We investigated the dynamic change of MR imaging in acute ischemic stroke with the tPA therapy in our hospital where 3.0T-MRI can support for 24 hours. The clinical data for 62 patients who received intravenous tPA for acute ischemic stroke and MR imaging before, during, and after the tPA of between April 2012 and December 2015. We investigated the change of MR imaging and clinical observation. Nineteen patients (24%) achieved early recanalization more than TICI 2A during tPA or TICI 2B within 8 hours of symptom onset. The DWI lesion reduction (DWI LR) was observed in 6 (10%) patients. In 30 minutes after the tPA, 63% of early recanalization group achieved TICI 2B, and DWI LR was observed in some cases. Early recanalization was related to the DWI LR, dramatic improvement of symptom and good outcome. NIHSS (22 in the LR group, and 16 in the non-LR group) and ASPECTS+W (7 in the LR group, and 8 in the non-LR group) were significantly different in early recanalization group. DWI lesion which disappeared in early phase might regrow between subacute and clonic phase. MR imaging changed dynamically in a short term after the tPA therapy. Early recanalization provides the dramatic improvement of symptom and good outcome, and reduces the DWI lesion of the relatively wide infarction range.

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Background and Purpose: To investigate the association between acute stroke and pseudogout and to identify the clinical characteristics of pseudogout complicated by acute stroke. Methods: We retrospectively analyzed 391 patients with acute stroke and 597 patients with other diseases. We compared the frequency of pseudogout complication and the clinical features of pseudogout between the stroke patients and the non-stroke patients. Results: Of the 391 patients with stroke, 13 developed pseudogout. The frequency of pseudogout in the patients with stroke tended to be higher than that in the non-stroke patients (3.3% and 1.5%, respectively, p=0.08), and likewise in the analysis of the definite or probable cases defined by McCarty criteria for pseudogout, the frequency of pseudogout complication was significantly higher in the stroke patients than in the non-stroke patients (1.8% and 0.3%, respectively, p=0.03). In all the 13 pseudogout patients with stroke, pseudogout occurred when the patients were confined to bed or a wheelchair. Of those patients, four had pseudogout on the hemiparetic side, one had pseudogout affecting both sides, and eight developed pseudogout on the non-paralyzed limbs. Eight of thirteen patients were initially treated with antibiotics before the diagnosis of pseudogout was made since they were first considered as having infections. Conclusion: This study revealed that patients with acute stroke are likely to develop pseudogout, and the arthritis occurs not only on the hemiparetic limbs, but also on the non-paralyzed limbs. Physicians need to recognize the possibility of pseudogout as a cause of fever in patients with acute stroke.

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An 82-year-old woman was presented with left hemiparesis and was admitted to the hospital. The MRI scan revealed acute infarction in the right hemisphere. The MRA scan showed the occlusion of the right middle cerebral artery. Tissue plasminogen activator (t-PA) was administered intravenously to the patient 3.5 hours after the onset of the event. Left hemiparesis improved within 15 minutes of administering t-PA; however, right hemiplegia occurred 55 minutes later. The MRA showed the occlusion of the left middle cerebral artery. Emergent endovascular thrombectomy achieved the recanalization of the left middle cerebral artery. When treating with intravenous thrombolysis, we should prepare for the interventional treatment.

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We report the case of an 84-year-old man with mild confusion and aphasia due to nonconvulsive status epilepticus (NCSE), giving special attention to chronological changes in the magnetic resonance imaging (MRI). The emergent diffusion-weighted imaging (DWI) showed slight hyperintensity, and the apparent diffusion coefficient map (ADC-map) showed decreased diffusion in the left pulvinar and hippocampus, which were the suspicious of acute cerebral infarction. Three days after the onset, DWI showed marked hyperintensity in the ipsilateral pulvinar, hippocampus, amygdala, uncus, and cerebral cortex. ADC-map showed combined decreased and increased diffusion. These signal changes indicated vasogenic and/or cytotoxic edema in the acute phase of NCSE. The arterial spin labeling and MR angiography demonstrated ipsilateral regional hyperperfusion. Follow-up MRI showed partial reversible brain damage. These images may reflect chronological changes in the cerebral edema due to hyperperfusion with NCSE.

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A 49-year-old female was transferred to our hospital with a sudden onset of confusion after headache. The patient was in a severely confused state, and the physical examination revealed tachycardia, tachypnea, fever, abnormal sweating, exophthalmos, and thyroid enlargement. Computed tomography (CT) of her head showed subarachnoid hemorrhage, and laboratory data revealed a high serum level of FT3 and FT4 and a low serum level of thyroid-stimulating hormone. We diagnosed the patient as having a subarachnoid hemorrhage complicated by thyroid storm. We made it a priority to control the thyroid storm and treat the subarachnoid hemorrhage conservatively at first. After the normalization of the thyroid hormone level, we performed surgical clipping. The patient had a favorable outcome. Thyroid storm is a life-threatening disease that requires emergency treatment. The symptoms of thyroid storm resemble those of subarachnoid hemorrhage; thus, the diagnosis of thyroid storm is difficult in the case of coexisting subarachnoid hemorrhage. Emergency surgery for subarachnoid hemorrhage with an oversight of thyroid storm can cause progressive exacerbation of the general condition, with the progression of thyroid storm. In the present case, we could reach a diagnosis of thyroid storm by suspecting Basedow disease based on vital signs and physical examinations. Priority treatment for thyroid storm and an elective surgery for subarachnoid hemorrhage led to a favorable outcome.

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Non-Vitamin K antagonist oral anticoagulants (NOACs) are fewer bleeding complication agents than Warfarin. So NOACs become widely used, but there has no established treatment guidelines for intracranial bleeding patients taking NOACs. We experienced a patient with traumatic acute subdural hematoma who had taken dabigatran etexilate and received craniotomy for the removal of hematoma with the administration of frozen fresh plasma (FFP). An 87-year-old woman was ambulanced to our ER for head injury. She had taken dabigatran etexilate 110 mg 6 hours before head injury and CT scans showed left traumatic acute subdural hematoma. Because her conscious was alert, and she did not have any neurological deficit, we treated conservatively. But 3 hours later after head injury, she developed coma and CT scans showed that the acute subdural hematoma was enlarged. So we performed a craniotomy for the removal of the hematoma with the administration of frozen fresh plasma. Bleeding tendency was not observed during the surgery. Her postoperative course was good and transferred to other nursing facility.

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We investigated the cognitive dysfunction associated with silent brain lesions in community-dwelling elderly subjects. Subclinical brain infarction (SBI) and chronic kidney disease conferred a risk of vascular cognitive impairment (VCI) or executive dysfunction. The physical inactivity is a major public health problem; however, the causative factors for the physical inactivity per se are poorly understood. We showed that the deep white matter lesions are one of the major factors that cause apathetic behavior, and that apathy or vascular depression has significant negative effects on the leisure-time physical activity in community-dwelling elderly subjects. Furthermore, the physical inactivity is one of the modifiable risk factors for hippocampal atrophy and Alzheimer disease. Path analysis based on structural equation modeling (SEM) indicated that the direct paths from the leisure-time activity to hippocampal atrophy and from hippocampal atrophy to memory dysfunction were significant. We are unable to infer a causal or temporal association among VCI, physical inactivity, and hippocampal atrophy from the present observational study. Nonetheless, based on the SEM scheme with acceptable model fit indices, we propose a hypothesis that vascular factors (i.e., VCI and vascular depression) would facilitate hippocampal atrophy or Alzheimer disease as a result of the physical inactivity.

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It is well recognized that statin has a possibility of plaque stabilization in coronary and carotid arteries, however, cardiac and cerebral adverse events might occur even in the patients undergoing aggressive statin therapy. Although n-3 polyunsaturated fatty acid (PUFA) such as EPA is reported to be able to reduce the risk of ischemic coronary artery disease, it remains unclear about the effect of n-3 PUFA on the carotid artery disease. In the current study, we analyzed the correlation of atherosclerosis-related factors and plaque vulnerability based on MRI black blood technique in carotid artery stenotic patients with normal LDL-C. As a result, most of the patients with carotid vulnerable plaque had a low blood ratio of eicosapentaenoic acid to arachidonic acid (EPA/AA ratio) of less than 0.4, and predominantly intraplaque hemorrhage in the affected carotid artery. Moreover, oral uptake of EPA 1,800 mg/day for 45 days (median) was able to stabilize specifically intraplaque hemorrhage through the upregulation of the EPA/AA ratio. Taken into consideration that our previous study demonstrated the combined oral administration of EPA and rosuvastatin leads to a beneficial effect on plaque composition of both intraplaque hemorrhage and lipid-rich necrotic core (Surg Cereb Stroke 41: 39–45, 2013), it is suggested that the mechanism of stabilization of carotid vulnerable plaque may be different between EPA and statin.

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It has been reported that cryptogenic ischemic strokes comprise about 25% of all ischemic strokes and considered that most cryptogenic strokes are thromboembolic. The causes of cryptogenic ischemic strokes are minor risk potential thromboembolic sources such as minor risk potential cardioembolic sources, convert paroxysmal atrial fibrillation, cancer-associated, arteriogenic emboli and paradoxical embolism. Advances in imaging techniques and improved understanding of stroke pathophysiology elucidate the causes of cryptogenic strokes, which however depend on the extent of diagnostic evaluation, making the definition of cryptogenic ischemic stroke to be vague and leading advances of its clinical research to be impeded. Embolic strokes of undetermined source (ESUS) recently are proposed, which are defined as a non-lacunar infarction without proximal arterial stenosis or cardioembolic sources. The definition of ESUS is distinct and a therapeutically relevant entity, comparing to cryptogenic strokes. Here we are going to deliberate the meaning and advantage of the rather simple definition of ESUS.

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Infective endocarditis (IE) has several complications, especially cerebrovascular disease which is the most common complication. Ischemic stroke occupies more than half of all neurological complications, and hemorrhagic stroke accounts for 6–18%. Stroke mainly occurs in the initial stage of IE, and ischemic stroke often develops as a first symptom of IE. The majority of cerebral infarctions is detected in the territory supplied by the cerebral cortical branches, and intracerebral hemorrhages are frequently found with multiple hematomas in the subcortical region. In the IE patients without stroke, asymptomatic infarctions, asymptomatic hemorrhages or both are often detected on magnetic resonance imaging or computed tomography. Stroke more frequently develops in the IE with Staphylococcus aureus to compare with in that with other types of the bacteria, and the size of vegetation detected on echocardiography is significantly associated with a risk of stroke.

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Atrial fibrillation (Af) can be the strongest risk of embolic stroke. Recently, some of the embolic strokes, which showed no embolic source such as Af or atherothrombotic lesion, have been focused on embolic stroke with undetermined source (ESUS). Although the guidelines recommend antiplatelet medication for the treatment of ESUS, clinical trials have been conducted to evaluate the effectiveness of anticoagulants against antiplatelets for ESUS. Therefore, we investigated the difference of outcome of patients between embolic stroke with and without Af, and both were treated with oral anticoagulants after acute ischemic stroke. The results reveal that the prevalence of risks was not different between patients with Af and without Af. The neurological deficit at onset was milder in patients without Af compared with persistent Af patients. The cumulative rate of ischemic stroke recurrence in 1 year was the same between patients with Af and without Af. The cumulative rate of adverse events (any death, brain hemorrhage and stroke recurrence) was lower in patients without Af compared with persistent Af patients. In conclusion, Af negative patients showed a milder neurological deficit at onset and better outcome compared with persistent Af patients, under the treatment of anticoagulants. These findings may suggest the existence of differences of pathological backgrounds between two stroke subtypes.

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