leptomeningeal enhancement
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Author(s):  
Mukesh Kumar Bhaskar ◽  
Mukta Meel ◽  
Kusum Mathur ◽  
Arpita Jindal ◽  
Mohit Khandelwal

AbstractHere we report a rare case of diffuse leptomeningeal glioneuronal tumor (DLGNT) in a 35-year-old man, who was misdiagnosed twice as having tuberculosis meningitis and later racemose neurocysticercosis. His delayed diagnosis of DLGNT might be due to prevalence of tuberculosis in our country, similarity in magnetic resonance imaging finding of prominent leptomeningeal enhancement in different cisterns of brain, and extreme rarity of DLGNT in the adults. So, it should be differentiated clinically and radiographically from granulomatous or infectious conditions. Hence, a timely histologic diagnosis through a leptomeningeal biopsy of the brain and spinal cord in case of unusual leptomeningeal enhancement with uncertain laboratory findings is essential because cytological examination of the cerebrospinal fluid in DLGNT is known to be negative.


2021 ◽  
Author(s):  
Benjamin Victor Ineichen ◽  
Charidimos Tsagkas ◽  
Martina Absinta ◽  
Daniel S Reich

Background: The lack of systematic evidence on leptomeningeal enhancement (LME) on MRI in neurological diseases, including multiple sclerosis (MS), hampers its interpretation in clinical routine and research settings. Purpose: To perform a systematic review and meta-analysis of MRI LME in MS and other neurologi-cal diseases. Materials and Methods: In a comprehensive literature search in Medline, Scopus, and Embase, out of 2292 publications, 459 records assessing LME in neurological diseases were eligible for qualitative synthesis. Of these, 135 were included in a random effects model meta-analysis with subgroup analyses for MS. Results: Of eligible publications, 161 investigated LME in neoplastic neurological (n=2392), 91 in neuroinfectious (n=1890), and 75 in primary neuroinflammatory diseases (n=4038). The LME proportions for these disease classes were 0.47 [95%CI: 0.37 to 0.57], 0.59 [95%CI: 0.47 to 0.69], and 0.26 [95%CI: 0.20 to 0.35], respectively. In a subgroup analysis comprising 1605 MS cases, LME proportion was 0.30 [95%CI 0.21 to 0.42] with lower proportions in relapsing-remitting (0.19 [95%CI 0.13 to 0.27]) compared to progressive MS (0.39 [95%CI 0.30 to 0.49], p=0.002) and higher proportions in studies imaging at 7T (0.79 [95%CI 0.64 to 0.89]) compared to lower field strengths (0.21 [95%CI 0.15 to 0.29], p<0.001). LME in MS was associated with longer disease duration (mean difference 2.2 years [95%CI 0.2 to 4.2], p=0.03), higher Expanded Disability Status Scale (mean difference 0.6 points [95%CI 0.2 to 1.0], p=0.006), higher T1 (mean difference 1.6ml [95%CI 0.1 to 3.0], p=0.04) and T2 lesion load (mean difference 5.9ml [95%CI 3.2 to 8.6], p<0.001), and lower cortical volume (mean difference -21.3ml [95%CI -34.7 to -7.9], p=0.002). Conclusions: Our study provides high-grade evidence for the substantial presence of LME in MS and a comprehensive panel of other neurological diseases. Our data could facilitate differential diagnosis of LME in clinical settings. Additionally, our meta-analysis corroborates that LME is associ-ated with key clinical and imaging features of MS. PROSPERO No: CRD42021235026.


2021 ◽  
Vol 12 ◽  
pp. 595
Author(s):  
George W. Koutsouras ◽  
Annelle Amsellem ◽  
Timothy Richardson ◽  
Harish Babu

Background: Primary spinal glioblastoma multiforme with multifocal leptomeningeal enhancement is rarely diagnosed or documented. We describe a rare case of multifocal spinal isocitrate dehydrogenase (IDH) wild type glioblastoma with leptomeningeal carcinomatosis in an elderly male presenting with a chronic subdural hematoma, progressive myelopathy, and communicating hydrocephalus. Case Description: A 77-year-old male with a medical history of an acoustic schwannoma, anterior cranial fossa meningioma, and immune thrombocytopenic purpura presented with right-sided weakness after repeated falls. Magnetic resonance imaging of the brain and spine demonstrated a left-sided subdural hematoma, leptomeningeal enhancement of the brain and skull base, ventricles, and the cranial nerves, and along with florid enhancement of the leptomeninges from the cervicomedullary junction to the cauda equina. Most pertinent was focal thickening of the leptomeninges at T1 and T6 with mass effect on the spinal cord. A T6 laminectomy with excisional biopsy of the lesion was planned and completed. Findings were significant for glioblastoma the World Health Organization Grade IV IDH 1 wild type of the thoracic spinal cord. Subsequently, his mental status declined, and he developed progressive hydrocephalus which required cerebrospinal fluid diversion. Unfortunately, the patient had minimal improvement in his neurological exam and unfortunately died 2 months later. Conclusion: In a review of the limited literature describing similar cases of primary spinal glioblastoma, the prognosis of this aggressive tumor remains unfavorable, despite aggressive treatment options. The purpose of this report is to increase awareness of this rare condition as a potential differential diagnosis in patients presenting with multifocal invasive spinal lesions.


2021 ◽  
Vol 36 (11) ◽  
pp. 1042-1046
Author(s):  
Judith A. Gadde ◽  
David S. Wolf ◽  
Stephanie Keller ◽  
Grace Y. Gombolay

Introduction: Myelin oligodendrocyte glycoprotein antibodies (MOG-abs) are associated with demyelinating diseases. Leptomeningeal enhancement occurs in 6% of adult MOG-abs patients but rates in pediatric MOG-abs patients are unknown. Methods: Retrospective review of pediatric MOG-abs patients was performed. Results: Twenty-one patients (7 boys, 14 girls) were included with an average age of 8.6 years (range 2-15 years). Seven of 21 (33%) pediatric MOG-abs patients had leptomeningeal enhancement. Two patients’ relapses were manifested by leptomeningeal enhancement alone and another patient presented with seizures, encephalopathy, and aseptic meningitis without demyelinating lesions. Cerebrospinal fluid pleocytosis was seen in both leptomeningeal (4/7 patients) and nonleptomeningeal enhancement (10/14 patients). Interestingly, 3 patients with leptomeningeal enhancement had normal cerebrospinal fluid white blood cell count. Cortical edema was more likely in patients with leptomeningeal enhancement ( P = .0263). Conclusion: We expand the clinical spectrum of anti-MOG antibody–associated disorder. Patients with recurrent leptomeningeal enhancement without demyelinating lesions should be tested for MOG antibodies.


Author(s):  
Keng Lam ◽  
Sameer K. Kulkarni ◽  
Manya Khrlobyan ◽  
Pamela K. Cheng ◽  
Caroline L. Fong

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