Table of contents
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Introduction
- Potential infections:
- Cerebral cortex --> encephalitis
- Meninges --> meningitis
- Potential abscesses:
- Crebral cortex --> Brain abscess
- Subdural Abscess --> (between arachnoid and dura)
- Epidural Abscess
- Blood brain barrier prevents entry of invading pathogens and toxic substances. However:
- Also prevents entry of Immunoglobulins, complement, and antibiotics.
- Therefore, if pathogen crosses BB barrier, CNS infections progress FAST and often SERIOUS.
- Maximal doses ("meningeal doses") of abx are often required.
- Also prevents entry of Immunoglobulins, complement, and antibiotics.
Meningitis
- See sub-page
Encephalitis
- See sub-page
Brain Abscess
- Symptoms:
- MOST COMMON: Severe headache at site of abscess.
- Sudden worsening = rupture of abscess into ventricles... high mortality rate (25-85%).
- Many present with triad:
- Headache
- Fever
- Focal Neuro Deficit
- Other Symptoms based on location:
- Neck stiffness only if occipital brain abscess or rupture into ventricle.
- altered mental status, lethargy, coma.
- Vomiting associated with incresed CSF pressure.
- MOST COMMON: Severe headache at site of abscess.
- Findings:
- Fever not present in 50%
- Neuro findings are late.
- Papilledema - late manifestation (25%)
- CN VI and III palsies from high ICP.
- Seizures if frontal brain abscess
- Two causes:
- 1. Direct spread from middle ear, frontal sinus, or dental infection
- 2. Hematogenous spread from chronic pulmonary/skin/pelvic/intra-abdo infection, endocarditis, cyanotic heart disease.
- 20-35% of patients --> do not find cause.
- Cerebritis (infammation and edema) --> necrosis, fibrotic capsule formation.
- Organisms:
- Organism provides clues on site of infection.
- Anaerobic bacteria (mouth/genital tract)
- Bacteroides fagilis, Prevotella, Propionibacterium, fusobacterium...
- Aerobic gram+ cocci (S. viridans, S. milleri, S. pneumo (rare), S. aureus)
- Aerobic gram- rods --> usually with neurosurg
- Immunocompromised:
- Toxoplasma, Nocardia, Aspergillus/cryptococcus/coccidioides.
- Immigrants (parasites)
- Cysticercosis parasite (85% of brain infections in Mexico City)
- Entamoeba hystolytica
- Schistosoma japonicum
- Paragonimus
- Diagnosis:
- Space occupying lesion (SOL) suggested by:
- Focal symptoms (even unilateral headache)
- signs (neuro deficits)
- papelledema
- LP CONTRAINDICATED, unless SOL excluded. (If papilledema or focal findings --> NO LP!! CT first)
- MRI better than CT (more sensitivity in picking up lesions) (Diffusion weighted MRI help discriminate abscess vs. neoplasms). CT only if unable to do MRI.
- Stages on CT:
- Early cerebritis
- irregular lesion of low density - no contrast enhancement.
- Later cerebritis
- Thick diffuse ring enhancement (enlarging) on contract injection.
- Late cerebritis
- Necrosis, Pre-contrast: ring of higher density surrounding edematous brain.
- Contrast: thin ring, non-uniform in thickness.
- Healed abscess
- Collagen capsule becomes isodense. No enhancement on contrast.
- Early cerebritis
- Stages on CT:
- Space occupying lesion (SOL) suggested by:
- Treatment:
- Neurosurg consult to drain abcess if >2.5cm lesion.
- (Excision or stereotactic aspiration), culture specimens.
- IV abx 6-8weeks
+/- prolongued oral therapy if appropriate agent is available.
(IV empiric therapy based on predisposing condition and presume pathogensis)- Generally:
- Ceftriaxone (enterobacterciae) + metronidazole (anaerobic lytic due to mouth flora)
- IF Dental Abscess: use penicillin + metronidazole to cover mouth flora
- IF concerned of pseudomonas (neurosurg)
- Use ceftazidime or cefepime
- IF trauma (worry about S.aureus) add vancomycin (MRSA) or oxacillin/nafcillin (MSSA) depending on resistance patterns... aminoglycosides, erythromycin, tetracycline, 1st gen cefs also used.
- IF hematogenous spread:
- Typically vanco + gentamycin for empiric therapy.
- Generally:
- Steroids:
- if mass effect + mental status change.
- IV dexamethasone (load 10mg then 4mg q6h)
- Do not worry about immunocompromise...
- DC as soon as possible.
- Reduce contrast enhancement on CT (hard to monitor)
- Decrease antibiotic penetration
- Slow capsule formation (can rutupre into ventricles)
- Repeat Neuroimaging
- IMPORTANT*, every other week up to 3months after completing therapy.
- To monitor for expansion of abscess or failure to respond.
- Neurosurg consult to drain abcess if >2.5cm lesion.
- Prognosis:
- Depends on stage:
- 0-30% generally
- 60-100% if stupor/coma
- 80-100% if ruptures into ventricle.
- Depends on stage:
Cranial Subdural Empyema
- Most common predisposing condition is in 40-80% of pts.
- Organisms (in sinuses): Aerobic Streptococci, Staphylococci, Aerobic gram negatives, and Anerobic streptococci (+ other anerobes). Polymicrobial infection is common.
- Symptoms and signs:
- Common: Rapidly progressive headache localized then generalized as progresses.
- Increased ICP: nausea, vomiting etc..
- Meningeal Irritation: meningitis-type symptoms.
- Focal cortical inflammation
- Diagnosis:
- MRI prefered to CT.
- Better clarity of morphologic detail.
- MRI better because:
- Can see empyemas not seen on CT, esp those in base of brain, falx cerebri, and those in the posterior fossa.
- Extra-axial empyemas from sterile effusions from subdural hematomas.
- MRI better because:
- Treatment:
- Surgical emergency.
- Decompress the brain and evacuate the empyema.
- Often craniotomy (better than craniectomy or burr holes based on a study).
- Empiric antimicrobial therapy with vancomycin, metronidazole and 3rd or 4rth cephalosporin.
- Surgical emergency.
Spinal Epidural Abscess
- Spinal canal has anterior and posterior epidural space
- Mechanism: of infection:
- Spread from osteomyelitis or disk space
- Spinal surgery or epidural catheter.
- Hematogenous spread from:
- Skin
- UTI
- IV drug use.
- Organisms:
- S. aureus (most common)
- Can see GN's or anaerobes if GU or GI source.
- 4 stages of clinical presentation:
- Back Ache and focal vertebral pain
- Nerve root pain (radiculopathy/parasthesias)
- Spinal Cord dysfunction
- Paraplegia
- Symptoms:
- Low back pain, fever, radicular pain, lower motor deficits, cord compression signs, spinous process tenderness.
-
- Back pain + fever --> consider epidural abscess
- MRI is test of choice.
- Diagnosis:
- MRI with Gadolinium --> procedure of choice!!!
- Can see spinal cord + epidural space in saggital and transverse sections.
- Can identify accompanied osteomyelitis, intra-medullary spinal cord lesions and diskitis.
- MRI with Gadolinium --> procedure of choice!!!
- Treatment
- If spinal cord compression:
- URGENT surgery.
- Can return function if done in 24-36hrs following neurological change.
- Emergency surgical drainage.
- Empiric Abx:
- Usually anti-staphylococcal agent (cloxacillin, nafcillin, oxacillin etc..)
- Usually (in US and MKSAP) vancomycin for empric MRSA coverage pending susceptibility testing.
(HIGH MRSA rates > 50% in some cases, vanco considered first line in US and MKSAP). - PLUS + antipseudomonal cephalosporin or carbapenem (for GN bacilli, esp for IVDU or spinal procedure).
(I.e. MKSAP answer is vancomycin + ceftazidime)
- Usually (in US and MKSAP) vancomycin for empric MRSA coverage pending susceptibility testing.
- Usually need prolongued (4-6weeks) tx with nafcillin, oxacillin, metronidazole, ceftriaxone.
- Usually anti-staphylococcal agent (cloxacillin, nafcillin, oxacillin etc..)
- Antimicrobial therapy alone can be considered in patients without long tract signs (i.e. if only pain and radicular symptoms), frequent follow-up, neuro exams, serial MRI studies to demonstrate abscess resolution are important.
- TB can be the cause.
- If spinal cord compression:
Generalized Neuropathy Causes
Botulism
- Two types of exposures:
- Preformed Toxin:
- home-canned foods
- In-vivo toxin Production: (After ingestion and spore germination)
- Honey (infants)
- Wound contamination.
- Preformed Toxin:
- Symptoms (1-5 days post ingestion) --> Classic Triad:
- Symmetric descending flaccid paralysis with prominent bulbar palsies:
- 4 D's of bulbar palsy:
- Diplopia
- Dysarthria
- Dysphonia
- Dysphagia
- 4 D's of bulbar palsy:
- Normal body temperature
- Clear sensorium
- Symmetric descending flaccid paralysis with prominent bulbar palsies:
- Diagnosis:
- Toxin in serum, stool, gastric aspirate or suspect foods.
- Treatment:
- Supportive
- Passive immunization using trivalent equine antitoxin (A, B, and E).
- MONITOR RESPIRATORY STATUS
Guillain-Barre Syndrome
-
Symptoms:
-
Typically: Antecedent infection (gastroenteritis from Campylobacter)
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Ascending paralysis and parasthesias
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Can have oculomotor findings (like botulism).
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Paralytic Shellfish Poisoning
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Ingestion of any type of filter-feeding molluscan shellfish (i.e. clams, oysters, scallops, muscles)
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Specific neurotoxin (saxitoxin) produced by algae accumulated.
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Symptoms hours to days post-ingestion
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Tinging of lips + tongue. ---> progresses to parasthesias of hand digits and feet.
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Eventually can lose control of hands and feet.
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If lots of toxin ingested: thorax and abdo muscles can paralyze causing respiratory difficulty.
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Tick Paralysis
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Associated with Dermacentor ticks (U.S. Pacific Northwest)
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Symptoms:
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Ascending paralysis (proximal large muscles).
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Prion Diseases of CNS
- Prions are novel, composed of transmissable proteins that lack genetic material.
- Cause 5 syndromes in humans.
- Kuru
- Gerstmann-Straussler-Scheinker Syndrome
- Fatal Familial Insomnia
- Sporadic Creutzfeldt Jakob Disease (two most common)
- Variant Creutzfeldt-Jakob Disease
-
Diagnosis:
- Progressive neurologic impairment
- Absence of inflammatory CSF findings
- Presence of spongeform changes on neuropathologic exam (biopsy). [often post-mortem :( ]
- No treatments available... fatal.
Creutzfeldt-Jakob Disease
- Classified as:
- Sporatic (most common) 85%
- Familial
- Iatrogenic (~1%)
- Variant (~1%)
- Probable Sporatic CJD criteria
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WHO Probable CJD: (must meet all criteria)
- 1. Progressive dementia
- 2. Clinial Signs
- 3. Lab or EEG findings
- 4. NO alternative diagnosis found on routine investigations.
-
- Clinically:
- Psych symptoms, cognitive decline, motor dysfunction.
- Extrapyramidal signs in >65%.
- Myoclonus, rapidly progressive dementia are hallmarks on disease.
- Median survival after onset is 5 months.
- Labs:
- Unrevealing.
- CSF usually acellular (normal), maybe slight protein elevation.
- 14-3-3 protein - specific neuronal protein in CSF fluid is elevated = indirect marker of sporatic CJD.
- Low Sn + Sp, only available in one lab.
- EEG - some findings.
- MRI - focal cortical hyperintensity on DWI or FLAIR = predictive of infection.
- Neural biopsy - spongiform changes - histopathologic staining for PRCSC prion protein (usually made post-mortem)
- Surgical procedures discouraged - can contaminate surgical instruments... exposes healthcare workers.
- Normal autoclaves do not remove prions!
- Need special procedures.
Variant Creutzfeldt-Jakob Disease
- In 1990's cluster of cases in UK --> had variant CJD.
- They were younger, psychiatric presentations, less rapid disease progression.
- Found that this outbreak is unique.
- ON biopsy: heavy concentrations of amyloid plaque in cerebrum + cerebellum
- Stain for a type of prion protein - PRPSC Type 4 pattern in tonsillar tissue...unique. Allows premortem dx.
- Consumption of beef during an epidemic of bovine spongiform encephalopathy supports animal to human transmission.
- Diagnosis:
- Radiographic + neuropathologic exam.
- MRI - pulvinar sign.
- Identification of prion protein (on stains) in tonsillar tissue allowing for pre-mortem histopathologic diagnosis.
- Radiographic + neuropathologic exam.
- Changes of animal feeding and buchering practices lead to decline in variant CJD.
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