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The Neurologic Disorders in Film
Published in Eelco F. M. Wijdicks, Neurocinema—The Sequel, 2022
Surprisingly, few films deal with meningitis and only with outbreaks. The main difficulty for screenwriters, I suppose, is that meningitis affects just one person, and diseases are more compelling when they affect and kill many (and do so in short order). Such outbreaks (usually a virus of some kind) occasionally appear as Hollywood themes. The ultimate medical disaster movie about a prevalent virus is Contagion (2011) directed by Steven Soderbergh. The fictional virus MEV-1 is a mix of bat and pig virus (“somewhere the wrong bat met up with the wrong pig”) and is modeled after the Nipah virus outbreak of April 1999 in Malaysia, when 265 cases of febrile encephalitis were reported. Because the virus is neurotropic, the initial symptoms are headache and dizziness followed by respiratory symptoms, seizures, and rapid-onset coma. Contagion does not show specific neurologic manifestations or neurologic involvement except for one terminal seizure. The filmmakers consulted Ian Lipkin, an epidemiologist and Professor of Neurology at Columbia University, before devising the imaginary virus. The film asks the important questions of how the public health organizations respond in such a disaster scenario and how quickly vaccines would be developed.
Yellow Fever: Emergence and Reality
Published in Jagriti Narang, Manika Khanuja, Small Bite, Big Threat, 2020
Neelam Yadav, Bennet Angel, Jagriti Narang, Surender Singh Yadav, Vinod Joshi, Annette Angel
The 17D vaccine is the most efficient vaccine till date. However, vaccination with 17D produces some side effects such as pain or redness at the injection site, headache, malaise, and myalgia. There are two categories of severe side effects related to the aforementioned vaccination: (i) vaccine-associated neurotropic disease (YEL-AND) (Merlo et al., 1993; Schoub et al., 1990) and (ii) vaccine-associated viscerotropic disease (YEL-AVD) (Belsher et al., 2007; CDC, 2002).
Neurological Dengue
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Encephalopathy is often caused by infections, metabolic derangements, alcohol or drugs. Many extra-cranial infections result in encephalopathy, not through central nervous system penetration, but as a result of a systemic inflammatory response. In contrast, encephalitis is a histological diagnosis of inflammation of the brain parenchyma, commonly due to viral infection. Organisms with the capacity to infect neurons are described as neurotropic, and those causing disease are neurovirulent. The typical clinical features of encephalitis are fever (if infective), reduced consciousness, headache, seizures, and focal neurological signs. Thus, encephalitis is one of the causes of encephalopathy, albeit not the most common
Cerebral toxoplasmosis in HIV-infected patients: a review
Published in Pathogens and Global Health, 2023
Sofiati Dian, Ahmad Rizal Ganiem, Savira Ekawardhani
In immunocompetent individuals, toxoplasmosis is an asymptomatic infection or manifests only as mild clinical symptoms such as fever, malaise, or lymphadenitis. However, when immunocompromised patients, such as those with AIDS, are infected, bradyzoite can reactivate and transform into cytotoxic tachyzoites and cause an intracerebral mass lesion. Lau et al. reported the median time from HIV diagnosis to cerebral toxoplasmosis diagnosis was 22.1 months (0–338.7) in 38 HIV-infected patients in Dallas, USA [36]. There is doubt about the neurotropism of T. gondii since the concentration in the brain is low compared to other organs in mice. Slow shedding of the parasite from the CNS, allowing chronic reactivation infection, could be considered neurotropism. Brain tissue is one of the significant structures in which abnormalities caused by the multiplying parasites have been noted. The parasite infection leads to necrotic foci and profound inflammation that can block the Sylvian aqueduct and cause hydrocephalus in the lateral ventricles [2,3].
Pathophysiology and mechanism of long COVID: a comprehensive review
Published in Annals of Medicine, 2022
D. Castanares-Zapatero, P. Chalon, L. Kohn, M. Dauvrin, J. Detollenaere, C. Maertens de Noordhout, C. Primus-de Jong, I. Cleemput, K. Van den Heede
Our review has provided arguments to support several mechanisms potentially involved in long COVID. First, virus-driven cellular alterations related to its neurotropism have been suggested to possibly contribute to the pathophysiology of long COVID. This mechanism could account for olfactive disorders or manifestations related to autonomous nervous system dysfunction. Second, a dysregulated immune reaction in response to either initial infection or occult viral persistence is thought to possibly provoke deleterious disorders, including autoimmune manifestations, coagulation and fibrosis pathway activation, or metabolic disturbances. Importantly, empirical studies on patients gave rise to the possibility of organ dysfunctions through inflammatory or autoimmune mechanisms. Moreover, several studies brought about elements regarding the hypothesis of persistent and occult virus presence, as based on the identification of viral particles in several organs after the acute infection [77,78,102,104]. Hence, our review clearly revealed that the clinical picture of long COVID could presumably not be ascribed to a single pathophysiological mechanism, and that responsible mechanisms were probably numerous and intertwined.
The potential association between COVID-19 disease and Guillain-Barré syndrome
Published in Neurological Research, 2022
Ozlem Ergin Beton, Ozlem Ozturk Tan, Sule Bilen
In earlier coronavirus epidemics (Middle East respiratory syndrome coronavirus [MERS-CoV] and severe acute respiratory syndrome coronavirus [SARS-CoV-1]), studies reported an association between infection with these viruses and subsequent neurological diseases, even if this association was tentative. [2–5] Viruses in this group are known to exhibit neurotropism[6]. There is compelling evidence indicating that COVID-19 has neurological consequences, with neurological symptoms accompanying or following COVID-19 within a few weeks [7,8]. Guillain-Barré syndrome (GBS), which is characterized by acute paralytic neuropathy, has diverse clinical and pathological forms and can have a relatively severe course[8]. GBS is the most common cause of acute flask paralysis, with an incidence rate of around 0.8 to 1.9/100,000[9]. The incidence rate increases by about 20% for each decade increase in age. In 20–30% of cases, the disease has a severe course and may become generalized and lead to respiratory distress[9].