Takeshi Yoshimoto

[Reversible changes on MR images in a patient with metronidazole-induced encephalopathy].

A 66-year-old woman was diagnosed with a brain abscess. The abscess was drained by sterotactic catheter insertion. She was administered metronidazole at a dose of 2 g/day. On the 30th day of treatment, she had nausea that gradually progressed. On the 45th day, she developed a disturbance of consciousness and was admitted to our department. She was in stuporous state, and had slight vestibular and cerebellar dysfunctions. Diffusion-weighted and FLAIR brain MR images showed bilateral symmetrical high signals in the splenium of the corpus callosum (SCC), cerebellar dentate nucleus, and inferior colliculus. The apparent diffusion coefficient (ADC) map was reduced in the SCC, but not in the other locations. The peak of lactate on MR spectroscopy was increased in the SCC. The clinical presentation and image changes of the patient were thought to be most consistent with metronidazole toxicity. Metronidazole was discontinued, and her condition improved rapidly. She was discharged 14 days later. The lesions in her cerebellar dentate nucleus and inferior colliculus, suspected to be vasogenic edema, had disappeared 5 to 10 days later, whereas the lesion in the SCC, which gradually diminishing, could still be faintly detected 40 days later, which corresponded to our suspicion of cytotoxic edema.

Two-Year Outcomes of Anticoagulation for Acute Ischemic Stroke With Nonvalvular Atrial Fibrillation ― SAMURAI-NVAF Study ―

BACKGROUND We determined the 2-year long-term risk-benefit profile in patients with stroke or transient ischemic attack (TIA) receiving warfarin or direct oral anticoagulants (DOACs) for nonvalvular atrial fibrillation (NVAF) using a prospective, multicenter, observational registry in Japan.Methods and Results:NVAF patients within 7 days after onset of ischemic stroke/TIA were enrolled in 18 stroke centers. Outcome measures included ischemic and bleeding events and death in the 2-year follow-up period. We enrolled 1,116 patients taking either warfarin (650 patients) or DOACs (466 patients) at acute hospital discharge. DOAC users were younger and had lower National Institutes of Health Stroke Scale, CHADS2and discharge modified Rankin Scale scores than warfarin users (P<0.0001 each). Incidences of stroke/systemic embolism (adjusted hazard ratio, 1.07; 95% CI, 0.66-1.72), all ischemic events (1.13; 0.72-1.75), and ischemic stroke/TIA (1.58; 0.95-2.62) were similar between groups. Risks of intracranial hemorrhage (0.32; 0.09-0.97) and death (0.41; 0.26-0.63) were significantly lower for DOAC users. Infection was the leading cause of death, accounting for 40% of deaths among warfarin users. CONCLUSIONS Stroke/TIA patients receiving DOACs for secondary prevention were younger and had lower stroke severity and risk indices than those receiving warfarin. Estimated cumulative incidences of stroke and systemic embolism within 2 years were similar between warfarin and DOACs users, but those of death and intracranial hemorrhage were significantly lower among DOAC users.

Early Achievement of Blood Pressure Lowering and Hematoma Growth in Acute Intracerebral Hemorrhage: Stroke Acute Management with Urgent Risk-Factor Assessment and Improvement-Intracerebral Hemorrhage Study

Background: Previous studies have revealed that hematoma growth mainly occurs during the first 6 h after the onset of spontaneous intracerebral hemorrhage (ICH). Early lowering of blood pressure (BP) may be beneficial for preventing hematoma growth. However, relationships between timing of BP lowering and hematoma growth in ICH remain unclear. We investigated associations between timing of BP lowering and hematoma growth for ICH. Methods: The Stroke Acute Management with Urgent Risk-factor Assessment and Improvement (SAMURAI)-ICH Study was a multicenter, prospective, observational study investigating the safety and feasibility of early (within 3 h from onset) reduction of systolic BP (SBP) to < 160 mm Hg with intravenous nicardipine for acute hypertension in cases of spontaneous ICH. The present study was a post hoc analysis of the SAMURAI-ICH study. We examined relationships between time from onset, imaging, and initiation of treatment to target SBP achievement and hematoma growth (absolute growth ≥6 mL) in ICH patients. Target SBP achievement was defined as the time at which SBP first became < 160 mm Hg. Results: Among 211 patients, hematoma growth was seen in 31 patients (14.7%). The time from imaging to target SBP and time from treatment to target SBP were significantly shorter in patients without hematoma growth than in those with (p = 0.043 and p = 0.032 respectively), whereas no significant difference was seen in time from onset to SBP < 160 mm Hg between groups (p = 0.177). Patients in the lower quartiles of time from imaging to target SBP and time from treatment to target SBP showed lower incidences of hematoma growth (p trend = 0.023 and 0.037 respectively). The lowest quartile of time from imaging to target SBP (< 38 min) was negatively associated with hematoma growth on multivariable logistic regression (OR 0.182; 95% CI 0.038–0.867; p = 0.032). Conclusions: Early achievement of target SBP < 160 mm Hg is associated with a lower risk of hematoma growth in ICH.

Cerebral Venous Sinus Thrombosis: Incidence and Hyperhomocysteinemia as a Risk Factor in Japanese Patients

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.

Paroxysmal dysarthria and ataxia in chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids

We describe the clinical and imaging features of a unique case of chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids. A 58‐year‐old man presented with development of mild ataxia. Magnetic resonance imaging showed punctate enhancement in the pons, brachium pontis, midbrain and cerebral white matter. Midbrain lesions involved the bilateral red nuclei with ring‐like enhancement. Treatment with steroids resulted in improvements in mild ataxia and brain lesions. However, several days after steroid therapy, the patient presented with paroxysmal dysarthria, and limb ataxia recurred a couple of dozen times each day. Single photon emission computed tomography showed hypoperfusion in the bilateral parietal lobes. After treatment with carbamazepine, symptoms and parietal hypoperfusion improved. Late‐onset paroxysmal dysarthria‐ataxia and parietal hypoperfusion might have been caused by interruption of the cerebellothalamocortical tract at the level of the ring‐like enhancing red nuclei lesions in chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids.