Hypereosinophilia is a rare condition, defined as a persistent elevation of absolute eosinophil count greater than 1.5x109/L and/or tissue eosinophilia. This condition can be caused by numerous different etiologies, both hematological (clonal) and non-hematological (reactive). Reactive hypereosinophilia encompasses all disorders, including infections. Patients with hypereosinophilia may experience a spectrum of clinical consequences due to multiple organ damage, including neurologic and thrombotic complications, associated with organ dysfunction and potentially life-threatening sequelae. Cerebral venous thrombosis (CVT) is the term used to describe thrombotic occlusion of veins and/or venous sinuses in the brain. This condition can occur at all ages and CVT related to hypereosinophilia is a rare disease. Diagnosis of the disease must be done quickly because thrombosis causes blockage of cerebral drainage, venous congestion, disruption of cerebrospinal fluid reabsorption, ischemic neuronal damage, cerebral edema, and hemorrhage, leading to severe neurological complications. Management of intracranial hemorrhage from CVT due to hypereosinophilia is a challenging task for clinicians, based on anticoagulation therapy, systemic corticosteroid, management of elevated intracranial pressure, and potentially progressive hemorrhage due to anticoagulant. The outcome of the patient generally relies on early detection, prompt, and appropriate treatment. In this case report, we discuss a rare case of CVT with hypereosinophilia and positive dengue serology in a child, in the context of intracranial hemorrhage, enlightening the importance of considering a personalized strategy in the management of this complex scenario.

UNASSIGNED: Factor XIII (FXIII) deficiency, a rare coagulation disorder resulting from F13A1 gene mutations, can lead to severe bleeding episodes, especially in infants. The authors\' case study featuring a 16-year-old female with a history of this deficiency revealed intracranial hemorrhage necessitating immediate medical intervention. The text emphasizes the importance of understanding the epidemiology and genetics of FXIII deficiency, as well as the challenges in diagnosis and management.
UNASSIGNED: A 16-year-old female with FXIII deficiency presented to the Emergency Department (ER) after a fall, experiencing weakness on her right side, headache, seizures, and altered consciousness. Neurological examination showed weakness and increased tone on the right side of the body. Computed tomography (CT) scan revealed an intracranial subdural hemorrhage overlying the superior parietal lobe. Treatment included IV fluids, sodium valproate, antibiotics, fresh frozen plasma, and mannitol. Serial neurological assessments were normal, and the patient remained stable. MRI later confirmed hemorrhage. Upon discharge, she was prescribed medication and physiotherapy, leading to significant improvement at the 6-month follow-up.
UNASSIGNED: The prevalence of FXIII deficiency, a rare disorder, is higher in populations with consanguineous marriages, particularly in regions like Pakistan, India, Tunisia, Finland, and Iran due to specific genetic mutations. Diagnosis involves thorough evaluation and specific lab tests, with varied clinical symptoms including prolonged bleeding, especially in newborns. FXIII deficiency can also develop in association with conditions like hepatic failure and leukemia, complicating diagnosis. Treatment options include blood products and recombinant FXIII, with management of intracranial bleeding requiring a multidisciplinary approach.
UNASSIGNED: The case underscores the critical need for early identification and specialized care for individuals with FXIII deficiency to mitigate life-threatening complications like intracranial hemorrhage, promoting tailored treatment approaches and improved patient outcomes.

BACKGROUND: Intracranial hemorrhage (ICH) is a potential complication associated with extracorporeal membrane oxygenation (ECMO), which has been increasingly utilized in recent years. A paucity of data exists describing patient outcomes following invasive neurosurgical interventions in patients receiving ECMO therapy. The purpose of this study was to assess the clinical and functional outcomes in patients who underwent cranial neurosurgery for the management of an ECMO-associated intracranial complication.
METHODS: This was a single-institution retrospective review of adult patients who underwent craniotomy or craniectomy after sustaining an intracranial hemorrhagic complication of ECMO therapy from 2008-2023. Anticoagulation status, operative indication, surgical details, post-operative course, and functional outcome were recorded. A systematic review of the prior literature was performed to contextualize our institutional results within previous reports.
RESULTS: Four adult patients were identified at our institution who underwent craniotomy or craniectomy for the neurosurgical management of an ECMO-associated ICH. One patient (25%) ultimately made a satisfactory recovery (mRS 3 at one year). The surviving patient had a notably higher GCS (7T vs 3T), had not received anticoagulation at the time of surgery, and did not experience post-operative re-accumulation or expansion of their hemorrhage, distinguishing factors from the other three included. Review of the existing literature identified 15 adult patients who underwent craniotomy while receiving ECMO therapy, of which four (26.7%) had a long-term favorable neurologic outcome.
CONCLUSIONS: The overall prognosis following neurosurgical intervention for the management of ECMO-associated intracranial complications was poor in our case series, which was corroborated by our literature review.

Neoplastic cerebral aneurysms (NCAs) are rare. This study reported a case of an NCA secondary to a poorly differentiated carcinoma of the parotid gland. An 84-year-old Japanese woman undergoing treatment for parotid gland cancer was admitted to our hospital with headache and progressive loss of consciousness. Based on computed tomography (CT) and CT angiography (CTA), a diagnosis of subarachnoid hemorrhage due to rupture of a left posterior inferior cerebellar artery aneurysm was made, and emergency aneurysmectomy was performed. Pathological examination of the resected aneurysm showed an NCA secondary to parotid carcinoma. After the aneurysmectomy, her condition stabilized; however, 33 days later, the patient developed an intracerebral hemorrhage, and a new aneurysm was confirmed in the right middle cerebral artery. To the best of our knowledge, there have been no previous reports on cases of NCAs secondary to parotid carcinoma. The pathology and clinical course strongly suggest that NCAs derived from malignant tumors may have an aggressive course.

A 40-year-old woman presented with mediastinitis, necrotizing pancreatitis, and severe acute respiratory distress syndrome with refractory acidemia (pH 7.14) and hypercapnia (PaCO2 115 mmHg), requiring veno-venous extracorporeal membrane oxygenation (ECMO). Eight hours after cannulation, and rapid correction of PaCO2 to 44 mmHg, she was found to have bilaterally fixed and dilated pupils. Imaging showed a 60 mL left-sided temporoparietal intracranial hemorrhage with surrounding edema, 8 mm midline shift, intraventricular hemorrhage, and impending herniation. Decompressive hemicraniectomy was not offered due to concern for medical instability. After receiving a dose of mannitol, her pupillary and motor exam improved. An intracranial pressure (ICP) monitor was placed to guide hyperosmolar therapy administration, hemodynamic targets, and sweep gas titration. On hospital day (HD) 5, her ICP monitor was removed. Follow-up imaging revealed resolution of mass effect and no brainstem injury. She was subsequently extubated (HD 9) and discharged home (HD 40). One year after hospitalization, she is living at home with minimal residual deficits. This case highlights the utility of targeted, medical ICP management and importance of assessing response to conservative therapies when considering prognosis in patients on ECMO with severe acute brain injury.

BACKGROUND: Although contrast extravasation on follow-up head computed tomography (CT) is frequently visualized after endovascular treatment, this phenomenon is rare after intravenous thrombolytic treatment in patients with acute ischemic stroke (AIS). Here, we report a case of contrast extravasation mimicking intracerebral hemorrhage (ICH) with intraventricular extension after intravenous thrombolytic treatment and computed tomography angiography (CTA).
METHODS: A 52-year-old man presented with right-sided hemiparesis and hypoesthesia. Initial non-contrast head CT was negative for intracranial hemorrhage and acute ischemic changes. He received intravenous treatment with tenecteplase 3.8 h after the onset of stroke. CTA of the head and neck was performed at 4.3 h after stroke onset. It showed no stenosis or occlusion of the carotid and major intracranial arteries. At about 1.5 h after CTA, the right-sided hemiparesis deteriorated, accompanied by drowsiness, aphasia, and urinary incontinence. Immediate head CT showed hyperdense lesions with mild space-occupying effect in the left basal ganglia and both lateral ventricles. The hyperdense lesions were reduced in size on follow-up CT after 5 h. Two days later, CT showed that the hyperdense lesions in the lateral ventricles almost completely disappeared and only a small amount remained in the infarcted area.
CONCLUSIONS: Contrast extravasation into the brain tissue and lateral ventricles, mimicking ICH with intraventricular extension, could occur after intravenous thrombolytic treatment and CTA in a patient with AIS, which might lead to misdiagnosis and wrong treatment of the patient. The rapid resolution of intracranial hyperdense lesions is key to differentiate contrast extravasation from ICH on serial non-enhanced CT.

BACKGROUND: Cavernous malformations (CMs), also known as cavernomas or cavernous angiomas, are vascular malformations characterized by sinusoidal spaces lined by endothelial cells. Giant CMs (GCMs) are extremely rare, with limited understanding of their presentation and management. We present a case of symptomatic GCM in a newborn and review the literature on this rare entity.
METHODS: A 1-month-old newborn presented with focal seizures and signs of increased intracranial pressure. Imaging revealed a massive right frontal-parietal GCM, prompting surgical resection. Histopathological examination confirmed the diagnosis of cerebral cavernous malformation. The patient recovered well postoperatively with no neurological deficits.
CONCLUSIONS: GCMs are exceedingly rare in children and have not been reported in newborns until now. Symptoms typically include seizures and mass effects. Gross total resection is the standard treatment, offering favorable outcomes. Further research is needed to understand the natural history and optimal management of GCMs, particularly in newborns, emphasizing the importance of heightened clinical awareness for timely diagnosis and appropriate management.

Scuba diving has become a common and popular activity, and adverse events can occur following this activity. Among those events, intracranial hemorrhage is very rare, and only intracerebral hemorrhage and subarachnoid hemorrhage are reported. However, the occurrence of chronic subdural hematoma (CSDH), possibly as an adverse event following scuba diving, has not been described. A 49-year-old man with no significant medical history visited our hospital complaining of memory disturbance and aphasia. He had experienced a minor head trauma five months before and had gone scuba diving six times between the traumatic episode and the visit to our hospital. A brain computed tomography scan revealed a left CSDH. The patient underwent burr-hole surgery to remove the CSDH, and his symptoms resolved. We report the first case of CSDH possibly related to scuba diving. No recurrence of CSDH was observed at 28 months postoperatively.

This case report discusses the intricate diagnostic and therapeutic challenges faced by a 23-year-old Indian male who presented with altered consciousness, a holo-cranial headache, right-sided hemiparesis, and subsequent neurological symptoms. The patient\'s dietary habits, leading to vitamin B12 and folic acid deficiencies resulting in hyperhomocysteinemia, along with binge alcohol drinking leading to dehydration, were identified as the main causes of cerebral venous sinus thrombosis (CVST) in this case. The case was complicated by an additional cerebral hemorrhage. The patient received a comprehensive treatment regimen involving antiepileptic medications, intravenous fluids, and anticoagulation therapy. A decline in the Glasgow Coma Scale score prompted further interventions. Collaborative decision-making, involving neurologists, neurosurgeons, and the patient\'s relatives, steered the treatment course, ultimately favoring continued medical management over decompression surgery. Notably, the patient exhibited remarkable progress in mobility, achieving the ability to walk with support by the end. This case report contributes valuable insights to the understanding of CVST, emphasizing the significance of nutritional considerations, especially in vegetarians, and underscoring the importance of thorough diagnostic evaluations in complex clinical scenarios.

BACKGROUND: Cerebral Cavernous Malformation (CCM) is one of the most common types of vascular malformation of the central nervous system. Intracerebral hemorrhage, seizures, and lesional growth are the main clinical manifestations. Natural history studies have tried to identify many risk factors; however, the clinical course remains highly unpredictable.
OBJECTIVE: Here, we have analyzed a multicenter CCM cohort looking for the differential clinical data regarding the patients harboring supra and/or infratentorial cavernous malformations in order to better understand risk factors involved in the anatomical location of the unique neurosurgical disease.
METHODS: We have presented a multicenter, Propensity Score Matched (PSM), case-control study including 149 consecutive CCM cases clinically evaluated from May 2017 to December 2022 from three different neurosurgical centers. Epidemiological data were defined at each clinical assessment. Logistic regression was used to identify the independent contribution of each possible risk factor to the bleeding risk. To balance baseline covariates between patients with and without symptoms, and specifically between those with and without symptomatic bleeding, we used a PSM strategy. The Kaplan-Meier curve was drawn to evaluate if patients with infratentorial lesions had a greater chance of bleeding earlier in their life.
RESULTS: The presence of infratentorial lesions was a risk factor in the multivariate analysis comparing the bleeding risk with pure asymptomatic individuals (OR: 3.23, 95% CI 1.43 - 7.26, P = 0.005). Also, having an infratentorial CCM was a risk factor after PSM (OR: 4.56, 95% CI 1.47 - 14.10, P = 0.008). The presence of an infratentorial lesion was related to precocity of symptoms when the time to first bleed was compared to all other clinical presentations in the overall cohort (P = 0.0328) and in the PSM group (P = 0.03).
CONCLUSIONS: Here, we have provided some evidence that infratentorial cerebral cavernous malformation may have a more aggressive clinical course, being a risk factor for symptomatic haemorrhage and precocity of bleeding.