Infectious disorders of the nervous system

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  1. Routes of infection
    • 1. Hematogenous spread - most common - arterial circulation, retrograde venous travel
    • 2. Direct implantation (trauma)
    • 3. Local expansion (adjacent structures - paranasal sinus, teeth, bone)
    • 4. Peripheral nervous tranport (predominantly virus - herpes)
  2. Viral syndromes (7)
    • 1. Acute aseptic meningitis acute onset: headache, fever, malaise, meningismus
    • 2. Recurrent meningitis
    • 3. Acute encephalitis and meningoencephalitis invasion beyond the meninges; more likely to have focal neuro deficits
    • 4. Ganglionitis - reactivation of latent virus in somatosensory ganglion
    • 5. Chronic invasion of neural tissue (slow, steady toxicity)
    • 6. Acute anterior poliomyelitis syndromes - motor nerve cell bodies
    • 7. Chronic infection without toxicity
  3. Herpes simplex encephalitis
    • Onset: rapid - subacute (several days)
    • Presentation: headache, fever, lethargy, altered level of consciousness
    •  - more variable: seizures  amnesia, aphasia, other focal signs

    Mortality can exceed 50%, even with treatment

    *Preferentially involves medial and inferior temporal and orbital gyri of frontal lobes

    CSF: lyphocytic pleocytosis, elevated RBC (40%), elevated protein, normal glucose

    Demographics: children and young adults (most commonly)

    Tx: empirical treatment w/ IV acyclovir (Toxicity: crystalline nephropathy)
  4. Bell's palsy
    (hypothesized) reactivation of herpes in geniculate ganglion

    • Clinical: hrs to days of LMN facial paralysis
    • 85% have near complete or complete recovery

    Tx: systemic corticosteroids within the first week of activation (more rapidly resolve sx)
  5. HSV1 and HSV2
    • Infection can remain dormant in peripheral somatosensory ganglia
    • intermittent reactivation

    • Thought to cause...
    • 1. Bell's palsy
    • 2. Vestibular neuritis
    • 3. Labial herpes (oral; 'cold sores') typically HSV1
    • 4. Genital herpes - typically HSV2

    Tx: labial and genital herpese cannot be cured; antivirals (acyclovir and famcyclovir) can be used to decrease frequency of outbreaks
  6. Vestibular neuritis
    ...may be due to reactivation of HSV

    • Subacute vertigo (days)
    • hearing can be affected

    most have complete recovery

    Tx: reassurance, corticosteroids, vestibulosuppressants (short-term only)
  7. Shingles
    (herpes zoster)
    reactivation of latent varicella zoster virus in the peripheral somatosensory ganglia

    • Presentation: unpleasant dysesthesia in a discrete dermatomal distribution
    • -erythematous rash
    • -cluster of clear vesicles
    • -neuropathic pain

    Postherpetic neuralgia

    Adult vaccination at age 60 lowers the risk of shingles by 2/3rds

    Tx: antivirals; acyclovir shorten the duration of pain and speeds the resolution of dermatomal eruption
  8. AIDS dementia complex
    (HIV encephalopathy)
    (HIV associated dementia)
    chronic infection with chronic toxicity

    • -Rare presenting manifestation of AIDS in adults
    • -More common presentation of children. 2/3 children are affected

    Untreated: pts rarely survive >6months

    Pathology: widespread inflammatory infiltrates

    Tx: responds well to HAART therapy
  9. HIV vacuolar myelopathy
    HIV pts manifest variable degree of myelopathy

    Pathology: vacuolization of dorsal columns and lateral corticospinal tracts with foamy macrophagesSimilar pathology to B12 deficiency

    • Presentation: spasticity, weakness, sensory and autonomic dysfunction
  10. Aseptic meningitis
    Early HIV seroconversion... pts often get meningitis with mild lyphocytic pleocytosis and mild increase CSF protein (usually asymptomatic)
  11. HIV myopathy syndrome
    diffuse weakness w/o pain or sensory changes

  12. Polio
    Invasion of neural structures, including anterior horn cells, brainstem motor nuclei, and motor cortex... resulting in LMN weakness and atrophy

    Infection is common --> <3% develop neurological weakness

    Post polio syndrome: 30-40 years after acute poliomyelitis -> rapid onset of LMN weakness and muscle atrophy, and pain in corresponding dermatome

    Hypothesis: Normal neuronal drop out occurs by aging
  13. Aseptic Meningitis
    nonspecific viral meningitis (most often non-bacterial)

    CSF: lymphocytic pleocytosis and elevated protein

    Clinical: most cases resolve completely; only mild inflammation in subarachnoid space mild meningitis syndrome: headache, fever, malaise
  14. Bacterial Meningitis
    Kernig's sign
    Brudzinski's sign
    • Rapid, subacute, progressiveClinical: fever, headache, meningismus, decreased level of consciousness due to local effects of bacterial toxin and inflammatory cytokines
    • late effects include cerebral infarction, seizures, hydrocephalus

    Kernig's/Brudzinski's signs: inability to extend the legs fully with the hips flexed/flexion of the hips and knees with flexion of the neck
  15. Bacterial meningitis
    • 1. H. influenza - kids (unvaccinated)
    • 2. N. meningitides - adolescents and young adults
    • 3. Streptococcus pneumoniae - any age

    Brain abscesses are most commonly caused by virulent streptococci Staphylococci also commonly cause brain abscess. (1-3 don't usually cause brain abscesses)Rapid empiric treatment with broad spectrum antibiotics

    Pneumococcal meningitis is improved with corticosteroids + Abx

    CT (check for abscess), LP to culture

    CSF: decreased glucose, increased protein, increased leukocytes (predominantly neutrophils)

    Prophylaxis tx of close contacts: H. influenza with rifampin
  16. Bacterial Abscesses
    Presentation: progressive focal deficits or seizures (rather than typical meningismus) most spread by hematological spread from remote sources (i.e. endocarditis) septic emboli some spread through local expansion and erosion (paranasal sinus, ear, and oropharyngeal cavity infections)

    • Pathology: inflammatory infiltration of the CSF in subarachnoid space
    • 1. meningeal vasculature becomes hyperemic and permeable
    • 2. Plasma cells and macrophages --> fibrin deposits can lead to loculation of exudate

    • 3. Liquifactive necrosis
    • 4. Small and medium sized arteries show endothelial hypertrophy and adventitial necrosis

    Mass effect --> provoked edema, neurological signs and sx, obstruction of drainage...
  17. Bacterial cerebritis
    paramenigneal abscess
    infection within the cerebral parenchyma

    Clinically less severe; less common. non-specific headache, fever, and malaise

    Micro: Mycoplasma, Lysteria, Legionella, catscratch, anthrax, brucellosis

    Parameningeal abscesses are often related to infection in the sinuses or trauma. hematogenous seeding is far less likely
  18. Tuberculousis Meningitis
    subacute or chronic meningitisClinical: low grade fever, headaches, lethargy and malaise, intracranial hypertension (papilledema and cranial neuropathies)

    -10% mortality in infected adults; higher in HIV pts

    Pathology: white tubercles form in subarachnoid space, basilar cistern - enhancement of basilar meninges on MRI. Penetrates the brain causing meningoencephalitis

    *Spread through hematogenous means: 2/3rds of patients show activity of disease in other organ system
  19. Cryptococcus
    variable clinical picturesubacute meningitis syndrome - meningismus is a much less common presenting sign

    • Immunocompetent => indolent
    • AIDS => explosive development of sx and progression over 1-2 days

    Pathology: meninges are thickened, causing obstruction of CSF circulation

    Gelatinous cystic lesions within expanded perivascular space -->"Soap-bubble" appearance
  20. Coccioides immotis
    fungal meningitis, similar to cryptococcus

    • Clinical: mild, influenza like non-bacterial pneumonia (<0.2% get disseminated disease including meningitis)
    • 50% mortality in pts who develop full meningitic phenotype

    • Risk factors
    •  *Exposure to overturned soil - California Central Valley or Imperial Valley
  21. Toxoplasmosis
    • Pt with AIDS => toxoplasmosis untill proven otherwise
    • subacute focal or multifocal brain lesionsmild infectious symptoms: headache, malaise, fever
    • Pathophysiology obligate intracellular parasite, toxoplasma gondii
    • Patholgoy abscesses near gray/white junction with eosinophilic coagulative necrosis

    Risk factors: cat feces. Can cause catastrophic injury to the fetus
  22. Cysticercosis
    • Infection with the larval stage of the pork tapeworm, Taenia solium
    • Variable presentation: Most assymptomatic, late complications include symptomatic epilepsy or obstructive hydrocephalus

    Pathophysiology larvae form encysted lesions, then die and are slowly calcified, leaving small calcified lesions in the brain parenchyma

    Tx: only treat when acutely ill, because tx can cause cysts to rupture, leading to explosive edema
  23. Syphilis 
    • Treponema pallidum invades the CNS within 3-18 months post inoculation
    • pathology

    • Subtypes: 
    • 1. meningovascular is the most common mild inflammatory perivascular change

    • Clinical: often asymptomatic, but can cause occlusion of arteries and formation of gummas
    • Gummas- plasma cell rich mass lesions

    2. paretic neurosyphilis - parenchyma is invaded --> neuronal death, microglial deposition, iron deposits

    3. Tabes dorsalis - axon and myelin loss in the ascending dorsal column
  24. Lyme disease
    Infection with spirochete Borrelia burgdorferi

    Clinical: mild meningoencephalitis with associated mononeuropathies of cranial and radicular nerves, lasts for months but not beginning until months after the skin lesion has resolved

    Classic history of outdoor activity, tick bite with target lesion...
  25. Leprosy
    Infectious neuritis caused by direct invasion by Mycobacterium leprae. Most common cause of polyneuropathy worldwide

    Clinical: hypesthesia leads to repetitive cutaneous injury, causing characteristic skin wounds

    Hypesthesia - diminished capacity for sensation
  26. Trichinosis
    nematode Trichinella spiralis

    Clinically: non-specific myalgia, fever, eosinophilia and malaise complex, often self limited
  27. Jakob-Creutzfeld disease
    Pathognomonic spongiform transformation of the cerebral cortex is seen in this prion disease

    Kuru plaques surrounded by spongiform changes ***picture***

    Rapid progression; multisystem dysfunction. Cognitive, motor, sensory deficits ...Invariably fatal within 1 year.

    Transmission through infected tissue, surgical instruments, corneas, growth hormone, environmentally
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Infectious disorders of the nervous system
2013-01-23 23:00:39

Infectious disorders of the nervous sytem
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