Qizhong Luo

Endoscopic versus microscopic transsphenoidal pituitary adenoma surgery: a meta-analysis

BackgroundEndoscopic transsphenoidal surgery has gradually come to be regarded as a preferred option in the treatment of pituitary adenomas because of its advantages of improved visualization and its minimal invasiveness. The aim of this study was to compare and evaluate the outcomes and complications of endoscopic and microscopic transsphenoidal surgery in the treatment of pituitary adenomas.MethodsWe performed a systematic literature search of MEDLINE, EMBASE, the Cochrane Library and the Web of Science between January 1992 and May 2013. Studies with consecutive patients that explicitly and fully compared endoscopic and microscopic approaches in the treatment of pituitary adenomas were included.ResultsA total of 15 studies (n = 1,014 patients) met the inclusion criteria among 487 studies that involved endoscopic surgery and 527 studies that dealt with microscopic surgery. The rate of gross tumor removal was higher in the endoscopic group than in the microscopic group. The post-operative rates of septal perforation were less frequent in patients who underwent endoscopic surgery. There was no significant difference between the two techniques in the incidence rates of meningitis, diabetes insipidus, cerebrospinal fluid leak, epistaxis or hypopituitarism. The post-operative hospital stay was significantly shorter for the endoscopic surgery group compared with the microscopic surgery group (P < 0.05). There was no significant difference in the length of the operation (P > 0.05).ConclusionsThe present study indicates that the endoscopic transsphenoidal approach is safer and more effective than microscopic surgery in the treatment of pituitary adenomas.

Mice lacking glutamate carboxypeptidase II develop normally, but are less susceptible to traumatic brain injury

Glutamate carboxypeptidase II (GCPII) is a transmembrane zinc metallopeptidase found mainly in the nervous system, prostate and small intestine. In the nervous system, glia‐bound GCPII mediates the hydrolysis of the neurotransmitter N‐acetylaspartylglutamate (NAAG) into glutamate and N‐acetylaspartate. Inhibition of GCPII has been shown to attenuate excitotoxicity associated with enhanced glutamate transmission under pathological conditions. However, different strains of mice lacking the GCPII gene are reported to exhibit striking phenotypic differences. In this study, a GCPII gene knockout (KO) strategy involved removing exons 3–5 of GCPII. This generated a new GCPII KO mice line with no overt differences in standard neurological behavior compared to their wild‐type (WT) littermates. However, GCPII KO mice were significantly less susceptible to moderate traumatic brain injury (TBI). GCPII gene KO significantly lessened neuronal degeneration and astrocyte damage in the CA2 and CA3 regions of the hippocampus 24 h after moderate TBI. In addition, GCPII gene KO reduced TBI‐induced deficits in long‐term spatial learning/memory tested in the Morris water maze and motor balance tested via beam walking. Knockout of the GCPII gene is not embryonic lethal and affords histopathological protection with improved long‐term behavioral outcomes after TBI, a result that further validates GCPII as a target for drug development consistent with results from studies using GCPII peptidase inhibitors. The peptide neurotransmitter N‐acetylaspartylglutamate (NAAG) suppresses glutamate transmission through selective activation of pre‐synaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3) after traumatic brain injury (TBI). However, synaptically released NAAG is hydrolyzed to form N‐acetylaspartate and glutamate mainly by Glutamate carboxypeptidase II (GCPII), losing neuroprotective effect. In this study, we found that knock out of the GCPII gene is not embryonic lethal and affords histopathological protection with improved long‐term behavioral outcomes after TBI.

Glutamate carboxypeptidase II gene knockout attenuates oxidative stress and cortical apoptosis after traumatic brain injury.

BackgroundGlutamate carboxypeptidase II (GCPII) inactivates the peptide co-transmitter N-acetylaspartylglutamate following synaptic release. Inhibition of GCPII elevates extracellular levels of the peptide, inhibits glutamate release and is neuroprotective in an animal model of traumatic brain injury. GCPII gene knockout mice were used to examine the cellular mechanisms underlying the neuroprotective efficacy of this transmitter system.ResultsFollowing controlled cortical impact injury, GCPII knockout (KO) mice exhibited reduced TUNEL-positive nuclei in the contusion margin of the cerebral cortex relative to wild type mice. Impact injury reduced glutathione levels and superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde. Each of these effects was moderated in KO mice relative to wild type. Similarly, the injury-induced increases in cleaved caspase-3, cytosolic cytochrome c levels and Bcl-2/Bax ratio observed in wild type mice were attenuated in the knockout mice.ConclusionsThese data support the hypothesis that the neuroprotective efficacy of GCPII KO in traumatic brain injury is mediated via a reduction in oxidative stress.

Blockade of N-acetylaspartylglutamate peptidases: a novel protective strategy for brain injuries and neurological disorders.

The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) is reported to suppress glutamate release mainly through selective activation of presynaptic Group II metabotropic glutamate receptor subtype 3 (mGluR3). Therefore, strategies of inhibition of NAAG peptidases and subsequent NAAG hydrolysis to elevate levels of NAAG could reduce glutamate release under pathological conditions and be neuroprotective by attenuating excitotoxic cell injury. A series of potent inhibitors of NAAG peptidases has been synthesized and demonstrated efficacy in experimental models of ischemic–hypoxic brain injury, traumatic brain injury, inflammatory pain, diabetic neuropathy, amyotrophic lateral sclerosis and phencyclidine-induced schizophrenia-like behaviors. The excessive glutamatergic transmission has been implicated in all of these neurological disorders. Thus, blockade of NAAG peptidases may augment an endogenous protective mechanism and afford neuroprotection in the brain. This review aims to summarize and provide insight into the current understanding of the novel neuroprotective strategy based on limiting glutamate excitotoxicity for a wide variety of brain injuries and neurological disorders.

Effects of Dose-Response of Topical Administration of Nimodipine on Cerebral Vasospasm After Subarachnoid Hemorrhage in Rabbits

Background:To explore the dose-response effects of topical administration of nimodipine on cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH) in rabbits. Methods:The CVS model was established by injection of fresh autologous nonheparinized arterial blood into the subtemporal area of basilar cisterns. The 24 CVS animals were randomly divided into 4 groups, group I (n = 7): nimodipine original stock solution/normal saline = 1/19 (0.01 mg/mL); group II (n = 6): nimodipine original stock solution/normal saline = 1/9 (0.02 mg/mL); group III (n = 5): nimodipine original stock solution/normal saline = 1/4 (0.04 mg/mL); and group IV (n = 6) with no nimodipine, but 5% ethanol dissolved in normal saline as the control group. The operative area was administrated with nimodipine at different concentrations or alcohol–saline at 3 days after SAH. The blood flow velocity of middle cerebral artery was measured at 5, 15, 30, and 60 minutes after topical administration of nimodipine by transverse cerebellar diameter monitoring. Results:Blood flow velocity of middle cerebral artery in group II (0.02 mg/mL) and in group III (0.04 mg/mL) significantly decreased at 60 and 15 minutes, respectively, after topical administration of nimodipine (P < 0.05), and even more significantly at 30 and 60 minutes after topical administration of nimodipine in group III (0.04 mg/mL) (P < 0.01). Conclusion:Topical administration of nimodipine at the concentrations of 1:5 (0.04 mg/mL) and 1:10 (0.02 mg/mL) significantly alleviates CVS after SAH, which indicates that topical administration of nimodipine may be useful for CVS of patients with SAH during surgical clip of intracranial aneurysms.

Intracranial choriocarcinoma occurrence in males: Two cases and a review of the literature

Choriocarcinomas generally develop in females. Non-gestational choriocarcinoma in males is extremely rare. The present study describes two cases of young males who were diagnosed with intracranial choriocarcinoma. One case was of an aggressive choriocarcinoma with multiple metastases to the brain, but with an unidentified origin. The patient was admitted in the terminal stage of the cancer. Although a tumor resection was performed, the condition of the patient rapidly deteriorated and chemotherapy was not recommended. The patient succumbed nine days after the surgery. The second case was of a primary ventricular choriocarcinoma. The patient was hospitalized for acute hydrocephalus caused by a mass that was located in the ventricle. Following a tumor resection, the patient underwent a course of whole-brain and spinal radiotherapy. The patient was followed up for more than half a year and remained in a good condition. The present study describes the two cases and a comprehensive review of the literature that was performed to identify similar studies that document choriocarcinomas in males.

Intramedullary conus medullaris metastasis from prostate carcinoma: A case report and review of the literature.

Intramedullary spinal cord metastases (ISCMs) are rare and account for 4–8.5% of central nervous system metastases. Only one case of biopsy-proven ISCM due to prostate cancer has previously been reported. The current study presents an additional unique case of a 74-year-old male who developed symptoms from an intramedullary conus medullaris metastasis as the first manifestation of prostate adenocarcinoma. To the best of our knowledge, this scenario is even more rare and has not previously been reported. The tumor was radically resected, followed by androgen blockade treatment. The patient’s neurological deficit significantly improved, with no tumor recurrence during the follow-up period. In addition, the present study provides an overview of the previous literature concerning ISCMs from prostate cancer, and discusses the treatment options.

Endoscopic Fenestration of Twenty-Six Patients With Middle Fossa Arachnoid Cyst.

AbstractMiddle fossa arachnoid cyst (MFAC) is the most common kind of arachnoid cyst. The objective of this study was to assess the efficacy of endoscopic fenestration for MFACs. The authors report 26 patients of MFAC with variety symptoms such as macrocrania, epilepsy, headache, and development delay. The authors performed surgery with a neuroendoscope to drain and fenestrate the cyst to obtain nearby cystocisternal communications under general anesthesia. All of the 26 patients had a successful fenestration, most of them had an improvement of at least 1 of their pretreatment symptoms with the substantial reduction of the cyst postoperatively. The authors conclude that endoscopic fenestration may be an acceptable and minimally invasive option for the management of symptomatic MFACs.

Improved neurite outgrowth on central nervous system myelin substrate by siRNA-mediated knockdown of Nogo receptor

Purpose To investigate the in vitro effect of short interfering RNAs (siRNAs) against Nogo receptor (NgR) on neurite outgrowth under an inhibitory substrate of central nervous system (CNS) myelin. Methods Three siRNA sequences against NgR were designed and transfected into cerebellar granule cells (CGCs) to screen for the most efficient sequence of NgR siRNA by using reverse transcription polymerase chain reaction (RT-PCR) and immunofluorescence staining. NgR siRNA sequence 1 was found the most efficient which was then transfected into the CGCs grown on CNS myelin substrate to observe its disinhibition for neurite outgrowth. Results Compared with the scrambled control sequence of siRNA, the NgR siRNA sequence 1 significantly decreased NgR mRNA level at 24 h and 48 h (p < 0.05), which was recovered by 96 h after transfection. NgR immunoreactivity was also markedly reduced at 24 and 48 h after the transfection of siRNA sequence 1 compared with that before transfection (p < 0.05). The NgR immunoreactivity was recovered after 72 h post-transfection. Moreover, the neurite outgrowth on the myelin substrate was greatly improved within 72 h after the transfection with siRNA sequence 1 compared with the scrambled sequence-transfected group or non-transfected group (p < 0.05). Conclusion : siRNA-mediated knockdown of NgR expression contributes to neurite outgrowth in vitro.

A child with uncontrollable bursts of laughter

Hypothalamic hamartomas (HH) are rare (1:200,000), nonneoplastic heterotopic congenital malformations formed by neurons and glial cells located close to the posterior hypothalamus, tuber cinereum, or mammillary bodies [1]. The condition was first described in 1873 as a seizure presenting with laughter [2]. Later, Daly and Mulder named this condition ‘‘gelastic epilepsy’’ [3]. Gelastic seizures, central precocious puberty, and cognitive impairment are the predominant manifestations of HH in infancy [4]. The typical MRI features of HH are isoor hypo-intensity on T1weighted images and isoor slight hyper-intensity on T2-weighted images. A lack of contrast enhancement in the tuber cinereum region is valuable for radiological diagnosis to distinguish tumors from other lesions in this field, such as third-ventricular ependymomas, hypothalamic astrocytomas, germ cell tumors, Langerhans cell histiocytosis, and papillomas. Our patient was diagnosed with HH due to the similarity with previous case reports. The electroencephalogram showed interictal focal (mostly right frontal and temporal) paroxysmal activity (more frequently slow spike-andwave complexes) consistent with HH lateralization. Recent reports have demonstrated the intrinsic epileptogenicity of HH. The mechanism of gelastic epilepsy may be the spontaneous firing of gamma-aminobutyric acid (GABA)-ergic small HH neurons, which project synaptic connections onto the larger adjacent pyramidal-like HH neurons. The combination of these neurons acts as a pacemaker that synchronizes the numerous output neurons to mediate seizure activity in the brain, and this action results in the observed clinical symptoms. This groupof lesionshas been classifiedbyDelalandeas I through IV, based onmorphology onMRI [5]. Type I has a horizontal orientation and may be lateralized to one side. Type II has a vertical orientation and an intraventricular location. Type III is a combination of types I and IIwith a vertical plane of attachmentwithin the ventricle and a horizontal plane of attachment on the underside of the hypothalamus. Type IV is a giant hamartoma. In our patient, the lesion was located in its entirety in the third ventricle (Fig. 2 of Images in Neuroscience: Question) and was thus classified as type II. Due to the insufficient number of clinical reports, there is no consensus regarding the various therapeutic options. Despite the use of higher doses and several combinations of antiepileptic drugs, freedom from seizures or good seizure control is rarely achieved in HH patients [6]. At present, surgical resection, stereotactic endoscopic disconnection, Gamma Knife radiosurgery (Elekta AB, Stockholm, Sweden), and radiofrequency thermocoagulation appear to be useful and safe approaches, particularly for the treatment of small HH [7–9]. In our patient, numerous antiepileptic drugs were utilized in various combinations for approximately 4 years; however, none of these treatments exhibited any efficacy. Subsequently, the patient underwent Gamma Knife radiosurgery and long-term follow-up. Further studies are needed to assess the prognosis.