Cervical Artery Dissection


  • Dissection = separation of structural components of the arterial wall
  • Classification:
    • vertebral vs carotid
    • extra vs intracranial
    • spontaneous vs traumatic
  • Most frequent is EC ICA dissection typically 2-3 cm above CCA bifurcations
  • Intimal tear –> blood penetrates arterial wall –> creation of intramural hematoma –> rupture of vasa vasorum (between adventitia and media causing pseudoaneurysm or between intima and media causing stenosis) –> ischemic stroke via 2 mechanisms:
    THROMBOEMBOLIC – endothelium damage / intimal flap / wall irregularities –> formation of thrombus –> artery-to-artery embolism –> ischemic stroke
    HEMODYNAMIC – mural hematoma enlargement –> arterial lumen compression –> hemodynamic ischemia

Triad of cervical artery dissection symptoms

  • pain (ipsilateral, head neck and face)
    • Headache in 65-80% – frontal or periorbital if carotid, occipital if vertebral
    • Neck pain
  • Horner’s syndrome
  • Ischemic symptoms (cerebral / retinal)

Other findings:

  • CN 7, 11, 10 damage
  • Tinnitus
  • Ataxia
  • N/v
  • posterior neck pain or occipital headache
  • Vertigo
  • Ipsilateral facial dysesthesia

Risk factors:

  • young age
  • Current smoker
  • Increased WBC
  • Shortened aPTT
  • Some genetic variants


⁃ CAD – generally good, mortality rate 2-5%, majority achieve functional independence at 3 months after symptom onset, recurrence <5-7%, usually within first 2 months



  • Flame sign most common finding (tapered occlusion)
  • Double barrel / double lumen sign – subadventitial lesions separating true and false lumen between intima and media
  • ADVANTAGE: detects wall irregularities and intimacy tears
  • LIMITATIONS: invasive, difficult to visualize lesions within arterial wall

Figure: DSA imaging

1 = double lumen sign / lifted intima

2 = ICA stenosis

3 = flame-shaped occlusion

4 = dissecting aneurysm

5= intima flap


  • FS-MR (fat-sat MR sequence) to visualize intimacy hemorrhage – hyper intense signal or crescent sign in T1W imaging (corresponds to methemoglobin concentration)
  • *NOTE: takes 72h for oxyHb and deoxyHb to convert to methHb, so initially IH is indistinguishable from surrounding tissue
  • 3D BB (Black Blood) T1 sequence useful

Figure: MR imaging

1 = FS T1W MR, arrow points to intramural hematoma / crescent sign in R ICA

2 = T2W MR, arrow points to intramural hematoma and intimal flap


  • Most commonly used modality
  • Long stenosis of arteries
  • Increased wall thickness and diameter
  • Intimate flaps and multi vessel lesions in trauma
  • CBCTA (cone-beam CTA) – provides high spatial resolution n each plane, superior for detection of intimacy flap and double lumen signs especially in VAD diagnosis

Figure: CTA finding

*arrow points to long narrowing of the ICA (clue to dissection)

Neck US

  • Detect abnormal blood flow velocity, irregular artery stenosis, presence of IH (eccentric echo genie lesions, luminal thrombus, mobile flaps and double lumen sign
  • NOTE: difficulties examining distal vA
  • Contrast-enhanced US (CEUS) – uses micro bubbles as a contrast agent; detection of high-intensity transient microemboli signals may be a factor for choice of proper antithrombotic therapy

Figure: US imaging

1 = intima-media complex

2 = intramural hematoma

3 = echogenic intraluminal thrombus formation

4 = intimal flap

5 = residual arterial lumen

6, 7 = intramural hematoma

**** = impaired blood flow


  • tPA is efficacious and safe in CAD-related IS
  • Use of antiplatelet or anticoagulant agents to prevent ischemic stroke is reasonable; duration of 3-6 months (no official recommendations)
    • Favor AP therapy if contraindications to AC, or area of infarction is large, when dissection extends to intracranial or intramural regions and in cases of spinal cord trauma
    • Favor AC if severe stenosis, occlusion or multiple ischemic lesions in single arterial territory and if luminal thrombus or microembolism is detected
    • *5 studies compare AP vs AC therapies, also studies compare NOAC with VKAs — nothing conclusive.
  • interventional treatment – effectiveness of thrombectomy similar to ischemic stroke from atherosclerotic lesions
    • Indications for endovascular treatment: recurrent ischemic events despite pharmacotherapy, C/I to antithrombotic therapy, pharmacological treatment failure, significant flow limitation from intramural hematoma, pseudo aneurysm, coexistence of embolism and hypoperfusion
    • No clear recommendations on EVT in tandem occlusion


Marciniec, M., Sapko, K., Kulczyński, M., Popek-Marciniec, S., Szczepańska-Szerej, A., & Rejdak, K. (2019). Non-traumatic cervical artery dissection and ischemic stroke: A narrative review of recent research. Clinical Neurology And Neurosurgery, 187, 105561. doi: 10.1016/j.clineuro.2019.105561

Algorithm: Management of Cervical Artery Dissection

*ACT = anticoagulant therapy

*AP = antiplatelet therapy

*CAD = cervical artery dissection

*EVT = endovascular treatment

*IH = intramural hematoma

*IS = ischemic stroke

*IVT = IV thrombolysis

*MT = mechanical thrombectomy

*TO = tandem occlusion

*CBCTA = cone-beam CTA

*FS-MR = fat saturation MR sequence

*BB-MR = black blood MR sequence


Marciniec, M., Sapko, K., Kulczyński, M., Popek-Marciniec, S., Szczepańska-Szerej, A., & Rejdak, K. (2019). Non-traumatic cervical artery dissection and ischemic stroke: A narrative review of recent research. Clinical Neurology And Neurosurgery, 187, 105561. doi: 10.1016/j.clineuro.2019.105561

Measuring Decompressive Hemicraniectomy

Three new CT measurements after decompressive hemicraniectomy:

Solid lines indicate measurements. Dash lines are the skull midline, and lines perpendicular to calvarium edges.

  • Barrier thickness to transcalvarial herniation – measure from brain surface to skin surface perpendicular to skin surface (27.3mm)
  • Anterior and posterior extents of infarcts measured parallel to midline from edge of calvarium to furthest extents of the infarct (17.0 mm and 12.5mm, respectively)

**Extension of cerebral infarcts beyond craniectomy bed is associated with progressive brain herniation.

**how useful these measurements are is still subject to future studies


Verma, U., Grabowska, M., Batchala, P., Abay, S., Shah, M., & Haughey, H. et al. (2019). New CT measurements to assess decompression after hemicraniectomy: A two-center reliability study. Clinical Neurology And Neurosurgery, 188, 105601. doi: 10.1016/j.clineuro.2019.105601

Ultrasound Techniques for Central Venous Catheter Insertion


  • Sweep probe over the path of the vessel like a broom
  • If path of probe is not following the longitudinal axis of the vein, the vein moves toward the edge of the vessel (W)
  • If the path of the probe follows the axis of the vein, the vein stays at the center of the image (R)


  • Swing the probe like a fan (about 30 degrees)
  • If the US probe is not perpendicular to long axis of vein, vein will move to the edge (W)
  • If the probe is perpendicular to the vein, the vein stays at the center of the image (R)


  • A – needle about to puncture skin, not seen in US image
  • B – needle punctures skin, point of brightness appears (needle tip)
  • C – move US (or tilt US) to advance scan plane, needle tip disappears
  • D – needle is again advanced slowly and point of brightness reappears
  • E – repeat A to D until needle reaches the vein
  • F – when tip touches anterior wall of target vein, it creates a dimple; needle is pushed with a snapping motion (penetrates anterior wall)
  • G – anterior wall returns to original shape, needle tip not seen (bright point is now the shaft)
  • H – move scan plane forward to see needle tip in the vein


  • Use this technique to identify center of vein
  • Align probe with long axis of vein
  • Turn probe to right (yellow arrow), US image of vein becomes like a bullet (end of vein tapers) – tip represents the right lateral wall of vein
  • Turn probe to left to identify the opposite lateral wall (left)
  • Estimate the center of the vein
  • Needle can be advanced within the ultrasound beam (LONG-AXIS IN-PLANE TECHNIQUE) to prevent anterior to lateral wall penetration


Practical guide for safe central venous catheterization and management 2017. (2019). Journal Of Anesthesia. doi: 10.1007/s00540-019-02702-9

PFO – To Close Or Not To Close

Patent Formaen Ovale (PFO)

  • seen in ~25% of adults
  • Risk of Paradoxical Embolism (RoPE) Score to calculate risk

Percutaneous PFO closure

  • introduced in 1992
  • initial trials did not demonstrate benefit, but recent trials show reduction in recurrent stroke risk in carefully selected patients.
    • reduces recurrent stroke in well-selected young crypto genie stroke patients of ~0.6% per year.
  • small risk of major procedural complication and atrial fibrillation (see table)


CLOSURE I: RCT of PFO closure (2012)

  • 909 patients, cryptogenic stroke and PFO
  • PFO (STARFlex device) vs ASA/warfarin/both
  • Stroke rate: no difference (2y f/u 2.9 vs 3.1% HR 0.90 CI 0.41-1.98 p=0/79)
  • Risk of Afib: increased with PFO closure (5.7 vs 0.7%, p<0.001)
  • PC Trial: PFO and Cryptogenic Embolism Trial (2013)
    • 414 patients with cryptogenic stroke and PFO
    • PFO (Amplatzer Occluder) vs antiplatelet/anticoagulation
    • Stroke rate: favor closure but not significant (4y f/u 0.5 vs 2.4% HR 0.20, 95% CI 0.02-1.72, p=0.14)

    RESPECT Trial: Randomized Evaluation of Recurrent Stroke Comparing PFO Closure to Established Current SOC Treatment (2013)

    • 980 patients with cryptogenic stroke and PFO
    • PFO (Amplatzer occluder) vs medical therapy
    • Stroke rate: favor closure, but statistically no difference (2.5y f/u 1.8 vs 3.3% HR 0.49 95% CI 0.22-1.11; p=0.08)
      • *per protocol analysis demonstrated reduction in recurrent stroke rates (1.3 vs 3.0% HR 0.37 95% CI 0.14-0.96, p=0.03)
      • *meta-analysis of RESPECT and PC (2016) indicated benefit of PFO over medical therapy (HR 0.39 95% CI 0.19-0.82, p=0.013)
    • Stroke rate: lower with PFO closure in primary ITT analysis (6y f/u, 3.6 vs 5.8%, HR 0.55 95% CI 0.31-0.99, p=0.046), PE more likely in closure arm (HR 3.48 95% CI 0.98-12.34, p=0.04)

    (2016) FDA approved use of St. Jude Aplatzer Septal Occluder for secondary stroke prevention in patients with PFO and cryptogenic stroke

    REDUCE Trial: (2017)

    • 664 patients with cryptogenic stroke and PFO —> required strokes to be “embolic-appearing” (i.e. exclude small deep strokes)
    • PFO Closure (Helen septal occluder) vs antiplatelets
    • Stroke risk: reduced (3y f/u, 1.4 vs 5.4% HR 0.23 95% CI 0.09-0.62, p=0.002)

    CLOSE Trial: (2017)

    • 663 patients with cryptogenic stroke and PFO, limit to either large shunt or atrial septal aneurysm, exclude single small drop stroke
    • 3 arms, antiplatelet vs anticoagulation vs closure with any CE-marked device (most commonly used Amplatzer device in 51%)
    • Stroke risk: reduced (5y f/u, 0 vs 6% HR 0.03 95% 0-0.26 P<0.001), no difference between anticoagulation and antiplatelet therapy

    DEFENSE-PFO Trial: Device Closure vs Medical Therapy for Cryptogenic Stroke Patients with High-Risk PFO (2018)

    • 120 patients, including up to 80y, with large PFO or concomitant ASA
    • PFO Closure (Amplatzer occluder) vs medical therapy (anticoagulation / antiplatelet)
    • Stroke rate: reduced (2y f/u 10.5% vs 0% p=0.02)

    Meta analysis of 6 trials = NNT 30 to prevent 1 stroke at 5 years, 6 fold increase in risk of Afib

    2 PFO Closure Devices approved in US:

    1. St. Jude Amplatzer PFO Occluder
    1. Gore Cardioform Septal Occluder


    • Age: most trials excluded >60y
    • +/- atrial septal aneurysm
    • Shunt Size: large R-to-L shunt associated with greater benefit from PFO closure
    • Infarct pattern: PFO related stroke likely to be superficial, c/w embolism rather than small and deep
    • +/- anticoagulation: among those deemed appropriate for anticoagulation, there is no benefit of PFO closure


    1. BMJ rapid review guidelines – in patients <60y with stroke and PFO without alternative stroke mechanism, strong recommendation for PFO closure (and antiplatelet meds) rather than antiplatelet alone).
    1. European Medical Societies guideline – strong recommendation in favor of PFO closure over medical therapy in cryptogenic stroke patients <=65y

    Bottom line: offer PFO closure if (+) PFO with cryptogenic stroke, consistent infarct pattern, age <60y, not amenable to anticoagulation.

    Other important trials (antiplatelet vs anticoagulation):


    Favilla, C., & Messé, S. (2019). Patent foramen ovale and stroke. Current Opinion In Neurology, 1. doi: 10.1097/wco.0000000000000782

    Types of Cerebral Edema

    Types of cerebral edema:


    • Teal shapes = neurons and axons with myelin sheaths
    • white circles with arrows = water molecules
    • yellow circles = glial cells.


    A.  normal relationship between brain cells and extracellular space, which contains water molecules with freedom of movement


    B.  brain tissue in a vasogenic edema situation, with an increased number of water
    molecules occupying the extracellular space but maintaining freedom of movement:

    C.  cytotoxic brain edema, represented by the swelling of brain cells (increased volume) without primarily affecting the extracellular space.  Water molecules inside the brain cells lose their freedom of movement:



    D.  intramyelinic edema, swelling of periaxonal space and spaces between myelin layers, without primarily affecting other extracellular spaces or involving brain cells. Water molecules inside the myelin layers cannot move to other extracellular spaces, losing their freedom of movement.




    de Oliveira, A., Paulino, M., Vieira, A., McKinney, A., da Rocha, A., & dos Santos, G. et al. (2019). Imaging Patterns of Toxic and Metabolic Brain Disorders. Radiographics39(6), 1672-1695. doi: 10.1148/rg.2019190016

    MOA: Vasopressin and Vaptans

    Vasopressin binds to the vasopressin 2 receptor (V2R), leading to an increase in intracellular cyclic adenosine monophosphate (cAMP), which activates protein kinase A (PKA). The latter leads to translocation of preformed vesicles containing aquaporin 2 (AQP2) along cytoskeletal elements toward the apical membrane, where exocytic insertion of AQP2 into the apical membrane renders the membrane permeable to water. Using the osmotic gradient from tubular lumen to medullary interstitium, tubular water can now move to the interstitium through constitutively activated basolateral AQP3 and AQP4 channels.

    Vasopressin receptor antagonists (vaptans) compete with vasopressin for the V2 receptor–binding site.

    Illustration below: Vasopressin–induced increase in water permeability in the collecting duct.


    Seay, N., Lehrich, R. and Greenberg, A. (2019). Diagnosis and Management of Disorders of Body Tonicity—Hyponatremia and Hypernatremia: Core Curriculum 2020. American Journal of Kidney Diseases.

    Sodium Formulae

    Selected Formulas Useful for the Classification and Management of Dysnatremias

    Plasma osmolality, mOsm/kg H2O: (2 × [Na+] (mEq/L)) + SUN (mg/dL)/2.8 + glucose (mg/dL)/18

    Plasma tonicity, mOsm/kg H2O Measured plasma osmolality (mOsm/kg H2O) − SUN (mg/dL)/2.8 or (2 × [Na+] (mEq/L)) +glucose (mg/dL)/18

    Edelman formula, simplified: [Na+] = (eNa++ eK+)/TBW

    *Urine to serum electrolyte ratio: (UNa+ UK)/[Na+]

    Electrolyte-free water excretion: Urine Volume × (1 − (UNa+ UK)/[Na+])

    Infusion rate, hypertonic saline solution: 1 mL/kg/h can be expected to increase [Na+] 1 mEq/L/h

    Infusion rate, D5W, to relower [Na+]: 3 mL/kg/h

    **Free-water deficit: TBW (L) × (([Na+]/140 mEq/L) − 1)

    Note: The formula for calculated plasma osmolality does not reflect the contribution of ethanol, methanol, or other toxic ingestions. Measured plasma osmolality should not be used for decision making in hyponatremia if an ingestion is suspected. A difference between plasma osmolality calculated with this formula and measured plasma osmolality can be used to infer the presence of a foreign substance. Infusion rates are approximations and do not take into account ongoing losses of water or solute;

    [Na+] should be monitored frequently during infusion.

    Abbreviations: D5W, 5% dextrose in water; eK+, exchangeable potassium content; eNa+, exchangeable sodium content; [Na+], serum sodium concentration; SUN,serum urea nitrogen; TBW, total-body water; UNa, urine sodium concentration; UK, urine potassium concentration.

    *Ratio > 1 predicts treatment failure with fluid restriction alone and worsening of hyponatremia in response to normal saline solution.

    **TBW = 0.6 × body weight (kg)


    Seay, N., Lehrich, R. and Greenberg, A. (2019). Diagnosis and Management of Disorders of Body Tonicity—Hyponatremia and Hypernatremia: Core Curriculum 2020. American Journal of Kidney Diseases.

    DVT Statistics In Neurosurgical Patients

    *% given in ranges (data pooled from multiple studies)

    Rate of DVT formation in neurosurgical patients without prophylaxis – 0% to 34%

    Incidence of DVT in neurosurgical patients receiving at least 1 form of DVT prophylaxis who underwent screening Doppler US – 3% to 16%

    Rates of symptomatic DVTs – 1% to 4%.

    DVT formation after cranial surgery – 3.4%

    • DVT formation among patients undergoing cranial procedures for tumor – 2% to 10%
    • DVT formation in SAH patients – 3.5% to 18%
    • DVT formation after DBS surgery – 1%

    DVT formation after spinal surgeries – 1.1%

    • DVT formation after surgery for spine trauma – 0% to ⼀9%
    • DVT formation after surgery deformity – 2% to 14%
    • DVT formation after surgery degenerative spine surgery – 0% to 9%

    Overall rate of PE in neurosurgical patients (+/- prophylaxis) – 0% to 5%, mortalities ranging from 9% to 50%

    Incidence of PE among neurosurgical patients receiving mechanical prophylaxis +/- chemoprophylaxis – 0.3% to 0.8% with associated mortality of 0% to 18%

    Risk factors associated with DVT formation in neurosurgical patients

    • Malignancy
    • Prior DVT / PE
    • Type of surgery (cranial, spinal, cerebrovascular)
    • Duration of surgery
    • OCP use
    • Stroke
    • Sepsis
    • Heart failure
    • Radiation therapy
    • Paraparesis
    • AMS
    • Heart failure
    • Smoking
    • Obesity
    • Presence of deep venous catheters
    • Age
    • Inherited hypercoagulable disorders

    Risk factors specific for patients undergoing spine surgery

    • Combined anterior-posterior approaches
    • Multilevel surgeries
    • Surgery for trauma
    • Surgery for deformity correction


    Shaikhouni, A., Baum, J., & Lonser, R. (2018). Deep Vein Thrombosis Prophylaxis in the Neurosurgical Patient. Neurosurgery Clinics Of North America, 29(4), 567-574. doi: 10.1016/j.nec.2018.06.010

    EDEMA and Modified EDEMA Scores for Predicting Malignant Brain Edema

    EDEMA Score is calculated based on the following 5 predictors

    • Basal cistern effacement (3)
    • MLS (mm)
      • 0-3 (1)
      • 3-6 (2)
      • 6-9 (4)
      • >9 (7)
    • Glucose >=150 mg/dL (2)
    • No previous stroke (1)
    • No acute intervention (1)

    Score ranges from 0-14.

    EDEMA = Enhanced Detectin of Edema in Malignant Anterior Circulation Stroke

    The Modified EDEMA Score:

    Modified EDEMA score adds NIHSS, and yields better AUC (0.72 vs 0.80).

    EDEMA Score AUC 0.72 (95% CI 0.67-0.76), NIHSS score AUC 0.74 (95% CI 0.70-0.78), modified score AUC 0.80 (95% CI 0.76-0.84)

    Other risk scores to predict malignant brain edema / infarction – Kasner Index Score, DASH score, MBE score, E-score.


    Cheng, Y., Wu, S., Wang, Y., Song, Q., Yuan, R., & Wu, Q. et al. (2019). External Validation and Modification of the EDEMA Score for Predicting Malignant Brain Edema After Acute Ischemic Stroke. Neurocritical Care. doi: 10.1007/s12028-019-00844-y

    Ong, C., Gluckstein, J., Laurido-Soto, O., Yan, Y., Dhar, R., & Lee, J. (2017). Enhanced Detection of Edema in Malignant Anterior Circulation Stroke (EDEMA) Score. Stroke, 48(7), 1969-1972. doi: 10.1161/strokeaha.117.016733