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Scientific Reports Jun 2024
PubMed: 38858541
DOI: 10.1038/s41598-024-64285-0 -
Spinal Cord Series and Cases Jun 2024Syringomyelia, or the formation of fluid-filled cysts within the spinal cord, associated with delayed spinal arachnoiditis is an uncommon complication of aneurysmal...
BACKGROUND AND IMPORTANCE
Syringomyelia, or the formation of fluid-filled cysts within the spinal cord, associated with delayed spinal arachnoiditis is an uncommon complication of aneurysmal subarachnoid haemorrhage. To date, about 18 cases have been reported in medical literature, with just two reported in patients under the age of 35 years.
CLINICAL PRESENTATION
A 27-year-old female patient complained of sudden, severe headaches in the occipital region, nuchal rigidity, and drowsiness when she presented at our institution. A head computed tomography scan revealed intraventricular bleeding in the lateral and fourth ventricles with more extensive haemorrhaging in the frontal horns. A left posterior inferior cerebellar artery (PICA) aneurysm was confirmed via digital subtraction angiogram, and endovascular embolization was done. Two years later, the patient reported intense pain in the lower back along with symptoms suggestive of spinal cord compression. Spinal magnetic resonance imaging (MRI) showed spinal adhesions from C1 to L4, syringomyelia with some vasogenic oedema extending from T3 to T9 level, and a cyst in the lumbar region. Consequently, a right hemilaminectomy was performed along with microsurgical release of arachnoid adhesions and placement of a subdural drain. Radiological and symptomatic improvements were observed. Since then, the patient's clinical condition has remained stable during the past three years of follow-up visits.
CONCLUSIONS
Literature on optimal treatment modalities and patient prognosis is scarce and debated. The time for symptom improvement depends on the level and extent of spinal cord involvement. Rehabilitation may be required for most patients, as complete symptomatic recovery may not be attainable.
Topics: Humans; Female; Arachnoiditis; Adult; Syringomyelia; Subarachnoid Hemorrhage
PubMed: 38858362
DOI: 10.1038/s41394-024-00654-1 -
World Neurosurgery Jun 2024A retrospective study of cases of endovascular treatment of dissection of the vertebral artery with subarachnoid hemorrhage was conducted.
INTRODUCTION
A retrospective study of cases of endovascular treatment of dissection of the vertebral artery with subarachnoid hemorrhage was conducted.
MATERIAL AND METHODS
Data were 11 cases of vertebral artery dissecting aneurysm (VADA)s among 291 consecutive SAH patients who underwent clipping or endovascular treatment at Ota Memorial Hospital. Classified into four patterns based on the location of the dissection and posterior inferior cerebellar artery (PICA): Pre-PICA, post-PICA, involved PICA, and non-PICA. And one of the case had bilateral vertebral artery dissection, and Computational fluid dynamics (CFD) analysis was included in the study.
RESULTS
Ruptured VADA occurred in 11 of the 291 patients (3.8%). Endovascular treatment was performed in 8 of these 11 patients. Postoperative diffusion-weighted imaging (DWI) detected no high intensity lesions and no postoperative ischemic complications or rebleeding occurred in any patient. In a case of bilateral VADA, computational fluid dynamics (CFD) analysis very low or high wall shear stress (WSS) at the dissection, low aneurysm formation indicator (AFI), and high oscillatory shear index(OSI) may be considered rupture factors.
CONCLUSION
Treatment strategies for each branching pattern of PICA can prevent rupture and avoid ischemic complications. And prediction of the rupture side is important in patients with bilateral dissection to consider the appropriate treatment and timing.
PubMed: 38857867
DOI: 10.1016/j.wneu.2024.06.007 -
Frontiers in Neurology 2024Cerebrovascular disease, among the most prevalent neurological disorders, poses a substantial threat to human health with its elevated mortality and disability rates,...
BACKGROUND
Cerebrovascular disease, among the most prevalent neurological disorders, poses a substantial threat to human health with its elevated mortality and disability rates, placing considerable strain on healthcare systems. Although several studies in recent years have suggested a potential association between digestive system diseases and cerebrovascular diseases, the findings remain inconsistent.
METHODS
Genome-wide association study (GWAS) summary data for 12 digestive diseases and cerebrovascular diseases were used to conduct Mendelian randomization (MR) analysis. In this investigation, we endeavored to elucidate the causal relationship between digestive system diseases and cerebrovascular diseases. Employing a comprehensive approach, including two-sample MR (TSMR), multivariate MR (MVMR), and two-step MR analysis, we leveraged summary statistics data obtained from published GWAS. The primary analysis method employed was inverse variance weighted (IVW), with MR-Egger and weighted median (WM) as secondary methods. Sensitivity analysis included heterogeneity testing, horizontal multivariate testing, MR-PRESSO, and a "leave-one-out" method. Additionally, the -statistic was utilized to assess the strength of instrumental variables, ensuring robust results.
RESULTS
In the TSMR analysis, this study found a significant causal relationship between genetically predicted gastroesophageal reflux disease (GERD) and any stroke (AS), any ischemic stroke (AIS), large-artery atherosclerotic stroke (LAS), intracranial aneurysm (IA), and subarachnoid hemorrhage (SAH). In MVMR analysis, this study found that even after adjusting for systolic blood pressure (SBP), body mass index (BMI) and type 2 diabetes (T2D), the causal relationship remains exist. In the two-step MR mediation analysis, it was found that BMI, SBP and T2D play mediating role in the causal relationship between GERD and cerebrovascular diseases.
CONCLUSION
This study indicates a clear positive causal relationship between GERD and cerebrovascular diseases, and this causal association remains significant even after adjusting for BMI, SBP and T2D. The mediation MR analysis suggests that BMI, SBP and T2D may mediate the causal relationship between GERD and the risk of cerebrovascular diseases.
PubMed: 38854966
DOI: 10.3389/fneur.2024.1389352 -
Cureus May 2024Cerebral venous thrombosis (CVT) is a cerebrovascular condition characterized by cerebral venous sinus thrombosis, resulting in venous infarction. The condition can...
Multifaceted Cerebral Venous Thrombosis With Extensive Intra-cerebral Hemorrhage in a Young Man With Mitral Valve Replacement Due to Thrombosis and IgA Nephropathy: A Challenging Case Report From Saudi Arabia.
Cerebral venous thrombosis (CVT) is a cerebrovascular condition characterized by cerebral venous sinus thrombosis, resulting in venous infarction. The condition can manifest through a range of signs and symptoms such as headaches, benign intracranial hypertension, subarachnoid hemorrhage, localized neurological deficits, seizures, unexplained changes in consciousness, and meningoencephalitis. Its causes are linked to numerous different conditions and factors. We report a complicated case and course of antiphospholipid antibody syndrome in a young patient. The case began two years prior, involving a 33-year-old man who had chronic kidney disease due to IgA nephropathy, pneumonia, and a large mass on his native mitral valve. He developed deep vein thrombosis (DVT) in his upper limb, for which he was prescribed warfarin. He was transferred to our hospital with a five-day history of severe headaches followed by a decrease in consciousness and seizures requiring intubation. He was found to have a subdural hematoma with a high international normalized ratio (INR). He underwent hematoma evacuation and a right decompressive craniotomy. CT of the brain via CT venography revealed intracerebral haemorrhage along with ischemic infarction in the right frontal-parietal and temporal lobes and cerebral venous thrombosis. He was treated with heparin infusion but later developed heparin-induced thrombocytopenia (HIT) and was switched to fondaparinux. Plasma exchange and intravenous methylprednisolone were given. His hospital course was complicated by recurrent infections, a new left intraparenchymal hemorrhage with intraventricular extension, and the need for extra ventricular drainage (EVD). The diagnosis of antiphospholipid antibody syndrome was confirmed. This case report provides invaluable insights into managing a complex scenario that requires balanced decisions between anticoagulation in the context of severe ICH and the necessity of immunosuppressive therapy. The emphasis is on the significance of using a personalized and multidisciplinary strategy to address CVT situations and their issues.
PubMed: 38854275
DOI: 10.7759/cureus.60016 -
European Journal of Pharmacology Jun 2024Nimodipine is used to prevent delayed ischemic deficit in patients with aneurysmal subarachnoid hemorrhage (aSAH). Spreading depolarization (SD) is recognized as a...
Nimodipine is used to prevent delayed ischemic deficit in patients with aneurysmal subarachnoid hemorrhage (aSAH). Spreading depolarization (SD) is recognized as a factor in the pathomechanism of aSAH and other acute brain injuries. Although nimodipine is primarily known as a cerebral vasodilator, it may have a more complex mechanism of action due to the expression of its target, the L-type voltage-gated calcium channels (LVGCCs) in various cells in neural tissue. This study was designed to investigate the direct effect of nimodipine on SD, ischemic tissue injury, and neuroinflammation. SD in control or nimodipine-treated live mouse brain slices was induced under physiological conditions using electrical stimulation, or by subjecting the slices to hypo-osmotic stress or mild oxygen-glucose deprivation (mOGD). SD was recorded applying local field potential recording or intrinsic optical signal imaging. Histological analysis was used to estimate tissue injury, the number of reactive astrocytes, and the degree of microglia activation. Nimodipine did not prevent SD occurrence in mOGD, but it did reduce the rate of SD propagation and the cortical area affected by SD. In contrast, nimodipine blocked SD occurrence in hypo-osmotic stress, but had no effect on SD propagation. Furthermore, nimodipine prevented ischemic injury associated with SD in mOGD. Nimodipine also exhibited anti-inflammatory effects in mOGD by reducing reactive astrogliosis and microglial activation. The results demonstrate that nimodipine directly inhibits SD, independent of nimodipine's vascular effects. Therefore, the use of nimodipine may be extended to treat acute brain injuries where SD plays a central role in injury progression.
PubMed: 38849040
DOI: 10.1016/j.ejphar.2024.176718 -
Heliyon Jun 2024Serum concentration of soluble growth stimulation expressed gene 2 (sST2) appears to have prognostic value in patients with aneurysmal subarachnoid hemorrhage (aSAH) by...
BACKGROUND
Serum concentration of soluble growth stimulation expressed gene 2 (sST2) appears to have prognostic value in patients with aneurysmal subarachnoid hemorrhage (aSAH) by now. This study aimed to investigate the relationship between cerebrospinal fluid (CSF) sST2 concentration and outcome in patients with aSAH.
METHODS
A total of 65 aSAH patients who met the inclusion criteria in the Neurosurgery Department of Jining No.1 People's Hospital from March 2021 to August 2022 were selected as the research objects. 35 patients with the third month Modified-Rankin-Scale (mRS) score of 0-2 were divided into good prognosis group, and 30 patients with the third month mRS score of 3-5 were divided into poor prognosis group. CSF was collected by lumbar puncture for the first 5 days after aneurysm surgery. CSF sST2 concentration was determined using an enzyme-linked immunosorbent assay.
RESULTS
In all patients, CSF sST2 concentrations initially increased, peaked on day 2, and then decreased. Compared with the good prognosis group, the sST2 concentration was significantly increased in the poor prognosis group at 1, 2, 3, 4 and 5 days after aSAH surgery. CSF sST2 concentration exhibited good diagnostic performance for predicting outcome (area under the receiver operating characteristic curve = 0.988). Additionally, CSF sST2 concentration has good performance for predicting cerebral edema, but only in the poor prognosis group (area under the curve = 0.93).
CONCLUSIONS
Elevated CSF sST2 concentration is associated with poor outcome in aSAH patients. CSF sST2 may have a role as a predictive biomarker in these patients.
PubMed: 38845883
DOI: 10.1016/j.heliyon.2024.e31745 -
Journal of Clinical Neuroscience :... Jun 2024Ventriculostomy-related infections (VRIs) are reported in about 10 % of patients with external ventricular drains (EVDs). VRIs are difficult to diagnose due to clinical...
BACKGROUND
Ventriculostomy-related infections (VRIs) are reported in about 10 % of patients with external ventricular drains (EVDs). VRIs are difficult to diagnose due to clinical and laboratory abnormalities caused by the primary neurological injury which led to insertion of the EVD. Polymerase chain reaction (PCR) of the cerebrospinal fluid (CSF) may enable more accurate diagnosis of VRI. We performed a prospective cohort study to measure the incidence of VRI as diagnosed by 16S rRNA PCR.
METHODS
Patients admitted to intensive care with a primary diagnosis of subarachnoid haemorrhage (SAH), traumatic brain injury (TBI), or intracerebral haemorrhage (ICH), who required an EVD, were assessed for inclusion in this study. Data were extracted from the electronic medical record, bedside charts, or from a prospectively collected database, the Neuroscience Outcomes in Intensive CarE database (NOICE). 16S rRNA PCR was performed on routinely collected CSF as per laboratory protocol. VRI was also diagnosed based on pre-existing definitions.
RESULTS
237 CSF samples from 39 patients were enrolled in the study. The mean patient age was 55.7 years, and 56.4 % were female. The most common primary neurological diagnosis was SAH (61.5 %). The incidence of a positive PCR was 2.6 % of patients (1 in 39) and 0.8 % of CSF samples (2 in 237). The incidence of VRI according to pre-published diagnostic criteria was 2.6 % - 41 % of patients and 0.4 % - 17.6 % of CSF samples. 28.2 % of patients were treated for VRI. Pre-published definitions which relied on CSF culture results had higher specificity and lower false positive rates for predicting a PCR result when compared to definitions incorporating non-microbiological markers of VRI. In CSF samples with a negative 16S rRNA PCR, there was a high proportion of non-microbiological markers of infection, and a high incidence of fever on the day the CSF sample was taken.
CONCLUSIONS
The incidence of VRI as defined as a positive PCR was lower than the incidence of VRI according to several published definitions, and lower than the incidence of VRI as defined as treatment by the clinical team. Non-microbiological markers of VRI may be less reliable than a positive CSF culture in diagnosing VRI.
PubMed: 38843672
DOI: 10.1016/j.jocn.2024.05.034 -
Delays and misdiagnosis of aneurysmal subarachnoid hemorrhage: The impact of socioeconomic barriers.Surgical Neurology International 2024
PubMed: 38840601
DOI: 10.25259/SNI_300_2024 -
Neurotherapeutics : the Journal of the... Jun 2024Calcium influx and subsequent elevation of the intracellular calcium concentration ([Ca]) induce contractions of brain pericytes and capillary spasms following...
Calcium influx and subsequent elevation of the intracellular calcium concentration ([Ca]) induce contractions of brain pericytes and capillary spasms following subarachnoid hemorrhage. This calcium influx is exerted through cation channels. However, the specific calcium influx pathways in brain pericytes after subarachnoid hemorrhage remain unknown. Transient receptor potential canonical 3 (TRPC3) is the most abundant cation channel potentially involved in calcium influx into brain pericytes and is involved in calcium influx into other cell types either via store-operated calcium entry (SOCE) or receptor-operated calcium entry (ROCE). Therefore, we hypothesized that TRPC3 is associated with [Ca] elevation in brain pericytes, potentially mediating brain pericyte contraction and capillary spasms after subarachnoid hemorrhage. In this study, we isolated rat brain pericytes and demonstrated increased TRPC3 expression and its currents in brain pericytes after subarachnoid hemorrhage. Calcium imaging of brain pericytes revealed that changes in TRPC3 expression mediated a switch from SOCE-dominant to ROCE-dominant calcium influx after subarachnoid hemorrhage, resulting in significantly higher [Ca] levels after SAH. TRPC3 activity in brain pericytes also contributed to capillary spasms and reduction in cerebral blood flow in an in vivo rat model of subarachnoid hemorrhage. Therefore, we suggest that the switch in TRPC3-mediated calcium influx pathways plays a crucial role in the [Ca] elevation in brain pericytes after subarachnoid hemorrhage, ultimately leading to capillary spasms and a reduction in cerebral blood flow.
PubMed: 38839450
DOI: 10.1016/j.neurot.2024.e00380