It is important to detect non-convulsive seizures in the treatment of critically ill children in ICU. Acute encephalopathy with biphasic seizures and late reduced diffusion (AESD) is characterized by a febrile status epilepticus as the initial neurological symptom, followed by secondary seizures and subcortical white matter edema at day 4 to 6. As MRI shows no acute abnormality at the onset, EEG is useful to distinguish AESD from febrile status epilepticus in early stage. Recently therapeutic hypothermia is applied as a treatment of AESD, and continuous EEG monitoring during the therapy is also important. Amplitudeintegrated EEG (aEEG) and dense spectral array (DSA) are useful for the identification of non-convulsive seizures in long-term EEG monitoring in ICU.

To evaluate the role of a comprehensive stroke center in community medicine, the achievements of a stroke emergency care system at our institute and the Yokohama City Bureau were reviewed. The Yokohama-shi Cerebrovascular Disease Emergency Care System was developed in 2008 in cooperation with the City Medical Bureau, emergency services, and thirty participating medical institutions. This system specialized in stroke care and treated the patients suspected of having acute stroke based on assessments made by emergency services. After being transferred to participating hospitals, 3-400 patients in the whole city area per year were diagnosed as having an acute brain infarct and were treated with alteplase for thrombolysis. From April 2016 to March 2017, our institute treated 22 patients with thrombolysis out of 127 hospitalized stroke patients through stroke hot line from emergency service. Our stroke hot line is connected to the Yokohama-shi Cerebro-vascular Disease Emergency Care System and is clinically informative, particularly for intensive therapy of acute brain infarcts. However, many non-stroke patients have been encountered through the stroke hot line, and some true stroke patients have conditions mimicking general emergency diseases. To avoid clinical errors which are pitfall so-called, neuro-emergency specialists must have a broad unbiased diagnostic perspective.

Acute stroke is the leading cause of morbidity and mortality. The emergency medical technicians (EMTs) must confirm acute stroke rapidly at the scene and transport these patients to the applicable medical facilities for treatment. Acute stroke presents with neurologic deficits, and many conditions may present with stroke-like symptoms, known as stroke mimics. This study aims to analyze the characteristics of stroke mimics affecting prehospital identification transported to Wakayama Medical University by helicopter emergency medical service during 7.5 years. Totally 349 patients were identified as potential strokes by EMTs, of which 284 (81.4%) had a definitive diagnosis of acute stroke, and 65 (18.6%) were stroke mimics. Epileptic Seizure was the most likely to be misdiagnosed as acute stroke. While all cases of acute stroke required admission to hospital, 10 patients of stroke mimics needed no hospitalization due to dramatic symptomatic recovery. The major symptoms of stroke mimics judged as acute stroke by EMTs were consciousness disturbance, hemiparesis, eye deviation. In these cases, there were 5 cases of the ipsilateral hemiparesis with eye deviation following seizure. Overtriage for potential strokes by EMTs should be acceptable. However, follow-up medical inspection is educationally important for EMTs to improve the quality of prehospital emergency care.

Guillain-Barré syndrome (GBS) is an autoimmunological demyelinating polyneuropathy that may occur after a traumatic event. We describe a case of suspected GBS following a traumatic brain injury. A 49-year-old man was transferred to our hospital after a motor cycle accident. On arrival, his consciousness level was GCS 14 and he had no motor weakness. Head CT revealed left acute subdural hematoma, cerebral contusion and traumatic subarachnoid hemorrhage. Conservative treatment was chosen, but right upper and lower limb weakness developed and his consciousness level worsened. Hematoma removal and craniotomy were performed 2 days after the trauma. The postoperative course was uneventful and the patient was extubated 3 days after the operation. However, respiratory failure, hypoxemia and circulatory disorder developed 3 days after the extubation, with accompanying loss of the deep tendon reflex and bilateral limb weakness. Neuromuscular disorder was suspected, and a spinal tap and motor conduction test revealed cyto-albuminological dissociation and axonal peripheral polyneuropathy. GBS was diagnosed and intravenous immunoglobulin was started 20 days after the trauma. The patient was weaned from the ventilator on the next day, and cerebrospinal fluid findings and clinical symptoms recovered gradually. He was discharged 6 months after the accident. The correct diagnosis of GBS in this case contributed to recovery of the patient.

Simultaneous onset of ruptured intracranial and intra-abdominal aneurysms are rare. We report the case of a patient who suffered from a subarachnoid hemorrhage (SAH), coexisting intra-abdominal hematoma. A 51-year-old man was transferred from another hospital for consciousness disturbance with hemodynamic instability. The contrast computed tomography (CT) showed SAH caused by the left ruptured vertebral artery dissecting aneurysm and intraabdominal hematoma caused by the ruptured posterior superior pancreaticoduodenal artery aneurysm. On CT examination of abdomen with contrast, another finding of the compression of celiac artery by midline arcuate ligament in were revealed. He was diagnosised with median arcuate ligament syndrome. Transcatheter arterial embolization (TAE) of the ruptured posterior superior pancreaticoduodenal artery was first attempted to control the bleeding. After successful of abdominal hemostasis was achieved by TAE, a coil embolization with stent combination was performed for the left ruptured vertebral artery dissecting aneurysm. He was transferred to a rehabilitation hospital at modified rankin scale 1 after treatment. We should be considered the possible of the coexisting of intra-abdominal hematoma for severe SAH with hemodynamic instability.

Introduction: We reported a case of primary central nervous system lymphoma after craniotomy for organized chronic subdural hematoma. Case: A 62-year-old man. History: The patient was diagnosed with chronic subdural hematoma in a neurosurgical clinic 10 years ago. Six years ago, head magnetic resonance imaging (MRI) was performed in our hospital and he was diagnosed with organized chronic subdural hematoma, but there was no intervention. He presented with right paralysis and was transported to our hospital. On physical examination, consciousness was clear and right upper and lower limb was mildly paralyzed. Based on head computed tomography (CT) and MRI results, he was diagnosed with organized chronic subdural hematoma. Because his symptoms were mild and not representative of acute onset hematoma, he was started on tranexamic acid and had scheduled follow-ups in the outpatient clinic. Two months later, he experienced a seizure and was transported to our hospital. Course: The cause of seizure was judged to be organized chronic subdural hematoma; craniotomy was performed. Size of the organized hematoma decreased, and pathological examination did not show any malignant findings. He was transferred for rehabilitation 2 months after craniotomy. He continued rehabilitation but his consciousness level declined; thus head MRI was performed 6 months after craniotomy. A tumor mass lesion in the cerebral hemisphere was suspected; he was admitted to our hospital. We suspected a primary brain tumor and performed craniotomy. Pathological examination showed malignant lymphoma diffuse large B-cell type. We started chemotherapy, but he died after 4 months. Conclusions: Organized chronic subdural hematoma with long term hematoma can cause malignant lymphoma and requires caution.

Background: Cervical level posterior spinal artery infarction is very rare among spinal cord infarcts. Case: The patient was a 69-year-old male with paroxysmal atrial fibrillation and high blood pressure under treatment with oral apixaban, pilsicainide and azilsartan. He became aware of numbness and movement disorder of the left arm, and visited our hospital. He presented with Horner syndrome; hypoesthesia of the left anterior chest, left face and left upper limb; mild motor paralysis; and deep sensory disturbance of the left upper limb. Diffusionweighted MRI showed a high signal on the dorsal medial side at the first cervical level. The diagnosis was cervical posterior spinal artery syndrome. A cerebral angiogram showed no abnormality in surrounding blood vessels, including the posterior spinal artery. Paralysis improved relatively quickly, and sensory disorders improved with a delay. His only risk factor was paroxysmal atrial fibrillation. Discussion: Posterior spinal artery syndrome causes symptoms such as deep sensory disorder, total sensory depletion at the medullary level, and motor paralysis. In this case, we speculate that Horner syndrome manifested due to an effect on the posterior lateral cord. Thus, cerebral infarction in the posterior spinal artery region can have various symptoms and care is needed for diagnosis.

A 42-year-old male patient was admitted to our hospital because of generalized convulsive status epilepticus (GCSE), disturbance of consciousness, and shock. He had cardiopulmonary arrest after arrival our hospital, but he was return of spontaneous circulation as soon as cardiopulmonary resuscitation. He had disseminated intravascular coagulation (DIC) and multiple organ dysfunction. From the time of admission, we managed about the patient's breathing, circulation, body temperature. We also administrated sodium valproate 400mg, levetiracetam 1,000mg daily, and continuous use of midazolam to status epilepticus. In addition, he underwent continuous renal replacement therapy because of acute renal failure. The electroencephalogram showed scattered delta waves. Brain MR images showed hyper-intense lesions at bilateral pallidum and thalami, which led to a diagnosis of hypoxic encephalopathy associated with long-term GCSE. On day 13, he started tracking our fingers with his eyes. On day 34, he was able to obey commands and he was transferred to the general ward. GCSE is known to exhibit various organ dysfunctions. In this case, there was a history of epilepsy and had developed on GCSE, but as a result of the clinical examination, it was considered epilepsy-related organ dysfunction because the cause of multiple organ dysfunction was not clear.

In recent years, brain-dead organ donation has been increasing in Japan, but the number is still extremely low compared to Western countries. To date, we have encountered 8 brain-dead organ donation cases at Hamamatsu Medical Center. To enhance brain-dead organ donation, it is important to develop a sustainable system for the organ donation process rather than employ a temporary approach for an individual case. From this point of view, we intended to share many roles with many doctors and staffs in order to escape excess burden to particular persons. Additionally, we adjusted the schedule of brain death determination and organ donations in order not to disturb routine hospital functions. However, some staffs still took on the heavy burden during these processes. And some problems related to privacy protection appeared. These efforts clarified the importance to share the knowledge accumulated through such experiences.