ABSTRACT
Aneurysmal subarachnoid hemorrhage (SAH) has increased with the aging of the population, but the outcome for elderly SAH patients is very poor. Therefore, predicting the outcome is important for determining whether to pursue aggressive treatment. Pigment epithelium-derived factor (PEDF) is a matricellular protein that is induced in the brain, and the plasma levels could be used as a biomarker for the severity of metabolic diseases. This study investigated whether acute-phase plasma PEDF levels could predict outcomes after aneurysmal SAH in the elderly. Plasma samples and clinical variables were collected over 1-3 days, post-SAH, from 56 consecutive elderly SAH patients ≥75 years of age registered in nine regional stroke centers in Japan between September 2013 and December 2016. The samples and variables were analyzed in terms of 3-month outcomes. Acute-phase plasma PEDF levels were significantly elevated in patients with ultimately poor outcomes, and the cutoff value of 12.6 µg/mL differentiated 3-month outcomes with high sensitivity (75.6%) and specificity (80.0%). Acute-phase plasma PEDF levels of ≥12.6 µg/mL were an independent and possibly better predictor of poor outcome than previously reported clinical variables. Acute-phase plasma PEDF levels may serve as the first biomarker to predict 3-month outcomes and to select elderly SAH patients who should be actively treated.
Subject(s)
Serpins , Subarachnoid Hemorrhage , Aged , Humans , Biomarkers , Eye Proteins , Nerve Growth Factors , Serpins/blood , Serpins/chemistry , Subarachnoid Hemorrhage/blood , Subarachnoid Hemorrhage/diagnosis , Treatment OutcomeABSTRACT
The diagnosis of dural arteriovenous fistulas(DAVF)has advanced with the development of imaging techniques. The indication for treatment of DAVF is generally based on classification according to the venous drainage pattern, which determines whether the presentation is benign or aggressive. In recent years, with the introduction of Onyx, transarterial embolization has been increasingly used, and outcomes have improved, although some conditions are more suitable for transvenous embolization. It is important to select an optimal approach based on location and angioarchitecture. Since DAVF is a rare vascular disease with limited evidence, further validation of clinical results is needed to provide more established treatment guidelines.
Subject(s)
Central Nervous System Vascular Malformations , Embolization, Therapeutic , Humans , Polyvinyls/therapeutic use , Central Nervous System Vascular Malformations/diagnostic imaging , Central Nervous System Vascular Malformations/surgery , Embolization, Therapeutic/methods , Vascular Surgical Procedures , Treatment OutcomeABSTRACT
PURPOSE: Cerebellar hypoplasia and atrophy (CBHA) in children is an extremely heterogeneous group of disorders, but few comprehensive genetic studies have been reported. Comprehensive genetic analysis of CBHA patients may help differentiating atrophy and hypoplasia and potentially improve their prognostic aspects. METHODS: Patients with CBHA in 176 families were genetically examined using exome sequencing. Patients with disease-causing variants were clinically evaluated. RESULTS: Disease-causing variants were identified in 96 of the 176 families (54.5%). After excluding 6 families, 48 patients from 42 families were categorized as having syndromic associations with CBHA, whereas the remaining 51 patients from 48 families had isolated CBHA. In 51 patients, 26 aberrant genes were identified, of which, 20 (76.9%) caused disease in 1 family each. The most prevalent genes were CACNA1A, ITPR1, and KIF1A. Of the 26 aberrant genes, 21 and 1 were functionally annotated to atrophy and hypoplasia, respectively. CBHA+S was more clinically severe than CBHA-S. Notably, ARG1 and FOLR1 variants were identified in 2 families, leading to medical treatments. CONCLUSION: A wide genetic and clinical diversity of CBHA was revealed through exome sequencing in this cohort, which highlights the importance of comprehensive genetic analyses. Furthermore, molecular-based treatment was available for 2 families.
Subject(s)
Exome , Nervous System Malformations , Child , Humans , Exome/genetics , Mutation , Nervous System Malformations/genetics , Atrophy/genetics , Folate Receptor 1/genetics , KinesinsABSTRACT
Aneurysmal subarachnoid hemorrhage (SAH) is a poor-outcome disease with a delayed neurological exacerbation. Fibulin-5 (FBLN5) is one of matricellular proteins, some of which have been involved in SAH pathologies. However, no study has investigated FBLN5's roles in SAH. This study was aimed at examining the relationships between serially measured plasma FBLN5 levels and neurovascular events or outcomes in 204 consecutive aneurysmal SAH patients, including 77 patients (37.7%) with poor outcomes (90-day modified Rankin Scale 3-6). Plasma FBLN5 levels were not related to angiographic vasospasm, delayed cerebral ischemia, and delayed cerebral infarction, but elevated levels were associated with severe admission clinical grades, any neurological exacerbation and poor outcomes. Receiver-operating characteristic curves indicated that the most reasonable cut-off values of plasma FBLN5, in order to differentiate 90-day poor from good outcomes, were obtained from analyses at days 4-6 for all patients (487.2 ng/mL; specificity, 61.4%; and sensitivity, 62.3%) and from analyses at days 7-9 for only non-severe patient (476.8 ng/mL; specificity, 66.0%; and sensitivity, 77.8%). Multivariate analyses revealed that the plasma FBLN5 levels were independent determinants of the 90-day poor outcomes in both all patients' and non-severe patients' analyses. These findings suggest that the delayed elevation of plasma FBLN5 is related to poor outcomes, and that FBLN5 may be a new molecular target to reveal a post-SAH pathophysiology.
Subject(s)
Brain Ischemia , Subarachnoid Hemorrhage , Vasospasm, Intracranial , Humans , Subarachnoid Hemorrhage/complications , Brain Ischemia/complications , Cerebral Infarction/complications , ROC Curve , Vasospasm, Intracranial/complicationsABSTRACT
BACKGROUND: The pathogenesis of abdominal symptoms in premature infants with hypothyroxinemia is not understood; therefore, we investigated changes in gut hormones before and after levothyroxine sodium (T4-Na) supplementation in preterm infants with abdominal symptoms and hypothyroxinemia. METHODS: In eight preterm study subjects and 14 gestational age-matched controls, fasting serum concentration of leptin, glucose-dependent insulinotropic polypeptide (GIP), glucagon-like peptide-1 (GLP-1), peptide YY (PYY), pancreatic polypeptide, insulin, amylin and ghrelin was measured using a bead array system. RESULTS: Serum GLP-1, GIP and PYY in the subjects before T4-Na supplementation were lower than in controls at age 2 weeks. After improvement of abdominal symptoms and free thyroxine, serum levels of the three gut hormones in the subjects were increased and were not different from those in the control patients. CONCLUSIONS: In preterm infants with abdominal symptoms, serum GLP-1, GIP and PYY might be related to thyroid function.
Subject(s)
Gastrointestinal Hormones/blood , Infant, Premature, Diseases/blood , Infant, Premature/blood , Thyroxine/deficiency , Female , Humans , Infant, Newborn , Male , Retrospective Studies , Thyroxine/bloodABSTRACT
We studied the cytokine profile of two siblings with neonatal lupus erythematosus (NLE) born to a mother positive for serum anti-Ro and -La antibodies, who did not receive any medication during the two pregnancies. The first sibling was found to have complete atrioventricular block in utero and became severely ill after birth. He fulfilled the diagnostic criteria for hemophagocytic lymphohistiocytosis on day 2. The second sibling did not have any fetal symptoms. He was generally stable after birth, but with typical skin rash. Laboratory data suggested that they both had hypercytokinemia during the neonatal period, requiring corticosteroid treatment. Interleukin (IL)-6, interferon-γ, IL-8 and monocyte chemotactic protein-1 were elevated in both cases, while IL-12, IL-13 and IL-17 were elevated only in the second sibling. Comparison of the cytokine profiles suggests the potential roles of different cytokines in the onset and clinical manifestations of NLE.
Subject(s)
Cytokines/blood , Lupus Erythematosus, Systemic/congenital , Pregnancy Complications/blood , Siblings , Adult , Female , Humans , Lupus Erythematosus, Systemic/blood , Lupus Erythematosus, Systemic/embryology , PregnancyABSTRACT
Retinal neurodegeneration, characterized by retinal ganglion cell (RGC) death, is a leading cause of vision impairment and loss in blind diseases, such as glaucoma. Müller cells play crucial roles in maintaining retinal homeostasis. Thus, dysfunction of Müller cells has been implicated as one of the causes of retinal diseases. Yes-associated protein 1 (YAP), a nuclear effector of the Hippo pathway, regulates mammalian cell survival. In this study, we investigated the role of YAP in Müller cells during N-methyl-D-aspartic acid (NMDA)-induced excitotoxic RGC injury in rats. We found that YAP expression increased and was activated in Müller cells after NMDA-induced RGC injury. This YAP response was partly due to an increase in Yap mRNA levels, although it may be independent of the Hippo pathway and ß-TrCP-mediated YAP degradation. Morphological analysis revealed that verteporfin, a selective YAP inhibitor, exacerbated NMDA-induced RGC degeneration, suggesting that YAP activation in Müller cells contributes to RGC survival in NMDA-treated retinas. Studies in the rat Müller cell line (rMC-1) demonstrated that overexpression of YAP increased the levels of Bcl-xL, while verteporfin decreased the levels of Bcl-xL and cell viability and increased the levels of cytochrome c released from mitochondria and cleaved caspase-3. Finally, we found that Bcl-xL expression increased slightly in NMDA-treated retinas, whereas intravitreal injection of verteporfin suppressed this increase. Our findings suggest that activated YAP in Müller cells protects against NMDA-induced RGC injury by upregulating Bcl-xL expression.
ABSTRACT
BACKGROUND: The opportunities to treat elderly patients with aneurysmal subarachnoid hemorrhage (aSAH) are increasing globally, but the outcome remains poor. This study seeks to investigate treatment-related factors that can modify functional outcomes in patients with aSAH aged ≥75 years. METHODS: A total of 202 patients with aSAH aged ≥75 years prospectively enrolled in 9 primary stroke centers from 2013 to 2021 were retrospectively analyzed. Clinical variables including treatments for hydrocephalus, angiographic vasospasm, and delayed cerebral ischemia were compared between patients with good (modified Rankin Scale [mRS] score 0-2) and poor (mRS score 3-6) outcomes at 90 days from onset, followed by multivariate analyses to find independent outcome determinants. A modifiable treatment-related variable was evaluated after propensity score matching with adjustments for age, sex, pre-onset mRS score, aSAH severity, and treatment modality. RESULTS: More than half of patients showed World Federation of Neurological Societies grades IV-V on admission. Univariate analyses showed that advanced age, worse pre-onset mRS score, more severe neurologic status on admission, higher modified Fisher grade on admission computed tomography scans, and acute and chronic hydrocephalus were associated with poor outcomes. In contrast, administration of a phosphodiesterase type III inhibitor, cilostazol, was associated with good outcomes in both univariate (P = 0.036) and multivariate analyses (adjusted odds ratio, 0.305; 95% confidence interval, 0.097-0.955; P = 0.042). Propensity score matching analyses showed that patients treated with cilostazol had better outcomes (P = 0.016) with fewer incidences of delayed cerebral infarction (P = 0.008). CONCLUSIONS: Even in patients with aSAH aged ≥75 years, cilostazol administration may lead to better outcomes by suppressing the development of delayed cerebral infarction.
Subject(s)
Hydrocephalus , Subarachnoid Hemorrhage , Vasospasm, Intracranial , Aged , Humans , Cilostazol/therapeutic use , Subarachnoid Hemorrhage/complications , Retrospective Studies , Propensity Score , Cerebral Infarction/etiology , Phosphodiesterase 3 Inhibitors/therapeutic use , Vasospasm, Intracranial/etiology , Hydrocephalus/complications , Treatment OutcomeABSTRACT
Cerebellar and/or vermis atrophy is recognized in various types of childhood disorders with clinical and genetic heterogeneity. Although careful evaluation of clinical features and neuroimaging can lead to correct diagnosis of disorders, their diagnosis is sometimes difficult because clinical features can overlap with each other. In this study, we performed family-based whole exome sequencing of 23 families including 25 patients with cerebellar and/or vermis atrophy in childhood, who were unable to be diagnosed solely by clinical examination. Pathological mutations of seven genes were found in ten patients from nine families (9/23, 39.1 %): compound heterozygous mutations in FOLR1, C5orf42, POLG, TPP1, PEX16, and de novo mutations in CACNA1A, and ITPR1. Patient 1A with FOLR1 mutations showed extremely low concentration of 5-methyltetrahydrofolate in the cerebrospinal fluid and serum, and Patient 6 with TPP1 mutations demonstrated markedly lowered tripeptidyl peptidase 1 activity in leukocytes. Furthermore, Patient 8 with PEX16 mutations presented a mild increase of very long chain fatty acids in the serum as supportive data for genetic diagnosis. The main clinical features of these ten patients were nonspecific and mixed, and included developmental delay, intellectual disability, ataxia, hypotonia, and epilepsy. Brain MRI revealed both cerebellar and vermis atrophy in eight patients (8/10, 80 %), vermis atrophy/hypoplasia in two patients (2/10, 20 %), and brainstem atrophy in one patient (1/10, 10 %). Our data clearly demonstrate the utility of whole exome sequencing for genetic diagnosis of childhood cerebellar and/or vermis atrophy.
Subject(s)
Cerebellum/pathology , Mutation , Adolescent , Atrophy/diagnosis , Atrophy/genetics , Child , Child, Preschool , DNA Mutational Analysis , Exome , Humans , Male , Tripeptidyl-Peptidase 1 , Young AdultABSTRACT
A 65-year-old man developed progressive worsening of right-sided limb-kinetic apraxia and extrapyramidal dysfunction. His left internal carotid artery was found to be occluded, and there was general atrophy and severely decreased cerebral blood flow in the left hemisphere. He had experienced an acute infarction in the left watershed area before superficial temporal artery to middle cerebral artery bypass surgery. After surgery, the cerebral blood flow in the left hemisphere was remarkably improved. Unilateral internal carotid artery occlusion may result in clinical manifestations similar to corticobasal degeneration.
Subject(s)
Apraxias/etiology , Carotid Artery, Internal/surgery , Carotid Stenosis/complications , Gait Disorders, Neurologic/etiology , Aged , Apraxias/surgery , Atrophy/complications , Carotid Stenosis/surgery , Gait Disorders, Neurologic/surgery , Humans , Male , Syndrome , Treatment OutcomeABSTRACT
OBJECTIVE: Although snares are useful devices to retrieve an intravascular foreign body, the control of snares is often difficult. We present a safe and effective technique to adjust snare position in the tortuous vessel for coil retrieval during endovascular coil embolization. METHODS: We describe a case of a protruding coil during coil embolization that was successfully retrieved using a unique technique to adjust snare position and discuss additional intraprocedural bailout strategies for retrieving a coil during endovascular coil embolization. RESULTS: The patient was a 44-year-old female with unruptured right internal carotid artery (ICA) aneurysm that had grown over a 1.5-year period. Coil embolization was performed. After detachment of final coil and microcatheter removal, the final coil protruded into the ICA and floated. Coil retrieval using a snare was attempted, but the snare could not be placed around the coil tail and coil retrieval could not be achieved. The following technique was used to allow adjustment of snare position. First, a microguidewire and a microcatheter were guided into the M2 and M1 segment of the middle cerebral artery as monorail guides of the snare, respectively. Next, the snare was advanced over the microcatheter. Around C2 segment of the ICA, the microcatheter and the snare were manipulated as a unit. Thus, the snare could be placed around the protruding coil tail and the coil was retrieved successfully. CONCLUSIONS: This technique may be widely adapted for various situations when using a snare.
Subject(s)
Carotid Artery Diseases , Embolization, Therapeutic , Foreign Bodies , Intracranial Aneurysm , Female , Humans , Adult , Embolization, Therapeutic/methods , Intracranial Aneurysm/diagnostic imaging , Intracranial Aneurysm/surgery , Middle Cerebral Artery , Carotid Artery, Internal/diagnostic imaging , Carotid Artery, Internal/surgeryABSTRACT
OBJECTIVE: To elucidate the relationship between abnormal lung function (LF) at school age and neonatal respiratory support in very low birth weight children with bronchopulmonary dysplasia (BPD). STUDY DESIGN: We retrospectively examined 78 BPD children whose LF was evaluated at 8-9 years. LF abnormalities were defined by reduced values of spirometric parameters. Adjusted odds ratios (aORs) for abnormal LF by the type and postmenstrual age (PMA) of respiratory support were calculated using logistic regression analysis after controlling perinatal factors. RESULTS: Overall, 24 (31%) patients had LF abnormalities. Antenatal steroid use was associated with a decreased risk of abnormal LF [aOR, 0.31; 95% CI, 0.09-0.92]. Requiring positive-pressure support at 37 weeks' PMA correlated with abnormal LF [aOR, 4.58; 95% CI, 1.15-21.90]; whereas only low-flow oxygen at any PMA did not. CONCLUSION: Requiring positive-pressure support at 37 weeks' PMA could be an indicator of abnormal LF at school age.
Subject(s)
Bronchopulmonary Dysplasia , Infant, Newborn , Humans , Child , Female , Pregnancy , Bronchopulmonary Dysplasia/complications , Infant, Premature , Retrospective Studies , Infant, Very Low Birth Weight , LungABSTRACT
Matricellular proteins have been implicated in pathologies after subarachnoid hemorrhage (SAH). To find a new therapeutic molecular target, the present study aimed to clarify the relationships between serially measured plasma levels of a matricellular protein, secreted protein acidic and rich in cysteine (SPARC), and delayed cerebral ischemia (DCI) in 117 consecutive aneurysmal SAH patients with admission World Federation of Neurological Surgeons (WFNS) grades I-III. DCI developed in 25 patients with higher incidences of past history of hypertension and dyslipidemia, preoperative WFNS grade III, modified Fisher grade 4, spinal drainage, and angiographic vasospasm. Plasma SPARC levels were increased after SAH, and significantly higher in patients with than without DCI at days 7-9, and in patients with VASOGRADE-Yellow compared with VASOGRADE-Green at days 1-3 and 7-9. However, there were no relationships between plasma SPARC levels and angiographic vasospasm. Receiver-operating characteristic curves differentiating DCI from no DCI determined the cut-off value of plasma SPARC ≥ 82.1 ng/ml at days 7 - 9 (sensitivity, 0.800; specificity, 0.533; and area under the curve, 0.708), which was found to be an independent determinant of DCI development in multivariate analyses. This is the first study to show that SPARC is upregulated in peripheral blood after SAH, and that SPARC may be involved in the development of DCI without angiographic vasospasm in a clinical setting.
Subject(s)
Brain Ischemia , Subarachnoid Hemorrhage , Humans , Osteonectin , Brain Ischemia/etiologyABSTRACT
BACKGROUND: The influence of neurological or balance dysfunction on cognitive impairment has not been well studied. We compared the results of the balance test, measured by either head or foot sway to consider whole body sway, with those of the cognitive impairment test. METHODS: Individuals of either gender, aged over 60 years, underwent a 30 s balance test. We measured sway while standing on one-leg or two-legs. Sway was evaluated by the distance or area of movement of the head or foot pressure. We also evaluated the effect of visual condition: eyes-open (EO) or -closed (EC). The Mini-Mental State Examination (MMSE) was used to evaluate the degree of cognitive impairment. RESULTS: The head sway area standing on one leg was significantly correlated to MMSE score with EO (correlation r = -0.462). In standing on two legs, no sway test results showed a significant correlation to MMSE scores with EO. With EC, the magnitude of sway became greater, and was significantly correlated to MMSE scores in the head distance. CONCLUSION: Although the correlation between head sway and MMSE was not strong, head sway showed a stronger correlation than did foot pressure sway. Standing on one leg, as measured by head sway area, may thus predict cognitive impairment.
ABSTRACT
Objective: We aimed to evaluate the efficacy of the "improved motion-sensitized driven-equilibrium (iMSDE)"-prepared T1-weighted black blood (T1-BB) MRI for monitoring treatment effect with a flow diverter (FD) for cerebral aneurysms. Methods: Following the exclusion of concomitant coiling and retreatment cases from 60 consecutive cases of cerebral aneurysms treated with FDs at our institution, 32 with imaging data were included in the analysis. Detectability of residual blood flow within the aneurysms was validated as follows: 1) comparison of MRI sequences (iMSDE-prepared T1-BB images, T1-weighted images [âT1WI], and time-of-flight [âTOF]-MRA) in cases of incompletely occluded aneurysms and 2) comparison of angiography and MRI sequences in the same period. Results: 1) The probability of diagnosing intra-aneurysmal blood flow was significantly higher with iMSDE-prepared T1-BB (iMSDE-prepared T1-BB vs. T1WI, p <0.001; iMSDE-prepared T1-BB vs. TOF-MRA, p <0.001). 2) The diagnostic accuracy of residual aneurysmal blood flow was significantly higher with iMSDE-prepared T1-BB than that with T1WI (p = 0.032). Furthermore, in cases of incomplete occlusion, the probability of detecting intra-aneurysmal blood flow was significantly higher with iMSDE-prepared T1-BB (iMSDE-prepared T1-BB vs. T1WI, p <0.001; iMSDE-prepared T1-BB vs. TOF-MRA, p = 0.023). Conclusion: Our results demonstrated that iMSDE-prepared T1-BB could help distinguish between blood flow and thrombus within the aneurysms after FD treatment, especially in the early stages of FD treatment.
ABSTRACT
Subtelomeric deletions of 1q44 cause mental retardation, developmental delay and brain anomalies, including abnormalities of the corpus callosum (ACC) and microcephaly in most patients. We report the cases of six patients with 1q44 deletions; two patients with interstitial deletions of 1q44; and four patients with terminal deletions of 1q. One of the patients showed an unbalanced translocation between chromosome 5. All the deletion regions overlapped with previously reported critical regions for ACC, microcephaly and seizures, indicating the recurrent nature of the core phenotypic features of 1q44 deletions. The four patients with terminal deletions of 1q exhibited severe volume loss in the brain as compared with patients who harbored interstitial deletions of 1q44. This indicated that telomeric regions have a role in severe volume loss of the brain. In addition, two patients with terminal deletions of 1q43, beyond the critical region for 1q44 deletion syndrome exhibited delayed myelination. As the deletion regions identified in these patients extended toward centromere, we conclude that the genes responsible for delayed myelination may be located in the neighboring region of 1q43.
Subject(s)
Agenesis of Corpus Callosum/diagnosis , Agenesis of Corpus Callosum/genetics , Chromosome Deletion , Chromosomes, Human, Pair 1 , Microcephaly/diagnosis , Microcephaly/genetics , Brain/metabolism , Brain/pathology , Child , Child, Preschool , DNA Copy Number Variations , Facies , Female , Humans , Infant , Karyotyping , Magnetic Resonance Imaging , Male , Myelin Sheath/physiology , Phenotype , Syndrome , TelomereSubject(s)
Adrenergic beta-Antagonists/therapeutic use , Kasabach-Merritt Syndrome/drug therapy , Liver Neoplasms/drug therapy , Propranolol/therapeutic use , Humans , Infant, Newborn , Kasabach-Merritt Syndrome/congenital , Kasabach-Merritt Syndrome/diagnosis , Liver Neoplasms/congenital , Liver Neoplasms/diagnosis , MaleABSTRACT
Aneurysmal subarachnoid hemorrhage (SAH) is a stroke type with a high rate of mortality and morbidity. Post-SAH brain injury as a determinant of poor outcome is classified into the following two types: early brain injury (EBI) and delayed cerebral ischemia (DCI). EBI consists of various acute brain pathophysiologies that occur within the first 72 hours of SAH in a clinical setting. The underlying mechanisms of DCI are considered to be cerebral vasospasm or microcirculatory disturbance, which develops mostly 4 to 14 days after clinical SAH. Glutamate is the principal neurotransmitter in the central nervous system, but excessive glutamate is known to induce neurotoxicity. Experimental and clinical studies have revealed that excessive glutamates are released after SAH. In addition, many studies have reported the relationships between excessive glutamate release or overactivation of glutamate receptors and excitotoxicity, cortical spreading depolarization, seizure, increased blood-brain barrier permeability, neuroinflammation, microthrombosis formation, microvasospasm, cerebral vasospasm, impairments of brain metabolic supply and demand, impaired neurovascular coupling, and so on, all of which potentially contribute to the development of EBI or DCI. As glutamates always exert their functions through one or more of 4 major receptors of glutamates, it would be valuable to know the mechanisms as to how glutamates cause these pathologies, and the possibility that a glutamate receptor antagonist may block the pathologies. To prevent the mechanistic steps leading to glutamate-mediated neurotoxicity may ameliorate SAH-induced brain injuries and improve the outcomes. This review addresses the current knowledge of glutamate-mediated neurotoxicity, focusing on EBI and DCI after SAH.
Subject(s)
Brain Injuries , Subarachnoid Hemorrhage , Vasospasm, Intracranial , Humans , Subarachnoid Hemorrhage/complications , Glutamic Acid , Vasospasm, Intracranial/etiology , Microcirculation , Brain Injuries/etiologyABSTRACT
OBJECTIVE: The objective was to clarify predisposing factors of recurrence after coil embolization for internal carotid-posterior communicating artery (IC-Pcom) aneurysms. METHODS: The medical records were retrospectively reviewed and patients harboring IC-Pcom aneurysms treated with coil embolization between June 2004 and June 2020 were identified. Aneurysms whose 3-dimensional images were available, whose initial treatment was performed during the study period, and whose follow-up term was more than 1 year were included. Information of the patients, the aneurysms and Pcoms, the initial treatment, and angiographic outcomes were collected. The IC-Pcom aneurysms were divided into Pcom-incorporated when their neck mainly rode on the Pcom or non-Pcom-incorporated when their neck mainly rode on the internal carotid artery or the classification was equivocal. Relationship between these factors and recurrence was analyzed. RESULTS: Fifty-seven IC-Pcom aneurysms from 55 patients were recruited. Fifteen of the 57 aneurysms were categorized into Pcom-incorporated. Eighteen of the 57 aneurysms recurred. Mean follow-up term was 74.3 months and mean duration between the initial treatment and recurrence was 47.9 months. On univariate analyses, ruptured (P = 0.004), fetal-type Pcom (P = 0.002), and Pcom-incorporated (P < 0.001) were significantly correlated with recurrence. Multivariate analysis demonstrated that Pcom-incorporated aneurysms were significantly associated with recurrence (P < 0.001) along with ruptured (P = 0.027). Kaplan-Meier estimate demonstrated that cumulative recurrence-free rate was significantly lower in Pcom-incorporated aneurysms compared with non-Pcom-incorporated aneurysms (log-rank P < 0.001). CONCLUSIONS: Pcom-incorporated IC-Pcom aneurysms were susceptible to recur after coil embolization, especially when ruptured and the incorporated Pcom was fetal-type.
Subject(s)
Embolization, Therapeutic , Intracranial Aneurysm , Angiography , Blood Vessel Prosthesis , Carotid Artery, Internal/diagnostic imaging , Embolization, Therapeutic/adverse effects , Humans , Intracranial Aneurysm/complications , Intracranial Aneurysm/diagnostic imaging , Intracranial Aneurysm/therapy , Retrospective Studies , Treatment OutcomeABSTRACT
OBJECTIVE: The risk of embolization to distal territory or to new territory in mechanical thrombectomy remains a major issue despite advancements in technological device. This condition can be caused by a large and firm dropped thrombus without passing through a guiding catheter during stent retriever or aspiration catheter withdrawal. This report introduced a novel technique referred to as retrograde angiography to detect dropped thrombus. METHODS: The retrograde angiography to detect dropped thrombus technique is a kind of retrograde angiography that consists of a contrast medium injection via a distal microcatheter and aspiration through an inflated balloon-guiding catheter. This method was used to detect dropped thrombus at the balloon-guiding catheter tip when back flow was blocked from the balloon-guiding catheter after stent retriever or aspiration catheter withdrawal. We retrospectively reviewed four consecutive patients who underwent the retrograde angiography to detect dropped thrombus technique during mechanical thrombectomy for acute ischemic stroke due to large vessel occlusion in the anterior circulation between January 2018 and January 2021. RESULTS: Three of four patients had dropped thrombus, which was diagnosed with the technique and retrieved completely with subsequent procedures while maintaining the balloon-guiding catheter inflated. None of the patients experienced embolization to distal territory/embolization to new territory, and a successful reperfusion was achieved in all four cases. CONCLUSIONS: The retrograde angiography to detect dropped thrombus is a technique to detect a dropped thrombus at the balloon-guiding catheter tip and allows us to retrieve it with subsequent mechanical thrombectomy procedures while maintaining the balloon-guiding catheter inflated and it may be useful for reducing the risk of embolization to distal territory/embolization to new territory.