Cerebrovascular Diseases and Infections Flashcards
What vascular deficits causes UMN weakness, cortical-type sensory loss and contralateral hemiplegia (initially)
ACA (anterior cerebral artery)
What vascular deficit causes contralateral leg > arm and face?
ACA
Injury to what causes alien hand syndrome?
ACA
semiautomatic movements of contralateral arm not under voluntary control
What vascular deficit causes contralateral homonymous hemianopia (only see one side of eye in both eyes)?
PCA
What is the most common vascular place for infarct and ischemia? Why?
MCA (middle cerebral artery)
larger territory
What vascular defect causes aphasia, hemineglect, hemianopia, face/arm (more common) or face/arm/leg sensorimotor loss?
MCA
MCA ischemia/infarct causes gaze preference toward….
toward side of lesion
Define lacunes
small, deep infarct involving penetrating branches of MCA (lenticulostriae vessels)
What is the third leading cause of death in US?
cerebrovascular disease
heart, cancer, then brain dz
What are the 3 major categories of cerebrovascular diseases?
Thrombosis
Embolism
Hemorrhage
What cerebrovascular disease condition does stroke apply to clinically?
All (thrombosis, embolism, hemorrhage)
especially acute symptomatology
What is an infarction in terms of stroke?
resultant lesion of brain parenchyma from thrombosis, embolism or hemorrhage
What are the most common cerebrovascular disorders?
Global ischemia (whole brain)
Embolism
Hypertensive Intraparenchymal Hemorrhage (most common, people don’t take meds or not treated)
Ruptured Aneurysm
Does oxygen or metabolic substrate limit brain oxygenation?
oxygen
When blood flow is reduced, survival depends on ……
collateral circulation (circle of willis)
duration of ischemia (TIA vs stroke)
magnitude and rapidity of flow reduction (slow blood loss or hypoxia vs fast)
What are 2 types of reduction in blood flow to brain?
global ischemia–> generalized reduction of perfusion
~~~cardiac arrest, shock severe hypotension
focal ischemia–> localized area
~~~embolic or thrombotic arterial occlusion (atherosclerosis in HTN!!!!!!)
What is a watershed infarct?
blood supply to two adjacent cerebral arteries are compromised
**region between 2 vessels are most susceptible to ischemia and infarction
Describe the type of necrosis in a watershed infarct
sickle-shaped band of necrosis over cerebral convexity (goes to back of brain lateral to separation of hemispheres)
Occlusion of what arterial connection causes higher-order visual processing deficits?
MCA-PCA
What would be the sx of a ACA-MCA watershed infarct?
Proximal arm and leg weakness
transcortical aphasia (language issues)
What is a typical patient that would have an ACA-MCA watershed infarct?
occlusion of INTERNAL CAROTID artery (MCA is terminal branch of internal carotid)
patient with hypotension and carotid stenosis
Cartoid stenosis is seen with what progressive disease?
Atherosclerosis
leads to stenosis of internal carotid artery just beyond bifurcation
With atherosclerosis–> carotid stenosis, you hear _______ into ________
bruit that continues into diastole
Thrombi formed in carotid artery d/t atherosclerosis can embolize and travel _______
distally to MCA, ACA and ophthalmic artery (vision problems)
What are classic sx of carotid stenosis?
contralateral face-arm weakness
contralateral sensory changes
contralateral visual field defects
aphasia
What are the most common sites of thombus formation?
branch points:
carotid bifurcation
origin of MCA (terminal branch of internal carotid)
either end of basilar artery
What most often causes thrombotic occlusions?
atherosclerosis
What is an atheroma?
intimal lesion with lipid core covered by fibrous cap in vessels
–> will cause clot or thrombus if ruptured d/t exposure of thrombotic substance (lipid core) to blood
What clot/thrombus would you get from A-fib?
left atrial appendage clot
What clot/thrombus would you get from an MI?
clot in hypokinetic or akinetic areas
What clot/thrombus would you get from valvular disease in heart?
form on diseased leaflets or prosthetic parts
Where is the origin of an artery-to-artery emboli?
vertebral or internal carotid artery stenosis
What clot/thrombus would cause a dissection?
carotid or vertebral emboli
atherosclerosis of aortic arch
What clot/thrombus would you get from a patent foramen ovale?
paradoxical embolus (bypass lungs to brain)
What causes air emboli?
deep sea divers
iatrogenic introduction into circulation
What causes septic emboli?
bacterial endocarditis
What causes fat/cholesterol emboli?
trauma to long bones
What causes marantic emboli?
proteinaceous emboli from non-bacterial thrombotic endocarditis
hypercoag states (malignancy, amniotic fluid emboli in childbirth)
What artery is most affected by embolic infarct?
MCA
Where do emboli typically lodge?
branch point or luminal stenosis
What is a shower emboli?
multiple emboli from fat after long bone fracture
What can cause hypercoagulable states?
heritable coag factor disorders (protein S, C, antithrombin III deficiency)
dehydration
adenocarcinoma/malignancies
surgery, trauma, childbirth
DIC (disseminated intravascular coag)
Hematologic disorders (sickle cell, leukemia, polycythemia)
vasculitis
What are sx of TIA?
+ or -
motor, sensory, visual auditory, olfactory, kinesthetic, emotional, cognitive (pretty much anything neuro)
What can cause sx of TIA?
migraines
seizures
non-neuro conditions (cardiac arrhythmia, hypoglycemia in elderly)
Describe the criteria to label sx as a TIA
neuro deficit less than 24 hours caused by temporary brain ischemia
more typical is less than 10 minutes (more–>permanent cell death)
TIAs that last longer than 1 hour are d/t what?
small infarcts
complete recovery can occur within 1 day
Are TIAs a neurological emergency?
yes!!!
warning sign for potentially larger ischemic injury to the brain
Why do TIAs need emergent evaluation?
15% TIAs will have full on stroke–> persistent defects within 3 months
half of those patients have stroke within first 48 hours
How does a TIA happen?
embolus temporarily occludes then dissolves
in situ thrombus formation
vasospasm
ALL TEMPORARY
What are the 2 types of strokes?
hemorrhagic (red, emboli)
–> intracerebral or subarachnoid hemorrhage secondary to reperfusion of damaged vessels (directly via collateral or dissolution of occlusion)
ischemic (pale/anemia, thrombus)
–> no blood, however can have hemorrhagic conversion if fragile vessels rupture
What causes an ischemic stroke?
inadequate blood supply–> infarction/death of brain tissue
emboli (formed elsewhere, moves), thrombi (local formed) in large vessel or small vessel, lacunar infarcts
Lacunar infarcts are associated with _________
HTN
Lacunar infarcts affect that arteries?
lenticulostriate arteries
What does malignant HTN cause in the CNS?
hypertensive encephalopathy
deep brain parenchymal hemorrhages
What causes vascular dementia and what are the sx of it?
malignant HTN
dementia, gait abn, pseudobulbar signs (sudden uncontrollable laughing/crying)
What is binswanger disease?
large area of subcortical white matter with myelin and axon loss
caused by HTN
What are Charcot-Bouchard Microaneurysms?
CHRONIC HTN
minute aneurysms in basal ganglia
Cerebral amyloid angiopathy (CAA) is associated with Alzheimer’s and ______
hypertensive lobar hemorrhage
amyloid deposits in wall of vessels–> microbleeds
What is CADASIL?
Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy
recurrent strokes and dementia around 35 years (younger than infarcts just d/t HTN)
NOTCH 3 gene
PAS+
What are stroke risk factors?
HTN DM HLD smoking family hx valvular dz, a-fib, PFO prior hx hypercoag
What is the most frequent cause of the most clinically significant hemorrhage?
Saccular/berry aneurysm in ANTERIOR circulation most common—> subarachnoid hemorrhage
What is a basilar subarachnoid hemorrhage?
fusiform rupture
d/t atherosclerosis of circle of willis
Are aneurysms present at birth?
no
develop over time d/t defect in media of vessel (usually at bifurcations)
What age is most common for aneurysms to rupture?
50s
more frequent in females
(over 10mm have 50% risk of bleeding per year)
What are situations where aneurysms can rupture?
if over 10mm–> 50% chance of bleeding per year
1/3 d/t increased ICP:
straining at stool
orgasm
The worst headache I’ve ever had corresponds to________-
ANEURYSM–> subarachnoid hemorrhage
What is the prognosis of aneurysm with subsequent subarachnoid hemorrhage?
25-50% with first rupture
repeat bleeding common in survivors
first few days after hemorrhage, increased risk for vasospam (brain doesn’t like blood there, so causes edema)–> more ischemic injury
Where are AV malformations in the brain?
subarachnoid space but can extend into brain tissue
more often occur in MCA and posterior branches
What are 4 principle routes of CNS infection?
blood–> most common (arterial, retrograde facial veins)
direct implantation–> trauma, congenital (meningomyelocele)
local extension-> teeth, sinuses
peripheral nervous system–> viruses (rabies, herpes zoster)
What produces CSF?
choroid plexus of lateral 3rd and 4th ventricles
exchanged every 3-4 hours
Does the CSF have lymphatics?
NO, in epidural space
How do herpes simplex and zoster spread to brain?
latent in sensory ganglia, replicate in schwaan cells and ascent within sensory nerves to brain
How does rabies spread to brain?
bind near acetylcholine receptors at NMJ, ascend to brain via motor nerves
Infections of retropharyngeal, peritoneal or mediastinal spaces may produce ________ via spread through epidural lymphatics
spinal epidural abscesses
Tuberulous meningitis develops by ______
seeding CSF from subepidural or submeningeal GRANULOMAS
What is an important anatomical feature that prevents most antibiotics, immunoglobulins and complement from going into the brain?
capillaries (surrounded by astrocyte foot processes that make BBB)
What causes aseptic meningitis?
acute or subacute viral infection
What causes chronic meningitis?
TB
spirochetes (neurosyphilis, neuroborreliosis)
cryptococcus
What is pyogenic meningitis and what can cause it?
suppurative exudate that covers brainstem and cerebellum
thickened leptomeninges
TB or neurosyphilis
What happens to the BBB in cerebral edema?
lost
How does cerebral edema develop?
accelerated by products of living bacteria and abx-lysed bacteria
How to slow/reverse cerebral edema
corticosteroids
Sx of acute suppurative meningitis
ha
meningeal irritation signs (Kernig, Brudzinski)
high fever
confusion and coma
Brudzinski sign
lift head, legs come up with it
meningitis test
Kernig sign
supine, flex leg at hip and knee
try to extend leg while hip is flexed–> + is pain or spasm in hamstring
Where would you see pus from meningitis in the brain?
follows subarachnoid space in sulci (near vessels)
Pneumonococcal meningitis vs H influenzae exudate location
Pneumo: over convexities near sagittal sinus
H influ: basal location
What fills what space when you have a suppurative/bacterial meningitis?
neutrophils fill subarachnoid space
What is focal cerebritis?
inflammatory cells infiltrate veins and go from subarachnoid space down into brain parenchyma
What is ventriculitis?
infection of brain that extends into ventricles
What is phelbitis?
venous thrombi–> hemorrhagic infarcts of brain
Leptomeningeal (between arachnoid and pia where CSF flows) fibrosis leads to _______
hydrocephalus
Pneumococcal meningitis can cause __________
chronic adhesive arachnoiditis (thick d/t capsular polysaccharide of bacteria–> gel-like)
Complications of bacterial meningitis
seizures
encephalitis
hearing loss, blindness, paralysis
meningococcemia and rash
–> adrenal hemorrhage and
death
——–> AKA Waterhouse-Friderichsen Syndrome
LP gram stain: gram negative diplococci
Neisseria meningitidis
LP gram stain: gram positive diplococci
Strep pneumoniae (#1 cause meningitis)
LP gram stain: gram negative pleomorphic
Haemophilus influenzae
LP gram stain: gram positive cocci
Staph aureus
Staph epidermidis
Strep
LP gram stain: gram negative bacilli
E coli
others
Where to perform LP
between L3 and L4
CSF findings in bacterial meningitis
very increased neutrophils (over 100)
very decreased glucose (half serum level)
increased protein
cloudy/turbid
CSF findings in viral meningitis
increased lymphocytes (may see neutrophils early on)
increased protein (not as much as bacterial)
clear/colorless
normal glucose
Who is at increased risk of meningitis?
below 5 or above 60
DM
immunosuppressed/HIV
contiguous infection (like sinusitis that can retrograde)
IV drug abuse
bacterial endocarditis
sickle cell anemia
Common causes of acute meningitis in neonate
E coli
Group B Strep
Common causes of acute meningitis in 3m-2 year UNVACCINATED kids
H influenze type B
Common causes of acute meningitis in adolescents and YA
Neiserria meningitidis
Common causes of acute meningitis in elderly
Strep pneumo
Listeria monocytogenes
What are examples of acute focal suppurative infections?
brain abscess
subdural empyema
extradural abscess
Describe how a brain abscess forms
same route as meningitis:
endocarditis–> multiple
abscesses
R–>L shunt
bronchiectasis
immunosuppression
strep and staph in non-immuno
Brain abscess sx
progressive focal neuro deficits
increased ICP signs
LIQUEFACTIVE NECROSIS
CSF of brain abscess
high WBC
high protein
normal glucose
Complications of brain abscess
rupture with ventriculitis or meningitis, venous sinus thrombosis
Treatment for brain abscess
surgical drainage and abx
What is a subdural empyema?
bacteria/fungal infection of skull bones OR sinuses that spread to subdural space
What is evidence of a subdural empyema?
thickened dura
What is the sx and CSF findings of subdural empyema?
same as abscess
- -> progressive focal neuro def
- -> increased ICP signs
- -> high WBC, protein, normal glucose
Treatment for subdural empyema
surgical drainage
Sx of untreated subdural empyema
focal neuro signs, lethargy, coma
What are extradural abscesses usually associated with?
osteomyelitis
What can extradural abscess cause?
cord compression if in spine–> neuro emergency
What can you see with subdural empyema?
thrombophlebitis of bridging veins–> infarct
How does Neisseria meningitidis colonize?
colonizes oropharynx of asymptomatic carriers
spread via direct contact with respiratory secretions
occurs in 2-3% of healthy individuals
Where is there a higher proportion of Neisseria?
crowded populations–> dorms, barracks, prisons
Clinical sx of neisseria meningitidis
rapidly progressive septicemia with F, hypotension, IDC, petechial and purpuric lesions
purpura fulminans can occur–> gangrene in distal limbs
Waterhouse-Friderichsen syndrome: hemorrhagic infarction of adrenal glands with above sx
What gram stain is Neisseria and where is it located?
gram negative diplococci
in and out of cells
CSF of chronic meningitis
elevated protein
lymphocytes
low glucose
How do you diagnose chronic meningitis?
meningitis sx and CSF findings progress for at least 4 weeks
What causes chronic meningitis?
TB
Neuroborreliosis (lyme disease)
Neurosyphilis
Where does mycobacterium tuberculosis cause chronic meningitis?
subarachnoid space with gelatinous or fibrinous exudate
likes base of brain, obliterates cisterns and encases cranial nerves–> arachnoiditis, hydrocephalus, CN sx
What is a tuberculoma?
well-circumscribed intraparenchymal mass with central caseous necrosis
may calcify
see with mycobacterium tb chronic meningitis
What bacteria can you see obliterative endarteritis with?
mycobacterium tb (chronic meningitis)
What bacteria can you see with acid-fast stain?
mycobacterium TB
Describe sx and CSF seen in chronic meningitis caused by borrelia burgdordferi
AKA lyme disease
neuro sx follow rash by 4 weeks (central clearing/bullseye)
CN palsy and peripheral neuropathies
CSF have antibodies, see with PCR
Ab cross-react with infectious mono, RA, SLE, syphilis (cause false +)
What is neurosyphilis and how many patients develop it?
TREPONEMA PALLIDUM
tertiary stage, only 10% of untreated syphilis patients develop it
What is meningovascular neurosyphilis?
chronic meningitis that involves the base of the brain and causes communicating hydrocephalus
will see obliterative/Heubner endarteritis
What is paretic neurosyphilis?
Delusions of grandeur with severe dementia (general paresis of the insane)
perivasuclar iron deposits
hydrocephalus with granular ependymitis
Describe tabes dorsalis
damage to sensory nerves in dorsal roots d/t neurosyphilis
loss of pain sensation, ataxia, joint damage with lightening pains (Charcot joints)
absence of deep reflexes
What is treponema pallidum?
spirochete
causes syphilis
What causes 80% of aseptic meningitis?
enteroviruses
Describe aseptic meningitis
no recognizable organism with meningeal irritation, F, altered LOC, relatively acute onset
less fulminant c/t bacterial
CSF findings in aseptic meningitis
lymphocytic pleocytosis
moderate increase in protein
normal glucose
Treatment for aseptic meningitis
self-limiting
symptomatic tmt
How do viruses enter the CNS and cause meningitis and encephalitis?
via blood
nerves (olfactory, trigeminal sensory or motor nerves)
brain mounts response with lymphocytes that have been sensitized by the virus
latency
What causes epidemic encephalitis?
arthropod-borne (mosquito vectors) viruses
What causes a polio-like syndrome with paralsysi?
West Nile virus
CSF of West Nile
colorless
slight increased pressure
increased protein
normal glucose
starts out with neutrophils–> rapidly progresses to lymphocytes
Histology seen in West Nile encephalitis
multiple foci of necrosis in white and gray matter
neuronophagia (microglia around dying neuron)
microglial nodules (aggregate around necrosis)
HSV-1 is seen in who?
children and young adults
What effect does HSV-1 have on the brain?
necrotizing and hemorrhagic changes to inferior and medial TEMPORAL lobes in kids and young adults
also orbital gyri of frontal lobes
What intranuclear inclusions are seen with HSV-1 infection?
Cowdry type A in neurons and glia
HSV-2 infection of CNS is seen in who?
neonates born via vaginal delivery to moms with active HSV-2
What does HSV-2 do to the brain?
in neonates (vag delivery with infected mothers)–> severe encephalitis
Where is herpes zoster latent?
sensory or dorsal root of trigeminal ganglia
Reactivation of herpes zoster causes ________
shingles
single or limited dermatome
What is persistent postherpetic neuralgia syndrome?
persistent pain following nonpainful stimuli
seen in shingles: skin brushed with clothing is painful
Where is cytomegalovirus found?
fetuses and AIDS patients
What is the histology of CMV found in utero?
periventricular necrosis–> severe brain destruction–> microcephaly and periventricular calcification
What does CMV cause in AIDS/immunocompromised patients?
subacute encephalitis (localizes in paraventricular subependymal regions)
can also see radiculoneuritis in lower spinal cord and roots
What inclusions are seen with CMV?
intracytoplamic and intranuclear
prominent enlarged cells
Sx of poliomyelitis
mononuclear cell perivascular cuffs and neuronophagia of anterior horn motor neurons–> FLACCID PARALYSIS
What is post-polio syndrome?
25-35 years later: decreased muscle mass and pain
What is the incubation period for rabies?
Lyssavirus of rhabdoviridae family
1-3 months
How does rabies infect/cause sx?
ascend along peripheral nerves from wound–> negri bodies in purkinje cells
*paresthesia around wound is diagnostic sx (pins and needles)
nonspecific sx: malaise, ha, fever
flaccid paralysis, respiratory center failure
hydrophobia (foaming at mouth, aversion to swallowing)
What can HIV cause in CNS?
aseptic meningitis within 1-2 weeks of seroconversion
dementia
primary CNS lymphoma
IRIS (immune reconstitution inflammatory syndrome) after antiviral therapy, paradoxical exacerbation of sx from opportunistic infections
Histology of HIV aseptic meningitis
acute: perivascualr inflammation
chronic: microglial nodules with multinucleated giant cells
white matter: pallor, axonal welling, gliosis
What is progressive multifocal leukoencephalopathy (PML)?
via JC polyomavirus (reactivated during immunosuppression)
affects oligodendrocytes–>demyelination
exclusively in IMMUNOSUPPRESSED people
subcortical area of demyel with lipid-laden macrophages in center (decreased # of axons)
What is subacute sclerosing panencephalitis (SSPE)?
paramyxovirus
progressive cognitive decline, spasticity of limbs, seizures
children or YA that aren’t immunized: months to year after measles (rubeola) in youth
Histology of subacute sclerosing panencephalitis (SSPE)
widespread gliosis and myelin degeneration
viral inclusions (paramyxovirus/measles)
neurofibrillary tangles
What is fungal meningoencephalitis caused by?
candida albicans
mucor
aspergillus
–> ALL vascular invasion
cryptococcus
–>AIDS
What causes fungal meningoencephalitis in DM patients?
mucormycosis
What does cryptococcus look like on histo?
soap bubbles
CSF finding of cryptococcal polysaccharide antigen points to what diagnosis?
chronic meningitis caused by cryptococcus neoformans
AIDS, immunosuppressive therapy
shows up on india ink stain
What CNS infector is huge in HIV and pregnant patients?
toxoplasmosis gondii
What does toxoplasmosis gondii cause in CNS?
brain abscess near gray-white junction and deep gray nuclei
central foci of necrosis with petechial hemorrhages and vascular proliferation
free tachyzoites and encysted bradyzoites at periphery of necrosis
What is the brain-eating ameba?
naegleria fowleri
contaminates when water enters brain through nose
warm freshwater and soil
What ameba causes chronic granulomatous meningoencephalitis?
acanthamoeba
What does plasmodium falciparum (parasite) cause?
long-term cognitive defects if survive
type of malaria
What causes Creutzfeldt-Jakob disease?
prion (PRP)
Describe sx of Creutzfeldt-Jakob disease
rapidly progressive neurodegen disorder–> dementia
spongiform change with intracellular vacuoles
Mad cow disease is
Creutzfeldt-Jakob disease
Bovine spongiform encephalopathy was seen where?
UK in young adults, 1995
slower progression c/t CJD
kuru plaque (congo red and PAS+ )
When do you see CJD?
70s
iatrogenic
rapidly progressive dementia with myoclonus
7 month survival
little evidence of brain atrophy but have microscopic spongiform changes
Describe fetal familial insomnia
sleep disturbances cause this
less than 3 year survival
ataxia, autonomic disturbances, stupor
