Renato Hoffmann Nunes

High Signal Intensity in Globus Pallidus and Dentate Nucleus on Unenhanced T1-weighted MR Images: Evaluation of Two Linear Gadolinium-based Contrast Agents.

PURPOSE To determine if a correlation exists between the number of previous enhanced magnetic resonance (MR) imaging examinations and high signal intensity in the globus pallidus (GP) and dentate nucleus (DN) in patients who received gadodiamide (Omniscan), a linear nonionic gadolinium-based contrast agent, and in those who received gadobenate dimeglumine (MultiHance), a linear ionic contrast agent. MATERIALS AND METHODS Institutional review board approval was obtained for this single-center retrospective study, with waiver of informed consent. The study population included 69 patients divided into two groups: Group 1 included patients who underwent gadodiamide-enhanced MR imaging, and group 2 included patients who underwent gadobenate dimeglumine-enhanced MR imaging. Two radiologists conducted a quantitative analysis of unenhanced T1-weighted images by using region of interest measurements. The GP-to-thalamus (TH) signal intensity ratio, DN-to-middle cerebellar peduncle (MCP) signal intensity ratio and relative percentage change (Rchange) between the first and last examinations for each patient were calculated. Relation between the signal intensity ratios and Rchange and the number of enhanced MR imaging examinations was analyzed by using a generalized additive model. Inter- and intraobserver agreement was evaluated with the Lin concordance correlation coefficient test. RESULTS Group 1 included 23 patients (19 female), with a mean of 5.0 doses ± 2.4 (standard deviation) (range, 3-11 doses) administered. Group 2 included 46 patients (24 female) with a mean of 4.6 doses ± 2.2 (range, 3-11 doses) administered. The interval between the first and last examination was 1500.1 days ± 780.2 (range, 98-3097 days) for group 1 and 1086.2 days ± 582.9 (range, 94-2633) for group 2. All patients had normal liver and renal function. Gadodiamide showed a significant increase in DN:MCP and GP:TH (P < .001 for both) and in Rchange (P = .001 for GP:TH, P < .001 for DN:MCP). In group 2, there was no significant increase in DN:MCP or GP:TH over time or in Rchange for GP:TH, but there was a significant trend toward an increase in Rchange for DN:MCP (P = .013). Interobserver agreement was almost perfect (0.99; 95% confidence interval: 0.99, 0.99) for all evaluated structures. Intraobserver agreement was substantial to almost perfect for both readers. CONCLUSION A significant increase in GP:TH and DN:MCP is associated with multiple gadodiamide-enhanced studies but not with gadobenate dimeglumine-enhanced studies, likely reflecting differences in stability and elimination of both contrast agents. Rate-of-change data indirectly suggest gadolinium deposition in the DN with gadobenate dimeglumine use, although it is considerably less than that with gadodiamide use.

Gadolinium-Based Contrast Agent Accumulation and Toxicity: An Update

SUMMARY: In current practice, gadolinium-based contrast agents have been considered safe when used at clinically recommended doses in patients without severe renal insufficiency. The causal relationship between gadolinium-based contrast agents and nephrogenic systemic fibrosis in patients with renal insufficiency resulted in new policies regarding the administration of these agents. After an effective screening of patients with renal disease by performing either unenhanced or reduced-dose-enhanced studies in these patients and by using the most stable contrast agents, nephrogenic systemic fibrosis has been largely eliminated since 2009. Evidence of in vivo gadolinium deposition in bone tissue in patients with normal renal function is well-established, but recent literature showing that gadolinium might also deposit in the brain in patients with intact blood-brain barriers caught many individuals in the imaging community by surprise. The purpose of this review was to summarize the literature on gadolinium-based contrast agents, tying together information on agent stability and animal and human studies, and to emphasize that low-stability agents are the ones most often associated with brain deposition.

T1 Signal-Intensity Increase in the Dentate Nucleus after Multiple Exposures to Gadodiamide: Intraindividual Comparison between 2 Commonly Used Sequences

The authors performed intraindividual qualitative and quantitative comparison between T1-weighted spin-echo and 3D MPRAGE images in 18 patients who had multiple exposures to gadodiamide. Differences in signal between the 2 sequences for both baseline and last examination dentate nucleus/middle cerebellar peduncle ratios were statistically significant. They conclude that T1-weighted spin-echo and MPRAGE sequences cannot be used interchangeably for qualitative or quantitative signal intensity analysis of the dentate nucleus in patients who received gadodiamide. BACKGROUND AND PURPOSE: Different T1-weighted sequences have been used for qualitative and quantitative evaluation of T1 signal intensity related to gadolinium deposition in the dentate nucleus in patients who underwent several enhanced MR imaging studies. Our purpose was to perform an intraindividual qualitative and quantitative comparison between T1-weighted spin-echo and 3D magnetization-prepared rapid acquisition of gradient echo sequences in patients who had multiple exposures to gadodiamide. MATERIALS AND METHODS: Our retrospectively selected population included 18 patients who underwent at least 3 administrations of gadodiamide and had a baseline and a final MR imaging performed with both T1-weighted sequences. Qualitative and quantitative analyses were independently performed. Dentate nucleus/middle cerebellar peduncle signal-intensity ratios and signal changes between the baseline and final examinations were compared by using the Wilcoxon signed rank test. Correlation between quantitative and qualitative evaluations was assessed by using a polyserial correlation test. RESULTS: The differences between the 2 sequences for both baseline and last examination dentate nucleus/middle cerebellar peduncle ratios were statistically significant (P = .008 and P = .006, respectively); however, the signal-intensity changes of the ratios with time were not (P = .64). The correlation between the qualitative and quantitative analysis was very strong (near-perfect) (r = 0.9) for MPRAGE and strong (r = 0.63) for spin-echo sequences. CONCLUSIONS: T1-weighted spin-echo and MPRAGE sequences cannot be used interchangeably for qualitative or quantitative analysis of signal intensity in the dentate nucleus in patients who received gadodiamide. Baseline and final examination ratios should be evaluated across time by using the same sequence. Qualitative analysis performed with MPRAGE correlated better with quantitative analysis and may offer advantages over spin-echo sequences for research purposes.

Recognizing Autoimmune-Mediated Encephalitis in the Differential Diagnosis of Limbic Disorders

SUMMARY: Limbic encephalitis is far more common than previously thought. It is not always associated with cancer, and it is potentially treatable. Autoantibodies against various neuronal cell antigens may arise independently or in association with cancer and cause autoimmune damage to the limbic system. Neuroimaging plays a key role in the management of patients with suspected limbic encephalitis by supporting diagnosis and excluding differential possibilities. This article describes the main types of autoimmune limbic encephalitis and its mimic disorders, and emphasizes their major imaging features.

Imaging of Creutzfeldt-Jakob Disease: Imaging Patterns and Their Differential Diagnosis

Diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD) remains a challenge because of the large variability of the clinical scenario, especially in its early stages, which may mimic several reversible or treatable disorders. The molecular basis of prion disease, as well as its brain propagation and the pathogenesis of the illness, have become better understood in recent decades. Several reports have listed recognizable clinical features and paraclinical tests to supplement the replicable diagnostic criteria in vivo. Nevertheless, we lack specific data about the differential diagnosis of CJD at imaging, mainly regarding those disorders evolving with similar clinical features (mimicking disorders). This review provides an update on the neuroimaging patterns of sCJD, emphasizing the relevance of magnetic resonance (MR) imaging, summarizing the clinical scenario and molecular basis of the disease, and highlighting clinical, genetic, and imaging correlations in different subtypes of prion diseases. A long list of differential diagnoses produces a comprehensive pictorial review, with the aim of enabling radiologists to identify typical and atypical patterns of sCJD. This review reinforces distinguishable imaging findings and confirms diffusion-weighted imaging (DWI) features as pivotal in the diagnostic workup of sCJD, as these findings enable radiologists to reliably recognize this rare but invariably lethal disease. A probable diagnosis is justified when expected MR imaging patterns are demonstrated and CJD-mimicking disorders are confidently ruled out. ©RSNA, 2017.

Toxic and Metabolic Myelopathies

Myelopathy describes any neurologic deficit related to the spinal cord. It is most commonly caused by its compression by neoplasms, degenerative disc disease, trauma, or infection. Less common causes of myelopathy include spinal cord tumors, infection, inflammatory, neurodegenerative, vascular, toxic, and metabolic disorders. Conditions affecting the spinal cord must be recognized as early as possible to prevent progression that may lead to permanent disability. Biopsy is rarely performed, thus the diagnosis and management rely on patient׳s history, physical examination, laboratory results, and imaging findings. Here we review the clinical presentations, pathophysiological mechanisms, and magnetic resonance imaging findings of myelopathies related to metabolic or toxic etiologies.

Familial striatal degeneration: New mutation and neuroimaging clues

Autosomal dominant striatal degeneration (ADSD) (MIM 609161) is a rare genetic disease caused by mutation in the PDE8B gene.1,2 The disease, with onset in the fourth to fifth decade, is characterized by slowly progressive dysarthria, mild parkinsonism but no tremor, brisk deep tendon reflexes, poor response to levodopa treatment, and distinctive brain MRI findings.1,2 Heterozygous mutations in the PDE8B gene, first identified in a German family,2 result in loss of protein cyclic nucleotide phosphodiesterase (PDE) function. PDEs are responsible for the breakdown of cyclic nucleotides, cyclic adenosine monophosphate, and cyclic guanosine monophosphate, and play a major role in striatal neuron regulation.3 The PDE superfamily consists of 11 families (PDE1–PDE11), each of which has 1 to 4 subtypes. Some neuropsychiatric and neurodegenerative diseases, including depression, schizophrenia, Parkinson disease, Alzheimer disease, and Huntington disease, have changes in phosphodiesterase expression in the brain.3 PDE8B expression is higher in specific brain regions affected by ADSD (putamen, caudate nucleus, and nucleus accumbens), producing peculiar lesions in the striatum.2,3

Neuromyelitis Optica Spectrum Disorders: Spectrum of MR Imaging Findings and Their Differential Diagnosis

Neuromyelitis optica (NMO) is an autoimmune demyelinating disorder for which the aquaporin-4 (AQP4) water channels are the major target antigens. Advances in the understanding of NMO have clarified several points of its pathogenesis, clinical manifestations, and imaging patterns. A major advance was the discovery of the AQP4 antibody, which is highly specific for this disorder. Descriptions of new clinical and radiologic features in seropositive patients have expanded the spectrum of NMO, and the term NMO spectrum disorder (NMOSD) has been adopted. NMOSD is now included in a widening list of differential diagnoses. Acknowledgment of NMOSD imaging patterns and their mimicry of disorders has been crucial in supporting early NMOSD diagnosis, especially for unusual clinical manifestations of this demyelinating disease. This pictorial review summarizes the wide imaging spectrum of NMOSD and its differential diagnosis, as well as its historical evolution, pathophysiology, and clinical manifestations. ©RSNA, 2018.

Imaging in Endoscopic Cranial Skull Base and Pituitary Surgery

Endoscopic endonasal approaches have widely accepted techniques for managing benign and malignant processes along the entire ventral skull base with similar or better results compared with open procedures, but with lower rates of complication. Managing pathology affecting the skull base can be challenging because of complex anatomy and the proximity of critical neurovascular structures. Postoperative imaging can be challenging, because of surgical alterations of normal anatomy and the now common use of complex reconstruction techniques. Understanding the normal imaging appearance of skull base reconstruction is important for accurate postoperative interpretation and delineation between normal reconstructive tissue and recurrent neoplasm.

A distinct imaging phenotype in amyotrophic lateral sclerosis confidently detected on T1 MTC

A 57-year-old woman presented with a progressing asymmetric (left to right) weakness and wasting that spread in the next 3 months from her lower to upper limbs; she exhibited mild hyper-reflexia in all four limbs. No cognitive or sensory impairment was detected. Cerebrospinal fluid and blood analyses were unremarkable. Electromyography showed pathological signs of denervation and chronic reinnervation with spontaneous activity at rest, consistent with a motor neuron disease. The presence of upper motor neuron (UMN) and lower motor neuron (LMN) signs together in multiple regions, on clinical and …