Micro- and macrovascular changes as the direct cause of parenchymal destruction in congenital murine hydrocephalus

1975 ◽  
Vol 43 (5) ◽  
pp. 535-545 ◽  
Author(s):  
Maciej Wozniak ◽  
David G. McLone ◽  
Anthony J. Raimondi

✓ Microangiotomography was used to identify the normal and pathological pattern of cerebral vessels in the hy-3 murine mutant mouse (normal and hydrocephalic) at various developmental stages from birth through 21 days of life. The technique employed allows resolution, in the range of 7 to 10 µ of the surface and in-traparenchymal (perforating) microvasculature. Ventricular enlargement causes displacement of primary cerebral arteries, followed by both stretching and a decrease in the caliber of primary, secondary, and tertiary vessels (arterial and venous). Ultimately, there is a reduction in the number and caliber of the microvasculature, resulting in diminished cerebral blood flow and cerebral edema. Tissue destruction leading to ependymal rupture, parenchymal cavitation, and the formation of porencephalic cysts within the edematous parenchyma ensues. External ventricular drainage, by decompressing the ventricles, resulted in rapid restoration of the filling of the primary and secondary vessels, thereby suggesting the primary role of vascular changes in the production of brain damage. This study offers experimental evidence that early diversion of the cerebrospinal fluid interrupts this chain of events in congenital murine hydrocephalus.

1998 ◽  
Vol 89 (2) ◽  
pp. 289-296 ◽  
Author(s):  
Chul-Jin Kim ◽  
Kee-Won Kim ◽  
Jin-Woo Park ◽  
Jung-Chung Lee ◽  
John H. Zhang

Object. This study was undertaken to explore whether erythrocyte lysate, a proposed cause of vasospasm, produces vasoconstriction by activation of tyrosine kinase in rabbit cerebral arteries. Methods. Isometric tension was used to monitor contractions in rabbit basilar arteries induced by erythrocyte lysate, 5-hydroxytryptamine (5-HT), or KCl in the absence or presence of tyrosine kinase inhibitors. Erythrocyte lysate, 5-HT, or KCl produced concentration-dependent contractions in rabbit basilar arteries. Preincubation with the tyrosine kinase inhibitors tyrphostin A23 and genistein (30 and 100 µM), but not diadzein, an inactive analog of genistein, attenuated significantly the contraction induced by erythrocyte lysate (p < 0.05). Tyrphostin A23, genistein, and diadzein (30 µM) failed to reduce the contraction caused by 5-HT. Genistein, but not tyrphostin A23 or diadzein (30 µM), attenuated significantly the contraction induced by KCl (p < 0.05). In another series, arterial rings were initially contracted with erythrocyte lysate, 5-HT, or KCl and the relaxant effect of genistein was then tested. Genistein relaxed rabbit basilar arteries that had been contracted by exposure to erythrocyte lysate, 5-HT, or KCl (30–100 µM; p < 0.05). Conclusions. These data indicate that tyrosine kinase may play a role in the regulation of cerebral arterial contraction and tyrosine kinase inhibitors may be useful in the management of cerebral vasospasm.


1981 ◽  
Vol 55 (6) ◽  
pp. 877-883 ◽  
Author(s):  
Lennart Brandt ◽  
Bengt Ljunggren ◽  
Karl-Erik Andersson ◽  
Bengt Hindfelt ◽  
Tore Uski

✓ In small human cerebral arteries preincubated with indomethacin, contractions induced by cerebrospinal fluid (CSF), from patients with subarachnoid hemorrhage were markedly increased. Also contractions induced by noradrenaline, but not 5-hydroxytryptamine, were augmented. Prostacyclin and its metabolite 6-keto-prostaglandin (PG)E1 reversed the contractions induced by CSF, as well as by noradrenaline, 5-hydroxytryptamine, and PGF2α. The findings suggest that these substances are able to counteract the influence of vasoconstrictor material in hemorrhagic CSF. If the capacity to synthesize these “protective” arachidonic acid metabolites is reduced, the resulting imbalance between contractile and relaxant forces acting on the vessel wall may lead to sustained cerebral vasoconstriction.


1992 ◽  
Vol 76 (4) ◽  
pp. 635-639 ◽  
Author(s):  
Shigeru Nishizawa ◽  
Nobukazu Nezu ◽  
Kenichi Uemura

✓ 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.


1980 ◽  
Vol 53 (3) ◽  
pp. 300-304 ◽  
Author(s):  
Toshisuke Sakaki ◽  
Kazuhiko Kinugawa ◽  
Tatsuo Tanigake ◽  
Seiji Miyamoto ◽  
Kikuo Kyoi ◽  
...  

✓ Embolism from an aneurysm is one of the mechanisms involved in the pathogenesis of ischemic symptoms associated with intracranial aneurysms. Four cases are reported in which aneurysms of the internal carotid arteries and middle cerebral arteries were the source of emboli resulting in cerebral infarction. In the treatment of these aneurysms, it is best to clip the neck of the aneurysm with great care to avoid embolism due to extrusion of clot into the distal artery.


1998 ◽  
Vol 89 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Abhaya V. Kulkarni ◽  
Abhijit Guha ◽  
Andres Lozano ◽  
Mark Bernstein

Object. Many neurosurgeons routinely obtain computerized tomography (CT) scans to rule out hemorrhage in patients after stereotactic procedures. In the present prospective study, the authors investigated the rate of silent hemorrhage and delayed deterioration after stereotactic biopsy sampling and the role of postbiopsy CT scanning. Methods. A subset of patients (the last 102 of approximately 800 patients) who underwent stereotactic brain biopsies at the Toronto Hospital prospectively underwent routine postoperative CT scanning within hours of the biopsy procedure. Their medical charts and CT scans were then reviewed. A postoperative CT scan was obtained in 102 patients (aged 17–87 years) who underwent stereotactic biopsy between June 1994 and September 1996. Sixty-one patients (59.8%) exhibited hemorrhages, mostly intracerebral (54.9%), on the immediate postoperative scan. Only six of these patients were clinically suspected to have suffered a hemorrhage based on immediate postoperative neurological deficit; in the remaining 55 (53.9%) of 102 patients, the hemorrhage was clinically silent and unsuspected. Among the clinically silent intracerebral hemorrhages, 22 measured less than 5 mm, 20 between 5 and 10 mm, five between 10 and 30 mm, and four between 30 and 40 mm. Of the 55 patients with clinically silent hemorrhages, only three demonstrated a delayed neurological deficit (one case of seizure and two cases of progressive loss of consciousness) and these all occurred within the first 2 postoperative days. Of the neurologically well patients in whom no hemorrhage was demonstrated on initial postoperative CT scan, none experienced delayed deterioration. Conclusions. Clinically silent hemorrhage after stereotactic biopsy is very common. However, the authors did not find that knowledge of its existence ultimately affected individual patient management or outcome. The authors, therefore, suggest that the most important role of postoperative CT scanning is to screen for those neurologically well patients with no hemorrhage. These patients could safely be discharged on the same day they underwent biopsy.


1974 ◽  
Vol 41 (1) ◽  
pp. 107-112
Author(s):  
Shigeaki Hori ◽  
Williamina A. Himwich

✓ A technique for exposing the vessels in the anterior part of the circle of Willis in the dog is described. Some of the physiological and anatomical characteristics of the anterior communicating and the anterior cerebral arteries are discussed.


1980 ◽  
Vol 52 (6) ◽  
pp. 776-781 ◽  
Author(s):  
George Tyson ◽  
W. Ellis Strachan ◽  
Peter Newman ◽  
H. Richard Winn ◽  
Albert Butler ◽  
...  

✓ A consecutive series of 48 adult patients with a chronic subdural hematoma is reported. These patients were treated according to a protocol consisting of a sequence of conventional surgical procedures ranging from simple burr-hole drainage to craniotomy and subdural membranectomy. Seven patients (15%) continued to demonstrate severe neurological dysfunction, or suffered acute neurological deterioration after completion of this protocol. However, after undergoing excision of the cranial vault overlying the hematoma site, six of these seven patients demonstrated a significant clinical improvement. Based on analysis of these seven cases, the authors suggest that craniectomy be considered in those patients who suffer a symptomatic reaccumulation of subdural fluid following craniotomy and membranectomy, or who demonstrate further neurological deterioration as a result of cerebral swelling subjacent to the hematoma site. However, this procedure probably has no efficacy once extensive cerebral infarction has occurred.


1995 ◽  
Vol 83 (4) ◽  
pp. 575-582 ◽  
Author(s):  
Giuseppe Cinalli ◽  
Dominique Renier ◽  
Guy Sebag ◽  
Christian Sainte-Rose ◽  
Eric Arnaud ◽  
...  

✓ The incidence of chronic tonsillar herniation (CTH) was evaluated with magnetic resonance imaging in 44 patients with Crouzon's syndrome and 51 with Apert's syndrome; the incidence was 72.7% in Crouzon's syndrome and 1.9% in Apert's syndrome. All the patients with Crouzon's syndrome and progressive hydrocephalus had CTH, but of 32 individuals with Crouzon's syndrome and CTH, only 15 had progressive hydrocephalus. Five patients with Apert's syndrome were treated for progressive hydrocephalus; none had CTH. The patterns of suture closure in these two groups of patients were studied, and significant differences in coronal, sagittal, and lambdoid sutures were found between patients with Crouzon's and Apert's syndromes. In Crouzon's syndrome, significant differences in the pattern of lambdoid suture closure were found between the groups with and without CTH; in the group with CTH, the lambdoid closure appeared earlier. The authors propose that the high incidence of individuals with CTH who have Crouzon's syndrome is related to the premature synostosis of the lambdoid suture in the first 24 months of age.


2000 ◽  
Vol 93 (4) ◽  
pp. 594-604 ◽  
Author(s):  
Michael Bitzer ◽  
Thomas Nägele ◽  
Beverly Geist-Barth ◽  
Uwe Klose ◽  
Eckardt Grönewäller ◽  
...  

Object. In a prospective study, 28 patients with 32 intracranial meningiomas were examined to determine the role of hydrodynamic interaction between tumor and surrounding brain tissue in the pathogenesis of peritumoral brain edema.Methods. Gadolinium—diethylenetriamine pentaacetic acid (Gd-DPTA), an extracellular contrast agent used for routine clinical imaging, remains strictly extracellular without crossing an intact blood—brain barrier. Therefore, it is well suited for investigations of hydrodynamic extracellular mechanisms in the development of brain edema. Spin-echo T1-weighted magnetic resonance images were acquired before and after intravenous administration of 0.2 mmol/kg Gd-DPTA. Additional T1-weighted imaging was performed 0.6, 3.5, and 6.5 hours later. No significant Gd-DPTA diffused from tumor into peritumoral brain tissue in 12 meningiomas without surrounding brain edema. In contrast, in 17 of 20 meningiomas with surrounding edema, contrast agent in peritumoral brain tissue was detectable after 3.5 hours and 6.5 hours. In three of 20 meningiomas with minimum surrounding edema (< 5 cm3), contrast agent effusion was absent. After 3.5 hours and 6.5 hours strong correlations of edema volume and the maximum distance of contrast spread from the tumor margin into adjacent brain parenchyma (r = 0.84 and r = 0.87, respectively, p < 0.0001) indicated faster effusion in larger areas of edema.Conclusions. The results of this study show that significant contrast agent effusion from the extracellular space of the tumor into the interstitium of the peritumoral brain tissue is only found in meningiomas with surrounding edema. This supports the hypothesis that hydrodynamic processes play an essential role in the pathogenesis of peritumoral brain edema in meningiomas.


1999 ◽  
Vol 91 (1) ◽  
pp. 1-11 ◽  
Author(s):  
Michael G. Fehlings ◽  
Charles H. Tator

Object. The authors conducted an evidence-based review of the literature to evaluate critically the rationale and indications for and the timing of decompressive surgery for the treatment of acute, nonpenetrating spinal cord injury (SCI). Methods. The experimental and clinical literature concerning the role of, and the biological rationale for, surgical decompression for acute SCI was reviewed. Clinical studies of nonoperative management of SCI were also examined for comparative purposes. Evidence from clinical trials was categorized as Class I (well-conducted randomized prospective trials), Class II (well-designed comparative clinical studies), or Class III (retrospective studies). Examination of studies in which animal models of SCI were used consistently demonstrated a beneficial effect of early decompressive surgery, although it is difficult to apply these data directly to the clinical setting. The clinical studies provided suggestive (Class III and limited Class II) evidence that decompressive procedures improve neurological recovery after SCI. However, no clear consensus can be inferred from the literature as to the optimum timing for decompressive surgery. Many authors have advocated delayed treatment to avoid medical complications, although good evidence from recent Class II trials indicates that early decompressive surgery can be performed safely without causing added morbidity or mortality. Conclusions. There is biological evidence from experimental studies in animals that early decompressive surgery may improve neurological recovery after SCI, although the relevant interventional timing in humans remains unclear. To date, the role of surgical decompression in patients with SCI is only supported by Class III and limited Class II evidence. Accordingly, decompressive surgery for SCI can only be considered a practice option. Furthermore, analysis of the literature does not allow definite conclusions to be drawn regarding appropriate timing of intervention. Hence, there is a need to conduct well-designed experimental and clinical studies of the timing and neurological results of decompressive surgery for the treatment of acute SCI.


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