Effect of initially limited resuscitation in a combined model of fluid-percussion brain injury and severe uncontrolled hemorrhagic shock

2000 ◽  
Vol 93 (2) ◽  
pp. 305-314 ◽  
Author(s):  
Susan A. Stern ◽  
Brian J. Zink ◽  
Michelle Mertz ◽  
Xu Wang ◽  
Steven C. Dronen
Keyword(s):  
Brain Injury ◽  
Physiological Parameters ◽  
Content Type ◽  
Group Iii ◽  
Fluid Percussion ◽  
Group I ◽  
Group Ii ◽  
Goal Map ◽  
Uncontrolled Hemorrhage ◽  
Fine Print

Object. Studies of isolated uncontrolled hemorrhage have indicated that initial limited resuscitation improves survival. Limited resuscitation has not been studied in combined traumatic brain injury and uncontrolled hemorrhage. In this study the authors evaluated the effects of limited resuscitation on outcome in combined fluid-percussion injury (FPI) and uncontrolled hemorrhage.Methods. Twenty-four swine weighing 17 to 24 kg each underwent FPI (3 atm) and hemorrhage to a mean arterial pressure (MAP) of 30 mm Hg in the presence of a 4-mm aortic tear. Group I (nine animals) was initially resuscitated to a goal MAP of 60 mm Hg; Group II (nine animals) was resuscitated to a goal MAP of 80 mm Hg; and Group III (control; six animals) was not resuscitated. After 60 minutes, the aortic hemorrhage was controlled and the animals were resuscitated to baseline physiological parameters and observed for 150 minutes.Mortality rates were 11%, 50%, and 100% for Groups I, II, and III, respectively (Fisher's exact test; p = 0.002). The total hemorrhage volume was greater in Group II (69 ± 32 ml/kg), as compared with Group I (41 ± 18 ml/kg) and Group III (37 ± 3 ml/kg) according to analysis of variance (p < 0.05). In surviving animals, cerebral perfusion pressure, cerebral blood flow (CBF), cerebral venous O2 saturation (ScvO2), and cerebral metabolic rate of O2 did not differ among groups. Although CBF was approximately 50% of baseline during the period of limited resuscitation in Group I, ScvO2 remained greater than 60%, and arteriovenous O2 differences remained within normal limits.Conclusions. In this model of FPI and uncontrolled hemorrhage, early aggressive resuscitation, which is currently recommended, resulted in increased hemorrhage and failure to optimize cerebrovascular parameters. In addition, a 60-minute period of moderate hypotension (MAP = 60 mm Hg) was well tolerated and did not compromise cerebrovascular hemodynamics, as evidenced by physiological parameters that remained within the limits of cerebral autoregulation.

Role of estrogen deficiency in the formation and progression of cerebral aneurysms. Part I: experimental study of the effect of oophorectomy in rats

2005 ◽  
Vol 103 (6) ◽  
pp. 1046-1051 ◽  
Author(s):  
Mohammad A. Jamous ◽  
Shinji Nagahiro ◽  
Keiko T. Kitazato ◽  
Junichiro Satomi ◽  
Koichi Satoh
Keyword(s):  
Cerebral Aneurysm ◽  
Cerebral Aneurysms ◽  
Bilateral Oophorectomy ◽  
Gelatinase Activity ◽  
Content Type ◽  
Group Iii ◽  
Group I ◽  
Group Ii ◽  
Fine Print

Object. Estrogen has been shown to play a central role in vascular biology. Although it may exert beneficial vascular effects, its role in the pathogenesis of cerebral aneurysms remains to be determined. To elucidate the role of hormones further, the authors examined the effects of bilateral oophorectomy on the formation and progression of cerebral aneurysms in rats. Methods. Forty-five female, 7-week-old Sprague—Dawley rats were divided into three equal groups. Group I consisted of intact rats (controls). To induce cerebral aneurysms, the animals in Groups II and III were subjected to ligation of the right common carotid and bilateral posterior renal arteries. One month later, the rats in Group II underwent bilateral oophorectomy. Three months after the experiment began all animals were killed and cerebral vascular corrosion casts were prepared and screened for cerebral aneurysms by using a scanning electron microscope. Plasma was used to determine the level of estradiol and the gelatinase activity. Hypertension developed in all rats except those in the control group. The estradiol level was significantly lower in Group II than in the other groups (p < 0.01). The incidence of cerebral aneurysm formation in Group II (60%) was three times higher than that in Group III (20%), and the mean size of aneurysms in Group II (76 ± 27 µm, mean ± standard deviation) was larger than that in Group III (28 ± 4.6 µm) (p < 0.05). No aneurysm developed in control animals (Group I), and there was no significant difference in plasma gelatinase activity among the three groups. Conclusions. The cerebral aneurysm model was highly reproducible in rats. Bilateral oophorectomy increased the susceptibility of rats to aneurysm formation, indicating that hormones play a role in the pathogenesis of cerebral aneurysms.

Microsurgical C-2 ganglionectomy for chronic intractable occipital pain

1998 ◽  
Vol 89 (3) ◽  
pp. 359-365 ◽  
Author(s):  
Andres M. Lozano ◽  
Graham Vanderlinden ◽  
Robert Bachoo ◽  
Peter Rothbart
Keyword(s):  
Axonal Regeneration ◽  
Excellent Result ◽  
Spontaneous Pain ◽  
Content Type ◽  
Group I ◽  
Experienced Pain ◽  
Pain Outcome ◽  
Group Ii ◽  
Fine Print

Object. The authors evaluated the effectiveness of microsurgical C-2 ganglionectomy in 39 patients with medically refractory chronic occipital pain. In this procedure the neurons transmitting sensory inputs from the occiput are removed and, unlike peripheral nerve ablation, axonal regeneration is not possible. Methods. The patients in this series had symptoms for 1 to 43 years. In 22 patients the occipital pain was caused by trauma; in 17 patients the pain was spontaneous. Pain relief failed in 17 patients who had undergone a previous occipital neurectomy or C-2 rhizolysis. Twenty-three patients experienced pain that was described as shocklike, electric, shooting, jabbing, stabbing, sharp, or exploding (Group I). Eight patients described their pain as dull, pounding, aching, throbbing, or pressurelike (Group II). The patients underwent unilateral or bilateral C-2 open microsurgical ganglionectomies. The postoperative follow-up period ranged from 19 to 48 months. Nineteen patients experienced an excellent result (> 90% reduction in pain). Pain caused by trauma or that described using Group I terms responded best to ganglionectomy (80% good or excellent response). In contrast, the majority of the patients with nontraumatic pain or those described using Group II descriptors did not achieve favorable results. Conclusions. The authors conclude that: 1) patients who suffer from chronic occipital pain after having sustained injury obtain worthwhile benefit from microsurgical C-2 ganglionectomy; 2) patients suffering from migraine, tension, and vascular headaches involving the occipital area are most often not helped by this operation; and 3) terms such as “shock,” “electric,” “shooting,” “jabbing,” and “sharp” used to describe occipital pain predict a favorable pain outcome following a C-2 ganglionectomy.

Failure of third ventriculostomy in the treatment of aqueductal stenosis in children

1999 ◽  
Vol 90 (3) ◽  
pp. 448-454 ◽  
Author(s):  
Giuseppe Cinalli ◽  
Christian Sainte-Rose ◽  
Paul Chumas ◽  
Michel Zerah ◽  
Francis Brunelle ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Aqueductal Stenosis ◽  
Third Ventriculostomy ◽  
Content Type ◽  
Group I ◽  
Endoscopic Guidance ◽  
Group Ii ◽  
Fine Print

Object. The goal of this study was to analyze the types of failure and long-term efficacy of third ventriculostomy in children.Methods. The authors retrospectively analyzed clinical data obtained in 213 children affected by obstructive triventricular hydrocephalus who were treated by third ventriculostomy between 1973 and 1997. There were 120 boys and 93 girls. The causes of the hydrocephalus included: aqueductal stenosis in 126 cases; toxoplasmosis in 23 cases, pineal, mesencephalic, or tectal tumor in 42 cases; and other causes in 22 cases. In 94 cases, the procedure was performed using ventriculographic guidance (Group I) and in 119 cases by using endoscopic guidance (Group II). In 19 cases (12 in Group I and seven in Group II) failure was related to the surgical technique. Three deaths related to the technique were observed in Group I. For the remaining patients, Kaplan—Meier survival analysis showed a functioning third ventriculostomy rate of 72% at 6 years with a mean follow-up period of 45.5 months (range 4 days–17 years). No significant differences were found during long-term follow up between the two groups. In Group I, a significantly higher failure rate was seen in children younger than 6 months of age, but this difference was not observed in Group II. Thirty-eight patients required reoperation (21 in Group I and 17 in Group II) because of persistent or recurrent intracranial hypertension. In 29 patients shunt placement was necessary. In nine patients in whom there was radiologically confirmed obstruction of the stoma, the third ventriculostomy was repeated; this was successful in seven cases. Cine phase-contrast (PC) magnetic resonance (MR) imaging studies were performed in 15 patients in Group I at least 10 years after they had undergone third ventriculostomy (range 10–17 years, median 14.3 years); this confirmed long-term patency of the stoma in all cases.Conclusions. Third ventriculostomy effectively controls obstructive triventricular hydrocephalus in more than 70% of children and should be preferred to placement of extracranial cerebrospinal shunts in this group of patients. When performed using ventriculographic guidance, the technique has a higher mortality rate and a higher failure rate in children younger than 6 months of age and is, therefore, no longer preferred. When third ventriculostomy is performed using endoscopic guidance, the same long-term results are achieved in children younger than 6 months of age as in older children and, thus, patient age should no longer be considered as a contraindication to using the technique. Delayed failures are usually secondary to obstruction of the stoma and often can be managed by repeating the procedure. Midline sagittal T2-weighted MR imaging sequences combined with cine PC MR imaging flow measurements provide a reliable tool for diagnosis of aqueductal stenosis and for ascertaining the patency of the stoma during follow-up evaluation.

Cerebral protection by intermittent reperfusion during temporary focal ischemia in the rat

1996 ◽  
Vol 85 (5) ◽  
pp. 923-928 ◽  
Author(s):  
Carlos A. David ◽  
Ricardo Prado ◽  
W. Dalton Dietrich
Keyword(s):  
Arterial Occlusion ◽  
Focal Ischemia ◽  
Global Ischemia ◽  
Cerebral Injury ◽  
Histopathological Analysis ◽  
Content Type ◽  
Group I ◽  
Group Ii ◽  
Temporary Clipping ◽  
Fine Print

✓ Temporary arterial occlusion has been routinely used as an adjunct in intracranial aneurysm surgery. This has commonly been performed using a protocol of multiple short periods of occlusion alternating with periods of restoration of normal circulation. Recently, the logical basis of this method has come under scrutiny. There is extensive experimental evidence to suggest that repetitive, brief periods of global ischemia may cause more severe cerebral injury than an equivalent single period of global ischemia. Only recently has this issue begun to be addressed with regard to focal ischemia. Hence, despite the common use of temporary clipping, little experimental data are available regarding the ischemic consequences of temporary arterial occlusion with periods of reperfusion versus uninterrupted temporary occlusion. To investigate this issue, a protocol of occlusion/reperfusion that simulates the temporal profile that occurs during surgery was performed in a rat model of focal ischemia. Sixteen anesthetized Sprague—Dawley rats were divided into two groups. The animals in Group I underwent 60 minutes of uninterrupted middle cerebral artery occlusion and the animals in Group II were subjected to six separate 10-minute occlusion periods with 5 minutes of reperfusion between occlusions. Histopathological analysis was performed 72 hours postischemia. Group I had significantly increased mean infarction volumes (50.0 ± 12.1 mm3) compared to Group II (8.7 ± 3.1 mm3) (p = 0.008). Injuries in Group I occurred in both the cortex and striatum, whereas Group II showed only striatal injuries. Furthermore, the extent of the injuries in Group II was less severe, characterized by ischemic neuronal injury rather than frank infarction. The results indicate that intermittent reperfusion is neuroprotective during temporary focal ischemia and support the hypothesis that intermittent reperfusion is beneficial if temporary clipping is required during aneurysm repair.

Changes in CSF pressure after mannitol in patients with and without elevated CSF pressure

1988 ◽  
Vol 69 (6) ◽  
pp. 869-876 ◽  
Author(s):  
Patrick Ravussin ◽  
Mounir Abou-Madi ◽  
David Archer ◽  
René Chiolero ◽  
James Freeman ◽  
...  
Keyword(s):  
Intracranial Hypertension ◽  
Venous Pressure ◽  
Tumor Resection ◽  
Fluid Pressure ◽  
Content Type ◽  
Csf Pressure ◽  
Arterial Blood ◽  
Group I ◽  
Group Ii ◽  
Fine Print

✓ In view of the current concern that rapid infusion of mannitol might initially aggravate intracranial hypertension, the effects of a mannitol infusion on lumbar cerebrospinal fluid pressure (CSFP) were investigated in 49 patients. The studies were performed when the patients were under general anesthesia prior to elective craniotomy for tumor resection or intracerebral aneurysm clipping. The patients were divided into two groups: 24 patients with normal CSFP (Group I, mean CSFP 10.5 mm Hg) and 25 with raised CSFP (Group II, mean CSFP 20.8 mm Hg). Measurements of CSFP, mean arterial blood pressure (MABP), and central venous pressure (CVP) were made serially during and after the infusion of 20% mannitol (1 gm ⋅ kg−1 infused over a 10-minute interval). In both groups, mannitol infusion provoked a fall in MABP and an increase in CVP. An immediate increase in CSFP was observed in Group II, whereas CSFP increased transiently but significantly in Group I. Analysis of the arterial and venous driving pressures which contribute to CSFP suggests that the transient increase in CSFP after mannitol in Group I was partly due to the increase in CVP. The presence of intracranial hypertension may thus alter the CSFP response to arterial and venous pressure changes. Cerebral blood volume (CBV) was measured in dogs in a separate study analogous to the human protocol. The CBV increased approximately 25% over control values after mannitol infusion both in the normal animals and in those with CSFP raised by an epidural balloon. The response of the CSFP to mannitol infusion differed between both groups in a fashion similar to that observed in the human subjects. Thus, differences in CBV changes after mannitol do not account for the difference in CSFP response between normal subjects and those with raised CSFP.

Subthalamic nucleus stimulation for Parkinson disease: benefits observed in levodopa-intolerant patients

2001 ◽  
Vol 95 (2) ◽  
pp. 213-221 ◽  
Author(s):  
Yoichi Katayama ◽  
Masahiko Kasai ◽  
Hideki Oshima ◽  
Chikashi Fukaya ◽  
Takamitsu Yamamoto ◽  
...  
Keyword(s):  
Parkinson Disease ◽  
Subthalamic Nucleus ◽  
Large Dose ◽  
Daily Activity ◽  
Daily Activities ◽  
Content Type ◽  
Percentage Time ◽  
Group I ◽  
Group Ii ◽  
Fine Print

Object. A blinded evaluation of the effects of subthalamic nucleus (STN) stimulation was performed in levodopaintolerant patients with Parkinson disease (PD). These patients (Group I, seven patients) were moderately or severely disabled (Hoehn and Yahr Stages III–V during the off period), but were receiving only a small dose of medication (levodopa-equivalent dose [LED] 0–400 mg/day) because they suffered unbearable side effects. The results were analyzed in comparison with those obtained in patients with advanced PD (Group II, seven patients) who were severely disabled (Hoehn and Yahr Stages IV and V during the off period), but were treated with a large dose of medication (500–990 mg/day). Methods. The patients were evaluated twice at 6 to 8 months after surgery. To determine the actual benefits afforded by STN stimulation to their overall daily activities, the patients were maintained on their medication regimen with optimal doses and schedules. Stimulation was turned off overnight for at least 12 hours. It was turned on in the morning (or remained turned off), and each patient's best and worst scores on the Unified Parkinson's Disease Rating Scale during waking daytime activity were recorded as on- and off-period scores, respectively. The order of assessment with respect to whether stimulation was occurring was determined randomly. The STN stimulation markedly improved daily activity and total motor scores in Group I patients. The percentage time of immobility (Hoehn and Yahr Stages IV and V) became 0% in patients who were intermittently immobile while not receiving stimulation. Improvements were demonstrated in tremor, rigidity, akinesia, and gait subscores. The STN stimulation produced less marked but still noticeable improvements in the daily activity and total motor scores in Group II patients. The percentage time of immobility as well as the LED was reduced in patients who displayed intermittent immobility with pronounced motor fluctuations while not receiving stimulation. Improvements were demonstrated in tremor, rigidity, and dyskinesia subscores in these patients. In contrast, STN stimulation did not improve the overall daily activities at all in patients who had become unresponsive to a tolerable dose of levodopa and were continuously immobile, even though these patients' tremor and rigidity subscores were still improved by stimulation. Conclusions. Consistent with earlier findings, the great benefit of STN stimulation in levodopa-intolerant patients is that STN stimulation can reduce the level of required levodopa medication. This suggests that STN stimulation could be a therapeutic option for patients with less-advanced PD by allowing levodopa medication to be maintained at as low a dose as possible, and to prevent adverse reactions to the continued use of large-dose levodopa.

Loss of forebrain cholinergic neurons following fluid-percussion injury: implications for cognitive impairment in closed head injury

1995 ◽  
Vol 83 (3) ◽  
pp. 496-502 ◽  
Author(s):  
Richard H. Schmidt ◽  
M. Sean Grady
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Head Injury ◽  
Cholinergic Neurons ◽  
Nucleus Basalis ◽  
Neuron Loss ◽  
Content Type ◽  
Fluid Percussion ◽  
Concussive Injury ◽  
Fine Print

✓ Disturbances in memory, concentration, and problem solving are common after even mild to moderate traumatic brain injury. Because these functions are mediated in part by forebrain cholinergic and catecholaminergic innervation, in this study the authors sought to determine if experimental concussive injury produces detectable morphological damage to these systems. Fluid-percussion head injury, sufficient to cause a 13- to 14-minute loss of righting reflex, was produced in rats that had been anesthetized with halothane. Injury was delivered either at midline or 2 mm off midline and compared with appropriate sham-injured controls. After 11 to 15 days, the rat brains were stained in serial sections for choline acetyltransferase, tyrosine hydroxylase, dopamine β-hydroxylase, acetylcholinesterase, and nicotinamide adenine dinucleotide phosphate diaphorase. Cell counts were determined for the entire population of ventrobasal forebrain cholinergic cells. Midline injury produced a bilateral loss of cholinergic neurons averaging 36% in area Ch1 (medial septal nucleus), 45% in Ch2 (nucleus of the diagonal band of Broca), and 41% in Ch4 (nucleus basalis of Meynart), (p ≤ 0.05). Lateralized injury resulted in cholinergic neuron loss of similar magnitude ipsilaterally (p ≤ 0.05), but a smaller contralateral loss of between 11% and 28%. No loss of neurons was detected in the pontomesencephalic cholinergic groups Ch5 and Ch6. There was no visible effect of head injury on forebrain dopamine or noradrenergic innervation. A significant and apparently selective loss of ventrobasal forebrain cholinergic neurons following brief concussive injury in rats is demonstrated in this study. This type of injury is known to produce significant disturbance in cognitive tasks linked to neocortical and hippocampal cholinergic function. It remains to be determined how this neuron loss occurs, whether it can be prevented with neuroprotective agents, how it affects innervation in target tissues, and whether it occurs in human victims of traumatic brain injury.

Apnea testing for the determination of brain death: a modified protocol

1992 ◽  
Vol 76 (6) ◽  
pp. 1029-1031 ◽  
Author(s):  
Edward C. Benzel ◽  
Jay P. Mashburn ◽  
Steven Conrad ◽  
Denise Modling
Keyword(s):  
Brain Death ◽  
Apnea Test ◽  
Content Type ◽  
Group I ◽  
The Mean ◽  
Group Ii ◽  
Safe Approach ◽  
Apnea Testing ◽  
Fine Print

✓ The absence of spontaneous respirations at a PaCO2 of 60 mm Hg or above has traditionally been accepted as the respiratory criteria for the determination of brain death. The testing of patients for the presence or absence of apnea has been complicated because the rate of PaCO2 elevation may vary substantially from patient to patient, and a nonlinear relationship exists between the rate of PaCO2 increase and the duration of apnea. In an attempt to refine the apnea test and to further elucidate the physiology of hypercapnia in humans, 11 patients who met all but the respiratory criteria for brain death were evaluated using a modification of a previously utilized apnea testing protocol. All patients were brought to a PaCO2 of 40 mm Hg or above prior to the apnea test. Baseline PaCO2 ranged from 40 to 45 mm Hg in six patients (Group I) and from 46 to 51 mm Hg in five patients (Group II). The mean rate of PaCO2 increase was 5.1 ± 1.4 mm Hg/min in Group I and 6.7 ± 3.1 mm Hg/min in Group II. No problems with cardiovascular instability or hypoxia were encountered during testing in this series. This refinement of the apnea test allows for a streamlined and safe approach to brain death detection.

Oculomotor nerve regeneration in rats

1987 ◽  
Vol 67 (3) ◽  
pp. 428-437 ◽  
Author(s):  
Eduardo Fernandez ◽  
Carlo Gangitano ◽  
Aurora Del Fà ◽  
Corrado Olivieri Sangiacomo ◽  
Giuseppe Talamonti ◽  
...  
Keyword(s):  
Nerve Regeneration ◽  
Vestibular Stimulation ◽  
Progressive Increase ◽  
Oculomotor Nerve ◽  
Plasma Clot ◽  
Content Type ◽  
Collateral Sprouting ◽  
Group I ◽  
Group Ii ◽  
Fine Print

✓ To study oculomotor nerve regeneration in rats, the oculomotor nerve was approached microsurgically and was sectioned at the base of the skull. The nerve stumps were reapproximated and affixed with a plasma clot in Group I animals and were separated by a gap in Group II animals. Visceral eye motility was evaluated weekly between 1 day and 40 weeks after surgery by recording the pupillary diameter under standardized photic stimulation. Somatic eye motility was assessed after 26 weeks by measuring the ocular displacement evoked by vestibular stimulation in the horizontal and vertical planes. Nerve regeneration was documented histologically and morphometrically at 8, 16, and 40 weeks after section. The selectivity of axonal regeneration to the extraocular muscles was investigated after 26 weeks by mapping (with injection of retrograde horseradish peroxidase) the motoneurons that supplied each reinnervated muscle. Between 6 and 20 weeks after section, the pupil diameter showed a progressive reduction in Group I rats, and no changes were observed in Group II rats. Compared with normal rats, the amplitude of horizontal and vertical ocular displacements was decreased, respectively, by 30% and 45% in Group I and by 65% and 80% in Group II. In Group I rats, the vestibular stimulation in the horizontal plane evoked anomalous eye movements with vertical components. On histological examination, regenerated nerves showed a progressive increase of axonal diameter and myelin-sheath thickness. Reinnervated muscles were associated with a less specific, bilateral representation in the midbrain compared with normal muscles, which have unilateral representation. The changes of the somatotopic organization were interpreted as being the result of the misdirected regrowth of axons in the postlesional nerve stump and of the collateral sprouting in the midbrain.

Expression of matrix metalloproteinases 2 and 9 in meningiomas associated with different degrees of brain invasiveness and edema

2001 ◽  
Vol 95 (5) ◽  
pp. 839-844 ◽  
Author(s):  
Ann-Christin Sandberg Nordqvist ◽  
Hubert Smurawa ◽  
Tiit Mathiesen
Keyword(s):  
Matrix Metalloproteinases ◽  
Clear Correlation ◽  
Consecutive Series ◽  
Tissue Samples ◽  
Content Type ◽  
Brain Invasion ◽  
Group Iii ◽  
Tumor Invasiveness ◽  
Group I ◽  
Fine Print

Object. Meningiomas display clinical characteristics that vary from very benign to clearly malignant with rapid invasive growth and metastasis. Benign meningiomas differ in their invasiveness and concomitant edema. This study was undertaken to analyze the expression of matrix metalloproteinases 2 and 9 (MMP-2 and MMP-9, respectively) in meningiomas associated with different degrees of brain invasion and edema. Methods. Tissue samples from 16 meningiomas were selected according to tumor invasiveness from a consecutive series of patients. Samples were analyzed for expression of both MMP-2 and MMP-9 by using in situ hybridization. The meningiomas consisted of three types: Group I, benign meningiomas that did not interfere with the arachnoid plane and exhibited no edema; Group II, benign meningiomas that invaded the arachnoid plane and caused edema; and Group III, aggressive and malignant meningiomas that caused edema and displayed brain invasion. In all 16 tumors analyzed, MMP-2 mRNA was identified. Levels of expression of MMP-2 mRNA were similar in all samples, and no correlation with increasing tumor invasiveness or associated edema could be detected. Expression of MMP-9 mRNA was identified in 14 of the 16 tumors, and a clear correlation with increasing tumor invasion into the brain was noted. Conclusions. Meningiomas express both MMP-2 and MMP-9. Tumor invasiveness, which ranged from minor with respect to the arachnoid membrane and progressed to frank brain invasion, correlated with the extent of MMP-9 expression. The findings indicate that MMP-9 expression and brain invasion are relevant mechanisms that must be interfered with in the treatment of aggressive and malignant meningiomas. No such correlation with MMP-2 was found.

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