Magnetic Resonance Imaging Signal Abnormalities Research Articles

Repurposing of the PET Probe Prototype PiB for Label and Radiation-Free CEST MRI Molecular Imaging of Amyloid.

Positron emission tomography (PET) probes are specific and sensitive while suffering from radiation risk. It is worthwhile to explore the chemical emission saturation transfer (CEST) effects of the probe prototypes and repurpose them for CEST imaging to avoid radiation. In this study, we used 11C-PiB as an example of a PET probe for detecting amyloid and tested the feasibility of repurposing this PET probe prototype, PiB, for CEST imaging. After optimizing the parameters through preliminary phantom experiments, we used APP/PS1 transgenic mice and age-matched C57 mice for in vivo CEST magnetic resonance imaging (MRI) of amyloid. Furthermore, the pathological assessment was conducted on the same brain slices to evaluate the correlation between the CEST MRI signal abnormality and β-amyloid deposition detected by immunohistochemical staining. In our results, the Z-spectra revealed an apparent CEST effect that peaked at approximately 6 ppm. APP/PS1 mice as young as 9 months injected with PiB showed a significantly higher CEST effect compared to the control groups. The hyperintense region was correlated with the Aβ deposition shown by pathological staining. In conclusion, repurposing the PET probe prototype for CEST MRI imaging is feasible and enables label- and radiation-free detection of the amyloid while maintaining the sensitivity and specificity of the ligand. This study opens the door to developing CEST probes based on PET probe prototypes.

Abnormal magnetic resonance imaging signal in the burr hole and the identification of the intracranial infection of a deep brain stimulation device: illustrative case.

Device infection is a critical postoperative complication in deep brain stimulation (DBS). However, intracranial infections are rare and lack specific findings, which lead to a challenging diagnosis. A 59-year-old female with generalized dystonia underwent bilateral globus pallidus internus and subthalamic nucleus (STN) DBS device implantation. One year earlier, a left STN-DBS extension wire disconnection was observed and replaced. The patient presented to our department because of tenderness along the extension wire that had persisted for 1 month. Magnetic resonance imaging (MRI) of the head indicated abnormal signals around the lead of the left STN and burr hole. Intraoperatively, the authors observed pus and infected granulation tissue in the burr holes. After device removal, antibiotics were administered, and the patient successfully progressed without complications. Moreover, the abnormal MRI signal disappeared. A characteristic abnormal MRI signal within the burr hole in DBS may suggest early infection even in the absence of other inflammatory findings. Clinicians should ensure that MRI is not limited to intracranial findings but extends beyond the extracranial space.

BBB opening with focused ultrasound in nonhuman primates and Parkinson's disease patients: Targeted AAV vector delivery and PET imaging.

Intracerebral vector delivery in nonhuman primates has been a major challenge. We report successful blood-brain barrier opening and focal delivery of adeno-associated virus serotype 9 vectors into brain regions involved in Parkinson's disease using low-intensity focus ultrasound in adult macaque monkeys. Openings were well tolerated with generally no associated abnormal magnetic resonance imaging signals. Neuronal green fluorescent protein expression was observed specifically in regions with confirmed blood-brain barrier opening. Similar blood-brain barrier openings were safely demonstrated in three patients with Parkinson's disease. In these patients and in one monkey, blood-brain barrier opening was followed by 18F-Choline uptake in the putamen and midbrain regions based on positron emission tomography. This indicates focal and cellular binding of molecules that otherwise would not enter the brain parenchyma. The less-invasive nature of this methodology could facilitate focal viral vector delivery for gene therapy and might allow early and repeated interventions to treat neurodegenerative disorders.

Juvenile-Onset Kufs Disease in a Chinese Consanguineous Family due to CLN6 Mutation

Objective: The aim of this study was to identify the genetic cause of two cases of Kufs disease in the same family. The two affected individuals exhibited different levels of severity under magnetic resonance imaging (MRI). Methods: Whole-exome sequencing was performed on affected individuals, and the candidate gene was confirmed by Sanger sequencing. Western blot analysis was used to evaluate the level of expression of CLN6 protein in 239T cells. Results: We identified a novel homozygous mutation of the CLN6 gene (c.14G>T, p.Arg5Leu) in a consanguineous Chinese family in which two people had Kufs disease. Both patients exhibited seizures and progressive psychomotor decline and mental deterioration without visual impairment. They had different ages of onset, although they carried the same missense mutation. The affected female showed a pronounced abnormal MRI signal in the bilateral hippocampus, while her younger brother only showed a very slight abnormal signal. Further study showed that this missense mutation could decrease the level of expression of CLN6 protein. Conclusions: A novel homozygous mutation of the CLN6 gene was identified, and patients with the same mutation showed different ages of onset and different levels of severity under MRI. Significance: Our study established that the same CLN6 mutation could produce different phenotypes in patients, and it has expanded the mutational and phenotypical spectrum of the CLN6 gene.

Incidence of Stroke and Other Brain Imaging Findings in Adult Patients with Sickle Cell Disease: A Retrospective Study

Background: Vaso-occlusion and hemolytic anemia are the main features of sickle cell disease. Central Nervous system complications of sickle cell disease (SCD) can include silent cerebral infarcts (SCI), hemorrhagic or ischemic strokes, seizures and Moyamoya syndrome. SCI is the most common neurological complications in SCD. SCI patients have abnormal Magnetic Resonance Imaging (MRI) of the brain with normal neurological examination and no history of stroke. More precisely, Casella et al in the Silent Cerebral Infarct Multi-Center Clinical trial (SIT) defined infarct as MRI signal abnormality that was at least 3 mm in one dimension and that was visible in two planes on fluid-attenuated inversion recovery T2 -weighted images, as determined by agreement of two of the three study neuroradiologists. SCI in children is associated with lower Intelligence Quotient and increased risk of stroke.Methods: In this retrospective study we reviewed 100 adult patients at our Comprehensive Sickle Cell Center. We looked at the incidence of documented stroke and other neurological complications in SCD patients. We reviewed the hospital records of SCD patients for any incidental brain imaging (MRI brain or Computed Tomography(CT) brain) findings, done as inpatient or in the emergency room as part of hospital visits.Results: Out of the 100 patients, 14 patients had documented stroke. On the review of other 86 patients, 10 patients had MRI brain, 23 patients had CT brain, and 53 patients had no brain imaging record. Out of the 10 patients with MRI brain, 7 patient had significant findings- 3 patients had small vessel ischemic changes, 1 patient with chronic petechial hemorrhage of cerebellar vermis, 1 patient with ischemic changes and Chiari malformation type 1 (CTM 1), 1 patient with CTM 1 and non-specific white matter changes and 1 patient with CTM 1 alone. Out of the 22 CT of the brain and 1 CT angiogram of brain, 2 imaging showed ischemic changes and the angiogram showed large cerebral vessel narrowing. Therefore, on our review, 19 patients out of 100 were found to have stroke and 24 out of 100 had significant neurological findings. However, only 14 out of 19 patients had documented stroke. 7 out the 10 patients with MRI brain had significant incidental neurological findings. The number of adult SCD patients with neurological findings in our cohort could have been higher, if we had brain imaging record for the 53 other patients.Conclusion: This study shows that there is a heavy burden of neurological complications in SCD patients and SCI is under-diagnosed. MRI brain is superior to CT brain in detecting neurological complications in SCD patients. SIT showed that regular blood-transfusion significantly reduced the recurrence of cerebral infarct in children with SCI. Finding of SCI in adults also warrants consideration for follow up brain imaging, neurology referral and discussion of treatment modalities including chronic blood transfusion and hydroxyurea therapy. CTM 1 can also be associated with SCD. In CTM 1, tonsil herniates 5 millimeter or below foramen magnum. SCD may cause increased thickness of calvarium from extramedullary hematopoiesis in skull, which can result in cranio-cephalic disproportion with cerebellar ectopia and subsequent CTM 1. Because of high incidence of neurological complications in SCD patients, routine screening with MRI brain should be considered in adult SCD patients. DisclosuresIdowu: Forma Therapeutics, Inc.: Research Funding; Pfizer: Research Funding; Novartis: Membership on an entity's Board of Directors or advisory committees, Research Funding; Global Blood Therapeutics: Membership on an entity's Board of Directors or advisory committees, Research Funding, Speakers Bureau; Ironwood: Research Funding.

Assessment of Magnetic Resonance Imaging Changes and Functional Outcomes Among Adults With Severe Herpes Simplex Encephalitis

Current guidelines recommend brain magnetic resonance imaging (MRI) for clinical management of patients with severe herpes simplex encephalitis (HSE). However, the prognostic value of brain imaging has not been demonstrated in this setting. To investigate the association between early brain MRI data and functional outcomes of patients with HSE at 90 days after intensive care unit (ICU) admission. This multicenter cohort study was conducted in 34 ICUs in France from 2007 to 2019 and recruited all patients who received a clinical diagnosis of encephalitis and exhibited cerebrospinal fluid positivity for herpes simplex virus DNA in the polymerase chain reaction analysis. Data analysis was performed from January to April 2020. All patients underwent a standard brain MRI during the first 30 days after ICU admission. MRI acquisitions were analyzed by radiologists blinded to patients' outcomes, using a predefined score. Multivariable logistic regression and supervised hierarchical classifiers methods were used to identify factors associated with poor outcome at 90 days, defined by a score of 3 to 6 (indicating moderate-to-severe disability or death) on the Modified Rankin Scale. Overall, 138 patients (median [interquartile range {IQR}] age, 62.6 [54.0-72.0] years; 75 men [54.3%]) with an admission median (IQR) Glasgow Coma Scale score of 9 (6-12) were studied. The median (IQR) delay between ICU admission and MRI was 1 (1-7) days. At 90 days, 95 patients (68.8%) had a poor outcome, including 16 deaths (11.6%). The presence of fluid-attenuated inversion recovery MRI signal abnormalities in more than 3 brain lobes (odds ratio [OR], 25.71; 95% CI, 1.21-554.42), age older than 60 years (OR, 7.62; 95% CI, 2.02-28.91), and the presence of diffusion-weighted MRI signal abnormalities in the left thalamus (OR, 6.90; 95% CI, 1.12-43.00) were independently associated with poor outcome. Machine learning models identified bilateral diffusion abnormalities as an additional factor associated with poor outcome (34 of 39 patients [87.2%] with bilateral abnormalities had poor outcomes) and confirmed the functional burden of left thalamic lesions, particularly in older patients (all 11 patients aged >60 years had left thalamic lesions). These findings suggest that in adult patients with HSE requiring ICU admission, extensive MRI changes in the brain are independently associated with poor functional outcome at 90 days. Thalamic diffusion signal changes were frequently observed and were associated with poor prognosis, mainly in older patients.

Practical recognition tools of immunoglobulin G serum antibodies against the myelin oligodendrocyte glycoprotein‐positive optic neuritis and its clinical implications

AbstractMyelin oligodendrocyte glycoprotein (MOG)‐associated disease is an autoimmune disease of the central nervous system, associated with the presence of immunoglobulin G serum antibodies against MOG. Recent data have allowed characterization of the clinical spectrum of MOG‐associated disease, which is now considered a new disease entity, distinct from multiple sclerosis and neuromyelitis optica spectrum disorders. Optic neuritis is the most common clinical presentation of MOG‐associated disease in adults, both at disease onset and during the disease course, and has several distinct clinical and paraclinical features. Immunoglobulin G serum antibodies against MOG‐positive optic neuritis is often bilateral and associated with optic disc swelling and a longitudinally extensive abnormal magnetic resonance imaging signal involving the retrobulbar portion of the optic nerve. The visual acuity during the acute attack is severely decreased, and the response to corticosteroids is often rapid and prominent. However, early relapses after steroid cessation are common, and a subset of patients is left with a permanent visual disability. In this review, we discuss the clinical and paraclinical features of immunoglobulin G serum antibodies against MOG‐positive optic neuritis in adults, and focus on the distinctive features that can enable its early diagnosis. Therapeutical considerations at the acute stage and for relapse prevention are further deliberated.

Early Predictors of Neurological Outcomes After Traumatic Spinal Cord Injury: A Systematic Review and Proposal of a Conceptual Framework.

Neurological outcomes after traumatic spinal cord injury are variable and depend on patient-, trauma-, and treatment-related factors as well as on spinal cord injury characteristics, imaging, and biomarkers. The aims of the study were to identify and classify the early predictors of neurological outcomes after traumatic spinal cord injury. The Medline, PubMed, Embase, and the Cochrane Central Database were searched using medical subject headings. The search was extended to the reference lists of identified studies. The study eligibility criteria were assessment of neurological outcomes as primary or secondary outcome, predictors collected during the acute phase after traumatic spinal cord injury, and multivariate design. The participants were adult patients with traumatic spinal cord injury followed at least 3 mos after injury. The quality of studies was assessed by two independent reviewers using the Study Quality Assessment Tools for Observational Cohort and Cross-sectional Studies. The studies' narrative synthesis relied on a classification of the predictors according to quantity, quality, and consistency of the evidence. Results were summarized in a conceptual framework. Forty-nine articles were included. The initial severity of traumatic spinal cord injury (American Spinal Injury Association Impairment Scale, motor score, and neurological level of injury) was the strongest predictor of neurological outcomes: patients with more severe injury at admission presented poor neurological outcomes. Intramedullary magnetic resonance imaging signal abnormalities were also associated with neurological outcomes, as the presence of intramedullary hemorrhage was a factor of poor prognosis. Other largely studied predictors, such as age and surgical timing, showed some inconsistency in results depending on cutoffs. Younger age and early surgery were generally associated with good outcomes. Although widely studied, other factors, such as vertebral and associated injuries, failed to show association with outcomes. Cerebrospinal fluid inflammatory biomarkers, as emerging factors, were significantly associated with outcomes. This study provides a comprehensive review of predictors of neurological outcomes after traumatic spinal cord injury. It also highlights the heterogeneity of outcomes used by studies to assess neurological recovery. The proposed conceptual framework classifies predictors and illustrates their relationships with outcomes.

Hippocampal Involvement With Vigabatrin-Related MRI Signal Abnormalities in Patients With Infantile Spasms: A Novel Finding.

In a subset of infants exhibiting typical vigabatrin-related magnetic resonance imaging (MRI) changes, the authors observed additional hippocampal signal abnormalities. The authors investigated occurrence and significance of additional signal abnormalities. A retrospective review of infantile spasms patients with typical vigabatrin-related MRI abnormalities was performed. Atypical features included signal changes unilaterally or at previously unreported sites. Comparisons were made between patients with and without atypical features. In all, 26/55 (47%) exhibited typical vigabatrin-related MRI changes, with additional signal abnormalities in the hippocampi in 6 of 26. On follow-up, evolution of hippocampal signal changes paralleled changes at typical locations in 4 patients. Two patients, clinically well, without follow-up MRI. Patients with and without additional hippocampal signal changes did not differ with respect to clinical factors, including seizure status. One patient had unilateral thalamic/cerebral peduncle signal abnormality along with typical vigabatrin changes. Hippocampal changes seen in subset of patients with typical vigabatrin-related changes may be attributable to vigabatrin exposure in the appropriate circumstance.

Structural and metabolic brain abnormalities in COVID-19 patients with sudden loss of smell.

ObjectivesSudden loss of smell is a very common symptom of coronavirus disease 19 (COVID-19). This study characterizes the structural and metabolic cerebral correlates of dysosmia in patients with COVID-19.MethodsStructural brain magnetic resonance imaging (MRI) and positron emission tomography with [18F]-fluorodeoxyglucose (FDG-PET) were prospectively acquired simultaneously on a hybrid PET-MR in 12 patients (2 males, 10 females, mean age: 42.6 years, age range: 23–60 years) with sudden dysosmia and positive detection of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on nasopharyngeal swab specimens. FDG-PET data were analyzed using a voxel-based approach and compared with that of a group of healthy subjects.ResultsBilateral blocking of the olfactory cleft was observed in six patients, while subtle olfactory bulb asymmetry was found in three patients. No MRI signal abnormality downstream of the olfactory tract was observed. Decrease or increase in glucose metabolism abnormalities was observed (p < .001 uncorrected, k ≥ 50 voxels) in core olfactory and high-order neocortical areas. A modulation of regional cerebral glucose metabolism by the severity and the duration of COVID-19-related dysosmia was disclosed using correlation analyses.ConclusionsThis PET-MR study suggests that sudden loss of smell in COVID-19 is not related to central involvement due to SARS-CoV-2 neuroinvasiveness. Loss of smell is associated with subtle cerebral metabolic changes in core olfactory and high-order cortical areas likely related to combined processes of deafferentation and active functional reorganization secondary to the lack of olfactory stimulation.

Report of a Case of Creutzfeldt-Jakob Disease With an Unusual Clinical Presentation.

We describe the clinical features, neuropsychological tests, laboratory, electroencephalography (EEG), magnetic resonance imaging (MRI) and positron emission tomography (PET) findings of a 59-year-old woman who presented to our Centre for cognitive impairment since few months, with language disturbances, particularly anomia, dyscalculia, and memory loss. The clinical and neuropsychological features were non-specific and overlapping with those of other rapidly progressing neurodegenerative disorders. However, brain MRI played a pivotal role in the diagnosis, showing cortical diffusion restriction, particularly in the parietal lobes and posterior cingulum, with sparing of the perirolandic cortex, typical of Creutzfeldt-Jakob disease (CJD). Brain MRI abnormalities were visible since the first evaluation and remained stable at 2 and 6 weeks follow up. Basal ganglia and thalami were never involved. PET showed left lateralized reduced glucose metabolism, with partial overlap with MRI signal abnormalities. Despite MRI were strongly indicative of CJD, clinical, laboratory and EEG findings did not fulfill the diagnostic criteria for CJD which applied at the time of clinical assessment. Indeed, neither myoclonus, visual or cerebellar signs or akinetic mutism were present. Also, the characteristic periodic sharp wave complexes were absent at baseline EEG, and the CSF assay for 14–3–3 was negative. We, therefore, performed a real-time quaking-induced conversion (RT-QuIC) assay on a frozen sample of corticospinal fluid (CSF), which showed a positive result. RT-QuIC is a prion protein conversion assay that has shown high diagnostic sensitivity and specificity for the diagnosis of CJD. RT-QuIC has been recently incorporated in the National CJD Research and Surveillance Unit and Center for Disease Control and Prevention (CDC) diagnostic criteria for CJD. The fatal evolution of the disease brought the patient to death 13 months after symptoms onset. Pathology proved the diagnosis of sporadic CJD, subtype MM/MV 2C.

Normal and pathological imaging of the hippocampus in geriatric patients.

The hippocampus is a small internal temporal cerebral structure which plays a primordial role in memory mechanisms. Magnetic resonance imaging (MRI) is the preferred method for analysing this structure. In older adults, dementia is the major cause of hippocampal anomalies, particularly atrophic anomalies, however, differential diagnoses involving other specific pathologies should also be recognised in this population. Most acute or recent hippocampal damage is detected based on MRI signal abnormalities. The aim of this article is to provide an iconographic review of normal and pathological hippocampal imaging in older adults with degenerative, infectious, vascular, inflammatory, tumoural, toxic, and metabolic disorders.

Normal and pathological hippocampal imaging in geriatric patients

The hippocampus is a small internal temporal cerebral structure, which plays a primordial role in the mechanisms of memory. Magnetic resonance imaging (MRI) is the reference imaging modality for the hippocampal analysis. In older adults, dementia represents the majority of hippocampal diseases, but other specific pathologies must be known in the differential diagnosis. Many hippocampal abnormalities are represented by a loss of substance (atrophy). However, most acute or recent hippocampal damage is detected by MRI signal abnormalities. The aim of this article is to offer a pictorial review of the normal and pathological hippocampal aspects of older adults, during degenerative, infectious, vascular, inflammatory, tumoral, toxic and metabolic disorders.

Coexistent Vestibular Schwannoma and Creutzfeldt–Jakob Disease: Recognition and Infection Control

We describe the first known case of coexistent vestibular schwannoma (VS) and Creutzfeldt-Jakob disease (CJD). Our objectives are to use this case as a general lesson for the subspecialist otolaryngologist to remain vigilant to alternative diagnoses, and to specifically improve understanding of the diagnosis and management of CJD as relevant to the practice of otolaryngology and skull base surgery. Retrospective case review performed in June 2016 at an academic, tertiary, referral center. A 55-year-old man presents with one month of worsening disequilibrium and short-term memory loss. Magnetic resonance imaging (MRI) (T1, T2) identified a 4 mm left VS which was then surgically resected. Postoperatively, his neurological status decline continued, and subsequent MRI identified patterns of FLAIR hyperintensity and diffusion restriction consistent with CJD. While CSF analysis (tau and 14-3-3) and EEG was inconclusive, serial imaging and the clinical course were highly suggestive of CJD. A probable diagnosis was made, surgical instruments quarantined, and infection control involved to minimize transmission risk. The patient died 6 months after symptom onset. Patients with CJD may initially present with otolaryngologic symptoms. MRI signal abnormality in the basal ganglia on diffusion weighted imaging and FLAIR sequences in conjunction with physical findings and clinical course may help make a probable diagnosis CJD. Prions are resistant to traditional sterilization and additional measures must be taken to prevent iatrogenic transmission. Level 4-Case series.

TSPO PET with [18F]GE-180 sensitively detects focal neuroinflammation in patients with relapsing–remitting multiple sclerosis

Expression of the translocator protein (TSPO) is upregulated in activated macrophages/microglia and is considered to be a marker of neuroinflammation. We investigated the novel TSPO ligand [18F]GE-180 in patients with relapsing-remitting multiple sclerosis (RRMS) to determine the feasibility of [18F]GE-180 PET imaging in RRMS patients and to assess its ability to detect active inflammatory lesions in comparison with the current gold standard, contrast-enhanced magnetic resonance imaging (MRI). Nineteen RRMS patients were prospectively included in this study. All patients underwent TSPO genotyping and were classified as high-affinity, medium-affinity or low-affinity binders (HAB/MAB/LAB). PET scans were performed after administration of 189 ± 12MBq [18F]GE-180, and 60-90min summation images were used for visual analysis and assessment of standardized uptake values (SUV). The frontal nonaffected cortex served as a pseudoreference region (PRR) for evaluation of SUV ratios (SUVR). PET data were correlated with MRI signal abnormalities, i.e. T2 hyperintensity or contrast enhancement (CE). When available, previous MRI data were used to follow the temporal evolution of individual lesions. Focal lesions were identified as hot spots by visual inspection. Such lesions were detected in 17 of the 19 patients and overall 89 [18F]GE-180-positive lesions were found. TSPO genotyping revealed 11 patients with HAB status, 5 with MAB status and 3 with LAB status. There were no associations between underlying binding status (HAB, MAB and LAB) and the signal intensity in either lesions (SUVR 1.87 ± 0.43, 1.95 ± 0.48 and 1.86 ± 0.80, respectively; p = 0.280) or the PRR (SUV 0.36 ± 0.03, 0.40 ± 0.06 and 0.37 ± 0.03, respectively; p = 0.990). Of the 89 [18F]GE-180-positive lesions, 70 showed CE on MRI, while the remainder presented as T2 lesions without CE. SUVR were significantly higher in lesions with CE than in those without (2.00 ± 0.53 vs. 1.60 ± 0.15; p = 0.001). Notably, of 19 [18F]GE-180-positive lesions without CE, 8 previously showed CE, indicating that [18F]GE-180 imaging may be able to detect lesional activity that is sustained beyond the blood-brain barrier breakdown. [18F]GE-180 PET can detect areas of focal macrophage/microglia activation in patients with RRMS in lesions with and without CE on MRI. Therefore, [18F]GE-180 PET imaging is a sensitive and quantitative approach to the detection of active MS lesions. It may provide information beyond contrast-enhanced MRI and is readily applicable to all patients. [18F]GE-180 PET imaging is therefore a promising new tool for the assessment of focal inflammatory activity in MS.

Magnetic resonance imaging features of Cryptococcus infection in central nervous system in patients with AIDS

To investigate the magnetic resonance imaging (MRI) features of Cryptococcus infection in central nervous system patients with acquired immune deficiency syndrome (AIDS). Methods: The retrospective study on magnetic resonance imaging (MRI) and clinical data of cryptococcal meningitis (CM) was carried out between July 2011 and March 2017. These patients had not received anti-retroviral treatment. Patients with other specific or suspicious diseases in the central nervous system were not included in the analysis. Results: A total of 39 patients were included in the analysis, with CD4 cell counts of 13.0×106/L [(0-205)×106/L], and 94.9% (37/39) of patients with CD4 cell count <100×106/L. Of the 39 patients, 26 patients showed abnormal MRI signals in the brain, which were most frequently involved in the basal ganglia (20/26, 76.9%). The basal ganglia lesions showed dilated Virchow-Robin space (VRS)/gelatinous spseudocysts (18/20, 90%). Postcontrast T1-weighted MRI revealed no significant enhancement (3/5, 60%) and mild enhancement (2/5, 40%). The incidence of cerebral cryptococcal granuloma were 35% (7/20). Nineteen of 26 patients with lesions outside the basal ganglia, of which 13 patients also complicated with basal ganglia lesions. Postcontrast T1-weighted MRI revealed no significant enhancement. The incidence of cryptococcal granuloma and meningeal thickening were 15.7% (3/19) and 26.3% (5/19), respectively. Postcontrast T1-weighted MRI meningeal thickening revealed enhancement (5/5, 100%). Conclusion: The incidence of brain MRI abnormality in AIDS complicated with central nervous system Cryptococcus infection may not be low, and the lesions are mostly located in the basal ganglia. It most frequently displays the dilated VRS/gelatinous spseudocysts. It can also be showed cryptococcal granuloma. Postcontrast T1-weighted MRI often reveals no enhancement or mild enhancement.

Evaluation and treatment of Langerhans cell histiocytosis patients with central nervous system abnormalities: Current views and new vistas

Central nervous system (CNS) involvement in Langerhans cell histiocytosis (LCH) can include mass lesions of the hypothalamic pituitary axis, choroid plexus, cerebrum, and cerebellum or magnetic resonance imaging (MRI) signal abnormalities of the cerebellum, pons, and basal ganglia. The term neurodegenerative (ND) CNS-LCH has been given to the MRI signal abnormalities and neurologic dysfunction, although initially patients may have no clinical symptoms. Standardized evaluations to better understand the natural history and response to therapy are needed. We propose guidelines for clinical, radiologic, and physiologic tests as a framework for developing the best methods of evaluation, which can then be tested in prospective treatment protocols.

Intraoperative neuromonitoring loss in abnormal magnetic resonance imaging signal intensity from patients with cervical compressive myelopathy

PurposeOur objective of this study was to evaluate if cervical compressive myelopathy (CCM) patients with preoperative abnormal magnetic resonance imaging (MRI) might easily lead to intraoperative neuromonitoring (IONM) loss. MethodA consecutive series of 152 CCM patients who underwent cervical cord decompression were enrolled in this study between December 2013 and February 2017. All patients with abnormal MRI signal intensity were divided into 2 groups (group 1: T2-WIs hyperintensity; group 2: both T2-WIs hyperintensity and T1-WIs hypointensity). Relevant IONM changes were identified as significant transcranial motor evoked potentials (MEP) loss associated with surgical decompression of cervical cord. ResultsThere were 121 patients in group 1, and then 6 cases showed IONM degeneration; 31 patients in group 2, and then 13 cases showed IONM degeneration (6/121 versus 13/31, p=0.000). Moreover, one case presented transient new spinal deficits after surgery, no permanent spinal deficit in group 1; 5 cases presented transient new spinal deficits, 2 cases showed permanent spinal deficit in group 2. And in group 2 the MEP amplitude before and after decompression had significant difference (134μV±30.2 versus 65μV±26.2, *p<0.05). ConclusionOur results suggest that the IONM degenerations or postoperative spinal deficits are more likely to appear on patients with abnormal T2-WIs and T1-WIs. Appropriate and timely interventions are probably useful for IONM recovery.

Evaluation of Cognitive Deficits and Structural Hippocampal Damage in Encephalitis With Leucine-Rich, Glioma-Inactivated 1 Antibodies

Limbic encephalitis with leucine-rich, glioma-inactivated 1 (LGI1) antibodies is one of the most frequent variants of autoimmune encephalitis with antibodies targeting neuronal surface antigens. However, the neuroimaging pattern and long-term cognitive outcome are not well understood. To study cognitive outcome and structural magnetic resonance imaging (MRI) alterations in patients with anti-LGI1 encephalitis. A cross-sectional study was conducted at the Departments of Neurology at Charité-Universitätsmedizin Berlin and University Hospital Schleswig-Holstein, Kiel, Germany. Data on 30 patients with anti-LGI1 encephalitis and 27 healthy control individuals matched for age, sex, and educational level were collected from June 1, 2013, through February 28, 2015. Clinical assessment, cognitive testing, and high-resolution MRI data, including whole-brain, hippocampal and basal ganglia volumetry; white matter integrity (diffusion tensor imaging); gray matter density (voxel-based morphometry); and hippocampal microstructural integrity (mean diffusivity and fractional anisotropy). Of the 30 patients included in the study, 19 were male (63%); mean (SD) age was 65.7 (12.3) years. Patients with anti-LGI1 encephalitis had incomplete recovery with significant and persisting verbal (mean [SE] Rey Auditory Verbal Learning Test [RAVLT], delayed recall: patients, 6.52 [1.05]; controls, 11.78 [0.56], P < .001) and visuospatial (Rey-Osterrieth Complex Figure Test [ROCF], delayed recall: patients, 16.0 [1.96]; controls, 25.86 [1.24]; P < .001) memory deficits. These deficits were accompanied by pronounced hippocampal atrophy, including subfields cornu ammonis 2/3 (CA2/3) and CA4/dentate gyrus (DG), as well as impaired hippocampal microstructural integrity. Higher disease severity correlated with larger verbal memory deficits (RAVLT delayed recall, r = -0.40; P = .049), decreased volumes of left hippocampus (r = -0.47; P = .02) and left CA2/3 (r = -0.41; P = .04) and CA4/DG (r = -0.43; P = .03) subfields, and impaired left hippocampal microstructural integrity (r = 0.47; P = .01). In turn, decreased volume of the left CA2/3 subfield (RAVLT delayed recall, r = 0.40; P = .047) and impaired left hippocampal microstructural integrity (RAVLT recognition, r = -0.41; P = .04) correlated with verbal memory deficits. Basal ganglia MRI signal abnormalities were observed in only 1 patient, but a longer duration of faciobrachial dystonic seizures correlated with a reduction of pallidum volume (r = -0.71; P = .03). In contrast, no abnormalities of cortical gray matter or white matter were found. The latency between disease onset and initiation of immunotherapy was significantly correlated with verbal (RAVLT recall after interference, r = -0.48; P = .02) and visuospatial (ROCF delayed recall, r = -0.46; P = .03) memory deficits. Anti-LGI1 encephalitis is associated with cognitive deficits and disability as a result of structural damage to the hippocampal memory system. This damage might be prevented by early immunotherapy.

Brain Herniation into Arachnoid Granulations: Clinical and Neuroimaging Features.

Brain herniation into presumed arachnoid granulations (BHAG) is an increasingly recognized entity. Though it has previously been described as isointense to brain matter on magnetic resonance imaging (MRI), we have encountered 21 cases in our clinical practice, many of which have signal abnormality in the herniated or adjacent parenchyma. We performed a systematic analysis on these cases to further understand the clinical significance. This is a retrospective analysis of cases collected from our clinical MRI practice. Each case was evaluated for location, size, lobe of origin, associated signal abnormality, symptoms, and the presence or absence of intracranial hypertension. Twenty-one cases of BHAG identified in 16 patients. Seven cases (7/21, 33%) demonstrated signal abnormality in the herniated or underlying parenchyma. On serial imaging, the size of herniation either fluctuated (2/10, 20%) or stayed the same (8/10, 80%). The associated signal abnormalities increased (1/5, 20%), decreased (1/5, 20%), or remained stable (3/5, 60%). Four patients (4/16, 25%) had signs/symptoms that could be associated with the BHAG. Ten patients (10/16, 63%) had either imaging findings or clinical signs that could be associated with intracranial hypertension. In contrast to previously reported cases, our study demonstrates that BHAG can be associated with MRI signal abnormalities of the herniated and adjacent brain. Symptoms are typically absent, though may be present in a small subset of patients, regardless of the presence of signal change or encephalomalacia of the involved brain. Indirect evidence of intracranial hypertension is present in a majority of patients but completely lacking in others.