Diagnosis of CNS Involvement Questioned

PEDIATRICS ◽  
1977 ◽  
Vol 60 (5) ◽  
pp. 782-783
Author(s):  
Stuart H. Walker

The report of Dr. Klimek et al. (Pediatrics 58:133, July 1976) concerning the relationship between infection with Mycoplasma pneumoniae and CNS disease recalls persisting difficulties in establishing the relationship between viral infection and CNS disease. Infection with a viral agent such as the varicella (VZ) virus may be associated with the detectable presence of the virus within the CNS (encephalitis, aseptic meningitis, etc.) or by inflammatory CNS disease in the absence of detectable evidence of the virus (parainfectious demyelinating disease or Reye's syndrome).1

Author(s):  
Stefan Bittmann

Since the outbreak near a fish market in Wuhan, China, in December 2019, researchers have been searching for an effective therapy to control the spreading of the new coronavirus SARS-CoV-2 and inhibit COVID-19 infection. Many countries like Italy, Spain, and the USA were ambushed by this viral agent. To date, more than 2.5 million people were infected with SARS-CoV-2. There is no clear answer, why SARS-CoV-2 infects so many people so fast. To date of April 2020, no effective drug has been found to treat this new severe viral infection. There are many therapy options under review and clinical trials were initiated to get clearer information, what kind of drug can help in this devastating and serious situation. The world has no time.


PEDIATRICS ◽  
1967 ◽  
Vol 39 (1) ◽  
pp. 43-48
Author(s):  
Preben Geertinger

THE PROBLEM of sudden, unexpected death in infancy (SUD) has become increasingly important in recent years in forensic medicine. Mortality in infancy from well defined causes has rapidly decreased, and the proportion of SUD of unknown cause has, therefore, been still more evident. Today SUD cannot be considered a problem for forensic medicine only; many other branches of medicine have an interest in this problem. In the past SUD has been attributed to suffocation by overlaying, by aspiration of vomitus, or by bedclothes. During the last 10 years it has widely been presumed that SUD is due to an overwhelming viral infection. Although much effort has been spent in an attempt to demonstrate the possible viral agent, the results have mainly been negative. Hypogammaglobulinemia as a possible cause of SUD was indicated by Harboe and Gormsen, and more recently it was suggested that SUD results from an anaphylatic reaction to cow's milk inhaled into the larynx or trachea. Many authors have pointed out that SUD might be connected with rickets or some more obscure kind of disorder in the calcium metabolism, and in 1962 Maresch demonstrated a significantly low content of calcium in heart musculature in these infants and presumed that one and the same basal disorder of metabolism might lead to rickets and spasmophilia as well as to SUD. However different the theories, two facts seem to be generally accepted by all authors in this field. Nearly all claim that SUD is significantly most frequent at the age of about 3 to 4 months.


2021 ◽  
Vol 26 (3) ◽  
pp. 34-39
Author(s):  
Z. A. Goncharova ◽  
Y. Y. Pogrebnova ◽  
N. M. Yarosh ◽  
S. M.M. Sehweil

The article presents the literature review and our experience in early diagnosis of multiple sclerosis based on the updated McDonald criteria of 2017. The study included 256 patients with clinic symptoms of probable idiopathic infl ammatory demyelinating disease, including rare and atypical forms of demyelination. As a result of the study the sensitivity and specifi city of the determination of oligoclonal immunoglobulin G in the population of Rostov-on-Don was described for the fi rst time, including dependence of the duration of the disease. The relationship of clinical and MRI features of the fi rst attack of the disease with the probability of determining oligoclonal IgG in the cerebrospinal fl uid is refl ected


1991 ◽  
Vol 9 (11) ◽  
pp. 1973-1982 ◽  
Author(s):  
T B Haddy ◽  
M A Adde ◽  
I T Magrath

Of 120 patients with small noncleaved-cell lymphoma who were entered sequentially on four National Cancer Institute (NCI) protocols, 29 (24%) had CNS involvement at some time in their clinical course. Seventeen had initial CNS involvement, and 12 developed CNS involvement at the time of first relapse. All 29 patients had extensive disease at presentation. The median serum lactate dehydrogenase (LDH) levels at presentation were 1,150 IU/L for patients with initial CNS involvement and 1,083 IU/L for patients with CNS involvement at relapse. CNS disease was significantly associated with serum LDH levels (P less than .0001), bone marrow involvement (P less than .0001), and jaw involvement (P = .018), but not involvement of the abdomen. There were nine long-term survivors among the 29 patients (31%). CNS disease did not appear to confer a worse prognosis on these patients than on patients without CNS involvement who had similar degrees of serum LDH elevation or who had bone marrow involvement, suggesting that extensive disease rather than CNS involvement was responsible for the poor prognosis. Event-free survival for patients with serum LDH levels above 500 IU/L was not different whether CNS disease was present or not (P = .29), nor was event-free survival different for patients with stage IV disease, whether CNS disease was present or not (P = .92). Although some patients had CNS radiation, there was no evidence that this was of therapeutic benefit. Intrathecal (IT) chemoprophylaxis effectively prevented spread to the CNS in patients without initial CNS involvement. Five of 18 patients (28%) who received no IT prophylaxis had CNS relapse (four isolated to the CNS), but only seven of the 85 patients (8%) who received IT prophylaxis had CNS relapse (two isolated to the CNS). The differences in overall and isolated CNS relapse rates were statistically significant (P = .034 and P = .008, respectively).


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Matthew D. Moore ◽  
Cassandra Suther ◽  
Yanjiao Zhou

PEDIATRICS ◽  
1982 ◽  
Vol 69 (1) ◽  
pp. 53-63
Author(s):  
G. Robert DeLong ◽  
Thomas H. Glick

The pathogenesis of Reye's syndrome encephalopathy was analyzed in terms of uniform criteria designed to clarify and assist evaluation of the leading hypotheses. Three of these hypotheses derive from known metabolic sequelae of hepatic mitochondrial dysfunction and the severe systemic catabolism of protein, fats, and carbohydrates that characterize the syndrome biochemically: hyperammonemia, hyperfattyacidemia, and hyperlactatemia. In addition, there is a fourth hypothesis of generalized mitochondrial insult affecting brain, muscle, and other organs as well as liver. The weight of evidence favors hyperammonemia as a sufficient factor while recognizing important interrelationships with the other observed biochemical derangements. How the catabolism and hepatic mitochondrial dysfunction are produced by the triggering viral infection remains unknown. Therapeutic efforts have thus far not succeeded in definitive metabolic intervention. Such reversal of the clinical syndrome would lead to confirmation of the necessary pathogenetic factors; this type of intervention remains the chief goal of metabolic research in Reye's syndrome.


PEDIATRICS ◽  
1978 ◽  
Vol 61 (2) ◽  
pp. 308-315
Author(s):  
J. Kenneth Herd ◽  
Muzaffar Medhi ◽  
Donald M. Uzendoski ◽  
Victor A. Saldivar

It is well recognized that systemic lupus erythematosus (SLE) masquerades as various other illnesses including neurologic disorders.1 Neurologic manifestations of SLE include seizures, organic brain syndromes (psychoses), aseptic meningitis, and a variety of focal neurologic syndromes, of which chorea is one example. Although chorea is reportedly a rare sign of CNS involvement in lupus, recent experience, such as the two cases reported here, suggests that it is more common than previously suspected, particularly in children. In 1975 Lusins and Szilagyi reviewed the cases of 28 patients with chorea associated with SLE.2 The majority of these patients were female, none were related to each other, and the youngest was 9 years old at the onset of lupus.


Metallomics ◽  
2020 ◽  
Author(s):  
Jemmyson Romário de Jesus ◽  
Tatianny de Araújo Andrade

Recently, the World Health Organization (WHO) declared a pandemic situation due to a new viral infection (COVID-19) caused by a novel virus (Sars-CoV-2).


Author(s):  
Samir Casseb ◽  
Karla de Melo

Dengue is an acute febrile disease caused by a virus of the genus Flavivirus, family Flaviviridae, endemic in tropical regions of the globe. The agent is a virus with single-stranded RNA, classified into four distinct dengue virus (DENV) serotypes: DENV-1, DENV-2, DENV-3, and DENV-4. The host’s innate and adaptive immune responses play an essential role in determining the natural history of viral infections, especially in dengue. In this context, it has observed in recent years that the presence of RNA interference (RNAi) in viral infection processes is increasing, as well as immune defense. The context microRNAs (miRNAs) go for stood out, as their presence during viral infection, both in the replication of the virus and in the defense against these infections, becomes increasingly noticeable, therefore, making it increasingly necessary to better understand the role of these small RNAs within viral infection by DENV and what their consequences are in aggravating the consequences of patients affected by this disease.


Blood ◽  
1997 ◽  
Vol 89 (3) ◽  
pp. 794-800 ◽  
Author(s):  
Elie Haddad ◽  
Maria-Luisa Sulis ◽  
Nada Jabado ◽  
Stephane Blanche ◽  
Alain Fischer ◽  
...  

Abstract We have retrospectively assessed the neurological manifestations in 34 patients with hemophagocytic lymphohistiocytosis (HLH) in a single center. Clinical, radiological, and cerebrospinal fluid (CSF ) cytology data were analyzed according to treatment modalities. Twenty-five patients (73%) had evidence of central nervous system (CNS) disease at time of diagnosis, stressing the frequency of CNS involvement early in the time course of HLH. Four additional patients who did not have initial CNS disease, who did not die early from HLH complications, and who were not transplanted, also developed a specific CNS disease. Therefore, all surviving and nontransplanted patients had CNS involvement. Initially, CNS manifestations consisted of isolated lymphocytic meningitis in 20 patients and meningitis with clinical and radiological neurological symptoms in nine patients. For these nine patients, neurological symptoms consisted of seizures, coma, brain stem symptoms, or ataxia. The outcome of patients treated by systemic and intrathecal chemotherapy and/or immunosuppression exclusively (n = 16) was poor, as all died following occurrence of multiple relapses or CNS disease progression in most cases. Bone marrow transplantation (BMT) from either an HLA identical sibling (n = 6) or haplo identical parent (n = 3) was performed in nine patients, once first remission of CNS and systemic disease was achieved. Seven are long-term survivors including three who received an HLA partially identical marrow. All seven are off treatment with normal neurological function and cognitive development. In four other patients, BMT performed following CNS relapses was unsuccessful. Given the frequency and the poor outcome of CNS disease in HLH, BMT appears, therefore, to be the only available treatment procedure that is capable of preventing HLH CNS disease progression and that can result in cure when performed early enough after remission induction.


Sign in / Sign up

Export Citation Format

Share Document