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Dive into the research topics where John P. Laurent is active.

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Featured researches published by John P. Laurent.


The Journal of Pediatrics | 1989

Chiari type I malformation in children

Leon S. Dure; Alan K. Percy; William R. Cheek; John P. Laurent

We reviewed the recent experience at Texas Childrens Hospital by examining the records of 11 children who underwent suboccipital decompression for symptomatic Chiari type I malformation. Presenting complaints included neck pain (1 child), scoliosis (4 children), back pain (1 child), torticollis (1), motor dysfunction (1), and apnea (3 children). Neurologic findings were normal in 7 of the 11 children. The craniocervical junction and medulla were studied by magnetic resonance imaging, which revealed anatomy consistent with Chiari type I malformation in all cases. At surgery, all patients had tonsillar herniation to the first cervical vertebra or below. Three patients had syringomyelia. Postoperatively, either the patients were symptom free or, in the cases of scoliosis and torticollis, there was no progression. Our experience suggests that Chiari type I malformation may occur in childhood with varied and unusual clinical findings. Magnetic resonance imaging was essential to the diagnosis; the presence of tonsillar herniation was confirmed at surgery. The results of suboccipital decompression were favorable in this series.


Neurology | 1975

Barbiturate attenuation of the clinical course and pathologic lesions in a primate stroke model

John I. Moseley; John P. Laurent; Gaetano F. Molinari

To evaluate the potential for clinical application, the reputed protective action of barbiturates in cerebral ischemia was tested in a controlled study after segmental middle cerebral artery occlusion in primates. Surviving treated animals promptly recovered consciousness, locomotion, and feeding behavior despite persistent hemiplegia, while control animals ran an indolent course, with slow recovery of poor quality. Cerebral lesions in treated animals were confined to the deep hemispheric structures, while control specimens showed larger deep lesions confluent with extensive areas of cortical infarction. These results are less dramatic than those reported by others, but the protective effect observed in fields of collateral circulation deserves further exploration as an adjunct to medical and surgical management.


Stroke | 1979

Attenuation of ischemic brain edema by pentobarbital after carotid ligation in the gerbil.

Pablo M. Lawner; John P. Laurent; Frederick A. Simeone; Eugene A. Fink; E Rubin

The efficacy of pentobarbital in the treatment of ischemic cerebral edema was evaluated in 160 gerbils. Animals underwent carotid ligation under ether or pentobarbital (50 mg/kg) anesthesia. The pentobarbital anesthetized group received an additional dose of 30 mg/kg 4 h after ligation. Animals were evaluated for neurologic deficit at 4 and 8 h post-ligation, then sacrificed. Water content of each hemisphere and swelling percentage were calculated from the wet and dry weights of the hemispheres. Swelling percentage in animals anesthetized with ether was 6.374 ± 0.89 SE, whereas gerbils who underwent sham carotid ligation showed a negligible (0.491 ± 0.15) swelling percentage (p < 0.01). Pentobarbital animals had a swelling percentage of 3.359 ± 0.68. This represents a significant edema reduction compared to ether-anesthetized animals (p < 0.01). Neurologic deficit was decreased by 56.7< (17/60 vs 30/60) in pentobarbital animals compared with ether animals (p ± 0.025). Mortality at 8 hours was reduced by 75< (2/60 vs 8/60) in pentobarbital animals (p < 0.05).


Journal of Neuropathology and Experimental Neurology | 1976

Primate Model of Cerebral Hematoma

John P. Laurent; Gaetano F. Molinari; John C. Oakley

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO2 in air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilated vessels surrounding the ischemic zones but without extravasations; when hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematomas involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantitative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.


Critical Care Medicine | 1993

Barbiturates and hyperventilation during intracranial hypertension

Penelope T. Louis; Jan Goddard-Finegold; Marvin A. Fishman; Johnny R. Griggs; Fernando Stein; John P. Laurent

OBJECTIVE The purpose of this study was to determine the effect of hyperventilation alone and hyperventilation plus barbiturate therapy on intracranial pressure, global and regional cerebral blood flow rates, cerebrovascular resistance, and cerebral perfusion pressure in adult dogs with and without intracranial hypertension induced by epidural balloon. DESIGN Prospective, randomized, controlled study. SETTING An animal laboratory of a university hospital. Four sequential global and regional cerebral blood flow determinations were made in each animal during monitoring of heart rate and systemic arterial pressure, during respiratory control and arterial blood gas monitoring, intracranial pressure monitoring, and with or without inflation of an epidural balloon catheter. SUBJECTS Acute mongrel dogs obtained from the Baylor Center for Comparative Medicine. Five groups of animals were studied. In group 1, the response to hyperventilation was assessed in dogs without increased intracranial pressure. In group 2, the response to hyperventilation was assessed in animals with acute intracranial hypertension. In group 3, the response to hyperventilation plus barbiturate therapy was assessed in dogs without increased intracranial pressure. In group 4, the response to hyperventilation plus barbiturate therapy was assessed in dogs with acute increased intracranial pressure. In group 5, a group of dogs with increased intracranial pressure was treated with neither hyperventilation nor barbiturates. INTERVENTIONS Hyperventilation, hyperventilation plus barbiturate therapy, or no interventions were studied in these experimental paradigms. MEASUREMENTS AND MAIN RESULTS The main outcome measures were changes in intracranial pressure and/or changes in regional or total cerebral blood flow. A significant decrease in intracranial pressure and cerebral blood flow rate was produced by hyperventilation alone in groups with intracranial hypertension. Combined hyperventilation and barbiturate therapy resulted in a significant further decrease in cerebral blood flow rate in animals with normal and increased intracranial pressure, but no greater decrease in intracranial pressure was seen compared with treatment with hyperventilation alone. Cerebral perfusion pressures remained normal despite significant decreases in cerebral blood flow rates. CONCLUSIONS These studies suggest that barbiturate administration in this model of intracranial hypertension was no more effective in reducing increased intracranial pressure than hyperventilation alone.


Pediatric Neurosurgery | 1988

Postradiation Meningioma in a Child

Chidambaram Balasubramaniam; Dawna L. Armstrong; William R. Cheek; John P. Laurent

Tumors caused by radiation treatment are not unknown. They may be benign or malignant. Among these, postradiation meningiomas (PRM) are considered to be a distinct entity. A case of a child who developed a PRM is presented. She received radiation therapy for a presumed thalamic glioma 11 years earlier. An unusual and interesting aspect of this tumor was its attachment to the membrane of the old subdural hematoma, following a shunting procedure. There was no dural attachment. The pathology of PRMs and meningiomas in children are discussed in light of our recent experience.


Journal of Neuroscience Nursing | 1991

Brachial plexus birth injury.

Janet M. Brucker; John P. Laurent; Rita Lee; Saleh M. Shenaq; Julie T. Parke; Itzel Solis; William R. Cheek

&NA; Brachial plexus birth injuries occur at a frequency of 1–2 per 1000 births. Many of these injuries spontaneously resolve. Should spontaneous recovery not occur within the first 4–6 months of life, the prognosis for attaining movement and function of the affected appendage is significantly impaired. The child demonstrates a lifelong disfiguring and functional handicap. With advances in technology, diagnosis and microsurgical techniques, surgical exploration of the brachial plexus has been revived. A multidisciplinary approach has provided dynamic results. At present only one institution in the United States utilizes this innovative protocol. This article addresses the collaborative perioperative nursing implications for a child with brachial plexus birth injury.


Surgical Neurology | 1982

Qualitative measurement of cerebral infarction using ultraviolet fluorescence

John P. Laurent; Pablo M. Lawner; Frederick A. Simeone; Eugene A. Fink; L.B. Rorke

A reliable method of macroscopically determining the volume of cerebral infarction using ultraviolet fluorescence was developed in an animal model. Cerebral infarction was induced in 40 dogs by occluding the distal internal carotid and middle cerebral arteries. No barbiturates were administered. Intravenous sodium fluorescein was given before the animal was killed. Following fixation, 1 cm coronal sections were evaluated with ultraviolet light of 366 nm wavelength. The area of induced fluorescence for each section was determined using a grid overlay. Microscopic examination revealed that the areas of ischemic cell necrosis corresponded to areas of maximal fluorescence. This is an easily reproducible method to determine the volume of cerebral infarction.


Electroencephalography and Clinical Neurophysiology | 1976

EEG changes after acute cerebral embolism

John C. Oakley; John P. Laurent; Gaetano F. Molinari

Embolism of the right middle cerebral artery regularly failed to induce clinical or electrical seizure activity during acute ischemia in primates. This negative correlation casts some doubt on the popular interpretation of seizures at the outset of clinical stroke as evidence of cerebral embolism.


Survey of Anesthesiology | 1994

Barbiturates and Hyperventilation During Intracranial Hypertension

Penelope T. Louis; Jan Goddard-Finegold; Marvin A. Fishman; Johnny R. Griggs; Fernando Stein; John P. Laurent

ObjectiveThe purpose of this study was to determine the effect of hyperventilation alone and hyperventilation plus barbiturate therapy on intracranial pressure, global and regional cerebral blood flow rates, cerebrovascular resistance, and cerebral perfusion pressure in adult dogs with and without intracranial hypertension induced by epidural balloon. DesignProspective, randomized, controlled study. SettingAn animal laboratory of a university hospital. Four sequential global and regional cerebral blood flow determinations were made in each animal during monitoring of heart rate and systemic arterial pressure, during respiratory control and arterial blood gas monitoring, intracranial pressure monitoring, and with or without inflation of an epidural balloon catheter. SubjectsAcute mongrel dogs obtained from the Baylor Center for Comparative Medicine. Five groups of animals were studied. In group 1, the response to hyperventilation was assessed in dogs without increased intracranial pressure. In group 2, the response to hyperventilation was assessed in animals with acute intracranial hypertension. In group 3, the response to hyperventilation plus barbiturate therapy was assessed in dogs without increased intracranial pressure. In group 4, the response to hyperventilation plus barbiturate therapy was assessed in dogs with acute increased intracranial pressure. In group 5, a group of dogs with increased intracranial pressure was treated with neither hyperventilation nor barbiturates. InterventionsHyperventilation, hyperventilation plus barbiturate therapy, or no interventions were studied in these experimental paradigms. Measurements and Main ResultsThe main outcome measures were changes in intracranial pressure and/or changes in regional or total cerebral blood flow. A significant decrease in intracranial pressure and cerebral blood flow rate was produced by hyperventilation alone in groups with intracranial hypertension. Combined hyperventilation and barbiturate therapy resulted in a significant further decrease in cerebral blood flow rate in animals with normal and increased intracranial pressure, but no greater decrease in intracranial pressure was seen compared with treatment with hyperventilation alone. Cerebral perfusion pressures remained normal despite significant decreases in cerebral blood flow rates. ConclusionsThese studies suggest that barbiturate administration in this model of intracranial hypertension was no more effective in reducing increased intracranial pressure than hyperventilation alone. (Crit Care Med 1993; 21:1200–1206)

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William R. Cheek

Boston Children's Hospital

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Pablo M. Lawner

University of Pennsylvania

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Alexander West

University of Washington

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Biagio Azzarelli

Indiana University Bloomington

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Cheryl A. Muszynski

Children's Hospital of Wisconsin

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Dennis H. Cotcamp

Cincinnati Children's Hospital Medical Center

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Eugene A. Fink

University of Pennsylvania

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Frederick A. Boop

University of Tennessee Health Science Center

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