[Anterior cervical fusion in the lower cervical spine. Locked vs nonlocked screw plate, pure cancellous bone vs tricortical strut]. / Vordere Spondylodesen an der unteren Halswirbelsäule. Winkelinstabile vs. winkelstabiler Platte, reine Spongiosa vs. trikortikalem Span.

Physical alterations in cervical fusions endanger healing. Experimentally we determined less stability loss in fixations using cancellous bone grafts than in those using tricortical grafts. Four hundred eighty-five Patients underwent anterior cervical fusion, for a total of 700 Segments. Patients were divided into four groups: (1) nonlocked H plate with autogenous cancellous bone, (2) nonlocked H plate with autogenous tricortical graft, (3) locked cervical plate with tricortical graft, and (4) stand-alone cage with cancellous bone. Evaluations included X-ray and random CT scan examinations. Our results suggest that anterior cervical fusions using nonlocked H screw plate systems with pure autogenous cancellous bone grafts provide the fastest (6 weeks) and most secure bone healing (P=0.00001), whereas fixations using nonlocked or locked screw plate systems and tricortical autograft require prolonged healing and develop nonunions more frequently. Complete consolidation was achieved using stand-alone cages filled with pure autogenous cancellous bone, but bony healing was delayed due to the cage. Rate of nonunions were: groups 1 and 4 0%, and groups 2 and 3 4.5% and 21%, respectively.

Kinetics of the cellular immune response following closed head injury.

BACKGROUND: The contribution of brain edema to brain swelling in cases of traumatic brain injury (TBI) remains a critical problem. We believe that inflammatory reactions may play a fundamental role in brain swelling following a head injury. Although possible roles of microglia activation and the release of mediators have been suggested, direct evidence of cellular immune reactivity in diffuse brain injury following closed head trauma is lacking. Accordingly, the objective of this study was to assess the temporal pattern of microglia activation and lymphocyte migration in an experimental model of TBI. METHOD: An impact acceleration TBI model was utilized to induce diffuse brain damage in adult Wistar rats. The animals were separated into three groups: unoperated controls, sham-operated controls and trauma group. At various times after TBI induction (5 min-24 h), rats were perfused transcardially. Sagittal brain sections were analyzed with immunohistochemical markers of CD3 to reveal the presence of T-lymphocytes, and by immunochemistry for the detection of CD11b to reveal microglia activation within the brain parenchyma. FINDINGS: In the control groups, scattered T-cells were found in the brain parenchyma. In the trauma group, TBI induced microglia activation and a transient biphasic T-cell infiltration of the brain parenchyma in all regions was found, beginning as early as 30 min post injury and reaching its maximum values at 45 min and 3 h after trauma induction. CONCLUSION: These results lead us to suggest that the acute response to severe head trauma with early edema formation is likely to be associated with inflammatory events which might be triggered by activated microglia and infiltrating lymphocytes. It is difficult to overestimate the clinical significance of these observations, as the early and targeted treatment of patients with severe head injuries with immunosuppressive medication may result in a far more favorable outcome.

Chlamydophila pneumoniae and human cytomegalovirus in atherosclerotic carotid plaques--combined presence and possible interactions.

The aim of our study was to investigate the combination of Chlamydophila pneumoniae and human cytomegalovirus (HCMV) as a pathogenic factor in atherosclerosis. Accordingly, we tested by means of PCR and immunohistochemistry the presence of these pathogens in the same atherosclerotic carotid specimen. The histology of the samples and the patients' antibodies against these pathogens were evaluated. Further, we examined the impact of C. pneumoniae and HCMV infection on the gene expression of the human monocytic cell line U937. Six of the 22 samples contained only C. pneumoniae, 4 contained only HCMV, 7 contained both C. pneumoniae DNA and/or antigens of both pathogens, and 5 samples were negative. No correlation was found between the presence of these microbes and either the cellular structure of the plaques, or the serostatus of the patients. The infection of U937 cells with HCMV and especially C. pneumoniae induced inflammation and atherosclerosis-related genes. Furthermore, the doubly-infected cells produced higher levels of the mRNA of pro-platelet basic protein and fatty acid binding protein 4. In conclusion, C. pneumoniae is often present in combination with HCMV in atherosclerotic carotid lesions. The in vitro coinfection model reveals that the doubly-infected monocytes are potent expressors of proatherosclerotic genes, suggesting that this coinfected population may accelerate the process of atherosclerosis.

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.

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.

Effect of axillary brachial plexus blockade on baroreflex-induced skin vasomotor responses: assessing the effectiveness of sympathetic blockade.

BACKGROUND: The combination of laser Doppler flowmetry and non-invasive blood pressure monitoring allows the continuous observation of cutaneous vascular resistance (CVR). Continuous recording of unmodulated skin blood flow (SBF) is very sensitive to artefacts, rendering the method unreliable. In contrast, intermittent short lasting challenges of the CVR by cardiovascular autonomic reflexes may provide information about the responsiveness of the sympathetic nervous system in the skin. METHODS: Eleven patients with below-wrist hand surgery (six males and five females; aged 35.2+/-7.1 years) performed Valsalva maneuver following axillary blockade. Skin blood flow was continuously monitored on the forearm of the side axillary blockade, as well as on the contra-lateral forearm, which was used as the control. The responses were expressed as changes compared with the baseline level derived from a resting period of 30 s. The maximal change in CVR was determined during the late strain phase of the Valsalva maneuver on both sides. For numerical comparison the change in CVR on the axillary blockade and control sides were simultaneously calculated. RESULTS: During the Valsalva maneuver a significant increase in CVR was observed on the control side with a maximum value during the late strain phase (baseline 0.18+/-0.1 and late strain phase 0.42+/-0.2 relative units; P<0.01). In contrast, only minimal changes were detected on the side of axillary blockade in CVR (baseline 0.17+/-0.8 and late strain 0.16+/-0.2 relative units; P=NS). CONCLUSIONS: Our findings support the disputed hypothesis that the human skin microvasculature is involved in baroreflex regulation under thermoneutral conditions. The determination of baroreflex stimulus-induced microvascular responses may serve as a feasible method for monitoring the effectiveness of sympathetic blockade.

[Results of surgical treatment in hemifacial spasm--the role of MR-angiography in detecting microvascular compression]. / Hemifacialis spasmus mútéti kezelésének eredménye MR-angiográfiával kimutatott microvascularis kompresszió esetén.

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.

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.

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.

Contrasting effects of dopamine therapy in experimental brain injury.

Management of cerebral perfusion pressure (CPP) is thought to be important for the treatment of traumatic brain injury (TBI). Vasopressors have been advocated as a method of increasing mean arterial blood pressure (mABP) and cerebral perfusion pressure (CPP) in the face of rising intracranial pressure (ICP). There are unresolved issues and theoretical risks about this therapy. This study therefore examined the effects of dopamine on physiological and MRI/MRS parameters in (1) a rodent model of rapidly rising intracranial pressure, caused by diffuse injury with secondary insult and (2) a model of cortical contusion. Dopamine was capable of restoring CPP in the model of rapidly rising ICP. This CPP restoration was associated with a partial restoration of CBF. Two profiles of change in the Apparent Diffusion Coefficient of water (ADCw) were seen; one in which ADCw recovered to baseline, and one in which ADCw remained persistently low. Dopamine did not alter these profiles. MRI assessed tissue water content was increased four hours after injury and dopamine increased cerebral water content in both subgroups of injury; significantly in the group with a persistently low ADCw (p < 0.01). In contusional injury, dopamine significantly worsened edema in both the ipsi- and contralateral hippocampus and temporal cortex. This occurred in the absence of ADCw changes, except in the contralateral hippocampus, where both water content and ADCw values rose with treatment, suggesting extracellular accumulation of water. In conclusion, although dopamine is capable of partially restoring CBF after injury, situations exist in which dopamine therapy worsens the swelling process. It is possible therefore that subgroups of patients exist who experience adverse effects of vasopressor treatment, and consequently the effects of vasopressor therapy in the clinical setting need to be more carefully evaluated.

[Surgical treatment of giant basilar artery aneurysm with induced hypothermia and circulatory arrest]. / Arteria basilaris óriásaneurysma mútéti kezelése hypothermiában végzett keringésmegállítás alatt.

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.

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.

Distinguishing between cellular and vasogenic edema in head injured patients with focal lesions using magnetic resonance imaging.

Having determined that edema and not vascular engorgement is the major factor leading to traumatic brain swelling, the objective of this study was to determine which type of edema, cellular or vasogenic, is responsible for increased tissue water in patients with focal lesions. Severely head injured patients (GCS 8 or less) were transported to imaging suites for measurement of brain water and apparent diffusion coefficient (ADC) using magnetic resonance technique. Cerebral blood flow by stable Xenon method was also measured in the regions of interest. Brain water was increased significantly in the hemisphere with lesion. The increase in water was associated with reduced ADC signifying a predominant cellular edema. The ADC in the contralateral hemisphere was near normal value. Cerebral blood flow values in the regions of interest were above ischemic levels suggesting that factors other than ischemia are responsible for the cytotoxic swelling in patients with focal injury.

The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury.

The contribution of blood brain barrier opening to traumatic brain edema is not known. This study compares the course of traumatic BBB disruption and edema formation, with the hypothesis that they are not obligately related. Sprague-Dawley rats were divided into three groups: Group A (n = 47)--Impact Acceleration (IAM); Group B (n = 104)--lateral cortical impact (CCI); Group C (n = 26)--IAM + hypoxia & hypotension (THH). BBB integrity was assessed using i.v. markers (Evan's Blue, or gadolinium-DTPA). Edema formation was evaluated with gravimetry, and T1-weighted MRI. In IAM, BBB opened immediately but closed rapidly, and remained closed for at least the next 36 hours whilst 24-hour hemispheric water content (HWC) rose by 0.9% (p < 0.01). In CCI, BBB opened in both hemispheres for up to 4 hours; four hour HWC in the uninjured hemisphere was indistinguishable from Sham, where HWC in the injured hemisphere rose by approximately 1.5% (p < 0.005). We distinguished two THH animals based on Apparent Diffusion Coefficient (ADC) recovery: in ADC-recovery animals 4 hour cortical water content (CWC) was 80.4 +/- 0.6%, cf 81.4 +/- 1.3% in ADC-non-recovery (p < 0.05). In all animals the BBB was open, however two populations of permeability were seen which likely related to flow-limited extravasation of gadolinium. In IAM edema forms despite only brief BBB opening. Although there is diffuse BBB opening with lateral contusion, edema only forms in the injured hemisphere. In THH, edema formation in the face of a widely permeable barrier is driven by ADC changes or cell swelling. Edema formation clearly does not correspond with BBB opening and an open BBB is clearly not required for edema formation. However we hypothesize that a permeable BBB permissively worsens the process, by acting as a low resistance pathway for ion and water movement. These findings are consistent with our general hypothesis that edema formation after TBI is mainly cytotoxic.

The effects of dopamine on edema formation in two models of traumatic brain injury.

The risk of vasopressors worsening cerebral edema has been raised. Previously we have reported that dopamine was able to restore cerebral blood flow in a model of monotonically rising intracranial pressure. In this study the effects of dopamine on cortical contusion and diffuse injury with secondary insult are examined. Adult male rats were divided into two groups: group 1 (n = 32)--Impact Acceleration Injury (IAM) with 30 minutes hypoxia and hypotension; group 2 (n = 12)--controlled cortical impact (6.0 m/sec, 3 mm depth). Dopamine was administered 2 hours post-injury (10-60 micrograms/kg/min i.v.). Cerebral water content and apparent diffusion coefficients (ADC) values were measured at baseline and four hours post-injury using MRI. Preinjury water content was the same in each group. Group 1 was subdivided into Groups 1A & 1B based on the ADC profile. Post-injury water content in Group 1A did not differ between saline or dopamine treated animals. Water content was higher in Group 1B-dopamine (83.4 +/- 1.1%) than Group 1B-saline animals (81.4 +/- 1.3%, p = 0.006). Contusion caused significant edema formation, however there was no significant difference between the dopamine treated or untreated group when considering either ipsilateral or contralateral cortex. Dopamine however significantly worsened edema in ipsilateral and contralateral hippocampus and both temporal cortices. ADC remained unchanged except in the contralateral hippocampus where both water content and ADC rose with dopamine suggesting precipitation of a vasogenic edema. In this study dopamine clearly worsened edema formation in two models of traumatic brain injury, and we conclude that there may be analogous clinical situations; therefore pressors should not be considered a 'blanket' therapy for all patients with a low cerebral perfusion pressure.

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.

Bronchus cardiacus accessorius dexter.

The diagnosis of bronchus cardiacus accessorius dexter (BCAD) has occurred in 25 cases during the bronchoscopic investigations of 30,000 adult patients of the authors. In most of the cases, this bronchial anomaly has been revealed as an accessory phenomenon, nevertheless, in one of the patients, it was the source of a considerable hemorrhage. In another case reported here in detail, it occurred together with multiple developmental anomalies, such as tracheobronchomegaly, mitral valve prolapse, pectus excavatum, hypoplasy of sinus frontalis on the right side, inguinal hernia on the left side and hyperlipidemia type IV. Family analysis did not confirm the presence of any chromosomal disorders or accumulation of similar developmental anomalies. The forms and frequency of associations of the anomalies are surveyed on the basis of literary data. The recognition of BCAD is of diagnostic importance, since it may explain the persistence of some bronchopulmonary symptoms; furthermore, the exploration of the associated abnormal vascular branches may be very useful in case of an eventual thoracic surgical intervention.

[Löfgren syndrome after silicone breast prosthesis implantation]. / Szilikongél emlöprotézis beültetése után kialakult Löfgren-szindróma.

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.

[Giant cell interstitial pneumonia]. / Oriássejtes interstitialis 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.

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.