Cerebrovascular Disease Mechanisms

• Lecture focuses on mechanisms involved in cerebrovascular disease & Atherosclerosis Obliterans (ASO)

Mechanisms in Cerebrovascular Disease

• Stenosis is the narrowing of a blood vessel due to ASO or plaque development
• Thrombosis is the formation of blood clots and is a common cause of stroke (CVA)
• Embolism is a foreign substance (solid, liquid, or gas) that lodges in a distal vessel causing obstruction, often embolized ASO in arteries
• Aneurysm is an abnormal dilation of a vessel wall (all 3 layers intact), rare in the cervical carotid, often from congenital defects, trauma, or ASO infection
• Dilation of greater than 50% in diameter compared to adjacent segments is considered aneurysmal

Mechanisms in Atherosclerosis Obliterans (ASO)

• Controllable risk factors include diabetes, smoking, HTN, and hyperlipidemia
• Uncontrollable risk factors include aging, genetics (family history), and male gender.
• Endothelial injury is caused by low-density lipoproteins (fats) upon the intima layer.
• Inflammatory response and smooth muscle proliferation thicken and harden arterial walls, reducing elasticity.
• Plaque accumulates on the intima, protrudes into the lumen, and causes stenosis and may be altered by hemorrhage, cell necrosis, or ulcerations.
• Plaque can proliferate into the media layer, damaging it and resulting in aneurysms

Common Locations for ASO Development

• Most common locations include bifurcations, branches, and origins of vessels.

Types of Plaque

• Fatty streak: the earliest form of plaque, hypoechoic and hard to identify
• Soft plaque: hypoechoic, hard to identify, requires color Doppler (CD)
• Dense Fibrous plaque: echogenic, easy to identify, fatty core surrounded by a protective capsule of smooth muscle
• Calcified plaque: hyperechoic, easy to identify with posterior shadowing
• Complicated lesion: necrosis leading to ulceration (open wound) where thrombi form, associated with emboli
• Homogenous plaque: uniform brightness (echogenicity), smooth/regular borders, brightness ranges from hyperechoic to hypoechoic
• Heterogeneous plaque: complex echo pattern, hypoechoic areas may be intra-plaque hemorrhage, hyperechoic areas may be intra-plaque calcifications
• Hollenhorst Plaque: originates elsewhere, occludes the retinal artery causing temporary/permanent blindness

Hollenhorst Plaque Route

• Common Carotid Artery (prox, mid, dist), bifurcation, Internal Carotid Artery (prox, mid, dist), bifurcation, Ophthalmic Artery, bifurcation, Retinal Artery

Formula for Hemodynamically Significant Lesion (HDSL)

• HDSL D.R ≥ 50% and A.R ≥ 75%
• True Lumen (TL)
• Residual Lumen (RL)
• Diameter Reduction (D.R)
• Area Reduction (A.R)

Diameter Reduction (D.R)

• D.R = 1 - (RL/TL) x 100

Area Reduction (A.R)

• A.R = 1 - (RL/TL)^2 x 100

Pathology in Arterial Circulation (Non-ASO Related)

• Dissection Aneurysm: dissection of the intima layer (usually from trauma)
• Fibromuscular Dysplasia (FMD): overgrowth of the medial layer of the muscle/collagen, and more common in young females, found primarily in the renal arteries, but rarely in the ICA (string of beads)
• Carotid Body Tumor (CBT): highly vascularized tumor between the ECA and ICA at the carotid body, regulates pH/blood pressure, may occur bilaterally, good prognosis but requires lengthy surgery, often mistaken for a goiter

Pseudoaneurysm

• May result from trauma/iatrogenic procedure (endarterectomy)
• Endarterectomy involves surgical removal of plaque and intima/media layers of the artery

HDSL

• Use this procedure if D.R ≥ 50% and A.R ≥ 75%. Formulas determine HDSL

Pseudoaneurysm

• False aneurysm: looks like an aneurysm, but has an opening (neck) to a blood pocket outside the vessel

Pseudoaneurysm Treatment

• Newly formed: compress with TX ~5 min for the ends to seal
• Older: inject thrombin to dissolve thrombus, compress with TX, or repair

Pseudoaneurysm Appearance via Ultrasound (U/S)

• Color doppler shows a Ying Yang pattern
• Pulsed wave doppler shows "to and fro" blood flow above/below the baseline
• Arteritis/Vasculitis is an autoimmune disease like Takayasu or temporal arteritis
• Arteritis/Vasculitis can arise from radiation therapy for cancer patients
• Ultrasound shows limited artery lumen blood flow with diffuse media thickening

Subclavian Steal Syndrome (SSS)

• Blood destined for the brain is redirected to the arms due to high-grade stenosis/occlusion of the proximal subclavian/innominate artery
• Suspect SSS when bilateral brachial BP differs by more than 15-20 mmHg
• Normal Vertebral Artery (VA): low resistance and antegrade flow
• Abnormal VA (SSS): high resistance and retrograde flow

Cerebrovascular Accident (CVA)

• Common term for stroke and the 3rd leading cause of death

CVA Types

• Ischemic: reduced blood flow to the brain
• Hemorrhagic: vessel rupture (aneurysm) causing reduced blood supply and increases skull pressure leading to coma.
• 80-85% of strokes are ischemic, resulting from a thromboembolic event involving ASO

Transient Ischemic Strokes

• Mini strokes characterized by sudden symptoms
• Transient Ischemic Attack (TIA): symptoms appear suddenly within minutes up to 24 hours max and the patient returns to normal
• Reversible Ischemic Neurological Deficit (RIND): symptoms appear suddenly and last 24-72 hours max and the patient returns to normal

Symptoms of TIA and RIND

• Amaurosis fugax (one eye blindness), dysphasia/aphasia (speech difficulty/loss), contralateral hemiparesis (paralysis), and behavioral disturbance
• Vertebrobasilar Insufficiency (VBI): disruption of the brain's posterior circulation, results in bilateral symptoms, unlike RIND and TIA

VBI Symptoms

• Ataxia (unstable walking), drop attacks (leg drop), paresthesia (numbness), vertigo (equilibrium problems), diplopia (double vision)

CVA Non-Localized Symptoms

• Include dizziness, syncope, headache, confusion, and speech difficulty
• CVA leads to persistent severe neurological deficit

CVA Symptoms

• Dysphasia/aphasia, hemiparesis, neurological deficit, and death

Stroke States

• Stroke in evolution: stroke is ongoing, unstable patient, changing symptoms and uncertain outcome
• Complete Stroke: completed, stable patient, fixed symptoms and persistent neurological deficit

Risk Factors for CVA Development

• Plaque build-up, HTN, diabetes, hyperlipidemia, age (55-60 years), genetics

Cerebrovascular Insufficiency (CVI)

• CVI is similar to CVA

CVI Causes

• Embolism, Stenosis, Aneurysms, Thrombosis, Trauma
• Anterior circulation symptoms always happen unilaterally, posterior circulation symptoms always happen bilaterally.
• Non-localized symptoms: include dizziness, syncope, aphasia/dysphasia & Confusion

Anterior CVI Symptoms

• Unilateral hemiparesis (muscle weakness/paralysis), hemiparesthesia (numbness), aphasia/dysphasia, behavioral abnormalities, and amaurosis fugax (vision loss)

Posterior CVI Symptoms

• Bilateral paresthesia, paresis (partial paralysis), vertigo (double vision), drop attacks (consciousness loss), and ataxia (impaired balance/gait)

Methods for Studying Arterial System Pathologies

• Indirect Cerebrovascular Circulation Testing: identifies HDSL in the ICA by assessing terminal branches.
• Indirect Cerebrovascular Circulation Testing: cannot differentiate between tight stenosis and occlusion and is only helpful when HDSL is present.

Oculopneumoplethysmography (OPG-GEE) Exam

• Exam functions to gather information regarding HDSL
• Limitations: cannot differentiate between a tight stenosis and an occlusion, cannot determine exact location of the obstruction, not helpful with well developed collaterals, or the monitoring of the progression of disease over time

OPG-GEE Contraindications

• Glaucoma, allergies to local anesthetics, history of retinal detachment, or eye surgery within the past 6 months

OPG-GEE Method

• Record bilateral BP, turn patient to supine, apply local anesthetic, place eye cups on one eye at a time, apply correct amount of pressure
• Increase intraorbital pressure, which stops blood flow from the ophthalmic artery into the retinal artery (temporary blindness)
• Release vacuum at 2 mmHg/sec. Record ophthalmic artery BP when vision returns.

OPG-GEE Results

• The vision returns when the ophthalmic artery pressure exceeds the intraorbital pressure and blood flows into the retinal artery and thereby into the eye.
• Obtained pressure also reflects the pressure of the distal ICA Ophthalmic systolic pressure (OSP) from RT to LT shouldn't vary by more than 5 mmHg. If it does, pathology is on the side with lower pressure
• OSP >0.43 to BSP indicates normal results, where OPS = ophthalmic systolic pressure (mmHg) brachial systolic pressure (mmHg)

Periorbital Exam

• Indirect ICA exam by testing the frontal artery
• Limitations: cannot differentiate tight stenosis/occlusion. Only confirm HDSL if present. Requires great skill
• Pt is supine, use CWD 8-10 MHz to locate frontal artery
• It will produce a blood flow velocity waveform Flow is antegrade, defined as flow towards the TX, waveform will be above the baseline.
• Perform series of compressions to determine blood supply to frontal artery It includes Facial, Superficial Temporal, Intraorbital (Supraorbital), CCA

Periorbital Exam Results

• Retrograde indicates disease in the ipsilateral ICA
• Blood diminishing or reversing when arteries is compressed indicates that compressed artery is source to frontal artery

Continuous Wave Doppler (CWD) Testing

• It can only produce a blood flow velocity waveform, it lacks ability to produce gray scale imaging.
• CWD (2 crystal) PWD (1 crystal). One crystal continuously transmits U/S, second is continuously receiving echoes Area of overlap is the whole cursor line, this is Range Ambiguity.
• Very accurate if blood flow is >2m/s
• Limitations are No imaging, Increased spectral broadening because large sample vol.
• May mistake ECA for ICA(High grade stenosis). Use Temporal Tap to confirm

CW Doppler Methods & Results

• Patient Supine, use doppler angle 45-60 degrees bilaterally CCAs feed blood to both ICA and ECA, therefore signal similar characteristics of both, moderate resistance, but refer as low. Should be end diastolic flow above baseline ICAs send to foreheads, eyes, and nose on spectral show sharp rise to diastole gradual deceleration without dicrotic notch, keep the flow above bass. *Low resistance feature
• ECAs send to scalp, face, and neck. A high-resistance waveform signal more pulsatile than ICA. Prominent dicrotic notch. The maneuver called Temporal tap

Temporal Tap

• Used differentiate between the ECA and ICA waveforms ICA No reaction to temporal tap and ECA oscillates to it VA-vertebral arteries supplies blood flow to the posterior portion of brain. Waveform same as ICA that Low Resistance Feature
• As with the ICA, the VA does not present with a dicrotic notch.

Transcranial Doppler (TCD)

• Measurement of blood flow velocities of intracranial Arteries Also can be used to assess Collatoral Pathways and r/o brain death or evaluate CVA.
• Use 8-10 MHz CWD probe for non-modality. 2-4 MHz for PWD probe

Transcranial Doppler (TCD) Windows

• Transorbital-Sockets, ICA(carotid siphon) ophthalmic Artery.
• Transtemporal-Temples, MCA, ACA, PCA & Terminal
• Suboccipital,Transforaminal-The Magnum, VA, & BA
• Submandibular- Under the Jaw for the distal ICA

Orbital/Transorbital Window

• Use to evaluate ophthalmic artery and carotid siphon Lower the power avoid lens damage. Place probe on eyelid, using PWD Flow from ophthalmic- 40-60mm, show blood with transducer, Carotid-found usually range between 60-80mm to the insonation

Transtemporal Window

• Middle Cerebral-supplies lateral surface the brain 30-60 mm & 65cm, with the low range.
• Anterior Cerebral Arteries(ACA-Front) usually at 60-80mm with velocity 50cm , low range blood
• Terminal ICA: Vessle located at 55-65mm with velocity=61 cm/s

Occipital/Suboccipital Window

• Used to evaluate the VA and BA, placing the probe on the base skull on hairline
• VA (Vertebral Arteries): located 60-80mm with velocity 40cm/s, low range blood
• BA (Basilar Arteries): can be found usually range-80-120mm velocity= 40cm,

Submandibular window

• Place the probe at the jaw of either side to find the Distal with range of 35-70 mm and can be found with 61cm high & range power

TCD Findings

• All vessels show low activity. Use scale of the MCA high to The VA low
• Vessels that show blood towards CCA, and that comes BA & VA
• For stenosis we use CCA Carotid Siphon, Terminal. Aneurysm AcoMA, MCA

Five Parameters for ID Specific Blood Vessels

• What Window we see? What Depth? What angle? What Means of velocities? & the DIrection of blood flow (The Beam)
• With an abnormal result for inclusion will always have collateration like a crossover where one feeds to other side
• ECA connects ICA, ophthalmic has super temporal, and facial artery to angular
• The posterior and wise better side to side collaterlzation is side for commicating Arteies

Explore key mechanisms in cerebrovascular disease, including stenosis from plaque development and the role of thrombosis in CVAs. Understand aneurysms as vessel dilations and the impact of medial calcinosis. Learn about the progression and initial stages of Atherosclerosis Obliterans (ASO).