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Inflammatory Disorders of the Nervous System
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Acute necrotizing encephalopathy/acute hemorrhagic necrotizing encephalopathy is a devastating parainfectious encephalopathy originally described as a childhood illness, usually in the context of influenza, but later recognized in adults.8 It presents similarly to AHLE, with a rapidly progressive encephalopathy, seizures, and motor deficits, and has a mortality of around 30%.
Emergence and Pathogenesis of Swine Influenza Viruses in Humans
Published in Sunit K. Singh, Human Respiratory Viral Infections, 2014
Jennifer L. Smith, Frederick T. Koster, Robert J. Hogan
Some cases of encephalopathy associated with influenza identified since 1994 have been severe and resulted in coma and death in 30% of patients. This condition is now known as acute necrotizing encephalopathy (ANE), and has also been described in SOIV-infected patients.140 ANE is most common in children under 6 but is occasionally seen in adults. The neurological symptoms begin within 1–3 days of the onset of respiratory signs, are followed by lethargy, seizures, and coma. Cerebrospinal fluid from influenza patients with ANE was characterized by increased pressure, no pleocytosis, normal glucose levels, and only occasional increased protein.141 MRI was normal or demonstrated areas of edema in basal ganglia, thalami, brainstem, cerebellar white matter, and cerebral white matter.140 Autopsies have demonstrated diffuse cerebral edema with necrosis in the same areas identified by MRI. These foci have necrotic cells, edema, congestion, and hemorrhages without inflammation.140 Treatments have included anti-influenza drugs, steroids, plasmapheresis, intravenous immunoglobulin, and anticonvulsants without success in preventing death or neurological sequelae.
Human Herpesvirus 6A, 6B, and 7 Encephalitis
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Joseph Ongrádi, Balázs Stercz, Valéria Kövesdi, Károly Nagy, Joshua Prichett, Dharam V. Ablashi, Steven Jacobson
Accumulating clinical and laboratory evidence on HHV-6 encephalitis has led to a diverse neuroradiographic subset of disease characteristics in both immunocompetent and immunocompromised patients. Initial case reports on pediatric patients with CNS complications of ES revealed CT findings of cerebral edema and hypodensities in the cortex, thalami, cerebellum, and brain stem. However, a series of imaging studies on pediatric immunocompetent patients with proven HHV-6 encephalitis using MRI subsequently revealed signal abnormalities (Yao et al. 2010) of the frontal/temporal—parietal—occipital lobes, cerebellum, brain stem, and deep gray nuclei. Restricted diffusion on MRI taken during the acute phase of illness was demonstrated in six pediatric patients, with frontal lobe hypoperfusion on single photon emission computerized tomography during the convalescent stage. In another series, acute MRI changes were found in the cerebellum/brain stem or thalami in six of seven children, with chronic necrotization of the affected regions several months after initial imaging (Crawford et al. 2009). In a 17-year-old ALL patient, HHV-6 reactivation and CNS dysfunction were documented. MRI revealed bilateral sub-cortical white matter edema with cortical involvement in the occipital lobes; hem-orrhage and thrombosis were excluded (Wittekindt et al. 2009). However, not all patients exhibit abnormalities upon MRI. In another case of HHV-6-associated acute necrotizing encephalopathy, CT showed hypodensities in the thalami (Kawabe et al. 2010). In HSCT patients with HHV-6 encephalitis, CT of the brain, especially obtained early in the course of illness, was often normal Acute abnormalities were more common in brain MRI studies, with abnormalities most commonly involving the temporal lobes and especially the medial temporal lobes (Zerr 2006). HHV-6 meningoencephalitis often involves both hippocampal and extrahippocampal structures including the amygdala, entorhinal cortex, hypothalamus, and deep forebrain structures (Singh and Paterson 2000; Yao et al. 2010).
Pathogenesis and Management of Acute Necrotizing Encephalopathy
Published in Expert Review of Neurotherapeutics, 2023
Ningxiang Qin, Jing Wang, Xi Peng, Liang Wang
Although many diseases that result from pathogenic infections, such as viral meningitis, are associated with direct pathogen invasion, the notion that viruses directly invade the nervous system and cause ANE is still a topic of debate. Viral encephalitis can be easily confused with acute necrotizing encephalopathy. It is worth mentioning that according to the definition of ANE, there should not be CSF pleocytosis or the presence of a CSF pathogen. These characteristics are typically present in viral encephalitis, which is an important differential diagnosis for ANE. For instance, in the case of COVID−19, this theory suggests that the virus penetrates the brain through the trigeminal nerve and olfactory nerve, causing a series of neurological symptoms. However, Frontera JA et al. [50,51] warned that the PCR tests used to amplify the contaminant could yield a false positive, particularly when the initial CSF test was negative. Stein, SR et al. detected SARS-CoV−2 in brain autopsies, but it is possible that the rough endoplasmic reticulum was misidentified as virions [52]. Despite the fact that ANE can be secondary to various pathogens, the theory that viruses directly invade the nervous system and cause ANE remains controversial. ANE is not regarded as a contagious brain disease, and viral RNA has not been found in the CSF of many ANE patients [5,10,53,54]. Therefore, ANE is unlikely to be caused by direct infection but rather by immune-mediated processes involving proinflammatory cytokines [10,39]. The cases above may represent atypical cases of ANE or viral encephalitis.
Potential neurological manifestations of COVID-19: a narrative review
Published in Postgraduate Medicine, 2022
Joseph V. Pergolizzi, Robert B. Raffa, Giustino Varrassi, Peter Magnusson, Jo Ann LeQuang, Antonella Paladini, Robert Taylor, Charles Wollmuth, Frank Breve, Maninder Chopra, Rohit Nalamasu, Paul J. Christo
The rates and presentation of encephalopathy and delirium in COVID-19 patients has not been studied. Delirium in COVID-19 patients may be under-reported to date, indeed delirium is thought to be widely under-reported for various conditions unless it is being specifically monitored [79–82]. Case studies of COVID-19-associated delirium appear in the literature [83,84]. Acute necrotizing encephalopathy, although relatively rare, has also been diagnosed in a hospitalized COVID-19 patient [85]. Overall, ICU patients on mechanical ventilation have rates of delirium as high as 70% to 75%, and delirium is associated with mortality and long-term cognitive impairment [86–88].