A Single-Center Experience of Mechanical Thrombectomy for Cancer-Associated Ischemic Stroke.

Objectives: Cancer-associated ischemic stroke tends to extend over multiple vascular territories and develops under poor general conditions. Owing to the rarity of such cases and poor prognoses, no comprehensive studies on mechanical thrombectomy for cancer-associated ischemic stroke have been reported in Japan. The present study investigated the radiological and clinical characteristics of mechanical thrombectomy in patients with cancer-associated ischemic stroke at our institution. Methods: We retrospectively reviewed 108 patients who underwent mechanical thrombectomy for large cerebral artery occlusion between January 1, 2021, and October 31, 2022, at our institution. The characteristics of mechanical thrombectomy in the cancer-associated ischemic stroke group were compared with those in the control group. Results: Of the 108 patients (112 procedures), seven patients (eight procedures) with clinically diagnosed cancer-associated ischemic stroke underwent mechanical thrombectomy. Of the eight procedures, six were performed during hospitalization. In contrast, only 10 of 104 procedures were performed in the control group. The in-hospital onset rate was higher in the cancer-associated ischemic stroke group (75.0%) compared to that in the controls (9.6%); p <0.001. The puncture-to-reperfusion time was significantly longer in the cancer-associated ischemic stroke group in comparison to that in the controls with a median interquartile range of 69 minutes (60.0-82.0 minutes) and 59.5 minutes (44.5-69.3 minutes), respectively (p <0.01). However, the rates of successful recanalization defined as thrombolysis in cerebral infarction ≥2b were not significantly different between the cancer-associated ischemic stroke group and controls with values of 62.5% and 79.8%, respectively (p = 0.250). Of the eight cases in the cancer-associated ischemic stroke group, only one (12.5%) had a good outcome on a modified Rankin Scale score of 0 to 2 at discharge, in contrast to 23 of the 104 (23.1%) cases in the controls (p = 0.523). Histopathological examination of six retrieved thrombi in the cancer-associated stroke group using hematoxylin and eosin staining revealed that only one case showed an erythrocyte-dominant thrombus while five displayed a fibrinoplatelet-dominant component. Conversely, 65 of 92 retrieved thrombi in the control group were erythrocyte dominant. Cancer was pathologically diagnosed in four of seven patients, all of which were adenocarcinomas. Conclusion: Cancer-associated ischemic stroke tends to occur during hospitalization. Coagulation disorders associated with cancer, especially adenocarcinoma, may be related to the formation of thrombi with fibrinoplatelet-dominant components, leading to ischemic stroke. The procedural time for mechanical thrombectomy in cancer-associated ischemic stroke tends to be longer.

Cerebrospinal fluid rhinorrhea with meningoencephalocele related to Sternberg's canal: A report of two cases.

Background: Cerebrospinal fluid (CSF) rhinorrhea with meningoencephalocele (MEC) associated with Sternberg's canal is rare. We treated two such cases. Case Description: A 41-year-old man and a 35-year-old woman presented with CSF rhinorrhea and mild headache worsening with standing posture. Head computed tomography showed a defect close to the foramen rotundum in the lateral wall of the left sphenoid sinus in both cases. Head magnetic resonance (MR) imaging and MR cisternography revealed that brain parenchyma had herniated into the lateral sphenoid sinus through the defect of the middle cranial fossa. The intradural and extradural spaces and bone defect were sealed with fascia and fat through both intradural and extradural approaches. The MEC was cut away to prevent infection. CSF rhinorrhea completely stopped after the surgery. Conclusion: Our cases were characterized by empty sella, thinning of the dorsum sellae, and large arteriovenous malformations that suggest chronic intracranial hypertension. The possibility of Sternberg's canal in patients with CSF rhinorrhea with chronic intracranial hypertension should be considered. The cranial approach has the advantages of lower infection risk and the ability to close the defect with multilayer plasty under direct vision. The transcranial approach is still safe if performed by a skillful neurosurgeon.

The effects of A1/A2 astrocytes on oligodendrocyte linage cells against white matter injury under prolonged cerebral hypoperfusion.

As oligodendrocyte precursor cells (OPCs) are vulnerable to ischemia, their differentiation to oligodendrocytes (OLG) is impaired in chronic cerebral hypoperfusion. Astrocyte-OLG interaction is important for white matter homeostasis. Recently, reactive astrocytes were separated into two types, A1 (cytotoxic) and A2 (neurotrophic). However, their role in prolonged cerebral hypoperfusion remains unclear. We analyzed the effects of interaction between A1-A2 astrocytes and OPC-OLG under hypoperfusion, focusing on mitochondrial migration. As an in vivo model, chronic hypoperfusion model mice were created by bilateral common carotid artery stenosis (BCAS) using microcoils. As a matching in vitro study, rat primary cells were cocultured with a nonlethal concentration of CoCl2 . At 28 days after hypoperfusion, the number of OPC and astrocytes increased, whereas that of OLG decreased. Increased astrocytes were mainly A1-like astrocytes; however, the number of A2-like type decreased. In cell culture, OPC differentiation was interrupted under mimic chronic ischemia, but improved after astrocyte-conditioned medium (ACM) was added. However, injured-ACM was unable to improve OPC maturation. Incubation with CoCl2 changed astrocytes from A2-like to A1-like, and mitochondrial migration was also reduced. A Trkß agonist was able to maintain astrocytes from A1-like to A2-like even under hyperperfused conditions, and aided in OPC maturation and memory impairment via mitochondrial migration and drug effects in cell culture study and BCAS model. The reduction of A1-like astrocytes protects against white matter injury. Trkß agonists may play an important role in the impairment under chronic ischemic conditions. Mitochondrial migration may be a broad therapeutic strategy for cerebrovascular diseases. MAIN POINTS: Prolonged cerebral hypoperfusion leads to impaired oligodendrocyte (OLG) maturation and increased numbers of A1 astrocytes. Mitochondria migration maintained A2 astrocyte morphology, mature OLG, and myelinated white matter in vivo/vitro.

The Effects of Astrocyte and Oligodendrocyte Lineage Cell Interaction on White Matter Injury under Chronic Cerebral Hypoperfusion.

Oligodendrocytes (OLGs) differentiate from oligodendrocyte-precursor-cells (OPCs) for myelination in white matter. This differentiation is maintained by cell-cell interactions through trophic factors such as brain-derived-neurotrophic-factor (BDNF). However, differentiation is impaired when white matter injury occurs in a chronic cerebral hypoperfusion model. Thus, we examined the effects of the interaction between astrocyte and oligodendrocyte lineage cells on myelination regarding the mechanism of impairment. A microcoil was applied to the bilateral common carotid arteries in male C57BL/6 mice as an in vivo cerebral chronic hypoperfusion model (BCAS model). A nonlethal concentration of CoCl2 was added to the primary cell culture from the postnatal rat cortex and incubated in vitro. White matter injury progressed in the BCAS model as myelin decreased. The numbers of OPCs and astrocytes increased after the operation, whereas that of OLGs decreased at day 28. BDNF continuously decreased until day 28. Differentiation was disrupted under the stressed conditions in the cell culture, but improved after administration of astrocyte-conditioned medium containing BDNF. Astrocytes with BDNF underwent differentiation, but differentiation was impaired under the stressed conditions due to the reduction of BDNF. We examined S100B regarding the mechanism of impairment. S100B is mainly expressed by mature astrocytes, and has neuroprotective and neurotoxic effects inside and outside of cells. GFAP-positive astrocytes increased in the corpus callosum in the BCAS model, whereas the number of mature astrocytes continued to decrease, resulting in reduced BDNF. The reduction in mature astrocytes due to the discharge of S100B in ischemic conditions caused the reduction in BDNF.

Endovascular parent artery occlusion of proximal posterior cerebral artery aneurysms: a report of two cases.

We report two cases of proximal posterior cerebral artery (PCA) aneurysms treated with endovascular parent artery occlusion (PAO) with coils. In both cases, selective injection from the 4 F distal access catheter clearly showed the perforating arteries arising from the PCA. Case No 1, a 49-year-old woman, was successfully treated with preservation of a paramedian artery. Case No 2, a 54-year-old woman, was treated in the same manner. The patient underwent extensive thalamic infarction after the procedure because of paramedian artery occlusion. Endovascular PAO with coils is feasible for proximal PCA aneurysms; however, preservation of perforating arteries arising from the PCA is mandatory.