Path - Cerebrovascular Disease Flashcards
what are the symptomatic effects of an anterior cerebral artery ACA) infarction
upper motor neuron-type weakness and cortical-type sensory loss
contralateral leg is affected more than the arm or face
“alien hand” syndrome (semiautomatic movements of the contralateral arm are not under voluntary control)
what are the symptomatic effects of a posterior cerebral artery (PCA) infarct
contralateral homonymous hemianopia
loss of half vision in both eyes on the contralateral half
what are the symptomatic effects of a middle cerebral artery (MCA) infarct
1) aphasia
2) hemineglect (patients fail to be aware of items to one side of space)
3) hemianopia
4) face-arm or face-arm-leg sensorimotor loss
5) gaze preference is toward the side of the lesion
what are causes of global ischemia
cardiac arrest, shock, severe hypotension
what are causes of focal ischemia
1) embolic or thrombotic arterial occlusion
2) atherosclerosis in HTN
damage to a watershed area produces what kind of necrosis
sickle-shaped band of necrosis
infarction in the ACA-MCA watershed area produces what sx
proximal arm and leg weakness
transcortical aphasia (language issues)
infarction in the MCA-PCA watershed area produces what sx
higher-order visual processing deficits
how do ACA-MCA watershed area infarcts occur
occlusion of the internal carotid a.
hypotension in a pt with carotid stenosis
what is the main cause of stenosis of the internal carotid a.
atherosclerosis
sx of carotid stenosis
1) contralateral face-arm or farm-arm-leg weakness
2) contralateral sensory changes
3) contralateral visual field defects
4) aphasia or neglect
thrombi formed in the internal carotid a. can embolize where?
MCA, ACA, ophthalmic artery
what are the primary sites of thrombosis
1) carotid bifurcation
2) origin of MCA
3) either end of basilar a.
describe how atherosclerosis can cause thrombosis
atheroma (intimal lesion, lipid core covered by fibrous cap) –> ruptures –> exposes blood to thrombogenic substance –> thrombosis/clot
rupture of an atherosclerotic plaque resulting in thrombosis causes what kind of infarct
wedge-shaped
describe paradoxical embolus and what can cause it
thromboembolus formed in the venous system travels to the arterial system
- patent foramen ovale (PFO)
describe causes of:
- air emboli
- septic emboli
- fat or cholesterols emboli
- merantic emboli
- amniotic fluid emboli
- air emboli: deep sea divers
- septic emboli: bacterial endocarditis
- fat or cholesterols emboli: trauma to long bones
- merantic emboli: noninfectious endocarditis (NBTE)
- amniotic fluid emboli: childbirth
list causes of hyper coagulable states that can cause thrombosis
1) heritable (protein S and C deficiency, antithrombin III deficiency)
2) dehydration
3) adenocarcioma/malignancies
4) surgery, trauma, childbirth
5) DIC
6) hematologic disorder (sickle cell, leukemia, polycythemia)
7) vasculitis
causes of TIAs
- migraines
- seizures
- cardiac arrhythmias
- hypoglycemia in elderly
what is the duration of TIAs
how do different durations cause different brain deficits
less than 24 hours
- typically ~10 mins tho
> 10 mins: some permanent cell death
> 1 hour: usually small infarcts, complete functional recovery can occur within 1 day
what are the potential mechanisms behind a TIA
1) an embolus temporarily occludes, then dissolves
2) in situ thrombus formation
3) vasospasm
compare the two types of stroke
1) hemorrhagic (red): emboli associated
2) ischemic (pale): thrombus associated
compare thrombus and emboli
thrombus: blood clot that forms in a vein
emboli: anything that travels through the blood vessels until it reaches a vessel that is too small to let it pass
what event can occur with an ischemic stroke causing more severe consequences
hemorrhagic conversion
- fragile vessels rupture leading to secondary hemorrhage
with what disease do lacunar infarcts occur
hypertensive cerebrovascular dz
what are slit hemorrhges
small caliber penetrating vessels causing slit-like cavities
- the slit is surrounded by pigment laden macrophages and gliosis
- seen in HTN cerebrovascular dz
sx of vascular multi-infarct dementia
- dementia
- gait abnormlaities
- pseudo bulbar signs (frequent, involuntary and uncontrollable outbursts of crying or laughing)
what is binswanger disease
a large area of arteriosclerosis and thromboembolism affecting the blood vessels that supply the white-matter and deep structures of the brain
–> large area of subcortical white matter w/ myelin and white matter loss
what are charcot-bouchard micro aneurysms
minute aneurysms in the basal ganglia
what is seen in cerebral amyloid angiopathy (lobar hemorrhage)?
beta amyloid deposition in the walls of vessels (same as Alzheimer’s) –> produces microbleeds
what is CADASIL (cerebral autosomal dominant arteriopathy w/ subcortical infarcts and leukoencephalopathy)
recurrent strokes and dementia
- first detectable around 35 y/o
Morphology: thickening of media and adventitia, loss of smooth muscle cells, and basophilic PAS+ deposits
what gene is associated with CADASIL
NOTCH 3
thickening of media and adventitia, loss of smooth muscle cells, and basophilic PAS+ deposits indicates _____
CADASIL (cerebral autosomal dominant arteriopathy w/ subcortical infarcts and leukoencephalopathy)
what is the most frequent cause of subarachnoid hemorrhage
rupture of saccular (berry) aneurysm
in what part of the circulation are saccular, mycotic, traumatic, and dissecting aneurysms most often seen
anterior
in what part of the circulation are atherosclerotic aneurysms most often seen
basilar a.
compare saccular, giant, fusiform, and mycotic aneurysms
saccular: bulges from one side of artery
giant: can involve more than one artery, over 2.5cm wide
fusiform: bulges from all sides of an artery, does not have a neck
mycotic: caused by infected artery
in the first few days after a subarachnoid hemorrhage, what are pts are risk for
additional ischemic injury from vasospasm affecting vessels bathed in extravasated blood
two tx for aneurysm
1) clipping
2) coiling
how do arteriovenous malformations affect the brain parenchyma
there is non-functional cortex under an AVM
most common route in CNS infection
hematogenous
how does TB meningitis develop
by seeding CSF from the sub-epidural or sub-meningeal granulomas
how do herpes simplex and zoster cause CNS infection
they produce latent infection of sensory ganglia –> replicate in Schwann cells –> and ascend to the CNS via SENSORY nerves
how does rabies cause CNS infection
bings at or near the acetylcholine receptors at the NMJ –> ascends to the CNS via MOTOR nerves
how does the structure of capillaries affect CNS infections
no fenestrations or intracellular clefts
they are relatively impermeable to antibodies, complement, and antibiotics
causes of chronic meningitis
1) TB
2) spirochetes (neurosyphilis or neuroborreliosis)
3) cryptococcus
what is the CNS response to infection
cerebral edema
how can you slow and reverse CNS edema in response to infection
corticosteroids
sx of acute (suppurative) meningitis
- HA
- meningeal irritation signs (kerning, brudzinski)
- high fever
- confusion and coma
compare locations between pneumococcal and H. influenzae in where their exudate occurs in meningitis
pneumococcal: often densest near sagittal sinus
h. influenzae: basal location
in acute meningitis, what fills the subarachnoid space
polymorphonuclear cells (PMNs)
describe the consequences of acute meningitis:
- ventriculitis
- focal cerebritis
- phlebitis
- ventriculitis: inflammation extending into ventricles
- focal cerebritis: inflammatory cells infiltrate walls of veins and extend into brain substance
- phlebitis: inflammation of veins leading to venous thrombosis and hemorrhagic infarction
what is a consequence that an occur with pneumococcal meningitis
chronic adhesive arachnoiditis
(thickening and adhesions of the leptomeninges in the brain or spinal cord)
“hand soap in your CSF”
what are the presumptive diagnosis from the following gram stains:
- gram negative diplococci
- gram positive diplococci
- gram negative pleomorphic
- gram positive cocci
- gram negative bacilli
- gram negative diplococci: Neiserria meningitidis
- gram positive diplococci: strep pneumonia
- gram negative pleomorphic: h. influenza
- gram positive cocci: s. aureus or s. epidermis, streptococci
- gram negative bacilli: e. ocli or other gram neg
what are the three tubes used to test in an LP
1st tube: most likely to be contaminated with skin/bacteria
2nd tube: chemistry
3rd tube: cell count
compare the following between an LP of bacterial and viral meningitis:
- gross appearance
- neutrophil count
- lymphs/mono count
- glucose
- protein
1) gross appearance:
- bacteria: cloudy, viral: clear
2) neutrophil count:
- bacteria: much higher
3) lymphs/mono count:
- viruses: much higher
4) glucose:
- greatly decreased in bacterial, normal in viral
5) protein:
- increased in both, but more increased in bacterial
describe the following in an LP of a fungal meningitis:
- CSF appearance
- dominant cell type
CSF appearance: clear
dominant cell type: early: PMNs, late: lymphocytes
list the common bacterial pathogens in acute meningitis for the following age groups:
- neonate
- 3m-2 y/o unvaccinated
- adolescent/young adult
- elderly
- neonate: E. coli, group B strep
- 3m-2 y/o unvaccinated: H. influenza type B
- adolescent/young adult: N. meningitides
- elderly: strep pneumonia and listeria monocytogenes
list the common bacterial pathogens in acute meningitis for the following conditions:
- immunocompromised
- basilar skull fracture
- head trauma: post neurosurgery
- CSF shunt
- immunocompromised: S. pneumonia, N. meningitidis, L. monocytogenes, P. aeruginosa
- basilar skull fracture: s. pneumonia, h. influenzae, group A beta hemolytic strep
- head trauma: post neurosurgery: s. aureus, s. epidermis, aerobic gram-neg bacilli (P. aeruginosa)
- CSF shunt: s. aureus, s. epidermis, aerobic gram-neg bacilli (P. aeruginosa), P. acnes
how does a congenital R –> L shunt increase risk for brain abscess
it removes the pulmonary filtration of organisms from the blood
most common bacterial causes of brain abscesses
strep and staph
sx of brain abscess
progressive focal neurological deficits with sx of increased ICP
what does the CSF show in a pt with brain abscess
high WBC, high protein, normal glucose
describe a subdural empyema
bacterial or fungal infection of the skull bones or sinuses that spreads to the subdural space
sx of untreated subdural empyema
focal neurological signs, lethargy, coma
thickened dura is indicative of ____
subdural empyema
osteomyelitis is associated with what type of abscess
extradural abscess
how does neisseria cause meningitis
colonization in crowded populations (dorms, Baracks, prisons)
–> colonizes the oropharynx and rhino pharynx of asymptomatic carriers –> spreads to CNS
clinical manifestations of N. meningitidis
rapidly progressive septicemia w/ fever, hypotension, DIC, petechial and purpuric lesions
- hemorrhagic skin lesions can progress to gangrene
- hemorrhagic infarction of adrenal glands
adrenal gland infarction due to n. meningitidis is characteristic of what dz process
waterhouse-friderichsen syndrome
sx of chronic meningitis
- fever
- headache
- lethargy
- confusion
- N/V
- neck stiffness
describe the CSF in chronic meningitis
- elevated protein
- lymphocytes
- low glucose level
gelatinous or fibrinous exudate in the subarachnoid space is indicative of ____
chronic meningitis from TB
obliterative endarteritis can occur with what dz processes
chronic meningitis from TB
meningovascular neurosyphilis
where does chronic meningitis from TB affect the brain
it has a predilection for the base of the brain
obliterates the cisterns and encases the cranial nerves
what is a tuberculoma
a well-circumscribed intraparenchymal mass of TB in the brain causing central caseous necrosis
seen in chronic TB meningitis
what kind of stain is used to diagnose TB
acid fast stain
sx of chronic meningitis from borrelia burgdorferi
rash then 4 weeks later neurological sx
- cranial nerve palsies
- peripheral neuropathies
what is seen in the CSF in chronic meningitis from borrelia burgdorferi
antibodies and polymerase chain reaction
compare paretic and meningovascular neurosyphylis
maningovascular: chronic meningitis at base of brain –> communicating hydrocephalus, obliterative endarteritis
paretic: progressive mental deficits w/ delusions of grandeur that terminate in severe dementia, has iron deposits
cause of tabes dorsalis
damage to sensory nerves in the dorsal roots
“Lightening pains”, absence of deep reflexes, loss of pain sensation, and joint damage (“Charcot joints”) indicate what dz process
tabes dorsalis
80% of viral causes of aseptic meningitis are caused by _____
enteroviruses
latent viral meningitis and encephalitis is indicative of what etiologies
- herpes zoster
- progressive multifocal leukoencephalopathy
perivascular lymphocytic cuffs are seen in what dz process
viral encephalitis
sx encephalitis from west nile virus
polio like syndrome w/ paralysis
CSF in encephalitis from west nile virus
colorless, increased pressure, increased protein, normal glucose
- initially exciting neutrophilic pleocytosis and then rapidly converts to lymphocytosis
describe the appearance of the parenchyma in arthropod-borne viral encephalitis (ex: west nile)
- multiple foci of necrosis in both white and gray matter
- neuronophagia
- microglial nodules
describe appearance of parenchyma in HSV-1 encephalitis
necrotizing and hemorrhagic in the inferior and medial temporal lobes
histological hallmark of HSC-1 encephalitis
cowry type A intranuclear viral inclusions in the neurons and glia
hemorrhagic temporal lobes indicates ____
HSV-1 encephalitis
what is persistent postherpetic neuralgia syndrome
persistent pain and painful sensation following non painful stimuli
- seen with shingles
describe how CMS affects the brain parenchyma in utero
periventricular necrosis –> severe brain destruction –> microcephaly and periventricular calcification
where does CMV localize
in paraventricular subependymal regions
describe how acute polio affects the spinal cord, and what sx does it elicit
mononuclear cel perivascular cuffs and neuronphagia of the anterior horn motor neurons on the spinal cord
–> flaccid paralysis
what is post-polio syndrome
occurs 25-35 years after resolution of initial illness
progressive weakness w/ decreased muscle mass and pain
how does rabies cause CNS effects
infection ascends along peripheral nerves from the wound site
sx rabies
- malaise, ha, fever
- local paresthesias around the wound
- CNS excitability, violent motor responses
- flaccid paralysis
- hydrophobia (foaming at the mouth, aversion to swallowing)
local paresthesia around a wound is indicative of what infectious agent
rabies
negri bodies indicate ___
rabies
compare morphology of acute and chronic HIV meningitis
acute: mild lymphocytic meningitis, perivascular inflammation, some myelin loss
chronic: microglial nodules w/ multinucleated giant cells
describe the vessels and white matter of the brain in HIV meningitis
vessels: abnormally prominent endothelial cells and perivascular foamy or pigment-laden macrophages
white matter: myelin pallor, axonal swelling, gliosis
what is IRIS (immune reconstitution inflammatory syndrome)?
occurs with antiviral therapy with HIV meningitis
- paradoxical deterioration after starting therapy
–> inflammatory response –> paradoxical exacerbation of symptoms from opportunistic infections
why does HIV associated dementia occur
because of inflammatory activation of microglial cells
increased incidence of primary CNS lymphoma is associated with ____
HIV
multinucleated giant cells are seen with what etiologies
- HIV
- herpes
- TB
what causes PML (progressive multifocal leukoencephalopathy)
JC polyomavirus
what happens in PML (progressive multifocal leukoencephalopathy)
JC polyomavirus infects oligodendroglial cells –> demyelination
what patients get PML (progressive multifocal leukoencephalopathy)
immunosuppressed (HIV+)
describe the morphology of the brain in PML (progressive multifocal leukoencephalopathy)
- ill defined destruction of white matter
- subcortical area of demyelination w/ lipid laden macrophages
- decreased number of axons
principle pathologic effect of PML (progressive multifocal leukoencephalopathy)
demyelination
what causes subacute sclerosing pancencephalitis (SSPE)
paramyxovirus
sx of subacute sclerosing pancencephalitis (SSPE)
cognitive decline, spasticity of limbs, seizures
what pts get subacute sclerosing pancencephalitis (SSPE)
non-immunized children or young adults following early-age infection w/ measles
morphology of subacute sclerosing pancencephalitis (SSPE)
- widespread gliosis
- myelin degneration
- neurofibrillary tangles (like Alzheimers)
what pts are at increased risk of getting a mucor infection
DM pts
what fungi cause vasculitis
what fungi cause parenchymal infection
vasculitis: nucor and aspergillosis
parenchymal: candida and crypto coccus
what histological hallmark is seen with cryptococcus infection
cryptococcal soap bubbles
what is seen in the CSF in cryptococcus meningitis
cryptococcal polysaccharide antigen
what test must be done on the CSF to diagnose cryptococcus
india ink preparation
what pts get toxoplasmosis gondii
HIV, immunosuppressed
pregnant pts
what happens to the brain parenchyma in toxoplasmosis infection
brain abscess near gray-white junction of cerebral cortex and deep-grey nuclei
histological hallmarks in toxoplasmosis infection
- central focus of necrosis
- petechial hemorrhages
- vascular proliferation
what is seen at the periphery of necrotic zones in toxoplasmosis gondii infection
free tachyzoites and encysted bradyzoites
what is naegleria fowleri
brain eating amoeba
- found in warm freshwater
acanthamoeba causes what
chronic granulomatous meningoencephalitis
what infectious agent causes cerebral malaria
plasmodium falciparum
sx of Creutzfeldt-jakob dz
- gerstmann-straussler-scheinker syndrome
- fatal familial insomnia
- kuru
what agent causes Creutzfeldt-jakob dz
prior protein (PrP)
morphology of Creutzfeldt-jakob dz
spongiform change: intracellular vacuoles in neurons and glia
what are causes of iatrogenic transmission of Creutzfeldt-jakob dz
- corneal transplant
- brain implant
- human growth hormone
describe fatal familial insomnia
seen in Creutzfeldt-jakob dz
- initially just sleep disturbances
- then ataxia, autonomic disturbances, stupor, then coma
- less than 3 year survival
what mutation is associated with fatal familial insomnia
aspartate substitution at codon 129
