scholarly journals Concentric and Eccentric Target MRI Signs in a Case of HIV-Associated Cerebral Toxoplasmosis

2018 ◽  
Vol 2018 ◽  
pp. 1-3 ◽  
Author(s):  
Adam D. Roche ◽  
Dominic Rowley ◽  
Francesca M. Brett ◽  
Seamus Looby

Cerebral toxoplasmosis is one of the most common causes of focal brain lesions in immunocompromised patients, such as those with human immunodeficiency virus (HIV). Differentiating toxoplasmosis from other central nervous system (CNS) lesions provides a significant clinical challenge. Magnetic resonance (MR) imaging of the brain is key to prompt diagnosis and treatment of cerebral toxoplasmosis. Several specific signs on MRI of brain have been described in recent literature including the “concentric target sign” and “eccentric target sign.” We report a case of successfully treated HIV-associated cerebral toxoplasmosis in which both MRI signs were present simultaneously.

1999 ◽  
Vol 73 (12) ◽  
pp. 10480-10488 ◽  
Author(s):  
M. Christine Zink ◽  
Kalachar Suryanarayana ◽  
Joseph L. Mankowski ◽  
Anding Shen ◽  
Michael Piatak ◽  
...  

ABSTRACT AIDS dementia and encephalitis are complications of AIDS occurring most frequently in patients who are immunosuppressed. The simian immunodeficiency virus (SIV) model used in this study was designed to reproducibly induce AIDS in macaques in order to examine the effects of a neurovirulent virus in this context. Pigtailed macaques (Macaca nemestrina) were coinoculated with an immunosuppressive virus (SIV/DeltaB670) and a neurovirulent molecularly cloned virus (SIV/17E-Fr), and more than 90% of the animals developed moderate to severe encephalitis within 6 months of inoculation. Viral load in plasma and cerebrospinal fluid (CSF) was examined longitudinally to onset of AIDS, and viral load was measured in brain tissue at necropsy to examine the relationship of systemic and central nervous system (CNS) viral replication to the development of encephalitis. In all animals, plasma viral load peaked at 10 to 14 days postinfection and remained high throughout infection with no correlation found between plasma viremia and SIV encephalitis. In contrast, persistent high levels of CSF viral RNA after the acute phase of infection correlated with the development of encephalitis. Although high levels of viral RNA were found in the CSF of all macaques (six of six) during the acute phase, this high level was maintained only in macaques developing SIV encephalitis (five of six). Furthermore, the level of both viral RNA and antigen in the brain correlated with the severity of the CNS lesions. The single animal in this group that did not have CNS lesions had no detectable viral RNA in any of the regions of the brain. The results substantiate the use of CSF viral load measurements in the postacute phase of SIV infection as a marker for encephalitis and CNS viral replication.


2010 ◽  
Vol 31 (6) ◽  
pp. 1469-1472 ◽  
Author(s):  
G.G. Sharath Kumar ◽  
A. Mahadevan ◽  
A.S. Guruprasad ◽  
Jerry M.E. Kovoor ◽  
P. Satishchandra ◽  
...  

2020 ◽  
pp. 102490792097607
Author(s):  
Hung-Lin Hsu ◽  
Wei-Jing Lee

A 37-year-old HIV-positive woman presented to the emergency department with fever, headache, confusion, and seizures for 3 days. Computed tomography of the head with contrast demonstrated multiple ring-enhancing masses. An eccentric mural nodule in ring-enhanced mass characterizes eccentric target sign, which is pathognomonic for cerebral toxoplasmosis. The patient received anti-toxoplasmic therapy and had marked clinical improvement.


QJM ◽  
2016 ◽  
Vol 109 (8) ◽  
pp. 555-555 ◽  
Author(s):  
S. Bansal ◽  
M. Goyal ◽  
M. Modi ◽  
C. Ahuja ◽  
V. Lal

Author(s):  
Michael S. Moore

This book assays how the remarkable discoveries of contemporary neuroscience impact our conception of ourselves and our responsibility for our choices and our actions. Dramatic (and indeed revolutionary) changes in how we think of ourselves as agents and as persons are commonly taken to be the implications of those discoveries of neuroscience. Indeed, the very notions of responsibility and of deserved punishment are thought to be threatened by these discoveries. Such threats are collected into four groupings: (1) the threat from determinism, that neurosciences shows us that all of our choices and actions are caused by events in the brain that precede choice; (2) the threat from epiphenomenalism, that our choices are shown by experiment not to cause the actions that are the objects of such choice but are rather mere epiphenomena, co-effects of common causes in the brain; (3) the threat from reductionist mechanism, that we and everything we value is nothing but a bunch of two-valued switches going off in our brains; and (4) the threat from fallibilism, that we are not masters in our own house because we lack the privileged knowledge of our own minds needed to be such masters. The book seeks to blunt such radical challenges while nonetheless detailing how law, morality, and common-sense psychology can harness the insights of an advancing neuroscience to more accurately assign moral blame and legal punishment to the truly deserving.


2021 ◽  
Vol 22 (16) ◽  
pp. 8876
Author(s):  
Pierre Layrolle ◽  
Pierre Payoux ◽  
Stéphane Chavanas

Peroxisome Proliferator-Activated Receptor gamma (PPARγ) is a master regulator of metabolism, adipogenesis, inflammation and cell cycle, and it has been extensively studied in the brain in relation to inflammation or neurodegeneration. Little is known however about its role in viral infections of the brain parenchyma, although they represent the most frequent cause of encephalitis and are a major threat for the developing brain. Specific to viral infections is the ability to subvert signaling pathways of the host cell to ensure virus replication and spreading, as deleterious as the consequences may be for the host. In this respect, the pleiotropic role of PPARγ makes it a critical target of infection. This review aims to provide an update on the role of PPARγ in viral infections of the brain. Recent studies have highlighted the involvement of PPARγ in brain or neural cells infected by immunodeficiency virus 1, Zika virus, or human cytomegalovirus. They have provided a better understanding on PPARγ functions in the infected brain, and revealed that it can be a double-edged sword with respect to inflammation, viral replication, or neuronogenesis. They unraveled new roles of PPARγ in health and disease and could possibly help designing new therapeutic strategies.


2015 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This chapter contains 4 highly rendered figures, 7 tables, 16 references, and 5 MCQs.


2018 ◽  
Author(s):  
Karen L. Roos ◽  
Jared R. Brosch

Acute viral meningitis refers to inflammation of the meninges of the brain in response to a viral pathogen. Viruses cause meningitis, encephalitis, myelitis, or a combination of these, meningoencephalitis or encephalomyelitis. Viral meningitis is typically a self-limited disorder with no permanent neurologic sequelae. This chapter reviews the epidemiology, etiology, diagnosis, differential diagnosis, treatment, complications, and prognosis. Tables describe Wallgren’s criteria for aseptic meningitis, important arboviral infections found in North America, herpes family viruses and meningitis, classic cerebrospinal fluid (CSF) abnormalities with viral meningitis, Centers for Disease Control and Prevention criteria for confirming arboviral meningitis, basic CSF studies for viral meningitis, and etiology of CSF pleocytosis. Figures depict common causes of viral meningitis, nuchal rigidity, examination for Kernig sign, and Brudzinski sign for meningeal irritation. This review contains 4 highly rendered figures, 8 tables, and 17 references.


Author(s):  
Dr. Ramakrishna Narra ◽  
Dr. Rajendra kumar Pamidi ◽  
Dr. Shaheen Syed

Author(s):  
Michael S. Moore

This paper examines a particular challenge to responsible agency thought to be mounted by contemporary neuroscience. The challenge stems from the alleged experimental demonstration that human choices, and the actions they putatively cause, are mere epiphenomena of one another, co-effects of common causes in the brain of the acting subject. Denied by this challenge is that choices cause the actions that are their objects, seemingly an indispensable requirement for there to be responsible agency. The force of this challenge is blunted by a showing that in certain cases we can control (and thus be responsible) for more than we cause—that (more specifically) we sometimes are in control of a harm that is one horn of an epiphenomenal fork by knowing of the fork’s existence and by being in control of the other horn of that fork, even while recognizing that of course there can be no causal relationship across the horns of such forks.


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