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REVIEW Pract Neurol 2007; 7: 285–302 Viral Encephalitis: a Clinician’S Guide Tom Solomon, Ian J Hart, Nicholas J Beeching

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REVIEW Pract Neurol 2007; 7: 285–302 Viral Encephalitis: a Clinician’S Guide Tom Solomon, Ian J Hart, Nicholas J Beeching Solomon, Hart, Beeching 285 REVIEW Pract Neurol 2007; 7: 285–302 Viral encephalitis: a clinician’s guide Tom Solomon, Ian J Hart, Nicholas J Beeching T Solomon Professor of Neurology and MRC Senior Clinical Fellow, University of Liverpool Divisions of Neurological Science and Medical Microbiology, and The Walton Centre for Neurology and Neurosurgery, Liverpool, UK I J Hart Consultant Clinical Microbiologist, Division of Medical Microbiology and Genitourinary Medicine, Royal Liverpool University Hospital, Liverpool, UK N J Beeching Senior Lecturer and Clinical Lead, Tropical and Infectious Diseases Unit, Royal Liverpool University Hospital, Liverpool, UK Correspondence to: Professor T Solomon University of Liverpool Divisions of Neurological Science and Medical Microbiology, 8th Floor Duncan Building, Daulby Street, Liverpool L69 3GA, UK; [email protected] www.practical-neurology.com 286 Practical Neurology The management of patients with suspected viral encephalitis has been revolutionised in recent years with improved imaging and viral diagnostics, better antiviral and immunomodulatory therapies, and enhanced neuro- intensive care. Despite this, disasters in patient management are sadly not uncommon. While some patients are attacked with all known antimicrobials with little thought to investigation of the cause of their illness, for others there are prolonged and inappropriate delays before treatment is started. Although viral encephalitis is relatively rare, patients with suspected central nervous system (CNS) infections, who might have viral encephalitis, are not. In addition, the increasing number of immunocompromised patients who may have viral CNS infections, plus the spread of encephalitis caused by arthropod-borne viruses, present new challenges to clinicians. This article discusses the Liverpool approach to the investigation and treatment of adults with suspected viral encephalitis, and introduces the Liverpool algorithm for investigation and treatment of immunocompetent adults with suspected viral encephalitis (available at www.liv.ac.uk/braininfections). here can be few things more frightening enkephalon, brain. Encephalitis can be caused than seeing an adult or child who was directly by a range of viruses, the herpes perfectly fit and well, progress from a viruses and some arboviruses being especially T flu-like illness to confusion, coma and important (table 1). Other microorganisms death within a few days, despite the best can also cause encephalitis, particularly treatment efforts. Even when treatment is protozoa such as Toxoplasma gondii, and successful and patients survive apparently bacteria such as Listeria monocytogenes and intact, in many cases the family say that the Mycobacterium tuberculosis (table 2). For person they took home with them is not the viruses such as HIV that infect the brain but same as the one they brought to hospital, with without causing inflammation, the term changes in personality, irritability, and poor ‘‘encephalitis’’ is not usually used. short-term memory. The management of Encephalitis can also occur as an immune- patients with suspected encephalitis has been mediated phenomenon—for example, acute revolutionised in recent years with improved disseminated encephalomyelitis (ADEM, imaging and viral diagnostics, better antiviral which follows infections or vaccinations), and immunomodulatory therapies, and paraneoplastic limbic encephalitis, and vol- enhanced neurointensive care settings. Despite tage gated potassium channel limbic ence- this, disasters in patient management are sadly phalitis.1 not uncommon. Although viral encephalitis is Strictly speaking, encephalitis is a patho- relatively rare, patients with suspected central logical diagnosis that should only be made if nervous system (CNS) infections, who might there is tissue confirmation, either at autopsy have viral encephalitis, are not. In addition, the or on brain biopsy. However, in practice most increasing number of immunocompromised patients are diagnosed with encephalitis if patients, who may have viral CNS infections, they have the appropriate clinical presenta- plus the spread of encephalitis caused by tion (febrile illness, severe headache reduced arthropod-borne viruses, present new chal- consciousness (see below)) and surrogate lenges to clinicians. This review aims to provide markers of brain inflammation, such as a rational approach to the investigation and inflammatory cells in the cerebrospinal fluid treatment of a patient with suspected viral (CSF), or inflammation shown on imaging, encephalitis. especially if an appropriate organism is detected. Encephalitis must be distinguished WHAT IS ENCEPHALITIS? from encephalopathy, the clinical syndrome Encephalitis means inflammation of the brain of reduced consciousness, which can be parenchyma, and comes from the Greek caused by viral encephalitis, other infectious 10.1136/jnnp.2007.129098 Solomon, Hart, Beeching 287 diseases, metabolic disorders, drugs and alcohol. Metabolic and toxic causes of TABLE 1 Causes of acute viral encephalitis (modified from Solomon and 58 encephalopathy can usually be distinguished Whitley ) from viral encephalitis by the lack of any acute febrile illness, more gradual onset, lack Sporadic causes of viral encephalitis (not geographically restricted) listed by of a CSF pleocytosis and absence of focal group l changes on brain MRI.2 Herpes viruses – Herpes simplex virus types 1 & 2, varicella zoster virus, Epstein-Barr Some of the organisms that cause ence- virus, cytomegalovirus, human herpes virus types 6 & 7 phalitis often also cause an associated l Enteroviruses meningeal reaction (meningitis), spinal cord – Coxsackie viruses, echoviruses, enteroviruses 70 & 71, parechovirus, inflammation (myelitis), or nerve root invol- poliovirus vement (radiculitis); these terms are some- l Paramyxoviruses times used in various combinations to reflect – Measles virus, mumps virus, whichever part of the neuraxis is affected—for l Others (rarer causes) example. meningoencephalitis, encephalo- – Influenza viruses, adenovirus, parvovirus, lymphocytic choreomeningitis myelitis, meningoencephalomyelitis, myelora- virus, rubella virus diculitis, meningoencephaloradiculitis. The Geographically restricted causes of encephalitis—mostly arthropod-borne* term ‘‘limbic encephalitis’’ refers to encepha- l The Americas – West Nile, La Cross, St Louis, Rocio, Powassan encephalitis, litis of the temporal lobes (and often of other Venezuelan, eastern & western equine encephalitis, Colorado tick limbic structures), while rhombencephalitis fever virus, dengue, rabies means hindbrain, or brainstem encephalitis. l Europe/Middle East – Tick-borne encephalitis, West Nile, Tosana, rabies, (dengue virus, PATHOGENESIS louping ill virus) l Africa Depending on the virus, the pathogenesis – West Nile, (Rift Valley fever virus, Crimean-Congo haemorrhagic fever, consists of a mixture of direct viral cyto- dengue, chikungunya), rabies pathology (that is, viral destruction of cells) l Asia and/or a para- or post-infectious inflamma- – Japanese encephalitis, West Nile, dengue, Murray Valley encephalitis, tory or immune-mediated response (fig 1). For rabies, (chikungunya virus, Nipah) most viruses, the brain parenchyma and l Australasia neuronal cells are primarily infected, but for – Murray Valley encephalitis, Japanese encephalitis (kunjin, dengue) some the blood vessels can be attacked giving a strong vasculitic component. Demyelination Rarer or suspected arboviral causes are shown in brackets. *All viruses are arthropod-borne, except for rabies and Nipah. following infection can also contribute. Herpes simplex virus (HSV) for example, primarily targets the brain parenchyma in around the mouth) or be asymptomatic the temporal lobes, sometimes with frontal or (serological studies show that up to 90% of parietal involvement. Mumps virus can cause healthy adults have been infected with HSV- an acute viral encephalitis, or a delayed 1). Following primary infection the virus immune mediated encephalitis. Measles virus travels centripetally along the trigeminal causes a post-infectious encephalitis, which nerve to give latent infection in the trigeminal can sometimes have a severe haemorrhagic ganglion, in most if not all those infected. component (acute haemorrhagic leukoence- About 30% of infected people have clinically phalitis). With influenza A virus, diffuse apparent herpes labialis, but even asympto- cerebral oedema is a major component in matic individuals have episodes or viral the pathogenesis, while for varicella zoster shedding. About 70% of cases of HSV-1 virus (VZV), vasculitis is a major pathogenic encephalitis already have antibody present, process. indicating that reactivation of virus must be How and when the virus crosses the blood the most common mechanism;3 however, it is brain barrier is a key issue in the pathogenesis not clear whether this is due to reactivation of any viral encephalitis. of virus in the trigeminal ganglion, or virus For example, primary infection with HSV that had already established latency in the type 1 (HSV-1) occurs in the oral mucosa, and brain itself.4 Why HSV sometimes reactivates may cause herpes labialis (vesicles and ulcers is not known. In contrast to adults, in younger www.practical-neurology.com 288 Practical Neurology TABLE 2 Diseases that may mimic viral meningoencephalitis (modified from Solomon and Whiteley58) Central nervous system infections Para/post-infectious causes Bacteria Guillain-Barre´ syndrome* –Bacterial
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