Microbiome composition comparison in oral and atherosclerotic plaque from patients with and without periodontitis.

There is no conclusive evidence regarding a causal relationship between periodontitis and atherosclerosis. In this study, we examined the microbiome in the oral cavity and atheromatous plaques from atherosclerosis patients with or without periodontitis to investigate the role of oral bacteria in the formation of atheromatous plaques. We chose four patients with and without periodontitis, who had undergone carotid endarterectomy. Bacterial samples were extracted from the tongue surface, from periodontal pocket (during the oral examination), and from the atheromatous plaques (APs). We investigated the general and oral conditions from each patient and performed next-generation sequencing (NGS) analysis for all bacterial samples. There were no significant differences between both groups concerning general conditions. However, the microbiome patterns of the gingival pocket showed differences depending on the absence or presence of periodontitis, while those of the tongue surface were relatively similar. The microbiome pattern of the atheromatous plaques was entirely different from that on the tongue surface and gingival pocket, and oral bacteria were seldom detected. However, the microbiome pattern in atheromatous plaques was different in the presence or absence of periodontitis. These results suggested that oral bacteria did not affect the formation of atheromatous plaques directly.

Acute Prevertebral Abscesses Caused by Bacterial-infected Traumatic Tooth Fractures.

We report a case of acute prevertebral abscess caused by traumatic tooth fractures in a 77-year-old Japanese man. After being transferred to our hospital the patient was initially diagnosed with a neck hematoma; however, blood culture showed Streptococcus parasanguinis, an oral bacterium, and an MRI examination suggested prevertebral abscesses. Tooth fractures, severe periodontitis, and peri-implantitis with Streptococcus parasanguinis were observed. Antibiotics were administered and fractured teeth were extracted. The patient's condition then gradually improved. We concluded that bacteremia caused by traumatic tooth fractures induced the acute prevertebral abscesses.

Warm Front Passage on the Previous Day Increased Ischemic Stroke Events.

BACKGROUND AND PURPOSE: The influence of a weather front passage is rarely evaluated on stroke events. We hypothesized that a weather front passage on the stroke onset day or during the previous days may play an important role in the incidence of stroke. METHODS: A multicenter retrospective study was conducted to evaluate the frequency of stroke events and their interaction with weather front passages. Consecutive acute stroke patients (n = 3935, 73.5 ± 12.4 years, 1610 females) who were admitted to 7 stroke hospitals in 3 cities from January 2012 to December 2013 were enrolled in this study. Multivariate Poisson regression models involving time lag variables were used to compare the daily rates of stroke events with the day of a weather front passage and the previous 6 days, adjusting for considerable influences of ambient temperature and atmospheric pressure. RESULTS: There were a total of 33 cold fronts and 13 warm fronts that passed over the 3 cities during the study period. The frequency of ischemic stroke significantly increased when a warm front passed on the previous day (risk ratio 1.34, 95% confidence interval 1.07-1.69, P= .016). CONCLUSIONS: This study indicated that a weather front passage on the previous days may be associated with the occurrence of stroke.

Serum 1,5-Anhydroglucitol: Risk Factor of Acute Ischemic Stroke and Transient Ischemic Attack in Well-Controlled Diabetes.

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-low) and >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. <14 µg/mL) and stroke was examined using multivariable logistic regression (MLR) with stepwise variable selection. In model 1, the OR and 95% CI was examined adjusted for age and gender. Known risk factors for stroke; hypertension, dyslipidemia, alcohol consumption, smoking, and estimated glomerular filtration rate were included in model 2. 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 (<14 µg/mL) 1,5-AG for stroke was statistically significant only in well-controlled diabetes (OR [95% CI] 2.19 [1.54-3.10]) in model 1 and (2.26 [1.56-3.28]) model 2. CONCLUSIONS: Low serum 1,5-AG levels could be a possible marker for AIS/TIA risk in patients with well-controlled DM.

Ischemic Stroke Mortality Is More Strongly Associated with Anemia on Admission Than with Underweight Status.

BACKGROUND: Underweight patients have recently been reported as a group with a high risk of poststroke death. Anemia also increases mortality rates in stroke patients. However, the causal associations between body weight and anemia resulting in stroke-related death remain unclear. We examined the association of weight status and hemoglobin levels with 3-month mortality after ischemic stroke. METHODS: The study enrolled all consecutive patients with acute ischemic stroke and no history of stroke admitted to our hospital between January 2010 and December 2013. The patients were categorized into 4 body mass index (BMI) categories (underweight, normal-weight, overweight, and obese). Anemia was evaluated according to the World Health Organization criteria (men, <13 g/dL; women, <12 g/dL). RESULTS: A total of 1733 acute ischemic stroke patients (149 underweight, BMI < 18.5 kg/m2; 1076 normal-weight, BMI = 18.5-24.9 kg/m2; 436 overweight, BMI = 25-29.9 kg/m2; and 72 obese, BMI > 30 kg/m2) were included. Death within 3 months occurred in 65 patients (underweight, 10.1%; normal-weight, 3.4%; overweight, 2.3%; and obese, 5.6%). Compared to nonanemic patients, those with anemia (n = 329, 19.0%) had lower BMI (21.8 kg/m2 versus 23.7 kg/m2, P <.001) and higher mortality rates (9.1% versus 2.5%, P <.001). Underweight status was associated with 3-month mortality after adjusting for age, sex, comorbidities, and initial stroke severity. However, in the models that included laboratory findings, it was anemia status (odds ratio, 2.81; 95% confidence interval, 1.46-5.43), not underweight status, that was independently associated with 3-month mortality. CONCLUSION: Anemia on admission was associated with stroke mortality independent of underweight status.

Vascular Risk Factors and Internal Jugular Venous Flow in Transient Global Amnesia: A Study of 165 Japanese Patients.

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.

Brain Natriuretic Peptide and Particular Left Ventricle Segment Asynergy Associated with Cardioembolic Stroke from Old Myocardial Infarction.

BACKGROUND: It is important to determine the usage of anticoagulants by defining the actual risk of cardioembolic stroke in patients with old myocardial infarction. In the present study, we aimed to more precisely evaluate the risks of each segment associated with cardioembolic stroke using a 16-segment model. The usage of the plasma brain natriuretic peptide (BNP) associated with cardioembolic stroke was also evaluated in comparison with a left ventricle ejection fraction less than 40%. METHODS: There were a total of 190 ischemic stroke patients who had premorbid myocardial infarction. The study included a total of 143 ischemic stroke patients with old myocardial infarction who were available for evaluation and excluded patients with atrial fibrillation or acute myocardial infarction. Their left ventricle wall motion abnormality and the level of plasma BNP at their admission were analyzed. RESULTS: Hypertension and a plasma BNP level of 206.9 pg/mL or higher, determined from the receiver operating characteristic curve, were independently associated with cardioembolic stroke (χ(2) = 35.6, R(2) = .30, P < .001). Adjusting for these factors, statistically independent high risk was observed at the basal-inferior, basal-inferolateral, mid-anterior, mid-anteroseptal, apical-anterior, and apical-septal left ventricles. CONCLUSION: High plasma BNP levels and left ventricular wall motion abnormalities in the segments perfused with left anterior descending coronary artery or right coronary artery show a high risk for cardioembolic stroke in patients with old myocardial infarction. Considering these factors, it could be possible to more precisely define the risk of cardioembolic stroke and to perform appropriate antithrombotic treatments in old myocardial infarction patients.

Association of HTRA1 mutations and familial ischemic cerebral small-vessel disease.

BACKGROUND: The genetic cause of cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL), which is characterized by ischemic, nonhypertensive, cerebral small-vessel disease with associated alopecia and spondylosis, is unclear. METHODS: In five families with CARASIL, we carried out linkage analysis, fine mapping of the region implicated in the disease, and sequence analysis of a candidate gene. We also conducted functional analysis of wild-type and mutant gene products and measured the signaling by members of the transforming growth factor beta (TGF-beta) family and gene and protein expression in the small arteries in the cerebrum of two patients with CARASIL. RESULTS: We found linkage of the disease to the 2.4-Mb region on chromosome 10q, which contains the HtrA serine protease 1 (HTRA1) gene. HTRA1 is a serine protease that represses signaling by TGF-beta family members. Sequence analysis revealed two nonsense mutations and two missense mutations in HTRA1. The missense mutations and one of the nonsense mutations resulted in protein products that had comparatively low levels of protease activity and did not repress signaling by the TGF-beta family. The other nonsense mutation resulted in the loss of HTRA1 protein by nonsense-mediated decay of messenger RNA. Immunohistochemical analysis of the cerebral small arteries in affected persons showed increased expression of the extra domain-A region of fibronectin and versican in the thickened tunica intima and of TGF-beta1 in the tunica media. CONCLUSIONS: CARASIL is associated with mutations in the HTRA1 gene. Our findings indicate a link between repressed inhibition of signaling by the TGF-beta family and ischemic cerebral small-vessel disease, alopecia, and spondylosis.

[A case of various illusion, and hallucination caused by occipital lobe infarction].

A 70-year-old right-handed man noticed that the right side of the screen on his television displayed a time lag compared to the other side. For five days before admission, he had characteristic polyopia, visual photopia, and complex hallucination. Upon neurological examination, he showed no abnormal findings except for right homonymous hemianopia. MRI showed acute infarction of the occipital gyri and part of the lingual gyrus in the left occipital lobe. After admission, he experienced various visual hallucinations and visual illusions, including metamorphopsia and micropia, many times. They gradually disappeared after 2 months. Various hallucination was caused by the release of visual information, and illusion was thought to be due to integration failure of visual information. The appearance of complex hallucination in the blind visual field is known due to the damage of the region on the left occipital gyrus. However, the cases with various symptoms such as visual photopia and micropsia are rare.

[Guillain-Barré syndrome following cytomegalovirus infection with increased level of antibody against moesin-a case report].

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.

[Transient, recurrent, white matter lesions in X-linked Charcot-Marie-Tooth disease with heterozygote mutation of GJB1 gene: case report of a female patient].

A 32-year-old woman showed transient central type facial nerve palsy and bulbar symptoms. Brain MRI revealed high intensity signals in the cerebral white matter, splenium of corpus callosum, and posterior limb of internal capsule. Two elder brothers of the patient had distal dominant peripheral neuropathies in four limbs. In this family, the point mutation of GJB1 gene, encoding connexin 32, was revealed and X-linked Charcot-Marie-Tooth disease (CMTX1) was diagnosed. The presented case was a heterozygote of this mutation. She showed severe transient central nervous system (CNS) symptoms and subclinical demyelinating peripheral neuropathy. The CNS symptoms and alterations of brain images were very similar among three siblings. There are many reports on male patients with CMTX1 who show associated CN symptoms, but female patients are very rare. There has been no previous report of a CMTX1 patient similar to the patient presented here. The trigger factors have been recognized at the onset of transient CN symptoms in these cases. The prevention of these factors is important for the management of such patients.

[CADASIL with cysteine-sparing NOTCH3 mutation manifesting as dissociated progression between cognitive impairment and brain image findings in 3 years: A case report].

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.

[Rapidly deteriorated lobar intracerebral hemorrhages: possible association of varicella zoster virus-vasculopathy].

A 75-year-old man having dementia and lifestyle related diseases developed a lobar intracerebral hemorrhage (LICH) in the left parietal and a small cerebellar infarction in the left occipital lobe. Many micro bleeds (MB) due to cerebral amyloid angiopathy (CAA) in the subcortical areas and multiple vascular stenosis were also found by MRI and MRA. He developed herpes zoster in his buttocks on day 6 of hospitalization and complicated with varicella zoster virus (VZV) meningitis with positive for VZV-DNA in the cerebrospinal fluid. Subsequently, LICHs occurred in the left frontal lobe and in the right parietal lobe for a short period of time and died on the day 18. We speculated that the repeating hemorrhages was primarily caused by VZV vasculopathy and additionally the subcortical MBs increased the hemorrhagic risk. The relationship between VZV vasculopathy and CAA should be studied in the future.

[Guillain-Barré syndrome associated with acute hepatitis A-A case report and literature review].

A 44-year-old female developed acute hepatitis A (HA) 5 weeks after ingesting raw oysters. She developed ascending motor weakness, bilateral peripheral facial nerve palsy, and bulbar symptoms. A diagnosis of demyelinating Guillain-Barré syndrome (GBS) was made on the basis of her clinical manifestations and the results of a nerve conduction study. The patient showed improvement following combination treatment with intravascular immunoglobulin and high dose methylprednisolone. No antibodies against specific gangliosides, sulfated glucuronyl paragloboside (SGPG), or sulfatide were detected. HA virus (HAV) RNA was isolated from her serum and its full-length genome sequence was determined. It revealed a homology of 99.9% or more with HAV genotype IA (HAV-IA) of the 2014 outbreak. No mutant virus RNA was detected.

[Clinical, epidemiological, and etiological studies of adult aseptic meningitis: a report of 12 cases of herpes simplex meningitis, and a comparison with cases of herpes simplex encephalitis].

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.

[Reversible cerebral vasoconstriction syndrome: a clinical study of 11 cases].

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.

Auditory agnosia associated with bilateral putaminal hemorrhage: A case report of clinical course of recovery.

A 45-year-old right-handed man with a past history (10 years) of putaminal hemorrage presented with auditory agnosia associated with left putaminal hemorrhage. It was suspected that the auditory agnosia was due to bilateral damage in the acoustic radiations. Generalized auditory agnosia, verbal and non-verbal (music and environmental), was diagnosed by neuropsychological examinations. It improved 4 months after the onset. However, the clinical assessment of attention remained poor. The cognition for speech sounds improved slowly, but once it started to improve, the progress of improvement was rapid. Subsequently, the cognition for music sounds also improved, while the recovery of the cognition for environmental sounds remained delayed. There was a dissociation in recovery between these cognitions. He was able to return to work a year after the onset. We also reviewed the literature for cases with auditory agnosia and discuss their course of recovery in this report.

[Hypogeusia and High Signals in the Nuclei of the Solitary Tract on MRI due to Varicella-Zoster Virus Infection: A Case Report].

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).

[A case of optic perineuritis-A literature review of Japanese cases and clinical problems].

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.

Anti-myelin oligodendrocyte glycoprotein (MOG) antibody-positive varicella-zoster virus myelitis presenting as longitudinally extensive transverse myelitis: a case report.

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.