CNS
Cranial Nerves
- Exit at base of the brain and pierce meninges to exit
- CNI (olfactory)- contact w/ external environment
- CNII (Optic)- directly visualized; w/in SAS if ↑ ICP
(papilledema)
- CNIII (oculomotor) passes under tentorium cerebella below
temporal lobe and is compressed by intracranial herniation
(presents as dilated pupil not reactive to light; ptosis, lateral
deviation)
- CNVI(abducens)- longest tract, sensitive indicator of ↑ ICP
(presents as failure to abduct the affected eye; ipsi)
- BBB- capillaries have tight junctions, no fenestrations,
surrounded by foot processes; difficult for organisms to
penetrate
CNS Infections- organisms enter via bloodstream, neuronal pathways, or direct inoculation
-
Encephalitis- infection of brain parenchyma
Meningitis- infection of leptomeninges; + parenchyma= meningoencephalitis; + SC= meningoencephalomyelitis
Myelitis- infection of the SC
Neuritis- infection of peripheral nerves
Acute bacterial meningitis- infection of meninges by bacteria w clinical present w/in 24-48 hrs (CSF LEUKOCYTOSIS)
Intracranial abscess: abscess in brain parenychema, may or may not be associated w/ meningeal involvement
50%: contiguous foci, 25%: hematogenous dissemination, 10%: direct inoculation, 15%: primary abscess
Pathogenesis:
- Frontal lobe: Sinuses, teeth, direct inoculation
- Temporal: otitis, mastoiditis, sphenoid sinusitis
- Cerebellum: otitis, astoiditis
- MCA circulation: hematogenous source for lung abscess, endocarditis
Stages of Abscess formation- early cerebritis: 1-3 days; late cerebritis: 4-9 days: early capsule: 10-13 days; late
capsule: >14 days
Diagnose w/ MRI or CT scan w/ contrast (MRI very sensitive avoid LP
Treatment: surgical drainage and management of increased ICP, search for source, culture abscess for
everything except viruses; empiric ATB: metronidazole + 3rd gen ceph + nafcillin or vancomycin
Encephalitis- inflammation of the brain, characterized by alteration in consciousness
Many non-infectious disease: drug rxns, vasculitis
Infectious is due to viral infection (bacteria, fungus, tubercular less common)
- Togavirus: EEE, WEE, VEE
- Flavi: SLE, West Nile
- Enteroviruses
- Paramyxo- measles (rare)
- Rabies
- Herpes: HSV 1, 2 and VZV (only treatable)
Pathogenesis: Hematogenous (viral, rickettsia, bac, fungi, TB), Retrograde (rabies, VZV), olfactory nerves (virus)
Diagnosis: EEG- slowing, MRI in HSV encephalitis shows temporal lobe involvement (PCR), LP w/ mild pleocytosis
Treatment: acyclovir effective for HSV1, 2, VZV (always give, in case of false negative); supportive care
Subdural Empyema- pyogenic infection of space between dura and arachnoid
Subdural space is crossed by small veins (emissary vessels); organisms reach subdural space this way or direct
extension of osteomylitis of the skull
Source: 50-80% frontal or ethmoid sinusitis; 10-20% otitis media/mastoiditis; 5% hematogenous dissemination
Bacteriology: Polymicrobic infections are common: aerobic strep, staph, S. pneumo, H, inf, anaerobes, GNR
4:1 male to female; usually in 2nd or 3rd decade of life
Diagnosis: MRI, very sensitive (diagnostic); CT scans will miss some; don’t do LP!
Treatment: neurosurgery for burr holes or craniotomy; management of ↑ iCP (dexamethasone), culture of
empyema fluid; simultaneous debridement of sinuses, mastoid, ear
Treatment AB: min of 3 wks- cover anaerobes, GNR, GPC (metronidazole+cefriaxone+nafcillin or vancomycin
Prognosis- 75% mortality if comatose, almost half develop seizures for life
Epidural abscess- located between bone and dura mater
Intracranial epidural abscess- spills over into subdural space and forms subdural empyema too
- Treat/diagnosis same as subdural empyema
Spinal epidural abscess- in spinal canal, epidural space-fat filled w/o emissary vessels, allows longitudinal spread
- Bacteria enter epidural space by direct extension (vertebral osteomyelitis) or hematogenous dissemin.
- Less often polymicrobial (S. aureus 60-90%, then streptococci, anaerobes, GNRs)
- Diagnosis: MRI, myelogram can visualize cord and look for compression, Blood cultures +, SED ↑
- Treatment: immediate surgical drainage; cover s. aureus, GNR and anaerobes pending cultures
(Vanco+3rd gen ceph+metronidazole); prognosis if treated prior to paralysis is good
Abscess
Lesion
Intracranial
Space occupying
Encephalitis
Focal deficit
Yes (neuro)
Yes (neuro)
Fever
Seizures
Altered Mental Status
N/V
Headache
<50%
Yes
Yes
Yes
Yes
Ataxia
Visual field deficit
Personality Changes
↓Consciousness
Hemiparesis
Papilloedema
Radiculopathy
Motor/sensory
deficits
Nuchal rigidity
Possible
Possible
Yes
Yes
Subdural Empyema
Rapidly expanding
mass
Yes (neuro)
spread/expand
Yes
Yes (later)
Yes
Yes
Focal, later
generalizes
Epidural
Yes (vertebral),
tenderness
Yes
Yes
Yes (later)
<50%
Yes
Yes ↑ paralysis
Yes
Presentation of Acute Bacterial Meningitis
Consider in patients w/ fever, neuologic symptoms, cerebral dysfunction
Typical: HA, fever, lethargy, confusion, vomiting, stiff neck (varies); nuchal rigidity*
- Kernig’s (leg resistant to passive extension on inflammation)*
- brudzinski’s sign (flexion of neck causes pelvic thrust)*
- papilledema <1%
- *not good predictors
Pathogenesis of Meningitis- The outcome is Increased intracranial pressure
Nasopharyngeal colonization somehow get local invasion causing bactermia meningeal invasion replication SAS
inflammation causes Increased BBB permeability (leads to vasogenic edema), cytotoxic edema, ↑ CSF outflow
resistance (leads to hydrocephalus interstitial edema), and cerebral vasculitis and or infarction
Workup of Bacterial Meningitis
CSF exam essential- Need to order WBC and DIFF, Glucose, Protein, Gram stain and Culture (special studies
possible= hold last tube)
Relative Contraindictation to LP (↑ ICP, platelet count <40,000, scoliosis, infected site over lumbar spine)
To check ICP fast:
- Look at eyes, PERRL
- Look at optic disc to see if bulging (bad)
- Get them to follow finger w/ eyes (good= they can do it)
Treatment of Bacterial Meningitis
If assessment for increased ICP is present you must obtain blood cultures, do empirical antimicrobial therapy
CT scan of head if no mass lesion can do lumbar puncture
If assessment for increased ICP is absent obtain blood cultures and perform lumbar puncture
After LP- if consistent w/ bacterial meningitis then start treatment w/ dexamethasone and empirical
antimicrobials by age if no positive gram stain and specific antimicrobials by agent if positive gram stain
Cover commonly encountered pathogens: tx for 10-14 days
Cause
Age
Risk
Vaccine
Diagnosis Treatment
S. agalactiae
(gr. B)
E. coli
L. mono
H. influenza
0-4 wks
0-4 wks
0-4 wks,
>50 yr
4 wks50 yrs
N. mening
> 4 wks
S. pneumo
> 4 wks
GNR
> 50
0-4wks
4wks-18 yrs
18 yrs- 50 yrs
50 yrs
Neonates, pregnant women, elderly,
immune-compromise
> 5 yo w/ sinusitis, otitis, epiglottis
pneumonia; Predisposing: DM,
ETOHism, asplenia, CSF leak, hypogammaglobenmia
MAC complement defect (less fatal)
#1 cause in 18-50 yo; w/ URTI, LRTI,
endocarditis; Predisposing: see H. inf
Type B type f
meningitis is ↑
A, C W135, Y; B
cause >50% infects
Covers most
common serotypes
Prime Bacteria
S. agalactiae, E. coli, L. monocytoes
H. inf, N. meningitides, S. pneumonia
H. inf, N. meningitides, S. pneumo
L. monocytoes, N. meningitidies, S. pneumo, GNR
+ bullet
coccus
Neg rod
+ rod,
catalase +
Neg rod
Amp or Pen G
3rd gen ceph
Amp or Pen G
(trimeth-sulfa)
3rd gen ceph
Neg
Amp or Pen G
diplococci
+ coccus
Vanco+ 3rd gen
ceph
Empirical treatment
Amp+ 3rd gen ceph; or amp+AG
Vancomycin + 3rd gen ceph
Vancomycin + 3rd gen ceph
Vancomycin + AG + 3rd gen ceph
Presentation of Acute Viral Meningitis
- Often aseptic meningitis
- Enteroviruses cause 80-85% of cases of viral meningitis; others include: arbovirus, herpes virus, HIV
Pathophysiology of Viral meningitis
- Muscosal colonization leads to viremia and virus crosses BBB (may travel along nerves)
- Virus enters SAS and spreads in the CSF inflammatory response specific for the virus (lymphocytes, Tcells)
Clinical Presentation of Viral meningitis
- Enterovirus in kids > 2 weeks old
- Sudden fever, frontal headache, photophobia, nuchal rigidity, and myalgias, d/v, anorexia, cough, sore throat
- Occurs more in summer months
- May be associated w/ enteroviral syndrome (classic rash, painful mouth vesicles)
- HSV 2 infection often associated w/ aseptic meningitis and signs of genital tract infections
- Initial episode of HIV may be associated w/ aseptic meningitis and AB may be negative
Treatment of Viral meningitis
- Enterovirus: consider use of gammaglobulin in extremely ill
- Herpes virus: acyclovir
- HIV: consider triple drug therapy
Presentation of Chronic Meningitis
Neurologic abnormalities or CSF abnormalities of > 4 wks duration
Infections from: TB, nocardia, Cryptococcus, toxoplasmosis, syphilis, lyme disease, CMV
Noninfectious causes: Behcet’s (autoimmune), carcinoma, vasculitis
Often Insidious in onset: wax and wanes over weeks but w/ gradual neurologic decline
Diagnosis and Treatment of Chronic Meningitis
Diagnostic workup is difficult: guide by history and PE plus lumbar punctures
Treatment is guided by most likely initial diagnosis if the patient is critically ill or preferably by confirmation
CSF Findings
WBC
Bacterial
> 1000; PMNs
Glucose
(abn. w/ AB)
Protein
Grain stain
Culture
< 45 or < 2/3
serum glucose
> 80
+ 80% of time
+ 80% of time
Viral
<1000 (almost always <3,000);
lymphs
Normal
(except HSV, LCM, mumps, EEE)
Mildly ↑
negative
Viral Culture difficult; PCR- HSV
Fungal
< 500; mononuclear
Tuberculosis
< 1000; mononuclear
Normal or low
< 45
Protein >60
negative
Special smears/culture
>>100
AFB smear
Culture +