Traumatic intracranial aneurysm in a distal posterior cerebral artery: A case report and literature review.

Background: Traumatic intracranial aneurysms (TICAs) are rare and known to rupture easily and have a high mortality rate. Case Description: An 87-year-old male patient with no neurological deficits presented to our hospital after head trauma. Computed tomography (CT) revealed a tentorial acute subdural hematoma (ASDH). The patient was managed conservatively and discharged home six days after hospitalization. Two days later, the patient returned with a severe headache. CT showed that the ASDH had enlarged and extended from the tentorium to the convexity. CT angiography and digital subtraction angiography revealed a pseudoaneurysm in a branch of the left posterior inferior temporal artery. The patient was diagnosed with an enlarged ASDH due to a ruptured TICA that arose from the P3 segment. We performed endovascular intervention with parent artery occlusion (PAO) using n-butyl-2-cyanoacrylate (NBCA). The parent artery was accessed through the left posterior communicating artery because left vertebral angiography revealed an aplastic left P1 segment. After navigating the microcatheter near the aneurysm, we injected 33% NBCA into the parent artery. The pseudoaneurysm disappeared after injection. The patient was discharged on hospital day 25 despite persistent delirium. Conclusion: This is the first report of a TICA arising from the P3 segment that was treated with PAO using NBCA. TICAs are rare; however, a TICA must be considered when an enlarged hematoma caused by head injury is detected.

Post-operative dexmedetomidine-based sedation after uneventful intracranial surgery for unruptured cerebral aneurysm: comparison with propofol-based sedation.

BACKGROUND: Clinical applications of dexmedetomidine (DEX) for neurosurgical procedures have not been adequately investigated. This study aimed to test the use of DEX infusion, alone or as an adjunct to propofol infusion, as compared to propofol infusion in patients with an unruptured cerebral aneurysm after uneventful intracranial procedures. METHODS: In this retrospective observational study from a single institute, of 184 patients who underwent uneventful intracranial procedures for an unruptured cerebral aneurysm between January 2003 and March 2007, we reviewed 50 managed with DEX-based sedation (DEX alone or as an adjunct to propofol infusion) between April 2005 and March 2007, and 50 managed with propofol-based sedation (propofol alone) between January 2003 and April 2005. With DEX-based sedation, both intubated and extubated patients received DEX infusion at an initial dose of 0.4 µg/kg/h, followed by a maintenance dose of 0.2-0.7 µg/kg/h. Propofol was used in both groups at a dose range of 0.5-5.0 mg/kg/h. Hemodynamic variables, including heart rate (HR) and blood pressure (BP), and adverse events were recorded and compared between the groups. RESULTS: HR during sedation and systolic BP at 2 h after beginning sedation were significantly lower in the DEX group. No serious adverse events were observed. In the DEX group, 66% were sedated in combination with propofol, of whom 94% were intubated. CONCLUSIONS: DEX could be used safely for both intubated and extubated patients following uneventful intracranial procedures for an unruptured cerebral aneurysm, though it significantly reduced HR. Our findings also indicate that it is preferable to add low-dose propofol to DEX for management of intubated patients.

Anterior cerebral artery notching on anterior optic pathways in a child with craniopharyngioma and progressive blindness.

We report the clinical significance of anterior cerebral artery (ACA) notching on the optic nerve and chiasm in a 3.5-year-old girl with a craniopharyngioma and progressive blindness. She presented with a headache and vomiting, followed by binocular blindness. Magnetic resonance imaging (MRI) studies demonstrated severely distended A1 segments and ill-depicted ACAs. Surgical decompression via a right subfrontal approach was performed to reverse blindness. Postoperative MRI studies showed good ACA visualization. A second operation via a right pterional approach revealed ACA notching, which appeared as a transverse groove on the right optic nerve and chiasm. ACA notching should be considered as a possible cause of progressive visual disturbance and a potential risk of ACA infarction in a child with a craniopharyngioma.

Pseudohypoxic brain swelling after elective clipping of an unruptured anterior communicating artery aneurysm.

A case of pseudohypoxic brain swelling, a newly defined entity, is described. The patient experienced generalized seizures and did not awake initially after a seemingly uneventful elective craniotomy for clipping of an unruptured anterior communicating artery aneurysm. Neuroimaging findings demonstrated diffuse brain swelling, especially in the bilateral basal ganglia and thalami. The rarity of this postoperative complication is addressed and the pathogenesis discussed.

Sequential and spatial profiles of apoptosis in ischemic penumbra after two-vein occlusion in rats.

OBJECT: The two-vein occlusion model is known to be useful for ischemic penumbra studies in vivo. It was applied here to examine sequential changes in the expression of Bax and Bcl-2 proteins and in apoptotic cells to assess the relationship between penumbra and apoptosis. METHODS: Two cortical veins were occluded photochemically by using rose bengal dye in 27 Wistar rats. The animals were killed with perfusion fixation at the following intervals: 4, 12, 24, 48, 96, and 168 hours after vein occlusion (four at each interval; three additional rats were sham-treated). Immunohistochemical analysis for the Bcl-2 family of proteins was performed along with the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) assay to examine the relationship to single-cell death. Cells positive for antiapoptotic proteins began to appear in the TUNEL assay for animals killed 24 hours after vein occlusion, with a peak at 48 hours. These cells were localized in the core of infarction. Immunohistochemical staining for Bax protein showed an increased presence around ischemic lesions at 4 hours after vein occlusion, and the amounts continued to rise until 24 hours, when the localization was diffuse around the core of infarction. Negative findings on immunohistochemical studies for Bcl-2 protein were seen at the early phase after two-vein occlusion. CONCLUSIONS: After vein occlusion, apoptosis appeared sequentially and widely in cortical lesions considered to be the penumbra. Therefore, control of apoptosis would be expected to offer a therapeutic window for treatment of venous infarction.

Persistent intracranial hypertension caused by superior sagittal sinus stenosis following depressed skull fracture. Case report and review of the literature.

Intracranial hypertension caused by a compound depressed skull fracture on the posterior part of the superior sagittal sinus is a rare condition, and nonspecific symptoms and signs can delay appropriate diagnosis and treatment. The authors report on a case of intracranial hypertension that persisted despite conservative treatment, including anticoagulation therapy, which did not improve severe flow disturbance related to the venous sinus compression. Management of this rare condition is discussed and the literature is reviewed.

Impairment of autoregulation following cortical venous occlusion in the rat.

Recent experiments showed an upward shift of the lower limit of autoregulation (AR) following photochemical occlusion of cortical veins in the rat. The goal of the present study was to prove the hypothesis that occlusion of cortical veins will be associated with impairment of the upper limit of autoregulation as well. In n = 28 Wistar rats unilateral frontoparietal cranial windows were drilled for transdural assessment of regional cerebral blood flow (rCBF) by laser Doppler scanning. The animals were allotted to two groups: (1) Group A (n = 5), control group for determination of the upper limit of autoregulation with stepwise induced arterial hypertension by intravenous administration of the alpha adrenergic drug methoxamine under continuous monitoring of mean arterial blood pressure (MABP); (2) Group B (n = 23), in which two cortical veins were photochemically occluded with rose bengal dye and fiberoptic illumination upon baseline CBF measurement. This was followed by repeated rCBF measurements under AR testing. Loss of AR in control Group A with passive increase of rCBF occurred at MABP of 147.5 +/- 2.9 mmHg. In Group B venous occlusion was followed by an initial phase of reduced rCBF, and then by pressure passive increases, thereby indicating loss of AR. Statistically significant changes of rCBF when compared to baseline MABP occurred at MABPbaseline + 10% (112.7 +/- 6.6 mmHg). We conclude that AR is impaired upon cortical venous occlusion with the propensity for hyperperfusion injury at a lower level of MABP when compared with a control group. In the context with earlier findings this may lead to narrowing of the corridor for MABP management following intra-operative occlusion of large cortical veins.