Partially thrombosed middle cerebral artery-lenticulostriate artery aneurysm with native radiological examinations suggesting proximal lenticulostriate artery aneurysm: A case report.

BACKGROUND: Preservation of the lenticulostriate artery (LSA) is crucial. LSAs usually cannot be spared with LSA aneurysms, when surgical clipping/excision or endovascular embolization of the LSA itself is performed. On the other hand, the LSA should be separated and preserved for proximal middle cerebral artery (M1)-LSA aneurysms. CASE DESCRIPTION: We report a case of M1-LSA aneurysm with native radiological examinations suggesting LSA aneurysm. The highlight of this unusual case was that during surgery, the aneurysm orifice was almost covered with thrombus and blood flow in an aneurysm that appeared separate from M1. Partial thrombectomy-clip reconstruction was performed, and M1 and LSAs were well preserved. CONCLUSION: Even with currently developed radiological modalities, thrombosed intracranial aneurysms may be misdiagnosed, depending on intraluminal flow conditions. Intraoperative findings from craniotomy sometimes contribute to a better understanding of the pathophysiology and decisions on appropriate treatment strategy.

Trauma may affect vasa vasorum to promote thrombosis and enlargement of intracranial aneurysms: A case report.

BACKGROUND: Thrombosed intracranial aneurysm (IA) is likely to occur in large or giant IAs. Almost all thrombosed IAs are found already in a thrombosed state, and few reports have depicted the process of thrombosis in unthrombosed aneurysm. Moreover, no reports appear to have described IA in which thrombosis accelerated after trauma. CASE DESCRIPTION: We report herein a case in which an unthrombosed large cerebral aneurysm rapidly thrombosed and grew within 3 months after trauma. The highlight in this unusual case was that during surgery, the aneurysm and anterior skull base were adherent and some blood vessels bridged between the aneurysm and dura mater. Histologically, intramural hemorrhage was seen in the tunica media of the aneurysm. CONCLUSION: Trauma may act as a "second hit" causing adhesion between IAs and surrounding tissues, accelerating inflammation of the vasa vasorum and aneurysmal walls, and thrombosis in IAs.

Cerebral Arteriovenous Malformations as Acquired Lesions: Case Reports and Review of the Literature.

Cerebral arteriovenous malformations (AVMs) are generally attributed to congenital lesions that arise from aberrant vasculogenesis between the fourth and eighth weeks of embryonic life. However, this dogma has been challenged by several recent observations, one of which is de novo formation of AVMs. Forty cases of de novo AVMs were published between 2000 and 2019, all of which involved a history of intracranial insult, such as vascular abnormalities or nonvascular conditions, prior to AVM diagnosis. We hereby present two unique operative cases of ruptured de novo AVMs in older adult patients. Case 1 is novel in the sense that the patient did not experience any kind of environmental trigger ("second hit") such as a previous intracranial insult, while Case 2 serves as the second report of a de novo AVM patient with a medical history of Bell's palsy. Although the exact mechanisms of AVM formation remain to be elucidated, it is likely to be a multifactorial process related to environmental and hemodynamic factors.

Lactate and Lactate Dehydrogenase in Cistern as Biomarkers of Early Brain Injury and Delayed Cerebral Ischemia of Subarachnoid Hemorrhage.

OBJECTIVE: The pathophysiology of delayed cerebral ischemia (DCI) following aneurysmal subarachnoid hemorrhage (aSAH) has not been fully evaluated. The aim of this study was to evaluate the dynamics of lactate and lactate dehydrogenase (LDH) in carotid cisternal cerebrospinal fluid (CSF), and to discuss their effectiveness as markers of early brain injury (EBI) and DCI following aSAH. PATIENTS AND METHODS: Among 91 consecutive aSAH patients treated between January 2012 and March 2019 at National Hospital Organization Beppu Medical Center, 19 patients (20.9%) were eligible for this retrospective study. Concentrations of lactate and LDH in carotid cisternal CSF within 14 days after onset of aSAH were evaluated. RESULTS: Six of the 19 patients (31.6%) had a history of DCI. Both lactate and LDH levels in carotid cisternal CSF were significantly higher in the DCI group than in the non-DCI group on postbleeding day (PBD) 1-2, 3-4, and 5-6. Interestingly, neither lactate nor LDH levels in blood differed significantly between DCI and non-DCI groups on PBD 1-2. CONCLUSIONS: Lactate and LDH concentrations in carotid cisternal CSF may vividly reflect the EBI and may thus represent predictive biomarkers of DCI following aSAH.

The Potentiality for Development of Multiple Dural Arteriovenous Fistulas after Ligation of the Internal Jugular Vein: A Case Report.

A 74-year-old male presented with an intracranial hemorrhage caused by multiple dural arteriovenous fistulas (DAVFs) in the left transverse sinus and right sigmoid sinus. Four months previously, the patient underwent tongue cancer removal with lymph node dissection and ligation of the right internal jugular vein. Endovascular embolization (transvenous and transarterial embolization) resulted in the complete disappearance of the fistulas. Follow-up angiography revealed new arteriovenous shunts at the superior sagittal sinus and right transverse sinus, and we treated the patient with staged transarterial embolization. Finally, venous congestion almost completely resolved and the DAVFs disappeared without any sign of recurrence. This case speculates the concept of DAVF as an acquired lesion caused by intravenous hypertension and alerts clinicians to take precautions against ligation of the internal jugular vein during a cervical operation.

Third nerve palsy caused by compression of the posterior communicating artery aneurysm does not depend on the size of the aneurysm, but on the distance between the ICA and the anterior-posterior clinoid process.

OBJECTIVE: Third nerve palsy (TNP) caused by a posterior communicating artery (PCoA) aneurysm is a well-known symptom of the condition, but the characteristics of unruptured PCoA aneurysm-associated third nerve palsy have not been fully evaluated. The aim of this study was to analyze the anatomical features of PCoA aneurysms that caused TNP from the viewpoint of the relationship between the ICA and the skull base. METHODS: Forty-eight unruptured PCoA aneurysms were treated surgically between January 2008 and September 2013. The characteristics of the aneurysms were evaluated. RESULTS: Thirteen of the 48 patients (27%) had a history of TNP. The distance between the ICA and the anterior-posterior clinoid process (ICA-APC distance) was significantly shorter in the TNP group (p<0.01), but the maximum size of the aneurysms was not (p=0.534). CONCLUSION: Relatively small unruptured PCoA aneurysms can cause third nerve palsy if the ICA runs close to the skull base.

Electroconvulsive seizure-induced VEGF is correlated with neuroprotective effects against cerebral infarction: Involvement of the phosphatidylinositol-3 kinase/Akt pathway.

The present study demonstrates the cytoprotective effect of electrical convulsive stimulation (ECS) as a potential neuroprotective vascular endothelial growth factor (VEGF) inducer against ischemic insult. Phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is thought to be an important factor that mediates neuroprotection. However, the signaling pathways in the brain in vivo after ECS remain unclear. We measured and compared infarction volumes to investigate the effect of ECS on cerebral infarction induced by permanent middle cerebral artery occlusion in rats. We evaluated the effects of pretreatment with Wortmannin (Wort), a specific PI3K inhibitor of ECS-induced neuroprotection against infarction volumes. To clarify the relationship between PI3K/Akt activation and neuroprotection, we used immunoblot analysis to determine the amounts of p-Akt and VEGF proteins present after ECS with or without Wort treatment. Neuroprotective effects of ECS (pretreatment with a single ECS 6h before ischemia) were prevented by Wort pretreatment, which indicates that the PI3K/Akt pathway may mediate ECS-dependent protection. ECS induced p-Akt and VEGF and ECS pretreatment enhanced ischemia-induced VEGF, both of which were prevented by Wort pretreatment. These results suggest that a single ECS induces p-Akt and that ECS plays an important role in neuroprotection against the cerebral ischemia through VEGF induction.

The phosphatidylinositol-3 kinase/Akt pathway mediates geranylgeranylacetone-induced neuroprotection against cerebral infarction in rats.

Previous studies demonstrated the cytoprotective effect of geranylgeranylacetone (GGA), a heat shock protein inducer, against ischemic insult. Phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is thought to be an important factor that mediates neuroprotection. However, the signaling pathways in the brain in vivo after oral GGA administration remain unclear. We measured and compared infarction volumes to investigate the effect of GGA on cerebral infarction induced by permanent middle cerebral artery occlusion in rats. We evaluated the effects of pretreatment with 5-hydroxydecanoate (5HD), a specific mitochondrial ATP-sensitive potassium (mitoK(ATP)) channel inhibitor; diazoxide (DZX), a selective mitoK(ATP) channel opener and wortmannin (Wort), a specific PI3K inhibitor of GGA-induced neuroprotection against infarction volumes. To clarify the relationship between PI3K/Akt activation and neuroprotection, we used immunoblot analysis to determine the amount of p-Akt proteins present after GGA administration with or without Wort treatment. Neuroprotective effects of GGA (pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia) were prevented by 5HD, DZX and Wort pretreatment, which indicates that the selective mitoK(ATP) channel and the PI3K/Akt pathway may mediate GGA-dependent protection. Oral GGA-induced p-Akt and GGA pretreatment enhanced ischemia-induced p-Akt, both of which were prevented by Wort pretreatment. These results suggest that a single oral dose of GGA induces p-Akt and that GGA plays an important role in neuroprotection against cerebral ischemia through the mitoK(ATP) channel opening.

Long-term suppression of tremor by deep brain stimulation of the ventral intermediate nucleus of the thalamus combined with pallidotomy in hemiparkinsonian patients.

Deep brain stimulation (DBS) of the ventral intermediate nucleus of the thalamus (VIM) is a powerful surgical option in the treatment of tremor-predominant Parkinson's disease. However, its therapeutic efficacy depends on the tremor distribution. DBS is highly efficient in relief of distal appendicular tremor but not other types of tremor. Also, it is generally thought that DBS of the VIM has no significant beneficial effects on other motor symptoms of Parkinson's disease. We report two hemiparkinsonian patients, in whom unilateral VIM DBS combined with posteroventral pallidotomy produced long-lasting suppression of not only hand tremor, but also leg or jaw tremor and other motor symptoms.

Severe postoperative vasculitis of the central nervous system in a child with arteriovenous malformation: case report.

BACKGROUND: Cerebral vasculitis is very rare complication after craniotomy. We report a case and discuss the etiology, diagnosis, and treatment of this complication. CASE DESCRIPTION: A 12-year-old boy was admitted because of a consciousness disturbance due to a ruptured AVM. Computed tomography revealed a left parietal subcortical hematoma. No apparent nidus was detected on the angiography findings, but AVM was suspected. After resection of the hematoma, the patient did not recover consciousness, and his high fever continued. Despite postoperative induced hypothermia, progressive multiple cerebral infarctions occurred. Postoperative angiography showed multiple arterial narrowing, and a "string of beads" phenomenon was observed in the anterior and posterior circulation in addition to the residual AVM. After administering steroid therapy, he recovered consciousness, but had a severe disability. After angiography, which was performed 1 year after onset, an improvement of the vasculitis and the complete occlusion of AVM were observed. CONCLUSION: We should therefore include cerebral vasculitis in the differential diagnosis when encountering a case with an unusual progressive stroke because a timely diagnosis and aggressive treatment are of critical importance for a successful recovery in such patients.

De novo appearance of cerebellar cavernous malformation in a patient with moyamoya disease: case report and review of the literature.

The authors report a case of cerebellar cavernous malformation associated with moyamoya disease. An adolescent male with moyamoya disease had undergone bilateral direct and indirect extracranial-intracranial anastomosis at 11 years of age, and the course had been uneventful until MRI detected the appearance of a cavernous malformation in the cerebellum 3 years later. The lesion had grown, bled, and caused headache and disturbance of consciousness 2 years after the initial detection. The cavernous malformation was removed surgically and pathologically verified. The patient has recovered without any neurological deficits. This is a quite rare case with cavernous malformation which appeared in a moyamoya disease patient. The association of the two different vascular disorders in a young patient may suggest the existence of some interaction in the pathogenesis of these diseases. Since cavernous malformations with a de novo appearance may grow and become clinically significant, careful observation is necessary.

Moyamoya disease associated with midaortic syndrome.

We report a 1-year-old girl who presented moyamoya disease associated with midaortic syndrome. She had been treated for cardiac failure and severe hypertension due to midaortic syndrome until she suffered seizure and repeated cerebral ischemic attack. Cerebral angiography revealed stenosis of the bilateral internal carotid artery at its terminal portion. She was successfully treated with encephaloduroarteriosynangiosis, and ischemic attack ceased postoperatively. This is the first report of moyamoya disease with midaortic syndrome. Although cerebral ischemic attack has been effectively managed by encephaloduroarteriosynangiosis, renovascular hypertension is still difficult to control.

Geranylgeranylacetone, a noninvasive heat shock protein inducer, induces protein kinase C and leads to neuroprotection against cerebral infarction in rats.

Previous studies demonstrated the cytoprotective effect of geranylgeranylacetone (GGA), a heat shock protein (HSP) inducer, against ischemic insult. Protein kinase C (PKC) is thought to be an important factor that mediates the expression of heat shock protein 70 (HSP70) in vitro. However, the signaling pathways in the brain in vivo after oral GGA administration remain unclear. We measured and compared infarction volumes to investigate the effect of GGA on cerebral infarction induced by permanent middle cerebral artery (MCA) occlusion in rats. To clarify the relationship between PKC induction and HSP70 expression, we determined the amounts of HSP70 and PKC proteins after GGA administration by immunoblotting. We evaluated the effects of pretreatment with chelerythrine (CHE), a specific PKC inhibitor, on expressions of PKC and HSP70 proteins with immunoblotting. Neuroprotective effects of GGA (pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia) were prevented by CHE pretreatment, which indicates that PKC may mediate the GGA-dependent protection. Oral GGA-induced HSP70 expression induced PKC delta, and GGA pretreatment enhanced ischemia-induced HSP70, both of which were prevented by CHE pretreatment. These results suggest that a single oral dose of GGA induces PKC delta and promotes HSP70 expression in the brain and that GGA plays an important role in neuroprotection against cerebral ischemia.

Neuroprotective effect of geranylgeranylacetone, a noninvasive heat shock protein inducer, on cerebral infarction in rats.

The present study evaluated the neuroprotective effect of geranylgeranylacetone (GGA), which is known as an antiulcer agent and more recently as a heat shock protein (HSP) inducer, against cerebral infarction induced by permanent left middle cerebral artery (MCA) occlusion. GGA was given orally in various regimens prior to MCA occlusion in rats. Pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia significantly attenuated cerebral infarction volume (81.7+/-18.4 mm3 versus 369.1+/-70.2 mm3; P<.01). A significant increase in HSP70 immunoreactivity was found in the neocortex in GGA-treated animals with or without ischemia. Pretreatment with a single oral dose of GGA provides an important tool for exploring the mechanisms of neuroprotection against cerebral ischemic neuronal damage.