Thung-Ming Su

Post-neurosurgical nosocomial bacterial meningitis in adults: microbiology, clinical features, and outcomes

The clinical data of 62 adult patients who suffered post-neurosurgical nosocomial bacterial meningitis, retrospectively collected over a 16-year period, were studied. Cases were divided into two groups based on the date of presentation, the first period being 1986-1993 and the second 1994-2001. Fever and progressive consciousness disturbance were the most consistent clinical features - signs that may also be attributed to other postoperative neurosurgical problems. The common pathogens included Staphylococcus aureus, coagulase negative Staphylococcus, Pseudomonas aeruginosa, Escherichia coli, and Acinetobacter baumannii. An increase in polymicrobial infections and multi-antibiotic resistance during the second period was identified. In the first half of the study, mortality was 22%, and in the second half 36%. Adult post-neurosurgical nosocomial bacterial meningitis has become an important clinical problem. The choice of appropriate empirical antibiotics is challenging and must be guided by an awareness of the relative frequency of various pathogens and the increasing incidence of resistant strains. Although high mortality rates may, in part, be related to the primary brain pathology, early diagnosis and the timely use of antibiotics based on antimicrobial susceptibility testing are essential for survival.

Contralateral acute epidural hematoma after decompressive surgery of acute subdural hematoma: clinical features and outcome.

BACKGROUND Delayed contralateral epidural hematoma (EDH) after decompressive surgery for acute subdural hematoma (SDH) is uncommon. If unrecognized, this delayed hematoma can cause devastating consequences. We present our experience with this group of patients and discuss the diagnosis and management of this dangerous condition. METHODS This study included 12 traumatic patients with acute SDH who developed delayed contralateral EDH after acute SDH evacuation. Clinical and radiographic information was obtained through a retrospective review of the medical records and the radiographs. RESULTS There were seven males and five females. Nine patients had severe head injury (Glasgow Coma Scale {GCS} score < or = 8). Ten patients underwent acute SDH evacuation within 4 hours after the trauma. Intraoperative brain swelling during SDH evacuation was noted in 10 patients. A skull fracture at the site of the EDH on computed tomography (CT) was noted only in 10 patients. However, a skull fracture overlying the EDH was found during EDH evacuation in all patients. Only three patients with less severe head injury (GCS > 8) had good recovery. Other patients with severe head injury (GCS < or = 8) had poor outcome. CONCLUSIONS Severe head injury, a skull fracture contralateral to the original hematoma, intraoperative brain protrusion, and a poor outcome are typical clinical findings in this disorder. In patients with acute SDH and a contralateral skull fracture, immediate postoperative CT scan is indicated to evaluate this rare but potentially lethal complication. According to the findings of the postoperative CT scan, the neurosurgeon can make an appropriate strategy of treatment promptly. Early detection and prompt treatment may improve the poor outcome in this group of patients.

Clinical features and predictive factors of intraventricular rupture in patients who have bacterial brain abscesses

Background: Intraventricular rupture of brain abscesses (IVRBA) remains a catastrophic and fatal complication of bacterial brain abscess (BBA). However, no information has been reported about the risk factors that are predictive of intraventricular rupture. Methods: This study was undertaken to determine the potential risk factors that are predictive of intraventricular ruptures in patients with BBA but without intraventricular rupture when arriving at the hospital. A comparison is also made between patients who already have IVRBA at the time of admission (initial IVRBA) and those who have the episode during hospitalisation (subsequent IVRBA). Results: 62 patients, including 45 who had initial IVRBA and 17 who had subsequent IVRBA, were examined. Stepwise logistic regression analysis showed that the adjusted risk of intraventricular rupture during hospitalisation for patients with multiloculated brain abscesses had an odds ratio (OR) of 4.2 (95% confidence interval (CI) 1.24 to 14.3; p = 0.02) compared with those without multiloculated brain abscesses (referent); a reduction of 1 mm in the distance between the ventricle and brain abscesses would increase the rupture rate by 10% (p = 0.006, OR 0.9, 95% CI 0.83 to 0.97). Conclusion: This study shows that if the abscess is deep seated, multiloculated and close to the ventricle wall, a reduction of 1 mm in the distance between the ventricle and brain abscesses will increase the rupture rate by 10%. Despite aggressive medical and surgical management shown in this series, many patients continue to progress poorly.

Intrathecally injected granulocyte colony-stimulating factor produced neuroprotective effects in spinal cord ischemia via the mitogen-activated protein kinase and Akt pathways

Granulocyte colony-stimulating factor (G-CSF) is a potent hematopoietic factor. Recently, this factor has been shown to exhibit neuroprotective effects on many CNS injuries. Spinal cord ischemic injury that frequently results in paraplegia is a major cause of morbidity after thoracic aorta operations. In the present study, we examined the neuroprotective role of G-CSF on spinal cord ischemia-induced neurological dysfunctions and changes in the mitogen-activated protein kinase (MAPK) and Akt signaling pathways in the spinal cord. Spinal cord ischemia was induced in male Wistar rats by occluding the descending aorta with a 2F Fogarty catheter for 12 min 30 s. Immediately after ischemia surgery, the rats were administered G-CSF (10 mug) or saline by intrathecal (i.t.) injection. The rats were divided into four groups: control, ischemia plus saline, ischemia plus G-CSF and G-CSF alone. The neurological dysfunctions were assessed by calculating the motor deficit index after ischemia surgery. The expressions of MAPK and Akt were studied using Western blotting and double immunohistochemistry. First, we observed that ischemia plus i.t. G-CSF can significantly reduce the motor function defects and downregulate phospho-p38 and phospho-c-Jun N-terminal kinase protein expressions-this can be compared with the ischemia plus saline group. In addition, G-CSF inhibited the ischemia-induced activation of p38 in the astrocytes. Furthermore, we concluded that i.t. G-CSF produced a significant increase in phospho-Akt and phospho-ERK in the motor neurons and exhibited beneficial effects on the spinal cord ischemia-induced neurological defects.

Neuroprotection by marine-derived compound, 11-dehydrosinulariolide, in an in vitro Parkinson’s model: a promising candidate for the treatment of Parkinson’s disease

Parkinson’s disease (PD) is a neurodegenerative disease characterized by tremor, rigidity, bradykinesia, and gait impairment. So far, very few pharmacological agents have been isolated or developed that effectively inhibit the progression of PD. However, several studies have demonstrated that inflammatory processes play critical roles in PD. Therefore, anti-inflammatory agents may suppress disease progression in PD. 11-Dehydrosinulariolide was isolated from cultured soft corals. The anti-inflammatory effect of this molecule has been observed through suppression of the expression of two main pro-inflammatory proteins: inducible nitric oxide synthase and cyclooxygenase-2, in lipopolysaccharide-stimulated macrophage cells. We also found that 11-dehydrosinulariolide significantly reduced 6-hydroxydopamine (6-OHDA)-induced cytotoxicity and apoptosis in a human neuroblastoma cell line (SH-SY5Y). The pharmacological activity of this compound has been studied, and it is associated with the inhibition of 6-OHDA-induced activation of caspase-3 and translocation of nuclear factor kappa B. 11-Dehydrosinulariolide increased the activation of survival-signaling phospho-Akt but not phospho-ERK. The neuroprotective effect of 11-dehydrosinulariolide was assessed here using 6-OHDA-treated SH-SY5Y cells, wherein neuroprotection is mediated through regulation of phosphatidylinositol 3-kinase (PI3K). Furthermore, 11-dehydrosinulariolide caused a significant decrease in caspase-3/7 activity in comparison to the 6-OHDA-treated group, indicating that 11-dehydrosinulariolide has neuroprotective properties. We conclude that 11-dehydrosinulariolide is a promising candidate for the treatment of Parkinson’s disease through its anti-apoptotic and anti-inflammatory action via PI3K signaling.

Suppressive effects of intrathecal granulocyte colony-stimulating factor on excessive release of excitatory amino acids in the spinal cerebrospinal fluid of rats with cord ischemia: role of glutamate transporters.

Recently, the hematopoietic factor, granulocyte colony-stimulating factor (G-CSF), has been shown to exhibit neuroprotective effects in CNS injuries. Our previous study demonstrated that intrathecal (i.t.) G-CSF significantly improved neurological defects in spinal cord ischemic rats. Considerable evidence indicates that the release of excessive amounts of excitatory amino acids (EAAs) plays a critical role in neuron injury induced by ischemic insult. In the present study, we used a spinal cord ischemia-microdialysis model to examine whether i.t. G-CSF exerted antiexcitotoxicity effects in a rat model of spinal cord ischemia. I.t. catheters and a microdialysis probe were implanted in male Wistar rats. The results revealed that spinal cord ischemia-induced neurological defects were accompanied by a significant increase in the concentration of EAAs (aspartate and glutamate) in the spinal dialysates from 30 min to 2 days after reperfusion. I.t administration of G-CSF immediately after the performance of surgery designed to induce ischemia led to a significant reduction in ischemia-induced increases in the levels of spinal EAAs. Moreover, i.t. G-CSF also brought about a significant reduction in the elevation of spinal EAA concentrations induced by exogenous i.t. administration of glutamate (10 microl of 500 mM). I.t. G-CSF attenuated spinal cord ischemia-induced downregulation of expression of three glutamate transporters (GTs), glial transporter Glu-Asp transporter (GLAST), Glu transporter-1 (GLT-1), and excitatory amino acid carrier 1 (EAAC1) protein 48 h after spinal cord ischemic surgery. Immunohistofluorescent staining showed that i.t. G-CSF significantly upregulated expression of the three GTs in the gray matter of the lumbar spinal cord from 3 to 24 h after injection. We propose that i.t. G-CSF possesses an ability to reduce the extent of spinal cord ischemia-induced excitotoxicity by inducing the expression of glutamate transporters.

Lumbosacral spinal subdural hematoma following burr hole craniotomy: Case report and literature review

Spinal subdural hematoma is a rare complication of cranial surgery. This study reports a case of postcraniotomy lumbosacral spinal subdural hematoma in the absence of predisposing factors. A review of the literature is also presented.

Concurrent chemoradiotherapy for primary cervical spinal cord germinoma

We report a rare case of primary intramedullary germinoma in the cervical spine of a 39-year-old woman without evidence of intracranial or disseminated disease. The germinoma was treated by a biopsy and follow-up concurrent chemoradiotherapy. This is the only reported case of primary spinal cord germinoma for which concurrent chemoradiotherapy was given. Furthermore, this is only the second reported case of histologically documented primary intramedullary cervical spinal cord germinoma. The patient was disease-free and there was near-complete resolution of the pre-operative neurological deficits at the 20-month follow-up examination.

Acute thrombosis and recanalization of a ruptured anterior communicating artery aneurysm

A 35-year-old man sustained a subarachnoid hemorrhage due to the rupture of an anterior communicating artery aneurysm. A second angiogram taken 8 hours later demonstrated that the ruptured aneurysm had thrombosed spontaneously with a small residual aneurysm stump at the neck. CT scans and conventional angiograms taken 2 days later demonstrated recanalization of the aneurysm, which was successfully treated by endovascular coiling. This case differs from previous reports of spontaneously thrombosed ruptured aneurysms because the aneurysm recanalized within 2 days. Thus a thrombosed ruptured aneurysm has the potential for recanalization, and should be considered at risk of further hemorrhage.

Predictors and outcome of acute symptomatic cerebral infarctions following aneurysmal subarachnoid hemorrhage

The leading cause of unfavorable outcomes following aneurysmal subarachnoid hemorrhage (SAH) is cerebral infarction. In this 3-year retrospective study, we have retrospectively evaluated 172 hospitalized patients with aneurysmal SAH, and compared those who developed a complicated cerebral infarction with those who did not. In this study, acute symptomatic cerebral infarctions accounted for 22.6% (39/172) of all episodes. Significant statistical analysis between the two patient groups included age at onset, hypertension as the underlying disease, presence of symptomatic vasospasm, mean hospitalization days and Glasgow Outcome Score at the time of discharge. After a minimum 1.5-year follow-up period, the median (interquantile range) Barthel index score was 75 (6–85) for those patients who had cerebral infarctions, and 80 (0–90) for those who had no cerebral infarctions. Multiple logistic regression analysis demonstrated that the presence of symptomatic vasospasm was independently associated with the presence of acute symptomatic cerebral infarctions. The presence of symptomatic vasospasm implies the danger of acute symptomatic cerebral events after aneurysmal SAH. Although our study demonstrates a worse short-term outcome and longer duration of hospitalization in this special group of patients, the functional outcome for patients with cerebral infarction was not inferior to those patients without cerebral infarction after a follow-up of at least 1.5-years.