Cerebrovascular Disease Lecture 04 PDF

6/24/2022 Lecture 04 Mechanisms involved in the development of cerebrovascular disease 1) Stenosis - is the narrowing of the blood vessel caused by the process of ASO (Atherosclerosis obliterans) or in other words plaque development. 2) Thrombosis - the formati...

6/24/2022 Lecture 04 Mechanisms involved in the development of cerebrovascular disease 1) Stenosis - is the narrowing of the blood vessel caused by the process of ASO (Atherosclerosis obliterans) or in other words plaque development. 2) Thrombosis - the formation of a blood clots, and is one of the most common causes of CVA (Cerebrovascular accident) or in other words stroke. 3) Embolism - is a foreign substance or a bit of thrombosis (solid, liquid, or gas) that moves through the circulatory system until it becomes lodged in a distal (smaller) vessel. - Result in partial or complete obstruction of the vessel. - Usually is embolized ASO in arteries 4) Aneurysm - is an abnormal dilation of the wall of a vessel, all 3 vessel walls are intact. - It is a rare finding in the cervical carotid. - It is the result of congenital defects, trauma, or ASO infection. - A dilation of greater than 50% in diameter as compared to adjacent segment is considered aneurismal. Mechanisms involved in the development of ASO - There are contributing risks factors in the development of ASO, “Controllable”; 1) Diabetes - contributes to the hardening of the arterial wall structure, which results in the loss of the elasticity of the vessel (medial calcinosis). - Blood will travel much faster down a stiff walled vessel vs. an elastic vessel. 2) Smoking - is a strong risk factor for the development of ASO. - It is the nicotine in the tobacco that will cause a recurrent vasoconstriction of the arteries and arterioles. - Blood travels much faster in these vessels. 3) HTN - Hypertension is high blood pressure. - Causes an increased stress on vessel walls. - With this added stress it contributes to the development of ASO. 4) Hyperlipidemia - high saturated lipids (fats) in the blood, which will increase the chances of development of ASO. - It will contribute to the progression of ASO accumulation. - There are non - contributing risk factors in the development of ASO, “NOT CONTROLLABLE”. 1) Aging, 2) genetics (family history), and 3) Male gender Page 1 of 14  6/24/2022 Lecture 04 ASO - Atherosclerosis Obliterans - Endothelial injury followed by deposition of low-density lipoproteins (fats) upon the intima layer. - There will be an inflammatory response with smooth muscle (media layer) proliferation. The arterial walls will thicken and harden, which will result in the loss of the vessel wall elasticity. - Plaque then accumulates upon the intima layer which will protrude into the vessel lumen causing stenosis. The plaque may become altered by hemorrhage, cell necrosis, or ulcerations. - Plaque can also proliferate into the media layer damaging it resulting in aneurysms. Most common locations for the development of ASO; 1) Bifurcations, of the 3 this is the most common 2) Branches 3) Origins of vessels. There are different types of plaques. 1) Fatty streak - this is the earliest form of plaque. - It is hypoechoic and is very difficult to identify even with CD. 2) Soft plaque - still hypoechoic difficult to identify, however because it is a bit more progressed we can/must use CD to identify it. 3) Dense Fibrous plaque - this is more echogenic and therefore easy to identify in grey scale. - There is a fatty core surrounded by a protective capsule, which is made up of smooth muscles. 4) Calcified plaque - hyperechoic, therefore very easy to identify, especially because it will cast a posterior shadow. 5) Complicated lesion - necrosis of the plaque will lead to ulceration (open wound) where thrombi will form. - This type of plaque is associated to emboli because of this. (Foreign substance made mobile). 6) Homogenous plaque - all echoes from the plaque are uniform in brightness (echogenecity). - Boarders are usually smooth and regular. - Brightness of the entire plaque can range from hyperechoic to hypoechoic. Page 2 of 14 6/24/2022 Lecture 04 7) Heterogeneous plaque - we find a complex echo pattern. Hypoechoic areas of the plaque may be related to intra-plaque hemorrhage. Hyperechoic areas of the plaque may be related to intra-plaque calcifications. 8) Hollenhorst plaque - It originates from somewhere and traveled to and is occluding the retinal artery. - Will result in temporary or permanent blindness. *Know the route: CCA prox, mid, dist, bifurcation, ICA prox, mid, dist, bifurcation, ophthalmic artery, bifurcation, retinal artery. HDSL = hemodynamically significant lesion. TL = True lumen RL = Residual lumen D.R = Diameter reduction A.R = Area reduction 𝑹𝑳 𝑹𝑳 D.R = 𝟏 − 𝒙 𝟏𝟎𝟎 A.R = 𝟏 − ( 𝑻𝑳 )2 x 100 𝑻𝑳 HDSL: D.R ≥ 50% & A.R ≥ 75% Mechanism of pathology found in the arterial circulation, not ASO related. 1) Dissection aneurysm - this is the dissection of the intima layer, usually the result of trauma. - May occur spontaneously in a patient with ASO development. - The U/S appearance presents with a fixed or mobile echogenic. 2) FMD - Fibromuscular dysplasia is the overgrowth of the medial layer, the collagen in the muscle. - More common in young females. - Primary found in the renal arteries, it is found as a rare secondary finding in the ICA’s. - Present in U/S as a string of beads: 3) CBT - Carotid body tumor is a highly vascularized tumor which arises between the ECA and ICA at the location of the carotid body. The carotid body is a location between ECA and ICA, and is a collection of nerves (ganglion), which serves to regulate pH and blood pressure and other blood factors. The tumor affects this area. - May occur bilaterally - Prognosis is good, but surgery is very long. May come back and another surgery may be required. - Often misdiagnosed as a goiter. Page 3 of 14  6/24/2022 Lecture 04 4) Pseudoaneurysm - may occur after a trauma, however it is usually the result of an iatrogenic procedure (surgical procedure) or a specific one designed to remove plaque in the carotid arteries (CCA, ICA, ECA) called endarterectomy. Endarterectomy is the surgical removal of the plaque and intima layer or plaque intima and media layers. - This procedure is used in case of an HDSL, D.R≥ 50%, and A.R≥ 75%. - Use formulas to determine HDSL - A pseudoaneurysm is a false aneurysm in that it looks like an aneurysm; however there is an opening (called the neck) connected to a pocket of blood outside of the vessel. - Treatment include; 1) If new, compress with TX for approximately ≃5 min and the ends seal. 2) If older, first the doctor injects the area with an enzyme, thrombin for example, in order to dissolve the thrombus accumulated, then can follow-up with compression with TX, or possible other method of repair. - U/S appearance will produce with CD in the sac a ying yang color Doppler signature and in the neck with PWD the waveform will present with “to and fro” (above and below baseline) blood flow. 5) Arteritis - also referred to as vasculitis, which is the result of an autoimmune disease, such as Takayasu arteritis, temporal arteritis. - This can also be the result of a patient undergoing radiation changes such as a patient undergoing cancer treatment. - The U/S appearance in a vessel has limited blood flow through its lumen, the result of diffuse concentric thickening of the media layer of the arteries. 6) SSS - Subclavian steal syndrome - In this case blood that is destined for the brain is shunted/redirected away from the cerebral circulation towards the blood flow of the arm. - This is the result of a high grade stenosis or an occlusion of the proximal subclavian arteries (one or the other) or the innominate artery/Brachiocephalic artery. - When suspecting an SSS we take bilateral brachial artery BP and compare RT to LT. The RT to LT BP must not differ by more than 15-20 mmHg from each other, should the difference be greater than 15-20 mmHg this could indicate SSS. Page 4 of 14 6/24/2022 Lecture 04 - Normal VA: blood flow characteristics will present with low resistance and antegrade flow. - Abnormal VA (SSS): blood flow characteristics will now present with high resistance because blood is no longer feeding the brain but the arms and therefore we find retrograde flow. 7) CVA - Cerebrovascular accident, in common terms this is a stroke and it is the 3rd leading cause of death. - There are 2 major types of CVAs; A) Ischemic - This is the result of decreased blood flow for the brain. B) Hemorrhage - This is the result of a vessel rupture. Usually an aneurysm that had ruptured which will result in 2 effects. First the blood supply to the tissue of the brain is now not being delivered. Second the pressure in the skull cavity will increase. This leads to coma. (High pressure in the brain and no blood supply). - 80% to 85% of all strokes are ischemic the result of a thromboembolic event (usually involving ASO). - There are 3 types of transient ischemic strokes, we call these mini strokes. A) TIA - Transient ischemic attack, where symptoms appear suddenly and last from a few minutes up to 24 hours max. - In this case the patient returns to normal B) RIND - Reversible ischemic neurological deficit, where symptoms appear suddenly and last at least 24 hours and up to 72 hours max. - In this case the patient returns to normal. Symptoms of TIA and RIND include; - Amaurosis fugax - blindness of one eye - Dysphasia or aphasia - difficulty speech or loss of speech. - Contralateral hemiparesis - opposite side of paralysis. - Behavioral disturbance Page 5 of 14 6/24/2022 Lecture 04 C) VBI - Vertebrobasilar insufficiency, symptoms are caused by a disruption to the posterior circulation of the brain, therefore as opposed to the RIND and TIA, symptoms in this case appear bilaterally. - Ataxia - unstable walking/walking like a drunk - Drop attacks - leg drop - Paresthesia - limbs are numb/needle like feeling - Vertigo - equilibrium problem - Diplopia - seeing double/double vision CVA - non localized symptoms Dizziness Syncope Headache Confusion Difficulty with speech CVA continued - is a persistent severe neurological deficit. - Some symptoms include; Dysphasia or aphasia Hemiparesis Other neurological deficit Death - Stroke in evolution Stroke is still occurring Patient is unstable Symptoms keep changing Outcome for patient is uncertain - Complete stroke Stroke is no longer occurring Patient is stable Symptoms are no longer changing Persistent neurological deficit. Page 6 of 14  6/24/2022 Lecture 04 - Risk factors in the development of a CVA include; Plaque build-up HTN Diabetes Hyperlipidemia Ages 55-60 years Genetics CVI - Cerebrovascular insufficiency is very similar to a CVA - Causes of CVI include: Embolism, stenosis, aneurysms, thrombosis, trauma - Symptoms of CVI regarding the anterior circulation of the brain Symptoms appear unilaterally - Hemiparesis - muscle weakness/partial paralysis on one side - Hemiparesthesia - numbness or abnormal sensation on one side of the body. - Aphasia and dysphasia - Behavioral abnormalities - Amaurosis fugax - loss of vision in one eye - Symptoms of CVI regarding the posterior circulation of the brain. Symptoms appear bilaterally - Paresthesia - pins and needles in arms and legs - Paresis - partial paralysis - Vertigo – double vision - Drop attacks with loss of consciousness - Ataxia - impaired balance, loss of gate - Symptoms of CVI Non localized Dizziness Syncope Aphasia/dysphasia Confusion There are several different methods for the study of the pathologies of the arterial system. - Indirect testing of the cerebrovascular circulation. These are exams that identify HDSL of the ICA by evaluating some of its terminal branches. These exams (like all exams) have some limitations; - Cannot differentiate between a tight stenosis and an occlusion. - Only helpful when HDSL is present. Page 7 of 14  6/24/2022 Lecture 04 I. OPG-GEE exam - oculopneumoplethysmography - This is one type of indirect testing which functions to gather information regarding HDSL of/in the ICA by testing the ophthalmic arteries. - Limitations of this exam include; Cannot differentiate between a tight stenosis and an occlusion. Cannot determine the exact location of the obstruction. Not helpful when well developed collaterals exist. Not helpful in the monitoring of the progression of disease over time. - Contraindications, reasons why not to perform this exam on a patient: Pt w/ glaucoma Pt w/ allergies to local anesthetics Pt w/ a history of retinal detachment Pt that has had eye surgery within the past 6 months - Method: we take pt’s bilateral BP and the pt is turned to a supine position. If the pt’s BP was less than 140 mmHg, then we will apply 300 mmHg vacuum. If the pt’s BP was greater than 140 mmHg, then we will apply 500 mmHg vacuum. A local anesthetic is applied to the eyes. Eye cups are placed over the eyes, one at a time. We apply the correct amount of pressure in the cup. This will increase the intraorbital pressure which will stop the blood flow from the ophthalmic artery to enter the retinal artery. The result is temporary blindness. The vacuum in the eye cups is released at a rate of 2 mmHg/sec, and when the pt indicates that their vision has returned then we read this pressure to be ophthalmic artery BP. - The vision returns when the ophthalmic artery pressure exceeds the intraorbital pressure and blood flows into the retinal artery and thereby into the eye. - This pressure we obtain also reflects the pressure of the distal ICA (supraclinoid segment). Page 8 of 14 6/24/2022 Lecture 04 - Results: 1) Ophthalmic systolic pressure (OSP) from RT to LT comparison should not differ by more than 5 mmHg. If the pressure difference is more than 5 mmHg then the pathology is on the side with lower pressure. 2) We also check this outcome with a ratio calculation, where normal results are indicated by OSP - 39 >0.43 BSP OPS = ophthalmic systolic pressure, units: mmHg BSP = brachial systolic pressure, units: mmHg - If this ratio calculation produces at greater than 0.43, it would indicate normal results for pt. - Must run this ratio twice because we have 2 eyes, one for the RT another for the LT. II. Periorbital exam - This is another indirect exam of the ICA by testing one of its terminal branches, in this case the frontal artery (branch off of the ophthalmic artery). - Limitations: cannot differentiate between a tight stenosis and an occlusion. Is not diagnostic if an HDSL is not present, therefore can only serve to confirm if HDSL is present. (HDSL: D.R ≥ 50% and A.R ≥ 75%) This study requires great skill. - Method, pt is supine and we use an 8-10 MHz CWD (continuous wave Doppler) Tx Locate with the TX the frontal artery in the inner canthus of the eye. This will produce a blood flow velocity waveform (CWD lacks the ability to produce a gray scale image). Flow should be antegrade, in this case is defined as being towards the TX, therefore waveform will appear above the baseline. Perform a series of compression on the following vessels to determine which is the supply to the frontal artery, : - Facial artery - Superficial temporal artery - Intraorbital artery (Supraorbital artery) - CCA Page 9 of 14 6/24/2022 Lecture 04 - Results - Retrograde blood flow in the frontal artery indicates disease in the ipsilateral (same side) ICA. - If blood flow diminishes or reverses while performing the compressions of the arteries mentioned, then that artery that was compressed is the blood supply for the frontal artery. III. CWD testing - continuous wave Doppler can only produce a blood flow velocity waveform, it lacks the ability to produce gray scale imaging. CWD uses 2 crystals where PWD uses 1. - With CWD one crystal is continuously transmitting U/S while the second crystal is continuously receiving the returning echoes. - Area of overlap is where the sample volume or gate is, however it is the entire cursor line and we lack the ability to place it at a location of our choosing, which is called Range ambiguity. - CWD is very accurate in measuring blood flow velocities greater than 2m/s - Limitations No imaging Increases spectral broadening not related to turbulent flow, but rather the result of a large sample volume. May mistake ECA for ICA in case of a high grade stenosis in the ICA, the ECA collateralization will have ECA waveform present with high resistivity, use temporal tap to confirm. - Methods Pt is supine Use Doppler Angle 45o- 60°, how? No imaging Obtain waveforms for; bilaterally - CCA (P, M, D) - ICA - ECA - Vas Page 10 of 14 6/24/2022 Lecture 04 - Results CCA - common carotid artery feeds blood flow for both ICA and ECA, therefore will present with a waveform characteristics of both. The CCA is moderate resistivity, yes, we still refer to it as low resistance. - End diastolic flow should be above the baseline. - Waveform (signal) should be very similar to contralateral CCA ICA - Internal carotid arteries provide blood supply for the anterior portion of the brain, forehead, eyes and nose. - This vessel’s waveform is present with low resistance characteristics. - On the spectral display we note a sharp rise to systole and a gradual deceleration as the heart cycle moves into diastole. - The waveform of this vessel does not present with a dicrotic notch. - The diastolic flow remains above the baseline. ECA - External carotid arteries provide blood flow for the scalp, deep and superficial structures of the face, and neck. - This vessel’s waveform presents with high resistance characteristics. - The signal (waveform) is more pulsatile than ICA. - The dicrotic notch is prominent with this waveform. - The maneuver called Temporal Tap is used to distinguish between the ECA and ICA waveform. The diastolic component of the ECA oscillates, and the ICA has no reaction to temporal tap. VA - Vertebral arteries supply blood flow for the posterior portion of the brain. - Waveform is very similar to ICA waveform, in that they are both low resistance, however the ICA has faster blood flow velocities (being larger) and the VA has slower blood flow velocities (being smaller). - As with the ICA, the VA does not present with a dicrotic notch. IV. TCD - Transcranial Doppler - This is a non-invasive technique that measures the blood flow velocities of the major intracranial arteries, the circle of Willis. - We use these exams to R/O brain death Measure blood flow velocities Assess collateral pathways Evaluate for CVA - Ischemic - Hemorrhage Page 11 of 14 6/24/2022 Lecture 04 - Method Use an 8-10 MHz CWD probe for non imaging modalities Use a 2-4 MHz PWD imaging probe Windows 1) Transorbital window - uses the eye sockets as an entry point for the sound beam. - Evaluate the ICA (carotid siphon) and ophthalmic artery 2) Transtemporal window - uses the temples as entry point for the sound beam. - Evaluate the MCA, ACA, PCA, and distal ICA (terminal) 3) Suboccipital/Transforaminal window -uses the foramen magnum. - Evaluate the VA and BA. 4) Submandibular window - also uses the foramen magnum - Evaluates the distal ICA 1) Orbital/Transorbital window This window is used to evaluate the ophthalmic artery and the carotid siphon. The power of the TX is lowered to avoid damage to the lens of the eye. - The TX is placed over the closed eyelid - We use a PWD probe - Flow direction may be away, towards, or even bidirectional. OA – Ophthalmic artery - Usually found at a depth of 40 – 60 mm - Blood flow should be towards the transducer. Carotid siphon – is usually found at a depth range between 60 – 80 mm - Direction of blood flow varies depending on insonation angle. 2) Transtemporal window is used to evaluate the MCA, ACA, PCA, and distal ICA; MCA - Middle cerebral artery - Supplies blood flow to the lateral surface of the brain. - Usually found at a depth range between 30-60 mm. - The flow direction must be towards the TX to indicate normal. - The blood flow velocities are ≃ 65 𝑐𝑚/𝑠 - The blood flow characteristics must be low resistance. ACA - Anterior cerebral artery - Usually found at a depth between 60-80 mm. - The direction of blood flow must be away from the TX to indicate normal. - The blood flow velocities are ≃ 50 𝑐𝑚⁄𝑠 - The blood flow characteristics must be low resistance. Page 12 of 14 6/24/2022 Lecture 04 PCA - Posterior cerebral artery - These are the terminal branches of the Basilar artery. - The PCA are located at a depth range of 60-70 mm. - The blood flow in the P1 segment is towards the TX and the P2 segment way from the TX. - The blood flow velocities are ≃ 40 𝑐𝑚⁄𝑠 - The blood flow characteristics must be low resistance. Distal ICA - distal (terminal) Internal carotid artery - This vessel is located at a depth range of 55-65 mm - The terminal ICA presents with low resistance waveforms. - The blood flow velocities are ≃ 61 𝑐𝑚⁄𝑠 3) Occipital/Suboccipital window - This window is used to evaluate the VA and BA. - With this approach the TX is placed at the base of the skull at the hairline. VA - Vertebral arteries - These arteries are located at a depth of 60-80 mm. - The blood flow direction must be away from the TX to indicate normal. - The blood flow velocities are ≃ 40 𝑐𝑚⁄𝑠 - The blood flow presents with low resistance. - The transition of the vertebral arteries confluence to form Basilar artery is ≃ 80 − 90𝑚𝑚. BA - Basilar artery - This vessel is usually found at a depth range between 80-120 mm. - The blood flow direction must be away from the TX. - The blood flow velocities are ≃ 40 𝑐𝑚⁄𝑠 - The blood flow waveform must be low resistance. 4) Submandibular window, place the TX under the jaw on either side. - Evaluate the distal ICA - This vessel is usually found at a depth range between 35 – 70 mm - Blood flow direction is away from TX. - Blood flow velocities ≃ 61 𝑐𝑚⁄𝑠 - Blood flow presents with low resistance characteristics. Page 13 of 14 6/24/2022 Lecture 04 TCD Findings - All vessels must present with low resistivity waveforms. - Vessels must fall within the following velocity scale: MCA＞ACA＞PCA = BA = VA - Vessels that must present with blood flow towards the TX: MCA, PCA (P1 segment) - Vessels that must present with blood flow away from the TX: ACA, PCA (P2 segment), BA, and VA. - For stenosis evaluate: MCA, carotid siphon, and terminal ICA - For aneurysm evaluate: AcomA, MCA and PCA. These are 5 parameters vital in the identification of specific vessels; 1) Window used 2) Depth Range 3) Direction of blood flow 4) Mean/Average blood flow velocities 5) Direction or angle of U/S beam Abnormal results will present because of occlusion, therefore collateralization will be present; 1) Crossover collateralization Such as RT hemisphere feeding LT hemisphere and vise versa. 2) ECA to ICA collateralization Via the ophthalmic artery branches 1) Supraorbital with superficial temporal artery 2) Frontal with superficial temporal artery 3) Angular/nasal with facial artery May see retrograde flow in the ipsilateral ophthalmic artery. 3) Posterior to anterior or vise versa collateralization via communicating arteries. Pg 99 – 114. Pay close attention to pg104 – 107, Table 22 on pg 112 Page 14 of 14