Background & Purpose: The diagnosis of the causes of sudden death using autopsy imaging has been in practice for many years. However, there are a few reports on autopsy imaging mainly focused on the stroke death. Postmortem CT scan as autopsy imaging in the emergency department reveals the trend in the causes of sudden death and the percentage of the stroke death in our autopsy imaging series. Methods: Postmortem CT scans from the head to the pelvis was conducted in 547 deceased cases between 2012 and 2014. Of them, the police requested postmortem CT scan for 246 cases. Among 337 patients taken by an ambulance as a cardiopulmonary arrest in our emergency department, 301 cases (89%) were conducted postmortem CT scan. Results: In the 547 autopsy-imaging series, 98 cases (18%) were diagnosed with internal death due to the several causes and 112 (20%) were external death. In the other 337 cases (62%), the cause of death could not be detected using postmortem CT scan. Twenty-nine cases (5%) were diagnosed with death from the stroke. Of them, 15 cases were diagnosed with subarachnoid hemorrhage, 13 were intracranial hemorrhage (4, pontine hemorrhage; 3, thalamo-putaminal hemorrhage; 3, subcortical hemorrhage; 1, putaminal hemorrhage; 1, cerebellar hemorrhage; 1, intraventricular hemorrhage), and only one case was diagnosed with large cerebral infarction due to occlusion of the internal cerebral artery. Conclusion: The frequency of stroke death was only 5% in 547 autopsy-imaging series using postmortem CT scan.
Generally, the majority of patients who complain of acute vertigo or dizziness end up being misdiagnosed with peripheral labyrinthine disorders in the emergency room and critical care center. Some patients with cerebellar infarcts are likely to be overlooked if imaging studies are not performed. The usual course of cerebellar infarction is benign; however, it may develop mass effect and cause brainstem compression, acute hydrocephalus, which could result in serious morbidity and mortality. Therefore, it is essential to differentiate cerebellar infarction from peripheral vertigo. However, it is difficult to precisely diagnose a patient who demonstrates isolated vertigo, particularly in an emergency room. Head MRI is required for the final confirmation of the diagnosis; however, some patients with acute stroke show no abnormal signal intensity on diffusion-weighted MR image in acute phase. We analyzed 50 patients with cerebellar infarction and assessed clinical features such as the involved vascular territories of cerebellar infarction. It was found later that 11 cases with cerebellar infarction were misdiagnosed at the initial stage. To distinguish between cerebellar infarction and peripheral vertigo is not always easy. During the examination, careful assessment of truncal ataxia as well as limb ataxia along with repeated examinations of head imaging is indispensable even if the initial CT or MRI does not find anything particularly noticeable.
Purpose and Method: Among nonvalvular atrial fibrillation aged 70 or older, 512 patients (75.5±5.7 years, 198 females) taking warfarin, relationships between the time in therapeutic range (TTR) to target the international normalized ratio of 1.6–2.6, and the occurrence of ischemic or hemorrhagic events were retrospectively investigated. Results: During the total follow-up period of 36,101 months, 60 ischemic events and 30 hemorrhagic events occurred. By multivariate analysis, TTR ≥55.6% were independently associated with ischemic events (hazard ratio, 0.54; 95% CI, 0.30–0.96; p=0.037), but, TTR had no association with hemorrhagic events. Conclusion: The quality of warfarin therapy is negatively correlated with ischemic events independently.
A 76-year-old female was presented to our hospital for consciousness disturbance and severe right hemiparesis that was developed one day before admission during the treatment of urinary infection. Any headache did not precede her neurological symptoms. Electroencephalogram revealed marked low activities in the wide area of the left cerebral hemisphere. Brain MRI revealed high intensity lesions in the left temporo-occipital lobes on diffusion weighted images. MR angiography revealed multiple stenosis on the left middle cerebral artery (MCA) and its branches. Cerebral ischemic injury by stenosis of the left MCA was diagnosed, and intravenous administration of argatroban was started. CT angiography taken the next day revealed the recovery of multiple stenotic lesions, and MR angiography taken 22 days after onset revealed no recurrence of arterial stenosis. Her cerebral ischemia was diagnosed as a reversible cerebral vasoconstriction syndrome (RCVS). She gradually improved and attained complete recovery. She had been suffering from dry mouth since 1 year prior to onset, and serum anti-SS-A antibody was positive. Labial salivary gland biopsy performed 40 days after the onset of RCVS revealed lymphocyte infiltration with foci of aggregation of >50 lymphocytes which were dominated by CD3(+) T-cells. Primary Sjögren syndrome associated with central nervous system (CNS) involvement was diagnosed. The pathophysiology underlying CNS in primary Sjögren syndrome includes the direct infiltration of mononuclear cells, vascular involvement, and small vessel vasculitis. Our case suggests that RCVS can be one of the pathogenic mechanisms for CNS involvement in the primary Sjögren syndrome. Argatroban has been shown to prevent cerebral vasospasm and may have therapeutic potential for RCVS.
A 43-year-old man was presented to our hospital with severe headache and seizures. A neurological examination revealed stupor and mild left hemiparesis. Head CT revealed a fresh infarction in the right parietal lobe and a hyperdensity spot in the posterior superior sagittal sinus (SSS). CT venography revealed the occlusion of the SSS. Since the patient had a history of Basedow disease, we examined the patient for hyperthyroidism, coagulation, and fibrinolytic system. His thyroid stimulating hormone (TSH) receptor antibody and thyroid stimulating antibody levels were found to have increased above normal levels (9.6 IU/l and 400%, respectively). The levels of von Willebrand (vW) factor and factor VIII procoagulant protein also showed a marked increase (>200% and 176.5%, respectively). Based on these findings, we made a diagnosis of cerebral venous sinus thrombosis due to Basedow disease. Hyperthyroidism should therefore be considered as a cause of cerebral venous sinus thrombosis. In addition, we should pay close attention to any changes in the levels of vW factor and factor VIII procoagulant protein. By doing so, it is possible to select the optimal treatment in a timely manner and predict the prognosis for patients with cerebral venous sinus thrombosis.
A 83-year-old man with a history of transient ischemic attack (TIA) was referred to our hospital with dysarthria, left-sided facial palsy, and weakness of the left arm. For the secondary prevention of ischemic stroke, warfarin was administered because he had non-valvular arterial fibrillation. Magnetic resonance imaging of the brain revealed multiple infarctions at the right middle cerebral artery. Carotid ultrasonography revealed severe stenosis at the right internal carotid artery with a mobile structure. After administration of combined antithrombotic therapy with dabigatran and aspirin, repeated carotid ultrasonography revealed serial reduction of the mobile structure, and disappeared on day 66. On day 101, the right internal carotid artery successfully underwent carotid artery stenting. After 1 year, neither recurrence of ischemic stroke nor new mobile structures had been noted. These findings allowed us to diagnose the mobile structure as thrombus. This case suggests that combination therapy with non-vitamin K oral anti-coagulant and aspirin is an appropriate therapeutic option for mobile plaques on carotid artery stenosis in patients with non-valvular arterial fibrillation.
It is believed that the development of cerebral vasospasm is unlikely after minor blood leakage and subarachnoid hemorrhage. Additionally, it is quiet common that cerebral vasospasm occurs at a high rate in double hemorrhage and vasospasm models based on animal experiments. We diagnosed a case of delayed diagnosis of subarachnoid hemorrhage in a 37-year-old man. He experienced two episodes of severe headache that was suspected to have resulted from minor blood leakage. Additionally, he developed cerebral infarction in the left middle cerebral artery territory caused by cerebral vasospasm. On admission, he had cerebral infarction with dysarthria and right hemiplegia. On magnetic resonance imaging (MRI), the infarction at the perforating branch of the left anterior choroidal artery was identified, and on magnetic resonance angiography, cerebral vasospasm at the left middle cerebral artery was identified. Additionally, an aneurysm was detected in the left internal carotid artery on angiography of the posterior communicating artery bifurcation. Initially, subarachnoid hemorrhage was not identified on head computed tomography. A fluid attenuation inversion recovery MRI image of the head showed a small hematoma in an ambient cistern. Clipping surgery was performed 16 days after the second headache. Intraoperatively, the left Sylvian fissure was covered with a thick arachnoid membrane that indicated xanthochromia. We performed clipping of the ruptured aneurysm in the left internal carotid artery at the posterior communicating artery bifurcation. After rehabilitation, the patient was able to walk independently and discharged. This case study indicates the possible occurrence of cerebral vasospasm after double hemorrhage, even with minor blood leakage.
In this article, a rare occurrence of a ruptured cerebral aneurysm complicated by glycogen storage disease (GSD) type 1a has been reported. A 34-year-old woman who suffered from GSD type 1a presented with a sudden disturbance in consciousness and left hemiparesis presented to the hospital. The computed tomography (CT) imaging of the patient revealed subarachnoid hemorrhage due to the rupture of a right middle cerebral artery saccular aneurysm. Neck clipping of the ruptured aneurysm was performed on the day of symptom onset. As an excessive brain swelling was encountered during the surgery, the external decompression was performed. During and post-surgery, intensive medical treatment was provided, especially for preventing hypoglycemia and metabolic (lactic) acidosis. The disturbance in consciousness and left hemiparesis gradually improved. Three months after the surgery, the patient was able to walk with a cane. GSD type 2 is known to manifest as cerebral arterial disorders, including aneurysms. However, to the best of our knowledge, there are no reports on concurrent GSD type 1a and cerebral aneurysms in the literature. Regarding the pathogenesis of the cerebral aneurysm in this case, the authors speculate that hyperlipidemia and hyperuricemia associated with GSD type 1a may have contributed to the formation of the aneurysm through atherosclerosis or inflammation in the arterial wall. The lactic acidosis during and after the clipping surgery may have contributed to excessive brain edema. Providing intensive care to control blood glucose levels and to avoid metabolic acidosis is thought to be important for preventing secondary cerebral damages, especially in the perioperative period.
Apraxia shows various serious effects on the activities of daily living. Although a few reports about apraxia have already been published, establishing rehabilitation methods to solve the effects of apraxia is difficult because of the variety and complexity of the symptoms. We examined the rehabilitation of an 82-year-old woman with ideational, ideomotor, and limb-kinetic apraxia, as well as very mild motor paralysis with moderate sensory disturbance in her right-side extremities due to atherothrombotic brain infarction in the left temporo-parietal lobe. Our focus was on her performance of eating with a spoon and fork using her right hand. During the training, we initially recommended her to use the spoon and fork with her left hand. Consequently, she was asked to use them with her right hand. After repetition of this task without error, she was finally able to eat perfectly with a spoon and fork using her right hand. The mechanism of this improvement may be due to the sensory abilities of her left hand covered with the sensory disturbance of her right hand. Use of the left hand may lead to the recognition of errors, access to manipulation/conceptual knowledge, and initiation of the correct motor program for use of the fork and spoon, resulting in accelerated motor learning and improved the use of the spoon and fork with the right hand.
Reversible cerebral vasoconstriction syndrome (RCVS) typically affects the bilateral medium-sized intracerebral arteries and their branches. We describe a woman with RCVS restricted to the ipsilateral hemisphere after carotid artery stenting (CAS). A 74-year-old woman presented with headache and left-sided weakness 17 days after undergoing right CAS. MR imaging showed borderzone infarcts and catheter-based angiography identified new irregularities of the right anterior cerebral and right middle cerebral artery. A follow-up angiography after about a month showed complete resolution of the cerebral arterial vasoconstriction. These results suggest that RCVS may occur after CAS. The mechanism is unclear, however, it may be due to the disturbance of cerebral autoregulation.
An 84-year-old man who had been administered anticoagulants after a previous transient ischemic attack associated with non-valvular atrial fibrillation (NVAF) was referred to our hospital with epigastric pain, dysphagia, and hoarseness. These complaints appeared after changing the anticoagulant regimen from warfarin to dabigatran. Upper gastrointestinal endoscopy revealed esophageal mucosal injuries with the pathological finding of erosion. His symptoms improved within a day of switching anticoagulation medication from dabigatran to apixaban without a proton pump inhibitor. Three months after the switch to apixaban, a second upper gastrointestinal endoscopy showed clear improvement of the esophageal mucosal injuries. These findings allowed us to diagnose “dabigatran-induced esophagitis”. A small number of case reports have described dabigatran-induced esophagitis, but none have provided the details of subsequent anticoagulation therapy with another non-vitamin K antagonist oral anticoagulant. We thus demonstrate that switching medication from dabigatran to apixaban may offer an effective choice with minimum risk of embolism for NVAF patients who cannot take dabigatran because of digestive symptoms.
Case: A 38-year-old woman had an intraventricular hemorrhage and was diagnosed with parasplenial arteriovenous malformation (AVM) of Spetzler-Martin grade I. V. After embolization with N-butyl-2-cyanoacrylate, Gamma Knife treatment was performed. One year and 7 months later, the patient had a second intraventricular hemorrhage. Cerebral angiography performed 3 months later showed an intranidal aneurysm, and contrast-enhanced magnetic resonance imaging (MRI) showed enhancement of the wall of the intranidal aneurysm. The patient had a third intraventricular hemorrhage 5 months after the second hemorrhage. After Onyx embolization, craniotomy and resection were performed. Conclusion: The incidence of hemorrhage in patients with AVM is higher in those with aneurysms than in those without. Intravascular therapy and radiation therapy are effective in reducing the nidus in patients with parasplenial AVMs with an intranidal aneurysm projecting towards the ventricle. However, strict follow-up is needed because of the higher risk of rebleeding into the ventricle. We could evaluate intranidal aneurysm within the ventricle using contrast-enhanced MRI. In this regard, frequent examination is important for assessing the risk of aneurysm enlargement and bleeding.
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