ACUTE NEUROLOGY

Acute neurological Key points

infections C The presentation of acute neurological infections varies
depending on the causative agent, anatomical involvement
Varun Sethi and host factors such as age, immune status and co-
Nicholas WS Davies morbidities; any recent travel history and patients vaccination
record should also be given due consideration

C Early diagnosis and treatment can help limit morbidity and

Abstract
mortality
Neuroinfection syndromes cause significant mortality and morbidity.
Clinical syndromes include meningitis, encephalitis, mass lesions
C Modern imaging and laboratory techniques aid diagnosis, but
(abscesses), myelitis, radiculitis, neuritis, myositis and neuromus-
a strong clinical suspicion of neuroinfection should warrant
cular junction dysfunction. Symptoms can develop rapidly (acute)
initiation of treatment pending definitive results
or over weeks (subacute) or longer (chronic). Viruses, bacteria,
fungi or protozoa can be causal. Timely diagnosis and initiation of
C Post-infectious autoimmune neurological conditions can mimic
treatment can reduce morbidity and mortality. This article briefly out-
neuroinfections and, in the case of herpes simplex virus en-
lines the common acute neuroinfection syndromes. As some patho-
cephalitis, be sequelae; these are beyond the scope of this
gens are more likely to be encountered in specific geographical
review
areas, information regarding travel to, and immigration from,
endemic areas must be carefully sought. Furthermore, different pop-
C All patients presenting with neuroinfections should be tested
ulations have varied susceptibility to infection because of specific
for HIV; Syphilis is a re-emerging infection and must be sought
defects in the host defence as a result of co-morbidities or treatment;
in individuals presenting with acute neurological
assessment of potential immunosuppression is mandatory in all
presentations
those presenting with neuroinfections. For more detailed discussion,
UK-specific guidelines are referenced.
Keywords Brain abscess; encephalitis; human immunodeficiency
virus (HIV); meningitis; meningoencephalitis; tuberculosis Acute meningitis
Acute meningitis presents with headache, neck stiffness, photo-
phobia, fever and altered mental status. Aetiological agents vary
based on host factors (Table 1). Hospital-acquired (nosocomial)
Definition and incidence meningitis must be considered as a complication of neurosurgical
Meningitis is an inflammation of the meninges, which can intervention. Complications of bacterial meningitis include sei-
involve the underlying cortex and spinal cord.1 Bacterial men- zures from cerebritis, hydrocephalus, venous sinus thrombosis,
ingitis is seen with an annual incidence of 2e6 per 100,000, vasospasm, ischaemic stroke, brain abscess and subdural em-
peaking in adolescence and at extremes of age. Viral meningitis pyema. Viral meningitis is usually benign and self-limiting, with
has an incidence of 10e15 per 100,000 per annum. Encephalitis minimal sequelae.2
is an inflammation of the brain parenchyma; the estimated Lumbar puncture and cerebrospinal fluid (CSF) analysis
incidence in England is 2.7e8.6 per annum. Meningo-encephalitis should be done as soon as clinically possible if there is no
describes meningitis with alteration in mental status, or en- contraindication (Table 2), and treatment for suspected bacterial
cephalitis with concomitant meningeal involvement. A brain meningitis initiated. As per the UK joint specialist guidelines, all
abscess is a focal collection of pus within the brain parenchyma, immunocompetent adults with suspected meningitis or menin-
and has an incidence of 0.3e0.9 per 100,000. Acute neuromus- gococcal sepsis should be given intravenous ceftriaxone 2 g every
cular weakness can result from involvement of the anterior horn 12 hours or cefotaxime 2 g every 6 hours. Patients aged 60
cells, nerve root, peripheral nerve, neuromuscular junction or years and immunocompromised patients should additionally be
muscle. given intravenous ampicillin/amoxicillin 2 g every 4 hours. In
immunocompetent adults, dexamethasone (intravenously, 10 mg
every 6 hours) should be given before or up to 12 hours after
initiating antibiotics. If Streptococcus pneumoniae (pneumo-
coccus) is identified as a cause, corticosteroids should be
Varun Sethi MD PhD is a Locum Consultant in Neurology at the continued for 4 days. Vancomycin or rifampicin can be added in
Department of Neurosciences, Charing Cross Hospital, Imperial
patients with history of recent travel to a country with high risk
College Healthcare NHS Trust, London, UK. Competing interests:
none declared.
of pneumococcal resistance to first-line antibiotics; if there is
anaphylaxis to penicillin or cephalosporins, chloramphenicol can
Nicholas WS Davies PhD FRCP is a Consultant Neurologist at the be added.
Department of Neurology, Chelsea and Westminster Hospital and
After initial empirical treatment, choice of appropriate anti-
Department of Neurosciences, Charing Cross Hospital, Imperial
College Healthcare NHS Trust, London, UK. Competing interests:
microbial is guided by Gram stain and polymerase chain reaction
none declared. (PCR) results. Fungal meningitis presents as subacute/chronic

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 MEDICINE xxx:xxx
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Infections associated with specific host defence defects5

Drug/infection Effect on immune system Associated pathogens

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Treatment related
Corticosteroids Inhibition of phagocytes and T-cell function Bacterial, herpes virus, Candida species infections
personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2023. Elsevier Inc. Todos los derechos reservados.

Cytotoxic drugs, i.e. methotrexate, Bone marrow suppression Gram-positive and Gram-negative bacteria, Candida species, invasive mould infections
DMP, 5-fluorouracil
Purine analogues, e.g. cladribine Neutropenia, lymphopenia, hypogammaglobulinaemia Encapsulated organisms, Gram-positive and Gram-negative organisms, herpes viruses
(HSV, VZV, CMV), mycobacteria, Candida species, Aspergillus species, Cryptococcus
Azathioprine Inhibition of B and T cell proliferation, decreased antibody Bacterial infections, VZV, CMV, PML, worsening of hepatitis B and C
production, myelosuppression
Ciclosporin, tacrolimus Inhibited production of interleukin-2 and cytokines by CD4 CMV, EBV, PTLD, PML, hepatitis C activation
cells
Mycophenolate Inhibition of B and T cell proliferation, decreased antibody Herpes viruses, hepatitis B and C activation, Candida species, cryptococcus, Aspergillus
production species
Phenytoin Immunoglobulin A deficiency, hypogammaglobulinaemia Bacteria including encapsulated organisms, respiratory viruses, enteroviruses, Giardia
Monoclonal antibodies
C Rituximab B cell depletion Hepatitis B reactivation, PML, possibly increased or severe complications of

ACUTE NEUROLOGY
mycobacterial disease
C Alemtuzumab Rapid but protracted peripheral lymphopenia (B and T cells) Infections caused by HSV, VZV and mycetes, Listeria monocytogenes
C Infliximab TNF inhibitors Reactivation of latent TB; hepatitis B, VZV, CMV infection
2

Related to co-morbidities and co-infections

HIV
C Acute HIV infection Self-limiting aseptic meningitis; rarely an acute encephalitis caused by HIV1/2
C Seroconversion Aseptic meningo-encephalitis, acute disseminated encephalomyelitis, transverse myelitis
or involvement of the peripheral nervous system with polymyositis, brachial neuritis or
cauda equina syndrome
C Early symptomatic phase VZV and peripheral neuropathy presenting during the early symptomatic phase
C With progressive CD4 decline AIDS-defining conditions including HAD, opportunistic infections (CMV, Toxoplasma,
Mycobacterium, Cryptococcus), PML, cerebral lymphoma, HIV cachexia
Diabetes mellitus Defects in humoral and cellular innate immunity Rhino-orbital-cerebral mucormycosis, non-tropical pyomyositis, pyogenic spinal
infections, Listeria meningitis, blastomycosis; infection with West Nile virus, VZV
Specific groups
Neonates Bacterial meningitis is often caused by group B Streptococcus, Listeria monocytogenes,
Escherichia coli (<3 months old) and pneumococcus, meningococcus, Haemophilus
Ó 2023 Published by Elsevier Ltd.

influenza type B (>3 months old)

Elderly individuals Streptococcus pneumoniae, Neisseria meningitidis, Listeria monocytogenes, aerobic
Gram-negative organisms
Pregnant women Bacterial meningitis caused by Listeria monocytogenes

DMP, 1,4-dimethyl pyridine; HAD, HIV-associated dementia; PTLD, post-transplant lymphoproliferative disease; TNF, tumour necrosis factor. For other abbreviations, see text.

Table 1
 ACUTE NEUROLOGY

meningitis but should be considered in the differential diagnosis,

Clear to turbid
especially in immunocompromised individuals.

Neutrophils
Increased

Negative
Elevated

Elevated
elevated
Aseptic

Acute encephalitis

Mildly

Low
Infectious encephalitis typically presents with acute onset of
fever, altered mental status and focal or generalized seizures.
Sporadic viral encephalitis in immunocompetent individuals is

Special tests, e.g. cryptococcal antigen

commonly caused by herpes simplex virus (HSV) type 1

Normal to mild increase, 0.2e0.5

(Figure 1), varicella-zoster virus (VZV) or enteroviruses. Sea-
sonal arthropod-borne encephalitis caused by flaviviruses such
as Japanese encephalitis virus, tick-borne encephalitis virus and

positive for Cryptococcus

West Nile virus depends on the geographical distribution of their
PCR (sensitivity, specificity for HSV >95% if Gram stain negative
vector. Other causes in immunocompromised individuals include
Culture positive
Listeria monocytogenes and cytomegalovirus (CMV).
Low to normal
High/very high

Lymphocytes

Imaging and CSF analysis are the mainstay of diagnosis. In

Clear/cloudy

viral encephalitis the CSF usually shows a lymphocytosis; an

0e1000
Normal
Fungal

initial polymorphonuclear response may be seen in the early

stages. Early (within 48 hours) neuroimaging and CSF exami-
nation may reveal normal findings and negative viral tests.
Repeat testing can be required. Readers are directed to other
sources for detailed guidance.
Normal to mild elevation, 0.5e1.0

In recent years there has been an increasing concern for

arthropod-borne encephalitides. Ticks, mites and mosquitoes act
as vectors leading to infections such as Japanese encephalitis,
Zika virus disease, tick-borne encephalitis, West Nile fever and
checked on day 2e10)

scrub typhus. Changing global ecological patterns are responsible

Normal to mild less
Normal to elevated

for these re-emerging infections and highlight the importance of

an up-to-date travel and vaccination history.
Lymphocytes
‘Gin’ clear

5e1000
Normal

Cerebral and epidural abscess

Viral

A subacute presentation of headache, fever, nausea and vomiting

High to very high, 1.0e1.5

with associated seizures or focal neurological signs should alert

Culture positive 50e80%
Low to very low (<30%)

clinicians to a possible space-occupying lesion (e.g. cerebral

ZiehleNeelsen stain

abscess). Biopsy or abscess drainage for microbiological studies

Elevated but <500

is not always possible. Appropriate imaging findings, clinical

Cloudy/yellow

in up to 80%
Lymphocytes
Tuberculosis

context and blood cultures help to refine the aetiological diag-

Increased

nosis. Risk factors include spread from local infection sites

Elevated
CSF findings in various central nervous system infections

positive

(sinusitis, otitis media), which often causes solitary abscesses,

and haematogenous spread from distant sites in patients with
endocarditis, etc (often multiple abscesses, at the greyewhite
Culture positive <80%
Blood culture positive

junction or vascular border zones). Complications of neurosur-

Gram stain positive

gical intervention, traumatic injury and other co-morbidities (see

Table 1) also predispose.
Turbid, cloudy

Low (<40%)
100e50,000

Lymphocytes Neutrophils

Common causes of pyogenic abscesses include Streptococcus

<60% PCR
Increased
Bacterial

Elevated

species, Haemophilus species, anaerobic organisms and Staphy-

<90%

lococcus aureus. In cases of penetrating trauma or neurosurgical

>1

complications, infection is caused by Staphylococcus species,

Streptococcus species, Enterobacteriaceae, Pseudomonas aerugi-
10e20 cm

50e66%

nosa and anaerobic organisms. An appropriate dose and duration

Normal

<0.45
Clear

of antimicrobial therapy (based on presumed aetiology or cul-

0e5
Nil

Nil

ture) must be given, in addition to eradication of the infection

source and anti-seizure medication if indicated. Surgical inter-
CSF/plasma glucose
White blood cells

vention can be required to drain abscesses associated with a

White blood cell
Red blood cells

Protein (g/litre)

mass effect or oedema. Corticosteroids can be used preopera-

CSF analysis

(cells/mm3)

tively to manage vasogenic oedema but prolonged use is

Pressure

avoided.
Others
Colour

types

Table 2

The triad of fever, back pain and neurological deficits should

highlight the possibility of a spinal epidural abscess (Figure 2),

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 ACUTE NEUROLOGY

Figure 1 Scans from a 67-year-old man with HSV encephalitis admitted after a seizure with a prodrome of a sore throat and memory impairment.
Magnetic resonance imaging on D3 shows an asymmetrical cortical and subcortical signal abnormality in the left more than right anteromedial
temporal lobe, amygdala, hippocampus and insula (chevrons) (a). Patchy restricted diffusion is noted as bright on diffusion-weighted imaging (b;
solid arrows), with hypointensity on apparent diffusion coefficient imaging (c; solid arrows) and lack of enhancement (d; open arrow).

increasingly seen in the context of spinal procedures, and intra- Other infectious causes of peripheral neuropathy/poly-
venous drug use e a prolonged course of appropriate antibiotics radiculopathy include infection with Corynebacterium diphther-
with surgical drainage is required. Co-infection with blood-borne iae, Borrelia burgdorferi (Lyme disease) and Mycobacterium
viruses such as HIV can further complicate the presentation and leprae. Bilateral cranial nerve abnormalities with descending
result in very rapid progression of the infectious process. weakness are seen in botulism. Clostridium tetani skin infection
can cause tetanus.
Acute neuromuscular weakness Inflammation of the spinal cord limited to the anterior horn
cells can present with a flaccid paresis syndrome caused classi-
Rapid onset of weakness progressing within days can be caused
cally by poliomyelitis viruses, but also by flaviviruses. HSV and
by acute infection although is better recognized as a post-
VZV can cause transverse myelitis. Infectious myositis can be
infectious condition in GuillaineBarre syndrome. The clinical
seen with dengue haemorrhagic fever and enterovirus infections.
syndrome depends on the site of involvement and can involve
the bulbar and respiratory muscles. Although the preceding
Tuberculosis (TB) neuroinfection
infection noted in GuillaineBarre syndrome is Campylobacter
jejuni (up to 50% cases), other infectious agents associated Central nervous system (CNS) infection with Mycobacterium
include CMV, EpsteineBarr Virus (EBV), influenza A, Myco- tuberculosis can cause tubercular meningitis (TBM), tuber-
plasma pneumoniae, Haemophilus influenza, HIV at serocon- culoma, tubercular abscess, and spinal involvement with a pre-
version, and hepatitis E, Zika, Japanese encephalitis, dilection for involving the bones with TB spondylitis. TBM can
chikungunya and severe acute respiratory syndrome coronavirus present similarly to bacterial/viral meningitis but typically is
2 viruses. more subacute. Because of the predilection for the basilar

Figure 2 Epidural abscess caused by methicillin-sensitive Staphylococcus aureus in a 28-year-old woman who presented with a week of shoulder
pain, progressing to weakness of the arms and legs. She needed catheterization on presentation. Magnetic resonance imaging of the cervico-
thoracic spine shows an extensive anterior and posterior epidural collection with subdural extension throughout the imaged spine on T2-weighted
(T2w) images (a; arrow), with T1 post-contrast enhancement (b; arrows).

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 ACUTE NEUROLOGY

meninges and cisterns, VIth, VIIth and IInd cranial nerve in the brain parenchyma causing seizures, focal neurological
involvement is often seen, as is the most common complication deficits, increased intracranial pressure and progressive paresis.
of TBM e stroke. Diagnostic tests depend on the disease stage. Direct detection
The diagnosis and treatment of CNS TB should follow the methods such as dark-field microscopy, fluorescent antibody
British Infection Association guidelines protocol. The recom- staining, immunohistochemistry and PCR can be used for in-
mended treatment regimen for CNS TB caused by fully sensitive dividuals presenting with a primary chancre. Serodiagnostic tests
M. tuberculosis is usually isoniazid, rifampicin, pyrazinamide have become the mainstay of diagnosing syphilis, including in
and ethambutol for 2 months, followed by rifampicin and asymptomatic patients:
isoniazid alone for a further 10 months. All immunocompetent  Non-treponemal tests (NTTs) measure immunoglobulin
patients with TBM should be given adjunctive corticosteroids (Ig) G and IgM in response to the lipidal material released
(dexamethasone 0.4 mg/kg per day reducing over 6e8 weeks). from dying cells. Commonly used NTTs include the rapid
Hydrocephalus, tuberculous cerebral abscess and vertebral TB plasma reagin (RPR) and Venereal Disease Research Labo-
with paraparesis are indications for neurosurgical referral. ratory (VDRL) tests. These do not become positive until
In patients with HIV infection, the British HIV Association about 15 days after infection, and are helpful in diagnosing
(bhiva.org) recommends the same antitubercular regimen. The active syphilis. When interpreting these results it is impor-
timing of the start of antiretroviral treatment involves balancing tant to know if the patient has previously been diagnosed
risks of drug interactions (hiv-druginteractions.org), immune with syphilis and if treatment for this was completed.
reconstitution disease and opportunistic infections. For patients  Treponemal tests include the treponemal enzyme immu-
with CD4 counts >100 cells/microlitre, initiation of antiretroviral noassay (EIA) or treponemal chemiluminescent assay,
treatment may be delayed. Adjunctive corticosteroids are advised fluorescent treponemal antibody absorbed test, micro-
for those with TBM and treated HIV infection. haemagglutination assay for antibodies to T. pallidum, T.
pallidum passive particle agglutination (TPPA) and T.
HIV pallidum haemagglutination (TPHA) assays, and T. pal-
lidum immunoblot. These tests detect antibodies to T.
In acute primary HIV infection (seroconversion), self-limiting
pallidum proteins and can be positive 6e14 days after a
aseptic meningitis and rarely meningoencephalitis can occur. In
primary ulcer appears; they thus help in diagnosing early
the period of chronic latent infection, recurrent VZV infection
syphilis missed by NTTs. However, these tests remain
(shingles) may be seen. HIV patients with CD4 counts <200
positive through life.
cells/microlitre are profoundly immunocompromised and are at
 T. pallidum-specific IgM antibody tests are the anti-
increased risk of HIV neuropathy and AIDS-defining illnesses
treponemal IgM EIA and immunoblot.
such as HIV-associated dementia; there is also greater risk of
The British Association of Sexual Health guidelines on syphilis
opportunistic neuroinfections including space-occupying lesions
suggest that an EIA/chemiluminescent assay, preferably detect-
caused by Toxoplasmosis gondii, EBV-driven primary CNS lym-
ing both IgM and IgG, is the screening test of choice. A positive
phoma, progressive multifocal leukoencephalopathy (PML) and
screening test should be confirmed with a different treponemal
Cryptococcus neoformans meningitis.
test using a second specimen. For monitoring the response to
In the post-highly active antiretroviral therapy era, immune
treatment, a quantitative RPR or VDRL test should be used. It
reconstitution inflammatory syndrome must also be in the dif-
must be remembered that serological tests can be falsely positive
ferential diagnosis if clinical deterioration is noted after starting
in autoimmune disease, in older age or after intravenous drug
treatment. This is a paradoxical worsening of clinical status
use, or falsely negative in the first 3 weeks after a chancre de-
resulting from recovery of the immune response after therapy (or
velops, and in secondary or latent syphilis because of the pro-
removal of immunosuppression). This can be with (or without)
zone phenomenon, especially in HIV-positive individuals. IgM is
opportunistic infections, which if present can be noted simulta-
negative in late syphilis.
neously or after a delay.3
A limitation of all syphilis serological tests is their inability to
distinguish between infection with T. pallidum subspecies pal-
Syphilis
lidum and the T. pallidum subspecies that cause (non-venereal)
In the current era of pre-exposure prophylaxis for HIV behaviour yaws, pinta or bejel. Positive screening tests must be confirmed
has changed and rates of Treponema pallidum infection are with a different treponema test. A quantitative RPR/VDRL test is
increasing. Although tertiary syphilis with presentations such as recommended for ascertaining the response to treatment.
tabes dorsalis and generalized paresis of the insane are now CSF must be examined in patients presenting with neuro-
extremely rare, other forms of neurosyphilis are seen. Pre- syphilis to look for pleocytosis and undertake a CSF RPR. The
sentations are protean, so in addition to HIV, syphilis serology interpretation and cut-offs of these results are also influenced by
should routinely be tested in any person presenting with a sus- HIV status. Lumbar puncture should be done in all individuals
pected acute neurological infection.4 with syphilis who have: (1) neurological signs, (2) ocular
Neurological involvement can occur across all stages of involvement, or (3) a CD4 count <350 cells/mm3, and (4) in HIV-
syphilis, including primary, secondary, early latent (early) and positive patients who are antiretroviral naive with an RPR >1:32.
late latent and tertiary (late) syphilis. Presentations include Neurosyphilis is suggested by a positive CSF test (VDRL, RPR,
meningitis, meningovascular syphilis presenting as stroke, TPHA, TPPA, PCR) or CSF pleocytosis >20 cells/mm3 if the pa-
ocular syphilis (papillitis, optic neuritis, uveitis) and otic syph- tient is antiretroviral naive, or >10 cells if the person is on an-
ilis. Gummatous syphilis can present as space-occupying lesions tiretroviral treatment.

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 ACUTE NEUROLOGY

Neurosyphilis treatment regimens include: (1) procaine E), schistosomiasis, TB and brucellosis can be long (>21 days),
penicillin 2.4 MU intramuscularly plus probenecid 500 mg orally and an intermediate incubation period is seen in Q fever, viral
four times daily for 10e14 days; (2) benzylpenicillin 10.8e14.4 g haemorrhagic fevers, malaria and African trypanosomiasis (10
daily given as 1.8e2.4 g intravenously every 4 hours for 10 e21 days).
e14 days; (3) doxycycline 200 mg orally twice daily for 28 days;
(4) amoxicillin 2 g orally three times daily plus probenecid Non- and partially immunized hosts
500 mg orally four times daily for 28 days; and (5) ceftriaxone 2 g A large number of diseases are now vaccine preventable,
intramuscularly or intravenously once daily for 10e14 days. including hepatitis B, polio, diphtheria and tetanus. However, in
After treatment the RPR and sometimes the CSF analysis should individuals who have not been vaccinated, are partially vacci-
be repeated to ensure complete treatment of infection.4 nated, have missed boosters or have conditions where require-
ment for the booster is accelerated (immunosuppression,
Patient groups warranting special attention immunomodulatory treatment), these aetiologies must be
considered with relevant presentations.
Children, pregnant women and elderly people The migration of populations can also influence the local
Changes in immune response and physiology makes these sub- epidemiology of disease; for example, as noted in parts of Lon-
groups more vulnerable to infection and rapid deterioration. VZV don, individuals moving from a region in which TB is not
reactivation, for instance, is commonly seen in elderly pop- endemic to one where it is may not have been vaccinated as
ulations. It is also important to remain cognisant of decreasing children with the BCG (Bacillus CalmetteeGuerin) as this may
immunity to infections (e.g. tetanus, diphtheria) in elderly people not be part of the local guidelines. A
after the protection from initial immunization in their youth has
waned away. Co-morbidities such as diabetes mellitus, malig-
nancy or prolonged corticosteroid usage can also facilitate the KEY REFERENCES
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FURTHER READING
Low-income societies Granerod J, Cousens S, Davies NWS, et al. New estimates of inci-
Lack of complete vaccination schedules with missed or delayed dence of encephalitis in England. Emerg Infect Dis 2013; 19:
boosters, together with limited access to diagnostic tests 175e8.
(computed tomography, magnetic resonance imaging, serolog- Kneen R, Michael BD, Menson E, et al. Encephalitis Guidelines
ical tests, etc) as well as appropriate therapy leads to differences Development and Stakeholder Groups. Management of suspected
in the epidemiology of infection in this subgroup. A good history viral encephalitis in children e Association of British Neurologists
and understanding of local epidemiology is important to limit and British Paediatric Allergy, Immunology and Infection Group
mortality and morbidity caused by neurological emergencies. national guidelines. J Infect 2011; 64: 449e77.
Lyons JL. Viral meningitis and encephalitis. Continuum 2018; 24:
Returning travellers 1284e97.
When relevant, a detailed travel history including dates of travel McGill F, Heyderman RS, Michael BD, et al. The UK joint specialist
in the context of considered incubation periods, together with societies guideline on the diagnosis and management of acute
information regarding immunization records, must be consid- meningitis and meningococcal sepsis in immunocompetent adults.
ered. Botulism, tetanus, Brucella, Borrelia, etc are known to J Infect 2016; 72: 405e38.
present with lower motor syndromes; Japanese B encephalitis, Solomon T, Michael BD, Smith PE, et al. National Encephalitis
viral haemorrhagic fevers such as Dengue and other viruses Guidelines Development and Stakeholder Groups. Management of
including Zika and hepatitis E must be considered. suspected viral encephalitis in adultsdAssociation of British Neu-
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