Neuronal damage in gerbils caused by intermittent forebrain ischemia

1999 ◽  
Vol 91 (5) ◽  
pp. 835-842 ◽  
Author(s):  
Takatoshi Sorimachi ◽  
Hiroshi Abe ◽  
Shigekazu Takeuchi ◽  
Ryuichi Tanaka
Keyword(s):  
Neuronal Damage ◽  
Cerebral Arteries ◽  
Ischemic Insult ◽  
Content Type ◽  
Ischemic Episode ◽  
Temporary Occlusion ◽  
Ischemic Depolarization ◽  
The Brain ◽  
Severe Ischemia ◽  
Fine Print

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.

Asymmetry of pressure autoregulation after traumatic brain injury

2003 ◽  
Vol 99 (6) ◽  
pp. 991-998 ◽  
Author(s):  
Eric A. Schmidt ◽  
Marek Czosnyka ◽  
Luzius A. Steiner ◽  
Marcella Balestreri ◽  
Piotr Smielewski ◽  
...  
Keyword(s):  
Head Injuries ◽  
Cerebral Arteries ◽  
Brain Lesion ◽  
Fatal Outcome ◽  
Midline Shift ◽  
Content Type ◽  
Arterial Blood ◽  
Left And Right ◽  
The Brain ◽  
Fine Print

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.

Real-time detection of vascular occlusion and reperfusion of the brain during surgery by using infrared imaging

2002 ◽  
Vol 96 (5) ◽  
pp. 918-923 ◽  
Author(s):  
Joseph C. Watson ◽  
Alexander M. Gorbach ◽  
Ryszard M. Pluta ◽  
Ramin Rak ◽  
John D. Heiss ◽  
...  
Keyword(s):  
Blood Flow ◽  
High Resolution ◽  
Real Time ◽  
Infrared Imaging ◽  
Cerebral Arteries ◽  
Infrared Camera ◽  
Collateral Flow ◽  
Content Type ◽  
The Brain ◽  
Fine Print

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.

Cerebral damage caused by interrupted, repeated arterial occlusion versus uninterrupted occlusion in a focal ischemic model

1994 ◽  
Vol 81 (4) ◽  
pp. 554-559 ◽  
Author(s):  
Gary K. Steinberg ◽  
Nariman Panahian ◽  
Go-Hua Sun ◽  
Carolina M. Maier ◽  
David Kunis
Keyword(s):  
Neuronal Damage ◽  
Rabbit Model ◽  
Total Duration ◽  
Arterial Occlusion ◽  
Focal Ischemia ◽  
Global Ischemia ◽  
Cerebral Injury ◽  
Content Type ◽  
Temporary Occlusion ◽  
Fine Print

✓ Temporary intracranial arterial occlusion is often utilized during the surgical treatment of intracranial aneurysms. Although numerous experimental studies have suggested that repetitive, brief periods of global ischemia cause more severe cerebral injury than a similar single period of global ischemia, this issue has not been extensively studied in relation to focal ischemia. It remains controversial whether it is safer to use brief periods of interrupted, temporary occlusion separated by reperfusion periods, or a more prolonged, single temporary occlusion. This question is addressed in studies on a rabbit model of transient, focal cerebral ischemia. Sixteen anesthetized rabbits underwent transorbital occlusion of the left internal carotid, middle cerebral, and anterior cerebral arteries, with one of two paradigms: uninterrupted occlusion (1 hour of temporary occlusion followed by 5 hours of reperfusion in eight rabbits), or interrupted occlusion (three separate 20-minute periods of occlusion, with 10 minutes of reperfusion between occlusions, followed by 4 hours, 40 minutes of reperfusion in eight rabbits). Histopathological evaluation for ischemic neuronal damage and magnetic resonance imaging studies for ischemic edema were conducted 6 hours after the initial arterial occlusion. The animals in the interrupted, repeated occlusion group showed a 59% decrease in the area of cortical ischemic neuronal damage (mean ± standard error of the mean 10.0% ± 1.7%) compared with the uninterrupted occlusion group (24.4% ± 5%, p = 0.016). There was no difference between the groups in the extent of striatal ischemic damage or area of ischemic edema. These results suggest that interrupted, repeated focal ischemia causes less cortical ischemic injury than uninterrupted transient ischemia of a similar total duration. Although caution should be exercised in extrapolating from these results to the clinical situation, they may have important implications for temporary arterial occlusion during intracranial surgery.

Cerebral aneurysms following radiotherapy for medulloblastoma

1989 ◽  
Vol 70 (4) ◽  
pp. 545-550 ◽  
Author(s):  
Peter J. Benson ◽  
Joo Ho Sung
Keyword(s):  
Cerebral Arteries ◽  
Cerebral Aneurysms ◽  
Content Type ◽  
Histological Features ◽  
Autopsy Examination ◽  
Cerebellar Medulloblastoma ◽  
Radiation Induced ◽  
The Brain ◽  
Fine Print ◽  
Saccular Aneurysms

✓ 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.

Norepinephrine in cerebrospinal fluid of patients with cerebral vasospasm

1982 ◽  
Vol 56 (3) ◽  
pp. 344-349 ◽  
Author(s):  
Taku Shigeno
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Arteries ◽  
Cerebral Aneurysms ◽  
Fluorometric Method ◽  
Content Type ◽  
Highly Sensitive ◽  
Secondary Phenomenon ◽  
Lumbar Cerebrospinal Fluid ◽  
The Brain ◽  
Fine Print

✓ 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.

The recurrent artery of Heubner: Otto Heubner's description of the artery and his influence on pediatrics in Germany

2000 ◽  
Vol 93 (6) ◽  
pp. 1084-1088 ◽  
Author(s):  
Raymond I. Haroun ◽  
Daniele Rigamonti ◽  
Rafael J. Tamargo
Keyword(s):  
Internal Medicine ◽  
Energy Metabolism ◽  
Cerebral Arteries ◽  
Early Research ◽  
Anterior Communicating Artery ◽  
Anatomical Studies ◽  
Content Type ◽  
Morphological Studies ◽  
The Brain ◽  
Fine Print

✓ Although the recurrent artery of Heubner is one of the best known cerebral arteries, little has been written in the neurosurgical or anatomical literature about its discovery. The artery is of primary importance to cerebrovascular surgeons, who identify it during clipping of anterior communicating artery aneurysms. Johann Otto Leonhardt Heubner (1843–1926), who described this artery in 1872, is better known as the father of German pediatrics. He was appointed to the first professorship in Germany exclusively devoted to pediatrics at the Charité Children's Clinic of Berlin University. Although he initially studied internal medicine in Leipzig under Carl Reinhold August Wunderlich and Ernst Leberecht Wagner, his early research involved anatomical studies of the circulation of the brain, from which he described syphilitic endarteritis (Heubner's disease). Finding morphological studies inconclusive, he turned to more physiological experiments. Together with the physiologist Max Rubner, Heubner performed important studies on energy metabolism in infancy, creating the notion of the nutrition quotient. In this article the authors review Heubner's life and scientific discoveries.

Delayed neurological deterioration following resection of arteriovenous malformations of the brain

1999 ◽  
Vol 90 (4) ◽  
pp. 695-701 ◽  
Author(s):  
Michael K. Morgan ◽  
Lali H. S. Sekhon ◽  
Simon Finfer ◽  
Verity Grinnell
Keyword(s):  
Arteriovenous Malformations ◽  
Cerebral Arteries ◽  
Venous Drainage ◽  
Neurological Deficits ◽  
Grading System ◽  
Content Type ◽  
Drainage Networks ◽  
Middle Cerebral Arteries ◽  
The Brain ◽  
Fine Print

Object. The aim of this study was to analyze delayed neurological deficits following surgical resection of arteriovenous malformations (AVMs).Methods. The authors report on a consecutive series of 200 patients with angiographically proven AVMs of the brain that were surgically resected between January 1989 and June 1998. The 30-day mortality rate for patients in this series was 1%, with one death caused by AVM resection and one death attributed to basilar artery aneurysm repair following successful AVM resection. The Spetzler—Martin grading system correlated well with the difficulty of surgery. No permanent incidence of morbidity resulted from resection of Grade I or II AVMs; the percentage of patients with a significant neurological deficit due to resection was 7.8% for those with Grade III lesions and 33.3% for those with Grade IV or V AVMs. However, this grading system did not accurately predict the development of delayed neurological deficits.Ten patients (5%) developed delayed neurological deficits after recovering from anesthesia and surgery. The delayed deficit was due to hemorrhage in four of the 10 patients and all four had undergone resection of AVMs measuring at least 4 cm in diameter. An increase in blood pressure during the first 8 postoperative days precipitated hemorrhage in these patients. Edema arising as a consequence of propagated venous thrombosis (two patients) was associated with extensive venous drainage networks rather than large AVM niduses. Both hemorrhagic and edematous complications can be included under the umbrella term of “arterial-capillary-venous hypertensive syndrome” to describe the common underlying pathogenesis accurately. An additional four patients developed a delayed deficit as a result of vasospasm. Vasospasm occurred when resection had involved extensive dissection of proximal anterior and middle cerebral arteries; in such cases the incidence of vasospasm was 27%.Conclusions. On the basis of their analysis of these complications, the authors recommend strict blood pressure control for patients with lesions measuring 4 cm or more in diameter (particularly those with a deep arterial supply). Thromboprophylaxis with aspirin and heparin is prescribed for patients with extensive venous drainage networks, and prophylactic nimodipine therapy and angiographic surveillance for vasospasm are suggested for patients in whom extensive dissection of proximal anterior or middle cerebral arteries has been necessary.

Possible control of intermittent cerebral ischemia by monitoring of direct-current potentials

2001 ◽  
Vol 95 (3) ◽  
pp. 495-499 ◽  
Author(s):  
Takayuki Sakaki ◽  
Rudolf Graf ◽  
Hiroyuki Nozaki ◽  
Gerhard Rosner ◽  
Wolf-Dieter Heiss
Keyword(s):  
Brain Injury ◽  
Direct Current ◽  
Cerebral Arteries ◽  
Laser Doppler Flow ◽  
Content Type ◽  
Dc Potential ◽  
Temporary Occlusion ◽  
Cerebral Ischemic ◽  
Cerebral Ischemic Damage ◽  
Fine Print

Object. Neurosurgically induced temporary occlusion of intracranial arteries carries the risk of cerebral ischemic damage. Because negative shifts in the cortical direct-current (DC) potential indicate tissue depolarization and, thus, critical ischemic stress, the authors hypothesized that recordings of these potentials could help to determine the optimal duration and frequency of induced intermittent focal ischemia to prevent brain injury. The investigators related the results of DC recordings both to simultaneously recorded decreases in extracellular Ca++ concentration ([Ca++]o), which reflect Ca++ entry into cells, and to histological outcome. Methods. In cats anesthetized with halothane the effects of intermittent brief (10 minutes long, six times [6 × 10-min group]) and prolonged (20 minutes long, three times [3 × 20-min group]) episodes of middle cerebral artery occlusions were compared with those of a single continuous episode (1 × 60-min group). Laser Doppler flow probes and ion-selective microelectrodes were used to measure cerebral blood flow, DC potentials, and [Ca++]o in cortical tissues of ectosylvian gyri. Negative shifts in DC potential were evaluated in the three groups during the entire 60-minute-long period of ischemia and were smallest in the 6 × 10-min group, larger in the 3 × 20-min group, and largest in the 1 × 60-min group. Accordingly, infarct volumes were smallest in the 6 × 10-min group, intermediate in the 3 × 20-min group, and largest in the 1 × 60-min group. Decreases in ischemic [Ca++]o were significantly greater in the 1 × 60-min group than in the two groups in which there were repetitive occlusions, and recovery of [Ca++]o after reperfusion normalized only in the 1 × 60-min group. Conclusions. The DC potential may provide a reliable measure to optimize intermittent ischemia and to achieve minimal ischemic brain injury during temporary neurosurgical occlusion of cerebral arteries.

Subarachnoid hemorrhage and cerebrovascular spasm

1981 ◽  
Vol 55 (6) ◽  
pp. 869-876 ◽  
Author(s):  
O. Petter Eldevik ◽  
Kristian Kristiansen ◽  
Ansgar Torvik
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Morphological Changes ◽  
Autologous Blood ◽  
Cerebral Arteries ◽  
Light And Electron Microscopy ◽  
Brain Vessels ◽  
Content Type ◽  
Perfusion Fixation ◽  
The Brain ◽  
Fine Print

✓ Artificial subarachnoid hemorrhage (SAH) produced by injection of autologous blood into the cisterna magna in dogs gave rise to considerable narrowing or spasm of the basilar artery and its branches, including the posterior cerebral arteries, as demonstrated by cerebral angiography. Repeated cisternal injections of blood at various intervals produced more severe spasm than a single injection. After perfusion-fixation of the brain, the cerebral arteries were examined by light and electron microscopy. None of the animals showed abnormalities in the intima or media of the vessel walls. Previously reported findings of morphological changes due to spasm could not be confirmed. Postmortem examination of brain vessels from nine patients with SAH and arterial spasm showed no specific changes that could be ascribed to spasm.

Ischemic depolarization monitoring: evaluation of protein synthesis in the hippocampal CA1 after brief unilateral ischemia in a gerbil model

2002 ◽  
Vol 97 (1) ◽  
pp. 104-111 ◽  
Author(s):  
Takatoshi Sorimachi ◽  
Hiroshi Abe ◽  
Shigekazu Takeuchi ◽  
Ryuichi Tanaka
Keyword(s):  
Protein Synthesis ◽  
Neuronal Damage ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Ischemic Damage ◽  
Content Type ◽  
Hippocampal Ca1 ◽  
Ischemic Depolarization ◽  
The Relationship ◽  
Fine Print

Object. The authors investigate whether depolarization monitoring is an accurate index of ischemic damage in a gerbil model of unilateral ischemia and assess the effects of brief cerebral ischemia on protein synthesis in this model. Methods. The authors evaluate the relationship between the duration of ischemic depolarization caused by unilateral carotid artery occlusion and ischemia-induced neuronal damage in the CA1 subregion 7 days after ischemia. When the depolarization period exceeded 210 seconds, some neuronal damage was detected, and almost complete neuronal damage was observed when the period exceeded 400 seconds. Uptake of [14C]valine was evaluated in ischemic and nonischemic CA1 subregions. Disturbances in protein synthesis were seen in all animals subjected to sublethal ischemia (≤ 210-second depolarization) after a 10-minute recirculation, and after 2 and 6 hours of recirculation in animals with 90 seconds or more of depolarization. Inhibition of protein synthesis was proportional to the length of the depolarization period. After 1 and 3 days of recirculation, protein synthesis returned to near normal, and some animals with depolarizations greater than 180 to 210 seconds showed an increase in protein synthesis. Protein synthesis in all animals returned to normal levels after 7 days of recirculation. Conclusions. In this study the authors demonstrate that monitoring of ischemic depolarization is a useful method to predict neuronal damage in the hippocampal CA1 in this model, and they identify subtle changes in protein synthesis after brief ischemia. Sublethal ischemia was divided into three categories by its depolarization period (< 90 seconds, 90–180 seconds, and > 180–210 seconds) with regard to changes in protein synthesis.

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