FLAIR Sequences Research Articles

Novel Pathways Correlating with MS-Related Tremor, A Case-Control Study (P10-3.001)

<h3>Objective:</h3> Identifying the white matter fiber pathways responsible for tremor in Multiple Sclerosis (MS). <h3>Background:</h3> MS-related tremor is characteristically resistant to treatment, affecting 25% and 58% of the patients with MS. <h3>Design/Methods:</h3> Patients with MS-related tremor (n=36) had 3.0 T MRI scans with T1-weighted, FLAIR, and diffusion-weighted (DWI) sequences. Subjects were gender and age-matched with a control MS group (n = 36) without tremor. Using regional brain diffusivity measures obtained from MRICloud and diffusion connectometry findings from DSI Studio, we identified 53 tracts-of-interest associated with MS-related tremor. Tractography of the identified tracts was performed in DSI Studio. The diffusion data were reconstructed using generalized q-sampling. A supervised atlas-based tractography method was used to segment the pathways using tract-specific parameters set based on neuroanatomical topology and standardized across subjects. We obtained the partial spearman correlation coefficients (r_s) for tremor severity with mean tract diffusivity measures adjusting for possible confounders. <h3>Results:</h3> Of the 53 tracts, 5 showed negative correlation between mean tract fractional anisotropy (FA) and tremor severity: the left medial lemniscus (r_{s =} −0.55, p = &lt; .001), the forceps minor of the corpus callusom (r_{s =} −0.45, p = 0.009), the right anterior corticostriatal tract (r_{s =} −0.413, p = 0.017), the forceps major of the corpus callusom (r_s = −0.376, p = 0.031), and the fornix (r_s = −0.367, p = 0.035). Of these tracts 3 had radial diffusivity (RD) values significantly correlating with tremor severity, namely the left medial lemniscus (r_s = 0.429, p = 0.013), the right anterior corticostriatal tract (r_s = 0.379, p = 0.029), and the forceps minor of corpus callosum (r_s = 0.369, p = 0.034). <h3>Conclusions:</h3> Using two independent techniques, we identified pathways associated with MS-related tremor. For the first time, we show that commissural, medial lemniscus, and striatal tracts correlate with tremor severity. <b>Disclosure:</b> Mr. Bayoumi has nothing to disclose. Khader Hasan has nothing to disclose. The institution of Dr. Lincoln has received personal compensation in the range of $5,000-$9,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Sanofi-Genzyme. Dr. Lincoln has received personal compensation in the range of $5,000-$9,999 for serving on a Speakers Bureau for Biogen. The institution of Dr. Lincoln has received research support from Deaprtment of Defense. The institution of Dr. Lincoln has received research support from National Institutes of Health. The institution of Dr. Lincoln has received research support from EMD-Serono. Dr. Lincoln has received intellectual property interests from a discovery or technology relating to health care.

An Atypical Manifestation of Lateral Medullary Syndrome (P12-5.011)

<h3>Objective:</h3> To describe a case of lateral medullary syndrome (LMS) presenting with ipsilateral hemiparesis and upper motor neuron (UMN)-type facial palsy. <h3>Background:</h3> LMS is a classical vascular syndrome involving the posterior inferior cerebellar artery, which presents typically with ipsilateral Horner syndrome, ipsilateral ataxia, and contralateral hemianesthesia. Motor weakness and facial palsy are not traditionally presented in LMS. <h3>Design/Methods:</h3> Case report. <h3>Results:</h3> A 62-year-old male with poorly controlled hypertension presented with sudden onset left hemiparesis. On presentation, initial blood pressure was 178/95 mmHg. The neurological exam showed dysarthria, left facial palsy sparing the forehead, left facial hypoesthesia, and left hemiparesis (NIHSS 8). Diffusion-weighted MR Brain showed acute infarct in the left lateral medulla. FLAIR sequence showed chronic infarct in the right thalamus. CT arteriogram revealed non-opacification of the left vertebral artery at the level of C2–C3 with opacification of the distal left V4 via retrograde flow, severe stenosis of the right M1 segment, and multifocal atherosclerosis of the bilateral internal carotid arteries. Initial labs showed elevated LDL (213 mg/dl) and normal hemoglobin A1c. Right hemianesthesia was reported during his hospitalization; dysphagia, frequent hiccups, and left dysmetria out of proportion to weakness were noted during the recovery. After acute interventions, he was started on dual antiplatelet treatments for 90 days and a single antiplatelet afterward given concerns of large vessel disease as stroke etiology. <h3>Conclusions:</h3> Atypical clinical presentation in this LMS case included the combination of ipsilateral hemiparesis and ipsilateral UMN-type facial palsy. LMS with ipsilateral hemiparesis is known as Opalski’s syndrome, which is explained by involving the post-decussating pyramidal tract at the lower medulla and upper cervical spine. The explanation of ipsilateral UMN-type facial palsy in our case remains unclear. One possible explanation is the aberrant caudal looping of facial corticobulbar fibers into medulla oblongata prior to synapsing with the pontine facial nucleus. <b>Disclosure:</b> Dr. Yu has nothing to disclose. Mr. Bluntson has nothing to disclose. Dr. Sharma has nothing to disclose.

HHV-7 Encephalitis: The Rare Infection and Its Outcome on a Child (P11-10.006)

<h3>Objective:</h3> The primary aims of this study were to relate HHV-7 infection with clinical manifestations of encephalitis, transient hip synovitis and hepatic changes in childhood and to evidence the effectiveness of early diagnosis and treatment in patients with encephalitis. <h3>Background:</h3> A 2-year-old male patient reported persistent high fever, coughing and rhinorrhea starting 1 week ago. They sought outpatient pediatric care and was prescribed ceftriaxone and prednisolone, with no satisfactory response. The symptoms evolved to vomiting and dehydration. During the physical exam, he showed irritation, with constant cervical stiffness and hyperextension, photophobia, and convergent strabismus. On arrival, he had been taking ceftriaxone, acyclovir and desloratadine. Laboratory tests were very altered in leukocytes, platelets, PCR, AST, ALT and GGT. During the ophthalmologic examination, a paresis of cranial nerve VI on the right was identified as secondary to a probable meningitis. After 21 days of treatment with acyclovir, the patient had a good prognosis, however, he had claudication upon movement of the left hip. <h3>Design/Methods:</h3> NA <h3>Results:</h3> The CSF results were colorless, cloudy, pH 8, Glucose 58, Leukocytes 40, Proteins 81. To confirm this observation, the molecular panel detected the presence of HHV-7. The imaging tests helped and added to the results of the blood count and CSF. Cranial MRI showed a hyperintensity in the FLAIR sequence of the perimesencephalic subarachnoid space and small accumulation of liquid. In addition, the abdomen CT found a bit of fluid in the hip region. <h3>Conclusions:</h3> Encephalitis is an inflammation of the brain parenchyma that leads to neurological dysfunction caused by infection or autoimmunity. In this occasion, the patient had a rare case of HHV-7 encephalitis. Basically, the treatment was carried out with acyclovir and ketoprofen, obtaining a progressive improvement of the clinical picture. Consequently, further research on the complications of HHV-7 is essential to develop a good characterization of this disease. <b>Disclosure:</b> Mr. Andrade has nothing to disclose. Miss MARQUES has nothing to disclose. Dr. Mota has nothing to disclose.

Neurological manifestations of scrub typhus: Encephalitis and Acute Inflammatory Demyelinating Polyneuropathy (AIDP) (P2-10.002)

<h3>Objective:</h3> We report a case of a young male with serologically confirmed scrub typhus presenting with fever, eschar, altered sensorium, and progressive quadriplegia to illustrate the neurological complications (central and peripheral) of scrub typhus. <h3>Background:</h3> A young male presented to the emergency with complaint of high-grade fever for the past 12 days and altered sensorium. From the 10th day of illness, he started complaining of worsening weakness in all four limbs. A black, crusted plaque with an erythematous halo, giving a ‘cigarette-burn’ appearance suggestive of an eschar, was noted on the right forearm. On neurological examination, the patient was disoriented to time and place. Neck rigidity was absent. Reduced power of 3/5 in upper limbs and 1/5 in lower limbs was noted. Deep Tendon Reflexes were absent, and plantars were mute. <h3>Design/Methods:</h3> N/A <h3>Results:</h3> CSF analysis revealed no cells, mildly raised proteins (75 mg/dl), and normal glucose. CSF Grams staining, culture, India Ink preparation, and GeneXpert for Tuberculosis, was negative. Blood cultures were sterile. Scrub typhus IgM antibodies were detected using Enzyme-Linked-Immunosorbent-Assay (ELISA). Abdominal ultrasound revealed hepatomegaly. MRI-Brain revealed diffuse gyral swelling and hyperintensity on T2-weighted and FLAIR sequences involving bilateral lobes with no diffusion restriction, consistent with encephalitis. No abnormal post-contrast enhancement was noted. MRI-Spine was normal. Nerve Conduction Studies (NCS) were suggestive Acute Motor Axonal Neuropathy (AMAN) variant of Guillain-Barré-Syndrome (GBS). The patient received doxycycline. IVIG was added after NCS results. His condition gradually improved, and there was regaining of muscle strength in the following weeks with physiotherapy. <h3>Conclusions:</h3> Scrub typhus induced neurological complications are widely reported, with meningoencephalitis being the most common manifestation. However, PNS complications such as GBS are infrequent, and a high degree of clinical suspicion with prompt appropriate therapy and supportive care may prevent morbidity and mortality. <b>Disclosure:</b> Ms. Sood has nothing to disclose. Mr. Modi has nothing to disclose. Dr. Arora has nothing to disclose. Dr. Moudgil has nothing to disclose.

Double inversion recovery to detect cervical spinal cord multiple sclerosis lesions.

Magnetic resonance imaging (MRI) plays a key role in diagnosing and monitoring multiple sclerosis (MS). Double inversion recovery (DIR) is a pulse sequence that has proven highly effective at detecting cortical lesions but is understudied in the spinal cord. We hypothesize that DIR images obtained during brain MRI can be of value in assessing the upper spinal cord of MS patients. We retrospectively examined brain MRI exams of 64 patients with established MS, who had also undergone cervical spine MRI. Two blinded MS expert readers, who assessed the scans for lesion numbers and rated lesion visibility and overall image quality, reviewed brain 3-dimensional DIR sagittal and coronal images. Standardized mean contrast-to-noise ratios (C/N) and standard deviation (SD) were calculated in representative lesions for each patient and compared to those of 3-dimensional FLAIR images. For the analysis of lesions categorized as "definite lesions," the sensitivity was 87%, specificity was 61%, and negative predictive value was 80%. On the other hand, for "definite" plus "probable" lesions, the sensitivity was 91%, the specificity was 54%, and negative predictive value was 86%. DIR demonstrated lesions with an average C/N of 7.56 with an SD of 1.77. FLAIR sequence demonstrated lesions with an average C/N of 0.67 and SD of 1.27. Sagittally acquired brain DIR can provide useful information on upper spinal cord lesions, with high C/N. In theory, this should facilitate the attainment of McDonald's or the Magnetic Resonance Imaging in MS (MAGNIMS) criteria in some cases, without a dedicated cervical spine MRI exam.

Tinnitus, Aural Fullness, and Hearing Loss in a Patient with Acoustic Neuroma and Pituitary Macroadenoma

We report the case of a 51-year-old woman with multiple otologic and vestibular symptoms. She presented with two different types of tinnitus in her right ear, vertigo, and fluctuating aural symptoms in the left ear. She also complained of disequilibrium; chronic headache; hyperhidrosis; amenorrhea; insomnia; broadened hands and feet; and widened, thickened, and stubby fingers. The patient underwent careful collection of medical history, otomiscroscopy, pure tone audiometry, tympanometry, reflex threshold measurements, vestibular assessments, blood tests, magnetic resonance imaging (MRI), and cone beam computed tomography (CBTC) of the head. The audiogram showed: (1) a mild low-to-mid frequency conductive hearing loss, and a sharply sloping sensorineural hearing loss above 4000 Hz in the right ear; (2) a mild low-frequency sensorineural hearing loss in the left ear. MRI with 3D FLAIR sequences detected an acoustic neuroma (7.4 mm × 5.2 mm) in the middle-third of the right internal auditory canal, a pituitary macroadenoma (13 mm × 10 mm × 10 mm) and left saccular hydrops. The CBCT scan documented an outbreak of otosclerosis (3 mm) around the fissula ante fenestram in the right ear. Therefore, acoustic neuroma (right ear), growth hormone-secreting macroadenoma of the pituitary gland, Menière’s disease (left ear), and otosclerosis (right ear) were diagnosed/strongly suspected. A watch-and-wait strategy was adopted for acoustic neuroma and otosclerosis, while transsphenoidal surgery was successfully performed to remove the pituitary macroadenoma. This case report confirms that multiple otologic disorders can occur simultaneously in the same patient, requiring prompt audiological and imaging evaluations.

Echocardiographic correlates of MRI imaging markers of cerebral small-vessel disease in patients with atrial-fibrillation-related ischemic stroke.

Atrial fibrillation (AF) has been linked to dementia risk, partly explained by cerebral small vessel disease (CSVD). Since AF and cardiovascular comorbidities were associated with cardiac dysfunction, we aimed to determine the association between echocardiographic parameters and neuroimaging markers of CSVD in patients with AF-related ischemic stroke. This cross-sectional study enrolled patients with AF-related ischemic stroke from March 2013 to December 2019 who underwent transthoracic echocardiography and brain 3T MRI, including T1, T2, Flair, and SWI imaging sequences. We assessed the presence of lacunes and cerebellar microbleeds (CMBs), the severity of white matter hyperintensity (WMH) scored by the Fazekas scale (0-6), and the severity of enlarged perivascular spaces (EPVS) in basal ganglia (BG) and centrum semiovale (CSO) classified into three categories (0-10, 10-25, and >25). CSVD burden was rated on a 0-to-4 ordinal scale. Generalized linear regression analysis and post hoc comparisons with Bonferroni correction were performed to assess the association between various echocardiographic parameters and these lesions, adjusted for demographics and potential confounders. 119 patients (68.38 ± 12.692 years; male 45.4 %) were included for analysis, of whom 55 (46.2%) had lacunes, 40 (33.6%) had CMBs, and median severity for WMH, BG-EPVS, CSO-EPVS, and CSVD burden were 2 (IQR: 1-3), 1 (IQR: 1-2), 1 (IQR: 0-1), and 1 (IQR: 1-2) respectively. In multivariable, fully adjusted models, left ventricular posterior wall thickness (LVPW) was associated with a higher risk of lacunes (RR 1.899, 95% CI: 1.342-2.686) and CSVD burden (RR = 2.081, 95%CI: 1.562-2.070). Right atrial diameter (RAD) was associated with greater CSO-EPVS (RR = 2.243, 95%CI: 1.234-4.075). No echocardiographic parameters were revealed to be associated with CMBs and WMH. In patients with AF-related ischemic stroke, LVPW is associated with a higher risk of lacunes and CSVD burden, while RAD was associated with greater CSO-EPVS. Larger studies are required to determine these associations and to elucidate if these associations can help facilitate cognitive evaluation and brain MRI screening.

The signal intensity variation of multiple sclerosis (MS) lesions on magnetic resonance imaging (MRI) as a potential biomarker for patients' disability: A feasibility study.

Although many lesion-based MRI biomarkers in multiple sclerosis (MS) patients were investigated, none of the previous studies dealt with the signal intensity variations (SIVs) of MS lesions. In this study, the SIVs of MS lesions on direct myelin imaging and standard clinical sequences as possible MRI biomarkers for disability in MS patients were assessed. Twenty seven MS patients were included in this prospective study. IR-UTE, FLAIR, and MPRAGE sequences were employed on a 3T scanner. Regions of interest (ROIs) were manually drawn within the MS lesions, and the cerebrospinal fluid (CSF) and signal intensity ratios (SIR) were calculated from the derived values. Variations coefficients were determined from the standard deviations (Coeff 1) and the absolute differences (Coeff 2) of the SIRs. Disability grade was assessed by the expanded disability status scale (EDSS). Cortical/gray matter, subcortical, infratentorial, and spinal lesions were excluded. The mean diameter of the lesions was 7.8 ± 1.97 mm, while the mean EDSS score was 4.5 ± 1.73. We found moderate correlations between the EDSS and Coeff 1 and 2 on IR-UTE and MPRAGE images. Accordingly, Pearson's correlations on IR-UTE were R = 0.51 (p = 0.007) and R = 0.49 (p = 0.01) for Coeff 1 and 2, respectively. For MPRAGE, Pearson's correlations were R = 0.5 (p = 0.008) and R = 0.48 (p = 0.012) for Coeff 1 and 2, respectively. For FLAIR, only poor correlations could be found. The SIVs of MS lesions on IR-UTE and MPRAGE images, assessed by Coeff 1 and 2, could be used as novel potential MRI biomarkers for patients' disability.

Anorexia nervosa and Wernicke-Korsakoff syndrome: case report an literature review

IntroductionWenicke-Korsakoff syndrome (WKS) is a neurological disorder caused by thiamine deficiency. Wernicke Encephalopathy (WE) is the acute phase and the chronic phase is called Korsakoff-syndrome (KS).ObjectivesTo review the current literature on the management of WKS in a patient with anorexia nervosa.MethodsWe report the case of a 63-year-old woman admitted to the Psychiatry Unit after weight loss in the last 3 months (from 39 kg to 33,500 kg). She only made one meal a day. By exploration and analysis, neoplastic disease is ruled out (thoraco-abdomino-pelvic CT without pathological findings). She has maintained restrictive intakes for more than 30 years. A long-term anorexia nervosa (AN) is suspected, with a worsening of restrictive behavior in recent months. Upon admission, she has a weight of 33,500 kg and a BMI of 14,10. She has a left palpebral ptosis and an alteration of the anterograde memory as well as affectation of executive functions. Progressive oral diet is started, and due to the suspicion of a WKS, thiamine ev is started for a week and then continued with oral thiamine. Thiamine levels are extracted once the ev treatment has begun, so we do not have previous levels to know if they were decreased. Brain MRI shows bilateral hyperintensities in white matter and at supratentorial level in T2 and FLAIR. After a month and a half of admission, the patient has progressively regained weight, has managed to make adequate intakes and has improvement in memory.ResultsAn adverse consequence of severe malnutrition in AN due to severe food restriction and purging behavior is thiamine deficiency, and also global cerebral atrophy and concomitant cognitive deficits can be found. Thiamine deficiency occurs in 38% of individuals with AN and is often unrecognized. WKS is caused by thiamine deficiency, and WE is the acute phase of this syndrome (presentation of triad can vary). The chronic phase is KS and consists in amnesia with confabulations. WKS typically develops after malnourishment in alcoholic patients but can be associated in nonalcoholic such as prolonged intravenous feeding, hyperemesis, anorexia nervosa, refeeding after starvation, thyrotoxicosis, malabsorption syndromes; hemodialysis; peritoneal dialysis; AIDS; malignancy. WKS is a clinical diagnosis, and no specific abnormalities have been found in cerebrospinal fluid, brain imaging or electroencephalograms. MRI has a sensitivity of 53%, but high specificity of 93%, and shows an increased signal in T2 and FLAIR sequences, bilaterally symmetrical in the paraventricular regions of the thalamus, the hypothalamus, mamillary bodies, the periaquedutal region, the floor of the fourth ventricle and midline cerebellum.ConclusionsIf the disorder is suspected, thiamine should be initiated immediately in order to prevent irreversible brain damage, with an estimated mortality rate of about 20%, or to the chronic form of the WE in up to 85% of survivorsDisclosure of InterestNone Declared

Deep learning based detection of enlarged perivascular spaces on brain MRI

Deep learning has been demonstrated effective in many neuroimaging applications. However, in many scenarios, the number of imaging sequences capturing information related to small vessel disease lesions is insufficient to support data-driven techniques. Additionally, cohort-based studies may not always have the optimal or essential imaging sequences for accurate lesion detection. Therefore, it is necessary to determine which imaging sequences are crucial for precise detection. This study introduces a deep learning framework to detect enlarged perivascular spaces (ePVS) and aims to find the optimal combination of MRI sequences for deep learning-based quantification. We implemented an effective lightweight U-Net adapted for ePVS detection and comprehensively investigated different combinations of information from SWI, FLAIR, T1-weighted (T1w), and T2-weighted (T2w) MRI sequences. The experimental results showed that T2w MRI is the most important for accurate ePVS detection, and the incorporation of SWI, FLAIR and T1w MRI in the deep neural network had minor improvements in accuracy and resulted in the highest sensitivity and precision (sensitivity = 0.82, precision = 0.83). The proposed method achieved comparable accuracy at a minimal time cost compared to manual reading. The proposed automated pipeline enables robust and time-efficient readings of ePVS from MR scans and demonstrates the importance of T2w MRI for ePVS detection and the potential benefits of using multimodal images. Furthermore, the model provides whole-brain maps of ePVS, enabling a better understanding of their clinical correlates compared to the clinical rating methods within only a couple of brain regions.

Abstract Number ‐ 115: A Case of Post‐Pipeline Headache : New Post‐Flow Diversion Headaches for Intracranial Aneurysm

Introduction Flow diversion using devices such as the “pipeline” stent is now a common treatment for unruptured intracranial aneurysms. Though much is known about the efficacy of the device, less is reported regarding potential side effects. We aimed to describe a case of giant aneurysm with new onset and severe headache Post‐ Pipeline flow diversion stent application. Methods A 70‐year‐old female patient was admitted to the neurology outpatient clinic with complaints of diplopia and drooping of the left eyelid that started three months ago. Neurological examination revealed decreased visual acuity and total ophthalmoplegia in the left eye. In neuroimaging,semi‐thrombosed aneurysm, 20*25*20 mm in size, compressing the optic nerve and cavernous structures was observed in the left internal carotid artery cavernous segment. In digital subtraction angiography, a narrow neck, 20*25*22 mm giant aneurysm was observed in the left ICA C4 segment in three‐dimensional imaging. In premedication, were started seven days ago acetylsalicylic acid 100 mg 1*1 and 48 hours ago ticagrelol 2*90 mg and Pipeline 4.25*30 mm flow diverter was applied to cover the aneurysm neck under general anesthesia. One day after the procedure, the patient developed a new headache behind the left eye, throbbing, sensitive to sound and light, unresponsive to paracetamol and non‐steroidal anti‐inflammatory agents.In contrast‐enhanced cranial MRI, an aneurysm causing a central thrombosed hypointense mass effect was observed in the left cavernous structure neighbor with a peripheral enhanced, hyperintense T2 Flair sequence compatible with peripheral vasogenic edema. Pulse 1 gram/day steroid treatment was applied to the patient for three days.The patient’s headache completely regressed at the end of the third month, and perianeurysmal inflammation disappeared in the same contrast‐enhanced cranial MRI.In the 12th month post‐procedure imaging of the patient, it was observed that the aneurysm was completely occluded. Results In the case, we reporta patient with neurologic worsening after flow‐diverter treatment for unruptured cerebral aneurysms. We found MR imaging evidence of perianeurysmal brain inflammation after the therapeutic thrombosis of the sac to be the main cause explaining clinical aggravation. Consequently, we may consider a perianeurysmal brain inflammation when encountering the association of a postprocedure headache with an increase in previous compressive signs, possibly associated with MR imaging signs of inflammation1,2. We tried pulse steroid therapy, which is accepted as the first‐line treatment for postimplantation syndrome after endovascular repair of aortic aneurysms in the literature for a patient who did not respond dramatically to nonsteroidal anti‐inflammatory therapy3.We experienced a significant improvement in the patient’s clinical findings and contrast‐enhanced MRI findings after steroid treatment. Conclusions An inflammatory reaction may aggravate, transiently, clinical symptoms after aneurysm treatment with a flow‐diverter device. Further research is needed to better understand the underlying mechanisms as well as to achieve better prevention strategies.

Glioblastoma, IDH-Wildtype, CNS WHO Grade 4, Associated with Deep Brain Stimulation in a Patient with Essential Tremor: Report of a Case with Molecular Characterization, and Review of the Literature.

Table S1. Summary of prior literature of Glioma post DBS placement. Figure S1. MRI: (A) FLAIR sequence showing normal brain at different levels pre-implantation of the deep brain stimulator system. (B) FLAIR sequences showing development of an ill-defined mildly expansile FLAIR hyperintensity in the high right frontoparietal lobe involving the cortex and white mater, body of the corpus callosum and extending to the left side. (C) T1 post-contrast images showing enhancement in the right frontal lobe white matter anterior and medial to the right DBS lead. (D) FLAIR and (E) T1 post-contrast images following radiation therapy showing a 5 mm rim enhancing lesion anterior to the right DBS lead. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

The presence of pachymeningeal hyperintensity on non-contrast flair imaging in patients with spontaneous intracranial hypotension.

Traditionally, in the work-up of patients for spontaneous intracranial hypotension, T1 post-contrast imaging is performed in order to assess for pachymeningeal enhancement. The aim of this study is to assess whether pachymeningeal hyperintensity can be identified on a non-contrast FLAIR sequence in these patients as a surrogate sign for pachymeningeal enhancement. The patient cohort was identified from a prospectively maintained database of patients with a clinical diagnosis of intracranial hypotension. Patients who had both a post-contrast T1 sequence brain as well as non-contrast FLAR sequence of the brain were reviewed. Imaging was retrospectively reviewed by three independent neuroradiologists. Each study was assessed for the presence or absence of pachymeningeal hyperintensity on the FLAIR sequence. From January 2010 to July 2022, 177 patients were diagnosed with spontaneous intracranial hypotension. In total, 121 were excluded as post-contrast imaging was not performed during their work-up. Twenty-four were excluded as the FLAIR sequence was performed after administration of contrast. Six were excluded as there was no pachymeningeal thickening present on T1 post-contrast imaging, although there were other signs of intracranial hypotension. The study group therefore consisted of 26 patients. Pachymeningeal thickening was correctly identified on the non-contrast FLAIR sequence in all patients (100%). Where present, diffuse pachymeningeal hyperintensity can be accurately identified on a non-contrast FLAIR sequence in patients with spontaneous intracranial hypotension. This potentially obviates the need for gadolinium base contrast agents in the work-up of these patients.

Usefulness of a Rim-Enhancing Pattern on the Contrast-Enhanced 3D-FLAIR Sequence and MRI Characteristics for Distinguishing Meningioma and Malignant Dural-Based Tumor.

Meningiomas are the most common type of extra-axial dural-based tumors; however, malignant dural-based tumors can mimic meningiomas on imaging. The aim of this study was to determine the efficacy of differentiating meningiomas from malignant dural-based tumors by using rim-enhancement patterns on a contrast-enhanced FLAIR sequence and MR imaging characteristics. This retrospective study included 102 patients with meningiomas and 31 patients with malignant dural-based tumors who underwent pretreatment MR imaging. The rim-enhancement patterns on contrast-enhanced FLAIR and MR imaging characteristics, including the dural tail sign, hyperostosis, bony destruction, leptomeningeal enhancement, peritumoral edema, T2-weighted signal intensity, and tumor enhancement were evaluated. Complete rim enhancement of the tumor-brain interface on contrast-enhanced FLAIR (contrast-enhanced-FLAIR rim sign) was present in most meningiomas (91/102, 89.2%) and at significantly greater frequency than in malignant dural-based tumors (2/31, 6.5%) (P < .001). Complete contrast-enhanced FLAIR rim enhancement provided high sensitivity (89.2%), specificity (93.5%), and accuracy (90.2%) for diagnosing meningioma. Additionally, hyperostosis was an MR imaging characteristic that suggested a diagnosis of meningioma. In contrast, bony destruction with cortical breakthrough and leptomeningeal enhancement suggested malignant dural-based tumors. There were limitations of meningiomas of <2.0 cm or at cavernous sinus locations that did not demonstrate contrast-enhanced FLAIR rim enhancement. The rim-enhancement pattern on contrast-enhanced FLAIR could help differentiate meningiomas and malignant dural-based tumors. The presence of complete rim enhancement on contrast-enhanced FLAIR was a robust predictive sign for meningioma.

Abstract TMP30: High Prevalence Of Unrecognized Cerebral Amyloid Angiopathy Related Inflammation Among Patients With Cerebral Amyloid Angiopathy And White Matter Disease

Introduction: Cerebral amyloid angiopathy related inflammation (CAARI) is an autoimmune inflammatory condition that occurs in patients with cerebral amyloid angiopathy (CAA) and can lead to rapidly progressive cognitive decline. Little is known about the prevalence of subclinical and clinical CAARI. We sought to determine the prevalence of subclinical and clinical CAARI among patients with CAA and white matter hyperintensities (WMH). Methods: In this multicenter, single healthcare system, retrospective cohort study, we reviewed electronic medical records and MRI brain scans of patients presenting with a diagnosis code for amyloidosis or CAA that were evaluated between 1/2010 - 6/2020. We included patients meeting modified Boston criteria for CAA who had WMH on T2 FLAIR sequences. Patients without available hemosiderin sensitive sequences (SWI or GRE) and T2 FLAIR sequences and those without WMH on T2 FLAIR imaging were excluded. Two independent vascular neurologists blinded to background clinical information reviewed each MRI brain scan for the presence of CAARI. The clinical course and outcomes were reviewed and reported. Results: Out of 1100 patients reviewed, 511 met modified Boston criteria for CAA and 193 met the final study inclusion criteria. 55 (28.5% of those with CAA and WMH, and 10.8% of all CAA) patients had MRI brain imaging suggestive of CAA-RI. 21 (38.2%) were male, 38 (69.1%) were Caucasian, and the mean (SD) age was 72.9 (8.9) years. CAA-RI was recognized in only 10 (18.2%) patients initially while 20 (36.4%) were diagnosed up to 9 months later (median 0, IQR 0-9 months). At time of earliest detection of CAARI on imaging, common concurrent findings were cognitive impairment (74.5%), macro-hemorrhages (52.7%), headache (30.9%), seizures (14.5%), and ischemic infarcts (14.5%). Only 18 (32.7%) patients were started on immunosuppression. Nineteen (34.5%) patients expired during the observation period of which only 8 (42.1%) were ever diagnosed with CAA-RI by their treating clinician. Conclusion: The prevalence of subclinical CAA-RI in our study was high. Most cases of radiographic CAARI went unrecognized and untreated. Further studies are needed to assess if treatment of subclinical CAARI may prevent cognitive decline in these patients.

Abstract WP97: Routine MRI Reveals Prior Stroke In The Same Vascular Territory In Half Of Patients Presenting With Acute Ischemic Stroke Due To Intracranial Atherosclerotic Disease

Introduction: In 2012, after SAMMPRIS demonstrated worse 30-day outcomes with Wingspan intracranial stent placement for intracranial atherosclerotic disease (ICAD), the FDA narrowed the “on-label” indication to a very specific subset of patients with symptomatic ICAD. The updated criteria require a prior stroke in the territory of the symptomatic vessel based on clinical history. Limitations in the accuracy of diagnosis of clinical stroke may be overcome with the use of MRI to identify any prior stroke - whether clinical or subclinical - which could expand the number of patients who are eligible for stenting. Methods: This was a retrospective analysis of consecutive cases of acute ischemic stroke attributable to ICAD with 50-99% stenosis in the symptomatic vessel from July 2019 - June 2022. MRI FLAIR sequences were reviewed for imaging evidence of prior infarction in the vascular territory of the symptomatic vessel. Subgroup analysis was performed based on stroke location, infarct pattern, degree of stenosis, and premorbid medication use. Results: 73 patients met inclusion criteria. Mean age was 72, and 41% were women. 37 patients (51%) exhibited MRI evidence of prior stroke in the same vascular territory. Of these, only 18/37 (49%) reported a prior clinical stroke. The frequency of prior stroke on MRI was similar with anterior (51%) and posterior (50%) circulation ICAD. Frequency of prior stroke based on infarct pattern was 64% for border zone infarction, 42% for thromboembolism, and 55% for branch atheromatous disease. Of the 31 patients who had degree of stenosis quantified on DSA, the frequency of prior infarction was 63% in patients with 70-99% stenosis versus 48% in those with &lt;70% stenosis. Only 1 patient (1.4%) met FDA on-label criteria for intracranial stenting. The most common reason for ineligibility was absent history of clinical stroke in the territory of the symptomatic vessel (75%). Conclusions: In patients presenting with acute stroke due to symptomatic ICAD, half exhibit MRI evidence of a prior stroke in the symptomatic arterial territory, and half of these prior strokes are not reported from clinical history. Routine MRI can be a valuable tool to identify prior stroke in the symptomatic territory, which may in turn expand therapeutic options for ICAD.

Anatomical Variations of the Willis Circle: A Risk Factor for Brain Lesions in Sickle Cell Patients

<i>Background and objective</i>: The brain lesions observed in sickle cell patients are often known to be due to vessels occlusions. But other factors could be associated with the genesis of these lesions. The objective of this study was to assess the association between the presence of anatomical variations in the Willis circle and that of brain lesions found on MRI in sickle cell patients. <i>Methods</i>: We conducted a bicentric cross-sectional study with retrolective analysis of images at the medical imaging departments of the HUDERF in Brussels (Belgium) and the Yaoundé General Hospital (Cameroon), over a period of 12 months from November 2020 to October 2021. We included 187 homozygous sickle cell patients with documented electrophoresis and brain MRI results. The MRI were carried out in T1, T2, T2*, FLAIR, Diffusion and 3D TOF sequences on Siemens^® 1.5 Tesla devices. The collected data were analyzed using SPSS^® software version 20.0 for Windows^® with a significant p<0.05. <i>Results</i>: The mean age of patients was 8.76 years with no significant difference between the sexes. Variations in the Willis circle were present in 20 cases (10.70%) with a predominance in the posterior hemicircle (6.96% versus 3.74% for the anterior hemicircle; p=0.04). The most common variation was type G corresponding to hypoplasia or absence of the anterior communicating artery in the anterior hemicircle, and hypoplasia or unilateral absence of a posterior communicating artery in the posterior hemicircle. At the parenchymal level, brain lesions were found in 11 cases (5.88%) including ischemic lesions (3.21%) and leukopathies (1.07%). In general, the existence of these lesions was significantly associated with the presence of the Willis circle variations (p=0.01). <i>Conclusion and recommendation</i>: The presence of anatomical variations of the Willis arterial circle in sickle cell patients is associated with the existence of brain lesions. We therefore conclude that anatomical variations of the Willis circle could be an unknown factor increasing the risk of brain damages and therefore morbidity in these patients. We recommend that a larger sample study be conducted to verify our findings.

MRI of unruptured infectious intracranial aneurysms in infective endocarditis. A case-control study

PurposeTo evaluate the usefulness of T2* and FLAIR sequences in the detection of unruptured infectious intracranial aneurysms (UIIAs) in infective endocarditis (IE) including the relationships between the lesion patterns within subarachnoid spaces and the presence of UIIA. MethodsRetrospective review of 15 consecutive patients with definite IE undergoing MR imaging (FLAIR, T2*, DWI, CE-MRA, 3D-T1, CE-3DT1 sequences), in whom DSA detected infectious intracranial aneurysms (IIA). Aneurysmal features (diameter, location, morphology on DSA) and signal patterns onT2*, FLAIR and conventional MR sequences at the site of the UIIA, follow-up MRI and IE background, were analyzed.A control-group of 15 IE-patients without IIA at DSA served for comparison. ResultsAmong 17 UIIAs studied, T2* sequence displayed a susceptibility vessel sign in 15/17 (88.2%), both distal and proximal, which matched with the IIA visualized on DSA. Three patterns of hyposignal areas were identified: (a) signet-ring or target-sign appearance (n = 7), (b) homogeneous, round-, oval- or pear-shaped area (n = 4), and (c) heterogeneous area (n = 4). A FLAIR hyperintensity of the lumen and of the adjacent cortex was present in 6 (35.3%) and 9 (53%) UIIAs, respectively. On T1 (12 UIIAs) a rounded hyposignal (n = 2), within the UIIA lumen matched with the FLAIR hypersignal.Using both T2* and FLAIR had an incremental value with 100% sensitivity and specificity. ConclusionThe susceptibility vessel sign is an MR imaging pattern frequently observed at the site of UIIAs in IE-patients.Both T2* and FLAIR may have the potential to depict UIIAs, regardless of their location and shape.

MRI radiomic features of peritumoral edema may predict the recurrence sites of glioblastoma multiforme.

As one of the most aggressive malignant tumor in the central nervous system, the main cause of poor outcome of glioblastoma (GBM) is recurrence, a non-invasive method which can predict the area of recurrence pre-operation is necessary.To investigate whether there is radiological heterogeneity within peritumoral edema and identify the reproducible radiomic features predictive of the sites of recurrence of glioblastoma(GBM), which may be of value to optimize patients' management. The clinical information and MR images (contrast-enhanced T1 weighted and FLAIR sequences) of 22 patients who have been histologically proven glioblastoma, were retrospectively evaluated. Kaplan-Meier methods was used for survival analysis. Oedematous regions were manually segmented by an expert into recurrence region, non-recurrence region. A set of 94 radiomic features were obtained from each region using the function of analyzing MR image of 3D slicer. Paired t test was performed to identify the features existing significant difference. Subsequently, the data of two patients from TCGA database was used to evaluate whether these features have clinical value. Ten features with significant differences between the recurrence and non-recurrence subregions were identified and verified on two individual patients from the TCGA database with pathologically confirmed diagnosis of GBM. Our results suggested that heterogeneity does exist in peritumoral edema, indicating that the radiomic features of peritumoral edema from routine MR images can be utilized to predict the sites of GBM recurrence. Our findings may further guide the surgical treatment strategy for GBM.

Snake bite-induced leukoencephalopathy

A 15-year-old girl was brought to the casualty with an alleged history of snake bite on the ring finger of her right hand (A), which showed digital ischemia. The patient was unresponsive with severe respiratory distress. Patient management was done through elective intubation, cardiopulmonary Resuscitation with lifesaving emergency medications were given followed by anti snake venom. Finger reconstructive plastic surgery was performed after the patient became stable. On MR Imaging of the brain, the T2 and FLAIR sequences (B) showed symmetrical hyperintensities in the bilateral caudate nucleus and lentiform nucleus. Diffusion-weighted imaging (C) shows the cortical rim of restriction in bilateral subcortical white matter and corpus callosum and with corresponding low signal intensity on A.D.C. There was no associated haemorrhage. Neurological signs and symptoms after a venomous snake bite are most often related to venom´s toxic effects, which are anticoagulant/procoagulant activity or neurotoxicity. Some patients develop neurological complications related to cerebral hypoxia, which are related to hypotensive shock that may accompany some snake bite envenomation. Neuromuscular disorders, that is, damage to the peripheral nervous system, occur most often after the bite of elapids but may also occur following a viper bite. The effect of neurotoxins may start from minutes to a few hours after the inoculation of venom, causing weakness related to a blockage of synaptic transmission at either presynaptic or postsynaptic levels.