Oculomotor Nerve Palsy in a Patient with a Ruptured Middle Cerebral Artery Aneurysm

We describe a case of acute oculomotor nerve palsy caused by a ruptured middle cerebral artery (MCA) aneurysm. A 59-year-old female presenting with headache and nausea was admitted to our hospital. Her consciousness was alert, and had no other neurological deficit without left oculomotor nerve palsy. A computed tomography (CT) showed SAH extending from left sylvian cistern to basal cistern. CT angiography revealed a left MCA aneurysm which protruded toward internal carotid artery. The patient was successfully treated with surgical clipping. The oculomotor nerve palsy resolved immediately after the surgery. Perioperative radiological evaluation revealed that there were no evidence of midbrain hemorrhage or stroke, vessel anomaly of basilar, posterior cerebral or superior cerebellar artery, vasospasm, and uncal herniation. Furthermore, intraoperative findings revealed that the aneurysm was projected toward the affected carotid cistern and oculomotor nerve. From these findings and time course of oculomotor nerve palsy, it is suggested that the jet flow of bleeding from the ruptured MCA aneurysm caused oculomotor nerve palsy in the patient

Upregulation of Relaxin after Experimental Subarachnoid Hemorrhage in Rabbits

Background. Although relaxin causes vasodilatation in systemic arteries, little is known about its role in cerebral arteries. We investigated the expression and role of relaxin in basilar arteries after subarachnoid hemorrhage (SAH) in rabbits. Methods. Microarray analysis with rabbit basilar artery RNA was performed. Messenger RNA expression of relaxin-1 and relaxin/insulinlike family peptide receptor 1 (RXFP1) was investigated with quantitative RT-PCR. RXFP1 expression in the basilar artery was investigated with immunohistochemistry. Relaxin concentrations in cerebrospinal fluid (CSF) and serum were investigated with an enzyme-linked immunosorbent assay. Using human brain vascular smooth muscle cells (HBVSMC) preincubated with relaxin, myosin light chain phosphorylation (MLC) was investigated with immunoblotting after endothelin-1 stimulation. Results. After SAH, RXFP1 mRNA and protein were significantly downregulated on day 3, whereas relaxin-1 mRNA was significantly upregulated on day 7. The relaxin concentration in CSF was significantly elevated on days 5 and 7. Pretreatment with relaxin reduced sustained MLC phosphorylation induced by endothelin-1 in HBVSMC. Conclusion. Upregulation of relaxin and downregulation of RXFP1 after SAH may participate in development of cerebral vasospasm. Downregulation of RXFP1 may induce a functional decrease in relaxin activity during vasospasm. Understanding the role of relaxin may provide further insight into the mechanisms of cerebral vasospasm

A case of lung cancer with osteoblastic metastasis diagnosed with visual impairment

Bone metastasis is relatively common in patients with lung cancers. Although there are some reports of osteolytic skull base metastasis in lung cancer, osteoblastic skull base metastasis is quite rare. A 56-year-old male presented with lung adenocarcinoma who developed vision loss due to papilledema in both eyes with intracranial hypertension. Magnetic resonance imaging revealed no obvious lesions in the intracranial space. Bone scintigraphy, magnetic resonance venography, and computed tomography showed left internal jugular vein stenosis with osteoblastic metastasis protruding into the left jugular foramen. Ventriculoperitoneal shunt surgery improved papilledema and ameliorated vision loss. This case is a reminder that a patient with lung cancer can demonstrate osteoblastic skull base metastasis, and ventriculoperitoneal shunt surgery is an effective and palliative method for such patients

Upregulation of Relaxin after Experimental Subarachnoid Hemorrhage in Rabbits

Background. Although relaxin causes vasodilatation in systemic arteries, little is known about its role in cerebral arteries. We investigated the expression and role of relaxin in basilar arteries after subarachnoid hemorrhage (SAH) in rabbits. Methods. Microarray analysis with rabbit basilar artery RNA was performed. Messenger RNA expression of relaxin-1 and relaxin/insulin-like family peptide receptor 1 (RXFP1) was investigated with quantitative RT-PCR. RXFP1 expression in the basilar artery was investigated with immunohistochemistry. Relaxin concentrations in cerebrospinal fluid (CSF) and serum were investigated with an enzyme-linked immunosorbent assay. Using human brain vascular smooth muscle cells (HBVSMC) preincubated with relaxin, myosin light chain phosphorylation (MLC) was investigated with immunoblotting after endothelin-1 stimulation. Results. After SAH, RXFP1 mRNA and protein were significantly downregulated on day 3, whereas relaxin-1 mRNA was significantly upregulated on day 7. The relaxin concentration in CSF was significantly elevated on days 5 and 7. Pretreatment with relaxin reduced sustained MLC phosphorylation induced by endothelin-1 in HBVSMC. Conclusion. Upregulation of relaxin and downregulation of RXFP1 after SAH may participate in development of cerebral vasospasm. Downregulation of RXFP1 may induce a functional decrease in relaxin activity during vasospasm. Understanding the role of relaxin may provide further insight into the mechanisms of cerebral vasospasm