Pathology - Cns - Infectious And Neurogenerative Diseases

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Inflammation of pia and arachnoid

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meningitis

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sparse exudate with numerous organisms with severe congestion of the leptomeninges characterizes what?

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hyperacute meningitis; death within 24 hrs

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most common infection of the CNS?

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bacterial acute meningitis secondary to hematogenous spread

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What is waterhouse-friderichsen syndrome?

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Septicemia with meningitis and adrenal gland hemorrhagic infarcion

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subacute/chronic meningitis is defined as?

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>1 week where PMNs are less and lymphocytes/plasma cells appear with macrophages

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complications of subacute/chronic meingitis?

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leptomeningeal fibrosis, hydrocephalus, and chronic adhesive arachnoiditis

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Most common meningeal bacterial in neonates?

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GBS and EColi

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MCC of meningitis in young adults?

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N. meningitides

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MCC of bacterial meningitis in adults and elders?

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Strep Pnemoniae and l monocytogenes

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Which is more fulminant? Viral or bacterial meningitis?

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Bacteiral

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MCC of viral meningitis?

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enterovirus (echovirus/ coxsackie/nonparalytic polio also)

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Pathologic finding in acute viral meningitis?

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lymphocytic infiltrate in leptomeninges and brain swelling

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Causative agents of brain abscesses?

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bacteria or fungi

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MCC of brain abcesses?

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strep and staph

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MCC of brain abcesses in IC?

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toxo, nocardia, listeria, GM-bacilli, mycobacteira, fungi

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Empyemas of epidural and subdural spaces caused by?

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local extension of infective process outside CNS MC steph or staph

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Inflammation of brain and spinal crod tissue?

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meningoencephalitis

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TB infections involve CNS how?

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meningoencephalitis

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Mycobacterial stain of CNS is how reliable?

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its only positive 5-30% of the time.

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complication of TB?

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obliterative endarteritis of meningeal vessels, causing infarcts

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What is seen in a tuberculoma?

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mass lesion of caseating necrosis surrounded by capsule of fibroblasts, epithelioid cells, giant cells, lymphocytes, with SPARSE bacilli in necrotic center

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what is TB in the vertebrae?

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Pott's Disease (spondylitis) where TB causes granulomatous processes in vertebral bodies and intervertebral discs

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Major forms of neurosyphilis?

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general paresis, meningovascular, and tabes dorsalis

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thickened meninges and atrophic brain with gradual impariment of cognition and attention, STD?

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general paresis ak aparetic neurosyphilis

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chronic meningitis and multifocal arteritis?

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heubner's arteritis of neurosyphilis

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lightning pains, loss of position and vibration, and paresthesias with syphilis?

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tabes dorsalis

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Perivascular and parenchymal mononuclear cell infiltrates?

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typical of viral meningoencephalitis

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neuronophagia and microglial nodules?

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typical of viral meningoencephalitis (macrophages eating infected neurons)

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important cause of epidemic encephalitis?

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arbovirus (EE WEE VEE, sLE, west nile, and california)

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hemorrhagic necorisis of temporal lobe? MCC?

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HSV-1

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eosinophilic cowdry Type A?

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HSV-1

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chronic phase of HSV-1?

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cavitaiton, glial scar, sparse lymphocytes

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HSV-2 causing meningitis in what instances?

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neonate passage through birht canal

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MC viral infection in AIDS pts?

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CMV

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Periventricular necrosis, microcephaly, and periventricular calcifications in a fetus?

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CMV infection

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predominant cell type infected by HIV in CNS?

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microglia (macrophage, CCR5)

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microglial nodule with multinucleated microglial cells?

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found in gray and white matter in HIV encephalitis

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vacuolation of white matter in AIDS patiens is called what?

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vacuolar myelopathy causing vib and prop deficits

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PML caused by and infects what?

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JC infection of oligodendrocytes to cause demyelination

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large astrocytes with bizzare pleomorphic hyperchromatic nuclei and intranuclear oligodendrocytic inclusions?

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progressive multifocal leukoencephalopathy

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Most common fungal meningitis

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crytococcus neoformans

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method of CNS infection by cryptococcus?

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infection by lungs and hematogenous spread to the brain

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diagnosis of cryptococcus?

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lumbar puncture, +lymphocytes, mild protein elevation, mild/normal glucose

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Multiple intraparenchymal cysts that resemble soap bubbles?

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cryptococcal CNS infection

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small buds and stain with mucicarmine?

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cryptococcal

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vascular CNS damage by fungi caused by?

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Mucormycosis and Aspergillus

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most common cause of CNS mass lesions in AIDS patients?

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toxoplasma

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most common cause of space occupying lesions in CNS?

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cryptococcus

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most common aids defining illness?

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crypto

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idiopathic spongiform encephalopathy?

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sporadic CJD

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what is GSS?

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inherited spongiform encephalopathy which is AD and onset is around 25 yrs.
gerstman-straussler-scheinker

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acquired/transmissible spongiform encephalopathy?

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iatrogenic CJD due to corneal transplants etc, OR dietary

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what is a prion?

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PRNP on chromosome 20 that becomes mutated to form the protein PrPsc which has a abnormal amyloid formation

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PRNP gene polymorphism?

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at 129 Met or Val.

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BSE?

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bovine spongiform encephalopathy

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rapidly progressive dementia in 7th decade, myoclonic jerking. What is used for proper Dx?

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EEG and MRI showing increased basal ganglia signals

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What are kuru plaques?

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amyloid plaques seen in spongiform encephalopathy

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what is notable about CJD histology?

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NO inflammatory response! only reactive astrocytosis and degeneration

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most common cause of dementia in elderly?

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alzheimer's

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Avg disease duration of alzheimer's?

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7 years (to tibet)

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CT showing diffuse symmetric cortical atrophy?

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alzheimers

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EEG only with mild generalized abnormality, imparied attention, no impared labs or CSf examination?

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alzheimers

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gross pathology of alzheimer's brain

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atrophy of gyri with wide sulci, decrease in brain weight (cortical atrophy)

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What is a senile plaque?

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an EXTRAcellular BA4 amyloid plaque derived from APP (amyloid precursor protein)

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What is tau?

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a microtubular associated protein that accumulates in neurons if abnormal. the abnormal form is called PHF (paired helical filament)

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what is diffuse plaque?

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betaA4 protein without PHF

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What is neuritic plaque

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betaA4 protein WITH PHF in axons and dendrites

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What kind of plaques are more closely associated with cognitive decline?

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neuritic plaque (the betaA4 with PHF)

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Hypothesized progression of plaque formations?

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diffuse forms first then neuritic plaques develop from diffuse ones.

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intraneuronal cytoplasmic aggregation of PHF. What is it and what does it look like?

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neurofibrillary tangles, flameshaped

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NFT occur first where?

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medial temporal lobe then cortex.

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The degree of cognitive impairment in AD is correlated to?

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NFT densities.

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pathological diagnosis of AD utilize what criteria?

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density of neuritic plaques and braak stage of NFT.

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What is the relationship between snile plaques and NFT?

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unknown

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AD pattern of inheritance?

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sporadic, nonmendelian inheritance, 1-2% familial AD which is autosomal dominant (AD!hehe)

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AD characterized how?

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familial or sporadic, early or late onset.

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what is early onset AD?

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less than 60 years age of onset

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most cases of FAD have mutation of?

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1) amyloid precursor protein gene
2) presenilin 1 gene
3) presenilin 2 gene

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APP is associated with?

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amyloid precursor protein is on chromosome 21 so many down's pts get AD mid 30's.

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What is amyloid precursor protein?

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a membrane glycoprotein. mutations of this yield betaA4 amyloid.

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how do mutations of preselilins affect APP?

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they are cofactors for proper gamma cleavage of APP

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where are betaA4 proteins located?

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extracellularly in plaques and also intraneuronal where it is toxic

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Responsible for 50% of all FAD?

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presenilin 1 on chromosome 14.

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What gene is associated with late onset AD?

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ApoE on Ch 19.

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which genotype influences an earlier onset of late AD?

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Apolipoprotein e4 homozygous.

mnemonic: e4 is beeee4

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What does Apo e4 do?

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increases deposition of betaamyloid

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severe atrophy of frontal and temporal lobes, sparing parietal and occipital?

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pick's disease

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Clinical presentation of pick's disease?

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behavioral and speech before memory disturbances

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What are pick bodies?

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tau protein cytoplasmic bodies (remember, tau is NORMAL but PFT are tangles of tau)

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Progressive supranuclear palsy presents how?

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50-70 yr old male with parkinsonial signs, impaired vertical gaze and some dementia

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lesions found in progressive supranuclear palsy?

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abnormal tau accumulations in subthalamic nucleus, substantia nigra, globus pallidus, basal ganglia, PAG.

and astrocytes!

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what are glial tangles?

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astrocytes with tau accumulations seen in progressive supranuclear palsy (not exclusively)

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What is vascular dementia?

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infarcs that cause diffuse white matter damage

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Pallor of substantia nigra in midbrain?

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parkinson's dz

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lewy bodies are?

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cytplasmic inclusions with a halo, composed of alpha synuclein

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what are lewy bWhat are alpha synuclein?odies made of

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alpha synuclein

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what causes dementia in parkinson's?

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lewy bodies in cortical neurons

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What is alpha synuclein?

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a normal presynaptic terminal protein

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Huntington's disease genetics?

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AD on Ch4, gene making huntingtin protein, paternal anticipation (only fathers go huntin)

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atrophy of caudate and putamen?

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huntington's dz

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Loss of GABA neurons?

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huntington's disease, loss of striatal inhibitory neurons

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Abnormality accounting for up to half of all hereditary ataxias?

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friedrich's: Ch9, a gene that codes for frataxin, a mitochondrial protein that regulates iron flow and ATP production

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GAA

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freidrich's ataxia

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CGG

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fragile X

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CAG

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huntington's

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Ataxia, loss of position and vibration sense before age 20?

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Friedrich's ataxia

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SOD1 mutation?

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ALS - fatal disorder of corticospinal degeneration.