Partial Endovascular Embolization of a Cerebral Arteriovenous Malformation in a Patient With Seizures Caused by a Steal Phenomenon: A Case Analysis.

Cerebral arteriovenous malformations (cAVMs) are developmental pathologic lesions of the blood vessels of the brain in which multiple arteries shunt blood directly into the venous drainage network. They are lesions with an unclear etiology and, if left untreated, can bear significant risks of complications such as migraines, seizures, neurological deficits, and intracranial hemorrhages. The diagnosis is based on several imaging methods, with angiography being the primary method. Treatment modalities include microsurgery, radiosurgery, embolization with the intent of obliteration, and various multidisciplinary approaches. We aim to introduce the case of an adult female patient with symptomatic cAVM who underwent partial endovascular embolization of the lesion and evaluate her recovery and the overall reliability of her treatment modality. A 22-year-old female patient has presented to the Neurosurgery Clinic with clinical manifestations with photosensitive seizures, migraines, and a history of sleep disturbances persisting for a period of one year. An appointed MRI and angiography revealed the presence of a glomerular cAVM of the anterior parietal branch of the middle cerebral artery located within the intraparietal sulcus of the left cerebral hemisphere (Spetzler-Martin grade 2). The venous drainage of the malformation led to a loss of nutrients in the surrounding brain parenchyma (a steal phenomenon), causing the seizures. The patient successfully underwent transarterial endovascular embolization with Onyx, which proved to be partial on a postoperative angiography, and refused further embolization procedures. There were no postoperative complications to be mentioned. The patient reported no seizures or sleep disturbances at the 12-month follow-up, with sporadic weak headaches remaining. cAVMs remain a pathology with significant morbidity and mortality when undiagnosed. Symptomatic cAVMs leading to a steal phenomenon and seizures can be reliably managed via endovascular embolization alone when the malformation has an appropriate angioarchitecture, location, size, and a low Spetzler-Martin score. However, further inquiry is required into the use of partial embolization in cases where further multiple-stage embolization procedures are declined and/or complete occlusion of the lesion is unfeasible. This case report emphasizes that partial endovascular embolization can be successfully utilized as a treatment modality for the symptoms caused by a steal phenomenon of the venous drainage of a cAVM, such as seizure disorders and migraines, in the rare instance when multiple-stage embolization is declined by the patient and occlusion of the lesion remains subtotal.

Cerebral Calcifications as a Result of Primary Hyperparathyroidism: A Report of a Rare Case.

Primary hyperparathyroidism (PHPT) is an extremely uncommon cause of cerebral calcification. A male patient, aged 45, was admitted to the neurosurgery clinic with a closed traumatic brain injury, namely a concussion, resulting in symptoms of headache and loss of balance. A CT scan was conducted, which detected bilateral calcifications on the basal ganglia and the tentorium. The blood tests revealed increased levels of serum calcium, phosphate, and parathyroid hormone (PTH), while vitamin D levels were within the normal range. The patient received symptomatic therapy for the cerebral concussion and was referred for further diagnostic procedures. Based on these exams, it was determined that the patient had a parathyroid adenoma, which was responsible for PHPT characterised by increased levels of calcium, phosphate, and PTH. The patient subsequently underwent a successful parathyroidectomy. Half a year following the surgical procedure, the patient remained free of any indications of neurological conditions, and the levels of PTH and calcium in their body were within the expected range. Whenever trying to identify the cause of cerebral calcification, it is important to explore several possible diagnoses. A possible cause that should be taken into account is PHTP.

Epileptic Seizures in a Pediatric Patient With Vein of Galen Aneurysmal Malformation and Obstructive Hydrocephalus: A Rare Case Report.

The vein of Galen aneurysmal malformation (VGAM) is a rare congenital arteriovenous fistula of the embryonic median prosencephalic vein of Markowski, resulting in its pathological dilation. If left untreated, it can lead to multiple severe complications in the neonatal period, among which obstructive hydrocephalus. We present a case report of a six-year-old male patient with severe status epilepticus and a clinical history of VGAM and obstructive hydrocephalus, diagnosed via an MRI and an MR-angiography. The hydrocephalus was treated via a ventriculostomy at the age of six months, while the VGAM underwent a partial transarterial endovascular embolization when the patient was four years old. The procedures were successful, and there were no significant post-operative complications observed. The epileptic seizures began at a later point and were successfully medicated with valproate. However, they resumed due to a lowering of the medication dosage by the patient's parents. The patient was given a new valproic acid regimen with an appropriate dosage, and his parents reported no further seizures. This case report emphasizes the use of appropriate prenatal and neonatal diagnostic methods for VGAM and explores the nature of the multi-procedural therapy approach towards the pathology and its complications in relation to a possibly idiopathic co-pathology, namely epilepsy.

Using antifibrinolytics to tackle neuroinflammation.

Plasmin is generally known as a promotor of inflammation. Recent advancement suggests that it has a complex role as immunity modulator. Pharmacological inhibition of plasmin production and activity has been proven to improve neurological outcomes in traumatic brain injury and subarachnoid hemorrhage, most probably by preventing re-bleeding. The immune-modulatory properties of antifibrinolytics, however, suggest that they probably have effects unrelated to fibrinolysis inhibition, which are currently not adequately harnessed. The present work aims to give an account of the existing data regarding antifibrinolytics as agents influencing neuroinflammation. Preclinical and clinical studies on the possible influence of antifibrinolytics on neuroinflammation are scarce. However, the emerging evidence suggests that inhibition of plasmin(ogen) activity can ameliorate neuroinflammation to some extent. This data demonstrate that plasmin(ogen) is not exclusively involved in fibrinolysis, but also has other substrates and can precipitate in inflammatory processes. Investigation on the role of plasmin as the factor for the development of neuroinflammation shows the significant potential of antifibrinolytics as pharmacotherapy of neuroinflammationm, which is worthy of further exploration.