Meningeal Enhancement Research Articles

Predictors of outcomes in children with Central Nervous System tuberculosis

BackgroundCentral Nervous system tuberculosis (CNS–Tb) is the most lethal form of extra-pulmonary tuberculosis in children. The lack of markers of outcome provides little information on the efficacy of the current treatment protocols for CNS–Tb and thus results in a higher mortality rate than other extrapulmonary manifestations of tuberculosis. This study aims to identify significant factors that will reliably predict the outcomes at discharge in children admitted with CNS–Tb. Methods and materialThis is a prospective observational study in children with neurotuberculosis admitted at a tertiary care hospital. Clinical presentations at the time of admission were studied. Outcomes at the end of in-patient care (completely cured, survival with some/severe disability or death) were correlated with clinical, laboratory, microbiological, and radiological parameters. Univariate and multivariate analyses were applied to study the parameters and a p-value ≤ 0.05 with a confidence interval (CI) of 95% was considered as statistically significant. FindingsThe study included 100 children between 4 months and 12 years of age with a mean of 5.84 (±3.5) years. At discharge, 55% of children recovered completely, 20% had some or severe disability and 25% died. On multivariate analysis, high CSF protein (p = 0.050) and drug resistance (p = 0.034) were highly associated with fatality. Meningeal enhancements with basal exudates (p = 0.021) and CSF lymphocyte count >90% were highly associated with survival with disability. Stage I disease at presentation (p < 0.0001) was the only variable associated with complete recovery. InterpretationReliable prognostic markers for CNS–Tb can aid in predicting the efficacy of the current treatment and the anticipated outcome in the children with this disease. FundingThis research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Teaching NeuroImage: Palindromic Rheumatoid Meningitis: A Tale of 2 Hemispheres

A 61-year-old man presented with right-sided somatosensory seizures and evidence of left-sided pachymeningeal enhancement on a cerebral MRI (figure, A–C). The patient had a seizure 12 years prior. Upon review of the previous MRI, similar inflammatory changes in the contralateral hemisphere were seen (figure, D–E). Serologic and cerebrospinal fluid analysis and a brain PET scan demonstrated no abnormality. Brain biopsy revealed chronic lymphohistiocytic meningitis. His episodic arthropathy prompted rheumatological workup that revealed elevated cyclic citrullinated peptide and rheumatoid factor, suggestive of palindromic rheumatism, with corresponding imaging findings reminiscent of those described with rheumatoid meningitis.1,2 He improved after a brief course of steroids with resolution of meningeal enhancement (figure, F).

Facial Nerve Palsy After Ear Infection: A Case Report

<strong>Introduction:</strong> The incidence of acute mastoiditis, a common complication of otitis media, has significantly decreased with the emergence of antibiotic therapy [1]. Classical symptoms of acute mastoiditis include fever, irritability, otalgia, swelling of the mastoid area, and retroauricular erythema [2]. Delay in appropriate antibiotic treatment of mastoiditis may lead to intracranial and extracranial complications. Facial nerve paralysis is a rare complication of otomastoiditis with different pathophysiologic mechanisms postulated [3]. Extensive literature search showed cases of lower motor neuron involvement of the facial nerve in affected patients. We report an unusual case of mastoiditis without fever complicated by epidural abscess and upper motor neuron facial nerve palsy in a previously healthy adolescent. <strong>Case Presentation:</strong> A 13-year-old male presented with painful progressive swelling behind his left ear of 5 days duration. Symptoms had started 2 weeks prior with complaints of left ear pain, and he was diagnosed with impacted cerumen and prescribed topical hydrogen peroxide. There was no history of fever, ear discharge, hearing loss or change in neurologic status. On admission, physical examination showed 4x4 cm tender swelling over the left mastoid region with forward displacement of the pinna and cerumen impaction. Neurological assessment was normal. Laboratory investigations showed peripheral leukocytosis (12,200 cells/uL) with neutrophilia (74%), and elevated c-reactive protein (87 mg/L). Head CT scan showed acute coalescent left mastoiditis with small left epidural abscess formation, displacing the left sigmoid sinus medially, and a developing left mastoid subperiosteal abscess (see <em><strong>Figure 1</strong></em>). A diagnosis of acute mastoiditis was made, and he was commenced on intravenous ceftriaxone and vancomycin with resultant decrease in size of the swelling and normalization of inflammatory markers. On the third day of admission, the patient developed mild right-sided facial asymmetry with sparing of the upper part of the face. Ceftriaxone was changed to piperacillin-tazobactam for broader-spectrum anerobic and gram-negative coverage. Otolaryngology evaluation revealed Bezold’s abscess requiring mastoidectomy. The father initially declined, given improvement in the patient’s symptoms, but consented to wide myringotomy and placement of a short-term myringotomy tube for further drainage and middle ear irrigation. Samples of pus collected were sent for aerobic, anaerobic, mycobacterial, and fungal cultures which all came back negative except for scant growth of Staphylococcus epidermidis. MRI done on the second post-operative day showed severe coalescent left otomastoiditis, mild meningeal enhancement compatible with meningitis along the left lateral temporal lobe, and a small sliver of epidural abscess along the left infratemporal fossa (see <em><strong>Figure 2</strong></em>). Antibiotic treatment was escalated from Piperacillin-tazobactam to meropenem to provide a broader gram-negative and anaerobic coverage. At this point, father consented, and patient underwent mastoidectomy with craniotomy and epidural abscess drainage. Patient received 14 days of parenteral antibiotics. He showed clinical and radiological improvement on repeat MRI, facial asymmetry resolved and patient was discharged home in stable condition to complete 1-month of oral antibiotics (levofloxacin + amoxicillin-clavulanate) with subsequent outpatient follow-up. <strong>Conclusion:</strong> Mastoiditis is a complication of otitis media that can lead to potentially life-threatening intracranial complications. Interestingly, the patient developed rightsided facial asymmetry sparing the upper part of the face suggesting a left upper motor neuron facial nerve palsy with involvement of the contralateral face. This finding is unique to our case, and to our knowledge has not been described in literature. A plausible anatomic explanation is the involvement of ipsilateral corticobulbar tract with subsequent interruption of the main input to the lower portion of contralateral facial nerve nucleus which controls the muscles of the lower face [4]. This results in sparing of the upper facial muscles characteristic of upper motor neuron lesion. Appropriate antibiotic treatment with surgical intervention led to complete resolution of symptoms.

Cerebral Amyloid Angiopathy-Related Inflammation/Vasculitis

Cerebral amyloid angiopathy (CAA) is a disorder characterized by the deposition of amyloid in the leptomeningeal and cortical blood vessels. Sporadic amyloid β (Aβ)-type CAA is the most common form of CAA. Although CAA is a well-known cause for recurrent cerebral lobar hemorrhage, inflammation, and vasculitis, CAA-related inflammation/vasculitis (CAA-ri/vasculitis) induced by Aβ deposition on vessel walls is emerging as a treatable condition. The estimated total number of cases of and prevalence of CAA-ri/vasculitis in Japan were 170 and 0.13 per 100 000 population, respectively. Patients with CAA-ri/vasculitis show acute or subacute-onset of cognitive impairment, behavioral changes, and headache. Brain magnetic resonance imaging, showing asymmetrical white matter abnormalities and occasional meningeal enhancement, is a useful tool for the diagnosis of CAA-ri/vasculitis. Moreover, elevation of anti-Aβ antibodies and inflammatory markers in the cerebrospinal fluid can help in clinical diagnosis. Although several clinical diagnostic criteria have been proposed, neuropathological examination of a brain biopsy remains the gold standard for detecting severe Aβ deposition and vasculopathic changes with lymphocytic infiltrations and/or granulomatous vasculitis. No validated treatment regimen has been established to date. Nearly 80% patients with CAA-ri/vasculitis improved after immunosuppressant therapy with corticosteroid and/or cyclophosphamide. Early treatment is essential to prevent irreversible sequelae in the brain.

Development and validation of a new scoring system for the early diagnosis of tuberculous meningitis in adults

We developed and validated a new diagnostic scoring system by simultaneously comparing 28 factors (including clinical, laboratory, and imaging) of HIV uninfected adult tuberculous meningitis (TBM) with viral meningitis (VM), bacterial meningitis (BM), and cryptococcal meningitis (CM). Predictors of TBM diagnosis obtained by logistic regression. A total of 382 patients with intracranial infection participated, and eight factors were independently associated with TBM diagnosis: symptom duration, evidence of extracranial tuberculosis, cerebrospinal fluid (CSF) leukocyte, CSF neutrophil, CSF protein, low serum sodium, meningeal enhancement, and tuberculomas. Factors are assigned according to weight, a score of ≥ 5 was suggestive of TBM with a sensitivity of 85.8% and a specificity of 87.7%, and the area under the receiver operating characteristic curve was 0.923. When applied to a prospective validation cohort, this scoring model showed robust performance. Our study suggests that the application of this score can help diagnose TBM more efficiently.

Bilateral trigeminal motor nucleus syndrome

A 48-year-old man was brought to our unit with deteriorating consciousness but no available history. His Glasgow Coma Scale score was 11/15 (E3, V4, M4). A limited neurological examination identified...

Imaging meningeal inflammation in CNS autoimmunity identifies a therapeutic role for BTK inhibition.

Leptomeningeal inflammation in multiple sclerosis is associated with worse clinical outcomes and greater cortical pathology. Despite progress in identifying this process in multiple sclerosis patients using post-contrast fluid-attenuated inversion recovery imaging, early trials attempting to target meningeal inflammation have been unsuccessful. There is a lack of appropriate model systems to screen potential therapeutic agents targeting meningeal inflammation. We utilized ultra-high field (11.7 T) MRI to perform post-contrast imaging in SJL/J mice with experimental autoimmune encephalomyelitis induced via immunization with proteolipid protein peptide (PLP139-151) and complete Freund's adjuvant. Imaging was performed in both a cross-sectional and longitudinal fashion at time points ranging from 2 to 14 weeks post-immunization. Following imaging, we euthanized animals and collected tissue for pathological evaluation, which revealed dense cellular infiltrates corresponding to areas of contrast enhancement involving the leptomeninges. These areas of meningeal inflammation contained B cells (B220+), T cells (CD3+) and myeloid cells (Mac2+). We also noted features consistent with tertiary lymphoid tissue within these areas, namely the presence of peripheral node addressin-positive structures, C-X-C motif chemokine ligand-13 (CXCL13)-producing cells and FDC-M1+ follicular dendritic cells. In the cortex adjacent to areas of meningeal inflammation we identified astrocytosis, microgliosis, demyelination and evidence of axonal stress/damage. Since areas of meningeal contrast enhancement persisted over several weeks in longitudinal experiments, we utilized this model to test the effects of a therapeutic intervention on established meningeal inflammation. We randomized mice with evidence of meningeal contrast enhancement on MRI scans performed at 6 weeks post-immunization, to treatment with either vehicle or evobrutinib [a Bruton tyrosine kinase (BTK) inhibitor] for a period of 4 weeks. These mice underwent serial imaging; we examined the effect of treatment on the areas of meningeal contrast enhancement and noted a significant reduction in the evobrutinib group compared to vehicle (30% reduction versus 5% increase; P = 0.003). We used ultra-high field MRI to identify areas of meningeal inflammation and to track them over time in SJL/J mice with experimental autoimmune encephalomyelitis, and then used this model to identify BTK inhibition as a novel therapeutic approach to target meningeal inflammation. The results of this study provide support for future studies in multiple sclerosis patients with imaging evidence of meningeal inflammation.

Hemispheric encephalitis secondary to HAV

A 2-year male child, presented to National Institute of Child Health (NICH), with acute onset high grade fever and focal left sided seizures for 1 day, followed by left hemiparesis and encephalopathy. Developmental and family history was unremarkable. On physical examination, patient’s body temperature rose up to 38.7 °C. Though he had pallor along with hepatomegaly, there were no signs of jaundice or ascites. Central nervous system examination showed encephalopathy as well as positive neck stiffness. Motor system examination revealed generalized decrease in bulk of upper and lower limbs, but rest of the findings were localized to left side of the body, showing hypertonia, decreased power, brisk muscle stretch reflex, and positive ankle clonus and left Babinski sign.&#x0D; Blood investigations showed anemia (hemoglobin 9.1g/dl), leukocytosis (white blood cells 22.1 cells/μL) and raised aspartate aminotransferase (AST) levels (826 IU/L). Total bilirubin and direct bilirubin levels were normal (0.3 mg/dL and 0.1 mg/dL, respectively). Serum ammonia (64 μg/dL) and lactic acid (1.6 μg/dL) levels were also within normal ranges. The cerebrospinal fluid (CSF) was also clear, with 0 leukocytes/μL, protein levels of 25 mg/dL, and normal glucose levels (82 mg/dL), no organism was seen on gram stain. Hepatitis A Ig M antibody came out to be reactive.&#x0D; Brain computed tomography showed large hypo density along with effacement of sylvian fissure, sulci, gyri on right side involving frontal, parietal, and temporal and occipital lobe on ipsilateral side. On post contrast, there was remarkable meningeal enhancement on right side. MRI brain revealed cortical and subcortical large area of abnormal signal intensity seen in fronto-parietal and occipital cortex on the right side along with laminar necrosis.&#x0D; Seizures were controlled by given intravenous injection phenytoin and leviteracetam in bolus and then maintenance doses. Intravenous acyclovir was started&#x0D; due to clinical suspicion of herpes encephalitis but was stopped after observing clinical improvement and identification of Ig M antibody of HAV. Patient conscious level improved after 2 weeks. AST levels also decreased to 20 IU/L and he was discharged with advice to follow up after 14 days

Cerebral amyloid angiopathy‐related inflammation and dementia

AbstractCerebral amyloid angiopathy (CAA) is a disorder characterized by deposition of amyloid on the leptomeningeal and cortical blood vessels. Sporadic amyloid β (Aβ)‐type CAA is the most common type of CAA. Although CAA is well known as a cause of recurrent cerebral lobar hemorrhage, inflammation and vasculitis (CAA‐related inflammation [CAA‐ri]) induced by deposited Aβ on the vessel walls is emerging as a treatable condition. Furthermore, dementia could develop regardless of the presence of Alzheimer's disease pathology. The estimated total number and prevalence of CAA‐ri in Japan was reported as follows: 170 and 0.13 per 100 000 population, respectively. The estimated total number of CAA‐related intracerebral hemorrhage was 5900. The crude prevalence rate of CAA‐related intracerebral hemorrhage was 4.64 per 100 000 population. The patients with CAA‐ri show acute or subacute‐onset cognitive impairment, behavioral changes and headache. Brain magnetic resonance imaging is a useful tool for the diagnosis of CAA‐ri, showing asymmetrical white matter abnormalities and occasional meningeal enhancement. Furthermore, elevation of anti‐Aβ antibodies and inflammatory markers in the cerebrospinal fluid would be useful for clinical diagnosis. Clinical diagnostic criteria were proposed; however, neuropathological examination obtained by brain biopsy is still warranted to confirm severe Aβ deposition and vasculopathic changes with lymphocytic infiltrations and/or granulomatous vasculitis. No validated protocol of treatment has been established. Nearly 80% of the patients with CAA‐ri improved after immunosuppressant therapy, including corticosteroid and cyclophosphamide. Early treatment is necessary to prevent the development of irreversible sequela in the brain.

COVID-19-associated meningoencephalitis: A care report and literature review.

Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may target the central nervous system and several neurological symptoms have been reported in patients with coronavirus disease 2019 (COVID-19). In the present study, a case of a SARS-CoV-2 complicated with meningoencephalitis was reported. Cerebrospinal fluid (CSF) analyses indicated hyperproteinorrachia but the specimen was negative for SARS-CoV-2 RNA. Furthermore, 10 published articles reporting on patients with COVID-19-associated meningitis/encephalitis were reviewed. Patients diagnosed with COVID-19-associated meningitis/encephalitis had diverse clinical neurological manifestations, including consciousness disturbance, epileptic attacks, psychotic syndrome and meningeal irritation signs. CSF tests revealed elevated protein, lymphocytes and cytokines. SARS-CoV-2 may be detected in the CSF of certain cases. Neuroimaging findings included hyperintense signal changes in the white matter and enhancement of meninges on brain MRI. Certain patients responded well to corticosteroid therapy and had a favorable prognosis, while elderly patients tended to have poor outcomes due to multiple organ dysfunction.

Reader Response: Clinical Significance of Anti-NMDAR Concurrent With Glial or Neuronal Surface Antibodies.

We welcome the study by Martinez-Hernandez et al.1 reporting antibody coexistence in anti-n-methyl-d-aspartate receptor (NMDA-R) encephalitis. The authors confirmed coexistence of aquaporin-4-IgG or myelin oligodendrocyte glycoprotein (MOG)-IgG as predictors of co-occurrence of anti-NMDA-R encephalitis and autoimmune CNS demyelination. By contrast, it was concluded that coexisting GFAP-IgG is “clinicoradiologically nonspecific.”1 The diagnosis of autoimmune GFAP astrocytopathy—AGA, a clinical-radiological-serological entity, characterized by an inflammatory steroid-responsive meningoencephalomyelitis—requires adherence to a 2-step CSF evaluation2–5 (figure): (1) detection—by optimized rodent tissue-based immunohistochemistry—of an astrocytic filamentous-appearing pattern of IgG staining of all of midbrain (meningeal, subpial, and periventricular), cerebellar white—but not gray—matter, hippocampal, and cortical brain regions, and myenteric plexus and (2) positivity by GFAPα isoform-transfected HEK293 CBA (figure). Serum testing is insensitive and generates nonspecific results, as occasionally does CSF if both tissue and cell-based assays steps are not followed. Two patients with coexisting GFAP-IgG reported by Martinez-Hernandez et al.1 had meningeal enhancement on MRI, but the authors attribute this to anti-NMDA-R encephalitis alone, although the question of these 2 IgGs coexisting was not addressed systematically. Deviations from published methods may explain the paucity of cases found by Martinez-Hernandez et al.—10 of 846 anti-NMDA-R encephalitis patients total, 1.2%.2 Since test “go-live” in June 2019, we have detected GFAP-IgG coexisting in 6% of NMDA-R-IgG positive CSF specimens. Martinez-Hernandez et al. reported universal nondetection of coexisting GFAP-IgG by immunohistochemistry.2 The authors did not state whether fixation and permeabilization were optimized for detection of IgGs reactive with cytoplasmic proteins, such as GFAP. Furthermore, the authors used a “live” GFAP-specific cell-based assay (CBA) to identify 10 patients with coexisting GFAP-IgG, yet the intracellular location of GFAP should preclude detection in live cells. Additional details pertaining to the GFAP isoform expressed, and the specimen types tested—CSF or serum—were lacking. All of these factors can impact the sensitivity and specificity of GFAP-IgG testing and frequency of coexistence with NMDA-R-IgG.2,6 To address the question of neurologic phenotype further, we reviewed data for 248 unique patients in whom CSF GFAP-IgG was detected and confirmed by our 2-step laboratory protocol2,6 over the course of 4.5 years (January 1, 2015–June 30, 2019). Median GFAP-IgG endpoint titer was 1:64 (range 4–512; normal, <2). Twenty-three (9%) had coexisting CSF NMDA-R-IgG detected, 11 with clinical information available. Six of 11 patients also had NMDA-R-IgG detected at high titer on tissue-based assay (median, 1:32 [range, 4–128; normal, <2], figure), confirmed by GluN1-specific CBA. Of those 6, 5 had typical anti-NMDA-R encephalitis clinical phenotype, 4 of whom had anti-NMDA-R encephalitis-typical (normal) MRI brain imaging, and 1had radial periventricular enhancement (AGA-typical). The 6th patient had an inflammatory encephalomyelitis clinically and radiologically (AGA-typical) but accompanied by orofacial dyskinesias (anti-NMDA-R encephalitis-typical). The remaining 5 patients had NMDA-R-IgG detected (robustly) by GluN1-specific CBA only. Four of 5 patients were AGA-typical radiologically and clinically—with headache and meningism prominent—and 1 was anti-NMDA-R encephalitis typical. Although the pathophysiology of AGA remains to be elucidated, GFAP-IgG is a biomarker of a treatable inflammatory CNS disorder, when appropriately evaluated for. Rigorous CSF evaluation permits clear AGA diagnosis, identification of clinically pertinent coexisting IgGs, avoidance of unnecessary brain biopsies, and facilitation of early treatment.

Isolated neurobrucellosis-characteristic clinical and laboratory features.

To report various neurological syndromes, CSF findings, imaging and diagnostic methods used in neurobrucellosis patients admitted in our Neurology department over a period of 6years. Case records of patients admitted to our department from August 2014 to May 2020 were searched for neurobrucellosis and data were obtained. A total of 19 patients were diagnosed as neurobrucellosis over a period of 6years. Ten patients had chronic meningitis, five had VIII nerve involvement, one had optic neuritis, two had acute meningitis, one had subacute meningitis, four had myelopathy, five had polyradiculitis and two had spondylodiscitis. CSF was abnormal in 17 patients. Neutrophilic pleocytosis was seen in 12 patients who included nine patients with chronic symptomatology.Brain imaging was abnormal in three chronic meningitis patients. One had diffuse meningeal enhancement, another had hydrocephalus while the third patient had meningeal enhancement with basal exudates and contrast enhancement of bilateral VIII nerve. One of the patients of acute meningitis had hydrocephalus while the other one had bilateral T2/FLAIR hyperintensities with enhancement of meninges and leptomeningeal vessels. Elevated antibody titers only in serum was seen in six patients while elevated antibody titers only in CSF was seen in seven patients. Four patients had elevated antibody titers in both serum and CSF. CSF culture was positive in three patients. Neurobrucellosis is a rare clinical complication of brucellosis but may pose a problem in diagnosis as it can mimic tuberculosis. Involvement of VIII nerve and neurophilic pleocytosis in CSF despite chronic symptomatology can be diagnostic clues favoring neurobrucellosis.

Neurological manifestations in scrub typhus from a case series in Southern India

Scrub typhus is an acute febrile illness caused by Orientia tsutsugamashi. CNS is the most crucial target in other rickettsial diseases and historically, the neurological disease burden was considered low in scrub typhus. However, there is growing evidence in literature that O. tsutsugamushi does invade the CSF and CNS invasion may be seen in 2–5 % cases of tsutsugamushi disease. O. tsutsugamushi parasitises endothelial cells both in the periphery as well as in the brain. The disease is characterized by focal or disseminated vasculitis and perivasculitis. Scrub typhus has protean manifestations. CNS involvement is rare but it should be considered as an important differential in the setting of known areas of scrub typhus outbreak. Meningoencephalitis with or without focal neurological deficits is the commonest clinical picture. However, the neurological manifestations can be highly variable. In our case series out of 81 patients who were diagnosed with scrub typhus, only 5 patients had neurological manifestations. All patients presented with altered sensorium. GCS was decreased in all patients. It was <10 in 60% cases. Neck rigidity and signs of meningeal irritation was present in 80% cases. There was no sign of papilloedema, cranial nerve involvement, focal neurological deficits. 2 of the patients had seizure which was GTCS in semiology. CSF in all cases showed lymphocytic predominance (between 150 and 400 cells/ mm3) with high protein and low to normal CSF sugar levels. NCCT brain was normal. MRI brain showed meningeal enhancement in 60% cases. Additionally, hyperintense signal on T2 was observed in 60% cases. Confirmation of the case requires serological evidence. CSF and neuroimaging picture are not pathognomonic. In the setting of acute fever, headache along with eschar or macular rash, scrub typhus must be ruled as a cause of neurological manifestations, such as altered sensorium, and seizure.

Predictors Modifying the Outcome of Tuberculous Meningitis (TBM) in Adults: A Hospital Based Study in Bangladesh

Background: Outcome of TBM can be modified by several predictors.&#x0D; Objective: This study was undertaken to evaluate the predictors of outcome of tuberculous meningitis (TBM) at 6 and 9 months.&#x0D; Methodology: This hospital based prospective cohort study was carried out from October, 2016 to September, 2017 (1 year) in the in-patient Department of Neurology at the National Institute of Neurosciences &amp; Hospital (NINS &amp; H), Dhaka, Bangladesh. All the patients with age 18 years or more of both sexes with features of TBM fulfilling the case definition criteria was included as the study population. The outcome was measured at 6 and 9 months by modified Rankin Scale (mRS) with no disability (score=0-1), mild disability (score = 2), moderate disability (score=3-4), severe disability (score=5) and dead (score=6). For statistical analysis outcome was classified as death and survival group. A number of clinical, laboratory and radiological parameters were evaluated initially by univariate and finally multiple regression analysis.&#x0D; Results: A total 54 TBM patients were included in this study. Over 70% of the patients were adolescent or young adult (&lt; 30 years) with mean age of 28.2 ± 12.3 years and 63% were female. Staging of the TBM showed that nearly half (48.1%) were at stage II and 37% cases were in stage III disease. Baseline imaging (CT-scan and MRI) showed basal meningeal enhancement in 40.7% cases, hydrocephalus in 40.7%, infarction 46.3% and tuberculoma in 29.6% cases. Final diagnosis was established as definite TBM in 3(5.6%) cases, probable TBM 30(55.6%) and possible TBM in 21(38.9%) cases. In terms of 6-months outcome, 16(29.6%) cases died and 10(18.5%) had recovered without any neurological sequelae; however, mild, moderate and severe disability were in11.1%, 27.8% and 13% cases respectively. At the 9 months of evaluation 13 (24.0%) had complete recovery without any neurological sequelae, 22 (40.9%) patients survived with various degree of disabilities like visual impairment, hemi or paraplegia, cognitive impairment, rests died giving a total mortality of 19(35.1%). In univariate analysis, age &gt;50 years (p=0.019), duration of illness before initiation of treatment (&gt;45 d) (p = 0.041), convulsion (p = 0.010), altered sensorium (p&lt;0.001), delayed initiation of treatment &gt;1 month (p=0.041) and stage III TBM (p&lt;0.001) were significantly associated with mortality. In multivariate analyses stage III TBM (p=0.004), altered sensorium (p=0.036), delayed initiation of treatment &gt;1 month (p=0.043) emerged as independent predictors of mortality.&#x0D; Conclusions: In conclusion stage III TBM, altered sensorium and delayed initiation of treatment more than 1 month are the independent predictors of mortality in TBM patients.&#x0D; Journal of National Institute of Neurosciences Bangladesh, January 2021, Vol. 7, No. 1, pp. 14-19

A study to assess the clinico-radiological presentation and outcome predictors in cases of tubercular meningitis

IntroductionTubercular bacterial meningitis continues to be an important cause of morbidity (especially neurologic handicap) in children from resource-poor countries. The present study was planned to assess the clinical and radiological presentation in cases of tubercular meningitis as well as to study the factors associated with mortality. MethodologyThis study was done over a period of 12 months on children between 5 years and 13 years with suspected TBM. Staging of tubercular meningitis was done according to RNTCP Pediatric TB guideline 2019. ResultThe study was conducted on a total of 47 pediatric patients with TBM. Mean age of children in present study was 8.77 ± 2.5 years. Our study documented male preponderance for TBM. Severe thinness was observed in 38.3% patients with TBM. Only 59.6% patients were immunized against tuberculosis and history of contact was documented in 40.5% patients. Maximum children belonged to stage I of TBM (59.6%) followed by stage III and stage II in 34% and 6.4% patients respectively. Montoux test positivity was observed in 14.9% patients only. CSF CBNAAT was positive in 6.4% patients. The most common finding was meningeal enhancement seen in 27.7% of patients followed by tuberculomas in 10.6%.Chest X ray was abnormal in 44.7% patients. In present study mortality was observed in 11 (23.4%) cases. Out of various risk factors, mortality was significantly associated with nutritional status and stage of TBM (p < 0.01). ConclusionTBM is associated with high morbidity and mortality in children especially in India where Burden of TB is high. Our study emphasized on the risk factors associated with mortality in children with TBM and need for early diagnosis and appropriate treatment.

Hearing Loss with Diffuse Meningeal Enhancement: A Rare Initial Presentation of Sarcoidosis

Background: Sarcoidosis is a systemic disease that can affect almost any organ system, with lungs being the most commonly involved. Other organ systems that may be affected include the skin, eyes, joints, heart, kidneys, or the gastrointestinal tract. Symptoms of sarcoidosis depend on the organ system involved. For instance, pulmonary involvement usually presents with cough and shortness of breath. Involvement of the joint usually presents with joint pain. Neurological manifestation, termed as neurosarcoidosis, is a relatively uncommon initial presentation of sarcoidosis. Patients with neurosarcoidosis can be asymptomatic or have multiple neurological findings such as numbness, paresthesias, hearing loss, vision changes, headaches etc. Case Report: We report a case of a young African American male who presented with hearing loss and bilateral lower extremity paresthesias. Subsequent imaging of his brain and spinal cord showed diffuse meningeal enhancement of the cerebrum, thoracolumbar spine, and cranial nerves (CN) V, VII, and VIII. Biopsy of calcified subcarinal lymph nodes seen on imaging showed non-caseating granulomas, consistent with the diagnosis of sarcoidosis. Conclusion: Neurosarcoidosis can present in many different ways, making it difficult to diagnose. There have been multiple studies that tried to find a pattern to this disease in order to make the diagnosis easier. However, no specific or sensitive findings to neurosarcoidosis could be concluded from those studies. To our knowledge, such a diffuse involvement of sarcoidosis in the nervous system has so far not been reported. Our case demonstrates yet another way neurosarcoidosis can present and the importance of keeping this diagnosis on the differential when dealing with patients presenting with similar symptoms.

Leptomeningeal, dura mater and meningeal vessel wall enhancements in multiple sclerosis

Background: Leptomeningeal contrast enhancement (LMCE) has previously shown potential to be an indirect marker for leptomeningeal inflammation in multiple sclerosis (MS). Dura mater (DME), inclusive falx cerebri (FCE) enhancement and meningeal vessel wall enhancement (VWE) represent two other meningeal enhancement patterns in MS that have not been extensively studied.Objectives: To investigate the frequency of LMCE, DME/FCE and VWE in patients with MS and their associations with demographic, clinical and MRI characteristics in a longitudinal retrospective study.Methods: 217 MS patients (193 relapsing-remitting MS, 24 progressive MS) were assessed at baseline and over 18 months follow-up using 3T 3D FLAIR pre- and post-contrast and subtraction images. Lesion and brain volume outcomes were additionally calculated. Analyses were adjusted for age, and corrected for multiple comparisons.Results: LMCE and VWE frequency was associated with higher age (p<0.02), but the presence of DME/FCE was not (p=0.402). 24% of MS patients revealed LMCE and VWE, respectively, and 47% showed DME/FCE. Presence of LMCE, VWE and DME/FCE was not significantly associated with clinical or imaging markers of disease severity. All three patterns of meningeal enhancement showed a high persistence in shape and size at follow-up.Conclusions: LMCE, DME/FCE and VWE can be identified by gadolinium-enhanced 3D FLAIR MR imaging. Meningeal enhancement is associated with higher age. DME/FCE is the most frequent meningeal enhancement pattern in MS, however further case-control studies should determine whether this represents abnormal lymphatic drainage in these patients or is an age-dependent physiologic phenomenon.

Role of magnetic resonance imaging (MRI) in tuberculous meningitis (TBM)

Background: Tuberculous meningitis (TBM) is a life-threatening disease which leads to a high mortality rate if not timely treated. On the other hand, if the treatment is started early the response is often good. Magnetic resonance imaging (MRI) is often one of the initial investigations performed in these cases. We aim to evaluate the role of MRI in the management of TBM. Methods and materials: This was a prospective study undertaken between 2007 and 2015 in which we studied all cases of TBM that underwent MRI which was performed with and without contrast. A total of 200 patients were diagnosed with TBM based on clinical criteria, cerebrospinal fluid analysis and response to anti-tuberculous treatment were included in this study and were analysed with MRI. Results: We studied 200 patients; all had subacute lymphocytic meningitis on CSF analysis. There were 180 patients who had various neuroimaging abnormalities and only 20 patients had normal MRI findings. Communicating Hydrocephalus and abnormal meningeal enhancement were the two common neuroimaging findings. Other major findings included basal exudates, vasculitic infarcts, enhancing tuberculomas, abscesses, oedema and less commonly calcified granulomas. Conclusion: MRI has a significant role in management of CNS tuberculosis. It not only aids in making the initial diagnosis but is also a valuable means of monitoring the course of the disease under treatment.

Brain MRI findings in relation to clinical characteristics and outcome of tuberculous meningitis.

Neuroradiological abnormalities in tuberculous meningitis (TBM) are common, but the exact relationship with clinical and inflammatory markers has not been well established. We performed magnetic resonance imaging (MRI) at baseline and after two months treatment to characterise neuroradiological patterns in a prospective cohort of adult TBM patients in Indonesia. We included 48 TBM patients (median age 30, 52% female, 8% HIV-infected), most of whom had grade II (90%), bacteriologically confirmed (71%) disease, without antituberculotic resistance. Most patients had more than one brain lesion (83%); baseline MRIs showed meningeal enhancement (89%), tuberculomas (77%), brain infarction (60%) and hydrocephalus (56%). We also performed an exploratory analysis associating MRI findings to clinical parameters, response to treatment, paradoxical reactions and survival. The presence of multiple brain lesion was associated with a lower Glasgow Coma Scale and more pronounced motor, lung, and CSF abnormalities (p-value <0.05). After two months, 33/37 patients (89%) showed worsening of MRI findings, mostly consisting of new or enlarged tuberculomas. Baseline and follow-up MRI findings and paradoxical responses showed no association with six-month mortality. Severe TBM is characterized by extensive MRI abnormalities at baseline, and frequent radiological worsening during treatment.

NIMG-61. UNUSUAL PRESENTATION OF NEUROSARCOIDOSIS: A CASE SERIES

Abstract INTRODUCTION Neurosarcoidosis is a rare diagnosis, and even with known systemic disease or history, often remains a diagnosis of exclusion. Typical imaging findings of neurosarcoidosis include white matter lesions coupled with meningeal enhancement, or “sugarcoating” near the skull base. Occasionally, imaging can be quite unusual and mimic other entities. Other diagnoses to rule out include neoplastic, autoimmune, or infectious pachymeningitis, neoplastic lesions, neurosyphilis or tuberculosis. METHODS Our neuropathology database was queried for neurosarcoidosis from January 2008 until December 2019. These cases were then reviewed for cases with unusual presentations for further review and discussion. RESULTS Here we present 16 cases of neurosarcoidosis with histories and/or imaging that did not conform to the typical appearance of neurosarcoidosis. Along with a rare radiographic presentation, these cases also lacked CSF, laboratory, or systemic findings to suggest a diagnosis of neurosarcoidosis. 15 of these cases presented intracranially while 1 case presented within the spinal cord. CONCLUSIONS Neurosarcoidosis presentations can vary greatly. A better understanding of some unique patient presentations can help improve noninvasive diagnosis, although biopsy often remains necessary for confirmation.