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  • 1
    Online Resource
    Online Resource
    Terson's syndrome in subarachnoid hemorrhage and severe brain injury accompanied by acutely raised intracranial pressure
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2001
    In:  Neurosurgical Focus Vol. 11, No. 4 ( 2001-10), p. 851-854
    Details
    In: Neurosurgical Focus, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 11, No. 4 ( 2001-10), p. 851-854
    Abstract: The syndrome of retinal or vitreous hemorrhage in association with subarachnoid hemorrhage (SAH) is known as Terson's syndrome. The authors' purpose was to determine whether intraocular hemorrhage occurs with similar incidence when caused by severe brain injury accompanied by acutely raised intracranial pressure (ICP). Methods Prospective ophthalmological examination was performed in 22 consecutive patients with SAH or severe brain injury and elevated ICP. Thirteen patients were admitted for SAH (World Federation of Neurological Surgeons Grades II–IV) and nine for severe brain injury (Glasgow Coma Scale scores 3–10). Monitoring of ICP was performed at the time of admission via a ventricular catheter. Initial ICP exceeded 20 mm Hg in all patients. Indirect ophthalmoscopy without induced mydriasis was performed within the 1st week after the acute event. Retinal or vitreous hemorrhage was seen in six (46%) of 13 patients with SAH and in four (44%) of nine patients with severe brain injury. Ocular bleeding was found bilaterally in three patients with SAH and in one patient with severe brain injury (18%). Six of the 10 patients with Terson's syndrome died as a result of their acute event. Conclusions The present results indicate that Terson's syndrome may be related to acute elevation of ICP, independent of its causes, and may occur with similar incidence in patients with severe brain injury and those with SAH. Because recognition and treatment of Terson's syndrome may prevent visual impairment and associated secondary damage to the eye, increased awareness of this entity in all patients with acute raised intracranial hypertension is recommended.
    Type of Medium: Online Resource
    ISSN: 1092-0684
    URL: Article
    DOI: 10.3171/foc.2001.11.4.3
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2001
    detail.hit.zdb_id: 2026589-X
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  • 2
    Online Resource
    Online Resource
    Analgesia by electrostimulation of the trigeminal ganglion in patients with trigeminopathic pain: a PET activation study
    Ovid Technologies (Wolters Kluwer Health) ; 2003
    In:  Pain Vol. 103, No. 1 ( 2003-05), p. 119-130
    Details
    In: Pain, Ovid Technologies (Wolters Kluwer Health), Vol. 103, No. 1 ( 2003-05), p. 119-130
    Type of Medium: Online Resource
    ISSN: 0304-3959
    URL: Article
    DOI: 10.1016/s0304-3959(02)00423-2
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2003
    detail.hit.zdb_id: 1494115-6
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  • 3
    Online Resource
    Online Resource
    Terson's syndrome in subarachnoid hemorrhage and severe brain injury accompanied by acutely raised intracranial pressure
    Journal of Neurosurgery Publishing Group (JNSPG) ; 1998
    In:  Journal of Neurosurgery Vol. 88, No. 5 ( 1998-05), p. 851-854
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 88, No. 5 ( 1998-05), p. 851-854
    Abstract: Object. The syndrome of retinal or vitreous hemorrhage in association with subarachnoid hemorrhage (SAH) is known as Terson's syndrome. The authors' purpose was to determine whether intraocular hemorrhage occurs with similar incidence when caused by severe brain injury accompanied by acutely raised intracranial pressure (ICP). Methods. Prospective ophthalmological examination was performed in 22 consecutive patients with SAH or severe brain injury and elevated ICP. Thirteen patients were admitted for SAH (World Federation of Neurological Surgeons Grades II–IV) and nine for severe brain injury (Glasgow Coma Scale scores 3–10). Monitoring of ICP was performed at the time of admission via a ventricular catheter. Initial ICP exceeded 20 mm Hg in all patients. Indirect ophthalmoscopy without induced mydriasis was performed within the 1st week after the acute event. Retinal or vitreous hemorrhage was seen in six (46%) of 13 patients with SAH and in four (44%) of nine patients with severe brain injury. Ocular bleeding was found bilaterally in three patients with SAH and in one patient with severe brain injury (18%). Six of the 10 patients with Terson's syndrome died as a result of their acute event. Conclusions. The present results indicate that Terson's syndrome may be related to acute elevation of ICP, independent of its causes, and may occur with similar incidence in patients with severe brain injury and those with SAH. Because recognition and treatment of Terson's syndrome may prevent visual impairment and associated secondary damage to the eye, increased awareness of this entity in all patients with acute raised intracranial hypertension is recommended.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.1998.88.5.0851
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 1998
    detail.hit.zdb_id: 2026156-1
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  • 4
    Online Resource
    Online Resource
    Inducible nitric oxide synthase: a possible key factor in the pathogenesis of chronic vasospasm after experimental subarachnoid hemorrhage
    Journal of Neurosurgery Publishing Group (JNSPG) ; 1999
    In:  Journal of Neurosurgery Vol. 90, No. 6 ( 1999-06), p. 1098-1104
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 90, No. 6 ( 1999-06), p. 1098-1104
    Abstract: Object. The role of nitric oxide (NO) in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage (SAH) is not well understood. Nitric oxide is a well-established vasodilatory substance; however, in SAH, NO may become a major source for the production of injurious free-radical species, leading to chronic cerebral vasospasm. Reactive overproduction of NO to counteract vascular narrowing might potentiate the detrimental effects of NO. The focus of the present study is to determine the extent of reactive induction of inducible nitric oxide synthase (iNOS) after experimental SAH. Methods. Chronic vasospasm was induced in male Wistar rats by an injection of autologous blood (100 µl) into the cisterna magna followed by a second injection 24 hours later. A control group of 10 animals was treated with injections of 0.9% sodium chloride solution. Vasospasm was verified by pressure-controlled angiography after retrograde cannulation of the external carotid artery 7 days later. In 11 of 15 animals radiographic evidence of cerebral vasospasm was seen. The animals were perfusion fixed and their brains were removed for immunohistochemical assessment. With the aid of a microscope, staining for iNOS was quantified in 40-µm floating coronal sections. Immunohistochemical staining for iNOS was markedly more intense in animals with significant angiographic evidence of vasospasm. Virtually no staining was observed in control animals. Seven days after the second experimental SAH, labeling of iNOS was found in endothelial cells, in vascular smooth-muscle cells, and, above all, in adventitial cells. Some immunohistochemical staining of iNOS was observed in rod cells (activated microglia), in glial networks, and in neurons. Conclusions. The present study demonstrates induction of iNOS after experimental SAH.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.1999.90.6.1098
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 1999
    detail.hit.zdb_id: 2026156-1
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  • 5
    Online Resource
    Online Resource
    Detection of hyperacute subarachnoid hemorrhage of the brain by using magnetic resonance imaging
    Journal of Neurosurgery Publishing Group (JNSPG) ; 2002
    In:  Journal of Neurosurgery Vol. 96, No. 4 ( 2002-04), p. 684-689
    Details
    In: Journal of Neurosurgery, Journal of Neurosurgery Publishing Group (JNSPG), Vol. 96, No. 4 ( 2002-04), p. 684-689
    Abstract: Object. The purpose of this study was to determine the diagnostic accuracy of high-field (1.5-tesla) magnetic resonance (MR) imaging in the assessment of hyperacute ( 〈 12 hours after onset of symptoms) subarachnoid hemorrhage (SAH). Methods. This investigation included 13 patients who were examined 2 to 12 hours posthemorrhage by using an MR imaging protocol consisting of T 2 -weighted and proton-density (PD)-weighted images, T 1 -weighted images, fast echoplanar—diffusion-weighted (EP-DW) images, and fluid-attenuated inversion-recovery (FLAIR) images. Subarachnoid hemorrhage had been diagnosed using computerized tomography (CT) scanning in all cases. In all 13 cases, SAH was reliably detected on both PD-weighted and FLAIR images. In contrast with FLAIR studies, the PD-weighted images were free of cerebrospinal fluid flow artifacts. The SAH was detected on T 1 -weighted images in only two cases and could not be detected on any T 2 -weighted or EP-DW images. Conclusions. Even hyperacute SAH can be diagnosed reliably from high-field MR images obtained using PD-weighted or FLAIR sequences. Use of these sequences in an emergency MR protocol may preclude the need for additional CT studies to rule out SAH.
    Type of Medium: Online Resource
    ISSN: 0022-3085
    URL: Article
    DOI: 10.3171/jns.2002.96.4.0684
    RVK:
    XA 10000
    RVK:
    XA 55270
    Language: Unknown
    Publisher: Journal of Neurosurgery Publishing Group (JNSPG)
    Publication Date: 2002
    detail.hit.zdb_id: 2026156-1
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  • 6
    Online Resource
    Online Resource
    Dexamethasone in the treatment of subarachnoid hemorrhage revisited: a comparative analysis of the effect of the total dose on complications and outcome
    Elsevier BV ; 2004
    In:  Journal of Clinical Neuroscience Vol. 11, No. 1 ( 2004-1), p. 20-24
    Details
    In: Journal of Clinical Neuroscience, Elsevier BV, Vol. 11, No. 1 ( 2004-1), p. 20-24
    Type of Medium: Online Resource
    ISSN: 0967-5868
    URL: Article
    DOI: 10.1016/S0967-5868(03)00155-3
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 2009190-4
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