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Define the disease
Encephalitis is known as brain tissue that becomes inflamed, usually caused by viral infections. Bacteria or Fungi can also cause encephalitis in rare cases. Encephalitis can be confused as meningitis, thus diagnosis is of utmost importance.
Encephalitis are divided into two main types:
Primary encephalitis
– Direct infection of the brain and the spinal cord.

Secondary encephalitis
– Infection that originates in different parts of the body, later on spreading to the brain and spinal cord.
(American Journal of Neuroradiology June 2017, 38 (6) 1070-1078)

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Bacterial pathogens, as Mycoplasma species are rare and invariably involve inflammation of the meninges.

In some cases transplantation of organs or blood can be an agent that cause Encephalitis.
There is also couple of animal vectors, including:
Encephalitis cause is of an infectious nature spread through person-to-person contact:
Viral agents
Measles virus
HSV types 1 and 2
Rubella virus
Mumps virus
Human herpes virus 6 may also be a causative agent
When we look at the pathophysiology the virus tends to replicate outside the Central Nervous System and later on gains entry to it, either by hematogenous spread or by travel alongside neuropathways. After crossing blood-brain barriers the virus enters neural cells, distrupting cell functions, hemorrhage and diffuse inflammatory response, effecting the grey matter.
(Clinical Infectious Diseases, Volume 15, Issue 2, 1 August 1992, Pages 211–222)

People with immune compromised diseases are more susceptible to obtain the virus. Also people that is not vaccinated against the disease, is more likely to get the virus. Susceptibility can differ from person to person, yet anyone can be infected. Susceptibility can only be determined by some external factors that influence obtaining the virus.

PathogenisisStage 1
Outcome dependent on:
– Viral factors
– Above plus site of entry, size of inoculum
Host factors:
Age, sex, immune status, genetic factors
Stage 2
– Respiratory, GI, GU, skin, ocular conjunctiva, blood
Entry into central nervous system
Hematogenous dissemination
Neural dissemination
Neurovirulence and Immunopathology
Stage 3
Neuronal infection
Latency, subtly altered function, apoptosis, necrosis
Anatomic location affects manifestations
Oligodendroglial cells Oligodendroglial cells
JC virus, PML (progressive multifocal leukoencephalopathy) z
Inflammatory reaction in meninges and in perivascular distribution within brain
Acute disseminated encephalomyelitis (ADEM)
(European Journal of Neuroscience ; HYPERLINK “” Volume32, Issue2,Glutamatergic Synapses July 2010 Pages 298-309)
Notifiable or not
Encephalitis is indeed notifiable, thus patients infected should seek medical attention immediately.

Clinical manifestations
Severe headache, fever, nausea, vomiting, lethargy and abnormal behaviour.
Alteration in level of consciousness, i.e. drowsiness, confusion, stupor and coma.

Generalised and/or focal convulsions.
Focal neurological deficits.
Abnormal movements
basal ganglia involvement.

Cranial nerve palsies (brainstem involvement)
loss of sphincter control
paresis of limbs and segmental sensory loss (spinal cord involvement).
Some patients may have signs of meningeal irritation.
Herpes encephalitis may have an acute and fulminant course. It can result from primary or recurrent infection.

Severe headache, fever, nausea, vomiting, lethargy and abnormal behaviour.

Alteration in level of consciousness
(Brain, Volume 123, Issue 7, 1 July 2000, Pages 1481–1494)
Other diagnostic test will be done, after clinical manifestations are analyzed. Sharp waves is shown in electoral activity of an ECG, usually in one or both temporal lobes.

Confusion and drowsiness are seen during the neuro examination. Irritation of the meninges causes a stiff neck, this is where meningitis can be diagnosed. By taking a sample of cerebrospinal fluid (lumbar puncture) there is an increased level of protein and white blood cells. If the patient has Encephalitis the results can be normal in some cases. If a CT scan is done, changes in the brain structure can be seen.

Doing a CT scan can also help ruling out:
MRI is the best diagnostic test to be done to detect or identify Encephalitis.

(American Journal of Neuroradiology June 2017, 38 (6) 1070-1078)

increased intracranial pressure
permanent neurological deficits
cerebral oedemaseizures
inappropriate antidiuretic hormone (ADH) secretion. (Brain, Volume 123, Issue 7, 1 July 2000, Pages 1481–1494)
Specific management
Laboratory tests are mostly unhelpful.
CSF may reveal:
slightly raised protein
normal glucose level
mild pleocytosis (mostly lymphocytes)
A specific virus is sometimes isolated. PCR is helpful, if available.
Red cells are seen with Herpes encephalitis
In some instances, the CSF may be completely normal.
A CT scan of the brain may reveal brain oedema. (CT findings may only be apparent after 3–5 days)
The herpes virus preferentially involves the temporal lobe and orbital surfaces of the frontal lobes
An EEG may demonstrate changes suggestive of herpes encephalitis
Nursing care
Evaluate patient for shock or hypotension
Airway protection
Seizure precautions
Oxygen and IV access secured
Administration of first dose or doses of Acyclovir
Collection of laboratory samples and cultures
Admit to high or intensive care unit, if appropriate.

Monitor, where indicated:

neurological status
heart rate
body temperature
blood pressure
haematocritblood glucose
acid-base status
blood gases
fluid balance, i.e. hydration
serum and urine osmolality
Ensure adequate nutrition by enteral feeding where possible.
Use a nasogastric tube if necessary.
If enteral feeding is not possible, give intravenous fluids: paediatric or neonatal maintenance solution with dextrose.(CHILDREN)
Raised intracranial pressure or cerebral oedema:
Elevate head of bed ± 20 degrees.
Maintain PaCO2 at 4–5 kPa; intubate and ventilate, if necessary.
Avoid fluid overload
( Diagnosis and treatment of central nervous system infections in the emergency department. Emergency Medical Clinics of North America. 2016;34:917.)
Medicine management
Adults Children
Paracetamol, oral, 1 g 4–6 hourly when required to a maximum of 4 doses per 24 hours.
Maximum dose: 15 mg/kg/dose.

Maximum dose: 4 g in 24 hours.

Ibuprofen, oral, 400 mg immediately then 8 hourly with meals, if needed. OR
Morphine, IV, to a total maximum dose of 10 mg (See Appendix II, for individual dosing and monitoring for response and toxicity).
Herpes simplex encephalitis:
Aciclovir, IV, 10 mg/kg 8 hourly for 21 days.

Start therapy as early as possible
Before results are available.

A negative herpes PCR usually excludes the diagnosis unless the specimen was taken within 72 hours of onset of symptoms, when false negatives have been described.
Treat seizures appropriately:
All suspected cases of herpes encephalitis should be discussed with a specialist.
EDL: chapter 14) p. 14.18
If herpes simplex virus or varicella zoster virus encephalitis:
Aciclovir, IV, 8 hourly administered over 1 hour for 21 days.

If 0–12 years of age: 20 mg/kg/dose.
If ; 12 years of age: 10 mg/kg/dose.

For fever:
Paracetamol, oral, 15 mg/kg/dose, 6 hourly until fever subsides.
Raised intracranial pressure or cerebral oedema:
Elevate head of bed ± 20 degrees.
Maintain PaCO2 at 4–5 kPa; intubate and ventilate, if necessary.
Avoid fluid overload.

Mannitol, IV, 250 mg/kg administered over 30–60 minutes.
Do not repeat without consultation with a paediatrician.
EDL) chapter 8p. 8.26
For neuro-imaging: patients not responding or worsening in condition, i.e. decrease in consciousness and cranial nerve palsies, despite appropriate therapy.

This is especially urgent in patients with tuberculous meningitis, who may develop hydrocephalus and require an urgent shunting procedure. (EDL
Deterioration of clinical condition despite adequate treatment.
Meningo-encephalitis with complications or loss of consciousness.(EDL
Measures against spread
Vaccination reduce the risk of encephalitis development:
Mosquito area’s measures should be taken to reduce risk of being bitten:
Wear long sleeve clothes
Use repellent
Mosquito nets
(Disease Control Priorities in Developing Countries. 2nd edition.)
Guideline Tunkel AR, Glaser CA, Bloch KC, Sejvar JJ, Marra CM, Roos KL, et al. The management of encephalitis: clinical practice guidelines by the Infectious Diseases Society of America. Clin Infect Dis. 2008 Aug 1. 47(3):303-27. Medline.

Dalmau J, Graus F, Villarejo A, et al Clinical analysis of anti-Ma2-associated encephalitis. Brain 2004;127:1831–44
Jamison DT, Breman JG, Measham AR, et al., editors.

B.P. Kelley, S.C. Patel, H.L. Marin, J.J. Corrigan, P.D. Mitsias and B. Griffith
American Journal of Neuroradiology June 2017, 38 (6) 1070-1078; DOI:
Bloch KC, Glaser C. Diagnostic approaches for patients with suspected encephalitis. Curr Infect Dis Rep. 2007 Jul. 9(4):315-22. Medline.

Dorsett M, et al. Diagnosis and treatment of central nervous system infections in the emergency department. Emergency Medical Clinics of North America. 2016;34:917.

Francesc Graus, Albert Saiz, Josep Dalmau, Journal of Neurology ,April 2010, Volume 257, Issue 4, pp 509–517
S. Humayun Gultekin, Myrna R. Rosenfeld, Raymond Voltz European Journal of Neuroscience Volume32, Issue2, Glutamatergic Synapses, July 2010, Pages 298-309
Joseph Eichen Jerome B. Posner Josep Dalmau, Brain, Volume 123, Issue 7, 1 July 2000, Pages 1481–1494,
Jerome B. PosnerSearch for other works by this author on:
Oxford Academic
Google Scholar
EDL chapter 14 (adult) p. 14.18
EDL chapter 8 (child) p. 8.26

Joseph EichenSearch for other works by this author on:
Oxford Academic
Google Scholar
Search for other works by this author on:
Oxford Academic
Google Scholar
Josep Dalmau

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