Vascular neurology requires an understanding of both neuroanatomy and vessel anatomy, as well as knowledge of up-to-date treatment protocols. This chapter review encompasses the pertinent information to excel with neurology exams. Real MRI, angiography, and gross specimens are available to aid in your study, and you may test your knowledge with our Question Bank and flashcards at the end!

Authors: Bradley Klein MD, Brian Hanrahan MD, Pouria Moshayedi MD

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Transient ischemic attack (TIA)

  • Defined as a transient episode (<24 hours) of neurologic dysfunction caused by focal ischemia, without acute infarction.
  • ABCD2 score is used to predict 7-day risk for stroke after TIA.
ABCD2 Score Table
ABCD2 Score Table
  • 7-day risk of stroke based on ABCD2 score:
    • 0-3 points: 1.2%
    • 4-5 points: 5.9%
    • 6-7 points: 11.7%

Ischemic stroke

Stroke subtypes (by TOAST criteria)

  • Large-artery atherosclerosis

    • The most common cause of ischemic stroke in the world.
    • Patients will have either 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.
      • 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, which presents with headaches, visual disturbances, and seizures. 
        • Occurs secondary to dysautoregulation of cerebral vessels in regions which been in chronic low-flow states.

  • Cardioembolism

    • The most common cause of ischemic stroke in the United States.
    • 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, etc.
 
L MCA Occlusion
L MCA Occlusion
    • The CHA2DS2-VASc Score helps to calculate the risk of stroke in patients with untreated atrial fibrillation.
CHA2DS2VASC Score Table
CHA2DS2VASC Score Table

  • Lipohyalinosis/small-vessel disease

    • Commonly occurs in the lenticulostriate vessels of deep cortical structure.
    • Also known as lacunar strokes, these are felt to be related to chronic hypertension, diabetes, and smoking.
Lacunar Stroke in Right Putamen
A relatively small cystic lesion in the putamen secondary to a lacunar ischemic stroke.

  • Stroke of Other Determined Etiology

    • Hypercoagulability 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.
        • Blood transfusions can decrease the risk of stroke in patients with sickle cell disease.
      • More likely to cause venous events than arterial.

    • Central nervous system (CNS) vasculitis
      • CNS vasculitis is a syndrome caused by a diverse spectrum of diseases that typically involves the gray/white matter junction.
      • Diffusion-weighted sequences on MRI will show multiple small focal areas of acute infarction in multiple vascular territories.
      • Vessel imaging will show marked beading and segmentation alongside numerous arterial structures.
        Primary CNS Vasculitis
        Primary CNS Vasculitis
      • 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 as a susceptibility gene for congenital moyamoya.
      • Secondary causes of Moyamoya disease include head/neck radiation, sickle cell disease, neurofibromatosis, and prothrombotic disorders.
      • Angiogram will show an 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 Disease
        Moyamoya Disease
      • Pathology:
        • Large vessel thickening of the intima, small overgrown dilated small arteries, and regions of ischemic and/or hemorrhagic infarct.
    • Arterial dissection
      • Dissections are due to a tear of the vessel wall intima leading to a formation of a false lumen.
      • Symptoms can include head/neck pain and Horner syndrome. Ischemic events occur due to thromboemboli formation and less often cerebral hypoperfusion.
      • A 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 syndrome).
      • Dissections are often extracranial and vessel imaging may show a “string sign” or flame-shaped occlusion in the area of the dissection.
        Right ICA Dissection
        Right ICA Dissection
    • Patent foramen ovale (PFO)
      • Seen in roughly 20% of people and its presence alone is not a strong risk factor for ischemic stroke. PFO’s 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.
      • While the standard of care for secondary stroke prevention in those with PFO is antiplatelet therapy, recent data suggest that surgical PFO closure for those with high-risk features reduces the risk of recurrent stroke, and should be considered if the patient is <60 years of age.
      • PFO closure in young stroke patients decreases the risk of secondary stroke. 
    • Air embolus
      • The entry of air into the vasculature can be related to surgery, trauma, intravascular catheters, and barotrauma.
      • If CTH is performed promptly after insult, air can be seen within the cerebral vessels.
      • Treatment includes emergent use of a hyperbaric oxygen chamber, but the prognosis is often poor.
    • Fat embolism syndrome (FES)
      • 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
      • Hypoperfusion can cause watershed regions between major vascular territories to become ischemic.
      • Imaging will show ischemia along border zone regions of the ACA-MCA and MCA-PCA territories.
        • Bilateral ACA-MCA border zone infarcts can cause “man in the barrel” syndrome: upper extremity paralysis with retained strength in lower extremities.
        • Bilateral MCA-PCA border zone infarcts can cause Balint’s syndrome: the triad of simultagnosia, oculomotor apraxia, and optic ataxia.
          Borderzone Infarcts
          Border zone Infarcts
    • Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like episodes (MELAS)
      • MELAS is a mitochondrial disease caused by a mitochondrial DNA mutation to the gene MT-TL1.
      • Symptoms of ischemic strokes, seizures, and headaches present before the age of 40.
      • Diagnostic testing will reveal elevated cerebral spinal fluid lactate levels, serum lactic acidosis, and ragged red fibers on muscle biopsy
    • Trauma
    • Drugs/Toxins
      • Common drugs that induce stroke include cocaine and amphetamines.

  • Stroke of Undetermined Etiology

    • A diagnosis that is given to patients in which a cause of a 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.

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
    • Acutely a gross examination will reveal 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
    • There will initially be 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)

    • Works by transforming plasminogen into plasmin, leading to fibrinolysis of the clot
    • Can be given within 4.5 hours from the time of last seen well.
    • Types include alteplase and tenecteplase.
    • Tenecteplase (TNK)
      • A modified form of human tissue plasminogen activator (tPA)
      • The 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
  • Ischemic stroke or severe head trauma in the previous three months
  • Previous intracranial hemorrhage
  • History of intracranial neoplasm
  • Gastrointestinal malignancy or hemorrhage in the previous 21 days
  • Intracranial or intraspinal surgery within the previous three months
  • Subarachnoid hemorrhage
  • Blood pressure ≥185 mmHg systolic or ≥110 mmHg diastolic
  • Active internal bleeding
  • Infective endocarditis
  • 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 seconds, or aPTT >40 seconds
  • Low molecular weight heparin (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
  • Minor or rapidly improving symptoms
  • Serum glucose <50 mg/dL
  • Serious trauma or major surgery in the previous 14 days
  • History of gastrointestinal bleeding or genitourinary bleeding
  • Seizure at stroke onset
  • Pregnancy
  • Arterial puncture at a noncompressible site in the previous 7 days
  • Large (≥10 mm), untreated, unruptured intracranial aneurysm
  • Intracranial vascular malformation

  • Intra-arterial therapy (IAT)

    • While initial trials (REVASCAT, SWIFT PRIME, EXTEND-IA, and ESCAPE) showed a benefit for 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 large vessel occlusion seen on CTA/MRA.
    • Patients with unclear or prolonged last known well should have a CT perfusion or MRI perfusion scan to identify the area that has already infarcted (the “core”) and the area 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

    • 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.
      • Herniation syndromes include transtentorial, subfalcine, tonsillar, ascending, and extracranial.
        • See our Neurocritical Care chapter for more details on herniation diagnosis and treatment.
    • Complete MCA territory infarcts can lead to transtentorial herniation and brainstem compression.
      • Decompressive hemicraniectomy is a life-saving intervention but has no 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.
    • While treatment with hyperosmolar therapy (hypertonic saline and/or mannitol) can reduce edema, it is only a temporizing measure.

  • 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.
    • The 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.
    • While there has been significant research to minimize free radical formation with reperfusion, there are no proven effective neuroprotectant therapies.
    • For these reasons, the decision to perform intra-arterial reperfusion should be made carefully, using the criteria mentioned above.

Secondary stroke prevention

  • Includes management of major risk factors such as diabetes, hyperlipidemia, hypertension, tobacco use, and utilization of antiplatelet and/or anticoagulation therapy.
    • Hypertension is the most common risk factor for stroke.

  • Antiplatelets

    • Aspirin:
      • Mechanism of action: Irreversible cyclooxygenase (COX-1 >> COX-2) inhibition. This leads to inhibition of platelet aggregation and secretion by preventing the synthesis of prostaglandins and thromboxane A2.
    • Clopidogrel: Adenosine diphosphate (ADP) (P2Y12) receptor inhibitor.
      • Clopidogrel is converted to its active metabolite by the cytochrome P450 system.
        • A minority of patients with CYP genetic variants are poor metabolizers of clopidogrel, and thus will have an inadequate antiplatelet function (i.e. inadequate conversion of clopidogrel to its active form).
      • Patients using omeprazole, a medication that also inhibits CYP, may also be at risk of inadequate clopidogrel activity. Omeprazole should be changed to an alternative to prevent an increase in stroke risk.
      • Can rarely cause thrombotic thrombocytopenic purpura (TTP).
      • Other ADP receptor inhibitors include prasugrel, ticagrelor, cangrelor, and ticlopidine.
    • A combination of aspirin and clopidogrel is 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.
    • Other rarely used antiplatelet medications include glycoprotein IIB/IIIA inhibitors (abciximab, eptifibatide, tirofiban) and adenosine reuptake inhibitors (dipyridamole).

  • Anticoagulants

    • Vitamin K antagonists: Warfarin
      • Used to be the first-line therapy for secondary stroke prevention for ischemic strokes caused by atrial fibrillation. However, now there are newer options.
        • Warfarin is still first-line for strokes caused by valvular atrial fibrillation.
      • Mechanism of action is related to the inhibition of the production of Vitamin K-driven coagulation factors: II, VII, IX, and X.
      • Requires periodic INR checks to maintain a “goal” level. The typical goal INR is 2.0-3.0 but varies by circumstance.
      • Reversal of warfarin is 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.
  • Novel oral anticoagulants (NOACs):
    • Direct thrombin inhibitors (dabigatran) or factor Xa inhibitors (rivaroxaban and apixaban)
    • NOACs have 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).
    • NOACs do not require INR/PT checks and have fewer drug interactions than warfarin.
      • Dabigritran activity can be assessed by checking thrombin time.
      • Rivaroxaban/apixaban activity can be assessed by checking anti-factor Xa.
    • Not indicated for valvular atrial fibrillation. Warfarin is the drug of choice for valvular atrial fibrillation.
  • Reversal agents:
    • Idarucizumab: Monoclonal antibody approved in 2015 for the reversal of dabigatran.
    •  Andexanet alfa: Recombinant modified Factor XA protein approved in 2018 for the reversal of rivaroxaban and apixaban.

HAS-BLED Score Table
HAS-BLED Score Table

CNS hemorrhagic lesions

Intraparenchymal hemorrhage

  • Causes

    • Trauma
      • Parenchymal contusions are a form of traumatic brain injury where multiple microhemorrhages are found on the interface between brain and bone.
      • Coup contusions occur beneath the site of impact
      • Countercoup contusions occur on the opposite side of the site of impact.
      • Patients will often have a concurrent skull or maxillofacial fracture.
        • Racoon eyes: Periorbital ecchymoses suggests a fracture of the orbital plate
        • Battle sign: Retromastoid ecchymosis suggests a fracture of the petrous portion of the temporal bone.
          • Leakage of CSF into the middle ear (CSF otorrhea) or sinus (CSF rhinorrhea) can occur. Samples of leaking fluid can be sent to the lab and tested with beta-2 transferrin assay to distinguish CSF from mucus.

    • Hypertension
      • The most common cause of non-traumatic IPH. High blood pressure leads to the rupture of small brittle blood vessels.
      • Lesions are located in deep cortical matter and brainstem.
    • Cerebral amyloid angiopathy (CAA)
      • The second most common cause of non-traumatic brain hemorrhage. Typically presents over the age of 60 with superficial lobar hemorrhages and cortical superficial siderosis.
      • Patients are also at risk of TIA-like attacks called “amyloid spells” also known as transient focal neurologic episodes (TFNEs). They are felt to be secondary to cortical irritation from blood products.
        • Can be differentiated from typical TIA based on blood products seen on neuroimaging.
      • Patients with Alzheimer’s disease are more likely to have CAA.
      • MRI will show multiple small silent cerebral microhemorrhages.
        Cerebral Amyloid Angiopathy
        Cerebral Amyloid Angiopathy
      • Pathology will show congophilic waxy pink material (amyloid) in cortical and leptomeningeal arteries with apple-green birefringence.
    • Vascular malformations
      • 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 intraluminal pressures.
        • Lesions are best appreciated with an angiogram.
        • Pathology will show arteries with fragmentation and reduplication of the elastic layer and thick-walled veins with a thin elastic layer.
        • While intraparenchymal bleeds are more common, superficial lesions may bleed into the subarachnoid space.
        • Gallery of radiographic images and pathology slides of AVMs:
      • Cavernous malformation (CM):
        • Also called cavernous hemangiomas or cavernomas.
        • Much less likely to cause catastrophic bleeding when compared to AVMs.
        • Commonly seen in young adults and can be either sporadic or familial.
          • CCM1 on chromosome 7q causes familial CMs in those with Hispanic heritage.
        • Symptoms include focal neurologic deficits secondary to hemorrhage or seizure.
          • If there is an associated developmental venous anomaly (DVA) there is a higher risk of hemorrhage.
        • Imaging will show an irregular partially calcified mass with a “popcorn appearance.”
        • Pathology will show 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
      • Atypical IPHs and/or patients with a 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 include melanoma, renal cell carcinoma > choriocarcinoma, thyroid (papillary) carcinoma > lung, and breast.
      • Glioblastomas are highly vascularized primary CNS tumors that can bleed.
      • See Tumors and Cysts for more information!
    • CNS infection (i.e herpes encephalitis)
    • Other
      • Hemorrhagic conversion of an ischemic stroke
      • Venous infarct
      • Vasculitis
      • Coagulopathy
      • Anticoagulants

  • Treatment

    • Blood pressure regulation (SBP 140-160)
    • Reversal of anticoagulation
      • If intracranial bleeding occurs with warfarin/NOAC use, treatment can be restarted ~7 to 30 days after the injury if the patient is at high risk for ischemic stroke based on the CHA2DS2VASc score.
    • Consideration for surgical intervention if a vascular malformation is found

Subarachnoid Hemorrhage (SAH)

  • Patients will present with the complaint of a thunderclap headache or “worst headache of my life”.
    • Thunderclap headache means the maximum intensity of the headache is reached in just seconds.
    • Other symptoms include nausea/vomiting, meningismus, or syncope at symptom onset.
  • SAH can be appreciated on CT but it is not as sensitive as lumbar puncture (LP) in an acute setting.
    • LP should be considered in patients when suspicion for SAH is high but the CTH was negative.
  • 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

    • Ruptured saccular/berry aneurysm
      • Hemodynamic stress in high blood flow junctions leads to a breakdown of the elastic lamina and eventual vessel outpouching and aneurysmal development.
      • Saccular aneurysms tend to be asymptomatic until they rupture, and are the most common and morbid cause of SAH.
      • 85% are located in the anterior circulation (Anterior communication artery, Posterior communicating artery, or bifurcation of MCA)
        • Posterior communicating artery aneurysms can cause compression of CN III leading to extraocular movement dysfunction and mydriasis secondary to dysfunction of superficial parasympathetic fibers.
      • Posterior circulation saccular aneurysms are found at the tip of the basilar artery.
    • 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.
        • The middle cerebral artery is most commonly affected.
    • Non-aneurysmal causes of SAH
      • Intracranial artery dissection, AVM, trauma, bleeding disorders, drugs, sickle cell disease, etc.
    • Gallery of radiographic images and pathology slides of SAH:

  • 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 include sensorineural hearing loss, cerebellar dysfunction, dementia, and pyramidal signs.
    • Imaging will show a widening of the cerebellar folia with atrophy and hemosiderin deposition.

Subdural hematoma (SDH)

  • Due to the tearing of the bridging veins from minor trauma, SDH is recognized as a blood collection between the dura and arachnoid space.
  • Elderly patients are at a higher risk due to brain atrophy.
  • CT head will show extra-axial, hyperdense (acute) or iso/hypodense (chronic), crescent-shaped blood that can cross suture lines but can not 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.
  • CTH will show a biconvex shaped hyperdense extra-axial lesion that does not cross suture lines.
    Right Epidural Hematoma
    Right Epidural Hematoma
  • Patients will usually have a history of recent head trauma with an initial asymptomatic period before a neurological decline (lucid interval).

Aging Hemorrhagic Lesions

  • The chart below can be used to determine the age of a brain bleed.
  • 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”).
  • Using the underlined words in the chart below, the following useful, albeit morbid, mnemonic is often used:
    • “I Bleed, I Die, Bleed Die, Bleed Bleed, Die Die”
Aging Intracranial Hemorrhages
Aging Intracranial Hemorrhages

Cerebral venous sinus thrombosis (VST)

  • Presenting signs/symptoms are non-specific 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.
  • Causes: Oral contraceptives, dehydration, hypercoagulable states, infection (meningitis, ENT infections), malignancy.
    • Ear infections have been associated with transverse sinus thrombosis.
  • Imaging:
    • CTV or MRV is the imaging of choice, which would show a filling defect in the venous system.
      Superior Sagittal Sinus Thrombosis
      Superior Sagittal Sinus Thrombosis
    • Digital subtraction angiography is the gold standard, but not often required.
    • CTH can show deep symmetric cortical hypodensities secondary to vasogenic edema.

  • 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 complications

  • 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

Long-term complications

  • Focal neurological deficits
  • Dysphagia 
  • Depression, increased risk of suicide
  • Post-stroke fatigue
  • Epilepsy

Hypoxic Ischemic injury (HIE)

  • Can present secondary to cardiac arrest, drug overdose, drowning, etc.
  • If severe HIE, 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.
  • EEG can have 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.

References

  1. Adams, H P, et al. “Classification of Subtype of Acute Ischemic Stroke. Definitions for Use in a Multicenter Clinical Trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment.” Stroke, vol. 24, no. 1, 1993, pp. 35–41., doi:10.1161/01.str.24.1.35.
  2. Adams RJ, McKie VC, Brambilla D, et al. Stroke prevention trial in sickle cell anemia. Control Clin Trials. 1998;19(1):110-129. doi:10.1016/s0197-2456(97)00099-8
  3. “Apixaban versus Warfarin in Atrial Fibrillation.” New England Journal of Medicine, vol. 366, no. 1, May 2012, pp. 88–90., doi:10.1056/nejmc1112500.
  4. Baharoglu, M Irem, et al. “Platelet Transfusion versus Standard Care after Acute Stroke Due to Spontaneous Cerebral Haemorrhage Associated with Antiplatelet Therapy (PATCH): a Randomised, Open-Label, Phase 3 Trial.” The Lancet, vol. 387, no. 10038, 2016, pp. 2605–2613., doi:10.1016/s0140-6736(16)30392-0.
  5. Balami, J S., Chen, R.L., Buchan, A.M., Stroke syndromes and clinical management, QJM: An International Journal of Medicine, Volume 106, Issue 7, July 2013, Pages 607–615.
  6. Campbell BCV, Mitchell PJ, Churilov L, et al.. Tenecteplase versus alteplase before thrombectomy for ischemic stroke. N Engl J Med 2018;378:1573–82. 10.1056/NEJMoa1716405.
  7. Delgado MG, Bogousslavsky J. Cerebral Hyperperfusion Syndrome and Related Conditions. Eur Neurol 2020;83:453-457.
  8. Fox, John L. “Systemic Aneurysms and Intracranial Aneurysms.” Intracranial Aneurysms, 1983, pp. 1429–1431., doi:10.1007/978-1-4612-5584-0_8.
  9. Howard RS, Holmes PA, Koutroumanidis MA. Hypoxic-ischaemic brain injury. Practical Neurology 2011;11:4-18.
  10. Johnston, S Claiborne, et al. “Validation and Refinement of Scores to Predict Very Early Stroke Risk after Transient Ischaemic Attack.” The Lancet, vol. 369, no. 9558, 2007, pp. 283–292., doi:10.1016/s0140-6736(07)60150-0.
  11. Kumar, N. “Neuroimaging in Superficial Siderosis: An In-Depth Look.” American Journal of Neuroradiology, vol. 31, no. 1, Mar. 2009, pp. 5–14., doi:10.3174/ajnr.a1628.
  12. Margaritescu O, Mogoanta L, Pirici I, Pirici D, Cernea D, Margaritescu C. Histopathological changes in acute ischemic stroke. Rom J Morphol Embryol. 2009;50(3):327–339.
  13. Morel, A., et al. “Mechanism of Ischemic Infarct in Spontaneous Cervical Artery Dissection.” Journal of Vascular Surgery, vol. 56, no. 3, 2012, p. 876., doi:10.1016/j.jvs.2012.07.018.
  14. Naidech AM. Intracranial hemorrhage. Am J Respir Crit Care Med. 2011;184(9):998–1006. doi:10.1164/rccm.201103-0475CI
  15. Pollack CV, Jr., Reilly PA, Eikelboom J, et al. Idarucizumab for Dabigatran Reversal. N Engl J Med 2015;373:511-520.
  16. Powers, W.j., et al. “2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association.” Journal of Vascular Surgery, vol. 67, no. 6, 2018, p. 1934., doi:10.1016/j.jvs.2018.04.007.
  17. Shah, Rahman, et al. “Device Closure Versus Medical Therapy Alone for Patent Foramen Ovale in Patients With Cryptogenic Stroke.” Annals of Internal Medicine, vol. 168, no. 5, Sept. 2018, p. 335., doi:10.7326/m17-2679.
  18. Stevens RD, Shoykhet M, Cadena R. Emergency Neurological Life Support: Intracranial Hypertension and Herniation. Neurocrit Care. 2015;23 Suppl 2(Suppl 2):S76–S82. doi:10.1007/s12028-015-0168-z
  19. Suzuki, J, and N Kodama. “Moyamoya Disease–a Review.” Stroke, vol. 14, no. 1, 1983, pp. 104–109., doi:10.1161/01.str.14.1.104.
  20. Wang, Y., et al. “Clopidogrel with Aspirin in Acute Minor Stroke or Transient Ischemic Attack.” Journal of Vascular Surgery, vol. 58, no. 4, 2013, p. 1140., doi:10.1016/j.jvs.2013.08.010.

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