Frequency, Characteristics, and Preventability of Adverse Drug Reactions in Perioperative Neurosurgery: Analysis Over 11 Years.

OBJECTIVE: Despite the importance of adverse drug reactions (ADRs), little is known about their role in perioperative neurosurgery. This study aimed to determine the prevalence of ADRs in perioperative neurosurgery and clarify the characteristics, severity, preventability, and risk factors of ADRs. METHODS: Data for all patients who underwent neurosurgical procedures over an 11-year period were analyzed. During the study period, 3648 surgical procedures were performed for 2695 patients. Demographic and clinical information documented included medical history, allergic history, diagnosis, surgical method, suspected drugs, concomitant medications, and drug details. Multivariate logistic regression analyses were performed to identify independent parameters that were correlated with ADRs. RESULTS: In total, 467 ADRs (18.3% ADRs/all neurosurgical procedures) were experienced by 401 patients. Anticonvulsants were associated with the highest number of ADRs (16.0%), followed by antibiotics (14.7%). Patients with ADRs were older than patients without ADRs (P<0.01). The total number of drugs in patients with ADRs was 8.8±3.6, compared to 5.2±2.4 for patients without ADRs (P<0.01). There were no significant differences in sex, allergic history, severe renal dysfunction (eGFR<30 ml/min/1.73 m2), hypertension, diabetes, urgency of surgery, and type of surgery. Multivariate analysis showed that a high total number of drugs (odds=3.2; 95%CI 1.9-5.1) and older age (odds=2.1; 95%CI 1.3-3.8) were independent risk factors for ADRs. CONCLUSIONS: The frequency of suspected and severe ADRs was higher than expected. Polypharmacy and older age were independent risk factors for ADRs in perioperative neurosurgery. To decrease ADRs during perioperative neurosurgery, polypharmacy must be discouraged, especially among older adult patients.

Association between Pericarotid Fat Density and Positive Remodeling in Patients with Carotid Artery Stenosis.

Background/Objectives: The underlying mechanism of the potential involvement of inflammatory crosstalk between pericarotid fat and vascular layers in atherosclerosis pathogenesis is unclear. We investigated the association between pericarotid fat density and positive remodeling and inflammatory markers in carotid stenosis. We hypothesized that pericarotid fat density might serve as a marker of plaque inflammation in a clinical setting. Methods: We evaluated the stenosis degree and pericarotid fat density in 258 patients with carotid plaques. Plaque composition was examined, and the correlation between pericarotid fat density and expansive remodeling was investigated. Pearson's product-moment correlation coefficient was used to examine the relationship between pericarotid fat density and the expansive remodeling ratio. We also evaluated the relationship of pericarotid fat density with plaque composition, degree of stenosis, and macrophage and microvessel counts by. The subgroup analysis compared these factors between symptomatic mild carotid stenosis. Results: The pericarotid fat density was -63.0 ± 11.1 HU. The carotid fat densities were -56.8 ± 10.4 HU in symptomatic and -69.2 ± 11.4 HU in asymptomatic lesions. The pericarotid fat density values in intraplaque hemorrhage, lipid-rich necrotic core, and fibrous plaque were -51.6 ± 10.4, -59.4 ± 12.8, and -74.2 ± 8.4 HU, respectively. Therefore, the expansive remodeling ratio was 1.64 ± 0.4. Carotid fat density and expansive remodeling ratio were correlated. Immunohistochemistry showed high macrophage and microvessel levels (143.5 ± 61.3/field and 121.2 ± 27.7/field, respectively). In symptomatic mild carotid stenosis, pericarotid fat density was correlated with other inflammatory factors. The pericarotid fat density and expansive remodeling ratio (2.08 ± 0.21) were high in mild stenosis (-50.1 ± 8.4 HU). Conclusions: Pericarotid fat and intraplaque components were well correlated. Carotid fat density may be a marker of plaque inflammation in carotid plaques.

Detection of Hyperdense Arterial Sign in Acute Ischemic Stroke with Dual-Energy Computed Tomography: Optimal Combination with X-ray Energy and Slice Thickness.

BACKGROUND: The hyperdense artery sign (HAS) in acute ischemic stroke (AIS) is considered an important marker of a thrombus on computed tomography (CT). An advantage of scanning with dual-energy CT (DECT) is its ability to reconstruct CT images with various energies using the virtual monochromatic imaging (VMI) technique. The aim of this study was to investigate the optimal combination of X-ray energy and slice thickness to detect HASs on DECT. METHODS: A total of 32 patients with confirmed occlusion of the horizontal (M1) portion of the middle cerebral artery were included in this study. Modified contrast-to-noise ratio (modified CNR) analysis was used as a method for evaluating HASs in AIS. A region of interest (ROI) was set as an HAS, the M1 portion, and an approximately 2 cm diameter ROI was set as the background including the HAS and measured. CT images with X-ray energies from 40 to 190 keV, with increments of 10 keV, were reconstructed based on VMI with 1, 2, and 3 mm slice thicknesses. RESULTS: The top five combinations of X-ray energy and slice thickness in descending order of the mean HAS-modified CNR were as follows: Rank 1, 60 keV-1 mm; Rank 2, 70 keV-1 mm; Rank 3, 60 keV-2 mm; Rank 4, 80 keV-2 mm; Rank 5, 60 keV-3 mm. CONCLUSIONS: Our study showed that the optimal combination to detect an HAS was 60 keV and a 1 mm slice thickness on DECT.

Diagnosis of a Dural Arteriovenous Fistula Involving the Superior Sagittal Sinus: The MMA Sign on Routine 3D-TOF MR Angiography.

BACKGROUND AND PURPOSE: The main feeding artery of a dural arteriovenous fistula (DAVF) involving the superior sagittal sinus (SSS) is the middle meningeal artery (MMA). MMA extends continuously from the proximal part to SSS in DAVF involving SSS. It is possible to diagnose DAVF involving SSS by evaluating the proximal part of MMA on routine three-dimensional time-of-flight MR angiography (MRA). We termed the finding in an anteroposterior maximum intensity projection (MIP) image of routine MRA in which MMA was continuously visualized at the top of the imaging slab (the upper corpus callosum level) without tapering as the MMA sign. The purpose of the present study was to examine the frequency of the MMA sign on routine MRA in patients with DAVF involving SSS and control patients. MATERIALS AND METHODS: Subjects comprised 18 patients with DAVF involving SSS confirmed by angiography and 871 control subjects who underwent routine MRA. The presence of the MMA sign was retrospectively evaluated using an anteroposterior MIP image of routine MRA in patients with DAVF involving SSS and control patients. RESULTS: The MMA sign was observed in 17 of the 18 (94%) patients with DAVF involving SSS. In one patient with DAVF involving the posterior part of SSS without the MMA sign, the main feeding artery was the occipital artery, not MMA. The MMA sign was observed in 13 of the 871 (1.5%) control patients. CONCLUSION: The MMA sign on routine MRA is useful, suggesting DAVF involving SSS.

Clinical Significance of Carotid Endarterectomy and Carotid Artery Stenting in Older Patients Over 80.

As the average life expectancy increases, neurosurgeons are likely to encounter patients aged 80 years and above with carotid stenosis; however, whether old age affects clinical post-treatment outcomes of carotid endarterectomy (CEA) or carotid artery stenting (CAS) remains inconclusive. Thus, this study aimed to evaluate the outcomes following CEA or CAS in patients aged 80 years and above. This study included older over 80 years (n = 34) and younger patients (<80 years; n = 222) who underwent CEA or CAS between 2012 and 2022. All of them were followed up for a mean of 55 months. All-cause mortality, the incidence of vascular events, ability to perform daily activities, and nursing home admission rates were assessed. During follow-up periods, 34 patients (13.3%) died due to coronary artery disease, malignancy, and pneumonia, and the incidence was significantly higher in the elderly group than in the younger group (P = 0.03; HR, 3.01; 95% CI, 1.53-5.56). The incidence of vascular events did not differ between the older group (29.5%) and the younger group (26.9%, P = 0.58); however, the incidence was significantly higher in patients with high-intensity plaques than in those without that (P = 0.008; HR, 2.83, 95%CI, 1.27-4.87). The decline in the ability to perform daily activities and increased nursing home admission rates were high in elderly patients (P < 0.01). Although the mortality rate was higher in the elderly group, subsequent vascular events were comparable to that in the younger group. The results suggest that CEA and CAS are safe and useful treatments for carotid stenosis in older patients, especially to prevent ipsilateral ischemic stroke.

Coil embolization for post-bypass aneurysm of middle meningeal artery for moyamoya disease - preservation of transdural anastomosis.

Background: Middle meningeal artery (MMA) pseudoaneurysm following revascularization surgery for moyamoya disease (MMD) is rare. Case Description: Here, a 29-year-old man presented with an MMA pseudoaneurysm after he underwent revascularization surgery (superficial temporal artery-to-middle cerebral artery bypass and encephalo-duro-myoarterio-pericranial synangiosis) for hemorrhagic MMD. At 3 months post-surgery, digital subtraction angiography showed a pseudoaneurysm in the right MMA. Transdural anastomosis to the parietal and occipital lobes was opacified at the distal MMA of the pseudoaneurysm. Intra-aneurysmal coil embolization was performed for preservation of transdural anastomosis. The postoperative course was uneventful. At 1 month post-embolization, angiography revealed an entirely occluded pseudoaneurysm. Conclusion: An increase in blood flow in the MMA due to bypass surgery may accelerate aneurysm development by increasing the hemodynamic stress. This case suggested that intra-aneurysmal embolization may be a potential treatment.

Therapeutic strategy of severe circular calcified carotid plaque with hemodynamic impairment: A patient treated by carotid endarterectomy following balloon angioplasty to prevent hyperperfusion.

Background: Cerebral hyperperfusion syndrome (HPS) is a serious complication. Recently, staged angioplasty has been reported as an effective strategy to avoid HPS. Severe calcification has been reported as contraindication of carotid artery stenting (CAS). In these cases, carotid endarterectomy (CEA) might be an alternative second stage treatment. We present a case of severe circular calcified plaque with hemodynamic impairments, treated with CEA following percutaneous transluminal angioplasty (PTA) to prevent HPS. Case Description: A 77-year-old woman presented with severe stenosis at the proximal left internal carotid artery. A CT scan of the neck demonstrated circular calcification. 123I-iodoamphetamine single-photon emission computed tomography (123I-IMP SPECT) showed reductions in cerebral blood flow (CBF) and cerebral vascular reserve in the left hemisphere. Staged therapy was subsequently performed as this patient had a high risk of HPS after conventional CAS or CEA. In the first stage, PTA was performed under local anesthesia. Two days after the procedure, 123I-IMP SPECT revealed improvements in CBF. There were no neurological morbidities. CEA was then performed under general anesthesia 7 days later, for the second stage. We found a calcified plaque with a large thrombus at its proximal end. A hematoxylin-eosin stain of the thrombus showed mostly intact and partially lytic blood cells. Postoperative 123I-IMP SPECT revealed CBF was improved, with no hyperperfusion immediately and 2 days after CEA. The patient was discharged with no neurological deficits. Conclusion: CEA following PTA for severe circular calcified plaque can be an alternative treatment strategy to prevent HPS. A disadvantage is the formation of thrombi. Early CEA should be considered if thrombus formation is suspected.

Impact of system approach and personal performance on preventable morbidity and mortality events in neurosurgery patients.

PURPOSE: Adverse events in neurosurgery are a serious problem. The approach for seeking solutions for adverse events has shifted from a personal approach to a systemic approach. However, to some extent, preventable morbidity events could be related to personal performance. This study aimed to clarify the impact of personal performance and systematic failure on the occurrence of morbidity and mortality events in neurosurgery patients. METHODS: All morbidity and mortality conference data stored within our department over a 9-year period were analyzed. There were 4580 admitted patients and 3262 surgical procedures performed. We performed a three-step classification of morbidity and mortality events based on the possibility of prevention, root of the event, and personal or systemic issues. RESULTS: As a result of the first step, 214 preventable and 278 unpreventable events were identified. Of the preventable events, two mortality and 212 morbidity events were analyzed. In the second step, 155 (72.4%), 34 (15.9%), 13 (6.1%), and 12 (5.6%) events were categorized as technical complications, critical events, judgment errors, and human factors, respectively. There were 179 events (83.6%) classified as personal performance issues and 35 events (16.4%) as systemic issues. The ratio of personal performance to systemic issues varied widely, with significant differences among the four categories (P < 0.01). CONCLUSIONS: Among neurosurgery patients who have preventable morbidity, issues related to personal performance were more frequent than systemic issues. Efforts to improve systems should be unwavering. However, the personal responsibility of neurosurgeons to avoid preventable complications should not be ignored.

Predictive Factors of Functional Outcome in World Federation of Neurosurgical Societies Grade V Subarachnoid Hemorrhage.

OBJECTIVE: Patients with World Federation of Neurosurgical Societies (WFNS) grade V subarachnoid hemorrhage (SAH) frequently have poor outcomes. The current understanding of the predictors of functional outcome only in WFNS grade V SAH is limited. METHODS: Patients with WFNS grade V SAH were retrospectively analyzed between April 2008 and August 2019. Surgical treatment is commonly delayed until clinical improvement is observed using a less aggressive approach. Clinical and radiologic data on admission were assessed, and disease-related characteristics were compared between patients with favorable outcomes (modified Rankin Scale score 0-3) and those with unfavorable outcomes (modified Rankin Scale score 4-6). RESULTS: A total of 144 patients were included, and 22 patients (15.3%) achieved favorable outcomes, whereas 122 patients (84.7%) had unfavorable outcomes. Surgical aneurysm repair was performed in all patients with favorable outcomes and in 21.3% of those with unfavorable outcomes. Multivariate analysis showed that Glasgow Coma Scale score of 3, high-grade Early Brain Edema Score, absence of bilaterally light reflex and neurologic improvement, and hypertension were significantly associated with unfavorable outcomes (odds ratio [OR], 9.54, P = 0.03; OR, 5.37, P = 0.04; OR, 11.80, P = 0.009; OR, 0.14, P = 0.02 and OR, 6.53, P = 0.04, respectively). CONCLUSIONS: The final outcome of patients with WFNS grade V SAH was still poor and highly predicted by Glasgow Coma Scale score of 3, high-grade Early Brain Edema Score, absence of bilaterally light reflex and neurologic improvement, and a history of hypertension. The efficacy of aggressive surgical treatment for these patients remains controversial, and the indications should be clearly defined in patients with desolate clinical status on admission.

Thin calcification (< 2 mm) can highly predict intraplaque hemorrhage in carotid plaque: the clinical significance of calcification types.

PURPOSE: Calcification pathogenesis and the relationship between calcification and plaque composition remain unclear. This study explored the calcification characteristics of vulnerable plaques, especially focusing on calcification thickness, using computed tomography angiography and magnetic resonance plaque imaging. METHODS: Demographic, computed tomography angiography, and magnetic resonance plaque imaging data were acquired from 178 patients with 229 lesions diagnosed with carotid stenosis. The calcification types were categorized by calcification thickness. We evaluated their features, including the anatomical location and the plaque composition compared with MR plaque imaging, and clarify the clinical characteristics. Furthermore, an immunohistochemical subgroup analysis was performed on 84 lesions treated with carotid endarterectomy. RESULTS: The result of the ROC analysis suggested the threshold between symptomatic and asymptomatic calcification was 2.04 mm (AUC;0.841, 95%CI; 0.771-0.894). Calcification with ≥ 2 mm thickness was classified as thick calcification and < 2 mm thickness as thin calcification. Multivariate analysis suggested the prevalence of symptomatic patients in the thin calcification group was significantly higher than others (P = 0.01; odds ratio, 4.1; 95% confidence interval 2.8-7.2). Plaques with thin calcification were associated with plaque with intraplaque hemorrhage (P < 0.01). The interobserver reliability (κ) of calcification type was 0.962 (95% confidence interval, 0.941-0.988). Immunohistochemical analysis demonstrated that the numbers of CD68-positive cells and CD31-positive microvessels in shoulder lesions were significantly higher in the thin calcification group than in the non-thin group (both P < 0.01). CONCLUSIONS: Thin calcification was associated with plaques with intraplaque hemorrhage and had different clinical implications than thick calcification.

Repeated recurrent intracerebral hemorrhage may be involved in cerebral amyloid angiopathy-related inflammation: An autopsy case.

We report an autopsy case of repeated recurrent intracerebral hemorrhage (ICH) diagnosed as having cerebral amyloid angiopathy-related inflammation (CAA-ri) in a 65-year-old woman. She had no history of hypertension or other risk factors for stroke. She had a history of lobar ICH in the right parietal lobe 30 months prior. Follow-up magnetic resonance imaging (MRI) performed 29 months after the initial ICH revealed superficial siderosis in the left frontal lobe. She initially presented with severe headache and dysarthria. An initial computed tomography (CT) revealed a subarachnoid hemorrhage on the left frontal lobe. One hour later, an epileptic seizure occurred, and another CT performed at the time revealed lobar ICH in the frontal lobe. Emergency surgical hematoma evacuation was performed. The cortical artery was removed from the surgical specimen. Hematoxylin and eosin (HE) staining revealed lymphocytic perivascular cuffs, and immunohistochemical staining revealed abundant amyloid-ß (Aß) deposits. The patient was diagnosed as having CAA-ri. On the next day, and 19, 46, 55, 78, 79, and 85 days after admission, ICH recurred. We did not administer immunosuppressive drugs, such as high-dose corticosteroids or cyclophosphamide, because of the patient's condition. Following the last ICH, the patient died on the 90th day after symptom onset. An autopsy was performed. Histologically, abundant Aß deposits were observed within the leptomeningeal and cortical arteries. Further dense-cored amyloid plaques were observed in the cortical samples. Our findings that ICH occurred initially three times in the left hemispheres and later five times in the right hemispheres were considered immune-mediated effects on vascular function. Further, superficial hemosiderosis in the left frontal lobe occurred before the first three ICH events, and hyperintensity of the white matter on MRI was identified in the right parietal lobe, a typical finding of CAA-ri. We hypothesize that the inflammatory process in CAA-ri may be related to recurrent ICH.

Negative Remodeling of Carotid Canal during Spontaneous Disease Progression in Moyamoya Disease.

OBJECTIVE: This study was designed to observe the changes in the carotid canal over time by measuring the carotid canal diameter longitudinally in adult patients with moyamoya disease in whom disease stage progressed spontaneously. METHODS: Of 70 adult patients with moyamoya disease, 10 adult patients on 15 sides with spontaneous progression of the disease stage during conservative follow-up were included in this study. Another 10 moyamoya cases on 15 sides were selected as the controls without disease progression. All patients were followed up for at least 60 months after the progression of disease stage was confirmed. In addition, 5 patients who underwent microvascular decompression were included as healthy controls. The carotid canal diameter was measured with bone window computed tomography (CT) and source images of time-of-flight magnetic resonance angiography at initial presentation, and then were serially monitored with the latter. RESULTS: There was a significant correlation between the values obtained from CT and magnetic resonance imaging (R2 = 0.992, P < 0.001). The carotid canal diameter in moyamoya disease at initial presentation was 4.29 ± 0.61 mm, being smaller than 5.20 ± 0.51 mm in healthy controls (P < 0.01). In response to disease progression, the carotid canal diameter started to decrease at 6 months after disease progression was confirmed, and reduced to about 85% of the original level during 60 months (P < 0.01). The phenomenon was not observed in patients without disease progression. CONCLUSIONS: The carotid canal diameter can decrease in response to disease progression even in adult moyamoya disease. "Negative" bone remodeling may play a key role in this unique phenomenon.

Oro-mandibular dystonia in pediatric moyamoya disease: Two cases report.

BACKGROUND: In this report, we describe rare two pediatric cases that developed oro-mandibular dystonia due to moyamoya disease. CASE DESCRIPTION: A 7-year-old boy presented with oro-mandibular dystonia and transient weakness of the left extremities, and was diagnosed as moyamoya disease. Another 7-year-old boy developed oro-mandibular dystonia alone and was diagnosed as moyamoya disease. In both, cerebral blood flow (CBF) was markedly decreased in the involved hemispheres, including the basal ganglia and cerebral cortex. They successfully underwent combined bypass surgery and experienced no further attacks of oromandibular dystonia during follow-up periods. CBF almost normalized through surgical collaterals through direct and indirect bypass. CONCLUSION: When treating patients with oro-mandibular dystonia, moyamoya disease should be listed as one of the differential diseases. The underlying mechanism of oro-mandibular dystonia in moyamoya disease is still unclear, but persistent cerebral ischemia in the basal ganglia and/or parietal lobe may play a key role to induce this rare symptom.

Complications of Endovascular Treatment of Intracranial Dural Arteriovenous Fistulas.

AIMS: To report the endovascular treatment and complications of intracranial and spinal dural arteriovenous (AV) fistulas. METHODS: A retrospective analysis of 863 cases with dural AV fistulas was completed in the nationwide registry study of the Japanese Society of Neuroendovascular Therapy. RESULTS: Treatments included transarterial/transvenous embolization (TAE/TVE), open surgery, stereotactic radiation, and their combinations. Modified Rankin Scale 0 (mRS-0) of the patients before and after treatment were 21% and 68%, and mRS 0-1were 69% and 86%, respectively. Mortality rate after treatment was 0.6%. Major complications of TAE and TVE were cranial nerve palsy and cerebral infarction. CONCLUSIONS: Major complications resulted from occlusion of vasa nervosum and material migration via dangerous intracranial and extracranial arterial anastomosis.

Impact of Perihematomal Edema on Infectious Complications after Spontaneous Intracerebral Hemorrhage.

OBJECTIVE: Intracerebral hematoma involves two mechanisms leading to brain injury: the mechanical disruption of adjacent brain tissue by the hematoma and delayed neurological injury. Delayed neurological injury involves perihematomal edema (PHE) formation. Infectious complications following intracerebral hemorrhage (ICH) are a significant contributor to post-ICH recovery. We sought to identify a correlation between PHE volumes and infectious complications following ICH. We also sought to explore the clinical impact of this association. MATERIALS AND METHODS: This retrospective study included 143 patients with spontaneous ICH. CT scans were performed on admission, and 3 h, 24 h, and 72 h following admission. Hematoma and PHE volumes were calculated using a semi-automatic method. The absolute PHE volume at each time point and changes in PHE volume (ΔPHE) were calculated. Neutrophil to lymphocyte ratio (NLR) and serum C-reactive protein (CRP) levels were measured from the obtained blood samples. Neurological deterioration (ND) was assessed in all patients. RESULTS: Infectious complications were associated with ΔPHE72-24 (P < 0.01), whereas there was no association between infectious complications and ΔPHE24-3 (P = 0.09) or ΔPHE3-ad (P = 0.81). There was a positive correlation between ΔPHE72-24 and NLR (r = 0.85, 95% CI: 0.79-0.90, P < 0.01) and between ΔPHE72-24 and CRP levels (r = 0.89, 95% CI: 0.84-0.92, P < 0.01). The ND rate in the group of patients with infectious complications comorbid with high ΔPHE72-24 was higher than the other patient groups (P < 0.01). CONCLUSIONS: This study revealed a correlation between ΔPHE72-24 and infectious complications after spontaneous ICH, which was associated with markers of systemic inflammation. This phenotype linkage is a negative cascade that drives ND.

[CT and MRI Findings of Cortical Venous Thrombosis and Cerebral Venous Sinus Thrombosis].

The author reports the cases of two young patients with cortical venous thrombosis(CVT)and cerebral venous sinus thrombosis(CVST)and demonstrates that CT and MRI investigations are critical for the diagnosis. The first case was an 18-year-old woman who developed symptoms of intracranial hypertension and, 20 days later, suffered from left hemiparesis and generalized seizures. A plain CT scan revealed an increased density of cortical veins("cord sign"). MR venography revealed superior sagittal sinus thrombosis and right frontal lobe cortical vein thrombosis. The second case was a 15-year-old boy who developed intracranial hypertension symptoms and went to various hospitals but the symptoms progressed. Six weeks after the onset, contrast-enhanced MRI showed an "empty delta sign" and superior sagittal sinus thrombosis was diagnosed. The patients had a history of protein-losing enteropathy and Behçet's disease. Both patients were treated with endovascular and anticoagulation therapy while also treating the primary disease, resulting in thrombus reduction in the sinus and good outcomes. CVT and CVST can lead to severe conditions, so a full understanding of the imaging findings is essential for an accurate diagnosis.

Ameliorative Effects of Combined Revascularization Surgery on Abnormal Collateral Channels in Moyamoya Disease.

OBJECT: Abnormal collateral channels, so-called moyamoya vessels, play a critical role to compensate cerebral ischemia, but carry the risk for hemorrhagic stroke in moyamoya disease (MMD). The present study was aimed to clarify if superficial temporal artery to middle cerebral artery (STA-MCA) anastomosis and encephalo-myo-duro-arterio-pericranial synangiosis (EDMAPS) can efficiently regress the abnormal collateral channels in MMD patients. METHODS: This study included 92 hemispheres of 61 MMD patients who underwent STA-MCA anastomosis combined with EDMAPS between 2013 and 2019. There were 17 children and 44 adults. We retrospectively analyzed the findings on cerebral angiography before and 3 to 6 months after surgery, including Suzuki's angiographical stage, the development of surgical collaterals, and the extent of abnormal collateral channels such as lenticulostriate, thalamic, and choroidal channels. RESULTS: Following surgery, no pediatric and adult patients experienced any stroke during follow-up periods (40.2±25.5 and 54.9±19.7 months, respectively). Suzuki's stage significantly advanced in both adult and pediatric patients after surgery (P=0.042 and P<0.001). In adult patients, all of the lenticulostriate, thalamic, and choroidal channels significantly regressed after surgery (P<0.001, P=0.012, and P=0.004, respectively). In pediatric patients, however, lenticulostriate and choroidal channels significantly regressed (P=0.005 and P=0.034, respectively). Correlation analysis revealed that the development of surgical collaterals determined the postoperative regression of choroidal channels (P<0.001). CONCLUSION: STA-MCA anastomosis and EDMAPS may be one of the most effective procedures to widely provide surgical collaterals to the operated hemispheres and prevent not only ischemic but also hemorrhagic stroke by regressing the hemorrhage-prone abnormal collateral channels in MMD.

Dilated microvessel with endothelial cell proliferation involves intraplaque hemorrhage in unstable carotid plaque.

BACKGROUND: The purpose of the present study was to clarify the characteristics of endothelial cell (EC) proliferation in intraplaque microvessels in vulnerable plaques and impact on clinical results. METHODS: The present study included 76 patients who underwent carotid endarterectomy. Patients were classified into three groups based on their symptoms: asymptomatic, symptomatic without recurrent ischemic event, and symptomatic with recurrent ischemic event. MR plaque imaging was performed and surgical specimens underwent immunohistochemical analysis. The number of CD31+ microvessels, and Ki67+ and CD105+ ECs in the carotid plaques was quantified, as measurements of maximum CD31+ microvessel diameter. RESULTS: MR plaque imaging yielded 41 subjects (54.0%) diagnosed with plaque with intraplaque hemorrhage (IPH), 14 subjects (18.4%) diagnosed with fibrous plaques, and 21 (27.6%) subjects diagnosed with lipid-rich plaques. The average largest diameter of microvessel in fibrous plaques, lipid-rich plaques, and plaque with IPH was 12.7 ± 4.1 µm, 31.3 ± 9.3 µm, and 56.4 ± 10.0 µm, respectively (p < 0.01). Dilated microvessels (>40 µm) were observed in 9.6% of plaques with IPH but only in 2.8% of lipid-rich plaques and 0% of fibrous plaques (p < 0.01). Ki67+/CD31+ ECs were identified in 2.8 ± 1.2% of fibrous plaques, 9.6 ± 6.9% of lipid-rich plaques, and in 19.5 ± 5.9% of plaques with IPH (p < 0.01). The average largest diameter of microvessels in the asymptomatic group was 17.1 ± 8.7 µm, 32.3 ± 10.8 µm in the symptomatic without recurrence group, and 55.2 ± 13.2 µm in the symptomatic with recurrence group (p < 0.01). CONCLUSION: Dilated microvessels with proliferative ECs may play a key role in IPH pathogenesis. Furthermore, dilated microvessels are likely related to clinical onset and the recurrence of ischemic events. The purpose of the present study was to clarify the characteristics of EC proliferation in intraplaque microvessels in vulnerable plaques and their impact on clinical results, focusing on dilated intraplaque microvessels.

Clinical and Radiological Features of Childhood Onset Adult Moyamoya Disease: Implication for Hemorrhagic Stroke.

Some of the pediatric moyamoya patients spend their childhood without diagnosed as moyamoya disease (MMD) because of their mild ischemic attacks and emerge again with ischemic or hemorrhagic stroke in their adulthood. This study was aimed to clarify the clinical characteristics of adult moyamoya patients with childhood onset and elucidate the impact of long disease period on their clinical features. Present study included 116 untreated hemispheres of 69 adult patients with MMD. They were divided into two groups: childhood onset group (26 hemispheres of 14 patients) and adult onset group (90 hemispheres of 55 patients). Clinical features were compared between the two groups. The incidence of hemorrhagic stroke was significantly higher in childhood onset group (P = 0.0091). Lenticulostriate and choroidal channels were more developed in childhood onset group (P = 0.044 and P <0.001, respectively). Vault moyamoya was more frequently observed in childhood onset group (P <0.001). The development of surgical collaterals through indirect bypass was more marked in childhood onset group (P = 0.0019). Multivariate analysis revealed that childhood onset and developed choroidal channels were significantly associated with the occurrence of hemorrhagic stroke (OR 4.31 [95% CI 1.21-15.4], P = 0.025 and OR 6.78 [95% CI 1.78-25.8], P = 0.0050, respectively). This study clearly shows that adult moyamoya patients with childhood onset have more developed spontaneous collaterals, which may, in turn, highly causes hemorrhagic stroke. Adult moyamoya patients with "childhood onset" should be recognized as a novel and important concept when elucidating the underlying mechanisms of hemorrhagic stroke in MMD.

High-intensity vessel sign on fluid-attenuated inversion recovery imaging: a novel imaging marker of high-risk carotid stenosis-a MRI and SPECT study.

BACKGROUND: Measurement of luminal stenosis and determination of plaque instability using MR plaque imaging are effective strategies for evaluating high-risk carotid stenosis. Nevertheless, new methods are required to identify patients with carotid stenosis at risk of future stroke. We aimed to clarify the mechanisms and clinical implications of the hyperintense vessel sign (HVS) as a marker of high-risk carotid stenosis. METHODS: We included 148 patients who underwent carotid stent (CAS) or carotid endarterectomy (CEA). MRI FLAIR was performed to detect HVS prior to and within 7 days after CAS/CEA. MR plaque imaging and 123I-iodoamphetamine SPECT was performed prior to CEA/CAS. Detailed characteristics of HVS were categorized in terms of symptomatic status, hemodynamic state, plaque composition, and HVS on time series. RESULTS: Forty-six of 80 symptomatic hemispheres (57.5%) and 5 of 68 asymptomatic hemispheres (7.4%) presented HVS (P < 0.01). Of the 46 symptomatic hemispheres with HVS, 19 (41.3%) presented with hemodynamic impairment and 27 (58.7%) presented without hemodynamic impairment. Of 19 hemispheres with hemodynamic impairment, 12 subjects (63.2%) showed high intensity and 7 (36.8%) showed iso-intensity plaques on T1WI. All 27 hemispheres without hemodynamic impairment showed high-intensity plaques. Of the five asymptomatic and HVS-positive hemispheres, one showed hemodynamic impairment; MR plaque imaging revealed T1 iso-intensity. The other four hemispheres that did not show hemodynamic impairment showed T1WI high-intensity plaques. CONCLUSION: There are two possible mechanisms of HVS, hemodynamic impairment due to severe carotid stenosis and micro-embolism from unstable plaques. HVS could be a radiological marker for high-risk carotid stenosis.