Vascular Neurology Flashcards
transient ischemic attack (TIA)
defined as a transient episode (<24 hours) of neurologic dysfunction caused by focal ischemia, without acute infarction
ABCD2 score
used to predict 7 day risk for stroke after TIA
Age, Blood pressure, Clinical features, Duration of TIA, Diabetes
No points: Age <60, BP <140/90, Clinically no speech deficit or unilateral weakness, duration <10 mins, no diabetes
1 point: Age >/=60, BP >/= 140/90, speech deficit without unilateral weakness, duration 10-59 mins, + diabetes
2 points: unilateral weakness, >/= 60mins
7 day risk of stroke based on ABCD2 score`
0-3 points: 1.2%
4-5 points: 5.9%
6-7 points: 11.7%
what does ABCD2 score not include
does not take into account severe carotid or intracranial stenosis which is also a risk for ischemic stroke after TIA
ischemic stroke subtypes
large-artery atherosclerosis
cardioembolism
lipohyalinosis/small-vessel disease
stroke of other undetermined etiology
stroke of undetermined etiology
large-artery atherosclerosis
most common cause of ischemic stroke in the world
patients will either have significant stenosis or occlusion of a major brain artery or branch cortical artery
symptomatic carotid
stenosis of the common carotid ipsilateral to a TIA or infarct
treatment for symptomatic carotid
carotid endarterectomy (CEA) or carotid artery stent (CAS) is indicated if the stenosis is 50-99% in men or 70-99% in women
asymptomatic carotid stenosis should be treated surgically if the stenosis is 80-99%
CEA has a higher risk of periprocedural myocardial infarction
CAS has a higher risk of periprocedural stroke
treatment with CEA or CAS can lead to cerebral hyperfusion syndrome
cerebral hyperfusion syndrome
presents with headaches, visual disturbances, and seizures
occurs secondary to dysautoregulation of cerebral vessels in regions which have been in chronic low flow states
cardioembolism
most common cause of ischemic stroke in the US
patients can present similarly with comparable imaging to those with large artery atherosclerosis but will have a cardiac source for the embolic phenomenon
sources of cardioembolism
atrial fibrillation, mechanical heart prosthetic valve, left atrial or ventricular thrombus, recent myocardial infarction, dilated cardiomyopathy, valvular heart disease, structural heart defects, tumors
CHA2DS2-VASc score
helps to calculate risk of stroke in patients with untreated atrial fibrillation
CHF, Hypertension, Age (>/=75), Diabetes, Stroke or TIA history, Vascular disease, Age (65-74), Sex category
CHA2DS2-VASc scoring
0 points: no CHF, BP </= 140/90, no diabetes, no history of stroke or TIA, no vascular disease, age <65, male
1 point: yes CHF, BP >140/90, yes diabetes, yes vascular disease, age 65-74, female
2 points: age >/= 75, yes stroke or TIA history
lipohyalinosis/small-vessel disease
commonly occurs in the lenticulostriate vessels of deep cortical structure
also known as lacunar strokes that are felt to be related to chronic hypertension, diabetes, and smoking
hypercoagulable states and coagulopathy
examples: Factor V Leiden, antiphospholipid antibody syndrome, protein S/C deficiency, prothrombin gene mutation, antithrombin III syndrome, sickle cell disease, thrombotic thrombocytopenic purpura (TTP), polycythemia, hyperhomocysteinemia, MTHFR gene mutations, and malignancy
more likely to cause venous events than arterial
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL)
autosomal dominant disease due to a mutation of the NOTCH3 gene on chromosome 19 leading to a vasculopathy affecting the small to medium-sized arteries of white matter
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) presentation
patient will present with recurrent stroke, headaches, seizures, and cognitive defects
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) pathology
granular osmiophilic material (GOM) in the basal lamina of small cutaneous arterioles on electron microscopy or will be PAS-positive and congo-red negative on staining
cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) imaging
scattered bihemispheric T2 FLAIR hyperintense lesions
CNS Vasculitis
caused by a diverse spectrum of diseases that typically involves the gray/white matter junction
CNS Vasculitis DWI
multiple small focal areas of acute infarction in multiple vascular territories
CNS vasculitis vessel imaging
marked beading and segmentation alongside numerous arterial structures
primary angiitis of the CNS (PACNS)
vasculitis confined only to the small-medium sized blood vessels in the brain, spinal cord, and meninges
moyamoya disease
congenital moyamoya disease is seen most often in patients of Asian descent
Mysterin/RNF213 is a susceptibility gene for congenital moyamoya
secondary causes of moyamoya
head/neck radiation, sickle cell disease, neurofibromatosis, and prothrombotic disorders
moyamoya on angiogram
abnormal vascular pattern of small net-like lenticulostriate vessels characterized as a “puff of smoke” with severe stenosis or occlusion of the distal internal carotid arteries
moyamoya pathology
large vessel thickening of the intima, small overgrown dilated small arteries, and regions of ischemic and/or hemorrhagic infarct
arterial dissection
due to a tear of the vessel wall intima leading to a formation of a false lumen
arterial dissection symptoms
head/neck pain and Horner syndrome
ischemic events occur due to thromboemboli formation and less often cerebral hypoperfusion
arterial dissection common
common cause of stroke in the young
should be considered in a patient with a history of neck trauma chiropractic neck manipulation/high-velocity neck injury, or connective tissue disease (fibromuscular dysplasia, Marfan syndrome, Ehlers-Danlos)
arterial dissection on imaging
often extracranial and vessel imaging may show a “string sign” or flame-shaped occlusion in the are of dissection
patent foramen ovale (PFO)
seen in roughly 20% of people and its presence alone is not a strong risk factor for ischemic stroke. PFOs shouldn’t be considered as an etiology for stroke unless a patient presents with a cryptogenic embolic stroke
- lesions that are large, have a significant right to left shunt or are accompanied by an atrial septal aneurysm have a higher risk of recurrent stroke
PFO standard of care for secondary stroke prevention
antiplatelet therapy
recent data suggests that surgical PFO closure for those with high-risk features reduces the risk of recurrent stroke, and should be considered if patient is <60 years of age
PFO closure in young stroke patients decreases the risk of secondary stroke
air embolus
entry of air into the vasculature can be related to surgery, trauma, intravascular catheters, and barotrauma
if CTH performed promptly after insult, air can be seen within the cerebral vessels
treatment includes emergent use of hyperbaric oxygen chamber, but the prognosis is often poor
fat embolism syndrome (FES)
occurs secondary to long bone or pelvic fractures leading to the release of fatty bone marrow into the systemic circulation
emboli obstruct pulmonary arteries leading to respiratory distress
microemboli can pass through the pulmonary circulatory system and extend into the systemic arterial system and brain leading to small, randomly distributed ischemic strokes
hypoperfusion
can cause watershed regions between major vascular territories to become ischemic
hypoperfusion on imaging
ischemia along border zone regions of the ACA-MCA and MCA-PCA territories
bilateral ACA-MCA border zone infarcts
man in the barrel syndrome: upper extremity paralysis with retained strength in lower extremities
bilateral MCA-PCA border zone infarcts
Balint’s syndrome: simultagnosia, oculomotor apraxia, and optic ataxia
mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS)
mitochondrial disease caused by a mitochondrial DNA mutation to the gene MT-TL1
MELAS symptoms
ischemic strokes, seizures, and headaches present before the age 40
MELAS testing
reveals elevated CSF lactate levels, serum lacic acidosis, and ragged red fibers on muscle biopsy
drugs/toxins that cause stroke
cocaine and amphetamines
stroke of undetermined etiology
diagnosis that is given to patients in which a cause of stroke cannot be determined with any degree of confidence
many patients with stroke of undetermined etiology will ultimately be found to have paroxysmal atrial fibrillation with prolonged heart monitoring
stroke risk factors
hypertension is the most important risk factor
others include diabetes, smoking, and hyperlipidemia
pathology of ischemic stroke
brain ischemia leads to excessive extracellular glutamate. this leads to hyperexcitation of neurons and activation of an apoptotic cascade that leads to cell death
gross pathology of stroke
acutely: swelling with effacement of the gray-white junction and cracking at the interface between the intact and infarcted brain tissue
over time: infarcted tissue becomes sharply demarcated and is eventually replaced by a cavity
micropathology of stroke
initially no changes on H&E stain for the first 8 hours
in the following days, hypereosinophilic anoxic neurons, also known as red dead neurons, develop
in the following weeks, the lesion undergoes liquefaction as macrophages enter the space and ingest necrotic tissue
thereafter, astrocytes will form a glial scar around the infarct. this is completed in the proceeding months after an ischemic insult
acute treatment of stroke
tissue plasminogen activator (tPA)
tenecteplase (TNK)
tissue plasminogen activator (tPA)
works by transforming plasminogen into plasmin, leading to fibrinolysis of clot
can be given within 4.5hrs from the time of last seen well
tenecteplase (TNK)
modified form of human tPA
EXTEND-IA TNK study showed that TNK was associated with a higher rate of reperfusion and better functional outcome than alteplase in patients with large vessel occlusions (LVO)
many institutions are transitioning from alteplase to TNK for acute IV thrombolytic therapy in patients with acute ischemic stroke
when to start aspirin and DVT prophylaxis after IV thrombolytics
24 hours as long as CT head shows no hemorrhagic conversion of an ischemic stroke
absolute IV thrombolytic exclusion criteria
ischemic stroke or severe head trauma in the previous three months
previous intracranial hemorrhage
history of intracranial neoplasm
GI malignancy or hemorrhage in the previous 21 days
intracranial or intraspinal surgery within the previous 3 months
subarachnoid hemorrhage
blood pressure >/=185 systolic or >/=110 diastolic
active internal bleeding
aortic arch dissection
acute bleeding diathesis, including but not limited to conditions defined as “hematologic”
platelet count <100,000/mm
current anticoagulant use with an INR >1.7, PT >15 secs, or aPTT >40secs
LMWH use within 24 hours for PE or DVT (not at prophylactic doses)
direct thrombin inhibitor, direct factor Xa inhibitor, or glycoprotein IIb/IIIa receptor inhibitor use
evidence of hemorrhage on CT head
extensive regions of hypodensity consistent with irreversible ischemic injury
relative IV thrombolytic exclusion criteria
minor rapidly improving symptoms
serum glucose <50mg/dL
serious trauma or major surgery in the previous 14 days
history of GI bleeding or GU bleeding
seizure at stroke onset
pregnancy
arterial puncture at a noncompressible site in the previous 7 days
large (>/=10mm), untreated, unruptured intracranial aneurysm
intracranial vascular malformation
intra-arterial therapy (IAT)
while initial trials (REVASCAT, SWIFT PRIME, EXTEND-IA, and ESCAPE) showed a benefit from mechanical thrombectomy in the first 6 hours of last seen well, more recent trials (DAWN and DEFUSE 3) have shown benefit up to 24 hours from last seen well in select patients
- patients who undergo IAT should have a LVO seen on CTA/MRA
IAT of unclear or prolonged last known well
should have CT perfusion or MRI perfusion scan to identify the area that has already infarcted (the “core”) and the are that is at risk of infarction but is not yet dead (the “penumbra”)
- good candidates for IAT have a small or no core and a significantly larger penumbra
on CT perfusion:
- low cerebral blood volume (CBV) and high mean transit time (MTT) suggests dead (core) tissue
- normal or high blood volume and high mean transit time (MTT) suggests at-risk tissue (penumbra)
secondary complications of ischemic stroke
malignant edema
hemorrhagic conversion
reperfusion injury
malignant edema
3-5 days after an ischemic event, large strokes will develop significant space-occupying cytotoxic edema which can lead to compression of normal tissues, hydrocephalus, and/or herniation
- treatment with hyperosmolar therapy (HTS and/or mannitol) can reduce edema, it is only a temporizing measure
herniation syndromes
transtentorial, subfalcine, tonsillar, ascending, and extracranial
complete MCA territory infarcts can lead to
transtentorial herniation and brainstem compression
- decompressive hemicraniectomy is a life-saving intervention but has on effect on the outcome of long-term neurological deficit, based on HAMLET, DECIMAL, and DESTINY trials
cerebellar strokes can lead to
ascending herniation, tonsillar herniation, and compression of the brainstem and the 4th ventricle, which may cause non-communicating hydrocephalus
- suboccipital decompressive craniectomy will reduce swelling to allow the re-emergence of normal CSF flow
hemorrhagic conversion
bleeding into the infarct bed is felt to be secondary to failure of vascular integrity
reperfusion injury
seen secondary to reperfusion of ischemic tissues due to effective thrombolytic or intervascular therapies
re-introduction of oxygen (via blood) to injured neurons with mitochondrial dysfunction leads to the formation of free radicals and eventual neuronal apoptosis and further damage
no proven effective neuroprotectant therapies
secondary stroke prevention
includes management of major risk factors such as diabetes, hyperlipidemia, hypertension, tobacco use, and utilization of antiplatelet and/or anticoagulation therapy
- HTN most common risk factor for stroke
antiplatelets
aspirin
clopidogrel
aspirin mechanism of action
irreversible cyclooxygnase (COX1»_space; COX2) inhibition which leads to inhibition of platelet aggregation and secretion by preventing the synthesis of prostaglandins and thromboxane A2
clopidogrel mechanism of action
adenosine diphosphate (ADP) (P2Y12) receptor inhibitor and is converted to its active metabolite by the cytochrome P450 system
clopidogrel metabolism
minority of patients with CYP genetic variants are poor metabolizers of clopidogrel, and thus will have inadequate antiplatelet function (i.e. inadequate conversion of clopidogrel to its active form)
omeprazole inhibits CYP and increase risk of inadequate clopidogrel activity and should be changed to an alternative to prevent increase in stroke risk
clopidogrel adverse effects
can rarely cause thrombotic thrombocytopenic purpura (TTP)
aspirin and clopidogrel
more effective than monotherapy for secondary stroke prevention after ischemic stroke in the first 90 days after stroke with intracranial atherosclerosis and likely for TIAs/mild strokes as well
anticoagulants
vitamin K antagonists: warfarin
novel oral anticoagulants (NOACs)
warfarin
used to be first-line therapy for secondary stroke prevention for ischemic strokes caused by atrial fibrillation, however now there are newer options
- still first line for strokes caused by valvular atrial fibrillation
warfarin mechanism of action
related to the inhibition of the production of Vitamin K-driven coagulation factors: II, VII, IX, and X
warfarin monitoring
requires periodic INR checks to maintain a “goal” level.
Typical goal si 2.0-3.0 but varies by circumstance
warfarin reversal
indicated in settings of intracranial or severe systemic bleeding
- Vitamin K replacement takes 6-24 hours to correct the INR
- fresh frozen plasma takes 12 to 32 hours for complete reversal
- prothrombin complex concentrate (PCC) takes only 15 minutes
anticoagulants and the dentist
holding anticoagulants, like warfarin, prior to minor dental procedures increases the risk of acute thrombotic events and doesn’t significantly reduce risk of bleeding complications
novel oral anticoagulants (NOACs)
direct thrombin inhibitors (dabigatran) or factor Xa inhibitors (rivaroxaban and apixaban)
NOACs efficacy
been shown to have comparable or superior efficacy in secondary stroke prevention and lower risks of bleeding complications when compared to warfarin
- apixaban was superior to warfarin in preventing stroke in nonvalvular atrial fibrillation and associated with lower bleeding and mortality risks (ARISTOTLE trial)
NOAC monitoring
do not require INR/PT checks and have fewer drug interactions than warfarin
- dabigatran activity can be assessed by checking thrombin time
- rivaroxaban/apixaban activity can be assessed by checking anti-factor Xa
NOAC in valvular atrial fibrillation
not indicated for valvular atrial fibrillation
warfarin is drug of choice
NOAC Reversal agents
idarucizumab: monoclonal antibody approved in 2015 for reversal of dabigatran
andexanet alfa: recombinant modified factor XA protein approved in 2018 for the reversal of rivaroxaban and apixaban
HAS-BLED score
used to assess the risk of hemorrhage for a patient who will start anticoagulation
- score >2 considered “high risk” but does not make anticoagulants contraindicated
- includes Hypertension, Abnormal renal/liver, Stroke history, Bleeding history, Labile INR, Elderly, “Drug” use
HAS-BLED scoring
0 points: </= 160 systolilc, normal renal/liver, no stroke history, no bleeding history, no labile INR, age </= 65, no aspirin, clopidogrel, NSAIDs, and <8 alcoholic drinks/week
1 point: >160 systolic, Renal (Cr>2.26) or liver disease, positive stroke history, positive bleeding history, High INR <60% time in therapeutic range, age >65, aspirin, clopidogrel, or NSAID use but <8 alcoholic drinks per week
2 points: renal and liver disease, aspirin, clopidogrel, or NSAID use AND >/= 8 alcoholic drinks per week
CNS hemorrhagic lesions
intraparenchymal hemorrhage
subarachnoid hemorrhage
subdural hematoma
epidural hematoma
intraparenchymal hemorrhage causes
trauma, hypertension, cerebral amyloid angiopathy, vascular malformations, cavernous malformation, charcot-bouchard aneurysms, brain tumor, CNS infection, other
trauma causing IPH
parenchymal contusions are a form of TBI where multiple microhemorrhages are found on the interface between brain and bone
coup contusions occur beneath the site of impact
countrecoup contusions occur on the opposite side of impact
patients will often have concurrent skull or maxillofacial fracture
- racoon eyes, battle sign
hypertension causing IPH
most common cause of nontraumatic IPH
High blood pressure leads to rupture of small brittle blood vessels
lesions are located in the deep cortical matter and brainstem
cerebral amyloid angiopathy causing IPH
second most common cause of nontraumatic brain hemorrhage
typically presents over age 60 with superficial lobar hemorrhages and cortical superficial siderosis
also at risk of TIA-like attacks called “amyloid spells” aka transient focal neurologic episodes (TFNEs) and felt to be secondary to cortical irritation from blood products
- differentiated from TIA based on blood products seen on neuroimaging
CAA patients and Alzheimer’s disease
patients with Alzheimer’s disease more likely to have CAA
CAA imaging
multiple small silent cerebral microhemorrhages
CAA pathology
congophilic waxy pink material (amyloid) in cortical and leptomeningeal arteries with apple-green birefringence
Arteriovenous malformation (AVM)
most likely vascular lesion to cause catastrophic morbidity/mortality
characterized by large abnormal arteries with surrounding thick-walled “arterialized” veins due to high luminal pressures
AVM diagnosed
best appreciated on angiogram
AVM pathology
arteries with fragmentation and reduplication of the elastic layer and thick-walled veins with a thin elastic layer
AVM complications
intraparenchymal bleeds more common, superficial lesions may bleed into the subarachnoid space
cavernous malformation (CM)
also called cavernous hemangiomas or cavernomas
much less likely to cause catastrophic bleed as compared to AVMs
cavernoma epidemiology
commonly seen in young adults and can be either sporadic or familial
CCM1 on chromosome 7q causes familial CMs in those with Hispanic heritage
cavernoma symptoms
focal neurologic deficits secondary to hemorrhage or seizure
- if associated developmental venous anomaly (DVA) there is a higher risk of hemorrhage
cavernoma imaging
irregular partially calcified mass with a “popcorn apperance”
cavernoma pathology
dilated, closely juxtaposed, thin-walled capillaries and a ring of hemosiderin consistent with remote microhemorrhages
Charcot-Bouchard aneurysms
associated with chronic hypertension, these lesions are located on small lenticulostriate arteries
rupture leads to deep cortical intraparenchymal bleeds
brain tumor and IPH
atypical IPHs and/or patients with history of cancer should have an MRI of the brain with and without contrast to evaluate for tumor
metastatic tumors that are likely to bleed
melanoma, renal cell carcinoma > choriocarcinoma, thyroid (papillary) carcinoma > lung, and breast
glioblastomas are highly vascularized primary CNS tumors that can bleed
CNS infection and bleeding
tends to occur in the temporal lobes, i.e. herpes encephalitis
other causes of IPH
hemorrhagic conversion of an ischemic stroke
venous infarct
vasculitis
coagulopathy
anticoagulants
treatment of IPH
BP regulation: SBP 140-160
reversal of anticoagulation
- if intracranial bleeding occurs with warfarin/NOAH use, treatment can be restarted ~7-30 days after the injury if the patient is at a high risk for ischemic stroke based on the CHA2DS2-VASC score
consideration for surgical intervention if a vascular malformation is found
subarachnoid hemorrhage presentation
complaint of thunderclap headache or “worst headache of my life”
- thunderclap means maximum intensity of the headache is reached in just seconds
- other symptoms include nausea/vomiting, meningismus, or syncope at symptom onset
SAH in acute setting
can be appreciated on CT but is not as sensitive as lumbar puncture in an acute setting
- LP should be considered in patients when suspicion of SAH is high but the CTH was negative
SAH complications
vasospasm is a serious complication that can cause multifocal infarctions or diffuse hypoxia/ischemia
- typically occurs between the 4th and 14th day after hemorrhage and may present with new focal neurologic deficits and drowsiness
- the oral calcium channel blocker nimodipine after SAH has been associated with better patient outcomes
causes of SAH
ruptured saccular/berry aneurysm
fusiform anuerysms
mycotic aneurysms
non-anuerysmal causes
ruptured saccular/berry aneurysm development
hemodynamic stress in high blood flow junctions leads to breakdown of the elastic lumina and eventual vessel outpouching and aneurysmal development
saccular aneurysm presentation
tend to be asymptomatic until they rupture and are the most common and morbid cause of SAH
saccular aneurysm locations
85% located in the anterior circulation (anterior communicating artery, posterior communicating artery, or bifurcation of MCA)
posterior circulation aneurysms found at the tip of the basilar artery
posterior communicating artery aneurysm
can cause compression of CN III leading to extraocular movement dysfunction and mydriasis secondary to dysfunction of superficial parasympathetic fibers
fusiform aneurysms
more common in posterior circulation vasculature
lesions are characterized as a dilation of the entire blood vessel and are less likely to rupture than berry aneurysms
mycotic aneurysms
secondary septic emboli from endocarditis
lesions are found in the distal branches of intracranial vessels and are best seen on angiography
- middle cerebral artery most commonly affected
non-aneurysmal causes of SAH
intracranial artery dissection, AVM, trauma, bleeding disorders, drugs, sickle cell disease, etc
superficial siderosis
chronic, slow, and intermittent SAH can lead to superficial siderosis
this is when there is chronic hemosiderin deposition of the brainstem, cerebellum, and cranial nerves leading to gliosis, neuronal apoptosis, and demyelination
symptoms of superficial siderosis
sensorineural hearing loss, cerebellar dysfunction, dementia, and pyramidal signs
superficial siderosis on imaging
widening of the cerebellar folia with atrophy and hemosiderin deposition
subdural hematoma (SDH)
due to tearing of the bridging veins from minor trauma, SDH is recognized as a blood collection between the dura and arachnoid space
SDH risk
elderly patients at higher risk due to brain atrophy
SDH on CT head
extra-axial, hyperdense (acute) or iso/hypodense (chronic), crescent-shaped blood that can cross suture lines but cannot cross the falx cerebri or tentorium cerebelli
epidural hematoma (EDH)
due to tearing of the middle meningeal artery caused by trauma/temporal bone fracture, EDH is recognized as a blood collection between the skull and dura
patients will usually have a history of recent head trauma with an initial asymptomatic period before a neurological decline (lucid interval)
EDH on CT head
biconvex shaped hyperdense extra-axial lesion that does not cross suture lines
aging hemorrhagic lesions: how to
compare the T1 and T2 brain MRI images and determine if the bleed is the same intensity as the brain parenchyma (isointense), hyperintense (“bright”), or hypointense (“dark”)
“I Bleed, I Die, Bleed Die, Bleed Bleed, Die Die” mnemonic
age of bleed <12 hours
T1 Isointense
T2 Bright
age of bleed 12-48 hours
T1 Isointense
T2 Dark
age of bleed 2-7 days
T1 Bright
T2 Dark
age of bleed 8-30 days
T1 Bright
T2 Bright
age of bleed >30 days
T1 Dark
T2 Dark
cerebral venous sinus thrombosis (VST) presentation
nonspecific and can include headache, seizures, decreased level of consciousness, nausea/vomiting, and papilledema and/or vision changes secondary to elevated intracranial blood pressures
- severe thrombosis can lead to hemorrhagic and less often ischemic strokes
VST causes
oral contraceptives, dehydration, hypercoagulable states, infection (meningitis, ENT infections), malignancy
- ear infections have been associated with transverse sinus thrombosis
VST imaging
CTV or MRV is imaging of choice, which would show filling defect in the venous system
digital subtraction angiography is the gold standard but not often required
CTH can show deep symmetric cortical hypodensities secondary to vasogenic edema
sagittal sinus thrombosis
can have empty delta sign where the contrast outlines the edges of the thrombus at the torcula on contrasted vessel imaging
on non-contrast CT it may appear as a triangular hyperdensity
VST management
heparin drip and aggressive IV fluid hydration
endovascular therapy has unclear utility but is sometimes used in patients with seizures and/or severe neurologic deficits
common post-stroke complications: acute
hemorrhagic transformation (ischemic stroke)
malignant edema
aspiration pneumonia (most common infection)
seizures
myocardial infarction, stress cardiomyopathy
urinary tract infections
deep venous thrombosis, secondary to immobility
common post-stroke complications: long-term
focal neurological deficits
dysphagia
depression, increased risk of suicide
post-stroke fatigue
epilepsy
hypoxic ischemic encephalopathy (HIE) presentation
can present secondary to cardiac arrest, drug overdose, drowning, etc
HIE on imaging
if severe, CT head will show generalized edema and loss of cortical sulcation while MRI will show diffuse restricted diffusion of the cortex and deep grey matter
HIE on EEG
variable patterns
favorable prognostic EEG findings are variability, reactivity to external stimuli, sleep patterns, and an increase in background frequencies
poor prognostic EEG findings are burst suppression, monorhythmic patterns, alpha coma (unless in the setting of reversible cause for coma such as metabolic dysfunction, sedative drugs, etc), generalized periodic discharges, and electrocerebral inactivity (ECI) defined as no EEG activity over 2 microvolts
