Biomedical subjects

P Barzó

Publications and source records attributed to P Barzó.

At least 19 recordsLinked to original sources

PubMed2006

Comparison of clinical symptoms and magnetic resonance angiographic (MRA) results in patients with trigeminal neuralgia and persistent idiopathic facial pain. Medium-term outcome after microvascular decompression of cases with positive MRA findings.

Neurovascular compression (NC) seems to have been confirmed as the major cause of classical trigeminal neuralgia (TN). In spite of the large number of surgically positive cases, however, there are still cases where no vascular compression of the trigeminal nerve can be found. To evaluate whether NC could be demonstrated preoperatively, high-resolution magnetic resonance angiography (MRA) was performed in 287 consecutive patients with TN and persistent idiopathic facial pain (PIFP) on a 0.5-T and a 1-T MR unit. Depending on the clinical symptoms, the TN cases were divided into typical TN and trigeminal neuralgia with non-neuralgic interparoxysmal pain (TNWIP) groups. Microvascular decompression (MVD) was performed in 103 of the MRA-positive cases. The patients were followed up postoperatively for from 1 to 10 years. The clinical symptoms were compared with the imaging results. The value of MRA was assessed on the basis of the clinical symptoms and surgical findings. The outcome of MVD was graded as excellent, good or poor. The clinical symptoms were compared with the type of vascular compression and the outcome of MVD. The MRA image was positive in 161 (56%) of the 287 cases. There were significant differences between the clinical groups: 66.5% of the typical TN group, 47.5% of the TNWIP group and 3.4% of the PIFP group were positive. The quality of the MR unit significantly determined the ratio of positive/negative MRA results. The surgical findings corresponded with the MRA images. Six patients from the MRA-negative group were operated on for selective rhizotomy and no NC was found. Venous compression of the trigeminal nerve was observed in a significantly higher proportion in the background of TNWIP than in that of typical TN on MRA imaging (24.1% and 0.8%, respectively) and also during MVD (31.2% and 1.2%, respectively). Four years following the MVD, 69% of the patients gave an excellent, 23% a good and 8% a poor result. The rate of some kind of recurrence of pain was 20% in the typical TN and 44% in TNWIP group. The rate of recurrence was 57% when pure venous compression was present. The only patient who was operated on from the PIFP group did not react to the MVD. The clinical symptoms and preoperative MRA performed by at least a 1-T MR unit furnish considerable information, which can play a role in the planning of the treatment of TN.

Adult↗

PubMed2004

Comparison of regional vasomotor responses to acetazolamide and CO2 in rabbit cerebrum and cerebellum, measured by a hydrogen clearance method.

AIM: Many investigators have proved the usefulness of acetazolamide provocation and the carbon dioxide test for assessment of the local cerebrovascular reactivity by measurement of the regional cerebral blood flow in patients with occlusive cerebrovascular disease. Data originating from a comparison of these two different vasomotor stimuli as concerns the differences in sensitivity to them in various parts of the central nervous system are scarce. Our aim was to compare the cerebral blood flow responses to hypercapnic and acetazolamide stimuli in different brain regions. METHODS: The cerebral blood flow was measured in the cerebrum (cortex and caudate nucleus) and cerebellum (cortex), as measured by a hydrogen clearance method in anaesthetized, artificially ventilated rabbits. RESULTS: In normocapnia, the cerebral blood flow values in the cerebrum and the cerebellum differed significantly. The cerebral blood flow responses to both vasodilatory stimuli were to be significantly higher in the cerebrum than in the cerebellum, but the relative increases, i.e. the mean relative reactivities, were similar in the different regions measured. CONCLUSION: The regional dissimilarity might explain to some extent the different sensitivities of the various brain areas to sudden blood pressure changes (infarction or haemorrhage). The results further suggest that heterogeneity in cerebrovascular reactivity should be considered in the assessment of vasoreactivity in patients with occlusive cerebrovascular disease. Since the comparison of the carbon dioxide and acetazolamide-induced cerebrovascular reactivities revealed a strong linear relationship, it was concluded that acetazolamide provocation is equivalent to the carbon dioxide test in the evaluation of cerebrovascular reactivity.

Acetazolamide↗

PubMed2001

[Surgical treatment of giant basilar artery aneurysm with induced hypothermia and circulatory arrest].

Surgical management of giant and complex posterior circulation aneurysms continues to be a technically difficult task with high operative morbidity. To minimize morbidity we have used cardiopulmonary bypass and circulatory arrest for the treatment of a giant basilar aneurysm. A 48-year-old woman presented with sudden headache. Magnetic resonance angiography revealed a giant basilar aneurysm. On the 2nd hospital day she developed right sided hemiparesis and cranial nerve deficits as a result of the second rupture of the aneurysm. The aneurysm was successfully treated and no significant neurological complications were related to this technique. This initial experience indicates that patients with giant posterior circulation aneurysm that cannot be treated using conventional techniques might benefit from a surgical approach that included the use of deep hypothermic circulatory arrest.

Aneurysm↗

PubMed2001

[Results of surgical treatment in hemifacial spasm--the role of MR-angiography in detecting microvascular compression].

The authors evaluated the follow-up results of microvascular decompression (sec. Janetta) in 8 patients with hemifacial spasm (HFS). Indication was based on there dimensional time of flight magnetic resonance angiography with 0.5T Elscint Gyrex V Dix equipment. Contrast material was administered in every case and maximum intensity projection and thin slice reconstruction were performed in three standard directions. Vascular contact with the facial nerve in the entry zone was identified on the symptomatic side in 10 patients. No contact was detected in 2 cases. Microvascular decompression was performed in 8 cases. The surgical and neuroradiological findings were identical in every cases. Five patients were completely free of HFS immediately after surgery, and another 2 patients became free of HFS during the next few weeks. Only 1 patient had uncured symptoms. In conclusion, the authors suggest that microvascular decompression of the facial nerve may evolve as the method of choice if vascular contact is proved by 3D TOF MRA.

Constriction, Pathologic↗

PubMed2001

Influence of nitrovasodilators and cyclooxygenase inhibitors on cerebral vasoreactivity in conscious rabbits.

Since the nitric oxide (NO) and cyclooxygenase pathways have been suggested to have important roles in most vasodilations, our aim was to study the influence of cyclooxygenase inhibitors and nitrovasodilators on cerebrovascular reserve capacity. Corticocerebral blood flow was measured by hydrogen polarography during hypercapnia and acetazolamide stimuli in conscious rabbits. The measurements were repeated in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) and indomethacin as nitric oxide synthase (NOS) and cyclooxygenase inhibitors. The effects of nitroglycerin and isosorbide-5-nitrate were also tested. L-NAME completely, while indomethacin markedly inhibited the hypercapnic corticocerebral blood flow response. Nitroglycerin and isosorbide-5-nitrate significantly attenuated hypercapnia elicited corticocerebral blood flow increase. The different treatments reduced only moderately the acetazolamide-induced corticocerebral blood flow response. These results lend support to the hypothesis that antithrombotic and antiinflammatory medication (cyclooxygenase inhibitors) and nitrovasodilator treatments could interfere with the measurement of cerebrovascular reactivity resulting in underestimation of the cerebrovascular reserve capacity in patients taking these drugs.

Acetazolamide↗

PubMed2001

Three-dimensional time-of-flight MR angiography in trigeminal neuralgia on a 0.5-T system.

The goal of this study was to analyze the diagnostic value of three-dimensional time-of-flight magnetic resonance angiography (3D TOF MRA), performed on a 0.5-T system in the detection of neurovascular compression in patients with trigeminal neuralgia (TN). One hundred seventy-two TN patients were examined using plain and contrast-enhanced 3D TOF MRA on a 0.5-T system. Maximum intensity projection (MIP) reconstruction was performed in three standard planes. Both the original and the reconstructed images were studied to search for vascular compression shown by close neurovascular contact and/or dislocation of the trigeminal nerve. Forty-two TN patients underwent surgical exploration of the posterior fossa. Results of MRA were compared with clinical data in all cases and to result of surgery in the surgically treated cases. Neurovascular contact at the root entry zone of the trigeminal nerve was detected on the symptomatic side in 94 patients, and on the asymptomatic side in 12 patients. Sensitivity, specificity, accuracy, as well as positive and negative predictive value of 3D TOF MRA in the detection of neurovascular compression in the patient group undergoing surgery, were 97.6, 92.5, 95.0, 93.0, and 97.4%, respectively. Three-dimensional TOF MRA performed on a 0.5-T system appears to be not less effective than similar examinations by higher field strength devices in the detection of neurovascular contact. This sequence accurately demonstrates the presence of neurovascular compression, and in this way valuable information may be achieved for the planning of surgical therapy of patients with trigeminal neuralgia.

Adult↗

PubMed2000

Contribution of edema and cerebral blood volume to traumatic brain swelling in head-injured patients.

OBJECT: The pathogenesis of traumatic brain swelling remains unclear. The generally held view is that brain swelling is caused primarily by vascular engorgement and that edema plays a relatively minor role in the swelling process. The goal of this study was to examine the roles of cerebral blood volume (CBV) and edema in traumatic brain swelling. METHODS: Both brain-tissue water and CBV were measured in 76 head-injured patients, and the relative contribution of edema and blood to total brain swelling was determined. Comparable measures of brain-tissue water were obtained in 30 healthy volunteers and CBV in seven volunteers. Brain edema was measured using magnetic resonance imaging, implementing a new technique for accurate measurement of total tissue water. Measurements of CBV in a subgroup of 31 head-injured patients were based on consecutive measures of cerebral blood flow (CBF) obtained using stable xenon and calculation of mean transit time by dynamic computerized tomography scanning after a rapid bolus injection of iodinated contrast material. The mean (+/- standard deviation) percentage of swelling due to water was 9.37+/-8.7%, whereas that due to blood was -0.8+/-1.32%. CONCLUSIONS: The results of this study showed that brain edema is the major fluid component contributing to traumatic brain swelling. Moreover, CBV is reduced in proportion to CBF reduction following severe brain injury.

Adolescent↗

PubMed1999

Intraventricular hemorrhage as a false localizing sign of a thoracolumbar arteriovenous malformation: case report.

BACKGROUND: Spinal arteriovenous malformation (SAVM) is a relatively rare disease characterized by a high incidence of intramedullary and subarachnoid haemorrhage. When the hemorrhage is profuse and the SAVM is in the cervical region the symptoms (disturbance of consciousness, papilledema, cranial nerve palsies, and convulsions) may be so severe and rapid in their onset that they may be mistaken for intracranial hemorrhage. We report here on a patient with a SAVM at T10-12, which bled intracranially, mainly intraventricularly, and resulted first in respiratory arrest and unconsciousness. CASE DESCRIPTION: The patient had been well until he was 28 years old when, during intercourse, he suffered a terrible headache and suddenly lost consciousness, with a transient respiratory arrest. He was also noted to have right hemiparesis. A computed tomography scan demonstrated intraventricular hemorrhage. After a 24-hour period of artificial ventilation the patient regained consciousness and the right arm paresis completely recovered, but a gradual worsening of the motor function of the left leg developed. Digital subtraction angiography did not demonstrate any intracranial source of bleeding, whereas spinal angiography revealed a SAVM located at the medullary cone, which was totally removed by surgery. CONCLUSION: The case reported here raises several important issues. First, the advisability of spinal magnetic resonance imaging in the investigation of intraventricular (and subarachnoid) hemorrhage in patients with no demonstrable intracranial source. Secondly, the benefits of early diagnosis and reestablishment of the spinal cord circulation before the onset of thrombosis and the progressive phase of myelopathy. Finally, the necessity of complete obliteration and treatment of SAVMs even in patients with fixed neurologic deficits, because rebleeding of lower thoracic or lumbar SAVMs can lead to impairment at a higher level with severe or lethal consequences.

Adult↗

PubMed1998

[Giant cell interstitial pneumonia].

GIP is a rarely occurring disorder. There is only few literature from its first description. Authors observed the course of GIP in the case of a 54 year old female patient in the form of bilateral disseminated microfocal pulmonary shadows, increased reticular outline with associated respiratory insufficiency. Open fine needle pulmonary biopsy proved giant cell desquamative alveolitis with help of light- and electronmicroscopical and histochemical examinations. Although possibility of exogenic, inhalative factor or/and infectious origin arose in causing the disease, disposition from the patient's actual immunological status could had helped the evolution of the disease. This fact seemed to be supported by the histologically proven associated dermatitis purpurica pigmentosa (Schamberg disease). With methylprednisolon therapy full radiological recovery occurred, while Schamberg disease was little influenced by the above mentioned therapy. The patient is pulmonologically symptom-free and without complaint after 1 year without any steroid-medication.

Cryptogenic Organizing Pneumonia↗

PubMed1998

[Löfgren syndrome after silicone breast prosthesis implantation].

The authors review the case of a 30-year old female hair-dresser, into the breasts of whom silicone-gel implants have been implanted for cosmetic reasons. Ten months after the operation Löfgren-syndrome evolved, which improved only temporarily after the removal of the implants. The present symptom-free state, existing for 6 months now, required a 17-month corticoid therapy. The authors share the view that in rare cases silicon-gel implants might induce an autoimmune reaction, which is unforeseeable. When it is rightly presumed that human adjuvant disease or some other specified systemic disease is evolving, it is advisable that the implants should be removed and the patient should be treated with immunological therapy.

Adrenal Cortex Hormones↗

PubMed1997

Detection of brain atrophy following traumatic brain injury using gravimetric techniques.

We hypothesized, that with atrophy, the correlation between water content and specific gravity of brain solids would break down signifying the onset of the atrophic process. The correlation between tissue water content, specific gravity of solids and ventricular size was studied in an impact acceleration model of closed head injury of the rat. Adult Sprague Dawley rats weighing 350 to 375 grams (n = 63) were separated into two groups: Group 1: Sham (n = 21), Group II: Trauma (n = 42). Water content was assessed using both gravimetric method and drying-weighing method at 1 hour, on days 1, 3, 7, 14, 28, and 42 in the trauma group as well as in the control group. Ventricular size was measured in cm2 on the MRI computer console in the coronal section at the coronal suture at the same time points. In the trauma group we found a significant increase (p < 0.01) in water content during the first week except on day 3 and there was a good correlation between the results of water content using both methods (p < 0.001). However, this relationship was poorly correlated after day 14 (p = 0.25). Although the ventricular size was the smallest at 1 hour post trauma, it significantly increased over the next 3 days (p < 0.001). On day 7 and 14 ventricular size decreased to normal size, yet gradually increased and then reached a significantly larger size on 42 days post trauma again (p < 0.01). We may consider, that brain edema following CHI begins immediately following trauma and resolves within 2 weeks. After 14 days degenerative change occurs in the cortex, as detected by specific gravity measurements which signifies the onset of the atrophic process and subsequent post traumatic ventricular dilatation.

Animals↗

PubMed1997

MRI diffusion-weighted spectroscopy of reversible and irreversible ischemic injury following closed head injury.

The objective of this study was to detect the threshold between reversible and irreversible secondary insult of hypoxia and hypotension following closed head injury as measured by MRI. Adult Sprague rats were separated into 3 groups: I: Sham (n = 6), II: Trauma and hypoxia coupled with mild hypotension of 40-50 mmHg (n = 6), III: Trauma and hypoxia coupled with severe hypotension of 30-40 mmHg (n = 6). The measurement of brain water content (BWC) was based on T1, whereas the differentiation between reversible and irreversible secondary insult on the measurement apparent diffusion coefficient (ADC). The ADCs in both trauma and secondary insult groups decreased rapidly from a control level of 0.68 +/- 0.5 x 10(-3) to significantly different minimum levels of 0.52 +/- 0.5 x 10(-3) in Group II and 0.42 +/- 0.5 x 10(-3) mm2/second in Group III at 30 minutes. In Group II rats there was a complete recovery in ADC as well as in their clinical conditions, whereas ADC in Group III rats remained at the minimum level and the animals were brain dead. The BWC was also significantly different at four hours post injury (Group II: 80.3 +/- 0.7%, Group III: 81.8 +/- 0.8%). The data lead the authors to suggest that the threshold between reversible and irreversible posttraumatic secondary insult is very narrow, and the measurement of ADC can provide information that will enable the clinician to identify critical threshold beyond which recovery is not possible.

Animals↗

PubMed1997

Biphasic pathophysiological response of vasogenic and cellular edema in traumatic brain swelling.

The objective of this study was to quantify the temporal water content changes and document the type of edema (cellular versus vasogenic) that is occurring during both the acute and the late stages of edema development following closed head injury. Adult Sprague rats (n = 50) were separated into two groups: Group I: Sham (n = 8), Group II: Trauma (n = 42). The measurement of brain water content (BWC) was based on T1, whereas the differentiation of edema on the measurement of the random, translational motion of water protons (apparent diffusion coefficients-ADC) by MRI. In trauma animals, we found a significant increase in ADC (105%) as well as in BWC (0.7 +/- 0.3%) during the first 60 minutes post injury indicating vasogenic edema formation. This transient increase; however, was followed by a continuing decrease in ADC beginning at 45 minutes post injury and reaching a minimum at days 7-14 (-103%). Since the BWC continued to increase during the next day (10.3%), it is suggested cellular edema formation started to develop soon after injury and became dominant between 1-2 weeks post injury. In conclusion we may consider, that there is a predominantly vasogenic edema formation immediately after injury and later a more widespread and slower edema formation due to a predominantly cellular swelling.

Animals↗

PubMed1997

Acute blood-brain barrier changes in experimental closed head injury as measured by MRI and Gd-DTPA.

The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury (CHI) and to what extent BBB is affected by secondary insult. The BBB disruption was quantified using T1-weighted MRI following administration of Gd-DTPA. The maximal signal intensity (SI) enhancement was used to calculate BBB disruption. A new CHI model was used to induce injury. Adult SD rats were separated into four groups: Group I: Sham (n = 4), II: Hypoxia and Hypotension (HH, n = 4), III: Trauma alone (n = 23), and IV: Trauma coupled with HH (THH, n = 14). Following trauma, a 30 minute insult of hypoxia (PaO2 = 40 mmHg) and hypotension (MABP = 30 mmHg) were imposed. In trauma animals, SI increased dramatically immediately following impact. By 15 minutes, permeability decreased exponentially and by 30 minutes was equal to that of control. In THH animals, SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically upon reperfusion and was equal to that of control after 60 minutes. In conclusion we may consider, that CHI is associated with a rapid and transient BBB opening which begins at the time of the trauma and lasts not more than 30 minutes. It has been also shown that addition of hypoxia and hypotension prolongs the time of BBB breakdown.

Animals↗

PubMed1997

Contribution of vasogenic and cellular edema to traumatic brain swelling measured by diffusion-weighted imaging.

The contribution of brain edema to brain swelling in cases of traumatic brain injury remains a critical problem. The authors believe that cellular edema, the result of complex neurotoxic events, is the major contributor to brain swelling and that vasogenic edema, secondary to blood-brain barrier compromise, may be overemphasized. The objective of this study, therefore, was to quantify temporal water content changes and document the type of edema that forms during the acute and late stages of edema development following closed head injury (CHI). The measurement of brain water content was based on magnetic resonance imaging-determined values of tissue longitudinal relaxation time (T1-weighted imaging) and their subsequent conversion to percentage of water, whereas the differentiation of edema formation (cellular vs. vasogenic) was based on the measurement of the apparent diffusion coefficient (ADC) by diffusion-weighted imaging. A new impact-acceleration model was used to induce CHI. Thirty-six adult Sprague-Dawley rats were separated into two groups: Group I, control (six animals); and Group II, trauma (30 animals). Fast ADC measurements (localized, single-voxel) were obtained sequentially (every minute) up to 1 hour postinjury. The T1-weighted images, used for water content determination, and the diffusion-weighted images (ADC measurement with conventional diffusion-weighted imaging) were obtained at the end of the 1st hour postinjury and on Days 1, 3, 7, 14, 28, and 42 in animals from the trauma and control groups. In the animals subjected to trauma, the authors found a significant increase in ADC (10 +/- 5%) and brain water content (1.3 +/- 0.9%) during the first 60 minutes postinjury. This is consistent with an increase in the volume of extracellular fluid and vasogenic edema formation as a result of blood-brain barrier compromise. This transient increase, however, was followed by a continuing decrease in ADC that began 40 to 60 minutes postinjury and reached a minimum value on Days 7 to 14 (10 +/- 3% reduction). Because the water content of the brain continued to increase during the first 24 hours postinjury (1.9 +/- 0.9%), it is suggested that the decreased ADC indicated cellular edema formation, which started to develop soon after injury and became dominant between 1 and 2 weeks postinjury. The study provides supportive evidence that cellular edema is the major contributor to posttraumatic swelling in diffuse CHI and defines the onset and duration of the increase in cellular volume.

Acceleration↗

PubMed1996

[Cerebral blood flow studied by SPECT and transcranial Doppler sonography in subarachnoid hemorrhage].

The detection of vasospasm plays an important role for the definition of the strategy of treatment in patients with subarachnoid hemorrhage (SAH). Besides the invasive contrast angiography, the non-invasive 99m-Tc-HMPAO brain perfusion SPECT and transcranial Doppler sonography (TCD) are recently used for this purpose. For the investigation of the possibilities of the last two methods, comparative studies were performed in 29 SAH patients in the subacute phase of the disease. In the detection of regional brain ischaemia the sensitivity of the SPECT study was 90%, the specificity was 28% and the accuracy was 50%, the corresponding values of TCD were 82%, 71% and 75%. In patients, in whom chronic neurological symptoms, or morphological abnormalities could be excluded, the specificity of the SPECT study was 67% at unchanged sensitivity. Based on the results it is concluded, that the brain perfusion SPECT and the TCD investigation are useful methods for the detection of vasospasm after SAH. The combination of the two methods is recommended for the correct diagnosis of vasospasm in SAH. Further investigations are necessary to clarify the prognostic impact of the result of these investigations.

Adult↗

PubMed1996

Use of transcranial Doppler sonography and acetazolamide test to demonstrate changes in cerebrovascular reserve capacity following carotid endarterectomy.

OBJECTIVES: To assess the effect of carotid endarterectomy on cerebrovascular reserve capacity. METHODS: Cerebral blood flow velocity (CBFV) and cerebrovascular reserve capacity (CVRC) were measured by transcranial Doppler sonography (TCD) and acetazolamide test in 40 patients who underwent uncomplicated unilateral carotid endarterectomy (CEA). Indication for operation was limited to stenoses > 70% as documented by angiography and/or Duplex scanning. The TCD studies were carried out 6 days (range 1-14 days) before and 8 days (range 5-12 days) after endarterectomy. RESULTS: Before endarterectomy, resting CBFV values and CVRC in the 40 patients were significantly different between the operated (51 +/- 19 cm/s; 20 +/- 16%) and the non-operated (60 +/- 19 cm/s; 34 +/- 24%) hemisphere (p < 0.05;p < 0.01). After CEA the overall increase of resting CBFV of the operated side was highly significant with preoperative CBFV values of 51 +/- 19cm/s and postoperative values of 62 +/- 15 cm/s (p < 0.01). Cerebrovascular reserve capacity after operation was increased on both sides significantly (non-operated side: from 34 +/- 24% to 43 +/- 19%, p < 0.05; operated side: from 20 +/- 16% to 51 +/- 18%, p < 0.001), and the preoperative asymmetry was no longer present. CONCLUSIONS: CEA has a beneficial effect on the cerebral circulation in most patients, even those who presented with asymptomatic carotid artery stenosis. Since CVRC has been assessed in the early postoperative period, our findings also suggest that cerebral vascular adaption occurs within 2 weeks after CEA.

Acetazolamide↗

PubMed1996

Characterization of edema by diffusion-weighted imaging in experimental traumatic brain injury.

The objective of this study was to use diffusion-weighted magnetic resonance imaging (DWI) to help detect the type of edema that develops after experimental trauma and trauma coupled with hypotension and hypoxia (THH). Reduction in the apparent diffusion coefficients (ADCs) is thought to represent cytotoxic edema. In a preliminary series of experiments, the infusion edema model and middle cerebral artery occlusion models were used to confirm the direction of ADC change in response to purely extracellular and cytotoxic edema, respectively. The ADCs increased (p<0.05) in the case of extracellular edema and decreased (p<0.001) in cytotoxic edema. Following these initial experiments, a new impact acceleration model was used to induce traumatic brain injury. Thirty-six adult Sprague-Dawley rats were separated into four groups; sham, trauma alone, hypoxia and hypotension (HH), and THH. Following trauma, a 30-minute insult of hypoxia (PaO2 of 40 mm Hg) and hypotension (mean arterial blood pressure (MABP) of 30 mm Hg) were imposed and the animals were resuscitated. The DWI was carried out at four 1-hour intervals postinjury, and MABP, intracranial pressure (ICP), cerebral perfusion pressure (CPP), and cerebral blood flow (CBF) were monitored. The ADCs in the control and HH groups remained unchanged. The ADCs in the THH group rapidly decreased from a control level of 0.68 +/- 0.05 x 10(-3) mm2/second to 0.37 +/- 0.09 x 10(-3) mm2/second by 3 hours posttrauma (p < 0.001). In this group, the decreased CBF and CPP during secondary insult remained low despite resuscitation, with the ICP increasing to 56 +/- 7 mm Hg by 3 hours. In the trauma alone group, the rise in ICP reached a maximum value (28 +/- 3 mm Hg) at 30 minutes with a significant and sustained increase in CBF despite a gradual decrease in CPP. The ADCs in this group were not significantly reduced. The data lead the authors to suggest that the rise in ICP following severe trauma coupled with secondary insult in this model is predominately caused by cytotoxic edema and that ischemia plays a major role in the development of brain edema after head injury.

Animals↗