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  • Journal of Neurosurgery Publishing Group (JNSPG)  (7)
  • 1
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    Online Resource
    Three-level and four-level anterior cervical discectomies and titanium cage—augmented fusion with and without plate fixation
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2004
    In:  Journal of Neurosurgery: Spine Vol. 1, No. 2 ( 2004-09), p. 160-167
    Details
    In: Journal of Neurosurgery: Spine, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 1, No. 2 ( 2004-09), p. 160-167
    Abstract: Object. Cage-assisted anterior cervical discectomy and fusion (ACDF) has proven to be a safe and effective procedure for the treatment of one- and two-level degenerative disc disease (DDD). To the authors' knowledge, clinical results after three- and four-level interbody cage—augmented ACDF have not been reported in the literature. The authors investigated the safety and effectiveness of titanium cages used in such procedures and evaluated the results in cases with or without plate fixation. Methods. Fifty-six patients suffering from cervical DDD were divided into two groups. Group 1 included 32 patients who underwent titanium cage—assisted ACDF; Group 2 included 24 patients who underwent the same procedure, supplemented with plate fixation. The cervical DDD was confirmed by radiography and magnetic resonance imaging. The patients underwent radiographic evaluation to assess cervical lordosis, segmental height of cervical spine, the height of the foramina, and spinal stability. Neurological outcomes were assessed using the Japanese Orthopaedic Association (JOA) scores. Neck pain was graded using a 10-point visual analog scale (VAS). The follow-up period ranged from 13 to 28 months (mean 17.2 months). In both Groups 1 and 2 significant increase (p 〈 0.001) was demonstrated in the JOA scores (preoperatively 10.7 ± 2.4 and 11.1 ± 2, postoperatively 13.9 ± 2.2 and 14.1 ± 2.3, respectively) and VAS pain scores (preoperatively 8.8 ± 0.9 and 8.5 ± 1, postoperatively 3.1 ± 2.1 and 2.8 ± 1.8, respectively); however, there was no significant intergroup difference. A significant increase in the cervical lordosis, foraminal height, and segmental height was observed in both groups. Good stability of cage fusion was obtained in both groups 12 months postoperatively (90.6% in Group 1 and 91.7% in Group 2); however, there were no statistically significant intergroup differences. The complication rate in Group 2 was higher than that in Group 1. The hospital length of stay in Group 1 was significantly lower than in Group 2 (p 〈 0.001). Conclusions. Analysis of these findings demonstrated that titanium cage—assisted ACDF provided long-term stabilization, increased lordosis, increased segmental height, and increased foraminal height. In both groups good neurological outcomes were achieved and donor site morbidity was avoided. The lower complication rate and shorter hospital stay, however, make the cage-assisted fusion without plate fixation better than with plate fixation.
    Type of Medium: Online Resource
    ISSN: 1547-5654
    URL: Article
    DOI: 10.3171/spi.2004.1.2.0160
    RVK:
    XA 55270.1
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2004
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  • 2
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    Online Resource
    Attenuation of experimental subarachnoid hemorrhage–induced cerebral vasospasm by the adenosine A2A receptor agonist CGS 21680
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2007
    In:  Journal of Neurosurgery Vol. 106, No. 3 ( 2007-03), p. 436-441
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 106, No. 3 ( 2007-03), p. 436-441
    Abstract: Impaired endothelium-dependent relaxation is present in vasospastic cerebral vessels after subarachnoid hemorrhage (SAH) and may result from deficient production of endothelial nitric oxide synthase (eNOS) or increased production and/or activity of inducible NOS (iNOS). Accumulating evidence demonstrates that adenosine A 2A receptors increase the production of NO by human and porcine arterial endothelial cells, which in turn leads to vasodilation. This study was designed to examine the effects of an adenosine A 2A receptor agonist, (2(4-[2-carboxyethyl]phenyl)ethylamino)-5′- N -ethylcarboxamidoadenosine (CGS 21680), in the prevention of SAH-induced vasospasm. Methods Experimental SAH was induced in Sprague–Dawley rats by injecting 0.3 ml of autologous blood into the cisterna magna of each animal. Intraperitoneal injections of CGS 21680 or vehicle were administered 5 minutes and 24 hours after induction of SAH. The degree of vasospasm was determined by averaging measurements of cross-sectional areas of the basilar artery (BA) 48 hours after SAH. Expression of eNOS and iNOS in the BA was also evaluated. Prior to perfusion–fixation, there were no significant differences among animals in the control and treated groups in any physiological parameter that was recorded. The CGS 21680 treatment significantly attenuated SAH-induced vasospasm. Induction of iNOS mRNA and protein in the BA by the SAH was significantly diminished by administration of CGS 21680. The SAH-induced suppression of eNOS mRNA and protein was also relieved by the CGS 21680 treatment. Conclusions This is the first evidence that adenosine A 2A receptor agonism is effective in preventing SAH-induced vasospasm without significant complications. The beneficial effect of adenosine A 2A receptor agonists may be, at least in part, related to the prevention of augmented expression of iNOS and the preservation of normal eNOS expression following SAH. Adenosine A 2A receptor agonism holds promise in the treatment of cerebral vasospasm following SAH and merits further investigation.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2007.106.3.436
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2007
    detail.hit.zdb_id: 2026156-1
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  • 3
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    Upregulation of estrogen receptor α and mediation of 17β-estradiol vasoprotective effects via estrogen receptor α in basilar arteries in rats after experimental subarachnoid hemorrhage : Laboratory investigation
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2008
    In:  Journal of Neurosurgery Vol. 109, No. 1 ( 2008-07), p. 92-99
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 109, No. 1 ( 2008-07), p. 92-99
    Abstract: The authors previously demonstrated that 17β-estradiol benzoate (E2) treatment prevents subarachnoid hemorrhage (SAH)–induced cerebral vasospasm and preserves endothelial nitric oxide synthase (eNOS) in male rats. Changes in the expression of estrogen receptor (ER) subtypes ERα and -β and their roles in the E2-mediated preservation of eNOS in SAH remain unknown. In the present study the effects of SAH on the expression of ERα and -β in the cerebral arteries were clarified, and the receptor roles in the E2-mediated preservation of eNOS expression in SAH were differentiated. Methods A 2-hemorrhage SAH model was induced by 2 autologous blood injections into the cisterna magna of adult male rats. The effect of SAH on ERα and -β expression was evaluated. Other rats subcutaneously received implanted Silastic tubes containing corn oil with E2 and daily injections of various doses of an ERα- (methyl-piperidinopyrazole [MPP]) or ERβ-selective antagonist (R,R-tetrahydrochrysene) after the first hemorrhage. The protein levels of ERα, ERβ, eNOS, and inducible nitric oxide synthase (iNOS) from basilar arteries were examined using Western blot analysis, and their mRNAs were evaluated by reverse transcription–polymerase chain reaction. Results The ERα but not the ERβ was upregulated in the basilar artery after SAH. Treatment with MPP eliminated E2-mediated effects in SAH, relieved cerebral vasospasm, preserved eNOS expression, and suppressed iNOS expression. Conclusions Estrogen receptor α is upregulated in the basilar artery after SAH. Note that E2 exerts its protective effects through ERα-dependent pathways to relieve cerebral vasospasm and preserve eNOS expression. A selective ERα agonist may be the drug of choice for the treatment of patients with SAH.
    Type of Medium: Online Resource
    ISSN: 0022-3085 , 1933-0693
    URL: Article
    DOI: 10.3171/JNS/2008/109/7/0092
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2008
    detail.hit.zdb_id: 2026156-1
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  • 4
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    Functions of G protein–coupled receptor kinase interacting protein 1 in human neuronal (NT2N) cells
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2006
    In:  Journal of Neurosurgery Vol. 105, No. 1 ( 2006-07), p. 103-110
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 105, No. 1 ( 2006-07), p. 103-110
    Abstract: Promotion of the repair and regeneration of damaged adult neurons is a major goal of neurological science. In this study, the effects of G protein–coupled receptor kinase interacting protein 1 (GIT1) overexpression in human neuron cells were tested in human neuronal cells by using an adenoviral vector. Methods A recombinant GIT1 and enhanced green fluorescent protein (EGFP) adenoviral vector (AdGIT1) was created by using a standard viral construction procedure. Human neuronal (NT2N) cells, which had been derived from an NT2 human teratocarcinoma cell line, were used in this experiment. Immunocytochemical methods were applied to identify NT2N cells with neural features and to probe the relationship among signaling proteins. Several biological activities were assessed, including neural spine formation, cell migration, and the levels of expression of growth-associated protein–43 (GAP-43) and active Cdc42. The number of cells with spine formation and the number of migrated cells were significantly higher in the AdGIT1-treated group of NT2N cells than in untreated (control) NT2N cells or in AdEGFP-treated NT2N cells. The levels of GAP-43 and active Cdc42 expression were significantly higher in the AdGIT1-treated group than that in the other two cell groups. Conclusions The results of this study demonstrate that GIT1 overexpression has the potential to promote neural spine formation and cell migration in human neuronal cells. At the same time, the increased level of GAP-43 in GIT1-overexpressed cells indicates that GIT1 may have the potential to improve growth and regeneration of damaged axons. The GIT1–β-PIX–Cdc42–PAK pathway may play an important role in neuronal outgrowth.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2006.105.1.103
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2006
    detail.hit.zdb_id: 2026156-1
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  • 5
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    Characterization of perioperative seizures and epilepsy following aneurysmal subarachnoid hemorrhage
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2003
    In:  Journal of Neurosurgery Vol. 99, No. 6 ( 2003-12), p. 978-985
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 99, No. 6 ( 2003-12), p. 978-985
    Abstract: Object. The reported incidence, timing, and predictive factors of perioperative seizures and epilepsy after subarachnoid hemorrhage (SAH) have differed considerably because of a lack of uniform definitions and variable follow-up periods. In this study the authors evaluate the incidence, temporal course, and predictive factors of perioperative seizures and epilepsy during long-term follow up of patients with SAH who underwent surgical treatment. Methods. Two hundred seventeen patients who survived more than 2 years after surgery for ruptured intracranial aneurysms were enrolled and retrospectively studied. Episodes were categorized into onset seizures (≤ 12 hours of initial hemorrhage), preoperative seizures, postoperative seizures, and late epilepsy, according to their timing. The mean follow-up time was 78.7 months (range 24–157 months). Forty-six patients (21.2%) had at least one seizure post-SAH. Seventeen patients (7.8%) had onset seizures, five (2.3%) had preoperative seizures, four (1.8%) had postoperative seizures, 21 (9.7%) had at least one seizure episode after the 1st week postoperatively, and late epilepsy developed in 15 (6.9%). One (3.8%) of 26 patients with perioperative seizures (onset, preoperative, or postoperative seizure) had late epilepsy at follow up. The mean latency between the operation and the onset of late epilepsy was 8.3 months (range 0.3–19 months). Younger age ( 〈 40 years old), loss of consciousness of more than 1 hour at ictus, and Fisher Grade 3 or greater on computerized tomography scans proved to be significantly related to onset seizures. Onset seizure was also a significant predictor of persistent neurological deficits (Glasgow Outcome Scale Scores 2–4) at follow up. Factors associated with the development of late epilepsy were loss of consciousness of more than 1 hour at ictus and persistent postoperative neurological deficit. Conclusions. Although up to one fifth of patients experienced seizure(s) after SAH, more than half had seizure(s) during the perioperative period. The frequency of late epilepsy in patients with perioperative seizures (7.8%) was not significantly higher than those without such seizures (6.8%). Perioperative seizures did not recur frequently and were not a significant predictor for late epilepsy.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2003.99.6.0978
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2003
    detail.hit.zdb_id: 2026156-1
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  • 6
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    Attenuation of cerebral vasospasm and secondary injury by 17β-estradiol following experimental subarachnoid hemorrhage : Laboratory investigation
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2009
    In:  Journal of Neurosurgery Vol. 110, No. 3 ( 2009-03), p. 457-461
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 110, No. 3 ( 2009-03), p. 457-461
    Abstract: Cerebral vasospasm remains a major complication in patients who have suffered a subarachnoid hemorrhage (SAH). Previous studies have shown that 17β-estradiol (E2) attenuates experimental SAH–induced cerebral vasospasm. Moreover, E2 has been shown to reduce neuronal apoptosis and secondary injury following cerebral ischemia. Adenosine A1 receptor (AR-A1) expression is increased following ischemia and may represent an endogenous neuroprotective effect. This study was designed to evaluate the efficacy of E2 in preventing cerebral vasospasm and reducing secondary injury, as evidenced by DNA fragmentation and AR-A1 expression, following SAH. Methods A double-hemorrhage model of SAH in rats was used, and the degree of vasospasm was determined by averaging the cross-sectional areas of the basilar artery 7 days after the first SAH. A cell death assay was used to detect apoptosis. Changes in the protein expression of AR-A1 in the cerebral cortex, hippocampus, and dentate gyrus were compared with levels in normal controls and E2-treated groups (subcutaneous E2, 0.3 mg/ml). Results The administration of E2 prevented vasospasm (p 〈 0.05). Seven days after the first SAH, DNA fragmentation and protein levels of AR-A1 were significantly increased in the dentate gyrus. The E2 treatment decreased DNA fragmentation and prevented the increase in AR-A1 expression in the dentate gyrus. There were no significant changes in DNA fragmentation and the expression of AR-A1 after SAH in the cerebral cortex and hippocampus in the animals in the control and E2-treated groups. Conclusions The E2 was effective in attenuating SAH-induced cerebral vasospasm, decreasing apoptosis in the dentate gyrus, and reducing the expression of AR-A1 in the dentate gyrus after SAH. Interestingly, E2 appears to effectively prevent cerebral vasospasm subsequent to SAH as well as attenuate secondary injury by reducing both apoptosis and a compensatory increase in AR-A1 expression in the dentate gyrus.
    Type of Medium: Online Resource
    ISSN: 0022-3085 , 1933-0693
    URL: Article
    DOI: 10.3171/2008.6.17622
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2009
    detail.hit.zdb_id: 2026156-1
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  • 7
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    Prognostic significance of annexin VII expression in glioblastomas multiforme in humans
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2003
    In:  Journal of Neurosurgery Vol. 99, No. 5 ( 2003-11), p. 886-892
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 99, No. 5 ( 2003-11), p. 886-892
    Abstract: Object. Glioblastoma multiforme (GBM) is the most common and lethal primary brain tumor in adults. It is nearly uniformly fatal, with a median survival time of approximately 1 year, despite modern treatment modalities. Nevertheless, a range of survival times exists around this median. Efforts to understand why some patients live longer or shorter than the average may provide insight into the biology of these neoplasms. The annexin VII (ANX7) gene is located on the human chromosome 10q21, a site long hypothesized to harbor tumor suppressor genes associated with prostate and other cancers. To test whether ANX7 expression might be a predictor for GBMs, we examined ANX7 expression, p53 accumulation, and the MIB-1 labeling index in a retrospective series of 99 GBMs. Methods. In all 99 cases, the patient's age, Karnofsky Performance Scale (KPS) score before surgery, extent of surgery, tumor location, and immunohistochemical features were analyzed using univariate and multivariate analyses to identify whether any significance exists among ANX7 expression, p53 accumulation, the MIB-1 labeling index, and survival time. Kaplan—Meier analyses demonstrated that a higher KPS score before surgery ( 〈 0.0001), total tumor excision (p = 0.0072), young patient age (p = 0.03), and ANX7 expression (p = 0.0006) correlated with longer survival. Multivariate Cox regression analyses demonstrated that ANX7 expression was the strongest predictor of outcome (p 〈 0.0001), independent of all other variables. In addition, ANX7 expression correlated with higher MIB-1 immunostaining, but did not correlate with p53 accumulation. Moreover, a significant positive correlation was observed between p53 and MIB-1 staining. Conclusions. These findings indicate that a higher KPS score before surgery, total tumor excision, young patient age, and ANX7 expression correlate with longer survival in patients with GBMs. Multivariate Cox regression analyses demonstrated that ANX7 expression was the strongest predictor of outcome (p 〈 0.0001) and was independent of all other variables.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2003.99.5.0886
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2003
    detail.hit.zdb_id: 2026156-1
    Location Call Number Limitation Availability
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