A new model of diffuse brain injury in rats

1994 ◽  
Vol 80 (2) ◽  
pp. 301-313 ◽  
Author(s):  
Montasser A. Abd-Elfattah Foda ◽  
Anthony Marmarou
Keyword(s):  
Brain Injury ◽  
Brain Stem ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Weight Drop ◽  
Group 2 ◽  
The Brain ◽  
Fine Print ◽  
Diffuse Brain ◽  
Group 1

✓ A new model producing diffuse brain injury, without focal brain lesions, has been developed in rats. This has been achieved by allowing a weight of 450 gm to fall onto a metallic disc fixed to the intact skull of the animal which is supported by a foam bed. Two levels of injury were examined by adjusting the height of the falling weight to either 1 m or 2 m. Two groups of animals were studied. Group 1 animals were separated into three subgroups: 10 received a 1-m weight drop, 58 received a 2-m weight drop, and 13 served as controls; all were allowed to breathe spontaneously. Group 2 animals were separated into the same subgroups: four received a 1-m weight drop, six received a 2-m weight drop, and four served as controls; all of these were mechanically ventilated during the procedure. In Group 1, morphological studies using light and electron microscopy were performed at 1, 6, 24, or 72 hours, or 10 days after insult; all Group 2 rats were studied at 24 hours after injury. Results from Group 1 animals showed that no mortality occurred with the 1-m level injury, while 59% mortality was seen with the 2-m level injury. On the other hand, no mortality occurred in Group 2 animals regardless of the level of trauma induced. However, the morphological changes observed in both groups were similar. Gross pathological examination did not reveal any supratentorial focal brain lesion regardless of the severity of the trauma. Petechial hemorrhages were noticed in the brain stem at the 2-m level injury. Microscopically, the model produced a graded widespread injury of the neurons, axons, and microvasculature. Neuronal injury was mainly observed bilaterally in the cerebral cortex. Brain edema, in the form of pericapillary astrocytic swelling, was also noted in these areas of the cerebral cortex and in the brain stem. Most importantly, the trauma resulted in a massive diffuse axonal injury that primarily involved the corpus callosum, internal capsule, optic tracts, cerebral and cerebellar peduncles, and the long tracts in the brain stem. It is concluded that this model would be suitable for studying neuronal, axonal, and vascular changes associated with diffuse brain injury.

Influence of oxygen therapy on glucose—lactate metabolism after diffuse brain injury

2004 ◽  
Vol 101 (2) ◽  
pp. 323-329 ◽  
Author(s):  
Michael Reinert ◽  
Benoit Schaller ◽  
Hans Rudolf Widmer ◽  
Rolf Seiler ◽  
Ross Bullock
Keyword(s):  
Brain Injury ◽  
Brain Tissue ◽  
Brain Metabolism ◽  
Arterial Line ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Lactate Levels ◽  
The Brain ◽  
Fine Print ◽  
Diffuse Brain

Object. Severe traumatic brain injury (TBI) imposes a huge metabolic load on brain tissue, which can be summarized initially as a state of hypermetabolism and hyperglycolysis. In experiments O2 consumption has been shown to increase early after trauma, especially in the presence of high lactate levels and forced O2 availability. In recent clinical studies the effect of increasing O2 availability on brain metabolism has been analyzed. By their nature, however, clinical trauma models suffer from a heterogeneous injury distribution. The aim of this study was to analyze, in a standardized diffuse brain injury model, the effect of increasing the fraction of inspired O2 on brain glucose and lactate levels, and to compare this effect with the metabolism of the noninjured sham-operated brain. Methods. A diffuse severe TBI model developed by Foda and Maramarou, et al., in which a 420-g weight is dropped from a height of 2 m was used in this study. Forty-one male Wistar rats each weighing approximately 300 g were included. Anesthesized rats were monitored by placing a femoral arterial line for blood pressure and blood was drawn for a blood gas analysis. Two time periods were defined: Period A was defined as preinjury and Period B as postinjury. During Period B two levels of fraction of inspired oxygen (FiO2) were studied: air (FiO2 0.21) and oxygen (FiO2 1). Four groups were studied including sham-operated animals: air-air-sham (AAS); air-O2-sham (AOS); air-air-trauma (AAT); and air-O2-trauma (AOT). In six rats the effect of increasing the FiO2 on serum glucose and lactate was analyzed. During Period B lactate values in the brain determined using microdialysis were significantly lower (p < 0.05) in the AOT group than in the AAT group and glucose values in the brain determined using microdialysis were significantly higher (p < 0.04). No differences were demonstrated in the other groups. Increasing the FiO2 had no significant effect on the serum levels of glucose and lactate. Conclusions. Increasing the FiO2 influences dialysate glucose and lactate levels in injured brain tissue. Using an FiO2 of 1 influences brain metabolism in such a way that lactate is significantly reduced and glucose significantly increased. No changes in dialysate glucose and lactate values were found in the noninjured brain.

Evaluation of brain-stem dysfunction following severe fluid-percussion head injury to the cat

1991 ◽  
Vol 74 (2) ◽  
pp. 270-277 ◽  
Author(s):  
Katsuji Shima ◽  
Anthony Marmarou
Keyword(s):  
Brain Stem ◽  
Content Type ◽  
Fluid Percussion ◽  
Fluid Percussion Injury ◽  
Brain Stem Injury ◽  
Group 2 ◽  
High Level ◽  
Subarachnoid Hemorrhages ◽  
Fine Print ◽  
Group 1

✓ The degree of brain-stem dysfunction associated with high-level fluid-percussion injury (3.0 to 3.8 atm) was investigated in anesthetized cats. Measurements were made of the animals' intracranial pressure (ICP), pressure-volume index (PVI), far-field brain-stem auditory evoked responses (BAER's), and cerebral blood flow (CBF). The animals were classified into two groups based on the severity of neuropathological damage to the brain stem after trauma: Group 1 had mild intraparenchymal and subarachnoid hemorrhages and Group 2 had severe intraparenchymal and subarachnoid hemorrhages. The ICP values in Group 1 were insignificantly lower than those in Group 2, while the PVI values in Group 2 were clearly lower (p < 0.05). Immediately after the injury, peaks II, III, and IV of the BAER's demonstrated a transitory and marked suppression. One Group 1 and two Group 2 animals showed the disappearance of peak V. In Group 1, the latencies of peak II, III, and IV gradually increased until 60 to 150 minutes postinjury, then returned to 95% of baseline value at 8 hours; however, the animals in Group 2 showed poor recovery of latencies. Two hours after brain injury, the CBF decreased to 40% of the preinjury measurement in both groups (p < 0.001). In contrast to Group 2, the CBF in Group 1 returned to 86.8% of the preinjury measurement by 8 hours following the injury. Changes in PVI, BAER, and CBF correlated well with the degree of brain-stem injury following severe head injury'- These data indicate that high-level fluid-percussion injury (> 3.0 atm) is predominantly a model of brain-stem injury.

Neurobehavioral protection by the neuronal calcium channel blocker Ziconotide in a model of traumatic diffuse brain injury in rats

2000 ◽  
Vol 93 (5) ◽  
pp. 821-828 ◽  
Author(s):  
Robert F. Berman ◽  
Bon H. Verweij ◽  
J. Paul Muizelaar
Keyword(s):  
Brain Injury ◽  
Calcium Channel ◽  
Cognitive Deficits ◽  
Channel Blocker ◽  
Neuroprotective Effects ◽  
Content Type ◽  
Diffuse Brain Injury ◽  
Severe Motor ◽  
Fine Print ◽  
Diffuse Brain

Object. Abnormal accumulation of intracellular calcium following traumatic brain injury (TBI) is thought to contribute to a cascade of cellular events that lead to neuropathological conditions. Therefore, the possibility that specific calcium channel antagonists might exert neuroprotective effects in TBI has been of interest. The focus of this study was to examine whether Ziconotide produces such neuroprotective effects.Methods. The authors report that the acceleration—deceleration model of TBI developed by Marmarou, et al., induces a long-lasting deficit of neuromotor and behavioral function. The voltage-sensitive calcium channel blocker Ziconotide (also known as SNX-111 and CI-1009) exerts neuroprotective effects in this model of diffuse brain injury (DBI) in rats. The dose and time of injection of Ziconotide chosen for the present study was based on the authors' previous biochemical studies of mitochondria. Rats were trained in a series of motor and memory tasks, following which they were subjected to DBI using the Marmarou, et al., model. At 3, 5, and 24 hours, all rats were injected with 2 mg/kg Ziconotide for a total cumulative dose of 6 mg/kg Ziconotide. Control brain-injured animals were injected with an equal volume of saline vehicle at each of these time points. The rats were tested for motor and cognitive performance at 1, 3, 7, 14, 21, 28, 35, and 42 days postinjury. Saline-treated rats displayed severe motor and cognitive deficits after DBI. Compared with saline-treated control animals, rats treated with Ziconotide displayed better motor performance during inclined plane, beam balance, and beam walk tests; improved memory while in the radial arm maze; and improved learning while in the Morris water maze.Conclusions. These results demonstrated that the acceleration—deceleration model, which had been developed by Marmarou, et al., induces severe motor and cognitive deficits. We also demonstrated that Ziconotide exhibits substantial neuroprotective activity in this model of TBI. Improvement was observed in both motor and cognitive tasks, even though treatment was not initiated until 3 hours after injury. These findings support the development of neuronal N-type calcium channel antagonists as useful therapeutic agents in the treatment of TBI.

A new model of diffuse brain injury in rats

1994 ◽  
Vol 80 (2) ◽  
pp. 291-300 ◽  
Author(s):  
Anthony Marmarou ◽  
Montasser A. Abd-Elfattah Foda ◽  
Wimer van den Brink ◽  
J. Campbell ◽  
H. Kita ◽  
...  
Keyword(s):  
Brain Injury ◽  
Mortality Rate ◽  
Cause Of Death ◽  
Skull Fracture ◽  
Guide Tube ◽  
Diffuse Brain Injury ◽  
Group 2 ◽  
The Impact ◽  
Diffuse Brain ◽  
Group 1

✓ This report describes the development of an experimental head injury model capable of producing diffuse brain injury in the rodent. A total of 161 anesthetized adult rats were injured utilizing a simple weight-drop device consisting of a segmented brass weight free-falling through a Plexiglas guide tube. Skull fracture was prevented by cementing a small stainless-steel disc on the calvaria. Two groups of rats were tested: Group 1, consisting of 54 rats, to establish fracture threshold; and Group 2, consisting of 107 animals, to determine the primary cause of death at severe injury levels. Data from Group 1 animals showed that a 450-gm weight falling from a 2-m height (0.9 kg-m) resulted in a mortality rate of 44% with a low incidence (12.5%) of skull fracture. Impact was followed by apnea, convulsions, and moderate hypertension. The surviving rats developed decortication flexion deformity of the forelimbs, with behavioral depression and loss of muscle tone. Data from Group 2 animals suggested that the cause of death was due to central respiratory depression; the mortality rate decreased markedly in animals mechanically ventilated during the impact. Analysis of mathematical models showed that this mass-height combination resulted in a brain acceleration of 900 G and a brain compression gradient of 0.28 mm. It is concluded that this simple model is capable of producing a graded brain injury in the rodent without a massive hypertensive surge or excessive brain-stem damage.

Arteriovenous malformations in the posterior fossa

1977 ◽  
Vol 47 (1) ◽  
pp. 50-56 ◽  
Author(s):  
Hiroshi Matsumura ◽  
Yasumasa Makita ◽  
Kuniyuki Someda ◽  
Akinori Kondo
Keyword(s):  
Arteriovenous Malformation ◽  
Brain Stem ◽  
Posterior Fossa ◽  
Arteriovenous Malformations ◽  
Cerebellopontine Angle ◽  
Anterior Part ◽  
Content Type ◽  
The Brain ◽  
Fine Print

✓ We have operated on 12 of 14 cases of arteriovenous malformation (AVM) in the posterior fossa since 1968, with one death. The lesions were in the cerebellum in 10 cases (three anteromedial, one central, three lateral, and three posteromedial), and in the cerebellopontine angle in two; in two cases the lesions were directly related to the brain stem. The AVM's in the anterior part of the cerebellum were operated on through a transtentorial occipital approach.

Predictive value of brain-stem auditory evoked potentials in children with post-traumatic coma produced by diffuse brain injury

1995 ◽  
Vol 11 (7) ◽  
pp. 400-405 ◽  
Author(s):  
J. Bosch Blancafort ◽  
M. Olesti Marco ◽  
J. M. Poch Puig ◽  
E. Rubio Garc�a ◽  
P. Nogu�s Bara ◽  
...  
Keyword(s):  
Brain Injury ◽  
Evoked Potentials ◽  
Brain Stem ◽  
Predictive Value ◽  
Auditory Evoked Potentials ◽  
Diffuse Brain Injury ◽  
Post Traumatic ◽  
Traumatic Coma ◽  
Diffuse Brain

Cervical spinal cord in experimental hydrocephalus

1972 ◽  
Vol 37 (5) ◽  
pp. 538-542 ◽  
Author(s):  
George J. Dohrmann
Keyword(s):  
Spinal Cord ◽  
Brain Stem ◽  
Cervical Spinal Cord ◽  
Central Canal ◽  
Content Type ◽  
Experimental Hydrocephalus ◽  
Physiological Pressure ◽  
The Brain ◽  
Shunting Procedure ◽  
Fine Print

✓ Adult dogs were rendered hydrocephalic by the injection of kaolin into the cisterna magna. One group of dogs was sacrificed 1 month after kaolin administration, and ventriculojugular shunts were performed on the other group. Hydrocephalic dogs with shunts were sacrificed 1 day or 1 week after the shunting procedure. All dogs were perfused with formalin at physiological pressure, and the brain stem and cervical spinal cord were examined by light microscopy. Subarachnoid granulomata encompassed the superior cervical spinal cord and dependent surface of the brain stem. Rarefaction of the posterior white columns and clefts or cavities involving the gray matter posterior to the central canal and/or posterior white columns were present in the spinal cords of both hydrocephalic and shunted hydrocephalic dogs. Predominantly in the dogs with shunts, hemorrhages were noted in the spinal cord in association with the clefts or cavities. A mechanism of ischemia followed by reflow of blood is postulated to explain the hemorrhages in the spinal cords of hydrocephalic dogs with shunts.

Predictive value of serum prolactin levels measured immediately after transsphenoidal surgery

2002 ◽  
Vol 97 (2) ◽  
pp. 307-314 ◽  
Author(s):  
Arun P. Amar ◽  
William T. Couldwell ◽  
Joseph C. T. Chen ◽  
Martin H. Weiss
Keyword(s):  
Prolactin Level ◽  
Serum Prolactin ◽  
Surgical Removal ◽  
Consecutive Series ◽  
Cure Rate ◽  
Content Type ◽  
Group 2 ◽  
Fine Print ◽  
Group 1

Object. Prolactin-secreting pituitary adenomas may be managed by surgery, medication, radiotherapy, or observation. The authors reviewed a consecutive series of patients who were followed for at least 5 years after surgery to assess the prognostic significance of preoperative factors (tumor size and prolactin level) and an immediate postoperative factor (prolactin level obtained the morning after surgery) on long-term hormonal outcome, thereby clarifying the indications for surgical removal of tumor, the definition of successful treatment outcomes, and the nature of “recurrent” tumors. Methods. Between 1979 and 1991, 241 patients with prolactinomas underwent transsphenoidal resection. Nineteen patients were lost to follow-up review, whereas the remaining 222 patients underwent measurement of their prolactin levels on postoperative Day 1 (POD 1), at 6 and 12 weeks, and every 6 months thereafter for a minimum of 5 years. On POD 1, prolactin levels in 133 patients (Group 1) were lower than 10 ng/ml, in 43 patients (Group 2) between 10 and 20 ng/ml, and in 46 patients (Group 3) higher than 20 ng/ml. At 6 and 12 weeks, normal prolactin levels (≤ 20 ng/ml) were measured in 132 (99%) of the 133 patients in Group 1 but only in 32 (74%) of the 43 patients in Group 2. By 5 years postoperatively, normal levels of prolactin were still measured in 130 patients (98%) in Group 1 compared with only five patients (12%) in Group 2. No patient with a prolactin level lower than 3 ng/ml on POD 1 was found to have an elevated hormone level at 5 years. The likelihood of a long-term chemical cure was greater for patients with microadenomas (91% cure rate) than for those with macroadenomas (33%). Preoperative prolactin levels also correlated with hormonal outcome. Conclusions. Prolactin levels lower than 10 ng/ml on POD 1 predict a long-term chemical cure in patients with microadenomas (100% cure rate) and those with macroadenomas (93% cure rate). In contrast, a cure is not likely to be obtained in patients with normal levels ranging between 10 and 20 ng/ml on POD 1 if they harbor macroadenomas (0% cure rate). A recurrence reported several years after surgery probably represents the presence of persistent tumor that was not originally removed. If the initial operation was performed by an experienced surgeon, however, reoperation is not likely to yield a chemical cure.

Cerebral cysticercosis with aqueductal obstruction

1980 ◽  
Vol 53 (2) ◽  
pp. 252-255 ◽  
Author(s):  
Tung Pui Poon ◽  
Edward J. Arida ◽  
Wolodymyr P. Tyschenko
Keyword(s):  
Intracranial Hypertension ◽  
Brain Stem ◽  
Normal Pressure Hydrocephalus ◽  
Signs And Symptoms ◽  
Normal Pressure ◽  
Content Type ◽  
Neurological Signs ◽  
Cerebral Cysticercosis ◽  
The Brain ◽  
Fine Print

✓ The authors report a case of cerebral cysticercosis which presented with generalized nonspecific neurological signs and symptoms attributed to acute aqueductal obstruction, with concomitant intracranial hypertension. These were characteristic intracranial calcifications along with angiographically demonstrated signs of hydrocephalus. Contrast encephalography clearly demonstrated aqueductal obstruction. Pathologically, the aqueductal obstruction was shown to be due to parasitic invasion of the brain stem with compression of the aqueduct. The presence of typical intracranial calcification in conjunction with either obstructive or normal-pressure hydrocephalus should alert the observer to the possibility of cerebral cysticercosis.

Odontoid compression of the brain stem in a patient with rheumatoid arthritis

1980 ◽  
Vol 53 (6) ◽  
pp. 841-845 ◽  
Author(s):  
Harold P. Smith ◽  
Venkata R. Challa ◽  
Eben Alexander
Keyword(s):  
Rheumatoid Arthritis ◽  
Brain Stem ◽  
Neurological Deficit ◽  
Neurological Symptoms ◽  
Direct Compression ◽  
Content Type ◽  
Vertical Subluxation ◽  
Progressive Neurological Deficit ◽  
The Brain ◽  
Fine Print

✓ Cervical spine involvement by rheumatoid arthritis is common; brain-stem compression secondary to vertical subluxation of the odontoid in patients with rheumatoid arthritis is rare. Vertical subluxation results from 1) destruction of the transverse atlantal, apical, and alar ligaments of the atlas and odontoid, and 2) bone resorption in the occipital condyles, lateral masses of the atlas, and basilar processes of the skull. Neurological symptoms result from direct compression of the brain stem or from ischemia secondary to compression of vertebral arteries, anterior spinal arteries, or small perforating arteries of the brain stem and spinal cord. A case is reported in which a slowly progressive neurological deficit developed in a woman with rheumatoid arthritis following a fall from a stretcher. Neurological symptoms represented direct compression of the medulla by the dens, a mechanism confirmed at operation and autopsy. Recognition of progressive neurological deficit is often difficult in patients with rheumatoid arthritis because of their inactivity and their atrophic and immobile joints, but is essential if appropriate decompressive or stabilizing procedures are to be done. In patients with vertical subluxation of the dens, the transoral approach with removal of the odontoid is recommended. Decompression should be extensive, including the fibrous capsule around the odontoid and overlying synovial tissue as well as the odontoid itself.

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