The role of intracranial hypotension in neonatal intraventricular hemorrhage

1983 ◽  
Vol 58 (2) ◽  
pp. 204-209 ◽  
Author(s):  
E. Scott Conner ◽  
Antonio V. Lorenzo ◽  
Keasley Welch ◽  
Brent Dorval
Keyword(s):  
Preterm Infants ◽  
Premature Infants ◽  
Intracranial Hypotension ◽  
Intraventricular Hemorrhage ◽  
Rabbit Model ◽  
Germinal Matrix ◽  
Content Type ◽  
Ventricular Hemorrhage ◽  
Fine Print

✓ Most preterm infants develop transient intracranial hypotension, which reaches its lowest level on the 2nd day of life. This corresponds to the time when most neonatal intraventricular hemorrhage (IVH) occurs. In order to test the hypothesis that intracranial hypotension may have an etiological role in the development of IVH in premature infants, the authors induced intracranial hypotension in the preterm rabbit by the intraperitoneal injection of glycerol. The rabbit model is well suited for this study because this animal is at risk of developing spontaneous germinal matrix and ventricular hemorrhage. Compared to control littermates, the glycerol-treated animals exhibited a greater than 3.5-fold incidence of germinal matrix and intraventricular hemorrhage.

The effect of furosemide on intracranial pressure and hemorrhage in preterm rabbits

1989 ◽  
Vol 70 (5) ◽  
pp. 785-792 ◽  
Author(s):  
Antonio V. Lorenzo ◽  
Clarence S. Greene ◽  
Gregory W. Hornig ◽  
L. Manuel Zavala ◽  
Keasley Welch
Keyword(s):  
Blood Pressure ◽  
Intracranial Hypotension ◽  
Intraventricular Hemorrhage ◽  
Fluid Loss ◽  
Tissue Pressure ◽  
Germinal Matrix ◽  
Content Type ◽  
Muscle Water ◽  
The Brain ◽  
Fine Print

✓ The hypothesis that intracranial hypotension due to excessive postnatal fluid loss places the premature infant at risk for germinal matrix and intraventricular hemorrhage (GM-IVH) was tested in preterm rabbits delivered at 28 and 29 days of gestation (term 32 days). Furosemide administered to newborn pups induced a diuresis that resulted in a 11% to 22% loss in body weight and a concomitant decline in muscle water (13% to 16%) and sodium (18% to 21%). Paradoxically, no change occurred in the water or electrolyte content of the brain even though cerebrospinal fluid and brain tissue pressure, but not blood pressure, declined. These changes were absent in littermates treated with saline. Microscopic examination of brain sections revealed a greater incidence of intracranial hemorrhage, particularly in the germinal matrix and choroid plexus, in furosemide-treated than in saline-treated preterm rabbit pups. These results are consistent with the hypothesis that intracranial hypotension promotes the incidence of GH-IVH in preterm animals.

Early death from rupture of an intracranial aneurysm

1982 ◽  
Vol 57 (6) ◽  
pp. 765-768 ◽  
Author(s):  
Albert Hijdra ◽  
Jan van Gijn
Keyword(s):  
Intracranial Aneurysm ◽  
Intraventricular Hemorrhage ◽  
Circulatory Arrest ◽  
Early Death ◽  
Intracerebral Hematoma ◽  
Brain Shift ◽  
Secondary Brain Damage ◽  
Content Type ◽  
Ventricular Hemorrhage ◽  
Fine Print

✓ The authors studied the clinical features and computerized tomography scans of 31 patients who died within 24 hours after the rupture of an intracranial aneurysm. Nine patients showed evidence of an intracerebral hematoma and brain shift, eight of a massive intraventricular hemorrhage, eight of both a hematoma and ventricular hemorrhage, and six of only subarachnoid hemorrhage (SAH). These anatomical types of hemorrhage could not be distinguished clinically. Four of the six patients with only SAH suffered initial apnea and circulatory arrest. In these cases, secondary brain damage may have been caused by anoxia, and therefore might have been reversible.

Intraventricular hemorrhage in the premature rabbit pup

1984 ◽  
Vol 60 (6) ◽  
pp. 1243-1245 ◽  
Author(s):  
David M. Coulter ◽  
Tim LaPine ◽  
W. Manford Gooch
Keyword(s):  
Animal Model ◽  
Normal Saline ◽  
Intraventricular Hemorrhage ◽  
Rabbit Model ◽  
Content Type ◽  
Bolus Infusion ◽  
Fine Print

✓ The authors used the premature rabbit model to examine the pathophysiology of intraventricular hemorrhage (IVH). They studied the brains of 167 control animals, of 45 animals after a hypertensive insult, of three animals after a bolus infusion of normal saline, and of 10 animals after both insults. In none of the brains was IVH identified. Limited reproducibility may restrict the use of this animal model.

Beagle puppy model of intraventricular hemorrhage

1982 ◽  
Vol 57 (2) ◽  
pp. 219-223 ◽  
Author(s):  
Laura R. Ment ◽  
William B. Stewart ◽  
Charles C. Duncan ◽  
Richard Lambrecht
Keyword(s):  
Blood Flow ◽  
Intraventricular Hemorrhage ◽  
Relative Volume ◽  
Low Flow ◽  
Flow Area ◽  
Germinal Matrix ◽  
Content Type ◽  
Carbon 14 ◽  
Neurological Problem ◽  
Fine Print

✓ Intraventricular hemorrhage (IVH) is a major neurological problem of the preterm infant and originates in the germinal matrix tissues of the developing brain. The newborn beagle pup has been demonstrated to provide an excellent model for this neonatal neuropathological condition. By the production of hemorrhagic hypotension followed by relative volume reexpansion, such hemorrhages can be produced in this animal. Carbon-14(14C)-iodoantipyrine was used for measuring the cerebral blood flow in this experimental model and demonstrated that, although the germinal matrix is a relatively low-flow area in the newborn beagle pup, the selective flow to this region increases significantly in animals with IVH.

Retinopathy of Prematurity and other Ocular Problems in Premature Infants Weighing less than 1500 g at Birth

2002 ◽  
Vol 12 (6) ◽  
pp. 506-511 ◽  
Author(s):  
I.C. Asproudis ◽  
S.K. Andronikou ◽  
E.A. Hotoura ◽  
C.D. Kalogeropoulos ◽  
G.K. Kitsos ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Premature Infants ◽  
Retinopathy Of Prematurity ◽  
Intraventricular Hemorrhage ◽  
Neonatal Intensive Care ◽  
Ocular Motility ◽  
Refractive Errors ◽  
Ophthalmological Examination ◽  
Retinal Hemorrhages

Purpose To estimate the incidence of retinopathy of prematurity and other ocular problems in a population of preterm infants. Methods This retrospective study included all infants with gestational age (GA) <32 weeks and birth weight (BW) <1500 g cared for in the neonatal intensive care unit (NICU) over a period of nine years (1992–2000). Ophthalmological examination was started the 4th week of life and included refractive examination, examination of the cornea and funduscopy under mydriasis. An ocular motility test was done after the 2nd month. Results The study included 194 infants. Stage I and II retinopathy occurred in 51 infants but regressed spontaneously. Five of the 194 (2.5%) had to undergo cryopexy. Optic disc atrophy was observed in association with peri-intraventricular hemorrhage (PIIVH) (grade IV) in seven infants. Fifteen infants (7.7%) had retinal hemorrhages which were absorbed by three months of age. Almost 20% of the study infants developed high refractive errors and 13.4% strabismus. Conclusions Not only retinopathy of prematurity, but other serious ocular problems were observed in this population of preterm infants. The role of PIIVH III-IV in the pathogenesis of certain ocular problems needs further elucidation.

Vasculature to the germinal matrix in rabbit pups

1986 ◽  
Vol 64 (4) ◽  
pp. 650-656 ◽  
Author(s):  
Edwin G. Fischer ◽  
Antonio V. Lorenzo ◽  
William J. Landis ◽  
Keasley Welch ◽  
Stephen K. Ofori-Kwakye ◽  
...  
Keyword(s):  
Methyl Methacrylate ◽  
Intraventricular Hemorrhage ◽  
Rabbit Model ◽  
Cerebral Vasculature ◽  
Brain Vessels ◽  
Germinal Matrix ◽  
Content Type ◽  
Vascular Casts ◽  
A Site ◽  
The Brain

✓ The authors report a study of the cerebral vasculature of premature rabbits pertaining to the germinal matrix (GM). A pigmented silicone material (Microfil) was injected into the carotid artery of anesthetized rabbits. Methyl methacrylate vascular casts of a similar group of premature rabbits were examined by scanning electron microscopy. The GM is supplied by arteries from both the basal and convexity surfaces of the brain. Vessels could be identified as arteries or veins by their typical patterns of branching and by the characteristic impressions made on the methyl methacrylate casts by endothelial nuclei. Specific evidence of structural weaknesses in the vasculature, which could be a site of predilection for GM bleeding, was not observed. The similarities in basal ganglia vasculature between premature rabbits and humans justifies using the rabbit model to study vascular aspects of the GM and intraventricular hemorrhage.

Acquired Chiari I malformation secondary to spontaneous spinal cerebrospinal fluid leakage and chronic intracranial hypotension syndrome in seven cases

1998 ◽  
Vol 88 (2) ◽  
pp. 237-242 ◽  
Author(s):  
John L. D. Atkinson ◽  
Brian G. Weinshenker ◽  
Gary M. Miller ◽  
David G. Piepgras ◽  
Bahram Mokri
Keyword(s):  
Cerebrospinal Fluid ◽  
Intracranial Hypotension ◽  
Chiari I Malformation ◽  
Csf Leak ◽  
Cerebrospinal Fluid Leakage ◽  
Content Type ◽  
Intracranial Hypotension Syndrome ◽  
Csf Leakage ◽  
Chiari I ◽  
Fine Print

Object. Spontaneous spinal cerebrospinal fluid (CSF) leakage with development of the intracranial hypotension syndrome and acquired Chiari I malformation due to lumbar spinal CSF diversion procedures have both been well described. However, concomitant presentation of both syndromes has rarely been reported. The object of this paper is to present data in seven cases in which both syndromes were present. Three illustrative cases are reported in detail. Methods. The authors describe seven symptomatic cases of spontaneous spinal CSF leakage with chronic intracranial hypotension syndrome in which magnetic resonance (MR) images depicted dural enhancement, brain sagging, loss of CSF cisterns, and acquired Chiari I malformation. Conclusions. This subtype of intracranial hypotension syndrome probably results from chronic spinal drainage of CSF or high-flow CSF shunting and subsequent loss of brain buoyancy that results in brain settling and herniation of hindbrain structures through the foramen magnum. Of 35 cases of spontaneous spinal CSF leakage identified in the authors' practice over the last decade, MR imaging evidence of acquired Chiari I malformation has been shown in seven. Not to be confused with idiopathic Chiari I malformation, ideal therapy requires recognition of the syndrome and treatment directed to the site of the spinal CSF leak.

Flushing in relation to a possible rise in intracranial pressure: documentation of an unusual clinical sign

2000 ◽  
Vol 92 (6) ◽  
pp. 1040-1044 ◽  
Author(s):  
Gregory W. Hornig
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intraventricular Hemorrhage ◽  
Pneumococcal Meningitis ◽  
Clinical Importance ◽  
Neurological Deterioration ◽  
Content Type ◽  
Transient Nature ◽  
Fine Print

✓ This report documents clinical features in five children who developed transient reddening of the skin (epidermal flushing) in association with acute elevations in intracranial pressure (ICP). Four boys and one girl (ages 9–15 years) deteriorated acutely secondary to intracranial hypertension ranging from 30 to 80 mm Hg in the four documented cases. Two patients suffered from ventriculoperitoneal shunt malfunctions, one had diffuse cerebral edema secondary to traumatic brain injury, one was found to have pneumococcal meningitis and hydrocephalus, and one suffered an intraventricular hemorrhage and hydrocephalus intraoperatively. All patients were noted to have developed epidermal flushing involving either the upper chest, face, or arms during their period of neurological deterioration. The response was transient, typically lasting 5 to 15 minutes, and dissipated quickly. The flushing reaction is postulated to be a centrally mediated response to sudden elevations in ICP. Several potential mechanisms are discussed. Flushing has clinical importance because it may indicate significant elevations in ICP when it is associated with neurological deterioration. Because of its transient nature, the importance of epidermal flushing is often unrecognized; its presence confirms the need for urgent treatment.

scholarly journals Direct evidence for a key role of protein kinase C in the development of vasospasm after subarachnoid hemorrhage

1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Direct Evidence ◽  
Control Group ◽  
Content Type ◽  
Kinase C ◽  
Protein Kinase C Activity ◽  
Fine Print

✓ Vascular contraction is induced by the activation of intracellular contractile proteins mediated through signal transduction from the outside to the inside of cells. Protein kinase C plays a crucial role in this signal transduction. It is hypothesized that protein kinase C plays a causative part in the development of vasospasm after subarachnoid hemorrhage (SAH). To verify this directly, the authors measured protein kinase C activity in canine basilar arteries in an SAH model with (γ-32P)adenosine triphosphate and the data were compared to those in a control group. Protein kinase C is translocated to the membrane from the cytosol when it is activated, and the translocation is an index of the activation; thus, protein kinase C activity was measured both in the cytosol and in the membrane fractions. Protein kinase C activity in the membrane in the SAH model was remarkably enhanced compared to that in the control group. The percentage of membrane activity to the total was also significantly greater in the SAH vessels than in the control group, and the percentage of cytosol activity in the SAH group was decreased compared to that in the control arteries. The results indicate that protein kinase C in the vascular smooth muscle was translocated to the membrane from the cytosol and was activated when SAH occurred. It is concluded that this is direct evidence for a key role of protein kinase C in the development of vasospasm.

Activation of complement by tissue plasminogen activator, but not acute cerebral ischemia, in a rabbit model of thromboembolic stroke

1997 ◽  
Vol 86 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Martin M. Bednar ◽  
Cordell E. Gross ◽  
Sheila R. Russell ◽  
David Short ◽  
Patricia C. Giclas
Keyword(s):  
Cerebral Ischemia ◽  
Plasminogen Activator ◽  
Complement Activation ◽  
Rabbit Model ◽  
Thromboembolic Stroke ◽  
Content Type ◽  
Acute Cerebral Ischemia ◽  
Tissue Plasminogen ◽  
Before And After ◽  
Fine Print

✓ Although complement activation is associated with tissue injury during inflammatory and ischemic states, complement activation in states of acute cerebral ischemia before and after administration of tissue plasminogen activator (TPA) has not yet been examined and is the focus of this investigation. Twenty-four New Zealand White rabbits weighing 3 to 3.5 kg were used for this study. Of these, 20 were subjected to intracranial autologous clot embolization via the internal carotid artery. Three hours postembolization, rabbits received an intravenous infusion of TPA (6.3 mg/kg, 20% bolus with the remainder infused over a 2-hour interval; 12 animals) or vehicle (eight animals). All animals were observed for a total of 7 or 8 hours postembolization. These two groups were compared to a cohort undergoing sham operation with subsequent TPA infusion (four animals). Plasma samples to quantify complement component C5 hemolytic activity (C5H5O) were obtained at the following time points: 30 minutes before and after clot embolization; 1 hour before and 1 hour after the initiation of therapy with TPA or vehicle and at the completion of the protocol; 7 to 8 hours after clot embolization. The C5 activation was not detected as the result of acute cerebral ischemia. However, animals receiving TPA with or without concomitant clot embolization exhibited C5 activation as assessed by a reduction in C5 hemolytic function, both 1 hour after initiation of TPA infusion (78.7 ± 10.3% and 77.5 ± 9.9% of baseline value, respectively; mean ± standard error of the mean [SEM]) and at the end of the protocol, 2 hours after the completion of the TPA infusion (72.5 ± 8.8% and 53.3 ± 8.1%, respectively; mean ± SEM, p < 0.05, each group). This study supports the conclusion that TPA, but not acute cerebral ischemia, may activate the complement cascade in this rabbit model of thromboembolic stroke.

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