CNS defeat in early congenital syphilis

2014 ◽  
Vol 5 (2) ◽  
pp. 65-68 ◽  
Author(s):  
Tamara Vladimirovna Melashenko ◽  
Irina Romanovna Milyavskaya ◽  
Igor Aleksandrovich Gorlanov ◽  
Larisa Mikhaylovna Leina

Early congenital syphilis, in 60 % of cases, accompanied by a specific lesion of the central nervous system. Clinical manifestations of neurosyphilis in newborns are usually absent. Diagnosis is based on serological examination of cerebrospinal fluid and MRI. The paper presents two cases of early syphilis with central nervous system.

Author(s):  
John J. Halperin

Nervous system involvement occurs in 10% to 15% of patients infected with Borrelia burgdorferi, B. afzelii, or B. garinii, the tick-borne spirochetes responsible for Lyme disease and its European counterparts. Common clinical manifestations include lymphocytic meningitis, facial and other cranial neuropathies, and painful mononeuropathies such as Lyme radiculitis. Diagnosis requires appropriate clinical, epidemiological, and laboratory evidence. Appropriately interpreted serologic testing is highly reliable; cerebrospinal fluid examination is often informative if the central nervous system is involved. Several week courses of widely available oral or parenteral antimicrobials are curative in most patients.


2021 ◽  
Vol 38 (4) ◽  
pp. 159-166
Author(s):  
Yu. V. Karakulova ◽  
N. E. Seksyaev ◽  
D. Yu. Sosnin

The authors of the article describe a case of the damage to the central nervous system by fungi of the genus Cryptococcus in a HIV-infected patient. The features of clinical manifestations and laboratory diagnostics are characterized. Special attention is paid to the discrepancy between the sharply changed appearance of the cerebrospinal fluid obtained during lumbar puncture and the clinical picture of the disease as well as the data of laboratory analysis of cerebrospinal fluid.


Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.


Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Petr Kelbich ◽  
Aleš Hejčl ◽  
Jan Krejsek ◽  
Tomáš Radovnický ◽  
Inka Matuchová ◽  
...  

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.


Author(s):  
Sara Gredmark-Russ ◽  
Renata Varnaite

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.


1927 ◽  
Vol 23 (11) ◽  
pp. 1182-1182
Author(s):  
D. K. Bogoroditsky

The technique of this reaction, suggested by two Japanese authors, Takata and Aga, in 1926, consists in adding 1 drop of a 10% Na carbonici solution and 0.3 of a freshly prepared mixture of equal parts 0.5% sulfa solution and 0.02% fuchsin (non-acid) solution to 1 cc of liquid. The mixture is shaken well and left in a test tube, and examined now after shaking, after h, after h, and after 24 h. Having tested this reaction in 60 patients, D.K. Bogoroditsky found that it is a very subtle indicator of the state of the central nervous system.


Neurosurgery ◽  
2015 ◽  
Vol 78 (3) ◽  
pp. 343-352 ◽  
Author(s):  
Arnault Tauziede-Espariat ◽  
Andre Maues de Paula ◽  
Melanie Pages ◽  
Annie Laquerriere ◽  
Emilie Caietta ◽  
...  

Abstract BACKGROUND: Primary leptomeningeal gliomatosis (PLG) is a poorly recognized tumor of the central nervous system. OBJECTIVE: To describe the histopathological, immunohistochemical, and molecular features of PLG. METHODS: Results of our multicentric retrospective study of 6 PLG cases (3 pediatric and 3 adult) were compared with literature data. RESULTS: The mean age was 54.7 years for adults and 8.7 years for children, with 3 males and 3 females. Clinical symptoms were nonspecific. Cerebrospinal fluid analyses showed a high protein level often associated with pleocytosis but without neoplastic cells. On neuroimaging, diffuse leptomeningeal enhancement and hydrocephalus were observed, except in 1 case. PLG was mostly misinterpreted as infectious or tumoral meningitis. The first biopsy was negative in 50% of cases. Histopathologically, PLG cases corresponded to 1 oligodendroglioma without 1p19q codeletion and 5 astrocytomas without expression of p53. No immunostaining for IDH1R132H and no mutations of IDH1/2 and H3F3A genes were found. Overall survival was highly variable (2-82 months) but seems to be increased in children treated with chemotherapy. CONCLUSION: This study shows the difficulties of PLG diagnosis. The challenge is to achieve an early biopsy to establish a diagnosis and to begin a treatment, but the prognosis remains poor. PLG seems to have a different molecular and immunohistochemical pattern compared with intraparenchymal malignant gliomas.


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