Radiographic and microsurgical characteristics of proximal (A1) segment aneurysms of the anterior cerebral artery

Background

Proximal A1 segment aneurysms of the anterior cerebral artery (ACA) radiologically resemble internal carotid artery bifurcation (ICBIF) aneurysms because of their anatomical proximity. However, proximal A1 aneurysms exhibit distinguishing features, relative to ICBIF aneurysms. We report our experience of managing proximal A1 aneurysms, then compare them to ICBIF aneurysms.

Methods

Among 2191 aneurysms treated between 2000 and 2016 in a single institution, we retrospectively reviewed 100 cases categorized as ICBIF or A1 aneurysms. We included aneurysms originating from the ICBIF and ACA, proximal to the anterior communicating artery (A1 segment) and divided them into two groups: proximal A1 (n?=?32) and ICBIF (n?=?50). If any portion of the aneurysm involved the ICBIF, it was classified as ICBIF. Aneurysms wholly located in the A1 segment were classified as proximal A1. Patient factors and angiographic factors were evaluated and compared.

Results

The proximal A1 group exhibited differences in aneurysm size (p?=?0.013), posterior aneurysm direction (p?=?0.001), and A1 perforators as incorporating vessels (p?=?0.001). The proximal A1 group tended to rupture more frequently when the aneurysm was smaller (p?=?0.046). One case of morbidity occurred in the proximal A1 group.

Conclusion

Compared to ICBIF aneurysms, proximal A1 aneurysms were smaller and directed posteriorly, with incorporating perforators. Because of these characteristics, it may be difficult to perform clipping with 360° view in microsurgical field. Therefore, when planning to treat proximal A1 aneurysms, different treatment strategies may be necessary, relative to those used for ICBIF aneurysms.

     

Acetylcholine precursor,citicoline (cytidine 5′‐diphosphocholine), reduces hypoglycaemia‐induced neuronal death in rats

Citicoline (cytidine 5′‐diphosphocholine) is an important precursor for the synthesis of neuronal plasma membrane phospholipids, mainly phosphatidylcholine. The administration of citicoline serves as a choline donor for the synthesis of acetylcholine. Citicoline has been shown to reduce the neuronal injury in animal models with cerebral ischaemia and in clinical trials of stroke patients. Citicoline is currently being investigated in a multicentre clinical trial. However, citicoline has not yet been examined the context of hypoglycaemia‐induced neuronal death. To clarify the therapeutic impact of citicoline in hypoglycaemia‐induced neuronal death, we used a rat model with insulin‐induced hypoglycaemia. Acute hypoglycaemia was induced by i.p. injection of regular insulin (10 U kg^‐1) after overnight fasting, after which iso‐electricity was maintained for 30 minutes. Citicoline injections (500 mg/kg, i.p.) were started immediately after glucose reperfusion. We found that post‐treatment of citicoline resulted in significantly reduced neuronal death, oxidative injury and microglial activation in the hippocampus compared to vehicle‐treated control groups at 7 days after induced hypoglycaemia. Citicoline administration after hypoglycaemia decreased immunoglobulin leakage via blood‐brain barrier disruption in the hippocampus compared to the vehicle group. Citicoline increased choline acetyltransferase expression for phosphatidylcholine synthesis after hypoglycaemia. Altogether, the present findings suggest that neuronal membrane stabilisation by citicoline administration can save neurones from the degeneration process after hypoglycaemia, as seen in several studies of ischaemia. Therefore, the results suggest that citicoline may have therapeutic potential to reduce hypoglycaemia‐induced neuronal death.     

Intra-arterial thrombectomy for acute ischaemic stroke patients with active cancer

Journal of Neurology - This study aimed to evaluate the efficacy of intra-arterial thrombectomy (IAT) and prognosis for acute ischaemic stroke patients with active cancer. We retrospectively...     

Dedifferentiated Schwann cells secrete progranulin that enhances the survival and axon growth of motor neurons

Schwann cells (SCs), the primary glia in the peripheral nervous system (PNS), display remarkable plasticity in that fully mature SCs undergo dedifferentiation and convert to repair SCs upon nerve injury. Dedifferentiated SCs provide essential support for PNS regeneration by producing signals that enhance the survival and axon regrowth of damaged neurons, but the identities of neurotrophic factors remain incompletely understood. Here we show that SCs express and secrete progranulin (PGRN), depending on the differentiation status of SCs. PGRN expression and secretion markedly increased as primary SCs underwent dedifferentiation, while PGRN secretion was prevented by administration of cAMP, which induced SC differentiation. We also found that sciatic nerve injury, a physiological trigger of SC dedifferentiation, induced PGRN expression in SCs in vivo. These results suggest that dedifferentiated SCs express and secrete PGRN that functions as a paracrine factor to support the survival and axon growth of neighboring neurons after injury.