scholarly journals Revisiting the Molecular Mechanism of Neurological Manifestations in Antiphospholipid Syndrome: Beyond Vascular Damage

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
M. Carecchio ◽  
R. Cantello ◽  
C. Comi

Antiphospholipid syndrome (APS) is a multiorgan disease often affecting the central nervous system (CNS). Typically, neurological manifestations of APS include thrombosis of cerebral vessels leading to stroke and requiring prompt initiation of treatment with antiplatelet drugs or anticoagulant therapy. In these cases, alterations of the coagulation system at various levels caused by multiple effects of antiphospholipid antibodies (aPL) have been postulated to explain the vascular damage to the CNS in APS. However, several nonvascular neurological manifestations of APS have progressively emerged over the past years. Nonthrombotic, immune-mediated mechanisms altering physiological basal ganglia function have been recently suggested to play a central role in the pathogenesis of these manifestations that include, among others, movement disorders such as chorea and behavioral and cognitive alterations. Similar clinical manifestations have been described in other autoimmune CNS diseases such as anti-NMDAR and anti-VGCK encephalitis, suggesting that the spectrum of immune-mediated basal ganglia disorders is expanding, possibly sharing some pathophysiological mechanisms. In this review, we will focus on thrombotic and nonthrombotic neurological manifestations of APS with particular attention to immune-mediated actions of aPL on the vascular system and the basal ganglia.

2016 ◽  
Vol 94 (5) ◽  
pp. 391-394
Author(s):  
A. V. Budnevskiy ◽  
V. A. Kutashov ◽  
Andrey Ya. Kravchenko

Antiphospholipid syndrome (APS) is one of the important but poorly known conditions. Its symptoms are ofparticular interest for neurologists since thrombi are most often localized in the cerebral blood vessels which leads to ischemic cerebrovascular accidents (AICS). APS can also manifest itself in the following symptoms: epileptic attacks, dementia, headache, chorea, peripheral neuropathy, myelo- and encephalopathy phenomenologically similar to multiple sclerosis. This article presents a clinical case of secondary APS with the neurological manifestations in a 25-year-old female patient.


Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto Javier Ramos

With confirmed COVID-19 cases surpassing the 8.5 million mark around the globe, there is an imperative need to deepen the efforts from the international scientific community to gain comprehensive understanding of SARS-CoV-2. Although the main clinical manifestations are associated with respiratory or intestinal symptoms, reports of specific and non-specific neurological signs and symptoms, both at presentation or during the course of the acute phase, are increasing. Approximately 25-40% of the patients present neurological symptoms. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the Central Nervous System (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood-brain barrier (BBB). Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for MERS-CoV. Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to dysbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this work we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV, explore the potential role for astrocytes and microglia in the infection and neuroinflammation, and compare them with the previously described human and animal CoV that showed neurotropism. We also propose possible underlying mechanisms by focusing on our knowledge of glia, neurons, and their dynamic intricate communication with the immune system.


2021 ◽  
pp. 155-161
Author(s):  
Zahoor Ahmad Parry ◽  
Swapnil Sunil Bumb ◽  
Santosh Kumar ◽  
Rohan Bhatt ◽  
Mohammed Irfan ◽  
...  

Introduction: COVID 19 often presents with flu-like symptoms. Elderly patients with systemic comorbidities are more likely to have severe COVID 19 infections and deaths. Severe neurological complications are frequently reported in severely and critically ill patients. In COVID-19, both central and peripheral nervous systems can be affected. The study aims to overview the spectrum, characteristics, and outcomes of neurologic manifestations associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Methods: A total of 1000 confirmed CoVID-19 patients were enrolled for the study. Demographic features and initial clinical manifestations were noted, and patients were followed during the hospital stay to develop any new neurological signs and symptoms. For analytical purposes, neurological presentations were grouped into the central nervous system, peripheral nervous system, and musculoskeletal system manifestations. Appropriate laboratory testing was employed as required on a case-to-case basis. Results: The mean age was 44.6 ± 14.3 years. 625 (62.5%) patients were male, while 375 (37.5%) were female. The neurological illness was a primary manifestation in 119 (11.9%) cases. These included encephalopathy (n=78), ischemic stroke (n=28), Guillain- Barre syndrome, (n=3), facial nerve palsy (n=4), and encephalitis (n=6). The most common neurological symptoms were headache 313 (31.3%) and hyposmia 52 (5.2%), followed by encephalopathy 78 (7.8%). More serious complications like seizures 18 (1.8%) and stroke 28 (2.8%) were also seen. Conclusion: CoVID-19 can present with a neurological illness, and we should remain vigilant to the possibility of neurological presentation of COVID-19 that can be thrombo-embolic, inflammatory, or immune-mediated. Bangladesh Journal of Medical Science Vol.20(5) 2021 p.155-161


ASN NEURO ◽  
2020 ◽  
Vol 12 ◽  
pp. 175909142095496 ◽  
Author(s):  
Veronica Murta ◽  
Alejandro Villarreal ◽  
Alberto J. Ramos

With confirmed coronavirus disease 2019 (COVID-19) cases surpassing the 18 million mark around the globe, there is an imperative need to gain comprehensive understanding of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the main clinical manifestations of COVID-19 are associated with respiratory or intestinal symptoms, reports of neurological signs and symptoms are increasing. The etiology of these neurological manifestations remains obscure, and probably involves several direct pathways, not excluding the direct entry of the virus to the central nervous system (CNS) through the olfactory epithelium, circumventricular organs, or disrupted blood–brain barrier. Furthermore, neuroinflammation might occur in response to the strong systemic cytokine storm described for COVID-19, or due to dysregulation of the CNS rennin-angiotensin system. Descriptions of neurological manifestations in patients in the previous coronavirus (CoV) outbreaks have been numerous for the SARS-CoV and lesser for Middle East respiratory syndrome coronavirus (MERS-CoV). Strong evidence from patients and experimental models suggests that some human variants of CoV have the ability to reach the CNS and that neurons, astrocytes, and/or microglia can be target cells for CoV. A growing body of evidence shows that astrocytes and microglia have a major role in neuroinflammation, responding to local CNS inflammation and/or to disbalanced peripheral inflammation. This is another potential mechanism for SARS-CoV-2 damage to the CNS. In this comprehensive review, we will summarize the known neurological manifestations of SARS-CoV-2, SARS-CoV and MERS-CoV; explore the potential role for astrocytes and microglia in the infection and neuroinflammation; and compare them with the previously described human and animal CoV that showed neurotropism to propose possible underlying mechanisms.


Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 971
Author(s):  
Noemí Cárdenas-Rodríguez ◽  
Cindy Bandala ◽  
América Vanoye-Carlo ◽  
Iván Ignacio-Mejía ◽  
Saúl Gómez-Manzo ◽  
...  

Coronavirus Disease 2019 (COVID-19), caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), is an emergent infectious disease that has caused millions of deaths throughout the world. COVID-19 infection’s main symptoms are fever, cough, fatigue, and neurological manifestations such as headache, myalgias, anosmia, ageusia, impaired consciousness, seizures, and even neuromuscular junctions’ disorders. In addition, it is known that this disease causes a series of systemic complications such as adverse respiratory distress syndrome, cardiac injury, acute kidney injury, and liver dysfunction. Due to the neurological symptoms associated with COVID-19, damage in the central nervous system has been suggested as well as the neuroinvasive potential of SARS-CoV-2. It is known that CoV infections are associated with an inflammation process related to the imbalance of the antioxidant system; cellular changes caused by oxidative stress contribute to brain tissue damage. Although anti-COVID-19 vaccines are under development, there is no specific treatment for COVID-19 and its clinical manifestations and complications; only supportive treatments with immunomodulators, anti-vascular endothelial growth factors, modulating drugs, statins, or nutritional supplements have been used. In the present work, we analyzed the potential of antioxidants as adjuvants for the treatment of COVID-19 and specifically their possible role in preventing or decreasing the neurological manifestations and neurological complications present in the disease.


2015 ◽  
Vol 62 (1) ◽  
pp. 59-63
Author(s):  
Camelia C. Diaconu ◽  
◽  
Giorgiana Dediu ◽  
Bianca Paraschiv ◽  
◽  
...  

Antiphospholipid syndrome is an acquired autoimmune disease characterized by the appearance of thrombosis (venous, arterial and microvascular) and/or complications during pregnancy, in the presence of antiphospholipid antibodies. The clinical spectrum of the disease is now more complex and include organ-specific and systemic symptoms induced not only by thrombotic mechanisms, but also immune-mediated. Patients diagnosed with antiphospholipid syndrome should be evaluated clinically and laboratory periodically to detect lung damage, cardiac, neurological, skin, eye, hematological, gastrointestinal complications.


Lupus ◽  
2017 ◽  
Vol 26 (5) ◽  
pp. 529-536 ◽  
Author(s):  
L C D de Amorim ◽  
F M Maia ◽  
C E M Rodrigues

Neurologic disorders are among the most common and important clinical manifestations associated with systemic lupus erythematosus (SLE) and antiphospholipid syndrome (APS), mainly those that affect the central nervous system (CNS). Risk of cerebrovascular events in both conditions is increased, and stroke represents one of the most severe complications, with an incidence rate between 3% and 20%, especially in the first five years of diagnosis. This article updates the data regarding the risk factors, clinical manifestations, neuroimaging, and treatment of stroke in SLE and APS.


2019 ◽  
Vol 2 (19) ◽  
pp. 29-33
Author(s):  
K. B. Manysheva ◽  
M. A. Akhmedov ◽  
A. A. Rakhmanova ◽  
S. M. Khutalieva

The article is devoted to the study of postoperative cognitive dysfunction — a syndrome that is often found in the postoperative period and does not depend on the volume of surgeon. Based on the analysis of the results of modern studies, the authors cite the most likely etiological causes of the syndrome, grouped according to different categories of risk factors. The pathogenetic algorithm for cognitive dysfunction includes the appearance of systemic inflammation, improving blood-brain barrier permeability with the endothelial dysfunction, the migration of inflammatory agents into the central nervous system, and the formation of oxidative stress. The clinical manifestations of cognitive deficit in the outcome of surgeon performed under general anesthesia, the authors illustrate with their own observations of patients with a neurosurgical profile with spinal pathology operated on with the use of propofol anesthesia, comparing the results of neuropsychological testing with an assessment of the level of anxiety. In conclusion, the authors outline a strategy for the prevention of postoperative cognitive dysfunction and recommend conducting neuropsychological rehabilitation as an important component of postoperative recovery for all patients with a diagnosed cognitive deficit that occurred after surgery.


2020 ◽  
Vol 21 (15) ◽  
pp. 5475 ◽  
Author(s):  
Manuela Pennisi ◽  
Giuseppe Lanza ◽  
Luca Falzone ◽  
Francesco Fisicaro ◽  
Raffaele Ferri ◽  
...  

Increasing evidence suggests that Severe Acute Respiratory Syndrome-coronavirus-2 (SARS-CoV-2) can also invade the central nervous system (CNS). However, findings available on its neurological manifestations and their pathogenic mechanisms have not yet been systematically addressed. A literature search on neurological complications reported in patients with COVID-19 until June 2020 produced a total of 23 studies. Overall, these papers report that patients may exhibit a wide range of neurological manifestations, including encephalopathy, encephalitis, seizures, cerebrovascular events, acute polyneuropathy, headache, hypogeusia, and hyposmia, as well as some non-specific symptoms. Whether these features can be an indirect and unspecific consequence of the pulmonary disease or a generalized inflammatory state on the CNS remains to be determined; also, they may rather reflect direct SARS-CoV-2-related neuronal damage. Hematogenous versus transsynaptic propagation, the role of the angiotensin II converting enzyme receptor-2, the spread across the blood-brain barrier, the impact of the hyperimmune response (the so-called “cytokine storm”), and the possibility of virus persistence within some CNS resident cells are still debated. The different levels and severity of neurotropism and neurovirulence in patients with COVID-19 might be explained by a combination of viral and host factors and by their interaction.


2021 ◽  
Vol 49 (5) ◽  
pp. 030006052110122
Author(s):  
Yimin Ma ◽  
Duanming Zhuang ◽  
Zhenguo Qiao

Celiac disease (CD) is a chronic immune-mediated intestinal disease that is characterized by production of autoantibodies directed against the small intestine. The main clinical manifestations of CD are typically defined as those related to indigestion and malabsorption. These manifestations include unexplained diarrhea or constipation, abdominal pain, bloating, weight loss, anemia, failure-to-thrive in children, and decreased bone density. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by heterogeneous clinical manifestations, which may also involve the gastrointestinal tract. Comorbidity of CD and SLE is rare, and the overlapping symptoms and nonspecific clinical presentation may pose a diagnostic challenge to clinicians. We report here a case of SLE with CD, which mainly manifested as recurrent diarrhea, uncorrectable electrolyte disorders, and severe malnutrition. Through review, we hope to further improve our understanding and diagnostic level of this combination of diseases.


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