Subcortical Hemorrhage Research Articles

Prophylactic Administration of Perampanel for Post-Stroke Epilepsy (PROPELLER Study): A Trial Protocol.

Post-stroke epilepsy can reduce patients' abilities to carry out various activities of daily living. Despite their importance in preventing the onset of post-stroke epilepsy, the prophylactic administration of antiepileptic drugs is controversial due to a lack of high-level clinical research. In this study, we initiated a prospective interventional study of prophylactic antiepileptic drug administration in patients with a subcortical hemorrhage, who are at the highest risk of developing epilepsy after experiencing a stroke. The study was conducted in a single-center setting and was a single-arm study with no control group; the case entry period started in November 2023 and is due to end in March 2025. Only cases with a subcortical hemorrhage will be included. The treatment regimen used in this study is 2 mg of perampanel per day. Perampanel will be administered for one year, followed by two years of follow-up, for a total study period of three years. The primary endpoint will be the development of epilepsy. Perampanel administration is expected to reduce the incidence of post-stroke epilepsy in comparison to the results of previous reports on the use of alternative treatments. The results of this study will provide new insights into the prevention of post-stroke epilepsy. The relatively small size of this study makes it difficult to provide strong evidence of the efficacy of perampanel, but it may serve as a basis for larger clinical trials.

Delayed levodopa-responsive parkinsonism following acute midbrain injury

Acute midbrain injury may cause both hyperkinetic movement disorders and parkinsonism. The temporal interval between the insult and the emergence of hyperkinetic disorders can last years. A delayed appearance of parkinsonism, on the other hand, was rarely described. We present three cases of male patients (50-, 58- and 28-year-old) who developed levodopa-responsive parkinsonism 20, 8 and two years, respectively, after acute brain insult involving the midbrain. Insults included subcortical intracerebral hemorrhage dissecting into the midbrain, embolic basilar occlusion and trauma. A fluorodopa scan, performed in two cases, revealed reduced striatal uptake. All individuals improved on low doses of levodopa and developed motor fluctuations shortly after levodopa was introduced. We conclude that delayed, levodopa-responsive parkinsonism following midbrain injury should be recognized in the relevant clinical setup. Possible mechanisms include age-related loss of dopaminergic neurons superimposed on acute injury and secondary neurodegeneration.

Prolonged hiccups induced by renal infarction: a case report

BackgroundHiccups are common symptoms that last for less than 48 hours. However, we encountered a case of renal infarction in a patient with prolonged hiccup. The relationship between hiccups and renal infarction is important in differentiating patients with prolonged hiccups.Case presentationAn 87-year-old Japanese man with atrial fibrillation and receiving antithrombotic therapy presented to the emergency department with prolonged hiccups. The patient discontinued antithrombotic therapy for atrial fibrillation due to subcortical bleeding, after which he experienced right back pain. He was diagnosed with right renal infarction based on computed tomography images, and the antithrombotic therapy was continued. The patient’s hiccups ceased, and he was discharged on hospital day 11.ConclusionHiccups can be induced by various clinical conditions. It is hypothesized that the inflammation of the right kidney infarction stimulated the diaphragm and induced prolonged hiccups in this patient; this theory is supported by the computed tomography images. This case report shows that internal organ diseases irritating the diaphragm can cause hiccups, and renal disease should be considered in patients with prolonged hiccups.

Isolated prosopagnosia caused by damage to the right inferior longitudinal fasciculus: a case report.

Prosopagnosia is a cognitive disorder in which facial recognition is severely impaired despite normal vision and intelligence. Prosopagnosia was first reported in the 1800s, but its cause remains unclear. Although other neurological symptoms are often present, some patients have pure prosopagnosia. The bilateral occipital lobes are believed to be associated with symptoms. Recent brain imaging techniques have identified the right fusiform gyrus (rFG), located at the junction of the right occipital temporal lobe, as the affected region. In this report, we present a case of associative prosopagnosia with no concomitant symptoms in a 76-year-old man. Brain magnetic resonance imaging detected a subcortical hemorrhage in the right temporal lobe. Using tractography based on diffusion tensor imaging, we visualized atrophy of the right inferior longitudinal fasciculus (ILF). This is the first time tractography has been used to show a clear association between associative prosopagnosia and ILF damage projecting from the rFG.

10214-COT-24 A RARE CLINICAL CASE OF LUMBAR METASTASIS FROM GLIOSARCOMA

Abstract Gliosarcoma (GS) is a variant of glioblastoma (GBM) and has been shown to be prone to extracranial metastasis. We report a rare case of lumbar metastasis of Gliosarcoma (GS) based on histopathological findings.37-year-old male.He underwent emergency surgery for a left frontal subcortical hemorrhage. Pathological diagnosis confirmed GS. Postoperatively, the patient underwent conventional radiation chemotherapy. Later, in conjunction with cranioplasty, the remaining lesion was additionally excised and maintenance therapy was administered for 9 months. Subsequently, a follow-up MRI revealed an intracranial disseminated lesion, although the primary site was not affected. At the same time, he had difficulty moving due to back pain, and MRI revealed extracranial metastases in the second lumbar vertebra and retroperitoneum. Lumbar biopsy confirmed the diagnosis of metastasis. Pathological findings at the initial surgery showed that the tumor consisted of GS and gemistocyte-like components, and immunostaining and genetic findings showed IDH wild type GBM. Additional tissue samples showed predominantly gemistocyte-like components and no GS component, and the genetic profile was similar.Lumbar biopsies showed predominantly GS and no gemistocyte-like components. MGMT methylation changed from methylation-negative to positive and then negative by immunostaining and MS-PCR. In a previous report, Feldheim et al. performed a meta-analysis of MGMT methylation changes in relapsing GBM and reported increased methylation after relapse. In addition, Jimenez et al. quantitatively analyzed MGMT methylation in recurrent GBM by pyrosequencing and found an increased rate of methylation in about half of the cases. These reports indicate that MGMT methylation is altered following therapeutic intervention. In the present case, it was hypothesized that an intracranial lesion that was initially unmethylated was methylated by the intervention, but an unmethylated, treatment-resistant GS component metastasized to the extracranial space. The clinical course of this case was a rare example of evidence of a change in MGMT methylation due to therapeutic intervention.

Subcortical hemorrhage caused by cerebral amyloid angiopathy compared with hypertensive hemorrhage

ObjectivesMost published reports on lobular hemorrhage in cerebral amyloid angiopathy (CAA) include patients diagnosed only by imaging studies. This study analyzed patients with subcortical hemorrhage histologically diagnosed as CAA or non-CAA (hypertensive). MethodsThis is a retrospective study analyzing data from 100 craniotomy cases. Tissue of hematoma cavity wall was collected for histological investigation in hematoma removal by surgery in patients with subcortical hemorrhage. Statistical analyses of blood pressure, hematoma location and volume, outcome, and mortality was performed in CAA and non-CAA groups. ResultsThere were 47 CAA and 53 non-CAA cases, and average age was significantly older in the CAA group (p < 0.01). Blood pressure was significantly lower (p < 0.01) but hematoma volume was significantly greater (p < 0.05) in the CAA group. Rebleeding occurred in two CAA cases and one non-CAA case, but no re-operations were required. Average score of modified Rankin Scale, which is used to measure the degree of disability in patients who have had a stroke, at three months after surgery was not significantly different between the two groups (CAA: 3.94 ± 1.28, non-CAA: 3.58 ± 1.50). There were seven deaths in the CAA and six in the non-CAA group, and intraventricular hemorrhage highly complicated in the death cases in both groups. In the CAA group, average age of the fatal cases was significantly older than that of the surviving cases (p < 0.05) and six cases demonstrated dementia before onset of hemorrhage. ConclusionsSurgical removal of a subcortical hemorrhage caused by CAA is not contraindicated. However, age > 80 years, complication with intraventricular hemorrhage, hematoma volume ≥ 50 ml, and dementia before onset of hemorrhage contribute to high mortality, and craniotomy should be carefully considered for such patients. A limitation of this study is that comparison between CAA and non-CAA groups was performed in the patients with only surgically indicated ICH, and does not evaluate entire ICH cases with CAA. However, this study appropriately compared pathologically diagnosed CAA and non-CAA in patients with moderate to severe lobular ICH with surgical indications.

Delayed Death Due to Methanol Poisoning: An Autopsy Case Report

Methanol is a non-drinking type of alcohol used for industrial and automotive purposes. Methanol itself is not dangerous, but its harmful metabolites may cause the accumulation of acid in the blood, leading to metabolic acidosis, permanent blindness, and death. In this case report study, the case was a 28-year-old Nepalese man who was admitted in a semi-unconscious state to the emergency department. A working diagnosis of methanol poisoning was made. After more than two weeks, he succumbed to death due to a worsening cerebral infarction. At autopsy, extensive hemorrhagic infarction was observed, involving bilateral cerebral hemispheres. Well-defined subcortical hemorrhages leading to laminar necrosis were seen at the frontoparietal lobes. Cystic or lacunar necrosis was present at the basal ganglia. The brainstem showed the presence of duret hemorrhage. The man died approximately three weeks after the methanol ingestion. This case highlights the important pathological changes and accumulating effects of methanol in the brain.

Secular trends and features of thalamic hemorrhages compared with other hypertensive intracerebral hemorrhages: an 18-year single-center retrospective assessment.

Trends regarding the locations of hypertensive cerebral hemorrhages are unclear. To clarify hypertensive hemorrhage trends, we investigated intracerebral hemorrhages (ICHs) over an 18-year period, focusing on thalamic hemorrhages compared with other sites of hemorrhages. We reviewed the cases of patients hospitalized for hypertensive ICH in 2004-2021 at our hospital; 1,320 eligible patients were registered with a primary ICH/intraventricular hemorrhage. After exclusion criteria were applied, we retrospectively analyzed 1,026 hypertensive ICH cases. The proportions of thalamic and subcortical hemorrhages increased over the 18-year period, whereas putaminal hemorrhage decreased. Multivariate logistic regression analyses revealed that for thalamic hemorrhage, ≥200 mmHg systolic blood pressure (p = 0.031), bleeding <15 mL (p = 0.001), and higher modified Rankin scale (mRS) score ≥ 4 at discharge (p = 0.006) were significant variables in the late period (2013-2021) versus the early period (2004-2012), whereas for putaminal hemorrhage, significant factors in the late period were triglyceride <150 mg/dL (p = 0.006) and mRS score ≥ 4 at discharge (p = 0.002). Among the features of the thalamic hemorrhages in the late period revealed by our group comparison with the putaminal and subcortical hemorrhages, the total and subcortical microbleeds were more notable in the thalamic hemorrhages than in the other two types of hemorrhage, whereas cerebellar microbleeds were more prominent when compared only with subcortical hemorrhages. Our findings revealed an increasing trend for thalamic hypertensive hemorrhage and a decreasing trend for putaminal hemorrhage. The thalamic hemorrhage increase was observed in both young and older patients, regardless of gender. The main features of thalamic hemorrhage in the late period versus the early period were decrease in larger hemorrhage (≥15 mL) and an increase in cases with higher systolic blood pressure (at least partially involved a small number of untreated hypertensive patients who developed major bleeding). The total and subcortical microbleeds were more notable in the thalamic hemorrhages of the late period than in the putaminal and subcortical hemorrhages. These results may contribute to a better understanding of the recent trends of hypertensive ICHs and may help guide their appropriate treatments for this condition.

Bilateral sudden sensorineural hearing loss due to subcortical cerebral hemorrhage in a patient with Moyamoya disease: case report

BackgroundMoyamoya disease (MMD) is a chronic cerebrovascular occlusive disease that can results in a variety of neurological deficits. We describe a very rare presentation of MMD in the form of bilateral sudden sensorineural hearing loss after a second attack of subcortical cerebral haemorrhage.Case presentationA 44-year-old female presented with bilateral sudden sensorineural hearing loss (SSNHL) secondary to an acute intracerebral haemorrhage in the left temporoparietal region. She had a previous haemorrhagic event in the right temporoparietal region two years ago. The two haemorrhagic events have apparently led to interruption of the auditory pathways bilaterally, resulting in sudden complete deafness. Digital subtraction angiography was done, and it showed bilateral occlusion of the internal carotid arteries, with the abnormal anastomotic vascular network at the base of the brain characteristic for MMD.ConclusionsSubcortical hemorrhage due to MMD is a potential cause of bilateral SSNHL that can be diagnosed with early proper imaging. Bilateral damage of the auditory pathways is the likely cause of cortical deafness in this clinical scenario.

Association of antithrombotic therapy with postoperative rebleeding in patients with cerebral amyloid angiopathy

BackgroundCerebral amyloid angiopathy is a common cause of subcortical hemorrhage in older adults. Although open hematoma removal may be performed for severe subcortical hemorrhage, its safety in patients with cerebral amyloid angiopathy has not been established, and postoperative rebleeding may occur. Therefore, this study aimed to investigate factors associated with postoperative rebleeding.MethodsOut of 145 consecutive patients who had undergone craniotomy for surgical removal of subcortical intracerebral hemorrhage between April 2010 and August 2019 at a single institution in Japan, we examined 109 patients with subcortical hemorrhage who met the inclusion criteria. After excluding 30 patients whose tissue samples were unsuitable for the study, the final study cohort comprised 79 patients.ResultsOf the 79 patients, 50 (63%) were diagnosed with cerebral amyloid angiopathy (cerebral amyloid angiopathy group) and 29 (37%) were not diagnosed with noncerebral amyloid angiopathy (noncerebral amyloid angiopathy group). Postoperative rebleeding occurred in 12 patients (24%) in the cerebral amyloid angiopathy group and in 2 patients (7%) in the noncerebral amyloid angiopathy group. Preoperative prothrombin time–international normalized ratio and intraoperative bleeding volume were significantly associated with postoperative rebleeding in the cerebral amyloid angiopathy group (odds ratio = 42.4, 95% confidence interval = 1.14–1578; p = 0.042 and odds ratio = 1.005, 95% confidence interval = 1.001–1.008; p = 0.007, respectively).ConclusionsPatients with cerebral amyloid angiopathy-related cerebral hemorrhage who are receiving antithrombotic therapy, particularly warfarin therapy, are at a high risk of postoperative rebleeding.Trial registrationRegistry and Registration Number of the study: 19–220, 2019/12/23, retrospectively registered.

Bold-S Signs on Computed Tomography Angiography Are Sensitive Markers for Diagnosing Subcortical Hemorrhage Due to Dural Arteriovenous Fistulae on Emergent Admission.

An optimal treatment strategy for subcortical hematomas caused by dural arteriovenous fistulae (dAVF) is important because of the high rebleeding rate. However, it is very difficult to diagnose that on admission. Therefore, an early sensitive predictive marker for subcortical hemorrhage caused by dAVF is necessary, especially during the first contact on admission. S-shaped dilated vessels around the hematoma (bold-S sign) on computed tomography angiography (CTA) performed during admission could be one such marker. Herein, we evaluated the characteristics of these vessels. Among 273 patients with intracerebral hemorrhage between April 2012 and March 2020, 67 patients with subcortical hematomas who underwent CTA on admission without arteriovenous malformations were included. The patients in the dAVF group (n = 7) showed fewer disturbances in consciousness, milder neurological deficits, and more frequent seizures than patients without dAVF (without dAVF group, n = 60). All patients in the dAVF group had dilated S-shaped vessels (2.59 ± 0.27 mm) around the hematomas, and only 20% of the patients in the without dAVF group had these vessels (1.69 ± 0.22 mm). The ratio of the ipsilateral S-shaped/contralateral largest vessels was 1.80 ± 0.29 in the dAVF group and 1.07 ± 0.16 in the group without dAVF. We called the dilated S-shaped vessels the "bold-S sign," with a cutoff ratio of 1.5. Bold-S sign findings are novel and help in diagnosing subcortical hematomas caused by dAVF on admission.

A spontaneous cerebral hemorrhage case in the right temporal lobe in a patient with hemophilia C (XI factor deficiency)

A 28-year-old man was taken to our hospital with sudden onset of severe headache. The computed tomography (CT) scan revealed subcortical hemorrhage of the right temporal lobe. The patient has past medical history of hemophilia C (XI factor deficiency). On neurological examination no deficit was observed (Glasgow Coma Scale (GCS) -15). 10 hours after admission, his GCS and CT scan of the brain were unchanged. After consultation with the hematologist, he received fresh frozen plasma, mannitol, tranexamic acid during the treatment. But 36 hours after admission, the neurological status was worsened (GCS -12)․ A decision was made to immediately perform a temporal craniotomy with evacuation of intracerebral hematoma. Surgery and the postoperative period were uneventful․ The patient was discharged without neurological deficit․ This case highlights the importance of adequate preparation of the patient presurgically as much as possible to minimizes the risk of complications (rebleeding) during the operation and in the postoperative period.

Two cases of hepatocellular carcinoma successfully treated by carbon ion radiotherapy after atezolizumab plus bevacizumab treatment.

We herein report two cases of huge hepatocellular carcinoma (HCC) that were successfully treated by carbon ion radiotherapy after atezolizumab plus bevacizumab treatment. Case 1, an 84-year-old man, was diagnosed with HCC (maximum diameter: 11cm) with portal invasion and presented HCC rupture. After obtaining hemostasis with transcatheter embolization, three cycles of atezolizumab-bevacizumab therapy were administered, and marked shrinkage of the HCC was confirmed. However, he developed jaundice, liver damage and cerebral subcortical hemorrhage. Thus, atezolizumab-bevacizumab therapy was discontinued. Total bilirubin, transaminase levels, and physical activity improved well with prednisolone, an antihypertensive agent, and rehabilitation. Thus, treatment with carbon ion radiotherapy (CIRT) was added, and the treatment effect at 4months after CIRT was judged as a complete response (CR) according to the modified response evaluation criteria in solid tumors (mRECIST). Case 2, a 68-year-old man, was diagnosed with HCC (maximum diameter: 14cm). Hepatic resection was difficult because the residual liver volume after treatment would be insufficient. Five cycles of atezolizumab-bevacizumab therapy were performed, and marked shrinkage of the HCC to a maximum diameter of 9cm was confirmed. The treatment was converted to CIRT, and atezolizumab-bevacizumab therapy resumed one month after CIRT. The treatment effect at 3months after CIRT was judged as CR according to mRECIST. Although conversion therapy after atezolizumab-bevacizumab therapy, including surgery and radiofrequency ablation, have been reported, CIRT may be a promising new tool for conversion therapy for HCC.

A case of cerebral amyloid angiopathy presented as subcortical brain hemorrhage in a young adult who underwent head trauma surgery using cadaveric dural graft in childhood

脳アミロイドアンギオパチー（CAA）は，55歳未満の発症は稀であり，その一部の症例において幼少期の脳外科手術との関連が報告されている．症例は，1歳時に頭部外傷手術に際して屍体硬膜を用いた硬膜再建を施行された37歳の男性．意識障害と運動性失語を認め，頭部CTで左側頭頭頂葉皮質下出血と診断された．脳血管撮影では，出血源となり得る有意所見は認めず，開頭血腫除去術を施行された．後日，創部感染から波及した左大脳実質の脳膿瘍に対して排膿術および骨弁除去術を施行され，その際に提出した脳表の病理組織診にて，血管壁へのアミロイドβ（Aβ）の沈着を認め，CAAの診断となった．CAAの遺伝的素因はなく，幼少期の屍体硬膜を用いた脳外科処置がAβの沈着とCAAの発症に関係していると考えられた．

A case of multiple small cerebral infarcts in the cerebellum and bilateral cerebrum, diagnosed with amyloid angiopathy by brain biopsy

An 82-year-old woman had been suffering from progressive forgetfulness and abnormal speech and behavior for One month. Findings of the MRI of the head indicated scattered small cerebral infarcts in the cerebellum and in bilateral cerebral cortex/subcortical white matter. After admission, she experienced a subcortical hemorrhage, and the percentage of small cerebral infarcts increased over time. Based on the suspicion of central primary vasculitis or malignant lymphoma, we performed a brain biopsy targeting the right temporal lobe hemorrhage site, and the patient was diagnosed with cerebral amyloid angiopathy (CAA). We conclude that CAA can cause multiple small progressive cerebral infarcts.

Blood Pressure and Spot Sign in Spontaneous Supratentorial Subcortical Intracerebral Hemorrhage

BackgroundSpontaneous intracerebral hemorrhage is a potentially devastating cause of brain injury, often occurring secondary to hypertension. Contrast extravasation on computed tomography angiography (CTA), known as the spot sign, has been shown to predict hematoma expansion and worse outcomes. Although hypertension has been associated with an increased rate of the spot sign being present, the relationship between spot sign and blood pressure has not been fully explored.MethodsWe retrospectively analyzed data from 134 patients (40 women and 94 men, mean age 62.3 ± 15.73 years) presenting to a tertiary academic medical center with spontaneous supratentorial subcortical intracerebral hemorrhage from 1/1/2018 to 1/4/2021.ResultsA spot sign was demonstrated in images of 18 patients (13.43%) and correlated with a higher intracerebral hemorrhage score (2.61 ± 1.42 vs. 1.31 ± 1.25, p = 0.002), larger hematoma volume (53.49cm3 ± 32.08 vs. 23.45cm3 ± 25.65, p = 0.001), lower Glasgow Coma Scale on arrival (9.06 ± 4.56 vs. 11.74 ± 3.65, p = 0.027), increased risk of hematoma expansion (16.67% vs. 5.26%, p = 0.042), and need for surgical intervention (66.67% vs. 15.52%, p < 0.001). We did not see a correlation with age, sex, or underlying comorbidities. The presence of spot sign correlated with higher modified Rankin scores at discharge (4.94 ± 1.00 vs. 3.92 ± 1.64, p < 0.001). We saw significantly higher systolic blood pressure at the time of CTA in patients with a spot sign (184 mm Hg ± 43.11 vs. 153 mm Hg ± 36.99, p = 0.009) and the highest recorded blood pressure (p = 0.019), although not blood pressure on arrival (p = 0.081). Performing CTA early in the process of blood pressure lowering was associated with a spot sign (p < 0.001).ConclusionsThe presence of spot sign correlates with larger hematomas, worse outcomes, and increased surgical intervention. There is a significant association between spot sign and systolic blood pressure at the time of CTA, with the highest systolic blood pressure being recorded prior to CTA. Although the role of intensive blood pressure management in spontaneous intracerebral hemorrhage remains a subject of debate, patients with a spot sign may be a subgroup that could benefit from this.

Hematoma expansion caused by trapped cerebrospinal fluid in subacute phase intracerebral hemorrhage: A case report

Background: Although hematoma expansion (HE) is caused by active bleeding in patients with intracranial hemorrhage in most cases, cerebrospinal fluid (CSF) trapped in the hematoma cavity is not a well-known cause of HE.Case Description: We present a case of subcortical hemorrhage in an 80-year-old woman who experienced neurological deterioration in the subacute phase because of HE caused by CSF pooling in the hematoma cavity. The patient was transferred to our hospital from a previous hospital for surgical treatment because the consciousness disturbance was likely caused by the perihematomal edema that occurred 4 days after onset. Head computed tomography (CT) at admission to our hospital showed a blend sign, and a part of the low-density area of the hematoma was enlarged compared with the CT at admission to the previous hospital. Although the hematoma was located adjacent to the lateral ventricle, no intraventricular hemorrhage was observed. Emergent hematoma evacuation was performed, and intraoperative findings indicated that the enlarged hematoma cavity was caused by CSF pooling. The patient’s postoperative course was uneventful. She was transferred to a rehabilitation hospital 16 days after admission to our hospital.Conclusion: Hematomas adjacent to the ventricle and showing a blend sign can expand in the subacute phase because of the trapped CSF.

Walking through a narrow opening improves collision avoidance behavior in a patient with stroke and unilateral spatial neglect: an ABA single-case design

ABSTRACT We investigated the effect of a 3-week intervention—wherein a patient with unilateral spatial neglect walks through a narrow opening while entering from the contralesional side—to improve walking ability or ADL. A 66-year-old man was diagnosed with right parietal subcortical hemorrhage. We used an ABA single-case design; period B was set as the intervention. The intervention improved the continuous walking distance and balance ability and decreased the number of collisions when walking through the narrow opening; however, it exerted minimal effect on ADL. Thus, the intervention may effectively improve continuous physical or spatial attention behavior, regardless of ADL improvement.

Evaluation of the Effectiveness of the Subacute Endoscopic Evacuation for Subcortical Hemorrhage in Elderly Patients under Local Anesthesia

Evaluation of the Effectiveness of the Subacute Endoscopic Evacuation for Subcortical Hemorrhage in Elderly Patients under Local Anesthesia

Subcortical Hemorrhage due to Cerebral Venous Sinus Thrombosis with Multiple Thrombotic Risks : A Case Report

Subcortical Hemorrhage due to Cerebral Venous Sinus Thrombosis with Multiple Thrombotic Risks : A Case Report