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Flashcards in 05-06 Brain Infections Deck (15):

Four cardinal manifestations of brain inflammation

  1. fever
  2. headache
  3. altered mental status
  4. focal neuro signs


Where does meningitis occur anatomically?

Inflammation of the membranes of the brain or spinal cord; infection involving the subarachnoid and Virchow-Robin spaces over the surface of the brain


Where does encephalitis occur anatomically?

Brain parenchyma


Where does myelitis occur anatomically?

Inflammation of the spinal cord


Define encephalopathy

Disorders/diseases of the brain that include non-infectious causes


Review: in what space is the CSF located?

CSF is in the sub-arachnoid space


Give example 1) cause(s) and 2) Major distinguishing sx at presentation for:

  • Meningitis: Acute
  • Meningitis: Subacute or chronic
  • Encephalitis: Acute a) Hematogenous
  • Encephalitis: Acute b) Neuronal
  • Encephalitis: Chronic
  • “Space-occupying lesions”
  • Toxin-mediated syndromes


What are the encephalitis viruses we worry most about?

Most concerning viral encephalidites:

  • Arboviruses: 1-50% cases are fatal
  • Herpes simplex viruses: > 70% untreated cases are fatal; 6-11% of treated cases are fatal.
  • Rabies: >99% cases are fatal without early post-exposure prophylaxis.


Clinical features of encephalitis

Acute febrile illness with h/a, AMS, focal neuro signs +/-:

  • a.Change in level of consciousness, disorientation, behavior change
  • b.Problems with speech
  • c.Seizures
  • d.Motor weakness
  • e.Hyper-reflexia and extensor plantar responses
  • f.Abnormal movements or tremor
  • g.Pituitary involvement: hypothermia, poikilothermy, diabetes insipidus, SIADH
  • h.Spinal cord involvement (myelitis): Flaccid paralysis, loss DTR’s, bladder and bowel dysfunction
  • i.Raised ICP (?papilledema)


Pathophysiology of Viral Encephalitis

  1. True encephalitis: Direct tissue destruction, vascular damage, and edema
    • a. Hematog.: e.g. Arboviruses (e.g. EEE, WEE, WNV StLE Cali-E)
    • b. Neuronal transmission: e.g. HSV, Rabies
  2. Post-infx encephalomyelitis: Autoimm demyelination


Host and vector for North American arboviruses?

North American arboviruses have an enzoonotic life cycle between the host (birds) and the vector (mosquitoes). Hu- mans and horses are accidental hosts.


West Nile

  • Presentation
  • Diagnosis
  • Treatment
  • Prevention


  • Ill 3-14 days after infected mosquito bite
  • West Nile fever (most viremic patients): Fatigue, fever, headache, muscle weakness; rash (50%)
  • Neuroinvasive disease (rare):
    • Encephalitis – (most common neuroinvasive form)
    • Meningitis
    • Flaccid paralysis
    • Other


  • Serology; PCR in blood banking
  • CSF: Lymphocytic pleocytosis/↑ prot; CSF Abs
  • Imaging: Often normal
  • EEG: Generalized slowing (frontal or temporal)


Prevention—mosquito control/insect repellants



HSV Encephalitis

  • Presentation
  • Routes of Infection
  • Where does HSV-1 cause dz? HSV-2?
  • Diagnosis
  • Treatment


  • F (89%), h/a (78%), AMS (96%), personality ∆ (61%), szs (38%), aphasia, hemiparesis

Routes of Infection—3 Routes

  1. 1/3 1° infx (usually via oropharynx) with CNS invasion via the trigeminal nerve or olfactory tract. Most patients with primary infection are <18 y.o.

  2. 1/3 CNS invasion after an episode of recurrent HSV-1 infection, likely viral reactivation with subsequent spread.

  3. 1/3 CNS infection without clinically obvious primary or recurrent HSV-1 infection, presumed reactivation of latent HSV in situ within the CNS.

​HSV-1 vs. HSV-2


  • HSV-1: Localized inflammation in medial-temporal, orbital-frontal lobes, limbic structures.
  • HSV-2: Can be more generalized encephalitis.


  • 1. CSF: High opening pressure, lymphocytic pleocytosis (0-1000 cells) + many RBC’s, raised protein; nl glucose
  • 2. HSV PCR: Sensitivity 75-98%; Specificity100% (compared to biopsy)
    • Expanded range of clinical presentations now documented using this sensitive test.
  • 3. EEG
  • 4. MRI
  • 5. Biopsy

Treatment—IV acyclovir – high dose




  • Pathophys
  • Clinical Course
  • Clinical Presentation
  • Management
  • Prevention


Replicates in muscles cells, taken up by unmyelinated periph nerve terminals and transported to CNS by retrograde axoplasmic flow at 8-20 mm a day.

  • Serum Ab develops in 10 days (but intraneural virus replicates undeterred).
  • After generalized CNS replication, centrifugal spread via peripheral nerves.

Clinical Course

The incubation from exposure to clinical rabies disease depends on the inoculation distance from CNS (average 20-60 days and range from 11 months to 6 yrs.) 

  • Sx onset occurs when virus reaches the spinal cord.

​Clinical Presentation

  • nonspecific prodrome that may include localized pain (?in the region of bite), parathesias, and myoedema.
  • most common presentation is “furious “(encephalitic) rabies = 80% cases
    • agitation
    • hydrophobia
    • excessive salivation (+ other autonom insuff.)
    • arrhythmias
    • coma, seizures, and death
  • “Paralytic” (dumb) rabies occurs in 20%
    • ascending paralysis
    • weakness
    • meningeal signs

Management is supportive.

Preventive measures include:

  • contact isolation precautions.
  • animal vaccination
  • management of human bite exposures (basic wound care)
  • human rabies vaccination (pre-exposure prophylaxis for vets and longterm travelers to high-endemicity areas) or post-exposure prophylaxis with rabies vaccine and rabies immunoglobulin



  • Stands for? What is it?
  • Typical Course?
  • Diagnosis
  • Incidence

Acute demyelinating encephalomyelitis (ADEM)

A.K.A. post-infectious encephalomyelitis

Autoimmune demyel. dz, mimics acute viral encephalitis.

Typical Course

Often h/o fever, rash, nonspecific respiratory, or GI illness in the days to weeks preceding illness.

  • Rarely, it follows vaccination or an atypical bacterial infection.


  • The CSF is normal or nonspecific.
  • MRI scanning shows enhancing multifocal white matter disease c/w demyelination


Uncommon, but kids > adults

  • incidence has been reduced dramatically by routine vaccination for childhood illnesses