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Delirium
Published in Henry J. Woodford, Essential Geriatrics, 2022
Herpes simplex encephalitis is the commonest form of infectious encephalitis in the UK. It typically starts as a flu-like illness with headache and fever, later followed by seizures, cognitive impairment/behavioural changes and sometimes with focal neurological signs.45 There is a bimodal distribution – one peak below age 20 and a second one over age 50. Aciclovir reduces mortality from 70% to around 20% overall. Treatment should start as soon as the diagnosis is suspected and continue for at least 14 days once confirmed. A case series of 12 people aged over 65 (mean age 76) found that 60% presented with seizures and 50% with headaches.46 The in-hospital mortality was 25% and 33% of survivors were judged to have a poor outcome at six months. MRI brain imaging is abnormal in 90%, showing unilateral or asymmetrical medial temporal lobe hyperintensities. A lumbar puncture will show a raised white cell count and be positive for herpes simplex virus polymerase chain reaction testing. EEG tests have a sensitivity around 80% and specificity around 30%, it can be used to exclude non-convulsive status epilepticus.45
Paper 2
Published in Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw, The Final FRCR, 2020
Amanda Rabone, Benedict Thomson, Nicky Dineen, Vincent Helyar, Aidan Shaw
Herpes simplex encephalitis is the most common cause of viral encephalitis. The typical features are bilateral temporal lobe involvement; however this can be asymmetrical, and involvement of the insular cortex, cingulate gyrus and frontal lobes is also common. There is frequently T2 and FLAIR hyperintensity involving the white matter and cortex and low T1 signal due to oedema. Areas of haemorrhage may develop, which will be high on T1 and low on T2 sequences. There is often restricted diffusion and gyral and leptomeningeal enhancement.
Encephalitis and Its Mimics in the Critical Care Unit
Published in Cheston B. Cunha, Burke A. Cunha, Infectious Diseases and Antimicrobial Stewardship in Critical Care Medicine, 2020
Herpes virus is the most commonly identified agent of sporadic encephalitis [26]. Herpes simplex virus (HSV) 1 and 2 are ubiquitous. Following initial infection, primarily via the mucous membranes, the virus generally establishes permanent residence in the innervating dorsal root ganglion neurons. Periodically, virus will migrate back down the axon, causing a recurrent cutaneous eruption. A similar mechanism is thought to underlie HSV1 encephalitis, the cause of the vast majority of herpes simplex encephalitis. The sensory neurons of the trigeminal nerve, which innervate the lips, also innervate the meninges of the middle and anterior cranial fossa. Experimentally, reactivating virus can be shown to migrate centrally, affecting the medial temporal and frontal lobes, the primary site of involvement in herpes simplex encephalitis.
Temporal pathway analysis of cerebrospinal fluid proteome in herpes simplex encephalitis
Published in Infectious Diseases, 2023
Anja Nääs, Peng Li, Clas Ahlm, Elisabeth Aurelius, Josef D. Järhult, Silvia Schliamser, Marie Studahl, Wenzhong Xiao, Jonas Bergquist, Gabriel Westman
Herpes simplex encephalitis (HSE) is a rare but severe manifestation of Herpes simplex virus, mainly caused by Herpes virus type 1 (HSV-1), with an incidence of 2–4 cases per million person-years [1,2]. HSE is a cytolytic infection causing an aggressive inflammation in brain tissue, mainly in the frontotemporal lobes. The major symptoms are fever, headache, altered mental status (confusion, reduced level of consciousness, changes in personality), seizures and focal neurological deficits. Many patients develop severe neurologic sequelae in spite of antiviral treatment, such as memory impairment, behavioral abnormalities, dysphasia and epilepsy [3,4]. It is not fully elucidated why some patients get struck by this severe manifestation of HSV-1 primary infection or reactivation, from a virus that in most people causes infection with mild skin symptoms, or no symptoms at all [5]. A minor part of HSE cases (ca 15%) can be linked to monogenic immune deficiencies, affecting TLR3 and interferon signalling [6–8].
Clinical Spectrum of Uveitis Induced by Herpes Simplex Virus with Posterior Pole Involvement at Initial Presentation: A Case Series and Literature Review
Published in Ocular Immunology and Inflammation, 2022
Feng Hu, Haicheng She, Xusheng Cao, Jiawei Wang, Caixia Lin, Xiaoyan Peng
HSV-induced ARN shows relatively different clinical features relative to VZV-induced ARN. HSV affects 20% to 30% of ARN patients, which is less common than VZV.6–8 HSV-induced ARN patients are reported mainly to be 20–40 years old or children,9 while VZV-induced ARN primarily occurs in individuals older than 50 years of age.7 Viral encephalitis is a well-known risk factor for ARN, especially for HSV-induced ARN.10 A retrospective survey from Japan including 67 HSV-ARN patients showed that 24% of HSV-ARN patients had histories of prior herpes simplex encephalitis (HSE). It is also noteworthy that in HSV-ARN after HSE, 31.3% of cases involved both eyes.11 Considering our present cases, cases 3 and 4 with viral encephalitis, both eyes were involved, while in cases 1 and 2, which were without a history of prior viral encephalitis, unilateral eyes were involved. The delay between the onset of herpetic encephalitis and ARN is usually one to 5 months, although much longer intervals of up to 20 years have also been described.12 In case 4, the interval between encephalitis and ocular onset was as short as 10 days. HSV-ARN is the most common presentation of herpetic viral encephalitis-associated uveitis, and posterior uveitis is rarely reported. Hideto Nakajima reported a case of HSV-2 encephalitis, with posterior uveitis in which multiple lesions located inside the vascular arch indicated choroidal inflammation, while no retinal necrotic lesions or inflammation in the anterior chamber or vitreous body was observed.13
Autoimmune encephalitis: novel therapeutic targets at the preclinical level
Published in Expert Opinion on Therapeutic Targets, 2021
Josefine Sell, Holger Haselmann, Stefan Hallermann, Michael Hust, Christian Geis
Some subtypes are associated to tumors and molecular mimicry with tumor presented neuronal antigens triggers the autoimmune reaction resulting in expansion of antigen-specific antibody-producing cells [25,26]. In about 25–40% of female patients with NMDA receptor encephalitis ovarian teratoma are found. Nearly all teratomas of patients with NMDAR AE were shown to contain nervous tissue, which was the case in only about 40% of non-NMDAR AE associated teratoma patients [27,28]. Such teratomas can account for aAB production by the induction of germinal center reactions, leading to NMDAR target-specific circulating B cells and aAB-producing plasma cells [29]. Therefore, once detected in NMDAR AE patients, tumor removal is obligatory to interrupt the immune response [7,30,31]. Neuronal damage together with inflammation induced by herpes simplex encephalitis has been identified as a second potential trigger of disease [32]. A recent study showed that 27% of patients after herpes encephalitis develop AE with IgG antibodies to neuronal antigens, most often to the NMDAR [33]. However, in the majority of patients no such events are present and the origin of antineuronal autoimmunity and breakdown of immune tolerance mechanisms in the pathogenesis of these diseases remains to be investigated [34]. In IgG4 aAB associated AE, e.g. LGI1 and CASPR2 as well as in IgLON5 disease association with human leucocyte antigen (HLA) genotypes have been described which might provide a link also toward T cell mediated immune mechanisms [35,36].