Norepinephrine in cerebrospinal fluid of patients with cerebral vasospasm

1982 ◽  
Vol 56 (3) ◽  
pp. 344-349 ◽  
Author(s):  
Taku Shigeno

✓ The content of norepinephrine (NE) in the ventricular, basal cisternal, and lumbar cerebrospinal fluid (CSF) was determined in 19 patients with ruptured cerebral aneurysms at different intervals according to the presence or absence of vasospasm. Twelve were operated on within 3 days after subarachnoid hemorrhage (SAH), prior to the occurrence of vasospasm. Postoperatively, CSF was continuously drained from a basal cistern or lateral ventricle. Norepinephrine was assayed by the highly sensitive automated fluorometric method. The concentration of NE increased in all sites of CSF sampling along with the appearance of vasospasm. Above all, the cisternal CSF of patients with vasospasm contained significantly higher NE (0.246 ± 0.049 ng/ml, mean ± SEM) compared to those without vasospasm (0.075 ± 0.001 ng/ml) (p < 0.001). However, since this increase cannot be considered to be high enough locally to constrict cerebral arteries, this might be only a secondary phenomenon due to release of NE into CSF from various sources in the brain.

1989 ◽  
Vol 70 (4) ◽  
pp. 545-550 ◽  
Author(s):  
Peter J. Benson ◽  
Joo Ho Sung

✓ Three patients, two males and one female aged 21, 14, and 31 years, respectively, developed cerebral saccular aneurysms several years after undergoing radiotherapy for cerebellar medulloblastoma at 2, 5, and 14 years of age, respectively. Following surgery, all three received combined cobalt-60 irradiation and intrathecal colloidal radioactive gold (198Au) therapy, and died from rupture of the aneurysm 19, 9, and 17 years after the radiotherapy, respectively. Autopsy examination revealed no recurrence of the medulloblastoma, but widespread radiation-induced vasculopathy was found at the base of the brain and in the spinal cord, and saccular aneurysms arose from the posterior cerebral arteries at the basal cistern or choroidal fissure. The aneurysms differed from the ordinary saccular aneurysms of congenital type in their location and histological features. Their locations corresponded to the areas where intrathecally administered colloidal 198Au is likely to pool, and they originated directly from a segment of the artery rather than from a branching site as in congenital saccular aneurysms. It is, therefore, concluded that the aneurysms in these three patients were most likely radiation-induced.


1978 ◽  
Vol 48 (4) ◽  
pp. 505-514 ◽  
Author(s):  
Jiro Suzuki ◽  
Hiro Ohara

✓ The origin and mechanism of rupture, repair, and growth of intracranial saccular aneurysms are reported in an investigation of 45 aneurysms (23 unruptured and 22 ruptured) found in 34 brain specimens. Gaps in the media at the bifurcations of cerebral arteries are important for aneurysmal formation. The walls of aneurysms smaller than 3 mm in diameter are mainly composed of endothelial cells, and fibrous tissue. When aneurysms grow larger than 4 mm, the walls become collagenous and extremely thin portions develop in their domes, forming potential rupture points. Immediately after the rupture, bleeding is stopped by clot and a new fibrin layer is formed around the rupture point. It is proposed that the cerebrospinal fluid has a special accelerating action in clot formation. This fibrin layer is weak, and repeat rupture occurs within 3 weeks after the initial hemorrhage. However, after 3 weeks, rebleeding is rare due to the reinforcement of this layer, and capillaries appear in this new wall. Hemorrhages from these capillaries occur within and outside the new wall caused by the constant impingement of blood flow. In severe cases, the aneurysm ruptures again, but when the hemorrhages are slight, the aneurysm grows as the wall is thickened by repeated hemorrhages and their absorption. This may explain the growth mechanism of the aneurysm.


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.


2005 ◽  
Vol 102 (2) ◽  
pp. 229-234 ◽  
Author(s):  
Rogier P. Schade ◽  
Janke Schinkel ◽  
Leo G. Visser ◽  
J. Marc C. van Dijk ◽  
Joan H. C. Voormolen ◽  
...  

Object. In the present study the authors compared the incidence and risk factors for external drainage—related bacterial meningitis (ED-BM) by using ventricular and lumbar catheters. Methods. A cohort of 230 consecutive patients with ED was evaluated. Cerebrospinal fluid samples were obtained daily for microbiological culture, and ED-BM was defined based on culture results in combination with clinical symptoms. The incidence of ED-BM was 7% in lumbar and 15% in ventricular drains. Independent risk factors included site leakage, drain blockage, and most importantly duration of ED. Despite a higher infection rate, ventricular catheters did not have a significant higher risk of infection after correcting for duration of drainage. Conclusions. Analysis of data in the present study showed that the incidence of ED-associated death is low (0.45%) in patients who do not receive continuous antibiotic prophylaxis during ED.


1977 ◽  
Vol 46 (2) ◽  
pp. 215-219 ◽  
Author(s):  
Gerald D. Silverberg ◽  
Christina B. Harbury ◽  
Edward Rubenstein

✓ A combination of concentrated platelets, thrombin, and fibrinogen was used to adhere a pericranial graft to surgically produced cerebrospinal fluid (CSF) fistulas in dogs. This sealant successfully stopped leakage of CSF in all fistulas produced in both acute and chronic preparations. All control animals leaked CSF acutely. In chronic control animals the CSF leaks sealed spontaneously but the grafts were not well incorporated. Histological examination of the grafts and underlying brain showed no injury to the brain or meningeal vessel from exposure to the platelet glue. Good fibrous union of the grafts to the dura was confirmed.


1979 ◽  
Vol 51 (1) ◽  
pp. 70-77 ◽  
Author(s):  
Jurjen Gazendam ◽  
K. Gwan Go ◽  
Annie K. van Zanten

✓ Edema fluid isolated from cats with cold-induced brain edema was subjected to analysis of electrolyte content, enzyme activities, colloid osmotic pressure and the radioactivity of intravenously injected 99mTc-labeled albumin. The findings corroborate the essential features of vasogenic edema, such as its origin from the blood plasma, its rapid propagation into the white matter of the brain as contrasted with the delayed spread into gray matter, and its contribution to composition of cerebrospinal fluid. Moreover, the elevated activities of cellular enzymes and K+ content of edema fluid point to the admixture with cellular contents due to the freezing damage.


1999 ◽  
Vol 91 (5) ◽  
pp. 835-842 ◽  
Author(s):  
Takatoshi Sorimachi ◽  
Hiroshi Abe ◽  
Shigekazu Takeuchi ◽  
Ryuichi Tanaka

Object. The purpose of this study was to investigate the possibility of preventing cumulative neuronal damage after repetitive severe ischemia.Methods. The authors monitored ischemic depolarization in the gerbil hippocampus, which has recently been shown to be a good experimental model of the effects of brief ischemia on the brain, and evaluated neuronal damage in the CA1 subregion 7 days after the ischemic insult. In a single-ischemia paradigm, the results indicate that induction of ischemia-induced neuronal damage depended on the duration of ischemic depolarization. Neuronal damage can be detected in the CA1 subregion after a period of depolarization lasting 210 seconds. Using a double-ischemia paradigm in which the animals were subjected to two periods of ischemia, there was apparently no accumulation of neuronal damage from the first ischemic episode to the second, provided the duration of the first period of ischemic depolarization did not exceed 90 seconds. Neuronal damage accumulated when the duration of the first ischemia episode exceeded 90 seconds, regardless of the duration of the reperfusion interval between the two ischemic insults. Finally, when the ischemic insult was spread over four separate episodes, each lasting 90 seconds (with a reperfusion interval of 5 minutes), neuronal damage was not found when the total depolarization period was less than 420 seconds.Conclusions. The authors conclude that cumulative neuronal damage may be avoided by adopting an intermittent ischemia approach. The implications of these results for human surgery requiring temporary occlusion of the cerebral arteries are discussed.


2003 ◽  
Vol 99 (6) ◽  
pp. 991-998 ◽  
Author(s):  
Eric A. Schmidt ◽  
Marek Czosnyka ◽  
Luzius A. Steiner ◽  
Marcella Balestreri ◽  
Piotr Smielewski ◽  
...  

Object. The aim of this study was to assess the asymmetry of autoregulation between the left and right sides of the brain by using bilateral transcranial Doppler ultrasonography in a cohort of patients with head injuries. Methods. Ninety-six patients with head injuries comprised the study population. All significant intracranial mass lesions were promptly removed. The patients were given medications to induce sedation and paralysis, and artificial ventilation. Arterial blood pressure (ABP) and intracranial pressure (ICP) were monitored in an invasive manner. A strategy based on the patient's cerebral perfusion pressure (CPP = ABP − ICP) was applied: CPP was maintained at a level higher than 70 mm Hg and ICP at a level lower than 25 mm Hg. The left and right middle cerebral arteries were insonated daily, and bilateral flow velocities (FVs) were recorded. The correlation coefficient between the CPP and FV, termed Mx, was calculated and time-averaged over each recording period on both sides. An Mx close to 1 signified that slow fluctuations in CPP produced synchronized slow changes in FV, indicating a defective autoregulation. An Mx close to 0 indicated preserved autoregulation. Computerized tomography scans in all patients were reviewed; the side on which the major brain lesion was located was noted and the extent of the midline shift was determined. Outcome was measured 6 months after discharge. The left—right difference in the Mx between the hemispheres was significantly higher in patients who died than in those who survived (0.16 ± 0.04 compared with 0.08 ± 0.01; p = 0.04). The left—right difference in the Mx was correlated with a midline shift (r = −0.42; p = 0.03). Autoregulation was worse on the side of the brain where the lesion was located (p < 0.035). Conclusions. The left—right difference in autoregulation is significantly associated with a fatal outcome. Autoregulation in the brain is worse on the side ipsilateral to the lesion and on the side of expansion in cases in which there is a midline shift.


2002 ◽  
Vol 96 (5) ◽  
pp. 918-923 ◽  
Author(s):  
Joseph C. Watson ◽  
Alexander M. Gorbach ◽  
Ryszard M. Pluta ◽  
Ramin Rak ◽  
John D. Heiss ◽  
...  

Object. Application of sensitive infrared imaging is ideally suited to observe blood vessels and blood flow in exposed organs, including the brain. Temporary vascular occlusion is an important part of neurosurgery, but the capacity to monitor the effects of these occlusions in real time is limited. In surgical procedures that require vascular manipulation, such as those involving aneurysms, arteriovenous malformations (AVMs), or tumors, the ability to visualize blood flow in vessels and their distribution beds would be beneficial. The authors recount their experience in the use of a sensitive (0.02°C), high-resolution (up to 50 µm/pixel) infrared camera with a rapid shutter speed (up to 2 msec/frame) for localizing cortical function intraoperatively. They observed high-resolution images of cerebral arteries and veins. The authors hypothesized that infrared imaging of cerebral arteries, performed using a sensitive, high-resolution camera during surgery, would permit changes in arterial flow to be be seen immediately, thus providing real-time assessment of brain perfusion in the involved vascular territory. Methods. Cynomolgus monkeys underwent extensive craniectomies, exposing the frontal, parietal, and temporal lobes. Temporary occlusions of the internal carotid artery and middle cerebral artery branches (30 events) were performed serially and were visualized with the aid of an infrared camera. Arteries and veins of the monkey brain were clearly visualized due to cooling of the exposed brain, which contrasted with blood within the vessels that remained at core temperature. Blood flow changes in vessels were seen immediately (< 1 second) in real time during occlusion and reopening of the vessels, regardless of the duration of the occlusion. Areas of decreased cortical blood flow rapidly cooled (−0.3 to 1.3°C) and reheated in response to reperfusion. Rewarming occurred faster in arteries than in the cortex (for a 20-minute occlusion, the change in temperature per second was 2 × 10−2°C in the artery and 7 × 10−3°C in the brain). Collateral flow could be evaluated by intraoperative observations and data processing. Conclusions. Use of high-resolution, digital infrared imaging permits real-time visualization of arterial flow. It has the potential to provide the surgeon with a means to assess collateral flow during temporary vessel occlusion and to visualize directly the flow in parent arteries or persistent filling of an aneurysm after clipping. During surgery for AVMs, the technique may provide a new way to assess arterial inflow, venous outflow, results of embolization, collateral flow, steal, and normal perfusion pressure breakthrough.


1982 ◽  
Vol 56 (4) ◽  
pp. 475-481 ◽  
Author(s):  
Nicholas T. Zervas ◽  
Theodore M. Liszczak ◽  
Marc R. Mayberg ◽  
Peter McL. Black

✓ Cerebral blood vessels are devoid of vasa vasorum. Therefore, the authors have studied the microarchitecture of the adventitia of large feline cerebral vessels and systemic vessels of the same size, in an effort to determine how the vessels are nourished. The cerebral vessels contain a rete vasorum in the adventitia that is permeable to large proteins and is in continuity with the subarachnoid space. This substructure may be analogous to the systemic vasa vasorum and may contribute to the nutrition of the cerebral arteries.


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