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Beagle puppy model of perinatal cerebral infarction

Acute changes in regional cerebral prostaglandins during hemorrhagic hypotension

Laura R. Ment, William B. Stewart, Charles C. Duncan, Judy Cole and Bruce R. Pitt

P erinatal cerebral infarction, or stroke, is a common finding in neonates who suffer severe asphyxial insult. 4, 6, 31, 32 Such infants may experience fetal bradycardias and are noted to remain profoundly hypotensive with heart rate changes in the first few postnatal days. 11, 42, 50 Neurodiagnostic imaging techniques reveal periventricular white matter abnormalities, 3, 12, 13, 23, 52 and, in those infants who come to postmortem studies, neuropathological examination demonstrates severe disorganization or even complete disruption of those regions. 2, 4, 6

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Beagle puppy model of perinatal cerebral infarction

Regional cerebral prostaglandin changes during acute hypoxemia

Laura R. Ment, William B. Stewart, Charles C. Duncan, Bruce R. Pitt and Judith S. Cole

P erinatal cerebral infarction, or stroke, is a common manifestation of perinatal asphyxia. 2–4, 6, 13, 14, 28, 33, 34, 51, 54 The incidence of severe perinatal asphyxia has been reported as between one in 50 and one in 500 live births, and infants with perinatal asphyxia suffer the consequences of both hypotensive and hypoxemic insults. 9–12, 42, 43, 48 Follow-up studies of infants surviving severe hypoxic insult demonstrate a 20% to 30% incidence of moderate or severe neurodevelopmental difficulties including cerebral palsy, mental retardation, and

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Toru Nagasaka, Shigemasa Hayashi, Takehiro Naito, Takeshi Okamoto, Hiroshi Ikeda and Suguru Inao

ig . 1. Axial neuroimages obtained in the patient. A and B: Computed tomography scans obtained at admission revealing a right caudate hemorrhage with intraventricular hematoma and acute hydrocephalus. C and D: Postoperative diffusion weighted magnetic resonance images showing hyperintense areas in the right frontal lobe, indicating cerebral infarction. Operation and Postoperative Course Endoscopic removal of the intraventricular hematoma and ventricular drainage were performed because of acute hydrocephalus progression. Angiograms showed stenosis of the

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Claudia S. Robertson, Robert G. Grossman, J. Clay Goodman and Raj K. Narayan

CT scans which were characteristic of cerebral infarction (Group 1). The location of the infarctions was typical of that described at autopsy in patients who die of their head injury. 11 Two patients had infarctions in the distribution of the posterior cerebral artery due to mesial temporal herniation secondary to extracerebral hematomas or diffuse swelling ( Fig. 1 ). Infarctions involving the middle cerebral artery (two patients) and anterior cerebral artery territories (one patient) developed following evacuation of intracerebral hematomas. One patient developed

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J. Michael Schmidt, Katja E. Wartenberg, Andres Fernandez, Jan Claassen, Fred Rincon, Noeleen D. Ostapkovich, Neeraj Badjatia, Augusto Parra, E. Sander Connolly and Stephan A. Mayer

detecting neurological decline. 7 It has been reported that clinically “silent” infarction may account for up to one-fourth of cases of DCI, and this complication of SAH has been associated with poor outcome. 17 , 30 Since detection of a new neurological deficit usually triggers the initiation of HHT, angioplasty, and other rescue therapies, 29 it is reasonable to assume that asymptomatic DCI may often go untreated. Asymptomatic cerebral infarction after SAH is likely to be an under-recognized clinical problem. We performed this study to identify the frequency, risk

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Seppo Juvela, Jari Siironen and Johanna Kuhmonen

, ICH, repeated hemorrhage, or hydrocephalus). Causes of poor clinical condition were determined by performing repeated CT studies, routine postoperative angiography, autopsy, or laboratory investigations. Outcome was assessed 3 months after SAH according to the GOS 10 and the mRS. 2, 19 A regularly scheduled follow-up CT scan was obtained 3 months after SAH to reveal permanent hypodense areas consistent with cerebral infarction; this scan was available for 155 patients (89%). Of the remaining 20 patients with a missing CT scan, 15 died before the planned CT study

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Tomoo Furui, Kyoko Satoh, Yoshio Asano, Sadashi Shimosawa, Michiaki Hasuo and Tony L. Yaksh

-endorphin immunoreactivity in cerebrospinal fluid (CSF) sampled from one of two patients with cerebral ischemic disease, in whom the neurological deficits were reportedly completely reversed by naloxone treatment. There has been no report of studies examining the alteration of endogenous opioid peptide levels in consecutive samples from patients with ischemic disease. We measured β -endorphin in the CSF and plasma of eight patients with cerebral infarction to ascertain whether, according to the suggested role of naloxone, levels of the endogenous opioid peptide, β

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Beagle puppy model of perinatal cerebral infarction

Acute changes in cerebral blood flow and metabolism during hemorrhagic hypotension

Laura R. Ment, William B. Stewart, Charles C. Duncan, Bruce R. Pitt, Aldo Rescigno and Judy Cole

P erinatal cerebral infarction with severe disorganization or even complete disruption of subcortical white matter structures may be secondary to embolic, thrombotic, or ischemic events. Stroke with discrete areas of cystic infarction is more commonly reported in full-term infants than in preterm patients, 5, 30, 31, 48, 50 in whom many small subcortical and brain-stem cystic lesions may be found and in whom this condition is known as “periventricular leukomalacia.” 1, 3, 4, 10, 24, 41, 52 Although Barmada, et al. , 5 reported a 5.4% incidence of cerebral

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Pava Popovic, Vojin Popovic, Richard Schaffer and Carl H. Sutton

T here is much speculation about the events that occur after cerebral infarction and about the kind of treatment one should adopt. Different experimental models give different results. Clinical data vary from patient to patient and are difficult to evaluate, especially because of differences in time of treatment, and the variability of the causes of infarction and their severity. Although one may expect striking pathophysiological changes induced by the damage to the blood vessels during severe brain ischemia caused by infarction, the picture is further

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Neurosurgical Forum: Letters to the Editor To The Editor Gabrielle M. de Courten-Myers , M.D. , Kenneth R. Wagner , Ph.D. , Ronald E. Myers , M.D., Ph.D. University of Cincinnati, College of Medicine Cincinnati, Ohio 146 148 We commend Hamilton, et al. (Hamilton MG, Tranmer BI, Auer RN: Insulin reduction of cerebral infarction due to transient focal ischemia. J Neurosurg 82: 262–268, February, 1995) for their careful investigation of independent effects of insulin and