Quality of life with special respect to depression after surgical treatment of hypertensive basal ganglia hemorrhage.

BACKGROUND: Hypertensive intracerebral hemorrhage is associated with high mortality and morbidity. Place of surgery in the primary supratentorial intracerebral hemorrhage is uncertain and the data on the long-term functional outcome of surgery in these patients is limited. AIM: The aim of the study was to determine long-term functional outcome of patients undergoing surgical treatment for hypertensive basal ganglia hemorrhage, especially in respect to depression. STUDY DESIGN AND SETTINGS: Retrospective analysis of database of 44 patients undergoing craniotomy for hypertensive basal ganglia hemorrhage between December 2002 and May 2007. MATERIALS AND METHODS: Long-term was defined as at least 18 months after craniotomy. Neurological status of the patients at admission was assessed by National Institute of Health Stroke Scale (NIHSS) and Glasgow Coma Scale (GCS). Outcome data consisted of the items including functionality, depression and quality of life. Tests applied included Barthel Index (BI), modified Rankin Scale (mRS), Beck Depression Inventory (BDI) and stroke-specific quality of life (SSQOL) scale. RESULTS: The long-term mortality rate was 29.5% (13/44). Of the 31 survivors, 21 (67.7%) patients had a BI >or= 60, 23 (74.2%) patients had a mRS <4 and 21 (67.7%) patients had a SSQOL >or= 60%, each representing a favorable outcome. In retrospect, 19 (61.3%) patients approved the surgery. Eighteen (58.1%) patients developed depression (BDI > 9), which was related to high NIHSS and low GCS score preoperatively, low BI, high mRS and low SSQOL postoperatively. CONCLUSIONS: The study reveals that depression is a common long-term complication after surgical treatment of hypertensive basal ganglion hemorrhage. Both the NIHSS and GCS scores before operation have critical roles in patient's quality of life associated with depression.

Endovascular embolization of small ruptured intracranial aneurysms using a biplane angiographic system with three-dimensional rotational digital subtraction angiography.

Endovascular coiling of small, ruptured intracranial aneurysms is controversial because of technical difficulties. We analyzed the clinical and angiographic effects of endovascular treatment of 39 small (5mm) ruptured intracranial aneurysms (in 37 patients) at our institution between March 2004 and March 2007. Procedures were carried out on a biplane angiographic system with three-dimensional rotational digital subtraction angiography. Immediately after embolization, 30 aneurysms were completely occluded and nine had a residual neck. The volumetric percentage occlusion was 45.2+/-9.7%. Angiographic and clinical follow-up was at 6.1 months and 15.9 months, respectively. Delayed rebleeding was not observed. Complications directly related to the procedure were encountered in two patients (one coil migration and one intraoperative rupture). For 34 patients, the final outcome was excellent or good, one suffered a moderate disability, one a severe disability and one patient died. The results suggest that endovascular embolization is effective and safe for patients with small ruptured intracranial aneurysms.

Experimental study on the correlation between abnormal muscle responses and F waves in hemifacial spasm.

OBJECTIVES: To investigate the correlation between abnormal muscle response (AMR) and F wave by establishing an animal model of hemifacial spasm (HFS). METHODS: Both demyelination in the main trunk of the facial nerve just distal to stylomastoid foramen and vascular compression were used to duplicate animal model of HFS in ten New Zealand white rabbits. AMR and F waves were elicited from the orbicularis oculi and mentalis muscles respectively by stimulating marginal mandibular branch of the facial nerve 6 weeks post-operatively. Correlation analyses were used to compare the relationship between AMR/M and F/M amplitude ratio and between the duration of AMRs and F waves. RESULTS: There was a linear correlation between the mean values of the AMR/M and F/M amplitude ratio (r=0.8602, p<0.01), which can also be found between the duration of AMRs and F waves (r=0.7702, p<0.01). DISCUSSION: Enhanced F waves and AMRs may have the same origin. The F wave can be regarded as a more direct index in the diagnosis pre-operatively, monitoring intraoperatively and follow-up post-operatively in patients with HFS.

The pre-treatment effect on brain injury during restoration of normal perfusion pressure with hemodilution in a new rat model of chronic cerebral hypoperfusion.

OBJECTIVES: To investigate the effect of hemodilution with high-concentration human serum albumin (HSA) on brain injury in a rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations. METHODS: The animal model was established by creating a fistula through an end-to-side anastomosis between the right distal external jugular vein and the ipsilateral common carotid artery, followed by ligation of the left vein draining the transverse sinus and bilateral external carotid arteries. The agent (20% HSA) or control solution (0.9% sodium chloride) was administered intravenously at a dosage of 1% body weight 24 hours before ligation of the fistula. Blood-brain barrier (BBB) disruption was judged by extravasation of Evans blue (EB) dye. EB, water content and the changes of myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in rat brains 24 hours after ligation of the fistula were determined. RESULTS: EB and water content in rat brains of the pre-treated group were significantly decreased compared with the control group accompanied by reduction of MPO activity and enhancement of SOD activity. DISCUSSION: Hemodilution with high-concentration HSA has a certain pre-treatment effect on brain injury after ligation of the fistula in rat model of chronic cerebral hypoperfusion, which may be resulted from improved microcirculation, decrease in inflammatory cell infiltration and inactivation of oxygen free radicals.

Treatment of atypical trigeminal neuralgia with microvascular decompression.

AIM: To explore the methods for achieving pain relief in patients with atypical trigeminal neuralgia (TN) using microvascular decompression (MVD). STUDY DESIGN AND SETTINGS: Retrospective study of 26 patients treated during the years 2000 to 2004. MATERIALS AND METHODS: Twenty-six patients in whom vascular compression of the trigeminal nerve was identified by high definition magnetic resonance tomographic angiography (MRTA) were treated with MVD for atypical TN in our department. Clinical presentations, surgical findings and clinical outcomes were analyzed retrospectively. RESULTS: In this study, single trigeminal division was involved in only 2 patients (8%) and two or three divisions in the other 24 patients (92%). Of prime importance is the fact that in 46.2% of the patients, several conflicting vessels were found in association. Location of the conflicts around the circumference of the trigeminal root was supero-medial to the root in 53.5%, supero-lateral in 30.8% and inferior in 15.7%. MVD for atypical TN resulted in complete pain relief in 50% of the patients with complete decompression, partial pain relief in 30.8% and poor pain relief or pain recurrence in 19.2% of the patients without complete decompression postoperatively. CONCLUSIONS: Complete decompression of the entire trigeminal root plays an important role in achieving pain relief in patients with atypical TN with MVD.

[Treatment of dural arteriovenous fistula by transarterial embolization with low dose of N-butyl-2-cyanoacrylate].

OBJECTIVE: To evaluate the efficacy of treatment of dural arteriovenous fistula (DAVF) by transarterial embolization with low dose of N-butyl-2-cyanoacrylate (NBCA). METHODS: Eighteen patients, 6 males and 12 females, aged 47.5 (23-72), with DAVF, 12 with carotid cavernous fistula and 6 with fistula in parietal lobe, underwent transarterial embolization with low dose of NBCA (10%-20%). The key point of transarterial embolization with low dose of NBCA was that low dose NBCA was injected and embolized the veins and then was reversed into the other supplying arteries. RESULTS: Seventeen patients with DAVF in cavernous region and 6 patients with DAVF in parietal lobe were cured anatomically, with the clinical syndromes disappearing. In 1 patient with DAVF in cavernous region the clinical syndrome were moderately improved after transarterial embolization, however, worsened 2 days later. Cerebrovascular angiography demonstrated that the vein was not completely embolized and the draining vein was broadened, and the clinical syndromes were moderately improved again after carotid artery compression therapy for 10 days. CONCLUSION: Convenient and fast, and with low cost and satisfying efficacy, transarterial embolization with low dose of NBCA is a better choice for treatment of DAVF in some cases. The key point of this approach is that the tip of microcatheter is close as much as possible to the fistulae, and NBCA is injected into the fistulae and make the vein diffused well. Attention should be paid to avoid dangerous anastomosis.

Chronic cerebral hypoperfusion and reperfusion injury of restoration of normal perfusion pressure contributes to the neuropathological changes in rat brain.

Restoration of normal perfusion pressure after resection of cerebral arteriovenous malformations (AVMs) is sometimes complicated by unexplained postoperative brain swelling and/or intracranial hemorrhage, which has been termed normal perfusion pressure breakthrough (NPPB). The precise mechanism of NPPB is still unclear. In this study, we investigated the time courses of blood-brain barrier (BBB) disruption, water content, neuronal apoptosis, myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in the brain during restoration of normal perfusion pressure in a new rat model of chronic cerebral hypoperfusion associated with AVMs. Male Sprague-Dawley rats were randomly divided into either a sham-operated group, a control group, or a model group with reperfusion assessed at 1, 12, 24 and 72 h after restoration of normal perfusion pressure. BBB disruption was judged by extravasation of Evans blue (EB) dye. We observed that EB and water content in rat brains of the model group with reperfusion were significantly increased compared with the other groups. The most predominant increase occurred at 1 h after reperfusion, and the next at 24 h after reperfusion, representing biphasic changes which are similar to the pathological processes of acute cerebral ischemia/reperfusion injury. There was no difference of the percentage of apoptotic cells in rat brains between the sham-operated group and the control group using flow cytometry. No prominent apoptotic cells were found in the model group with reperfusion at 1 h. However, the percentage of apoptotic cells increased significantly in rat brains of the model group with reperfusion at 12 h, peaked at 24 h, and decreased at 72 h after reperfusion. Apoptotic cells were confirmed with electron microscopy and terminal deoxynuleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). A significant enhancement of MPO activity in combination with reduction of SOD activity was seen at 12, 24 and 72 h in rat brains of the model group with reperfusion. Our data indicates that reperfusion after restoration of normal perfusion pressure with chronic cerebral hypoperfusion lead to secondary neuronal damage which may associate with cerebral ischemia/reperfusion injury.

Vascular endothelial growth factor expression and angiogenesis induced by chronic cerebral hypoperfusion in rat brain.

OBJECTIVE: In a rat model, we studied the time courses of vascular endothelial growth factor (VEGF) expression and angiogenesis induced by chronic cerebral hypoperfusion in the brain, and we investigated the histological basis of normal-perfusion pressure breakthrough. METHODS: Twenty-one Sprague-Dawley rats were randomly divided into a control group (n = 3) and a model group assessed at various time points after the creation of a carotid artery-jugular vein fistula (12 h, n = 3; 24 h, n = 3; 72 h, n = 3; 7 d, n = 3; 21 d, n = 3; 90 d, n = 3). The time courses of the expression of VEGF messenger ribonucleic acid (mRNA) and protein in rat brain were analyzed with semiquantitative reverse transcriptase-polymerase chain reaction and Western blot assays, respectively. Immunohistochemical techniques were used to evaluate VEGF protein localization with rabbit polyclonal anti-rat VEGF, VEGF receptor (VEGFR) expression with rabbit polyclonal antibodies to VEGFR-1 and -2, microvascular density with mouse monoclonal anti-rat CD31, and astrocytic reactivity with polyclonal anti-glial fibrillary acidic protein, in cerebral cortical tissue of the right middle cerebral artery territory. RESULTS: Three alternative splicing forms, i.e., VEGF(188), VEGF(164), and VEGF(120), were observed in cerebral cortical tissue of the right middle cerebral artery territory in semiquantitative reverse transcriptase-polymerase chain reaction analyses. VEGF(164) mRNA was the predominant isoform expressed in rat brain. VEGF(188) mRNA and VEGF(120) mRNA were also detected but at very low levels (not statistically significant). Low levels of VEGF(164) mRNA were observed in the control brains. However, VEGF(164) mRNA levels were significantly increased in the model brains at 24 hours postoperatively, peaked by 7 days, decreased by 21 days, and returned to basal levels by 90 days after fistula formation. VEGF protein expression, as measured in Western blot assays, was also increased in rat brains in the model group from 24 hours to 21 days postoperatively but returned to control levels by 90 days after fistula formation. VEGF immunohistochemical analyses indicated that this increased expression was mostly associated with endothelial cells. Consistent with the VEGF protein expression findings, up-regulation of VEGFR-1 but not VEGFR-2 expression on endothelial cells in the model brains was observed. Microvascular density in the rat brains began to increase significantly 7 days after fistula formation in the model group, as assessed immunohistochemically, and the increase was maintained for 90 days. Although no prominent astrocytic reactivity was observed in the rat brains throughout the experiments, there was an absence of astrocytic foot processes surrounding some cerebral capillaries 90 days after fistula formation in the model group. CONCLUSION: These results demonstrated that chronic cerebral hypoperfusion could induce sustained up-regulation of VEGF mRNA and protein expression in rat brain, which was correlated with angiogenesis. An absence of corresponding astrocytic reactivity during angiogenesis may be an important factor accounting for structural deficits of the blood-brain barrier and the occurrence of normal-perfusion pressure breakthrough.