hospitals. D-dimer, C-reactive protein (CRP), carcinoembryonic antigen (CEA), CA19-9, and CA 125 levels were measured. Of 120 AIS patients with active cancer, 47 were diagnosed with CAS. CA 125 had the strongest correlations with D-dimer and CRP (ρ = 0.543, p

Although associations between malnutrition status at stroke admission and poor stroke outcomes have been established, the effect of nutritional intake during the acute phase remains unclear. We aimed to evaluate the associations between nutritional intake one week after admission and the outcome at three months among acute ischemic stroke (AIS) patients.Consecutive AIS patients were investigated. Nutritional status at admission was evaluated using the Controlling Nutritional Status score, calculated from the serum albumin, lymphocyte count, and total cholesterol. We retrospectively evaluated nutritional intake (energy and protein) one week after admission, and the cutoff value of each nutritional intake level for good outcome was defined as the modified Rankin Scale 0-2 at three months after stroke onset using the receiver operating characteristic curve.Of the 205 patients, 146 patients had good outcomes. Mild initial neurological symptoms and good nutritional status at admission were associated with good outcome. The cutoff value of good outcome for protein intake was 0.812 g/kg/day (sensitivity: 0.884, specificity: 0.509) and that for energy intake was 19.0 kcal/kg/day (sensitivity: 0.918, specificity: 0.424). Those nutritional intake indicators were independently associated with good outcome after adjusting for baseline confounders, including stroke severity and nutritional status at admission (protein intake: odds ratio (OR), 4.04; 95% confidence intervals (CIs), 1.14-13.1, and energy intake: OR, 5.00; 95% CIs, 1.41-17.8, respectively).Adequate nutritional intake at one week after admission was independently associated with good outcome regardless of the nutritional status at admission or stroke severity.

A 65-year-old man presented with a slight headache and transient visual disturbance. Magnetic resonance imaging (MRI) revealed occlusion of the left internal carotid artery (ICA) and acute brain infarctions in both hemispheres, and a blood examination indicated inflammation. Gadolinium enhancement was observed in the walls of the temporal arteries and ICAs. After we diagnosed giant cell arteritis (GCA) by a temporal artery biopsy, aspirin and corticosteroids were administered. The typical symptoms of GCA, such as jaw claudication and temporal artery tenderness, were absent during the entire clinical course, and the findings of contrast-enhanced MRI contributed to the diagnosis.

Although hypercoagulability using D-dimer levels may be a useful marker for predicting outcomes in ischemic stroke patients with cancer, other biological markers for predicting outcomes are unclear. We aimed to investigate the associations between several biological markers and short-term or long-term outcomes among ischemic stroke patients with cancer.Consecutive acute ischemic stroke patients with cancer (n = 309) were registered. Biological markers such as hemoglobin, albumin, C-reactive protein and D-dimer levels were assessed. Stroke outcomes, namely, a 3-month modified Rankin Scale score indicating poor functional outcome (mRS score of 3-6) and 1-year survival, were assessed.Of the 277 patients who could be assessed for 3 months outcome, 131 patients (47.3%) had a poor outcome at 3 months. Multivariable analysis revealed that increased D-dimer levels and decreased albumin levels were independently associated with poor stroke outcomes (adjusted odds ratio [aOR]: 1.04, 95% confidence interval [CI]: 1.00-1.08, and aOR: 0.50, 95% CI: 0.31-0.80, respectively). Of 309 patients, 70 patients (22.7%) died during the follow-up period (median, 241 days). Multivariate Cox proportional hazard analyses showed that high D-dimer levels and hypoalbuminemia were independently associated with mortality (adjusted hazard ratio [aHR]: 2.65, 95% CI: 1.37-5.12, and aHR: 2.29, 95% CI: 1.21-4.49, respectively). The effect of each biological marker on mortality was notably observed among patients with active cancer but not among those with nonactive cancer.Low albumin levels were independently associated with short- and long-term outcomes, as were D-dimer levels, in acute ischemic stroke patients with cancer.

Wall shear stress (WSS) is the frictional force caused by viscous blood flowing along the vessel wall. Decreased WSS is associated with local vascular endothelial dysfunction and atherosclerosis. The vector flow mapping (VFM) technique detects the direction of intracardiac blood flow and WSS on the vessel wall with echocardiography. In this study, we examined carotid WSS by applying the VFM technique to the carotid arteries and evaluated its relationship with cerebral small vessel disease (SVD).This is a single-center, prospective, observational study. We investigated the association between carotid WSS and SVD imaging, and cognitive outcomes in consecutive 113 patients with acute lacunar infarction.Carotid WSS was negatively associated with age (r=-0.376, p＜0.001). Lower WSS was correlated with total SVD scores (ρ=-0.304, p=0.004), especially with enlarged perivascular space (EPVS) in the basal ganglia ＞10 (p＜0.001). The carotid intima-media thickness was not associated with the total SVD score (ρ=-0.183, p=0.052). Moreover, lower WSS was associated with executive dysfunction.EPVS has recently been reported as a marker of early SVD imaging, and executive dysfunction is common in vascular cognitive impairment. These results suggested that decreased carotid WSS based on vascular VFM, which can be measured easily, is associated with imaging and cognitive changes in the early stages of SVD.

There is accumulating evidence that periodontal disease is associated with atrial fibrillation (AF) or stroke, but it is unclear which causative species of periodontal disease are present in stroke patients with AF. We aimed to investigate the associations between AF and specific periodontal pathogens using serum titers of IgG antibodies of bacteria in acute stroke patients.Acute stroke patients were registered at two hospitals. Serum samples were evaluated for titers of antibodies against 9 periodontal pathogens (16 genotypes) using ELISAs. We identified AF in patients according to the following criteria: (1) a history of sustained or paroxysmal AF or (2) AF detection upon arrival or during admission. We carried out propensity score matching to categorize the patients as those with AF and those without.Of the 664 acute stroke patients, 123 (18.5%) had AF. After propensity score matching, 234 patients were selected. Patients with AF had a higher prevalence of positive serum titers of antibodies against Porphyromonas gingivalis (FimA type III) and Porphyromonas gingivalis (FimA type V) than those without AF (59.0% vs. 39.3%, p=0.004 and 58.2% vs. 40.2%, p=0.009, respectively).Porphyromonas gingivalis, especially FimA type III and type V, might be associated with AF in stroke patients.

Diffusion-weighted imaging hyperintensities are observed in intracerebral hemorrhage patients at times and might be associated with unfavorable functional outcomes. However, the suitable time to evaluate diffusion-weighted imaging hyperintensities to influence stroke outcome remains unclear. This study investigated the associations between acute and sub-acute diffusion-weighted imaging hyperintensities and functional outcomes among patients with acute intracerebral hemorrhage.Diffusion-weighted imaging hyperintensities were evaluated within 24 h (acute phase) and at 14 ± 5 days (sub-acute phase). An unfavorable functional outcome was a score of 5-6 on the modified Rankin Scale at 3 months.Among 268 intracerebral hemorrhage patients, diffusion-weighted imaging hyperintensities in the acute phase were observed in 32 (11.9%). Among 227 patients who underwent a second magnetic resonance imaging in the sub-acute phase, diffusion-weighted imaging hyperintensities were observed in 57 (25.1%). Multivariable analysis revealed that the baseline intracerebral hemorrhage volume, history of stroke, and severe white matter lesions were associated with sub-acute diffusion-weighted imaging hyperintensities. The patients with unfavorable outcomes (n = 37) had a higher frequency of sub-acute diffusion-weighted imaging hyperintensities than those without (n = 190) (51.4% vs. 20.0%, P 0.001); the frequencies of acute diffusion-weighted imaging hyperintensities were not significantly different between the groups (13.5% vs. 10.0%, P = 0.559). Sub-acute diffusion-weighted imaging hyperintensities were independently associated with unfavorable outcomes after adjusting for confounding factors (Odds Ratio, 3.35, 95% CI 1.20-9.35, P = 0.021).The rate of sub-acute diffusion-weighted imaging hyperintensities was higher than acute diffusion-weighted imaging hyperintensities among acute intracerebral hemorrhage patients and likely to be associated with unfavorable outcomes.

Objectives The present study aimed to examine the effectiveness of proton magnetic resonance spectroscopy (1HMRS) in determining the progression of neurological symptoms resulting in acute ischemic stroke in patients with lenticulostriate artery (LSA) infarction. Materials and Methods 1HMRS was performed within 72 h after neurological symptom onset. Voxel of interest was placed in tissue that included the pyramidal tract and identified diffusion weighted echo planar spin-echo sequence (DWI) coronal images. Infarct volume in DWI was calculated using the ABC/2 method. 1HMRS data (tNAA, tCr, Glx, tCho, and Ins) were analyzed using LCModel. Progressive neurological symptoms were defined as an increase of 1 or more in the NIHSS score. Patients who underwent 1HMRS after progressive neurological symptoms were excluded. Results In total, 77 patients were enrolled. Of these, 19 patients had progressive neurological symptoms. The patients with progressive neurological symptoms were significantly more likely to be female and had higher tCho/tCr values, higher rates of axial slices ≥ 3 slices on DWI, higher infarct volume on DWI, higher maximum diameter of infarction of axial slice on DWI, and higher SBP on admission compared to those without. Multivariable logistic analysis revealed that higher tCho/tCr values were independently associated with progressive neurological symptoms after adjusting for age, sex, and initial DWI infarct volume (tCho/tCr per 0.01 increase, OR 1.26, 95% CI 1.03–1.52, P = 0.022). Conclusions Increased tCho/tCr score were associated with progressive neurological symptoms in patients with LSA ischemic stroke. Quantitative evaluation of 1HMRS parameters may be useful for predicting the progression of neurological symptoms.

Strains of Streptococcus mutans expressing the cell surface collagen-binding protein, Cnm, encoded by cnm (cnm-positive S. mutans), are associated with hypertensive intracerebral hemorrhage (ICH) and the occurrence of cerebral microbleeds (CMBs). Small diffusion-weighted imaging (DWI) hyperintensities in patients with acute ICH are also associated with CMBs. However, the association between cnm-positive S. mutans and DWI hyperintensities is unclear. Hence, this study aimed to investigate the association between cnm-positive S. mutans and DWI hyperintensities in patients with acute ICH.Patients with acute ICH were prospectively registered at three hospitals. Dental plaque specimens were collected within 4 days after admission, and cnm-positive S. mutans was detected using the polymerase chain reaction. Magnetic resonance imaging at 14 ± 5 days after admission was used to evaluate DWI hyperintensities and CMBs.A total of 197 patients were enrolled in this study. cnm-positive S. mutans was detected in 30 patients (15.2%), and DWI hyperintensities were observed in 56 patients (28.4%). Patients with cnm-positive S. mutans had a higher frequency of DWI hyperintensities (50.0% vs 24.6%; p = 0.008) and a higher number of CMBs (5.5 vs 1.5; p 0.001) than those without cnm-positive S. mutans. Multivariable logistic analysis revealed that the presence of cnm-positive S. mutans was independently associated with DWI hyperintensities (OR 2.38; 95% CI 1.01-5.61; p = 0.047) after adjusting for several confounding factors.This study found an association between the presence of cnm-positive S. mutans and DWI hyperintensities in patients with acute ICH.

Aim The prediction of functional outcome is essential in the management of acute ischemic stroke patients. We aimed to explore the various prognostic factors with multivariate linear discriminant analysis or neural network analysis and evaluate the associations between candidate factors, baseline characteristics, and outcome. Methods Acute ischemic stroke patients (n=1,916) with premorbid modified Rankin Scale (mRS) scores of 0-2 were analyzed. The prediction models with multivariate linear discriminant analysis (quantification theory type II) and neural network analysis (log-linearized Gaussian mixture network) were used to predict poor functional outcome (mRS 3-6 at 3 months) with various prognostic factors added to age, sex, and initial neurological severity at admission. Results Both models revealed that several nutritional statuses and serum alkaline phosphatase (ALP) levels at admission improved the predictive ability. Of the 1,484 patients without missing data, 560 patients (37.7%) had poor outcomes. The patients with poor outcomes had higher ALP levels than those without (294.3±259.5 vs. 246.3±92.5 U/l, P＜0.001). Multivariable logistic analyses revealed that higher ALP levels (1-SD increase) were independently associated with poor stroke outcomes after adjusting for several confounding factors, including the neurological severity, malnutrition status, and inflammation (odds ratio 1.21, 95% confidence interval 1.02- 1.49). Several nutritional indicators extracted from prediction models were also associated with poor outcome. Conclusion Both the multivariate linear discriminant and neural network analyses identified the same indicators, such as nutritional status and serum ALP levels. These indicators were independently associated with functional stroke outcome.

Backgrounds Vascular compression of the rostral ventrolateral medulla (RVLM) has been associated with hypertension or blood pressure (BP) variability. For acute ischemic stroke patients, increased BP variability may cause poor functional outcomes. We tested the hypothesis that RVLM compression was associated with increased BP variability or stroke outcome in acute ischemic stroke patients. Methods Acute ischemic stroke patients (n = 622) with 24-h ambulatory BP monitoring during the subacute phase of stroke (median 9 days from onset) were retrospectively studied. Variability in BP was evaluated with the SD and coefficient of variation of SBP and DBP. The morning surge was also evaluated. The presence of RVLM compression was evaluated using time-of-flight three-dimensional MRI. A poor outcome was defined as a modified Rankin Scale score of 3-6 at 3 months. Results Patients with RVLM compression (n = 213) had significantly higher 24-h SBP mean, 24-h SBP SD, 24-h SBP coefficient of variation, 24-h DBP mean, 24-h DBP SD, and 24-h DBP coefficient of variation values and a higher prevalence of morning surge than those without (n = 409). Multiple regression analysis revealed that RVLM compression was associated with increased SBP variability, DBP variability, and morning surge. Despite the significant association between RVLM compression and BP variability, RVLM compression was not associated with poor stroke outcome. Conclusion Although RVLM compression was closely associated with BP variability in the subacute ischemic stroke phase, an effect of RVLM compression on stroke outcome was not observed.

Introduction The association of malnutrition on stroke subtypes has not been well established. We investigated the relationship between malnutrition and functional outcome according to stroke subtypes. Methods Acute consecutive ischemic stroke patients (n = 1915, 73 ± 12 years) were analysed. The nutritional status was evaluated using the Controlling Nutritional Status (CONUT) score, which was calculated from the serum albumin level, lymphocyte count, and total cholesterol level; malnutrition was defined as a CONUT score of 5 to 12. A poor outcome was defined as a modified Rankin Scale score ≥ 3 at 3 months. Results Of the 1518 patients, 113 (7.4%) had malnutrition, and 533 (33.1%) had a poor outcome. Among the patients with cardioembolic stroke and stroke of other etiologies, those with malnutrition had higher rates of poor outcomes than those without. After adjusting for age, sex, and baseline stroke severity, malnutrition was independently associated with poor outcomes in patients with cardioembolic stroke and other stroke etiologies (odds ratio 3.25, 95% confidence interval 1.02–10.4, p = .044; 6.22, 2.71–14.3, p Conclusions Considering stroke subtype, malnutrition determined using the CONUT score was independently associated with poor outcomes in the patients with cardioembolic stroke or stroke of other etiologies.

To assess the influence of periodontal disease on cerebral hemorrhage and its clinical course, we examined the association of the serum IgG titer of periodontal pathogens with hemorrhage growth and 3-month outcome. We consecutively enrolled 115 patients with acute cerebral hemorrhage (44 females, aged 71.3 ± 13.1 years) and used ELISA to evaluate the serum IgG titers of 9 periodontal pathogens: Porphyromonas gingivalis, Aggregatibacter (A.) actinomycetemcomitans, Prevotella intermedia, Prevotella nigrescens, Fusobacterium (F.) nucleatum, Treponema denticola, Tannerella forsythensis, Campylobacter rectus, and Eikenella corrodens. Significant hematoma growth was defined as an increase in the volume of >33% or an absolute increase in the volume of >12.5 mL. A poor outcome was defined as a 3 or higher on the modified Rankin Scale. We observed hemorrhage growth in 13 patients (11.3%). Multivariate analysis revealed that increased IgG titers of A. actinomycetemcomitans independently predicted the elevated hemorrhage growth (odds ratio 5.26, 95% confidence interval 1.52-18.25, p = 0.01). Notably, augmented IgG titers of F. nucleatum but not A. actinomycetemcomitans led to a poorer 3-month outcome (odds ratio 7.86, 95% confidence interval 1.08-57.08, p = 0.04). Thus, we demonstrate that elevated serum IgG titers of A. actinomycetemcomitans are an independent factor for predicting cerebral hemorrhage growth and that high serum IgG titers of F. nucleatum may predict a poor outcome in patients with this disease. Together, these novel data reveal how systemic periodontal pathogens may affect stroke patients, and, should, therefore, be taken into consideration in the management and treatment of these individuals.

Several cohort studies have shown that periodontal disease is associated with an increased risk for stroke. However, it remains unclear whether serum antibody titers for a specific periodontal pathogen are associated with outcome after ischemic stroke, and which kinds of pathogens are associated with ischemic stroke. We examined the relationship between serum IgG titers to periodontal pathogens and outcome in ischemic stroke patients. A total of 445 patients with acute ischemic stroke (194 female [44.0%], mean age 71.9±12.3 years) were registered in this study. Serum IgG titers to 9 periodontal pathogens (Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Prevotella nigrescens, Fusobacterium nucleatum, Treponema denticola, Tannerella forsythensis, Campylobacter rectus, Eikenella corrodens) were evaluated using the enzyme-linked immunosorbent assay (ELISA) method. An unfavorable outcome was defined as a 3 or higher on the modified Rankin Scale. The proportion of patients with unfavorable outcome was 25.4% (113 patients). Based on multivariate logistic regression analysis, numbers of IgG antibodies positive for periodontal pathogens (odds ratio 1.20, 95% CI 1.02-1.41, p = 0.03) were independent predictors of unfavorable outcome in ischemic stroke patients.

A 28-year-old man noticed sensory disturbance in the distal parts of his four extremities and muscle weakness of his hands two weeks after cytomegalovirus (CMV) infection. He had splenomegaly, impairment of hepatic function and peripheral neuropathy with decreased tendon reflexes. Protein-cell dissociation was observed in the cerebrospinal fluid, and the nerve conduction study (NCS) showed the changes due to demyelination. Intravenous immunoglobulin therapy was performed for 5 days after the diagnosis of Guillain-Barré syndrome. He did not show any severe symptoms such as bulbar palsy and was discharged on day 16. Anti-GM2 and anti-GalNAc-GD1a IgM antibodies were detected and acute inflammatory demyelinating polyneuropathy following the CMV infection was confirmed. NCS showed the abnormal changes were normalized after 4 months. The levels of antibodies against moesin, which is a protein existing in trace amounts in node of Ranvier, were increased. However, the antibodies were not detected 4 months after therapy. These changes were well correlated to his clinical course.

We treated 437 cases of adult aseptic meningitis and 12 cases (including 2 recurrent patients; age, 31.8 ± 8.9 years; 7 females) of herpes simplex meningitis from 2004 to 2016. The incidence rate of adult herpes simplex meningitis in the cases with aseptic meningitis was 2.7%. One patient was admitted during treatment of genital herpes, but no association was observed between genital herpes and herpes simplex meningitis in the other cases. The diagnoses were confirmed in all cases as the cerebrospinal fluid (CSF) was positive for herpes simplex virus (HSV)-DNA. For diagnosis confirmation, the DNA test was useful after 2-7 days following initial disease onset. Among other types of aseptic meningitis, the patients with herpes simplex meningitis showed relatively high white blood cell counts and relatively high CSF protein and high CSF cell counts. CSF cells showed mononuclear cell dominance from the initial stage of the disease. During same period, we also experienced 12 cases of herpes simplex encephalitis and 21 cases of non-hepatic acute limbic encephalitis. Notably, the patients with herpes simplex meningitis were younger and their CSF protein and cells counts were higher than those of the patients with herpes simplex encephalitis.

This study reports eleven cases of reversible cerebral vasospasm syndrome (RCVS). Of the 11 patients, two were males and nine were females, with the average age of 47.9 ± 14.1 years. Many of these patients were young. The rates of severe, intractable and pulsative headache, generalized convulsions, and motor hemiparesis were 64%, 27%, and 36%, respectively. As complications of intracerebral lesions in the early stage of disease onset, convexal subarachnoid hemorrhage, lobar intracerebral hemorrhage, and posterior reversible encephalopathy syndrome were observed in 63%, 9%, and 45% of cases, respectively. Cerebral infarction occurred in 45% of cases at around 1-3 weeks after onset. Improvement of cerebral vasoconstriction was recognized in several cases from about the first month of onset. The post-partum period, migraine, transfusion, rapid amelioration for anemia, renal failure, bathing, and cerebrovascular dissection were suspected as disease triggers. Abnormally high blood pressure at onset was confirmed in 55% of cases. It is important to analyze the pathophysiology of RCVS associated with these triggers from the viewpoint of the breakdown of the blood-brain barrier.

Neuronal intranuclear inclusion disease (NIID) is a slowly progressive neurodegenerative disorder with a wide range of clinical manifestations, including dementia and peripheral neuropathy.1 NIID is pathologically characterized by eosinophilic hyaline intranuclear inclusions found in the central and peripheral nervous systems and various organs, including the skin,1,2 which enables the confirmation of a diagnosis by skin biopsy.2 High-intensity signals along the corticomedullary junction on diffusion-weighted imaging (DWI) and bilateral leukoencephalopathy are also specific features of NIID1 and extend as the disease progresses.1,3 However, the clinical and pathophysiologic significance of cerebral blood flow remains undetermined. In this study, we present the case of a patient with NIID exhibiting dynamic perfusion changes on arterial spin labeling (ASL) before typical subcortical DWI signals. The patient's clinical manifestations and radiologic changes are very unique and remarkable for NIID. Her diagnosis was confirmed by skin biopsy and genomic analysis.

Background The etiology of transient global amnesia (TGA) remains unclear. We studied the pathophysiology of TGA in 165 Japanese patients. Subjects and Methods TGA was diagnosed in hospitalized patients from 2004 to 2015. We analyzed clinical characteristics, magnetic resonance imaging findings, and maximum intima-media thickness of the common carotid artery, and the reflux of internal jugular venous (IJV) flow by ultrasonography, and statistically compared patients with TGA with age-matched and sex-matched patients who have had a transient ischemic attack (TIA), small-vessel occlusion (SVO), and normal controls (each group, N = 165). Results Patients with TGA showed lower prevalence of vascular risk factors than patients with TIA and SVO did. Eleven patients (6.7%) had 2 episodes of TAG, but specific clinical variables could not be recognized in these patients. The maximum intima-media thickness was significantly thinner in TGA (1.1 ± .7 mm) than in SVO (1.6 ± .9 mm; P = .001). The percentages of cases whose IJV flow reflux was increased by Valsalva maneuver showed no difference ( P = .573) between TGA (26.0 %) and SVO (29.4%). MR diffusion-weighted imaging yielded small hyperintense signals in the hippocampus in 64 of 90 (71.1%) patients between 24 and 72 hours. Potential precipitating specific factors or events before the attacks could be recognized in 40 cases (24.2%) of 165 patients. Conclusion Arterial ischemia and IJV flow reflux might not contribute to TGA pathophysiology. The vulnerability of the hippocampus to physical or emotional stress might be suspected as an underlying mechanism in some patients with TGA.

A 64-year-old woman was admitted to our hospital owing to decreased visual acuity and visual field defect. She had a similar history of decreased visual acuity and received steroid therapy 10 years ago. Brain MRI revealed gadolinium-enhancement in the sheath of the optic nerve, called "tram-track" and "doughnut" signs. Optic perineuritis (OPN) was diagnosed on the basis of her clinical manifestations, which improved on treatment with high-dose methylprednisolone (mPSL). However, clinical manifestations relapsed 10 days post-discharge; hence, she was re-admitted. She was re-administered high-dose mPSL and subsequent oral administration of prednisolone. She had no relapse or recurrence for the last 2 years. We reviewed studies involving Japanese patients with OPN, including 17 idiopathic and 14 secondary cases and found that 43% of patients had recurrences and 30% of patients had poor outcome including severe residuals of visual acuity. Secondary OPN occurred owing to various diseases manifesting generalized systematic inflammation. Timely and suitable treatment was very important for clinical favorable outcomes in OPN.

AIM This study aimed to evaluate the associations of blood pressure (BP) variability in patients with ischemic stroke during the subacute phase using ambulatory blood pressure monitoring and the ankle-brachial index (ABI). METHODS We retrospectively examined 831 consecutive patients (women 44.8%, mean age 76 ± 12 years) with acute ischemic stroke who underwent 24-h ambulatory blood pressure monitoring during the subacute phase of stroke (median 9 days from onset) and an ABI examination. BP variability was evaluated by assessing the standard deviation and coefficient of variation of systolic BP and diastolic BP. A low ABI was defined as an ABI

Summary Stroke can be a cause of death, while in non-fatal cases it is a common cause of various disabilities resulting from associated brain damage. However, whether a specific periodontal pathogen is associated with increased risk of unfavorable outcome after stroke remains unknown. We examined risk factors for unfavorable outcome following stroke occurrence, including serum antibody titers to periodontal pathogens. The enrolled cohort included 534 patients who had experienced an acute stroke, who were divided into favorable (n = 337) and unfavorable (n = 197) outcome groups according to modified ranking scale (mRS) score determined at 3 months after onset (favorable = score 0 or 1; unfavorable = score 2–6). The associations of risk factors with unfavorable outcome, including serum titers of IgG antibodies to 16 periodontal pathogens, were examined. Logistic regression analysis showed that the initial National Institutes of Health stroke scale score [odds ratio (OR) = 1·24, 95% confidence interval (CI) = 1·18–1·31, P

Thus far, it is well known that increased blood pressure variability may exacerbate stroke outcomes. Blood pressure in the acute phase would be influenced by both reactive hypertension to stroke and intrinsic blood pressure reactivity. Thus, we aimed to evaluate the association between blood pressure variability and outcomes at 3 months using ambulatory blood pressure monitoring in ischemic stroke patients in the subacute phase after reactive hypertension subsided. We retrospectively examined 626 consecutive patients with acute ischemic stroke who underwent 24-hour ambulatory blood pressure monitoring during the subacute phase of stroke (median, 9 days from onset). The variability in blood pressure was evaluated by assessing the standard deviation and coefficient of variation of systolic and diastolic blood pressure. The primary outcome was functional status at 3 months. A poor outcome was defined as a modified Rankin scale score of 3 or more and a good outcome as 2 or less. We assessed the functional outcome at 3 months in 497 patients (79.4%). The mean systolic and diastolic blood pressure levels were not associated with functional outcome. The multivariable analysis revealed that increases in the standard deviations of systolic and diastolic blood pressure, coefficient of variation of diastolic blood pressure, and morning blood pressure surge were associated with poor outcome. Blood pressure variability during the subacute phase of ischemic stroke can be a useful prognostic indicator of poor functional outcome at 3 months in patients with acute ischemic stroke.

Introduction: Oral health conditions, including periodontal disease has been considered as a risk factor for cerebral or cardiovascular disease. Cerebral small vessel disease (SVD) such as white matter lesions (WMLs) or cerebral microbleeds (CMBs) are also associated with the incidence of stroke. However, it is unclear how oral health conditions are associated with the severity of SVD. Hypothesis: The purpose of this study is to examine the associations of oral health conditions (serum titer of periodontal pathogens or tooth loss) with the severity of SVD (WMLs or CMBs) in acute stroke patients. Methods: Acute stroke patients were enrolled in two stroke centers. Serum antibody titers of periodontal pathogens (16 pathogens) were evaluated within 3 days after stroke onset. The severity of WMLs was assessed by Fazekas classification; grade 0 and 1 were defined as mild and grade 2 and 3 as severe WMLs. The presence or numbers of CMBs was assessed by T2*-weighted MRI. The patients were evaluated for the numbers of tooth loss by a dentist in single center (Hiroshima university hospital). The severity of tooth loss was classified by the number 0 to 5 as mild and 6 or more as severe. Results: In total, 664 acute stroke patients were enrolled (ischemic, n=558 and hemorrhagic, n=106). No significant associations were detected between the grades of any serum antibody titers of periodontal pathogens and the severity of WMLs or CMBs. Of these, 124 patients were evaluated for the numbers of lost teeth. The patients with severe WMLs had severe tooth lost frequently compared to those with mild WMLs (70.7% vs. 39.4%, P=0.020). The patients with multiple CMBs (more than 2) had severe tooth lost frequently compared to those without (67.6% vs. 48.8%, P=0.048). After adjusting for age, sex, hypertension, diabetes, dyslipidemia and atrial fibrillation, severe tooth loss (odds ratio [OR] 2.82, 95% CI 1.23-6.47, P=0.014) were associated with the severity of WMLs. Similarly, severe tooth loss was also associated with the multiple CMBs after adjusting for those factors (OR 2.73, 95% CI 1.05-7.11, P=0.040). Conclusion: No association is detected between any serum antibody titer to periodontal pathogens and the severity of SVD. On the other hand, the severe tooth loss is associated with the severity of SVD.

Introduction: It has been reported that stroke is associated with periodontal disease, which is caused by many kinds of pathogens; however, the influence of periodontal disease on cerebral hemorrhage and its clinical course have not been investigated. Thus, we examined the association of the serum IgG titer of periodontal pathogens with hemorrhage growth and 3-month outcome. Methods: We consecutively enrolled 115 patients with acute cerebral hemorrhage (44 females, 71.3±13.1 years). The serum IgG titers of 16 periodontal pathogens ( P. gingivalis [5 strains], A. actinomycetemcomitans [3 strains], P . intermedia , P . nigrescens , F . nucleatum [ 2 strains], T. denticola , T. forsythensis , C. rectus , E. corrodens ) were evaluated using the ELISA method. Significant hematoma growth was defined as an increase in volume of >33% or an absolute increase of volume of >12.5 mL. A poor outcome was defined as a 3 or higher on the modified Rankin Scale. In the multivariate analysis, we used the following factors for adjustment: age, sex, BMI, NIHSS score on admission, drinking and smoking habits, comorbidities (hypertension, diabetes mellitus, dyslipidemia, atrial fibrillation, peripheral artery disease, and chronic heart failure), and CRP levels. Results: Hemorrhage growth was found in 13 patients (11.3%). On univariate analysis, hemorrhage growth was associated with NIHSS score, diabetes mellitus, chronic heart failure, and IgG titers of A. actinomycetemcomitans SUNY 67 . Multivariate analysis revealed that this IgG titer was independently associated with hemorrhage growth (odds ratio 3.18, 95% CI 1.13-8.95). Notably, the IgG titer of F. nucleatum10953 but not A. actinomycetemcomitans SUNY 67 was associated with a poor 3-month outcome (odds ratio 6.11, 95% CI 1.51-31.21). Conclusions: Higher serum IgG titer of A. actinomycetemcomitans SUNY 67 was an independent factor for predicting hemorrhage growth in patients with cerebral hemorrhage. Higher serum IgG titer of F. nucleatum10953 was associated with a poor outcome, which suggests the systemic negative impact on stroke patients apart from hemorrhage growth.

Background: The increased blood pressure (BP) variability may influence on the stroke outcome. However, in the acute phase of large stroke, reactive hypertension would occur and sustain for a few days. Therefore, in this phase, it is difficult to understand a cause of BP variability whether it is from reactive hypertension or original blood pressure reactivity. Thus, we aimed to evaluate the association of BP variability using ambulatory blood pressure monitoring (ABPM) in the subacute phase of ischemic stroke, when restoration from reactive hypertension can be observed, with 3-month outcomes. Method: We retrospectively enrolled a consecutive series of 840 patients hospitalized for acute ischemic stroke (55.2% males, age: 76 ± 12 years) performing 24-hour ABPM during the subacute phase of stroke (median 9 days from onset). Variability in BP was evaluated with the standard deviation (SD) and with the coefficient of variation (CV) of systolic (SBP) and diastolic BP (DBP). The primary outcome was evaluated from the 3-month functional status: poor outcome as a modified Rankin Scale score of 3 or more and good outcome as 2 or less. Results: Patients with dipper, non-dipper and riser type were 11.4%, 50.5%, and 38.1%, respectively among the total enrolled cohort. Of these, 651 patients (77.5 %) were assessed for the functional outcomes at 3 months. The rates of patients with poor functional outcome were higher in patients with non-dipper or riser type than in the dipper type (47.7%, 57.1%, and 35.1%, respectively). The mean level of SBP and DBP were not associated with functional outcome. The variability of SBP and DBP was significantly associated with poor functional outcome in univariate analysis. After adjusting for age, sex and initial stroke severity, one increase of SD value (odds ratio [OR] 1.08, 95% confidence interval [CI] 1.03 to 1.13, P Conclusion: The variability of BP in the subacute phase of ischemic stroke is expected to be a useful prognostic factor of a 3-month functional outcome.

Tooth loss, closely associated with malnutrition, increases the risk for cardiovascular disease. The aim of this study was to examine the link between tooth loss, nutritional status, and stroke outcomes.We retrospectively analyzed 195 consecutive patients with acute ischemic stroke who were evaluated for tooth loss. Tooth loss was classified as mild or severe. Nutritional status was evaluated using the Controlling Nutritional Status (CONUT) score. A poor neurologic outcome was defined as a score of 3 to 6 on the modified Rankin Scale at 3 mo post-stroke onset; a score of 0 to 2 was defined as a good outcome.A significant correlation was observed between tooth loss and the CONUT score at admission (ρ = 0.156; P = 0.034). Patients with poor outcomes had higher CONUT scores (P0.001) and a greater frequency of severe tooth loss (P = 0.025). On multivariate analysis, severe tooth loss (odds ratio [OR], 3.93; 95% confidence interval [CI], 1.31-11.8) and the CONUT score (OR, 1.33; 95% CI, 1.02-1.74) were independently associated with poor stroke outcomes.Nutritional status was associated with tooth loss among patients with acute ischemic stroke. Severe tooth loss and a higher CONUT score were independently associated with poor stroke outcomes.

We report the patient of a 53-year-old woman who developed subacute-onset marked tonge protrusion and bite. She was diagnosed as dementia with Lewy bodies (DLB) from the clinical features including progressive cognitive decline, visual hallucinations, parkinsonism, and severe insomnia and depression, and the radiological finding of low dopamine transported uptake in basal ganglia by Dat SCAN and low blood circulation in occipital lobe of cerebrum. The patient received 600 mg doses of levodopa for over a year, followed by rotigotine and ropinirole with a rapid increase of dosage. It is believed that these treatments stimulated and sensitized dopamine D1 receptors, thereby inducing lingual dystonia. Furthermore, the patient demonstrated dyspnea and attacks of apnea caused by the closure of bilateral vocal cords due to laryngeal dyskinesia. After initiation of the neuroleptic, olanzapine, for a short duration, the high dose of levodopa overlapped with neuroleptic sensitivity, suggesting DOPA-induced dystonia and dyskinesia. This interaction can sometimes lead to lethal adverse events, and must be considered very important when treating patients with DLB.

Oral health conditions and cerebral small vessel disease, such as white matter lesions or cerebral microbleeds (CMBs), are associated with the incidence of stroke. The purpose of this study was to examine the associations between oral health conditions (serum IgG titers of periodontal pathogens) with the presence or severity of CMBs in acute stroke patients. From January 2013 to April 2016, acute stroke patients were registered in two hospitals. Serum samples were evaluated for antibody titers against 9 periodontal pathogens using the ELISA method. The cut-off points for reactivity (the positive decision point) to each antigen were defined as more than a mean ELISA unit + 1 standard deviation (after logarithmic transformation) in all subjects. CMBs were evaluated on T2*-weighted MRI. In all, 639 patients were evaluated (ischemic, n = 533 and hemorrhagic, n = 106; 73.1 ± 12.9 years old). Among these patients, 627 were available for CMB evaluation. Among the 9 evaluated periodontal pathogens, only Campylobacter rectus (C. rectus) was associated with the presence of CMBs. the prevalence of positive serum antibody titers against C. rectus was higher among patients with CMBs than among those without CMBs (14.6% vs. 8.7%, P = 0.025). In addition, positive serum antibody titers against C. rectus remained one of the factors associated with the presence of CMBs in multivariate logistic analysis (odds ratio 2.03, 95% confidence interval 1.19-3.47, P = 0.010). A positive serum antibody titer against C. rectus was associated with the presence of CMBs in acute stroke patients.

A 55-year-old man with no history of stroke or migraine presented to the clinic with cognitive impairment and depression that had been experiencing for two years. Neurological examination showed bilateral pyramidal signs, and impairments in cognition and attention. Brain MRI revealed multiple lacunar lesions and microbleeds in the deep cerebral white matter, subcortical regions, and brainstem, as well as diffuse white matter hyperintensities without anterior temporal pole involvement. Cerebral single-photon emission computed tomography (SPECT) revealed bilateral hypoperfusion in the basal ganglia. Gene analysis revealed an arginine-to-proline missense mutation in the NOTCH3 gene at codon 75. The patient was administered lomerizine (10 mg/day), but the patient's cognitive impairment and cerebral atrophy continued to worsen. Follow-up testing with MRI three years after his initial diagnosis revealed similar lacunar infarctions, cerebral microbleeds, and diffuse white matter hyperintensities to those observed three years earlier. However, MRI scans revealed signs of increased cerebral blood flow. Together, these findings suggest that the patient's cognitive impairments may have been caused by pathogenesis in the cerebral cortex.

We experienced 13 cases (29.8 ± 7.0 years) of mumps meningitis and 365 cases of adult aseptic meningitis during 11 years from 2004 to 2014. A small epidemic of mumps occurred for 3-4 years, and the incidence rate of adult mumps meningitis coincided with the epidemic without seasonal fluctuation. Parotitis was observed in 8 of the 13 mumps meningitis patients (61.5%) and orchitis in 2 of 7 male patients (28.6%). There were no differences in clinical manifestations, laboratory findings, and outcome between patients with adult mumps meningitis and those with echovirus 9 meningitis (9 patients), except for the low frequency of nausea/vomiting and a high percentage of mononuclear cells of the cerebrospinal fluid in those with mumps. Eight patients had contact with persons with mumps before the symptomatic stage of meningitis. Only one patient had received mumps vaccination in childhood. On the basis of the values of the anti-mumps IgM and IgG antibodies, we speculated primary infection and the re-infection of mumps in 6 and 2 patients, respectively. Moreover, second vaccine failure was suggested in the vaccinated patient.

A 69-year-old man was admitted to our hospital because of disturbed consciousness and gait disturbance. He had herpes zoster (HZ) in his left thigh 10 days before admission, and motor paresis of four extremities developed. A dark red rash was observed in his left buttock and thigh (L2-3 region), which was also scattered in the right lower leg, chest wall, and both upper extremities. Brain MRI showed no lesions of demyelinating plaques. Spine MRI showed no abnormal signals in the lumbar region; however, high signals in the spinal cord from the bottom of the medulla oblongata to the upper (Th 2) thoracic region were observed. High signals were observed mainly in the central white matter. These lesions might correspond to longitudinally extensive transverse myelitis (LETM). Cerebrospinal fluid (CSF) showed increased protein and cell counts of lymphocytes and was positive for varicella-zoster virus (VZV)-DNA. His serum sample tested negative for anti-aquaporin (AQP)4 antibody but positive for anti-myelin oligodendrocyte glycoprotein (MOG) antibody (cell-based assay). Disseminated HZ was suspected on the basis of the widely scattered rash, and damage to the both lungs and liver. This is the first report of HZ-associated LETM with a high titer anti-MOG antibodies. Our case showed that HZ may trigger anti-MOG-IgG positive myelitis.

A 63-year-old man noticed hypogeusia after presenting hiccups for several days. He was serologically diagnosed with varicella-zoster virus (VZV) infection, but had no skin lesions typical of herpes (zoster sine herpete). Hypogeusia was confirmed by electrogustometry and the filter-paper disk method, which showed damage in the areas innervated by the cord of tympanum, glossopharyngeal nerve, and greater petrosal nerve. High signals in the nuclei of the solitary tract of the medulla oblongata and the enhancement of the bilateral intracranial segments of the cranial nerve IX and X complex were observed by magnetic resonance imaging (MRI). The signal changes in the nuclei of the solitary tract on MRI were seen for more than 2 months, and hypogeusia lasted for more than 7 months. Hypogeusia caused by VZV infection has rarely been reported; however, similar cases could have gone undiagnosed or underdiagnosed in patients with idiopathic hypogeusia. (Received August 18, 2016; Accepted September 29, 2016; Published February 1, 2017).

Background and Hypothesis: The effectiveness and safety of anticoagulants, which are widely used for preventing stroke recurrence, in stroke prevention is well established, they rarely cause severe adverse events, such as intracerebral hemorrhage (ICH). Direct oral anticoagulants (DOACs) have recently become an option for anticoagulation therapy. The incidence of hemorrhagic events in patients under DOAC therapy has been investigated in several studies, but it is unclear whether the severity of a hemorrhagic event is influenced by the use of DOACs. We hypothesized that the severity of ICH is different in patients under warfarin versus those under DOAC therapy. Method: We retrospectively reviewed medical records and computed tomography images of patients with ICH who were treated at our hospital during April 2011-May 2016. Patients’ clinical characteristics and ICH volume and location were compared between warfarin- and DOAC-treated patients. Result: Of the 1147 patients with ICH, 114 patients were taking anticoagulants on admission. Eighty-nine patients (78.1%) received warfarin, whereas 25 (21.9%) received DOACs. The following DOACs were used: dabigatran (two patients), rivaroxaban (10 patients), apixaban (12 patients), and edoxaban (one patients). Median ICH volume was significantly lesser in DOAC-treated patients than in warfarin-treated patients [8.1 (range, 0.05-160) ml vs 15.9 (range, 0.1-119) ml, respectively; p = 0.048). A significant correlation between ICH volume and HAS-BLED score was found only in the DOACs group (ρ= 0.560 p = 0.004) but not in the warfarin group (ρ= 0.025 p = 0.822). We found two patients with an ICH volume of >150 mL in the DOACs group. Their HAS-BLED score was 3, and they had experienced multiple stroke events (three or six times). Conclusion: ICH volume was lesser in DOAC-treated patients than in warfarin-treated patients. We also found that HAS-BLED can be a predictor of ICH volume in DOAC-treated patients.

Background: Serum 1,5-anhydroglucitol (1,5-AG) levels are a measure that provides information on daily glycemic variations. We evaluated whether 1,5-AG could be a possible marker of acute ischemic stroke (AIS) or transient ischemic attacks (TIA) in patients with diabetes mellitus (DM). Methods: We retrospectively reviewed electronic medical records of 5,294 AIS/TIA patients. Of the 5,294, 1,898 had diabetes and in 1,246, serum 1,5-AG levels were measured (group S). Group S was divided into 2 subgroups: hemoglobin A1c (HbA1c) 7% (S-high). As controls, 394 outpatients with diabetes (group C) without AIS/TIA were likewise divided into subgroups, C-low and C-high according to HbA1c level. In each HbA1c subgroup, the association between serum 1,5-AG (≥14 vs. Results: Overall, serum 1,5-AG levels were lower in group S than in group C. Serum 1,5-AG levels were low in subgroups S-high and C-high, showing no differences in mean values. However, mean serum 1,5-AG levels in S-low was statistically lower than that in C-low. MLR analysis showed that the OR for low (Conclusions: Low serum 1,5-AG levels could be a possible marker for AIS/TIA risk in patients with well-controlled DM.

Background: Cerebral venous sinus thrombosis (CVT) occurs commonly in young female adults and is caused by various risk factors. Our aim was to determine the incidence, clinical characteristics, and risk factors of Japanese CVT patients. Patients and methods: We performed a retrospective study of CVT patients from January 2010 to June 2015. In the patients who had hyperhomocysteinemia, vitamin levels were measured. To define the clinical characteristics in patients with hyperhomocysteinemia, we statistically compared them to those patients with normal levels of homocysteine. Results: Sixteen patients (aged 54.6 ± 17.7 years; 13 men and 3 women) were included. The incidence of CVT was 0.23% among all types of strokes or 0.30% of acute ischemic strokes, which was lower than previously reported. The patients were characterized by advanced age, low frequency of headaches, and few female patients, especially female patients using oral contraceptives. The predisposing conditions included a notably high incidence of hyperhomocysteinemia (56.3%). They also included deficiencies of folate, vitamin B12, vitamin B6, or combined deficiencies. Marked hyperhomocysteinemia over 100 nmol/ml was noted in combined deficiencies. Conclusions: CVT in Japan commonly occurred in older males. The prevalence of hyperhomocysteinemia as a risk factor of CVT was high, and the main underlying disorders were folate and vitamin B12 or B6 deficiencies. This is clinically important, because these acquired risks can be corrected by supplementation therapy to prevent the recurrence of CVT.

Introduction: Current guidelines set the goal of diabetes control to a glycated hemoglobin A1c (HbA1c) level of Hypothesis: 1,5AG can be used to evaluate the risk of CI in patients with well-controlled diabetes. Methods: We retrospectively reviewed the medical records of 1169 patients with diabetes who received treatment for CI at our hospital between 2009 and 2014. These patients were divided into the following two groups according to their HbA1c-based diabetes control status: a CI-low group (HbA1c Results: There was no difference in the 1,5AG level between the CI-high and nonCI-high groups (8.8±7.3% vs. 8.9±7.1%, p=0.83). However, the 1,5AG level was significantly lower in the CI-low group than in the nonCI-low group (12.5±8.1% vs. 15.2±8.8%, p Conclusion: The results of this study show that short-term glycemic control and glycemic variability have a significant relationship with existing CI especially in patients with good diabetes control. The 1,5AG level may be a surrogate measure of the risk of CI in patients with HbA1c levels that indicate good diabetes control.

Introduction: Cerebral microbleeds (CMBs) are considered as a risk factor for stroke. The incidence of post-tPA microbleeds have been reported in recent studies, however, it is not clear that whether hybrid procedure (the combination of tPA and endovascular thrombectomy) for ischemic stroke would increase risk of post-treatment CMBs more than treatment with tPA or endovascular thrombectomy alone. Objective of this study is to compare the incidence of post-treatment CMBs and symptomatic exraischemic hemorrhage by treatments: hybrid procedure, tPA alone, and endovascular thrombectomy alone. Hypothesis: Combined therapy of endovascular thrombectomy and tPA for ischemic stroke have higher incidence of post-treatment CMBs than tPA or endovascular thrombectomy alone. Methods: We retrospectively reviewed pre- and post-T2*-weighted MRI of ischemic stroke patients who received above treatments in our hospital during 2010 to 2014. The presence and number of CMBs were assessed according to the Brain Observer Microbleeds Scale. We compared the number of pre-treatment CMBs, incidence of newly-occurred post-treatment CMBs and symptomatic extraischemic hemorrhage within a year after treatments among hybrid procedure, tPA alone, and endovascular thrombectomy alone. Results: A total of 147 (hybrid procedure n=17, tPA alone n=90, endovascular thrombectomy alone n=40) patients’ pre- and post-treatment MRIs were reviewed. The average number of pre- treatment CMBs was 1.4±4.0 and there was no difference among treatments. The incidence of post-treatment CMBs was significantly higher in hybrid procedure (n=5, 29.4%) and tPA alone (n=18, 20.0%) than endovascular thrombectomy (n=1, 2.5%). However, there was no difference between hybrid procedure and tPA alone. Symptomatic extraischemic hemorrhage was found only one patient who received endovascular thrombectomy alone. Conclusion: The incidence of CMBs after treatments was increased in treatments using tPA. However, there was no difference in post-treatment incidence between hybrid procedure and tPA alone. This result suggests that additional thrombectomy after tPA would not increase the risk of CMBs.

A 63-year-old man was admitted to our hospital because of convulsive seizures. Radiological examinations revealed cerebral venous sinus thrombosis in the anterior part of the superior sagittal sinus. He had marked hyperhomocysteinemia (93.5 nmol/ml) due to combined deficiencies of folate and vitamin B12. He was T/T homozygous for methylene tetrahydrofolate reductase C677T polymorphism. He received a supplement therapy of vitamins. First, he was administered folate orally. After 3 months, the serum level of homocysteine decreased to 22.6 nmol/ml (an 86% reduction), but was still above the normal level. Next, an additional supplement therapy of vitamin B12 lowered the homocysteine level to normal (12.3 nmol/ml) after 4 months. These results showed that the increase of homocysteine levels in this patient was mainly caused by the deficiency of folate. Additionally, acquired risk factors like vitamin deficiencies increased the level of serum homocysteine to almost 100 nmol/ml.

We report the case of a 73-year-old woman presenting with hypersomnia and loss of appetite. She suffered from diabetic nephropathy without receiving dialysis, in addition to hypertension, which was well controlled without marked fluctuation. There were no objective neurological findings. Her laboratory findings showed renal failure with 3.7 mg/dl of serum creatinine and decreased serum sodium and potassium. Brain magnetic resonance imaging (MRI) showed posterior reversible encephalopathy syndrome (PRES) with vasogenic edema, which was distributed in the dorsal midbrain, medial thalamus, and hypothalamus. After we addressed the electrolyte imbalance and dehydration, her symptoms and MRI findings gradually improved, but faint high signals on MRI were still present 3 months later. Orexin in the cerebrospinal fluid was decreased on admission, but improved 6 months later. We diagnosed uremic encephalopathy with atypical form PRES showing functional disturbance of the hypothalamus.