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Flashcards in 05-06 Brain Infections Deck (15):
1

Four cardinal manifestations of brain inflammation

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

2

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

3

Where does encephalitis occur anatomically?

Brain parenchyma

4

Where does myelitis occur anatomically?

Inflammation of the spinal cord

5

Define encephalopathy

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

6

Review: in what space is the CSF located?

CSF is in the sub-arachnoid space

7

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

A image thumb
8

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.

9

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)

10

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

11

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.

12

West Nile

  • Presentation
  • Diagnosis
  • Treatment
  • Prevention

Presentation

  • 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

Diagnosis

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

Treatment—supportive

Prevention—mosquito control/insect repellants

 

13

HSV Encephalitis

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

Presentation

  • 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.

Diagnosis

  • 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

 

14

Rabies

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

Pathophysiology

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

15

ADEM

  • 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.

Diagnosis

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

Incidence

Uncommon, but kids > adults

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