Infectious disorders of the nervous system

• 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)

• 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

• 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)

(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)

• 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

...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)

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

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

HIV pts manifest variable degree of myelopathy

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

• Presentation: spasticity, weakness, sensory and autonomic dysfunction

Early HIV seroconversion... pts often get meningitis with mild lyphocytic pleocytosis and mild increase CSF protein (usually asymptomatic)

diffuse weakness w/o pain or sensory changes

myositis

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

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

• 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

• 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

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...

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

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

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

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

• 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

• 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

• 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

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...

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

nematode Trichinella spiralis

Clinically: non-specific myalgia, fever, eosinophilia and malaise complex, often self limited

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