Background and Purpose: The efficacy of thrombectomy in patients showing extensive signal hyperintensity on diffusion-weighted magnetic resonance imaging has not been established. We evaluated outcomes of thrombectomy in patients with a low diffusion-weighted imaging-Alberta stroke program early computed tomography score (DWI-ASPECTS). Methods: Among 167 patients who underwent thrombectomy at our hospital between January 1, 2015 and August 31, 2018, we enrolled 21 patients with a preoperative DWI-ASPECTS ≤ 5. Results: Preoperative DWI-ASPECTS was 2 in two, 3 in seven, 4 in five, and 5 in seven patients. Based on magnetic resonance angiography, vascular occlusion sites were the internal carotid artery in 14 patients and the middle cerebral artery in seven. Modified Rankin Scale (mRS) at discharge was 0 in two patients, 1–4 in one patient each, 5 in 11 patients, and 6 in four patients. When background factors were compared between patients with favorable outcomes (mRS 0–2) and those with unfavorable outcomes (mRS 3–6) at discharge, significantly fewer patients in the favorable outcome group showed signal hyperintensity in the M5 segment (favorable, 25%; unfavorable, 94.1%; P = 0.012) and occluded internal carotid artery (favorable, 0%; unfavorable, 82%; P = 0.006). Conclusion: After thrombectomy for acute cerebral infarction, outcomes at discharge were frequently unfavorable in patients with preoperative DWI-ASPECTS ≤ 5. To perform thrombectomy in patients with low DWI-ASPECTS, predictors of postoperative prognosis must be clarified.

The factors that affect the induction and progress of painful hemiplegic shoulder (PHS) in stroke patients with hemiplegia were examined in this retrospective cohort study. Our study included stroke patients with hemiplegia who underwent rehabilitation in our recovery phase rehabilitation ward. Age, sex, PHS, shoulder subluxation, paralysis side, paralysis degree of upper limbs and fingers, motor function, and activities of daily living ability were evaluated at the time of entering the ward and discharge. In our logistic regression analysis, only the degree of paralysis of the upper limb was extracted as a factor that affected the induction of PHS. Additionally, the degree of paralysis of the upper limb was worse in patients whose PHS persisted than in patients who recovered. Our results suggest that PHS might occur and remain, regardless of shoulder subluxation, in stroke patients with severe hemiplegia.

Background and Purpose: The aim of this study was to investigate the frequency of low skeletal muscle mass in acute ischemic stroke patients and to clarify the factors associated with them. Methods: We enrolled 122 patients with ischemic stroke within 48 h of onset between April 2017 and December 2018. Skeletal muscle mass was measured by bioelectric impedance analysis. We defined low skeletal muscle mass as skeletal muscle mass index <7.0 kg/m² in men, and <5.7 kg/m² in women. Results: Low skeletal muscle mass was evident in 82 patients (67%). Multivariate logistic regression analysis showed that age >77 years (odds ratio 3.8; 95% confidence interval 1.271–11.081, p = 0.017), past history of stroke (3.7; 1.080–12.686, 0.037), and body mass index <23.5 kg/m² (11.6, 4.023–33.186, <0.001) were independent factors associated with low skeletal muscle mass. Conclusions: Approximately 70% of acute ischemic stroke patients had low skeletal muscle mass, and older age, past history of stroke, body mass index <23.5 kg/m² were associated with low skeletal muscle mass.

We report a case of subarachnoid hemorrhage during chemotherapy with ramucirumab. A 64-year-old man who had a history of colon cancer treated with ramucirumab, an inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), was admitted to our hospital because of vomiting and disturbed consciousness. CT images showed a subarachnoid hemorrhage (SAH) in the left Sylvian fissure, and CT angiography showed a left middle cerebral artery (MCA) aneurysm. The diagnosis was an SAH due to a ruptured left MCA aneurysm. Because the side effects of ramucirumab include delayed skin healing and an increased risk of bleeding, the patient underwent coil embolization of the ruptured aneurysm rather than direct surgery. Postoperatively, he experienced a disturbance of consciousness, right hemiparesis and aphasia. MRI performed on postoperative 6 days showed multiple cerebral infarctions. Gradually his symptoms improved. He was discharged 53 days later after onset with a good clinical outcome (modified Rankin Scale, 0). We must carefully consider the best way to treat SAH during chemotherapy with an inhibitor of VEGFR and prepare for adverse events.

We used contrast-enhanced ultrasonography (CEUS) and volume isotropic turbo spin-echo acquisition (VISTA) to diagnose two cases of symptomatic, radiation-induced carotid stenosis (RCS). Because the lesions were high-grade, carotid ultrasonography (CUS) were not effective. Case 1: A 73-year-old man was diagnosed with RCS-induced infraction by VISTA after 2 years. Clopidogrel and rosuvastatin were administered. Case 2: An 82-year-old man was diagnosed with RCS-induced transient ischemic attack using CUS, three-dimensional computed tomography and angiography; cilostazol was administered. Follow-up with CUS was not performed, and recurrence was observed 2 years after diagnosis. The lesion was confirmed using CUS and cerebral angiography, and clopidogrel and rosuvastatin were administered. Follow-up using CUS and VISTA were conducted, and no recurrence was observed after 2 years. Two cases were examined using CEUS and VISTA, these are concluded to be useful techniques for diagnose of patients with RCS.

Congenital afibrinogenemia, which is one of the coagulation disorders, is an autosomal recessive inherited hemorrhagic disease. Incidence of this disease is extremely rare. We report a case of afibrinogenemia-related intracerebral hemorrhage and discuss about characteristics and management of this clinical situation. A 46-year-old male patient was followed up for congenital afibrinogenemia at our department of hematology. He was taken to the emergency department of a local hospital by ambulance because he had headaches and numbness of the whole body from 2 days ago. Although CT scan showed intracranial hemorrhage, he was thought necessary for intensive care, because of congenital afibrinogenemia, and was transferred to our hospital. CT scan showed a subcortical hematoma in the right parietal region and subarachnoid hematoma in the left fronto-temporal region. Result of his blood test shown as the following: PT-INR ≥ 10, APTT ≥ 360 s, fibrinogen < 30 mg/dL. He developed consciousness level reduction and appeared anisocoria with left hemiparesis. He underwent craniectomy and external decompression on the right frontotemporal area, and hematoma removal for the subcortical hemorrhage with fresh frozen plasma (FFP) transfusion. He had no postoperative hemorrhage in the perioperative period with FFP transfusion and fibrinogen administration. There are currently no definitive guidelines for the perioperative management of patients with congenital afibrinogenemia in a case of intracerebral hemorrhage. We found that it is necessary to control the fibrinogen value >50 mg/dL in the case of surgery for intracerebral hemorrhage, as other major surgery.

We herein report a 68-year-old male who had atrial fibrillation and was under anticoagulation with rivaroxaban at a dose of 15 mg/day. The baseline serum creatinine level was approximately 1.0 mg/dl. He developed urinary retention, and serum creatinine level was mildly elevated to 1.25 mg/dl (estimated creatinine clearance, 58.9 ml/min). Anticoagulation with rivaroxaban was not withdrawn. Two days later, he presented with suddenly impaired consciousness and was admitted to our institute. On admission, he had fever and left hemiparesis and head computed tomography revealed a right thalamic hematoma of 3.7 cm with intraventricular extension. Anticoagulation with rivaroxaban was discontinued. Serum creatinine level reached 2.88 mg/dl (estimated creatinine clearance, 27.9 ml/min) and pyuria was evident. Abdominal computed tomography revealed right hydronephrosis with a ureteral calculus and an atrophic left kidney. Antimicrobial therapy was effective, and the calculus was spontaneously excreted. The serum creatinine level improved to 0.94 mg/dl. Anticoagulation was resumed with edoxaban at a dose of 60 mg/day on day 16 after admission and the patient has remained stroke-free for 1 year. We assumed that acute kidney injury had led to elevated blood rivaroxaban level that had resulted in the intracerebral hemorrhage. When patients develop any symptom or sign suggesting renal dysfunction when under therapy with direct oral anticoagulant (DOAC), renal function should be monitored frequently and reduction of the DOAC dose or withdrawal of this agent must be considered.

The Angio-Seal^® (St. Jude Medical, St. Paul, MN) is a vascular closure device that is used to achieve hemostasis of a femoral arterial puncture site after endovascular procedures. This device is easy to use, enables an early start to walking, and decreases the length of hospital stay. However, it can rarely cause lower-limb ischemic complications. We used an Angio-Seal^® to achieve hemostasis after carotid artery stenting, but part of the collagen sponge entered the femoral artery despite correct usage. Surgical removal was performed on the same day. The femoral artery had mild stenosis and its diameter was around 5 mm. We made a tube model that reproduced mild stenosis and confirmed that the anchor of the Angio-Seal^® was caught in the stenosed portion and the collagen sponge strayed into the vessel. If a vascular wall irregularity exists and the diameter of the femoral artery is around 5 mm, clinicians should be aware of this possible complication. If lower-limb ischemia is suspected, rapid diagnosis and treatment will contribute to lower-limb preservation.

Thalamic pain, which is primarily located in the face, is highly refractory, and there are few reports of effective medical and surgical treatments. Four months following a small infarction in the right thalamus, the patient felt severe burning pain on the left side of his face (V1–3 region, especially V2). The pain did not alleviate with medical treatment, and eventually operative treatment was performed at the urge of the patient. First, an electrode was inserted into the spinal epidural space of the superior cervical vertebrae to stimulate the trigeminal spinal nucleus. This test stimulus was only partly effective in that paresthesia was limited to an area from the mandible downward to the neck. Next, thalamotomy was planned, but no response was noted on stimulation of the face in response to somatotopy by electrical stimulation targeting the vicinity of the infarct lesion. After changing the target area to the small infarct lesion for reconstruction of the neural circuit and then performing coagulation, the patient's pain symptoms were dramatically ameliorated. This pain-relieving effect has persisted for more than two and a half years after the procedure.

A 68-year-old man presented with acute cerebral infarction. At the time of admission, computed tomography angiography showed occlusion and anomalous reticular collateral artery only in the right M1 part of the middle cerebral artery (MCA) and there was no stenosis or occlusion in the terminus of the internal carotid artery. The patient was diagnosed with an aplastic or twig-like MCA. We planned superficial temporal artery-MCA anastomosis with low cerebrovascular reservation in the right MCA area. However, the patient developed right thalamic hemorrhage while waiting for the operation. A small aneurysm was present in collateral circulation. The rupture of this aneurysm or collateral vessels was suspected as a source of bleeding and antiplatelet agents introduced after cerebral infarction was also thought to be an influence. In this case, bypass surgery was performed, considering that improvement of hemodynamic cerebral ischemia is effective in preventing rebleeding. In the postoperative follow up, the aneurysm and collateral arteries disappeared and no cerebrovascular event occurred in 26 months.

We report our experience of great vein of Galen thrombosis after treatment consisted of Factor XIII (F XIII) concentrate. A 76-year-old woman presented with subarachnoid hemorrhage (SAH) caused by ruptured anterior communicating artery aneurysm and was successfully treated with direct surgery. Four days after operation, she was awake but presented with cerebrospinal fluid rhinorrhea and was found to be F XIII deficiency, therefore we performed intravenous injection of F XIII concentrate. Sixteen days after operation, she became drowsy without cerebrovascular spasms and hydrocephalus. CT angiography and digital subtraction angiography demonstrated the obstruction of great vein of Galen. She received the treatment with low-molecular-weight heparin (LMWH) and after that, direct oral anticoagulants (DOAC). The patient responded to the treatment, and followed an uneventful course without developing any hemorrhagic complication. To the best of our knowledge, this is the first case of cerebral venous thrombosis after the treatment of F XIII concentrate. The thrombosis can be attributed to the treatment of F XIII concentrate, and would be better served by treatment with LMWH and DOAC.