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1.
J Neurosurg ; 110(1): 94-100, 2009 Jan.
Article in English | MEDLINE | ID: mdl-18928358

ABSTRACT

OBJECT: Hydrogen peroxide (H2O2) is used as a hemostatic agent in many neurosurgery centers. The authors used a 3% H2O2 solution for final hemostasis after removal of a left insular tumor. Immediately afterward, air bubbles were observed within the lumen of the polar temporal artery. Postoperative MR imaging revealed punctate areas of infarction in the lenticulostriate artery territory. The authors designed an experimental study to elucidate the mechanism of remote O2 emboli and reactive O2 species-related vasoactive responses and thrombus formation. METHODS: In this study, H2O2 irrigation was used in mice with either an intact pial layer or after the pia mater was removed through a corticotomy. Normal saline irrigation was used in the corresponding control groups. Vessels were examined for intravascular O2 emboli under the microscope. Tissue sections were then obtained and stained with H & E and the 3-nitrotyrosine (3-NT) antibody to evaluate intravascular thrombus formation and peroxynitrite reaction, respectively. RESULTS: Multiple bubbles were observed within the lumen of the vessels after exposure to H2O2 regardless of whether the pial layer was destroyed or intact. Immunofluorescent staining for 3-NT showed an abundant positive reaction in the vessel walls of all animals exposed to H2O2 as well as vascular occlusion with acute thrombus formation. Samples taken from the animals that received saline showed no positive staining for 3-NT and no vascular occlusion. CONCLUSIONS: Exposure to H2O2 may cause serious ischemic complications. The formation of peroxynitrite may cause vasoactive responses to H2O2 and platelet aggregation/thrombus formation, and the free diffusion of H2O2 through the vessel walls and its conversion to water and O2 leads to O2 bubbles within the closed vessel lumen. If used intradurally, H2O2 may have deleterious ischemic effects, and it can only be used carefully in open extradural spaces.


Subject(s)
Hemostatics/adverse effects , Hydrogen Peroxide/adverse effects , Postoperative Complications/chemically induced , Stroke/chemically induced , Adult , Animals , Aphasia/etiology , Basal Ganglia Cerebrovascular Disease/chemically induced , Brain/pathology , Fluorescent Antibody Technique , Humans , Magnetic Resonance Imaging , Male , Mice , Paresis/etiology , Peroxynitrous Acid/toxicity , Pia Mater/pathology , Recovery of Function , Stroke/etiology , Stroke/pathology
2.
J Perinatol ; 26(1): 57-63, 2006 Jan 01.
Article in English | MEDLINE | ID: mdl-16319938

ABSTRACT

High-dosage, tocolytic magnesium sulfate (MgSO4) administered to pregnant women during preterm labor can be toxic, and sometimes lethal, for their newborns (Cochrane Database of Systematic Reviews (relative mortality risk 2.82, 95% confidence interval 1.2-6.6)). Based on the results of the Magnesium and Neurologic Endpoints Trial and the work of many others, a unifying triangular concept is proposed to account for the increased prevalence of brain lesions, with their likely resultant mortality, in neonates and infants exposed to high-dose MgSO4 in the context of preterm labor. We review the evidence that: (1) elevated circulating levels of serum ionized magnesium occurring in mothers, and therefore in their babies, at the time of delivery are associated with subsequent neonatal intraventricular hemorrhage (IVH); (2) neonatal IVH is strongly associated with lenticulostriate vasculopathy (LSV), an unusual mineralizing lesion involving the thalami and basal ganglia of the neonate; and, (3) exposure to 50 g or more of tocolytic MgSO4 during preterm labor is associated with the development of LSV.


Subject(s)
Basal Ganglia Cerebrovascular Disease/chemically induced , Cerebral Hemorrhage/chemically induced , Magnesium Sulfate/adverse effects , Prenatal Exposure Delayed Effects , Tocolytic Agents/adverse effects , Basal Ganglia Cerebrovascular Disease/epidemiology , Cerebral Hemorrhage/epidemiology , Cerebral Palsy/prevention & control , Female , Humans , Infant, Newborn , Magnesium Sulfate/blood , Magnesium Sulfate/therapeutic use , Obstetric Labor, Premature/drug therapy , Obstetric Labor, Premature/prevention & control , Pregnancy , Prenatal Exposure Delayed Effects/chemically induced , Prenatal Exposure Delayed Effects/epidemiology , Randomized Controlled Trials as Topic/adverse effects , Randomized Controlled Trials as Topic/mortality , Tocolytic Agents/blood , Tocolytic Agents/therapeutic use
3.
J Perinatol ; 25(2): 101-7, 2005 Feb.
Article in English | MEDLINE | ID: mdl-15496867

ABSTRACT

OBJECTIVE: To determine the antenatal risk factors associated with neonatal lenticulostriate vasculopathy (LSV). STUDY DESIGN: Women in preterm labor were randomized to magnesium sulfate (MgSO4), other tocolytic, or saline control. The surviving babies underwent head ultrasounds (HUS) (weeks of life 1, 2, and 4) and periodic developmental examinations (months 4, 8, 12, and 18). RESULTS: Of 140 infants, 17.1% (24) had neonatal intraventricular hemorrhage (IVH), and 10.0% (14) had LSV (half of the latter (7 of 14) had both IVH and LSV). In a regression model in which other risk factors were controlled for, the association between antenatal exposures to tocolytic MgSO4 >or=50 g and LSV were significant (adjusted odds ratio (OR), 8.3; 95% confidence interval (CI), 1.5 to 45.0; p=0.01). CONCLUSION: Based on our data and their analyses, we infer that antenatal exposure to high-dosage, tocolytic MgSO4 may be associated with LSV.


Subject(s)
Basal Ganglia Cerebrovascular Disease/chemically induced , Cerebral Hemorrhage/chemically induced , Magnesium Sulfate/adverse effects , Tocolytic Agents/adverse effects , Adult , Dose-Response Relationship, Drug , Female , Follow-Up Studies , Humans , Infant, Newborn , Magnesium Sulfate/administration & dosage , Obstetric Labor, Premature/drug therapy , Pregnancy , Prospective Studies , Risk Factors , Tocolytic Agents/administration & dosage
4.
Clin Imaging ; 25(1): 12-4, 2001.
Article in English | MEDLINE | ID: mdl-11435032

ABSTRACT

A case is reported of a young man who developed bilateral symmetrical basal ganglia infarcts after intravenous use of cocaine and heroin. Ischemic infarcts of the brain are a known complication of to cocaine use, alone or in combination with heroin (speed balling). This symmetrical occurrence of infarction, however, is unusual and has not been reported after cocaine use.


Subject(s)
Basal Ganglia Cerebrovascular Disease/chemically induced , Brain Infarction/chemically induced , Cocaine , Heroin , Substance Abuse, Intravenous/complications , Adult , Basal Ganglia/diagnostic imaging , Basal Ganglia Cerebrovascular Disease/diagnosis , Basal Ganglia Cerebrovascular Disease/diagnostic imaging , Brain Infarction/diagnosis , Brain Infarction/diagnostic imaging , Humans , Male , Tomography, X-Ray Computed
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