[Physico-chemical and toxicological profile of gadolinium chelates as contrast agents for magnetic resonance imaging]. / Physico-chimie et profil toxicologique d'agents de contraste pour l'imagerie par résonance magnétique, les chélates de gadolinium.

Gadolinium chelates (GC) are contrast agents widely used to facilitate or to enable diagnosis using magnetic resonance imaging (MRI). From a regulatory viewpoint, GC are drugs. GC have largely contributed to the success of MRI, which has become a major component of clinician's diagnostic armamentarium. GC are not metabolised and are excreted by the kidneys. They distribute into the extracellular compartment. Because of its high intrinsic toxicity, gadolinium must be administered as a chelate. GC can be classified according to two key molecular features: (a) nature of the chelating moiety: either macrocyclic molecules in which gadolinium is caged in the pre-organized cavity of the ligand, or linear, open-chain molecules, (b) ionicity: Gd chelates can be ionic (meglumine or sodium salts) or non-ionic. The thermodynamic and kinetic stabilities of the various GCs differ according to these structural characteristics. The kinetic stability of macrocyclic GCs is much higher than that of linear GCs and the thermodynamic stability of ionic GCs is generally higher than that of non-ionic GC, thus leading to a lower risk of gadolinium dissociation. This class of drugs has enjoyed an excellent reputation in terms of safety for a long time, until a causal link with a recently-described serious disease, nephrogenic systemic fibrosis (NSF), was evidenced. It is acknowledged that the vast majority of NSF cases are related to the administration of some linear CG in renally-impaired patients. Health authorities, worldwide, released recommendations which drastically reduced the occurrence of new cases.

Diffusion-weighted MR imaging within 24 h post-injury after traumatic spinal cord injury: a qualitative meta-analysis between T2-weighted imaging and diffusion-weighted MR imaging in 18 patients.

STUDY DESIGN: Only few studies have been published about diffusion-weighted imaging (DWI) within 24 h of traumatic spinal cord injury (tSCI). OBJECTIVES: The purpose of this study was to compare the imaging findings from conventional magnetic resonance imaging (MRI) and DWI in seven tSCI patients with findings in the existing literature. METHODS: Seven patients with tSCI at neurologic levels C2-T10 were examined with conventional MRI and DWI within 24 h post-injury. DWI was obtained with a b-factor of 1000 s mm(-2). American Spinal Injury Association (ASIA) scores and Spinal Cord Independence Measurement (SCIM) II item 12 after 12 months were collected. In addition, MEDLINE was searched from 1995 to 2010 to identify clinical tSCI studies reporting on MRI, DWI and apparent diffusion coefficient maps within 24 h post-injury to perform a meta-analysis. Images obtained with a b-factor of 1000 s mm(-2) were compared with lower b-factors. Differences were calculated using χ (2) tests. RESULTS: No associations were identified between the images of the seven tSCI patients and ASIA or SCIM II scores. Eighteen SCI patients (11 from the retrieved publications) were included in the meta-analysis. The detection rates of hyperintense signals on T2-weighted and DW imaging did not show significant differences at 94 and 72%, respectively. In addition, there were no significant differences in detection rates or diffusion abnormalities between subjects in whom DW images were obtained with a maximum b-factor of 1000 or <1000 s mm(-2). CONCLUSION: Our analysis suggests that T2-weighted and DW imaging have comparable detection rates for spinal cord damage in tSCI patients within 24 h post-injury.

Prostaglandin E2 and tumor necrosis factor alpha cooperate to activate human dendritic cells: synergistic activation of interleukin 12 production.

Interleukin (IL)-12 is a proinflammatory cytokine that contributes to innate resistance and to the development of antigen-specific T cell responses. Among other effects, prostaglandin E2 (PGE2) inhibits the production of IL-12 by macrophages activated with lipopolysaccharide (LPS). Here we investigated the effects of PGE2 on human dendritic cells (DCs) which develop in the presence of GM-CSF and IL-4. We demonstrate that in the absence of LPS, PGE2 dose dependently stimulated the production of IL-12 by DCs. Although PGE2 alone stimulated the production of low amounts of IL-12 only, it synergized with tumor necrosis factor (TNF)-alpha to induce high levels of IL-12 production by DCs. Addition of TNF-alpha in the absence of PGE2 had no effect on IL-12 production. Conversely, in the presence of LPS, PGE2 inhibited IL-12 production by DCs in a dose-dependent manner. The combination of PGE2 and TNF-alpha efficiently silenced mannose receptor-mediated endocytosis in DCs and readily induced neo-expression of the CD83 antigen. In addition, the expression of various surface antigens such as major histocompatibility complex class I and II, adhesion, as well as costimulatory molecules was upregulated by this treatment. The effects of PGE2 on IL-12 synthesis and CD83 expression could be mimicked by dibutyryl-cAMP and forskolin, indicating that they were due to the intracellular elevation of cAMP levels. DC treated with PGE2 and TNF-alpha were most potent in stimulating allogeneic T cell proliferation. Our data demonstrate that PGE2 contributes to the maturation of human DCs and that PGE2 can be a potent enhancer of IL-12 production by human DCs.

Susceptibility-Weighted MR Imaging Hypointense Rim in Progressive Multifocal Leukoencephalopathy: The End Point of Neuroinflammation and a Potential Outcome Predictor.

BACKGROUND AND PURPOSE: Progressive multifocal leukoencephalopathy (PML) represents a life-threatening demyelinating disorder of the brain caused by reactivation of a rare opportunistic infection with JC Polyomavirus. The aims of this study were to describe the incidence of a susceptibility-weighted imaging hypointense rim in patients with multifocal leukoencephalopathy and to explore the histologic correlates and prognostic value of the rim with regard to the clinical outcome. MATERIALS AND METHODS: This retrospective study included 18 patients with a definite diagnosis of progressive multifocal leukoencephalopathy. Ten patients were HIV-positive, 3 patients had natalizumab-associated progressive multifocal leukoencephalopathy, 1 patient had multiple myeloma, 3 patients had a history of lymphoma, and 1 was diagnosed with acute myeloid leukemia. Patients were divided into short- (up to 12 months) and long-term (>12 months) survivors. A total of 93 initial and follow-up MR imaging examinations were reviewed. On SWI, the presence and development of a hypointense rim at the periphery of the progressive multifocal leukoencephalopathy lesions were noted. A postmortem histologic examination was performed in 2 patients: A rim formed in one, and in one, there was no rim. RESULTS: A total of 73 progressive multifocal leukoencephalopathy lesions were observed. In 13 (72.2%) patients, a well-defined thin, linear, hypointense rim at the periphery of the lesion toward the cortical side was present, while in 5 (27.8%) patients, it was completely absent. All 11 long-term survivors and 2 short-term survivors presented with a prominent SWI-hypointense rim, while 5/7 short-term survivors did not have this rim. CONCLUSIONS: The thin, uniformly linear, gyriform SWI-hypointense rim in the paralesional U-fibers in patients with definite progressive multifocal leukoencephalopathy might represent an end-point stage of the neuroinflammatory process in long-term survivors.

Persistent repression of a functional allele can be responsible for galactosyltransferase deficiency in Tn syndrome.

A human hematopoietic disorder designated as Tn syndrome or permanent mixed-field polyagglutinability has been ascribed to a stem cell mutation leading to a specific deficiency of UDP-Gal:GalNAc alpha 1-O-Ser/Thr beta 1-3 galactosyltransferase (beta 3 Gal-T) activity in affected cells. To test for the possibility that an allele of the beta 3Gal-T gene might be repressed instead of mutated, we have investigated whether 5-azacytidine or sodium n-butyrate, both inducers of gene expression, would reactivate expression of beta 3Gal-T in cloned enzyme-deficient T cells derived from a patient affected by the Tn syndrome. Flow cytometry revealed that a single treatment induced de novo expression of the Thomsen-Friedenreich antigen (Gal beta 1-3GalNAc-R), the product of beta 3Gal-T activity. In addition, a sialylated epitope on CD43 (leukosialin), which is present on normal but not on beta 3Gal-T-deficient T cells, was also reexpressed. Although no beta 3Gal-T activity was detectable in untreated Tn syndrome T cells, after exposure to 5-azaC,beta 3Gal-T activity reached nearly normal values. Both agents failed to reactivate beta 3Gal-T in Jurkat T leukemic cells, which also lack beta 3Gal-T activity. These data demonstrate that Tn syndrome T cells contain an intact beta 3Gal-T gene copy and that the enzyme deficiency in this patient is due to a persistent and complete but reversible repression of a functional allele. In contrast, the cause of beta 3Gal-T deficiency appears to be different in Jurkat T cells.

Intracranial infections: clinical and imaging characteristics.

The radiologist plays a crucial role in identifying and narrowing the differential diagnosis of intracranial infections. A thorough understanding of the intracranial compartment anatomy and characteristic imaging findings of specific pathogens, as well incorporation of the clinical information, is essential to establish correct diagnosis. Specific types of infections have certain propensities for different anatomical regions within the brain. In addition, the imaging findings must be placed in the context of the clinical setting, particularly in immunocompromised and human immunodeficiency virus (HIV)-positive patients. This paper describes and depicts infections within the different compartments of the brain. Pathology-proven infectious cases are presented in both immunocompetent and immunocompromised patients, with a discussion of the characteristic findings of each pathogen. Magnetic resonance spectroscopy (MRS) characteristics for several infections are also discussed.

Nordihydroguaiaretic acid blocks secretory and endocytic pathways in human dendritic cells.

Nordihydroguaiaretic acid (NDGA), an antioxidant and inhibitor of the lipoxygenase arm of the arachidonic acid metabolism, was recently demonstrated to inhibit transport of secretory proteins to the Golgi complex. We have investigated the effects of NDGA on the secretory and endocytic activity of cultured human blood dendritic cells (DC). Treatment with NDGA strongly diminished cytokine secretion by DC. Moreover, NDGA reduced in a dose- and time-dependent fashion fluid phase as well as receptor-mediated endocytosis in DC. Zileuton and MK-886, specific inhibitors of 5-lipoxygenase and 5-lipoxygenase-activating protein, respectively, had no effect. Likewise, N-acetyl-L-cysteine, a thiol antioxidant precursor of glutathione, did not affect DC function. Finally, serum remarkably protected the cells from the inhibitory effects of NDGA. Our data demonstrate that NDGA not only disrupts vesicular transport along the secretory route but is also a potent inhibitor of the endocytic pathways in human DC and that NDGA has inhibitory properties different from those described.

Differences in the regulation of specific glycosylation in the pathogenesis of paroxysmal nocturnal hemoglobinuria and the Tn-syndrome.

Paroxysmal nocturnal hemoglobinuria (PNH) is an acquired hematologic disorder that resembles in several aspects the Tn-syndrome, in which bone marrow-derived cells are deficient in mucin-type beta 1,3 galactosyltransferase (beta 1,3Gal-T) due to the persistent repression of an intact allele. In the present study, we have investigated phytohemagglutinin (PHA)-activated T cells from the peripheral blood of an individual with the well-established clinical diagnosis of PNH. Only 10% of T cells were deficient in surface expression of the glycosylphosphatidylinositol (GPI)-linked CD48 antigen; in contrast, 95% of the patient's polymorphonuclear leukocytes harbored the defect. The cell-surface density of CD48 on unaffected T cells from this patient was two- to three-fold higher when compared to PHA-activated normal donor T cells. CD48-negative T cells were cloned and shown to belong to the CD4+ or the CD8+ antigenic subset. To test for the possibility that in PNH, as in Tn syndrome, gene repression may be responsible for the deficiency, CD48- T cell clones were treated with 5-azacytidine (5-azaC) and sodium n-butyrate (NaB). While such treatment reproducibly led to reexpression of a sialylated CD43 epitope on affected Tn-syndrome T cell clones, these drugs failed to induce reexpression of CD48 on affected PNH T cell clones. Our data suggest that despite many similarities, different pathogenetic mechanisms are responsible for PNH and Tn-syndrome. These CD48- T cell clones are the first to be described and may be useful to define the PNH lesion at a biochemical and genetic level.

In vitro generation of CD83+ human blood dendritic cells for active tumor immunotherapy.

There is increasing clinical interest in dendritic cells that are capable of initiating antitumor immune responses. Dendritic cells cultured from human blood mononuclear cells using granulocyte/macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4) are competent for antigen uptake but express relatively low levels of costimulatory molecules and thus correspond to immature resident tissue dendritic cells. In this study we took advantage of the new dendritic cell-specific marker CD83, which is expressed by mature dendritic cells, to delineate the maturation of cultured human blood dendritic cells. Although dendritic cells cultured with GM-CSF and IL-4 contained transcripts for CD83 as determined by reverse transcription PCR, CD83 protein was barely detectable by flow cytometry, confirming that dendritic cells obtained with this system are immature. However, treatment of dendritic cells with tumor necrosis factor-alpha (TNF-alpha) significantly increased the levels of CD83 transcripts and induced CD83 protein expression in dendritic cells. In contrast to the initiation of dendritic cell culture, which was facilitated by high cell density (5 x 10(6) cells/mL), differentiation into CD83+ dendritic cells required a low cell concentration (0.5 x 10(6) cells/mL). At higher cell density (1 x 10(6) cells/mL), CD83 expression was suppressed and was almost completely prevented at 2 x 10(6) cells/mL. Induction of CD83 expression was accompanied by a strong upregulation of the costimulator B7-2 (CD86) on dendritic cells. While untreated CD83(-) dendritic cells efficiently internalized fluoresceinated Dextran, TNF-alpha treated CD83+ dendritic cells excluded these molecules, confirming that maturation of dendritic cells was associated with the silencing of the antigen-capturing machinery. Morphologically, CD83+ dendritic cells presented with pronounced cytoplasmic projections (veils) characteristic of mature dendritic cells. In summary, we show that cell density critically regulates dendritic cell development. Knowledge of the appropriate conditions for dendritic cell generation and maturation will be important in clinical immunotherapy settings.

How to image patients with spine pain.

Different radiological methods play an important role in the work-up of patients complaining of spine pain. Depending on the symptoms and the suspected underlying etiology different methods are selected. In the following presentation we briefly present the different radiological and magnetic resonance tomography methods that are at hand, give some guidance in which method to use, and present the typical imaging findings in some of the most common conditions that presents with spine pain.

Inhibition of LncaP prostate cancer cells by means of androgen receptor antisense oligonucleotides.

Currently available methods for treatment of human prostatic carcinoma aim to inactivate the androgen receptor (AR) by androgen deprivation or blockade with anti-androgens. Failure of endocrine therapy and tumor progression is characterized by androgen-independent growth despite high levels of AR expression in metastatic disease. We inhibited AR expression in LNCaP prostate tumor cells by using antisense AR oligodeoxynucleotides (ODNs) and explored whether antisense AR treatment would be conceivable as a therapy for advanced prostate cancer. Among the various AR antisense ODNs tested, a 15-base ODN targeting the CAG repeats encoding the poly-glutamine region of the AR (as750/15) was found to be most effective. Treatment of LNCaP cells with as750/15 reduced AR expression to approximately 2% within 24 hours compared with mock-treated controls. AR down-regulation resulted in significant cell growth inhibition, strongly reduced secretion of the androgen-regulated prostate-specific antigen, reduction of epidermal growth factor receptor expression, and an increase in apoptotic cells. Mis-sense and mismatched control ODNs had no or only slight effects. Antisense inhibition was also very efficient in LNCaP-abl cells, a subline established after long-term androgen ablation of LNCaP cells, resulting in inhibition of AR expression and cell proliferation that was similar to that seen for parental LNCaP cells. This study shows that inhibition of AR expression by antisense AR ODNs may be a promising new approach for treatment of advanced human prostate cancer.

Use of O-glycosylation-defective human lymphoid cell lines and flow cytometry to delineate the specificity of Moluccella laevis lectin and monoclonal antibody 5F4 for the Tn antigen (GalNAc alpha 1-O-Ser/Thr).

The Tn antigen (GalNAc alpha 1-O-Ser/Thr) is a disease-related O-linked (mucin-type) carbohydrate neoantigen which is expressed in idiopathic Tn syndrome, AIDS, T-cell lymphoma and in many carcinomas. In the present study, we took advantage of a Tn antigen expressing T-lymphocyte clone derived from a patient with the idiopathic form of the Tn syndrome and the Tn+ Jurkat cell line to characterize new reagents that should identify Tn antigens (monoclonal antibody 5F4 and a lectin newly isolated from Moluccella laevis seeds). Flow cytometry revealed that both reagents strongly bound to Tn antigen expressing T lymphocytes but not to normal donor T cells, which are Tn negative. In contrast to mAb 5F4, Moluccella laevis lectin weakly bound to normal donor cells after sialidase pretreatment, indicating its broader specificity. N-Acetyl-D-galactosamine at a concentration of 100 mM significantly reduced antibody binding and abolished lectin binding, completely demonstrating the sugar specificity of both reagents. These reagents should be useful tools in glycobiology and for clinical purposes.

A clinically approved oral vaccine against pneumotropic bacteria induces the terminal maturation of CD83+ immunostimulatory dendritic cells.

Dendritic cells (DCs) are important antigen-presenting cells of the immune system that have attracted interest as cellular adjuvants to induce immunity in clinical settings. We have investigated the effects of Broncho-Vaxom, an oral vaccine composed of lysates from eight pneumotropic bacteria, on human monocyte-derived dendritic cells (moDCs). Broncho-Vaxom induced the terminal maturation of CD83+ moDCs. MoDCs stimulated with Broncho-Vaxom displayed a phenotype of activated DCs with high levels of major histocompatibility complex (MHC) molecules and increased levels of adhesion and co-stimulatory molecules. In addition, moDCs activated with Broncho-Vaxom exhibited enhanced T cell-stimulatory capacity in the allogeneic mixed leukocyte reaction. Broncho-Vaxom at 100 microg/ml was as potent as TNF-alpha at 1000 U/ml in activating human moDCs. Neither LPS-like activity nor bacterial DNA was found to be responsible for the maturation-inducing activity of Broncho-Vaxom, suggesting that Broncho-Vaxom contains other bacterial factors that are capable of inducing the terminal maturation of moDCs. In DC-based immunotherapy, Broncho-Vaxom could be used as a stimulus of DC maturation, which meets the standards of good manufacturing practice (GMP). In addition, vaccination with Broncho-Vaxom-loaded moDCs may be an attractive treatment option in preventing recurrent airway infection in predisposed individuals.

Relationship between coronary hemodynamic changes and the phasic events of rapid eye movement sleep.

Previous studies in dogs showed dramatic increases in coronary blood flow associated with episodes of sinus tachycardia during rapid eye movement (REM) sleep. The present study demonstrates that 90% of these surges in heart rate and coronary flow are concentrated during periods of phasic REM sleep and only 10% in tonic REM sleep. Intensely phasic REM was distinguished from moderately phasic REM sleep by the degree of phasic eye movement. The surges were three times more frequent during intensely phasic REM than in moderately phasic REM sleep. However, the magnitudes of heart rate (37% +/- 3%) and coronary flow (25% +/- 3%) surges were unaffected by the specific substage of REM sleep. The incidence of surge events was almost eleven times greater in epochs of phasic REM that also contained a muscle twitch than in those that did not. During REM sleep, muscle twitches accompanying surges were not associated with any additional elevations in coronary flow or myocardial demand. Our data indicate that the sinus tachycardia-associated surges in coronary flow represent integrated autonomic responses intrinsic to phasic periods of REM sleep in dogs.

Local and systemic reactions after lung contusion: an experimental study in the pig.

The present study was designed to investigate the consequences of isolated unilateral lung contusion on local alveolar and systemic inflammatory responses in an animal model in the pig. Isolated unilateral lung contusion was induced by bolt shot in eight mechanically ventilated animals under general anesthesia (sham: n=4). Plasma and bronchoalveolar lavage fluid were collected during a period of 8 h following lung contusion. Leukocytes, leukocyte neutral protease inhibitor (LNPI), terminal complement complex (TCC), thrombin-antithrombin-complex (TAT) as well as pulmonary microvascular permeability and surfactant function were determined. Within 30 min, lung contusion was found to cause a significant local and systemic increase in TCC and TAT concentrations and a systemic increase in LNPI concentrations. The latter was accompanied by a sequestration of leukocytes in the contused lung. Complement activation and leukocyte sequestration in the contused lung progressively increased during the investigation period. Although surfactant function decreased in the entire lung 30 min after contusion, TCC, TAT, and leukocyte sequestration was unchanged in the contralateral lung. The first indication of an involvement of the contralateral lung was obtained by an increase in leukocyte sequestration 8 h after lung contusion. Unilateral lung contusion initiates an early systemic activation of humoral and cellular defense systems. Involvement of the contralateral lung appears to be a secondary event caused by a systemic inflammatory reaction.

Initial and follow-up MR imaging findings in AIDS-related progressive multifocal leukoencephalopathy treated with highly active antiretroviral therapy.

BACKGROUND AND PURPOSE: Recent studies have shown the beneficial effect of highly active antiretroviral therapy (HAART) in AIDS-related progressive multifocal leukoencephalopathy (PML). The purpose of our study was to evaluate the initial and follow-up imaging findings and survival in patients with PML who were treated with HAART. METHODS: The clinical course and MR imaging findings on initial and follow-up MR studies in four consecutive AIDS patients with PML who were treated with HAART are described. RESULTS: Two patients were short-term survivors and died after 3 months. Two patients are still alive, with a survival time of 22 and 43 months, respectively. On initial MR studies, more extensive white matter changes were seen in the short-term survivors. Development of a mass effect and temporary enhancement (in one patient) was observed in two HAART responders on follow-up MR studies. Increased hypointensity on T1-weighted images with concomitant low signal on fluid-attenuated inversion-recovery fast spin-echo (FLAIR-FSE) images was seen in two responders, representing leukomalacia. Atrophic changes of the involved areas of the brain, consistent with burnt out PML lesions, were seen in two long-term survivors. In the short-term survivors, increased hypointensity was present on T1-weighted images with increased high signal on FLAIR-FSE images, representing progressive destructive disease. CONCLUSION: Our results suggest that a clinical and radiologic response can be seen in some patients with AIDS-associated PML on HAART while in others there may be no beneficial response. Development of a mass effect and temporary enhancement on MR images in the early phase of treatment might represent positive predictive factors for prolonged survival.

Comparison of T2-weighted and fluid-attenuated inversion-recovery fast spin-echo MR sequences in intracerebral AIDS-associated disease.

PURPOSE: To compare the value of fast fluid-attenuated inversion-recovery (FLAIR) with T2-weighted fast spin-echo MR imaging in the detection of acquired immunodeficiency virus (AIDS)-related lesions of the brain. METHODS: Forty-four human immunodeficiency virus (HIV)-positive patients were examined with both sequences on either a 1.0-T or a 1.5-T MR system. The number, size, location, and conspicuity of the lesions were evaluated by two independent observers. Contrast ratios between lesions and normal brain/cerebrospinal fluid were determined, and contrast-to-noise ratios were calculated. RESULTS: FLAIR was found to be superior to T2-weighted fast spin-echo in detection of small lesions and of lesions located in cortical/subcortical regions and deep white matter. The two techniques were equal in delineation of lesions larger than 2 cm and for lesions located in the basal ganglia and posterior fossa. In 24 patients, more lesions were detected with the FLAIR fast spin-echo technique. Lesion/cerebrospinal fluid contrast ratios and contrast-to-noise ratios were significantly higher for the FLAIR fast spin-echo sequences than for the T2-weighted fast spin-echo sequences. CONCLUSION: FLAIR allows early detection of small lesions in subcortical and cortical locations, especially in HIV encephalitis. Because of its improved lesion detection rate and greater overall lesion conspicuity, we believe FLAIR is useful in the evaluation of subtle changes in the brains of AIDS patients with central nervous system disease, and could even replace the T2-weighted fast spin-echo technique.

Highly active antiretroviral therapy for patients with AIDS dementia complex: effect on MR imaging findings and clinical course.

BACKGROUND AND PURPOSE: Recent studies have reported the clinical improvement in patients with AIDS treated with a combination of antiretroviral regimens. The purpose of our study was to describe the effects of highly active antiretroviral therapy on MR images in patients with HIV encephalopathy and to compare the clinical course with follow-up neuroimaging studies. METHODS: Initial and follow-up MR imaging findings are described in four patients with AIDS dementia complex at baseline and after antiretroviral therapy, and correlated with clinical and immunologic findings. RESULTS: Initial MR imaging revealed white matter signal abnormalities on long-TR images without mass effect and without enhancement on postcontrast images, consistent with HIV encephalopathy. Lesions were located in the basal ganglia and posterior fossa in two patients. All four patients showed progression of white matter disease on the first follow-up MR scan (mean, 6 months). On subsequent scans, regression was seen in three patients and stabilization of white matter disease was observed in one patient. Increases in CD4+ count and decreases in viral load below the limit of quantification were present in all patients. CONCLUSION: Although our patient population was small, the results suggest that disease regression in patients with AIDS dementia complex after treatment with highly active antiretroviral therapy can be characterized and monitored by MR imaging.

The postoperative spine.

During the last decade, magnetic resonance imaging (MRI) mostly has replaced computed tomography for evaluation of spinal surgery patients. The inherent advantages of MRI are obvious for this particularly difficult field of imaging. With MRI, it is possible to demonstrate anatomic as well as pathological and iatrogenic changes in three different imaging planes and countless neighboring planes and to obtain a superior view of the complex postoperative situation regardless of the spinal level imaged. Soft-tissue masses in particular can be identified more readily and located within three-dimensional space. One of the major advantages is that the nature and histology of the mass can be estimated precisely using different MR sequences in combination with intravenous contrast media. The most important benefit may be demonstration of inflammatory and hemorrhagic masses in the early postoperative periods (with special emphasis on alterations visible in the spinal cord itself) as well as repair processes and ongoing degeneration in later stages. This visualization is possible even when their extent is limited. In the postoperative spine, the application of MRI was facilitated with the advent of new materials, such as titanium alloys, used for surgical instrumentation. These new materials limit the amount of artifacts visible on MR images. Earlier implants made of other metallic material prohibit the use of computed tomography in the spine. This article provides a brief overview of the progress in spinal surgery and focuses on the developments in MRI techniques during the last decade. Technical questions about imaging of spinal instrumentation are discussed. "Normal" postoperative findings needed for interpretation of pathologic conditions are also discussed. Finally, the most important frequently asked questions from referring surgeons that radiologists must be able to answer by MRI are presented.