scholarly journals Long COVID Neuropsychological Deficits After Severe, Moderate or Mild Infection

2021 ◽  
Author(s):  
Philippe Voruz ◽  
Gilles Allali ◽  
Lamyae Benzakour ◽  
Anthony Nuber-Champier ◽  
Marine Thomasson ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Symptoms ◽  
Psychiatric Symptoms ◽  
Olfactory Dysfunction ◽  
Neuropsychological Deficits ◽  
Post Discharge ◽  
The Central Nervous System

Abstract Background: There is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms.Methods: Standardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 ± 22.54 days post-discharge following SARS-CoV-2 infection. Results: Deficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed.Conclusion: The data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.

scholarly journals Long COVID neuropsychological deficits after severe, moderate or mild infection

2021 ◽  
Author(s):  
P. Voruz ◽  
G. Allali ◽  
L. Benzakour ◽  
A. Nuber-Champier ◽  
M. Thomasson ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Severe Acute Respiratory Syndrome ◽  
Respiratory Symptoms ◽  
Psychiatric Symptoms ◽  
Olfactory Dysfunction ◽  
Neuropsychological Deficits ◽  
Post Discharge ◽  
The Central Nervous System

ABSTRACTBackgroundThere is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms.MethodsStandardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 ± 22.54 days post-discharge following SARS-CoV-2 infection.ResultsDeficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed.ConclusionThe data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.

scholarly journals Modern aspects of neuropathogenesis and neurological manifestations of COVID-19

2021 ◽  
Vol 17 (2) ◽  
pp. 6-15
Author(s):  
L.A. Dziak ◽  
O.S. Tsurkalenko ◽  
K.V. Chekha ◽  
V.M. Suk
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Psychiatric Symptoms ◽  
Clinical Manifestations ◽  
The Body ◽  
Altered Level ◽  
Wide Range ◽  
The Central Nervous System ◽  
The Brain

Coronavirus infection is a systemic pathology resulting in impairment of the nervous system. The involvement of the central nervous system in COVID-19 is diverse by clinical manifestations and main mechanisms. The mechanisms of interrelations between SARS-CoV-2 and the nervous system include a direct virus-induced lesion of the central nervous system, inflammatory-mediated impairment, thrombus burden, and impairment caused by hypoxia and homeostasis. Due to the multi-factor mechanisms (viral, immune, hypoxic, hypercoagulation), the SARS-CoV-2 infection can cause a wide range of neurological disorders involving both the central and peripheral nervous system and end organs. Dizziness, headache, altered level of consciousness, acute cerebrovascular diseases, hypogeusia, hyposmia, peripheral neuropathies, sleep disorders, delirium, neuralgia, myalgia are the most common signs. The structural and functional changes in various organs and systems and many neurological symptoms are determined to persist after COVID-19. Regardless of the numerous clinical reports about the neurological and psychiatric symptoms of COVID-19 as before it is difficult to determine if they are associated with the direct or indirect impact of viral infection or they are secondary to hypoxia, sepsis, cytokine reaction, and multiple organ failure. Penetrated the brain, COVID-19 can impact the other organs and systems and the body in general. Given the mechanisms of impairment, the survivors after COVID-19 with the infection penetrated the brain are more susceptible to more serious diseases such as Parkinson’s disease, cognitive decline, multiple sclerosis, and other autoimmune diseases. Given the multi-factor pathogenesis of COVID-19 resulting in long-term persistence of the clinical symptoms due to impaired neuroplasticity and neurogenesis followed by cholinergic deficiency, the usage of Neuroxon® 1000 mg a day with twice-day dosing for 30 days. Also, a long-term follow-up and control over the COVID-19 patients are recommended for the prophylaxis, timely determination, and correction of long-term complications.

scholarly journals Self-buffering capacity of a human sulfatase for central nervous system delivery

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yi Wen ◽  
Nazila Salamat-Miller ◽  
Keethkumar Jain ◽  
Katherine Taylor
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Buffering Capacity ◽  
The Self ◽  
High Concentration ◽  
Formulation Design ◽  
The Central Nervous System ◽  
Therapeutic Enzymes ◽  
Intrathecal Space

AbstractDirect delivery of therapeutic enzymes to the Central Nervous System requires stringent formulation design. Not only should the formulation design consider the delicate balance of existing ions, proteins, and osmolality in the cerebrospinal fluid, it must also provide long term efficacy and stability for the enzyme. One fundamental approach to this predicament is designing formulations with no buffering species. In this study, we report a high concentration, saline-based formulation for a human sulfatase for its delivery into the intrathecal space. A high concentration formulation (≤ 40 mg/mL) was developed through a series of systematic studies that demonstrated the feasibility of a self-buffered formulation for this molecule. The self-buffering capacity phenomenon was found to be a product of both the protein itself and potentially the residual phosphates associated with the protein. To date, the self-buffered formulation for this molecule has been stable for up to 4 years when stored at 5 ± 3 °C, with no changes either in the pH values or other quality attributes of the molecule. The high concentration self-buffered protein formulation was also observed to be stable when exposed to multiple freeze–thaw cycles and was robust during in-use and agitation studies.

Mycophenolate mofetil as induction and long-term maintaining treatment in childhood: Primary angiitis of the central nervous system

2017 ◽  
Vol 84 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Anna Rosati ◽  
Alessandra Cosi ◽  
Massimo Basile ◽  
Alice Brambilla ◽  
Renzo Guerrini ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Mycophenolate Mofetil ◽  
Primary Angiitis ◽  
The Central Nervous System

Long-term impact of neonatal inflammation on demyelination and remyelination in the central nervous system

Glia ◽  
2014 ◽  
Vol 62 (10) ◽  
pp. 1659-1670 ◽  
Author(s):  
Karelle Bénardais ◽  
Viktoria Gudi ◽  
Lijie Gai ◽  
Jasmin Neßler ◽  
Vikramjeet Singh ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
The Central Nervous System ◽  
Long Term Impact

scholarly journals Neurobrucellosis mimicking primary vasculitis of the central nervous system: we should perform a metagenomic analysis of the cerebrospinal fluid prior to brain biopsy

2021 ◽  
Author(s):  
Marina Barrionuevo Mathias ◽  
Fernando Gatti ◽  
Gustavo Bruniera ◽  
Vitor Paes ◽  
Gisele Sampaio Silva ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Psychiatric Symptoms ◽  
Brain Mri ◽  
Genetic Material ◽  
Clinical Manifestations ◽  
Brain Biopsy ◽  
Metagenomic Analysis ◽  
Normal Brain ◽  
The Central Nervous System

Context Primary angiitis of the central nervous system (PACNS) is characterized by the inflammation of small and medium CNS arteries; the clinical manifestations include headache, cognitive impairment and focal neurological deficits. The gold standard test for diagnosis is brain biopsy. Neurobrucellosis is an infection associated with cattle farming, which leads to neurological and psychiatric symptoms. We report a case of neurobrucellosis mimicking PACNS. Case report Male, 32 years old, with fever, headache, dizziness and cognitive impairments for 30 days. History of stroke 2 years before, with mild sequelae right hemiparesis; investigation showed suspected intracranial dissection. On physical examination, he had apathy, preserved strength, reduced reflexes with plantar flexor responses. General laboratory tests, autoantibodies and serology were normal. Brain MRI showed deep left nucleocapsular gliosis and cerebral angiography revealed stenosis of the ICA and MCA. CSF showed 42 cells/ mm³, glucose 46 mg/dL, protein 82 mg/dL. Blood PCR was negative for Brucella. Immunophenotyping of the CSF and PET-CT excluded neoplasia. Brain biopsy was inconclusive for vasculitis. Metagenomic analysis of the CSF detected 78% of Brucella genetic material. Serum agglutination test was 1:40 for brucella. Conclusions PACNS is diagnosed by exclusion. The patient filled criteria for possible PACNS, image compatible with vascular stenosis, but inconclusive brain biopsy. Brucellosis is an endemic disease in underdeveloped countries that can present as CNS vasculitis. Metagenomic analysis allows the detection of different pathogens using a single method. The case illustrates the use of metagenomics in rare diseases characterized by vasculitis, with change in clinical outcomes and conduct.

Hormonal-sympathetic interactions in long-term regulation of arterial pressure: an hypothesis

1995 ◽  
Vol 268 (6) ◽  
pp. R1343-R1358 ◽  
Author(s):  
V. L. Brooks ◽  
J. W. Osborn
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Circumventricular Organs ◽  
Feedback Signal ◽  
Salt Loading ◽  
Alternate Model ◽  
The Central Nervous System

The importance of the sympathetic nervous system in short-term regulation of arterial pressure is well accepted. However, the question of whether neural systems participate in long-term control of pressure has been debated for decades and remains unresolved. The principal argument against such a control system is that arterial baroreceptors adapt to sustained changes in arterial pressure. In addition, denervation of baroreceptors has minimal to no effect on basal levels of arterial pressure chronically. This argument assumes, however, that baroreceptors provide the primary chronic feedback signal to the central nervous system. An alternate model is proposed in which circulating hormones, primarily arginine vasopressin and angiotensin II, provide a long-term afferent signal to the central nervous system via binding to specific receptors in central sites lacking a blood-brain barrier (circumventricular organs). Studies suggest that the release of the hormones and the sympathetic response to alterations in their plasma concentrations are nonadaptive but may be gated by baroreceptor input. Evidence that this "hormonal-sympathetic reflex" model may explain the long-term alterations in sympathetic activity in response to chronic salt depletion and salt loading as well as congestive heart failure is presented. Finally, the role of an impaired hormonal sympathetic reflex in hypertension, specifically salt-dependent hypertension, is discussed.

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