Medical 273


1. Acute meningitis a. Acute aseptic (viral) meningitis i. Lep to meningeal inflammation due to viruses (enterovirus most frequent)

ii. Lymphocytic infiltration of leptomeninges and superficial cortex iii. Fever, signs of meningeal irritation, depressed consciousness iv. Low mortality b. Acute purulent meningitis i. Purulent lep to meningeal inflammation due to bacteria

• Neonates: group B streptococci, Escherichia coli

• Infants and children: Haemophilus influenzae

• Adolescents and young adults: Neisseria meningitidis

• Elderly: Streptococcus pneumoniae and Listeria monocytogenes ii. NeutrophOic infiltration of the leptomeninges, extending variably to cortex iii. Opaque leptomeninges iv. Diffuse cerebral edema: risk of fatal herniations v. Headache, fever, nuchal rigidity, cloudy sensorium, coma, and death vi. Sequelae due to organization of purulent exudate and fibrosis ■ Hydrocephalus

• Cranial nerve impairment (neural deafness)

2. Mycobacterial meningoencephalitis a. Can be caused by Mycobacterium tuberculosis or atypical mycobacteria b. Usually involves the basal surface of the brain c. Characteristic tuberculomas within the brain and dura mater d. Frequent in AIDS patients, particularly by Mycobacterium avium-intracellular (MAI)

Table 29-1. CSF Parameters in Different Forms of Meningitis



Glucose (pg/dl)

Proteins (mg/dl)

Pressure (mm H^O)

Normal values

<5 lymphocytes

45-85 (50-70% glycemia)



Purulent (bacterial)

Up to 90,000 neutrophils

Decreased (<45)

Increased (>50)

Markedly elevated

Aseptic (viral)

100-1,000 most lymphocytes


Increased (>50)

Slighdy elevated

Granulomatous (mycobacterial/ fungal)

100-1,000 most lymphocytes

Decreased (<45)

Increased (>50)

Moderately elevated

3. Viral encephalitides a. Common features: perivascular cuffs, microglial nodules, neuron loss, and neu-ronophagia b. Clinical manifestations: variable (mental status change, fever, and headache, often progressing to coma)

c. Specific forms i. Arthropod-borne: St. Louis, California, Eastern and Western equine, Venezuelan encephalitides ii. Herpes simplex type 1: characteristic hemorrhagic necrosis of temporal lobes iii. Rabies: characteristic Negri bodies in hippocampal and Purkinje neurons iv. HIV

• Cerebral involvement is frequent and leads to AIDS-dementia complex Dementia and other neurological abnormalities

Histopathology: microglial nodules and diagnostic multinucleated giant ; cells

• Spinal involvement leads to vacuolar myelopathy: similar to vitamin B12 deficiency-associated subacute combined degeneration d. Progressive multifocal leukoencephalopathy (PML)

i. Related to ]C virus (a polyomavirus)

ii. JC virus causes PML in immunocompromised patients (especially AIDS)

iii. Histopathology: demyelination, lymphohistiocytic, and astrogliosis iv. Astrocytes acquire bizarre shapes v. Oligodendrocytes in active lesions contain intranuclear inclusions

4. Fungal menin go encephalitides a. Candida, Aspergillus, Cryptococcus, and Mucor species most frequent agents b. Aspergillus and Mucor have a marked tropism for blood vessels: vasculitis, rupture of blood vessels, and hemorrhage c. Cryptococcus causes diffuse meningoencephalitis: invasion of the brain through Virchow-Robin and soap bubble lesions.

5. Toxoplasmosis a. Frequent in AIDS patients b. Cerebral abscess with central necrosis and chronic inflammation c. MRI/CT scan: characteristic ring-enhancing lesion

276 medical

6. Cerebral abscess a. Hematogenous dissemination or direct spread from contiguous foci b. Predisposing conditions i. Acute bacterial endocarditis, cyanotic heart disease (right-to-left shunt), and chronic pulmonary abscesses ii. Mastoiditis, paranasal sinusitis, acute otitis, open fracture, previous neurosurgery c. CT/MRI appearance: ring-enhancing lesion d. Clinical manifestations i. Signs of increased intracranial pressure (headache, vomiting, and papilledema)

ii. Focal neurological deficits (vary depending on site of lesion)

7. CreutzfeJdt-Jacob Disease (CJD)

a. Caused by a prion protein (PrP)

i. PrP is a 30-kD protein normally present in neurons ii. Encoded by a single-exon gene on chromosome 20

iii. Its normal conformation is an Ot-helix PrPf iv. In disease states, PrPc changes to a (i-pleated sheet conformation: PrPsc v. Low spontaneous change results in sporadic cases of CJD

vi. Mutations of PrP result in hereditary cases of CJD

vii. PrPsc facilitates conformational change of other PrPc molecules into PrPsc viii. PrPsc is responsible for cerebral pathologic changes b. Results in spongiform change i. Fine vacuolization of the neuropil in the gray matter (especially cortex)

ii. Due to large membrane-bound vacuoles within neuronal processes iii. Associated with neuronal loss and astrogliosis iv. Kuru plaques are deposits of amyloid of altered PrP protein c. What are the clinical manifestations of spongiform encephalopathies?

i. CJD: 85% cases are sporadic; 15% are familial ii. Middle-aged to elderly patients iii. Rapidly progressive dementia iv. Memory loss with startle myoclonus or other involuntary movements v. Typical EEG changes vi. Death widiin 6-12 months

Table 29-2. Prion Diseases

< Disease

Infectious Agent



: Kuru



Subacute Spongiform Encephalopathy (SSE); Fore Tribe - Mew Guinea; consuming infected brains

Creutzfeldt-Jakob Disease



Genetic predisposition





1 Fatal Familial Insomnia







SSE—scraping their wool off on fences

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