T2 Signal Hyperintensity Research Articles

An MRI-guided HIFU-triggered wax-coated capsule for supertargeted drug release: a proof-of-concept study

BackgroundExternally controlling and monitoring drug release at a desired time and location is currently lacking in the gastrointestinal tract. The aim of the study was to develop a thermoresponsive wax-coated capsule and to trigger its release upon applying a magnetic resonance imaging (MRI)-guided high-intensity focused ultrasound (HIFU) pulse.MethodsCapsules containing a lyophilised gadolinium-based contrast agent (GBCA) were coated with a 1:1 (mass/mass) mixture of lanolin and cetyl alcohol (melting point ≈43 °C) and exposed to simulated gastric and intestinal fluids (United States Pharmacopoeia) at 37 °C for 2 and 24 h, respectively. In a HIFU gel phantom, wax-coated capsules (n = 3) were tracked based on their T1- and T2-hypointensity by 1.5-T T1- and T2-weighted MRI pre- and post-exposure to an MRI-guided HIFU pulse.ResultsLanolin/cetyl alcohol-coated capsules showed high resistance to simulated gastrointestinal fluids. In a gel phantom, an MRI-guided HIFU pulse punctured the wax coating, resulting in the hydration and release of the encapsulated lyophilised GBCA and yielding a T1-hyperintense signal close to the wax-coated capsule.ConclusionWe provide the proof-of-concept of applying a non-invasive MRI-guided HIFU pulse to actively induce the disintegration of the wax-coated capsule, and a method to monitor the release of the cargo via T1-weighted MRI based on the hydration of an encapsulated lyophilised GBCA. The wax-coated capsule platform enables temporally and spatially supertargeted drug release via the oral route and promises to address a currently unmet clinical need for personalised local therapy in gastrointestinal diseases such as inflammatory bowel diseases and cancer.

The Magnetic Resonance Imaging Appearance of Endoscopic Endonasal Skull Base Defect Reconstruction Using Free Mucosal Graft

At our institution, skull base reconstruction using a free mucosal graft from the nasal cavity floor has been the standardized technique after pituitary adenoma resection via transsellar approach. In this study, the expected appearance of the reconstruction on postoperative magnetic resonance imaging (MRI) scans is described and its integrity and impact on the sinonasal cavity are assessed. Fifty patients were selected, and their electronic medical records were reviewed for postoperative course, Sino-Nasal Outcome Test-22 (SNOT-22) scores, and nasal endoscopy reports. A total of 116 postoperative MRI scans were available to evaluate 1) the appearance and thickness of the graft, 2) the enhancement of the graft, and 3) the T2 signal in sphenoid sinus as a potential indication for inflammatory disease. There was no significant change in the thickness of the graft over time. Except for the 7 scans that were obtained without intravenous contrast, all scans showed enhancement of the graft. About half of the patients showed persistent T2 hyperintense signal at 12 and 24 months. However, this finding was not clinically significant, because postoperative SNOT-22 scores showed minimal sinonasal impact. Postoperative MRI surveillance scans showed a stable appearance of the graft that mimics the native mucosa, with enhancement through time, reflecting its robust vascularization and integration to the skull base. Although persistent T2 hyperintense signal was detected in the sphenoid sinus, clinical evidence based on nasal endoscopy reports and SNOT-22 scores indicated minimal sinonasal morbidity.

Leukoencephalopathy due to variants in GFPT1-associated congenital myasthenic syndrome.

To determine the molecular etiology of disease in 4 individuals from 2 unrelated families who presented with proximal muscle weakness and features suggestive of mitochondrial disease. Clinical information and neuroimaging were reviewed. Genome sequencing was performed on affected individuals and biological parents. All affected individuals presented with muscle weakness and difficulty walking. In one family, both children had neonatal respiratory distress while the other family had 2 children with episodic deteriorations. In each family, muscle biopsy demonstrated ragged red fibers. MRI was suggestive of a mitochondrial leukoencephalopathy, with extensive deep cerebral white matter T2 hyperintense signal and selective involvement of the middle blade of the corpus callosum. Through genome sequencing, homozygous GFPT1 missense variants were identified in the affected individuals of each family. The variants detected (p.Arg14Leu and p.Thr151Lys) are absent from population databases and predicted to be damaging by in silico prediction tools. Following the genetic diagnosis, nerve conduction studies were performed and demonstrated a decremental response to repetitive nerve stimulation, confirming the diagnosis of myasthenia. Treatment with pyridostigmine was started in one family with favorable response. GFPT1 encodes a widely expressed protein that controls the flux of glucose into the hexosamine-biosynthesis pathway that produces precursors for glycosylation of proteins. GFPT1 variants and defects in other enzymes of this pathway have previously been associated with congenital myasthenia. These findings identify leukoencephalopathy as a previously unrecognized phenotype in GFPT1-related disease and suggest that mitochondrial dysfunction could contribute to this disorder.

Adhesive capsulitis: review of imaging findings, pathophysiology, clinical presentation, and treatment options.

Adhesive capsulitis, commonly referred to as "frozen shoulder," is a debilitating condition characterized by progressive pain and limited range of motion about the glenohumeral joint. It is a condition that typically affects middle-aged women, with some evidence for an association with endocrinological, rheumatological, and autoimmune disease states. Management tends to be conservative, as most cases resolve spontaneously, although a subset of patients progress to permanent disability. Conventional arthrographic findings include decreased capsular distension and volume of the axillary recess when compared with the normal glenohumeral joint, in spite of the fact that fluoroscopic visualization alone is rarely carried out today in favor of magnetic resonance imaging (MRI). MRI and MR arthrography (MRA) have, in recent years, allowed for the visualization of several characteristic signs seen with this condition, including thickening of the coracohumeral ligament, axillary pouch and rotator interval joint capsule, in addition to the obliteration of the subcoracoid fat triangle. Additional findings include T2 signal hyperintensity and post-contrast enhancement of the joint capsule. Similar changes are observable on ultrasound. However, the use of ultrasound is most clearly established for image-guided injection therapy. More aggressive therapies, including arthroscopic release and open capsulotomy, may be indicated for refractory disease, with arthroscopic procedures favored because of their less invasive nature and relatively high success rate.

Global Burden Related to Nitrous Oxide Exposure in Medical and Recreational Settings: An Individual Patient Data Meta-Analysis

Background: The risk of adverse effects of nitrous oxide (N2O) exposure is insufficiently recognised despite its widespread use. These effects are mainly reported through case reports. Methods: We conducted an individual patient data meta-analysis to assess the prevalence of clinical, laboratory, and magnetic resonance findings in association with N2O exposure in medical and recreational settings. We calculated the pooled estimates for the studied outcomes and assessed the potential bias related to population stratification using principal component analysis. Findings: Eighty-five publications met the inclusion criteria and reported on 100 patients with a median age of 27 years and 57% of recreational users. The most frequent outcomes were subacute combined degeneration (28%), myelopathy (26%), and generalised demyelinating polyneuropathy (23%). A T2 signal hyperintensity in the spinal cord was reported in 68% (57·2%-78·8%) of patients. The most frequent clinical manifestations included paraesthesia (80%; 72·0%-88·0%), unsteady gait (58%; 48·2%-67·8%), and weakness (43%; 33·1%-52·9%). At least one haematological abnormality was retrieved in 71·7% (59·9%-83·4%) of patients. Most patients had vitamin B12 deficiency: vitamin B12 15 µmol/L (90·3%; 79·3%-100%), and methylmalonic acid >0·4 µmol/L (93·8%; 80·4%-100%). Interpretation: N2O can produce severe outcomes, with neurological or haematological disorders in almost all published cases. More than half of them are reported in the setting of recreational use. The N2O-related burden is dominated by vitamin B12 deficiency. This highlights the need to evaluate whether correcting B12 deficiency would prevent N2O-related toxicity, particularly in countries with a high prevalence of B12 deficiency. Funding Statement: INSERM UMR_S 1256. Declaration of Interest: Authors declare no conflict of interest

Imaging features (CT, MRI, MRS, and PET/CT) of primary central nervous system lymphoma in immunocompetent patients

BackgroundBecause of the low incidence of primary central nervous system lymphoma (PCNSL) in non-HIV individuals and because of the lack of specific clinical manifestations and auxiliary examinations, the disease is easily missed or misdiagnosed.ObjectiveTo analyze the imaging features of PCNSL in non-HIV patients.MethodsThis was a retrospective study of patients with PCNSL treated between January 2001 and December 2011 at the Naval General Hospital (Beijing, China). All included patients were pathologically diagnosed with PCNSL. Specimens were obtained by stereotactic biopsy and diagnosed by pathological examination. Serological panel had to be negative for HIV.ResultsOut of the 118 patients, 73 (61.9%) were male and 45 (38.1%) were female. Median age was 54 (range 11–83) years. All patients had B cell lymphoma. The lesions showed slightly hyperintense shadows on computed tomography (CT) images, and mostly hyperintense T1 and iso- or hyperintense T2 signals on magnetic resonance imaging (MRI). Most lesions showed patchy enhancement after enhanced scanning, and some had the characteristic “butterfly sign” on enhanced MRI. The magnetic resonance spectroscopy of PCNSL manifested as increased Cho peak, moderately decreased NAA peak, and slightly decreased Cr peak. Positron emission computed tomography indicated high metabolism of 18F-FDG in PCNSL lesions.ConclusionMRI is important in the diagnosis of PCNSL. Understanding the imaging features of PCNSL will help improve its diagnosis in clinics.

Electrophysiological assessment of lower cranial nerve palsy triggered by spontaneous extracranial carotid dissection

A 43-year-old man was admitted to our department for the acute onset of unilateral right throbbing headache. Neurologic examination revealed right ocular myosis and ptosis, left displacement of the uvula, dysphonia, weak left-turning of the head, right scapular winging on arm abduction and right tongue deviation, suggesting 9th through 12th cranial nerve palsy and Horner’s syndrome. Neurophysiologic examination confirmed the unilateral involvement. EMG showed loss of motor unit recruitment and denervation activity in the right sternocleidomastoid, trapezius and genioglossus muscles. MEPs and C-MAP were not excitable from those muscles. MRI demonstrated a crescent-shaped hyperintense T1 and T2 signal within the wall of the distal extracranial portion of the right internal carotid artery (ICA), suggesting an intramural hematoma causing mass effect upon the internal jugular vein. A diagnosis of spontaneous extracranial carotid dissection was made. An extended CT angiogram showed extensive luminal irregularities in the main renal arteries, with aneurysm formation at its bifurcation. Ibromuscular dysplasia was hypothesized and genetic counseling for connective tissue was carried on. Cranial nerve palsy is an unusual presentation of extracranial ICA dissection, likely mediated by compression or stretching of the nerve by the expanded artery. Neurophysiological testing provides useful information to localize the damage and to better understand the pathophysiology of the disease.

ONDINE'S CURSE DUE TO OSMOTIC DEMYELINATION SYNDROME

SESSION TITLE: Critical Care 3 SESSION TYPE: Fellow Case Report Posters PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Osmotic Demyelination Syndrome is a life-threatening complication of sudden rise in serum osmolality after a chronic hypotonicity. The damage depends highly on the brains response to changing serum concentration and can present with many symptoms. Here we describe a patient treated for severe hyponatremia who later presented with Ondine’s curse. CASE PRESENTATION: A 67-year-old Caucasian male transferred to a tertiary facility from a rural hospital. Initially admitted and intubated for worsening shortness of breath; community-acquired pneumonia and alcohol withdrawal. History revealed a drinking habit of twelve or more bottles of alcohol daily, he also drank excessive amounts of water in the previous month with minimal eating. Laboratory data revealed serum sodium concentration was between 143 and 152 throughout hospitalization with no significant acute changes.One week after admission, multiple trails of extubation were unsuccessful and he was found to have no gag reflex, dysphagia or central hypoventilation. Therefore, Brain magnetic resonance imaging (MRI) was obtained; results showed early T2 hyperintense signal within the pons centrally in a pattern suggesting Osmotic Demyelination syndrome (ODS) (figures 1 & 2).Patient remained conscious and needed to be transferred to a long-term nursing facility after tracheostomy and percutaneous endoscopic gastrostomy. DISCUSSION: A hypotonic hyponatremia state in the body naturally forces fluid across the blood brain barrierincreasing water content. This decreased serum tonicity leads to swelling of many brain cells, mainly astrocytes. Astrocytes surround the brains capillaries with foot processes and contain the vital water channels that regulate cellular solutes and water across the blood-brain-barrier. If the brain were not able to adapt to a fall in tonicity, the cells would swell and burst causing irreversible damage. Additionally, any brain swelling would cramp the cranial cavity leading to herniation and further damage.Chronic hyponatremia leads to a more effective depletion of the osmotically active solutes that take time to replenish. So when we rapidly correct the hypotonic state in a chronically hyponatremicpatient the cells cannot osmotically compensate as well, causing them to shrink.This leads to a cascade o fapoptosis, disruption of oligodendrocytes, inflammatory cytokine release, and microglial activation. If the insult involved the respiratory center in the medulla or higher brainstem it can cause central hypoventilation syndrome which lead to decreased autonomic response to hypercapnia and hypoxiaalthough they are able to consciously control their ventilation normally and respond to non-chemoreceptive inputs for ventilation CONCLUSIONS: This case report underlines the importance of recognizing predisposing risk factors for osmotic demyelination syndrome and the potential complications if not done properly Reference #1: Jazeela Fayyaz, DO. Zab Mosenifar, M, ed. "Hypoventilation Syndromes". "Congenital central hypoventilation syndrome". Genetics Home Reference. U.S. National Library of Medicine. Reference #2: "Primary alveolar hypoventilation: Ondine's curse". A.D.A.M. Medical Encyclopedia. U.S. National Library of Medicine.Severinghaus JW; Mitchell, R. A. (1962). "Undine's curse — failure of respiratory center automaticity while awake". Clin Res. 10: 122 DISCLOSURES: No relevant relationships by Hani Badi, source=Web Response No relevant relationships by Ali Eltatawy, source=Web Response No relevant relationships by Zubair Khan, source=Web Response No relevant relationships by Tamer Said Ahmed, source=Web Response No relevant relationships by Young Sook Yoon, source=Web Response

WED 148 Imaging findings in autoimmune encephalitis: a retrospective review

BackgroundNeuroimaging findings in autoimmune encephalitis may include normal MRI as well as limbic and extra-limbic involvement. Prompt recognition allows early immunosuppression and improved outcomes.MethodsRetrospective review of patients with Autoimmune encephalitis over the last 5 years.ResultsWe identified N-methyl-d-aspartate receptor (NMDAR) n=8, voltage gated potassium channel (VGKC) n=11, and leucine-rich glioma inactivated 1 (LGI1) n=11 encephalitis patients. 1/8 NMDAR encephalitis patients had abnormal MRI findings of T2 hyper intense signal in right anterior temporal and bilateral frontal and left insular lobe. DWI sequence showed restricted diffusion. 4/11 with VGKC encephalitis had positive MRI findings. Two patients had limbic involvement while one also had involvement of basal ganglia. Two patients had modest cerebral atrophy. Four patients had normal MRI findings. MRI scan was not available for three patients. 5/11 LGI1 encephalitis patients had bilateral mesial temporal lobe changes. In one patient, MRI could not be done due to permanent pacemaker. Five patients had normal MRI findings.ConclusionsIn our series, 33% patients had abnormal MRI findings consistent with a diagnosis of autoimmune encephalitis, which is lower than reported in literature. High clinical suspicion should lead to prompt diagnosis even in the absence of typical encephalitic changes on MRI.

Apparent Diffusion Coefficient Levels and Neurodevelopmental Outcome in Fetuses with Brain MR Imaging White Matter Hyperintense Signal.

One of the perplexing findings of fetal brain MR imaging is white matter T2 hyperintense signal. The aims of our study were initially to determine the main etiologies associated with white matter T2 hyperintense signal, then to examine whether the different etiologies have different ADC values, and, last, to assess the association of white matter T2 hyperintense signal with developmental outcome. This was a prospective cohort study of 44 MR imaging scans of fetal brains obtained for suspected brain pathologies at a tertiary medical center during 2011-2015. Clinical data were collected from electronic medical charts. ADC values were measured and averaged in the frontal, parietal, occipital, and temporal lobes. Neurodevelopmental assessments were performed with the Vineland Adaptive Behavior Scales II. Half of the cases of MRI hyperintense T2 signal of the fetal brain were associated with congenital cytomegalovirus infection. The other half were mainly idiopathic. Thus, the study group was divided to subgroups positive and negative for cytomegalovirus. Both groups had hyperintense signal in the temporal lobe. The group positive for cytomegalovirus had involvement of the parietal lobe. Only this group had increased ADC values in the temporal and parietal lobes. There was no association between the neurodevelopment outcome and the etiologies or ADC values. T2 hyperintense signal in fetal brain MRI associated with positive cytomegalovirus infection has increased ADC values in the temporal and parietal lobes, suggestive of brain edema in these areas. However, the association between this finding and neurodevelopment outcome requires further evaluation.

Differentiation of Cerebellar Hemisphere Tumors: Combining Apparent Diffusion Coefficient Histogram Analysis and Structural MRI Features

We aimed to develop a diagnostic algorithm for differentiation of cerebellar hemisphere tumors, combining Apparent Diffusion Coefficient (ADC) histogram analysis and structural imaging features. Pretreatment MRI of patients with pathologically proven cerebellar hemisphere neoplasms were reviewed. Voxel-wise volumetric ADC histograms of tumor solid components were determined. Histogram variables, patients' age, and structural imaging features were applied to develop a differential diagnosis algorithm. Among 142 patients, the most common tumors were metastasis (n = 54), hemangioblastoma (n = 39), pilocytic astrocytoma (n = 18), and medulloblastoma (n = 9). On ADC histogram analysis, medulloblastomas had the lowest, and pilocytic astrocytomas had the highest ADC values. An ADC 15th percentile value < 580 × 10-6 mm2 /s could differentiate medulloblastomas from other cerebellar hemisphere tumors with receiver operating characteristic (ROC) area under the curve (AUC) of .98 (P < .001). Comparing the two most common adult cerebellar hemisphere tumors (metastases and hemangioblastomas), hemangioblastomas had higher ADC values; and an ADC 90th percentile value > 2000 × 10-6 mm2 /s could identify hemangioblastomas with ROC AUC of .82 (P < .001). Along with ADC histogram and patients' age, structural imaging features including enhancement pattern, prominent vascular flow voids, surrounding FLAIR hyperintensity, and solid component T2 signal hyperintensity were independent differentiation variables in the diagnostic algorithm. In pretreatment differentiation of cerebellar tumors, the ADC histogram analysis is particularly helpful for distinction of medulloblastomas from other subtypes, and differentiation of the two most common adult tumors (ie, metastases and hemangioblastomas) from each other. Combination of structural imaging features and ADC histogram analysis can help with pretreatment differentiation of cerebellar tumors.

Spinal Cord Hyperintensities in Neurofibromatosis Type 1: Are They the Cord Equivalent of Unidentified Bright Objects in the Brain?

Focal areas of T2 hyperintensity are seen on magnetic resonance imaging (MRI) in patients with neurofibromatosis type 1 (NF1). These lesions are commonly known as "unidentified bright objects" of the brain. We have seen similar lesions in the spinal cord of the same patient population. Our aim was to determine the prevalence and characterize the imaging features of these T2 hyperintense spinal cord lesions in children with NF1. A search of our hospital's medical imaging database yielded all children with NF1 and MRI of the brain and/or spine between February 2014 and April 2017. Medical imaging was reviewed for T2 hyperintense signal changes and medical records were reviewed of those children with T2 hyperintense spinal cord lesions. During the study period 155 children underwent a brain MRI and 72 had a spine MRI. One hundred twenty-three (79%) showed multiple cerebral T2 hyperintense lesions and six (8%) had non-contrast enhancing spinal cord T2 hyperintensities with five children having had a follow-up scan. The one child without follow-up imaging was not further pursued. Interval scanning showed stable appearance of the spinal cord lesions in four children and signal reduction in one child. All five children with T2 hyperintense changes in the spinal cord had an MRI brain and all (100%) also exhibited cerebral T2 hyperintensities. Focal areas of signal hyperintensity in the spinal cord are the corollary of the better described cerebral T2 hyperintensities in individuals with NF1.

Radiation-Induced Myelitis: Initial and Follow-Up MRI and Clinical Features in Patients at a Single Tertiary Care Institution during 20 Years.

Myelitis is a rare complication of radiation exposure to the spinal cord and is often a diagnosis of exclusion. A retrospective review of clinical records and serial imaging was performed to identify subjects with documented myelitis and a history of prior radiation. Eleven patients fulfilled the inclusion criteria. All patients had longitudinally extensive cord involvement with homogeneous precontrast T1 hyperintense signal in the adjacent vertebrae, corresponding to the radiation field. T2 signal abnormalities involving the central two-thirds of the cord were seen in 6/11 patients (55%). The degree of cord expansion and contrast enhancement was variable but was seen in 6 (54%) and 5 (45%) patients, respectively. On follow-up, 2 patients developed cord atrophy, while complete resolution was noted in 1. Clinical improvement was noted in 5 patients, with symptom progression in 2 patients. Our results suggest that radiation myelitis is neither universally progressive nor permanent, and some radiographic and clinical improvement may occur.

Acute Lumbar Pain - Football

HISTORY: A freshman collegiate football player presented to the athletic training facility after his first official practice, complaining of worsening, severe pain in his R greater than L lumbar region without radiation or radicular symptoms. He denied any injury during practice. He had previously reported mild low back tightness during summer conditioning workouts that resolved with rest. He and the sports health staff were aware that he has sickle cell trait. PHYSICAL EXAMINATION: Pt in severe distress with diaphoresis, agitation and restlessness Limited lumbar ROM. Tenderness in lumbar paraspinal muscles R greater than L. Non-tender abdomen, symmetric pulses x4 extremities, no neurologic deficits or costa-vertebral tenderness. HR and BP elevated. Afebrile. High-flow oxygen by mask initiated and athlete transported to ED. DIFFERENTIAL DIAGNOSIS: Lumbar muscle/myofascial strain Lumbar disc rupture Lumbar paraspinal myonecrosis Ureteral calculus Renal angiomyolipoma TESTS AND RESULTS: CMP Cr 1.7, Ca 10.6, Glu 140; otherwise normal WBC 11.8, Hgb 15.5, Hct 47.5, Plt 178 CK 747 U/L Urinalysis SpGr 1.010, Pro 30, Small blood, 2 RBC, 4 WBC, myoglobin negative MRI lumbar spine: T2 hyperintense signal in the paraspinous muscles bilaterally, R greater than L. Spine and nervous structures normal. Impression: Multifocal paraspinous muscular edema. Considerations would include strain, acute myonecrosis (given clinical history), or acute blood products FINAL DIAGNOSIS: Acute lumbar paraspinal myonecrosis in athlete with SCT TREATMENT AND OUTCOMES: 1. High-flow oxygen continued 2. IV fluids initiated and 3L NS bolus given by pressure infusion 3. IV hydromorphone prn for pain control 4. Rapid improvement in pain post IV fluid bolus 5. Inpatient admission, transitioned from IV hydromorphone to PO oxycodone 6. Peak CK of 10,169 approximately 13 hours post event 7. Discharged home hospital day 2 with CK down trending at 7,060 ,Cr 0.98, off all pain meds 8. Cleared for activity at 7 days post event 9. Completed return to play activities, returned to full practice at 11 days post event 10. No related medical issues, no visible loss of muscle bulk/tone and continued full team participation as of abstract submission

Effect of Myoarchitectonic Spinolaminoplasty on Concurrent Hypertension in Patients With Cervical Spondylotic Myelopathy.

ObjectiveWhen treating patients with cervical spondylotic myelopathy (CSM), we often note amelioration in concomitant hypertension after surgery. To assess the effects of surgery and the mechanisms thereof, blood pressure (BP) and parasympathetic nervous activity were monitored prospectively in CSM patients undergoing surgery. MethodsSixty-eight consecutive CSM patients who underwent surgery with myoarchitectonic spinolaminoplasty were enrolled. BP and electrocardiography were recorded preoperatively and at 1, 3, and 6 months postoperatively. Forty-six patients completed the scheduled follow-ups and were analyzed. Preoperatively, 17 had a mean BP higher than 100 mmHg (the HT group) and 12 had hypertension despite taking medication (the HT-refractory group). To evaluate alterations in parasympathetic function, the coefficient of variation of the RR interval (CVRR) was evaluated. ResultsA significant BP reduction was observed in the HT group 6 months after surgery, but not in the normotensive group (n=29). The effect was more remarkable in the HT-refractory group. A transient BP increase at 1 and 3 months after surgery was observed in all groups. Comparisons were made between groups classified by age (over 65 years or younger than 60 years) and the presence or absence of an intramedullary hyperintense T2 signal on magnetic resonance imaging, but no significant differences were detected. Measurements of CVRR did not significantly differ between the groups over the course of follow-up. ConclusionHypertension coexisting with CSM can be ameliorated after surgical treatment. The effect is likely to be mediated by moderation of sympathetic activity, rather than parasympathetic activation. We believe that a combination of adequate decompression of the spinal cord and relief from musculoskeletal stresses effectuate this moderation.

Magnetic Resonance Imaging Characteristics of Pituitary Abscess: A Review of 51 Cases.

To investigate pituitary abscess (PA) magnetic resonance imaging (MRI) features to improve the neuroradiologic and diagnostic knowledge of this rare disease and guide follow-up treatments. Clinical data were collected for 51 patients with PA, and MRI data were quantitatively reviewed in a retrospective analysis. Clinical factors were analyzed to investigate their relevance. PA neuroimaging showed special radiologic features, including hypointensity or isointensity on T1-weighted imaging (30 patients, 58.8%), isointensity or hyperintensity on T2-weighted imaging (39 patients, 76.5%), and disappearance of the posterior pituitary bright spot in most patients (44 patients, 86.3%). After gadolinium injection, rim or rimlike enhancement was observed in 82.4% of patients (n= 42). Half of those patients showed typical rim enhancement (profound peripheral enhancement with internal hypointensity); others showed atypical rim enhancement with special signs, such as enhanced, thick abscess wall and hyperintense flocculent or cottonlike foci within the internal hypointense region. Almost all patients (96.1%) presented at least 1 sign of adjacent anatomic structure invasion, including peripheral meninges enhancement, pituitary stalk thickening, and paranasal sinus mucosa enhancement. Rank correlation analysis of the clinical time course and MRI characteristics of PA showed a Spearman correlation coefficient of 0.270, indicating borderline significance (P= 0.055). Classic MRI characteristics of PA show T1 signal hypointensity or isointensity, T2 signal isointensity or hyperintensity, and peripheral rim enhancement after gadolinium injection. The MRI appearance of PA may reflect the abscess liquefaction and formation. Despite its profound significance for differential diagnosis, adjacent structure invasion is generally ignored by clinicians.

Clinical, radiological, and pathological features of extraskeletal osteosarcoma.

To evaluate clinical and radiological features of pathology-proven extraskeletal osteosarcomas. This retrospective study was IRB-approved and HIPAA-compliant. Our pathology database was queried for cases of extraskeletal osteosarcoma. Tumor location, size, imaging appearance, presence of metastases, and clinical outcome were documented. Nineteen patients met inclusion criteria (age 59 ± 15 (range 28-85) years; 15male, 4 female). Tumors occurred in the lower extremities (12 out of 19, 63%), pelvis/gluteal region (3 out of 19, 16%), upper extremity (2 out of 19, 5%), thorax (1 out of 19, 5%), and neck (1 out of 19, 5%). Two out of 19 (11%) patients had undergone radiation to the tumor site previously. According to pathology, 16 out of 19 tumors were high-grade (84%). Tumors presented as soft-tissue masses measuring 9.5 ± 6.8 (2-29) cm. Tumor mineralization was present in 5 out of 19 cases (26%) and local invasion was found in 1 out of 19 cases (6%). On MRI, tumors typically appeared hyperintense on T2-weighted sequences with enhancement in 15 out of 15 (100%) contrast-enhanced studies, and with central necrosis in 10 out of 19 (53%) cases. Low-grade tumors were smaller (<4cm; 3 out of 3, 100%) and lacked central necrosis (3 out of 3, 100%). 8 out of 19 patients (42%) had metastases, most commonly to the lung (7 out of 19, 37%) and bone (2 out of 19,11%). Two out of 8 patients (25%) with metastases and 8 out of 11 (73%) without metastases achieved recurrence-free survival (mean follow-up 3.8 ± 4.0 [0.2-14.2]) years. No metastases or deaths occurred in patients with low-grade histology. Extraskeletal osteosarcomas are rare, typically high-grade malignancies that commonly metastasize to lung and bones. Low-grade tumors and those without metastases have a good prognosis. MRI appearance is nonspecific, with T2 hyperintense signal and heterogeneous enhancement. Unlike conventional osteosarcoma, mineralization is rare.

A promising magnetic resonance stem cell tracer based on natural biomaterials in a biological system: manganese(II) chelated to melanin nanoparticles.

BackgroundMelanin and manganese are both indispensable natural substances that play crucial roles in the human body. Melanin has been used as a multimodality imaging nanoplatform for biology science research because of its natural binding ability with metal ions (eg, 64Cu2+, Fe3+, and Gd3+). Because of its effects on T1 signal enhancement, Mn-based nanoparticles have been used in magnetic resonance (MR) quantitative cell tracking in vivo. Stem cell tracking in vivo is an essential technology used to characterize engrafted stem cells, including cellular viability, biodistribution, differentiation capacity, and long-term fate.MethodsIn the present study, manganese(II) ions chelated to melanin nanoparticles [MNP-Mn(II)] were synthesized. The characteristics, stem cell labeling efficiency, and cytotoxicity of the nanoparticles were evaluated. MR imaging of the labeled stem cells in vivo and in vitro were also further performed. In T1 relaxivity (r1), MNP-Mn(II) were significantly more abundant than Omniscan. Bone marrow-derived stem cells (BMSCs) can be labeled easily by coincubating with MNP-Mn(II), suggesting that MNP-Mn(II) had high biocompatibility.ResultsCell Counting Kit-8 assays revealed that MNP-Mn(II) had almost no cytotoxicity when used to label BMSCs, even with a very high concentration (1,600 µg/mL). BMSCs labeled with MNP-Mn(II) could generate a hyperintense T1 signal both in vitro and in vivo, and the hyperintense T1 signal in vivo persisted for at least 28 days.ConclusionTaken together, our results showed that MNP-Mn(II) possessed many excellent properties for potential quantitative stem cell tracking in vivo.

T2-hyperintensity Signal along the Optic Tract in Pituitary Metastasis: Case Report

T2-hyperintensity Signal along the Optic Tract in Pituitary Metastasis: Case Report

MRI findings in glutamic acid decarboxylase associated autoimmune epilepsy.

Glutamic acid decarboxylase (GAD65) has been implicated in a number of autoimmune-associated neurologic syndromes, including autoimmune epilepsy. This study categorizes the spectrum of MRI findings in patients with a clinical diagnosis of autoimmune epilepsy and elevated serum GAD65 autoantibodies. An institutional database search identified patients with elevated serum GAD65 antibodies and a clinical diagnosis of autoimmune epilepsy who had undergone brain MRI. Imaging studies were reviewed by three board-certified neuroradiologists and one neuroradiology fellow. Studies were evaluated for cortical/subcortical and hippocampal signal abnormality, cerebellar and cerebral volume loss, mesial temporal sclerosis, and parenchymal/leptomeningeal enhancement. The electronic medical record was reviewed for relevant clinical information and laboratory markers. A study cohort of 19 patients was identified. The majority of patients were female (84%), with a mean age of onset of 27years. Serum GAD65 titers ranged from 33 to 4415nmol/L (normal < 0.02nmol/L). The most common presentation was medically intractable, complex partial seizures with temporal lobe onset. Parenchymal atrophy was the most common imaging finding (47%), with a subset of patients demonstrating cortical/subcortical parenchymal T2 hyperintensity (37%) or abnormal hippocampal signal (26%). No patients demonstrated abnormal parenchymal/leptomeningeal enhancement. The most common MRI finding in GAD65-associated autoimmune epilepsy is disproportionate parenchymal atrophy for age, often associated with abnormal cortical/subcortical T2 hyperintensities. Hippocampal abnormalities are seen in a minority of patients. This constellation of findings in a patient with medically intractable epilepsy should raise the possibility of GAD65 autoimmunity.