scholarly journals COVID-19 Accompanied with Intracerebral Hemorrhage: A Case Series

2020 ◽  
Vol 15 (4) ◽  
Author(s):  
Athena Sharifi-Razavi ◽  
Zahra Sedaghat ◽  
Mana Baziboroun ◽  
Narges Karimi

Introduction: The new coronavirus, also known as COVID-19, can potentially involve in the central nervous system. The most important neurological manifestations include dizziness, headache, hypogeusia, hyposmia, ataxia, seizure, ischemic stroke, cerebral hemorrhage, encephalopathy, encephalitis, meningitis, seizure, cerebral vein thrombosis, and Guillain-Barre syndrome. Case Presentation: In this case series, we reported five patients with consciousness alteration and focal neurological deficit and neuroimaging that is consistent with intracerebral hemorrhage. In all patients, there was an association with COVID-19 infection. Conclusions: While the neurological manifestation of COVID-19 has not been appropriately defined, it is possible that a number of patients, particularly those who suffer from a severe illness, had central nervous system involvement. Thus, the neurologists should be aware of the likelihood of any neurological symptoms of COVID-19 infection.

2020 ◽  
Vol 65 ◽  
pp. 47-53 ◽  
Author(s):  
Scott R. Beach ◽  
Nathan C. Praschan ◽  
Charlotte Hogan ◽  
Samuel Dotson ◽  
Flannery Merideth ◽  
...  

Parasitology ◽  
1985 ◽  
Vol 90 (2) ◽  
pp. 255-268 ◽  
Author(s):  
D. D. Whitelaw ◽  
J. E. Moulton ◽  
W. I. Morrison ◽  
M. Murray

Relapse of infection after trypanocidal drug treatment of trypanosome infections is normally attributed to drug resistance on the part of the parasite, under-dosage of the drug, or reinfection of the host. We have demonstrated relapse infections in goats arising from none of these. Fourteen goats infected with Trypanosoma brucei suffered severe illness and 3 died within 45 days. Despite treatment with the trypanocidal drug Berenil, a 4th goat died 2 days later. Recovery of the remainder followed chemotherapy, and in 2 goats, necropsiecl 45 days after treatment, no trypanosomes or abnormalities were detected. However 2–3 months after Berenil chemotherapy, despite trypanosomes being undetectable in the blood during the intervening period, infections in 4 of the remaining 8 animals relapsed. At all stages of the primary and relapse infections, trypanosomes isolated from the blood of the goats were completely susceptible to Berenil when tested in mice, as were parasites isolated from cerebrospinal fluid and brain tissue at necropsy. At the time of treatment, only minimal cellular infiltration was found in the central nervous system (CNS), but death from the relapse infection was associated with a very severe meningoencephalitis. We conclude that the relapse infections were caused by the re-emergence of trypanosornes from the CNS, where sequestered parasites were inaccessible to the trypanocidal effects of the drug.


Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 5704-5704 ◽  
Author(s):  
Ramiro Espinoza ◽  
Diana Berenice Nolasco ◽  
Sosa Alejandro ◽  
Zapata Nidia ◽  
Cervera Eduardo ◽  
...  

Abstract Extramedullary myeloma (EMM) is defined by the presence of plasma cells outside the bone marrow in a patient with multiple myeloma (MM) (Touzeau & Moreau, 2016). EMM is by itself a rare entity with cases involving central nervous system (CNS) being rarer, it has an estimated incidence of 1-1.8% of all MM cases (Majd et al, 2015). Its presentation in comparison to classical MM has an adverse prognosis including a shorter progression free survival (PFS) (Gozzetti et al, 2015) and overall survival (OS) with a mean life expectancy of 1.5-6 months (Majd et al, 2015). Currently there are not international treatment guidelines for this disease. The aim of this report is to illustrate our experience at a single institution in Mexico, presenting five cases of CNS-EMM treated with proteasome inhibitor (carfilzomib) in combination with thalidomide, dexamethasone plus radiotherapy. The patient's characteristics and the treatment regimen are shown in table 1 and 2. Within three months, following the criteria to the international multiple myeloma working group (IMMWG), all five patients accomplished a positive response (one partial response [PR] four very good partial responses [VGPR]), at sixth months two patients improved their response from previously PR to a VGPR and from VGPR to complete response (CR), one sustained its VGPR and after this period of time two patients had progressive disease (PD) and died due to infectious complications. After the tenth month a third patient also died of infectious complications. By the end of this report two patients still alive, one is being evaluated for autologous stem cell transplantation (ASCT) and the other one wasn't eligible according to European Group for Blood and Marrow Transplantation (EBMT) risk score and will continue treatment without ASCT. Previously reported cases in the literature with old chemotherapy regimens shown to have median survival of 1.5 months (Petersen et al 1999), nowadays the recommended therapy is based on triplet induction therapy followed by high-dose melphalan/ASCT, a triplet consolidation therapy and maintenance treatment with lenalidomide (Touzeau & Moreau, 2016); so far there is no evidence of proteasome inhibitors penetrating the blood brain barrier (Nooka et al, 2013) and this might be the reason why the literature strongly recommends the use of lenalidomide as this one does penetrate into the CSF after oral administration (Muscal et al, 2012), we did not use lenalidomide due to the high monetary cost of the treatment but instead we use thalidomide in combination with carfilzomib and dexamethasone with improved OS in three of our five patients (VGPR + CR). Despite the small number of patients presented in this report and the lack of cytogenetics or FISH information, we think this might be a good therapeutic approached in patients with CNS-EMM, especially in those scenarios with not accessible resources or absence of clinical trials. Further studies evaluating the addition of monoclonal antibodies (daratumumab, elotuzumab) need to be done in order to improve the OS and PFS in this group of patients. Disclosures No relevant conflicts of interest to declare.


2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
L. N. Wainaina Mungai ◽  
C. M. Njeru ◽  
L. A. Nyamai ◽  
M. Maina

Hunter syndrome, or mucopolysaccharidosis type 2 (MPS2), is a lysosomal storage disorder associated with the involvement of multiple organs such as the central nervous system, hepatomegaly, musculoskeletal, respiratory, cardiac, and hearing. This is due to the accumulation of glycosaminoglycans in body tissues leading to organ failure. Since the laboratories in Kenya do not screen for metabolic diseases, there is the likelihood of assumption that these patients do not exist. These first cases were referred from the eastern part of Kenya where the majority of inhabitants are from the same ethnic community. It was noted that there was increased mortality among boys below the age of 20 years, and hence, the families sought for help in the national referral and teaching hospital. The case series is meant to show that these cases exist and the majority of the patients may be dying before the diagnosis is made. There are no data on MPS2 from Kenya, and the prevalence and incidence are unknown. In this retrospective study, we present a case series of 6 Kenyan boys with MPS2 from a national referral hospital. They were part of 17 patients who had had their blood analyzed for metabolic diseases. All of them were symptomatic with varying degrees of central nervous system involvement. They had undetectable levels of iduronate-2-sulfatase (I2S) enzyme, and three genetic mutations were detected in the IDS gene.


Parasitology ◽  
1988 ◽  
Vol 97 (1) ◽  
pp. 51-61 ◽  
Author(s):  
D. D. Whitelaw ◽  
P. R. Gardiner ◽  
M. Murray

SUMMARYRelapse of parasitaemia after drug treatment of trypanosome infections is normally attributed to drug-resistance on the part of the parasite, under-dosage of the drug or reinfection of the host. In addition, inaccessibility of parasites to drug through sequestration in privileged extravascular sites has been shown in the past to occur withTrypanosoma brucei, and we have obtained evidence that extravascular foci ofT. vivaxcan also serve as a source of relapsing infections. Infection of goats with a West African stock ofT. vivaxresulted in severe illness, which was fatal if untreated. During the terminal stage of an acute infection, clinical signs of central nervous system involvement were apparent. Histologically, the choroid plexus was swollen and oedematous, and in some cases meningitis or meningoencephalitis was seen. Trypanosomes could be detected in the cerebrospinal fluid, and also extravascularly in the choroid plexus and meninges. In three cases they were present in the aqueous humor, associated with corneal cloudiness or opacity. Treatment of 2 goats with the trypanocidal drug diminazene aceturate eliminated parasitaemia, but infections in both relapsed about 6 weeks later, despite trypanosomes being undetectable in the bloodstream during the intervening period. We conclude that the relapse infections were caused by re-emergence of trypanosomes from the CNS and/or the eye, where sequestered parasites may have been inaccessible to the trypanocide.


2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi230-vi231
Author(s):  
Florencia Yorio ◽  
Lucas Alessandro ◽  
Naomi Arakaki ◽  
Nicolas Palomar ◽  
Alejandro Muggeri ◽  
...  

Abstract INTRODUCTION Ewing Sarcoma (ES) is defined by molecular markers, being t(11,22) the most frequent. Intracranial ES/pPNET usually represent metastases from extracranial sites. Primary Central Nervous System (CNS) lesions are extremely rare. MATERIAL AND METHODS Retrospective review of clinical records from patients with primary CNS ES/pPNET assessed at a neurological center in Argentina between 2007–2019. All confirmed with molecular marker. Clinical characteristics, imaging, histopathology, and treatment response were evaluated. Extensive workup included whole-body CT scan, skeletal-scintigraphy, and positron-emission tomography, excluding extracranial primary lesions in all cases. RESULTS Total 24p. Median age 22yo (2–65); M:F 2:1. Clinical presentation: intracranial hypertension, focal neurological deficit or seizures. In brain MRI 11 supratentorial lesions, 7 infratentorial and 6 diffuse leptomeningeal. Histopathology: diffuse pattern with small round blue cells 13/24p, other patterns were also described. CD99 marked positive in all cases and T(11.22) confirmed as well: 22 PCR and 2 FISH for EWSR1-rearrangement. Misdiagnosis lead to median delay for accuracy of 7,5mo (0–124); including other CNS primary tumors (n= 13), infectious diseases (n= 5) and other diagnoses (n= 4). Most patients (n= 10) were treated with Euro99-protocol (6 cycles plus local radiotherapy (RT)), 4 with Temozolomide, Irinotecan plus RT, 7 with other regimens and 2 received no treatment. Mean overall survival (OS): 58mo (0–132) and progression-free survival 22mo (0–85). Five year OS:41%. CONCLUSION Clinical behavior in primary CNS ES deferred from extraosseous ES, being necessary to apply a specific regimen for this pathology as there is no standard regime for intracranial ES/pPNET. Results showed two different groups of patients with long and very short survival. Presentation, histology, and outcomes are so uneven that we propose if a more specific molecular classification should be necessary. This is, to our knowledge, the largest case series reported describing a heterogeneous group despite the presence of accurate molecular diagnosis.


Blood ◽  
2021 ◽  
Vol 138 (Supplement 1) ◽  
pp. 4190-4190
Author(s):  
Selin Aytac ◽  
Gunay Balta ◽  
Baris Kuskonmaz ◽  
Tekin Aksu ◽  
Fatma Visal Okur ◽  
...  

Abstract The presence of central nervous system involvement has a profound impact on the prognosis, treatment, and clinical outcome of the primary hemophagocytic lymphohistiocytosis (pHLH). However, isolated CNS-HLH is a challenging disease with a high mortality and morbidity , possibly resulting from a spsecific neuroinflammation that leads to isolated disease only without systemic activation under some additional genetic modifiers. In this study, we retrospectively reviewed our isolated CNS-HLH cases and there were 73 patients (36 male, 37 female) with a median age of 20 months (range, 1- 226 months) diagnosed as primary hemophagocytic lymphohistiocytosis at Hacettepe University Faculty of Medicine, between January 2005 and June 2021. Among these, 39 (53%) patients had central nervous system involvement either on admission or during the recurrence. On admission, the number of patients who had both CNS and sytemic involvement was 19 (49%), moreover 2 had CNS infiltration both initially and during the course of relapse. 8 patient did show CNS involvement only during the relapse. Ten (25%) patients (5 male, 5 female) with isolated CNS involvement are the main subject of this study and none of them had infectious trigger. What we know is they were presented with mostly unexplained neurological findings and /or cranial nerve paralysis. In this group median age at presentation was 101 months ( range 6 - 180 months). They all had primary HLH associated patogenic mutation and in some of them diagnosed was also confirmed by brain biopsy. Neither family history and /or consanguinity nor HLH criteria are fullfilling in this devastating disorder. Cranial MRI gives many clues during admission in experienced hands. Two of our published cases were initially diagnosed as lymphomatoid granulomatosis and acute disseminated encephalomyelitis ; they were diagnosed as hemophagocytic lymphohistiocytosis after developing systemic symptoms 3 and 12 months later. Interestingly 6 of 10 patients in this group never developed systemic symptomps, 7 patients underwent allogeneic bone marrow transplantation. Spinal cord involvement was determined in 8 patients(20%), including 4 at diagnosis and 4 during follow up ; including one previously published case, 4 out of 8 had isolated cases did show spinal involvement as well. Even though few number of cases with isolated CNS-HLH has been reported in the recent years, we believe that the number of such cases is not limited to those who have been reported because it is rather difficult to diagnose patients with isolated CNS symptoms, which leads to misdiagnosis and/or mistreatment. What we don't know is how to specifically treat patients with CNS directed therapy, and exactly which mutations are associated with isolated CNS-HLH or whether there is a known tendency in this group and perhaps unknown mutations ? Does it have a facilitating effect ? Disclosures No relevant conflicts of interest to declare.


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