CCP2- Stroke By Dr.

David Sirois Transcribed by Matt Asaro

March 24, 2014

Hello, thank you for letting me narrate this stroke CCP since I wasnt able to present it to you in person. These CCPs are excellent opportunities to apply basic science principals into a clinical setting one that should influence your decision making so you see a connection between the facts and the patients. So lets talk about stroke. Chief complaint Lets start by introducing our 55 year old white male who desires a check up and cleaning but he does have the concern that hes finding it difficult to chew and swallow and clean his teeth and he suffered a stroke two years ago. History of Present Illness When you hear this you ask him to tell you a little more about his medical illness. He tells you that he suffered the stroke a little more than a year ago and he entered rehab. He has some residual upper limb and right facial paresis, which is facial paralysis. He notices oral bleeding and odor no doubt of that the result of impaired oral hygiene. He takes 4 meds, 2 of them are for hypertension, no doubt the risk factor for his stroke. Youll learn about these more but remember the more meds a patient takes the more difficult it is to control. Hes taking two, hes currently taking an anti depressant and as a mental illness, this can certainly be a consequence or the consequence. Its like asking him if he had pre or post stroke depression or only post stroke. A significant number of patients, particularly those with increasing deficits after stroke are depressed. Hes also taking Coumadin. Any patients are prescribed an anti coagulant after stroke in order to reduce the risk of a second event. Well be learning about blood thinners but its the most important life saving events or treatments that a patient who just had a stroke or heart attack can get. Social History His social history, Hes retired hes never smoked or used tobacco products and he does not drink alcohol. He denies recreational drug use . He is single without children has a family history of maternal diabetes and paternal death from a CVA. The moment youve heard this history so far the bells go off. Youre thinking risk factors here that are partly genetic or familial. Hypocholestemia, for example, and diabetes as well as environmental risk factors. Youre thinking about his oral health and its interactions with systemic health youre thinking about the meds hes taking and their adverse effects on oral health and their interactions. Youre already beginning to anticipate potential management problems from drug side effects including xerostomia to increase risk for bleeding should he require dental treatment that could result in bleeding. Not to mention the fat that hes only one year out from a stroke and whats the risk for another medical emergency right in your chair including a heart attack since many patients who had a stroke are at risk for heart attack.

Dental history He tells you hes had routine dental check ups and more recently has had bleeding and sore gums. Its more difficult to brush his teeth because he has a right arm paresis making it difficult to operate a tooth brush. Medical History So with his history of hypertension and his history of cerebrovascular accident and a history of depression you got to begin to think about the types of info you need in order to plan the proper treatment for this man. Review of Systems On review of systems he says he does have problems chewing and there certainly is reason to ask if he has issues swallowing. Patients who have reduced gag reflex that could result from a stroke are at increased risk for aspiration ammonia or oral fluids ending up in their lungs thats a real risk how your position a patient and how you control fluids during treatment, how you aerosolize when using high speed hand pieces is very important Ive seen very many patients need up in hospital from such complications. He has no unusual skin, sores or lesions. His Cardiovascular review, he has shortness of breath which may be related to his hypertension congestion and progressive heart failure. Certainly if this is the result of congestive heart failure and his right sided heart failure youd be concerned bout his cardiac capacity, his reserve to undergo dental treatment and since hes had a stork presumably because of peripheral vascular disease hes also at risk for having a hear attack since the myocardium would be subject to the same diminished blood supply as his brain. He denies chest pain or CP this is an important question to ask because if he indeed does have myocardial ischemia or diminished blood diffusion than end has angina and ad sig risk for hear attack. He doe describe prolonged bleeding after injury, which should come as no surprise since hes taking a anti coagulant. He has hemiparesis, which means he had a contralateral left hemisphere stroke since left side of brain controls right side of is body. Stroke So lets look at some definitions first. Stroke is an infarction of brain tissue due to diminished blood supply or ischemia. The slide is incorrect stroke is now the4th leading cause of death not the third which is a good sign and the consensus is that there are about 200,000 people or 1 in 3 that have a second stroke in the first year. There are about 3 million stroke survivors out there. Transient ischemic attacks are episodic recurring and transient events where there is diminished blood flow where the patient recovers. During that time he may have some neurological signs or symptoms well talk about but transient ischemic attacks are very important predictors of stroke. About 15% of strokes have a transient ischemic event in the weeks before the stroke. Thats a sig predictor so the short term relationship between say a stroke within two days of a TIA 1-% will have a stroke and within 90 days, 15 will have a stroke. Roughly 12% or roughly 1 in 8 patients who have TIA will die within a year so these are a very imp predictor and something to pay attention to. Hes taking therapy in general fro strokes are medications to block

blood flow. Anti coagulants and anti thrombotic simply stop platelets from sticking together. Anti coagulant stops tat platelet plug from becoming a fibronous clot. Well talk more about that. In patients with demonstrated significant atherosclerotic disease, we can do essentially rotor rooters where they are surgically opened and fatty plaques are removed and then immediately after a stroke the immediate interventions are focused don reversing the blood clot or a thrombolysis and administering medications to reduce the injury to the damaged nerve tissue. Hemostasis So keep in mind that hemostasis is always a balance between forming clots and breaking up clots and the first step in stopping bleeding is platelets that are sticking together via these glycoprotein complexes. But these complexes are only lasting for a few minutes. A platelet plug is only lasting minute before it breaks down or at best an hour and it gets consolidated by the compliment cascade to create fibronous clot so we can use anti thrombotic agents to stop platelet adhesions like aspirin or another class called ADP inhibits or anti coagulants like Coumadin or warfarin or heparin to stop the plaque form forming from the platelet plug so the platete plug will just break down. and youve learned about this factor phase where the compliment cascade results in a fibronous clot formation. Diagram of Circle of Willis and Brain When we think about the anatomy of the brain blood supply you already know here the arch of the aorta with the internal carotid arteries coming directly off or off the subclavian artery and these travel up and eventually brought he carotid canal where they enter in the brain and terminate here and enlarged in this view into the circle of Willis. You also are a posterior circulation called vertebral arteries coming up as branches of subclavian, which come off vertebra, combine into the basilar artery here, and the basilar artery supplies the posterior part of the circle of Willis. So vertebral basilar circulations are connected through a highway of connecting arteries creates the circle of Willis. This is important architecture because it allows for collateral blood supply Diminished flow can come from the other direction to make some oft hat up and it has limited capacity for that but its critical compensating mechanism. You can imagine that these blood vessels layered on top of the brain depending on the territory they supply here the middle cerebral artery going out to an entire hemisphere. Depending on where along this vascular tree you end up having a blockage resulting in stroke will determine how much brain tissue you will have affected. Brain image Here is another just transparency view with it layered again on top of the brain. The large internal carotid and circle of Willis, middle cerebral for instance coming up here Cerebral Ischemia The relationship between ischemia and infarction I already mentioned that 12% or 1 in 8 people will die within a year from a stroke and a short term risk of a stroke

after an ITA is 10% at 2 days and 15% at 90 days and these diminished blood flows are usually he result of occlusion, blockage in the vessel by a fatty plaque or a platelet collection or that thrombus which is that stationary obstruction which can be mobile which we call an embolus and it can travel to a vessel that it can block and cause a stroke. Of course theres is increased pressure in these vessels because of their diminished lumen. So another reason people have strokes is because of hemorrhage. So a hemorrhagic stroke is when a blood vessel bursts open and you lose the blood supply cause its in the extracellular space. These treatments are the opposite because you in one you want to reprofuse the brain and the other you want to stop bleeding so its very important to know which type of stroke it is. Risk factors are important to identify because they give you an opportunity to prevent disease and improve health. You should identify which risk factors you can help the patient influence. You cant change age gender and ethnicity but you can control exercise diet and the use of tobacco. So understand those factors which you can influence cause it can be important thing for you to do. Cerebral Hemorrhage Now I was just mentioning that small portion of strokes are hemorrhagic in nature, now look at his blood vessel getting smaller and smaller in diameter and its not so much the vessel its the lumen getting smaller because of atherosclerotic disease and if an embolus came along how quickly it could block the lumen or how it could blow out this wall an cause a hemorrhagic stroke. Most strokes occur in the mid brain basal ganglia thalamus area and the next most common area is around the pons. This thalamus area is a important ascending and descending tracts systems pass so it represents a high risk area for large scale neurological deficits. Brain Scan Images Here are some brain scan s to show the amount of necrotic brain tissue that can happen follow after stroke. Of course, some of these are incompatible with life. Angiography Images We can image the vessels using good old fashioned dye enhanced angiography here looking at the carotid blood supply and you can see how one is larger than the other or in this panel where one side is completely occluded there is no blood supply here and here you can see the carotid artery is engorged. Trying to manage a collateral circulation but not very effectively. So we can evaluate patients at risk by angiography just like we can with a cardiac angiogram in the cardiac blood vessels we can do angioplasties much more readily than we can in cerebral vessels. Image So imagine these vessels somewhere along getting blocked by a thrombosis or an embolus and depending on whether that a proximal or distal event youd have a larger of smaller area of brain getting affected. And here in the midbrain in the internal capsule area or basal ganglia area, the striate arteries are high-risk areas and when you get strokes here it affects many of the ascending and descending tracts. of the u can also see branching of middle cerebral artery coming out into the

cerebral cortex and in branching points these are high turbulence high flow areas with sig risk for plaque accumulation or hemorrhagic blowout so strokes typically happen at these intersection areas. Signs/Deficits of stroke symptoms Patients who are having a stroke who are having non-specific signs depends on where that stroke is occurring. They can complaining of headaches, be dizzy, unsteady on their feet, lose consciousness, have a sense of nausea and even vomiting, muscle abnormalities, altered speech, anything suddenly happening would be signs of a transient ischemic attack or a stroke. We have hemispheric specialization so depending on what area is involved will determine where they affected based on the anatomy of their stroke. Physical Exam So well go back to our patient and his physical exam. His Blood pressure is 136/94 thats an elevated pressure and keep in mind hes on two hypertensive still with high BP which gives you insight into the level of disease control and his risk as well as the reserve he has to tolerate increased exercise. The more compensated somebody is when theyre in for instance heat failure or they have hypertension hen the less capacity they have to tolerate physical stress. He has facial asymmetry as well as upper and lower extremity weakness because of the paresis. His salivary glands have diminished flow that could be the result of drugs medications and he drools on one side of his mouth because of the facial muscle paralysis and lip incompetency. We will talk about upper and lower motor neurons and how hey tell you I its a central or peripheral vent. Looking at his dentition we see he has gross plaque and calculus and bleeding, broken teeth and caries and so forth. Oral Health Considerations These are examples of what a paresis would look like the asymmetry and also his face. An don imaging I mentioned here that here the brain shows large areas of cerebral infarction on both CT and MRI> This is an imp thing to do immediately to identify hemorrhagic from obstructive strokes. X-Ray Image Keep in mind as a dentist you also have a responsibility in any imaging you obtain and dentists are using larger filed of view techniques like comb field CT you are responsible for more than just these teeth. If you see anything like this an atherosclerotic plaques or calcification of artery you need to detect that and inform the patient, Failure to do so would be below the standard of care. Upper and Lower Motor Neuron Findings I mentioned upper and lower motor neuron disease. The motor nerve axis is two neurons. The UMN whos cell body is in the pre central gyrus in cortex and it travels down sometimes as longa s three feet if its traveling to lumbar spinal cord where it will synapse in the grey horn and synapses with a lower motor neuron that will innervate the muscle. So if someone has a brain infarction it can affect the UMN and

usually its a traumatic event that affects a LMN. Wen a LMN is injured it removes all innervation to the muscle so it becomes flaccid and atrophic so its paralyzed and also with diminished reflexes. When a UMN lesion occurs, keep in mind that LMN is still intact and connected to the muscle. And so it has some local segmental spontaneous activity and that maintains the muscle tone and so when theres a UMN lesion, you dont see flaccid paralysis and atrophy of the muscle, Youll see paralysis but is sporadic and hypertensive because its lost central control. Youll see rigid paralysis because of spontaneous firing of segmental neurons. In a facial nerve its very unique and you can determine is something is upper or motor based on the clinical presentation and thats because the facial nerve the motor nucleus of 7 that part of the nucleus that just supplies the upper 3rd of the face receives bilateral cortical innervation whereas the LMN only receives contralateral innervation. So if you have a LMN lesion obviously it will affect all branches ranging from temporal zygomatic regions and youll get complete facial paralysis from top of the head to the bottom of the chin, so the LMN affects the entire side of the face evenly. If you have an UMN even if I blow out one side of the projection, keep in mind that part of the nucleus has bilateral innervation. So one side remains intact. So a patient how has a UMN region of facial nerve will have sparing on the upper part of his face because of the bilateral innervation of the motor nucleus. Study diagram and read slides to make sense to you. A patient who has sparing on the upper 1/3 of the face will reflect an UMN lesion, which could be a stroke versus somebody who has complete ipsilateral paralysis. Two mens face videos So here we are looking at these movies. If I ask the gentlemen to raise his eyes you see there is some paralysis of the entire face, he cannot raise his eyebrow or smile very well. His ability to raise his eyebrows and smile is from top to bottom of his face. That would be a LMN lesion. Here you see she can raise her eyelid and when you ask her to smile there is lower 2/3 paralysis and this would indicate a UMN lesion. Sparing of the forehead with paralysis to the lower face. So the lady on the right has an UMN lesion, could be a stroke. The man on the left has a LMN lesion. Tongue Videos These are just examples of looking at the tongue, when there is hypoglossal innervation or LMN lesion. Here you can see this is an UMN lesion with a lot of fasciculations and the muscle is hypertonic so there is a lot of fasciculations and motor activity and not that much atrophy of the tongue Compare that tot his side and right away see a lot of atrophy of the tongue and there is into nearly the same fine fasciculations you as on the other side so an UMN versus LMN lesion. Also importantly for the gag reflex and your ability to seal off the oral pharynx from your nasopharynx as well as protect your airway. Patients how have involvement of vagal nerves can have difficult swallowing so here you see this fasciculations and rapid movements and also the asymmetry in the drape of the palate which suggests an UMN lesion and over here, more of the case is a LMN lesion where if you ask the patient to raise the mouth, you can see that one entire side doesnt even move so it pulls away to the normal side and the effected side droops. Okay.

Corneal Blink Reflex Video Um and also in these I just want to point out what trigeminal nerve involvement would look like. Muscle atrophy of the temporalis, if you ask the patient to frown you see that he deviates to one side a bit. That can be a joint problem but sometimes its neurologic because the lateral pterygoids on this side are not operating while this side they are. So his innervation of masticatory muscles and hiss loss of it results in atrophy and deflection to the defective side in the pterygoids. If you asked this patient to do the corneal blink reflex, to stimulate the left pupil, both eyes blink so that tells you the motor component is intac.t SO when we touch the other side, nothing happens. So hes lost all sensory supply to the cornea and so the combination of sensory and motor loss tell you this is probably a CN V lesion. Looking at the cranial nerve exam, something youd do on a patient with risk of stroke or history of that we looked at CN V, VII, IX, and X. Now well look at the cranial nerves to the eyes, III, IV, and VI asking patient to look to cardinal gaze the left and both eyes go left. When you ask the patient to look to the right his left eye goes that way and the other doesnt move at all. You know thee are different muscles. Over here is the lateral rectus whereas over here is the medial rectus. The lateral rectus is innervated by sixth nerve whereas medial is innervated by third nerve. So you can localize where the lesion might be. The sixth nerve innervating the lateral rectus, the fourth innervating the superior oblique and the rest innervated by three. A simple clinical test like that will tell you. What more do you want to know? So heres our patient with his plaque and calculus and his ability to clean those areas because of his hemi paresis. So now you are developing a treatment plan and you realize and decide what you need to know to treat this guy. So you look at medical risk assessment to look at his risk for an acute event. Days months after a stroke there is a risk for a repeat event. Not mentioning the same thing happening in a coronary artery resulting in a heart attack so youre assessment is essential. Find out what his cardiac reserve is, what he can take, how its controlled, whats the effect of his blood thinning drugs. If youre doing surgery how you can control that bleeding. What other condition might contribute to his oral disease are this meds causing dry mouth that increase the risk for oral disease. Do any o these disease increase his risk for worsening systemic disease. Youve probably heard that relationships between periodontal diseases and cardiovascular status. So these are all things are you go through clinical education you get increasingly sophisticate youre thinking about atomically. How well can a patient clean his teeth and maintain health and prevent disease and what are his risk factors for local oral or system disease and what you can do to mitigate those risk factors. Hemostasis diagram Keeping in mind these patients are going to be on lifetime blood thinning meds so these drugs will reduce platelet adhesion like aspirin of the ADP inhibitors or they will be drugs that affect factors like Coumadin or low molecular weight coagulants that are coming out so understanding his hemostasis and changes in that will be

critical to patient management and post operative healing in surgery. Im skipping by some of these causes we dont need to talk about every detail in great length. Oral health considerations So in the end as you consider his oral health conditions, his anti coagulant therapy, xerostomia from drugs, what are his physical limitations in performing oral hygiene, loss of protective reflexes, youll be in there with high speed hand pieces and irrigation flying everywhere, how are you going to manage secretions to prevent an aspiration. If patient has impaired swallowing or chewing how will that affect his safety in the balance of the foods he can eat. His apraxia or muscle reflex may make it difficult for him to stay open, limited visits, limited opening. All of these are things that can happen in a post stroke patient. I summarized some of the management issues obviously youll be learning much more about this in your third year medicine courses and this gives you an idea here about anatomy and physiology and biochemistry because they really are used by the smart clinician in every decision he or she makes, Drugs with coagulation side effects Well skip by this cause we already talked about this. Just know there are plenty of drugs you might prescribe as a dentist and some of these drugs might interact with some of the drugs hes taking for instance Coumadin which ahs a very low therapeutic index. Youve changed that blood level a little bit the patient could die and that could happen very easily by a medication you prescribe and Ive seen patients die that way and it happens. This is it, obviously you cant ask me any question but if you have any burning questions send me an email. Thanks again for your time, and I hope you found this useful.