Analysis of cerebrospinal fluid in racemose form of neurocysticercosis

Bazan, Rodrigo; Odashima, Newton Satoru; Luvizutto, Gustavo José; Filho, Pedro Tadao Hamamoto; Zanini, Marco Antônio; Takayanagui, Osvaldo Massaiti

doi:10.1590/0004-282x20150120

Cited by 6 publications

(4 citation statements)

References 21 publications

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“…We did demonstrate a strong association between ventricular lesions and symptoms related to increased intracranial pressure that was just below the threshold of statistical significance ( p = 0.051). In a previously described subset of patients who underwent CSF analysis, we also could not demonstrate statistically significant differences related to sex, other demographic data, or cyst location [44]. …”

Section: Discussionmentioning

confidence: 56%

Clinical Symptoms, Imaging Features and Cyst Distribution in the Cerebrospinal Fluid Compartments in Patients with Extraparenchymal Neurocysticercosis

et al. 2016

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Extraparenchymal neurocysticercosis has an aggressive course because cysts in the cerebrospinal fluid compartments induce acute inflammatory reactions. The relationships between symptoms, imaging findings, lesion type and location remain poorly understood. In this retrospective clinical records-based study, we describe the clinical symptoms, magnetic resonance imaging features, and cyst distribution in the CSF compartments of 36 patients with extraparenchymal neurocysticercosis. Patients were recruited between 1995 and 2010 and median follow up was 38 months. During all the follow up time we found that 75% (27/36) of the patients had symptoms related to raised intracranial pressure sometime, 72.2% (26/36) cysticercotic meningitis, 61.1% (22/36) seizures, and 50.0% (18/36) headaches unrelated to intracranial pressure. Regarding lesion types, 77.8% (28/36) of patients presented with grape-like cysts, 22.2% (8/36) giant cysts, and 61.1% (22/36) contrast-enhancing lesions. Hydrocephalus occurred in 72.2% (26/36) of patients during the follow-up period. All patients had cysts in the subarachnoid space and 41.7% (15/36) had at least one cyst in some ventricle. Cysts were predominantly located in the posterior fossa (31 patients) and supratentorial basal cisterns (19 patients). The fourth ventricle was the main compromised ventricle (10 patients). Spinal cysts were more frequent than previously reported (11.1%, 4/36). Our findings are useful for both diagnosis and treatment selection in patients with neurocysticercosis.

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Section: Discussionmentioning

confidence: 56%

Clinical Symptoms, Imaging Features and Cyst Distribution in the Cerebrospinal Fluid Compartments in Patients with Extraparenchymal Neurocysticercosis

et al. 2016

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“…The CSF analysis is an important tool in the diagnosis and treatment of NCC in humans 3 . The most common findings in CSF of humans infected with T. solium include a lymphocytictype mononuclear pleocytosis and high protein concentration in the CSF 8,9 . We observed the same pattern in our animals after the inoculation: cell counting average showed a sharp increase in the first month, and the proteinorrachia was over twice as high in the same time period as it was before the cysts injection.…”

Section: Discussionmentioning

confidence: 99%

Cerebrospinal Fluid Changes in Experimental Model of Extraparenchymal Neurocysticercosis: preliminary results

Alves¹,

Filho²,

Ossuna³

et al. 2020

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Introduction: Neurocysticercosis (NCC) is the most common parasitic disease affecting the CNS and is considered a public health problem in many countries around the world, including Brazil. The cerebrospinal fluid (CSF) changes provoked by the disorder in humans are well defined in literature and were first described in 1940 by Lange. These modifications include pleocytosis, hyperproteinorrachia and eosinophilia. The majority of the experimental models of NCC published are focused on the parenchymal form of the disease. Few models studied the extraparenchymal form or analyzed the CSF parameters. Objective: To analyze the temporal modifications in the CSF of rabbits after the experimental induction of extraparenchymal NCC. Method: We included 14 male rabbits in this study. Each animal underwent a suboccipital injection of 50 cysts of T. crassiceps into the cisterna magna. Just before the inoculation, CSF samples were collected (sham). The animals were observed for 6 months, with monthly suboccipital punctures for CSF sample collection. Cellularity and protein concentration changes were analyzed throughout the observation period. Results: The initial cell counting average was only 1 (±0.88) cell/μL, raising to 1138.9 (±624.1) cells/μL in the first month and then dropping to 17.2 (±14.4) cells/μL in the sixth month. The differential analysis proved that, after the inoculation, lymphocytes were the most common cells in the CSF (85.1%, ±14.6). A similar pattern was identified with the proteinorrachia: an initial average of 25.8 (±8.3) mg/dL, increasing to 66.5 (±22.5) mg/dL one month later and then gradually decreasing to 40.2 (±15.6) mg/dL in the last month. Conclusion: It was possible to identify a substantial increase in cellularity and protein concentration in the CSF after the induction of NCC in rabbits, followed by a gradual fall over the remaining months. These variations are comparable to the findings in humans. The authors are currently giving continuity to this study, and stronger data will be released in future publications.

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“…In the CNS, TNF-α produced by migrated peripheral immune cells or by microglia and astrocytes in the presence of inflammation [ 39 , 40 ] plays an important role in inducing and maintaining inflammation that occurs in NCC. Evidence for this includes high levels of TNF-α reported in CSF samples from patients [ 12 , 41 – 47 ] and increased expression of the TNF-α gene in pericystic capsules in pigs treated with PZQ [ 17 , 48 , 49 ]. TNF-α has also been shown to be a key cytokine in maintaining inflammation in other inflammatory diseases involving the CNS, such as some causes of meningitis and autoimmune encephalitis [ 50 – 56 ].…”

Section: Discussionmentioning

confidence: 99%

TNF-α blockade suppresses pericystic inflammation following anthelmintic treatment in porcine neurocysticercosis

et al. 2017

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BackgroundNeurocysticercosis (NCC) is an infection of the brain with the larval cyst of the tapeworm, Taenia solium. Cysticidal treatment induces parasite killing resulting in a post inflammatory response and seizures, which generally requires corticosteroid treatment to control inflammation. The nature of this response and how to best control it is unclear. We investigated the anti-inflammatory effects of pretreatment with etanercept (ETN), an anti-tumor necrosis factor agent, or dexamethasone (DEX), a high potency corticosteroid, on the post treatment inflammatory response in naturally infected pigs with neurocysticercosis after a single dose of the cysticidal drug praziquantel (PZQ).Methodology/Principal findingsWe followed the methods from a previously developed treatment model of NCC in naturally infected swine. The four study groups of infected pigs included 3 groups treated with PZQ on day 0: PZQ-treated alone (100 mg/kg PO; n = 9), pretreated with dexamethasone (DEX, 0.2 mg/kg IM administered on days -1, +1 and +3; n = 6), and pretreated with etanercept (ETN, 25 mg IM per animal on days -7 and 0; n = 6). The fourth group remained untreated (n = 3). As measured by quantitative RT-PCR, ETN pretreatment depressed transcription of a wide range of proinflammatory, regulatory and matrix protease encoding genes at 120 hr post PZQ treatment in capsules of cysts that demonstrated extravasated Evans Blue (EB) (a measure of blood brain barrier dysfunction) compared to animals not receiving ETN. Transcription was significantly depressed for the proinflammatory genes tumor necrosis factor (TNF)-α, and interferon (IFN)-γ; the inflammation regulating genes cytotoxic T-lymphocyte-associated protein (CTLA)4, interleukin (IL)-13 and transforming growth factor (TGF)-β; the tissue remodeling genes matrix metalloprotease (MMP)1 and 9, tissue inhibitors of metalloproteases (TIMP)1 and 2, and the genes regulating endothelial function vascular endothelial growth factor (VEGF)1, angiopoietin (Ang)1, Ang 2, and platelet endothelial cell adhesion molecule (PECAM)-1. In contrast, transcription was only modestly decreased in the DEX pretreated pigs compared to PZQ alone, and only for TNF-α, IL-6, IFN-γ, TGF-β and Ang1. IL-10 was not affected by either ETN or DEX pretreatments. The degree of inflammation, assessed by semi-quantitative inflammatory scores, was modestly decreased in both ETN and DEX pretreated animals compared to PZQ treated pigs whereas cyst damage scores were moderately decreased only in cysts from DEX pretreated pigs. However, the proportion of cysts with EB extravasation was not significantly changed in ETN and DEX pretreated groups.Conclusions/SignificanceOverall, TNF-α blockade using ETN treatment modulated expression of a large variety of genes that play a role in induction and control of inflammation and structural changes. In contrast the number of inflammatory cells was only moderately decreased suggesting weaker effects on cell migration into the inflammatory capsules surrounding cysts than on release of modu...

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Analysis of cerebrospinal fluid in racemose form of neurocysticercosis

Cited by 6 publications

References 21 publications

Clinical Symptoms, Imaging Features and Cyst Distribution in the Cerebrospinal Fluid Compartments in Patients with Extraparenchymal Neurocysticercosis

Clinical Symptoms, Imaging Features and Cyst Distribution in the Cerebrospinal Fluid Compartments in Patients with Extraparenchymal Neurocysticercosis

Cerebrospinal Fluid Changes in Experimental Model of Extraparenchymal Neurocysticercosis: preliminary results

TNF-α blockade suppresses pericystic inflammation following anthelmintic treatment in porcine neurocysticercosis

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