Stroke Podcast 1/2

The subject of internal medicine is vast and voluminous. It's all encompassing and one needs to know right from the early days of MBBS of preclinical subjects like physiology, biochemistry and anatomy and going on to learn more about pathology, microbiology, pharmacology. And then comes the final MBBS years when you read actually the diseases and its management in the subject of medicine. The students have to read these topics in detail and cover a large number of disease conditions. With further subspecialization of medicine these topics have become even more vast and detailed which include common emergencies, acute and chronic conditions which have to be understood in detail by the students both for the purpose of answering questions in the exams and to understand the topic better to treat these conditions when faced with them later in life as doctors. Students both undergraduate and post graduates often find the enormity of the subject overwhelming and the teachers are unable to do justice to the topics being taught in the classes due to paucity of time and attention span of the students. This often makes the students resort to study material available online, the content of which is often not validated and the accuracy of which is often doubtful. Towards this end the Department of Intel Medicine at AFMC brings its expert faculty on an audio podcast in an interview format wherein important topics will be discussed in a Q&A format. These 20 to 30 minutes podcasts will serve as handy, reliable and well validated source of information for the students. We are starting this series of podcasts with surgeon Captain Vinny Wilson, Professor of Medicine and a neurologist of repute of more than a decade of experience. An alumnus of the F2 batch of AFMC, he did his post graduation from INHS Ashwini in Mumbai and then moved on to specialize in neurology from the prestigious PGI MER Chandigarh. An avid researcher, a popular teacher and a keen student of medicine, he has more than 50 publications of which 20 are international and these include a few in very premier journals like the New England Journal of Medicine. Today he will be discussing a very important and clinically relevant topic of stroke and its management for the benefit of the students and the topic will cover the basics of the pathophysiology, pathogenesis of stroke, the various mechanisms and its management in detail. I request these students to make notes as they go through this podcast in their mind and also get back to us in case they find certain issues which are of concern to them which they would like to know more details about and myself as well as surgeon Captain Vinny will be very happy to get back to you with the solutions to these questions. We hope that this podcast will serve as a genuine educational material for the students and ensure that when they appear in the exams or move on to become doctors future in life they shall be stronger to deal with patients and these questions. So Vinny medicine has evolved over years and I can understand that there are a lot of terminologies which have changed when I was a student we would call an entity cerebral vascular accident wherein part of the brain blood supply was lost and would lead to a neurological deficit. So are stroke and CVA one and the same and can they be used interchangeably? That's a great question because even today these two terms are used interchangeably. However stroke is the preferred term to be used now earlier terms like apoplexy, cerebral vascular accident and many other terms were being used but the current literature the consensus among world authorities and even journals is to use the term strokes. So how do you define stroke? Stroke is essentially a neurological expression of a vascular event in the brain and it is caused by one of the two mechanisms namely either an ischemia due to occlusion of a blood vessel or it's an hemorrhage due to a rupture of a blood vessel and stroke has two very important signatures clinically which are the abruptness with which the event occurs and this kind of stamps the event as vascular and the second important signature of stroke is the forkality of the neurological deficit and this often helps in differentiating a stroke from various other neurological disorders that may at times mimic a stroke. In olden terms where a time when functional neurology and functional imaging was not available stroke used to be learned the functional mapping of the brain used to be done stroke by stroke with the clinical symptoms when they were matched with autopsy findings. So yes stroke is a vascular event which has abruptness and forkality as essential signatures underlines. So what I would understand from what you just said is that all neurological events which are sudden in onset and have a distribution of deficit which is focal in nature would it mean that they can be labeled as stroke or do you think there's something more to it? Yes so the classical teaching is that anything that is sudden and is focal is unless proven otherwise a stroke. However one should keep in mind that there are some rare disorders which may manifest like this important among them being hemiplegic variant of migraine which may present like a stroke in the sense that there may be a focal hemiparesis but usually the condition is given away by a history of migraine in the past or a preceding headache. There is a variant of migraine called achephalgic migraine where the headache may not perceive the focal deficit and similarly in focal seizures with secondary generalization one may get tauts peresis which may also present with hemiparesis. Here again the presence of seizure which is not very common in acute strokes is usually the first event to occur. Sometimes a patient was recovered from stroke and is well compensated now may suddenly develop hemiparesis when there is a metabolic insult like hypoglycemia or hyponeutrimia. So these are some important stroke mimics that one should keep in the back of the mind but by and large when you have an abrupt event which is focal in nature think of stroke. Okay so stroke mimics are likely to be rarer than stroke itself however it should be kept in mind because the management is different. So when we talk about strokes I think the major subset is of ischemic stroke where the blood supply to a part of the brain is hampered. What are the pathological mechanisms which underlie ischemic strokes? It's a great question. The ischemic strokes that occur and ischemic strokes constitute by and large about 80 to 85 percent of the entire spectrum of strokes and among the ischemic strokes it is the atherosclerosis of the large vessels with superimposed thrombosis that constitute about 40 percent whereas embolism into the cerebral vessels mostly in the form blood clots they constitute another 30 percent whereas occlusion of the small vessels with the brain parenchyma which we often refer to as the lacuna strokes they constitute about 20 percent. However these are not the only mechanisms causing ischemic strokes there are some other rarer mechanisms like dissections. One may remember that australian cricketer had suffered a dissection of the neck vessel following a trauma of a cricket ball and had subsequently died so that is also a form of getting an ischemic stroke vascularitis especially takayasus in middle age women in the Indian population and also in high altitude thrombosis of the cerebral vein and the dural sinuses which may also occur in pregnancy and perperium is also an important cause. In situ thrombosis of the cerebral vessels without an underlying atherosclerotic substrate due to hypercoagulable state beat due to an inherited thrombophilia or any other cause are also and like COVID-19 was a condition where we had hypercoagulable states and a large number of patients used to present with large artery strokes and the second broad category other than ischemic stroke is of course hemorrhage which constitute about 10 percent of the entire stroke spectrum. Here the broad categories are either intracerebral hemorrhage or subarachnoid hemorrhage among the intracerebral hemorrhage the causes include hypertension, trauma, arterial venous malformations, coagulation disorders, even drug abuse like cocaine or the hemorrhage may result from the hemorrhagic transformation of an originally ischemic stroke whereas the subarachnoid hemorrhage usually either results from a trauma or is it is usually due to a rupture of a neurosome which may sometimes give us warning signs which we will discuss later. Okay so what I understand is that there are a large number of mechanisms which may underlie a patient developing a stroke so as a physician in charge of an emergency and I am encountering a patient with stroke do I look at the age of the patient and be able to decide that underlying mechanism is more likely to be this compared to somebody who comes at a different age? That again is a very important aspect of evaluating a patient of acute stroke because not all strokes are written with the same etiopathological mechanisms especially when you are encountering a child who has developed a stroke the spectrum or the pathology underlying the stroke is entirely different from somebody who is elderly. In childhood or in children we tend to see strokes rising out of congenital heart diseases, moa moa, infective endocarditis, sickle cell, even rare causes like mitochondrial disorders like malas, homocysteine urea and fibrous disease are considerations when you are dealing with a child who has suffered an acute stroke. On the other hand when you have a middle-aged person coming with stroke the most common cause is atherosclerosis of course and we discussed about embolism. It could also be an undiagnosed or uncontrolled hypertension which is hemorrhaged. The patient may be having a dissection or a ruptured aneurysm. In the elderly age group in addition to these causes that we discussed in the middle age there are some other rare causes like myeloid angiopathy that comes into consideration when dealing with people in the extremes of age. Okay now there's an entity called stroke in young because as you just mentioned when a patient presents with stroke at a younger age the likely mechanism and causes are likely to be different and hence the approach to their management. So how do you define stroke in young and what are the usual causes that you must look at? So it is very important to kind of recognize the stroke is happening in young and though there are no clear-cut age definitions of stroke in young but it is broadly agreed that the age group between 18 to 45 is the age where we should look for causes that are not common that we do not commonly investigate in a slightly elderly population. So among the pathological mechanisms that underlie a stroke in young can include a atherosclerotic large vessel or it could be a non-ethrosclerotic mechanism even cardiac embolism in hypercoagulable states can occur in the in this age group. Among atherosclerotic large vessel disease the usual risk factors like dyslipidemia, juvenile diabetes mellitus, homocysteineuria and even a past history of radiation injury or radiation exposure is a risk factor for a stroke in young and those in whom atherosclerosis is not a consideration the other rare causes like dissection of fibromuscle dysplasia or Moammar disease even vasculitis and certain infections are important considerations cardiac embolism either rising out of infective endocarditis, atrial fibrillation, a paradoxical embolism rising out of deep venous thrombosis in the leg or very rarely atrial mixoma can also be a cause of stroke in young and of course inherited thrombophilic conditions, sickle cell, apla and polycythemia vira can lead into a hypercoagulable states are also causes of stroke in young. So the gamut of the causes in the young are far wider than in the elderly or slightly age group so it is important to know and evaluate about it. Okay so in our part of the world infections are common and I can see that one of the non-atherosclerotic mechanisms that you mentioned of stroke is infections. So what are the infections as a physician should I be looking for in a patient who's resident with stroke in a young age? The especially in the Indian subsets the infections form a very important part of stroke in young population and the recent COVID-19 pandemic we saw a huge uptake in the causes of strokes in in the young population especially large vessel strokes which are amenable to intervention and mechanical thrombectomy. Apart from COVID-19 which has which has kind of weighed the other important infections that may cause strokes are myocombicosis, infective endocarditis by way of embolism, syphilis tuberculosis especially the arthritis of the circle of villus in the base of the brain certain herpes groboviruses like chickenpox can lead to strokes and dengue is infamous for causing strokes in the form of cerebral hemorrhage. These are important considerations in definitely in India when you're faced with stroke and infection as a possibility. Okay so from what I gather that we've shared till now is what is stroke and what are the different mechanisms and causes in stroke especially in various age groups. So as a physician working in the emergency and a patient lands up with me which appears to be a stroke what are the things that I should look for to recognize as this patient to be having an acute stroke? That's a great question because there is a common myth that to diagnose stroke one requires a neuroimaging of some kind as a CT scan or MRI but fortunately it doesn't require any kind of neuroimaging to diagnose stroke because stroke till date remains a clinical diagnosis and the best part is that you don't require a formal degree to diagnose stroke because it is very easy by the way of its presentation that one can pick up stroke and as we discussed earlier it is the abruptness of the event that points towards vascular etiology and it is the forkality that helps differentiate this condition from other stroke mimics. There is an acronym that is popular the world over and the acronym goes by the name BFAST where B stands for the balance if a patient complements a loss of balance that is abrupt in onset, E stands for eyes where the patient has difficulty in vision or patient is seeing double and F stands for a facial group and A stands for arm weakness or a arm drift and S stands for difficulty in speaking or any space difficulty and the T portion of the BFAST represents the time indicating that this is the patient who has to be rushed to an emergency without losing any minute or the precious seconds because every minute millions of neurons are at risk of dying. These are also the features the abruptness in the forkality and the pattern that we just discussed that differentiate a stroke from stroke mimics rarely the stroke may progress unlike the pattern that we discussed earlier the abruptness may not be as abrupt there are certain forms of stroke that tend to stutter in the sense that they progress over in a stepwise fashion over hours or maximum up to a day and also cerebral edema that usually follows an ischemic stroke or a hemorrhaging stroke may cause the neurological deficit to worsen for the next 48 to 72 hours. Okay so now we understand that strokes are basically because of arterial involvement does it mean that the size of the artery matters as in is it a large artery which is involved which is causing the stroke and is the management and the prognosis of the patient likely to differ in these cases. It's a great question and a very important question when faced with an acute stroke to determine whether this stroke is a large artery stroke or artery that involves a large vessel often abbreviated as a large vessel occlusion LBO or is it a small vessel stroke because if the patient is suffering from a large vessel occlusion this is the patient who is at risk for decompressive surgery because of edema that may ensue later and this is the patient who may benefit from a neurovascular or endovascular intervention for management of acute stroke whereas a small vessel stroke may not be as catastrophic as a large vessel stroke in terms of the extent of the damage that it causes and because of the small calibre of vessel interventional endovascular procedures are not usually done in small vessel stroke. The way one can pick up a large vessel stroke clinically when he presents to the emergency is to look for cortical symptoms like aphasia, agnosia, agnosia is the inability to recognize familiar objects in a particular sensory modality, apraxia refers to the loss of learned motor activity like brushing his or her teeth or wearing a shirt for example and or the presence of a cortical sensory loss that usually affects the phase and the dissonance as against this kind of a pattern of a large vessel stroke the small vessel strokes also referred as lacuna syndrome do not manifest in cortical symptoms in that they lack aphasia, agnosia or apraxia and the sensory loss that one encounters is usually a hemisensory kind of a sensory loss and involves a trunk of the patient and is due to the involvement of the thalamus and the hemiparesis or the hemiplegia that the patient suffers from in a small vessel stroke is usually a dense hemiplegia in that the the the degree of weakness is usually equal both in both the upper and the low limbs. Great so my understanding of neurology in clinical practice as a physician is that to localize the lesion in the brain or the rest of the nervous system requires one to understand the pattern of neurological deficit so does that apply to strokes as well as in by pattern of neurological involvement will I be able to sort of predict which arterial territories has been involved. Yes it's a as I said earlier in the earlier days the functional mapping of the brain and spinal cord was based on how the stroke used to present and how that stroke symptom used to correlate with the autopsy findings the stroke used to be learned the the neurology used to be learned stroke by stroke some important patterns that the emergency doctor should recognize include the dense hemiplegia that we already discussed where the weakness in the upper and the lower limb on the hemiparotic side is equal and this often localizes the lesion into the internal capsule and is usually the result of a lacuna stroke against this a different pattern where you have a differential weakness where the weakness in the upper arm is more than the lower limb or the lower the weakness in the lower limb is greater than the upper limb is referred often as a differential weakness and this kind of differential weakness usually arises from involvement of the of the corona radiator in conjunction with this differential weakness if there are cortical symptoms in the form of aphasia ignosia proxia or even cortical sensory symptoms then this kind of differential weakness in cortical sensory and cortical symptoms kind of fit into a vascular territory and a facial brachial weakness kind of a differential weakness is representative of a middle cerebral artery territory whereas a lower limb weakness that is greater than the upper limb weakness very sparsely involving the face is representative of an anterior cerebral artery kind of a territory you have one more pattern which is referred to as cross hemiparosis where one gets a lower motor neuron weakness of brain loss on one side and hemiparosis on the contralateral side this often localizes to the brainstem similarly if the patient presents with a taxia, dysarthria, diplopia or visual loss it is the posterior circulation the vertebral or the basilar or the posterior cerebral arteries that are that are to be blamed. Presence of a monocular vision loss with a contralateral hemiparosis usually implicates the carotid artery on the side of the vision loss and presence of headache, seizures at onset in a pregnant lady or somebody who's been exposed to a high altitude and especially when they manifest with papillodema should cerebral venous sombrosis should be suspected. These are some of the common patterns that everyone should recognize which will help them in a long way to localize the lesion. For example, if one does not recognize the presence of a posterior circulation involvement the radiologist may miss that territory at all because on a CT scan the posterior fossa structures are not so readily visible and unless you alert them to the possibility of a posterior fossa stroke or a posterior circulation stroke they may not actively look for such a stroke. That's very interesting and in fact I understand that what makes neurology interesting is that there is a lot of mathematical patterns which are involved and understanding them and predicting which territories involved can actually improve the pre-test probability when we are actually going into imaging. So similarly, while we take history in a patient with stroke is it possible for us to predict what is the underlying mechanism which has caused the stroke because the initial emergency management may differ in such cases even before imaging can confirm that mechanism. Absolutely. Though it is not categorically one may not be able to differentiate as to the exact etiology without doing an imaging. However, there are certain clues that one may gather from the initial presentation as to whether there's an hemorrhage or a or an ischemic event. Some of the clinical symptoms that point towards hemorrhage include severe headache, severe hypertension, presence of seizures at onset of stroke, loss of consciousness or any other feature of a raised intracranial tension. The intracerebral hemorrhage tends to be absolutely abrupt with the maximum deficit at onset which may progress steadily for minutes or hours at the most whereas the subarachnoid hemorrhage tends to be always instantaneous and maximal at onset. In contrast to the intracerebral hemorrhage, the embolism presents like a bolt from the blue and almost peaks at almost at once without further progression. Thrombosis on the other hand tends to stutter, progresses in a series of steps, first involving the upper limb, then the lower limb after some time and then may involve the face and this kind of series of step wise progression is also referred to as saltatory progression and this kind of progression is very different from that of a hemorrhage which tends to be a steady state of progression. Sometimes progression is noted in all these mechanisms that is secondary to development of edema. So edema may progress in all these hemorrhage embolism or thrombosis and this edema can cause the neurological deficit to worsen for up to 48 to 72 hours. So there is no clear cut way of differentiating clinically but there are these clinical clues that can give you some idea as to what could be the underlying etiology. Okay so a large subset of stroke is in fact ischemic stroke where the blood supply to a part of the brain has been blocked because the artery has got a blockage. Now this blockage as I understand can happen if there is a sudden rupture of the plaque and clot is formed which blocks the artery or there's an embolism which has come from a distant clot somewhere and lodges itself in these arteries. So considering these two different mechanisms are there any pointers in the history that can point towards this being either a thrombotic stroke versus an embolic stroke? Again there are pointers one cannot be absolutely certain so certain pointers that make you suspect that the underlying mechanisms embolism is a younger population. So whenever you're encountering a stroke in young think of embolism as the first cause. Also embolism tends to be like a bolt from the blue with absolutely no prodromal symptoms to kind of warn the patient or the relatives. It also tends the embolized material also tends to get arrested at the arterial bifurcations for example at the bifurcation of the middle cerebral artery or the bifurcation of the internal carotid into the MCA and the arterial cerebral artery. Whenever one encounters a hemorrhagic transformation of infarct on CT it is almost always embolism. Similarly when multiple vascular territories are involved think of an embolic cause either emanating from a common source like a cardiac chamber. Also most thrombotic strokes allow collateral whistles because of the solitary slow stepwise progression allow the collateral whistles to form and there is a kind of sparing of the distal territory. So when you see absolute no sparing of distal territory beyond the occlusion that is again is a hallmark for probably an embolic stroke. And the most important thing about embolic stroke is the setting. So in a patient who has atrial fibrillation or has valvular conditions like severe mitral stenosis or mitral valve prolapse has had a previous MIA with delvia neurasome is suffering from infective endocortitis or has been diagnosed with mixoma. These are some settings where again embolism comes with the forefront. Presence of a pulmonary hypertension allowed P2 may give you a clue to a probable possibility of a paradoxical embolism and very rarely when a patient meets with a road traffic accident with severe bone trauma and suffers a stroke one should consider fat embolism and recreations, scuba diving and abortions that have got complicated or sometimes even after cervical or thoracic surgery can lead to air embolisms. Despite extensive investigation up to 20 to 30 percent of such embolic strokes remain undiagnosed as to the source from where the embolism originated. Okay, so embolism is one mechanism. What about ethyl thrombotic blockage of the artery as a mechanism? Are there any pointers in history? So apart from the clue that we discussed earlier about the startling course where the progress may be in a stepwise manner, the stroke that occurs in sleep where the patient gets up from his bed and immediately falls with a stroke or they tend to be thrombotic. Also a transient ischemic attacks that are especially the ones that are repetitive and are the stereotype are the kind of presentation that underlie a thrombotic event and a partial stroke that often receipts temporarily to become completely alright and before proceeding again or before manifesting again with a completed stroke is likely to be thrombotic than embolic. And also ethromas tend to form at regions of branching points. The arteries are the curves of the brain and the sides include the internal carotid artery at its origin, the cervical part of the vertebral or its origin from the subclavian or its junction of the basilar. The middle cerebrular artery stem is a favorite site for thrombosis even its bifurcations as also the proximal posterior cerebral artery and the anterior cerebral arteries. The ancient and especially the Indian population tend to have more intracranial atherosclerosis than the extracranial atherosclerosis that one tends to see in the western population. And the mechanism that underlie thrombosis is not just occlusion but it could also lead to a watershed in fact for example if the thrombosis in the internal carotid artery the watershed between the ACA that is the anterior cerebral artery and the middle cerebral artery can the watershed areas between these two territories can show an infarction. Also the thrombosis forming in the internal carotid artery may embolize to a dislocation and sometimes the expanding thrombosis can occlude the penetrating vessels for example the penetrating vessels that go into the basal ganglia from the middle cerebral artery and can cause lacuna syndrome. Okay so there is a subset called transient ischemic attacks where the deficit may not complete itself and completely recover over a period of few hours. Now are these TIAs always a throat thrombotic or are there any other mechanisms also that may be involved? So TIAs usually TIAs though the classical definitions 24 hours where they reverse but a TIA for all functional purposes or practical purposes tends to reverse without leaving a trace either in the brain or in as the neurological deficit within one hour. When you get repetitive stereotype TIAs they are usually because of a throat thrombotic mechanisms however a single episode of TIA can also be due to embolism. TIAs that can take the form of repetitive limb shaking and may often be mistaken for seizures and it is important to recognize also TIAs can be a warning sign for an imminent stroke giving clinician valuable time to investigate such a patient and mitigate the risk factors so that he or she may prevent a stroke from occurring. In those who patients of TIA the in those who get stroke following a TIA the 20% will occur within a month and a 50% within a year. There is a score called ABCD score and the score is useful in predicting the stroke following a TIA and it's a very simple stroke that involves age blood pressure the clinical presentation and the duration of the TIA and everybody can do it bedside without getting any investigations done. And there are certain patterns of TIA that can give you a clue as to the underlying etiology for example a TIA that occurs after exercise is due to occlusion of the aorta or its branches which can occur in certain kinds of vascularitis like tachyosis arthritis or may even occur in dissection of carotid artery or the aorta similarly a TIA that is brought on by hyperventilation in a child is an indicator of a moya maya disease. Okay one important aspect of history taking is family history and most conditions that we look for we look for any inherited cause so when it comes to strokes are there any inherited conditions which can predispose or cause strokes? So the certain rare causes of strokes can be inherited and among them prominent among them include the sickle cell anemia it can be homocysteine urea it can be certain mitochondrial disorders like malars there is an autosomal dominant disorder called catacel that can cause stroke. Fabric disease can cause stroke and apart from this certain inherited thrombophilias can also cause stroke so whenever you get a family history of stroke in a younger age group which occurs in a cluster of either autosomal recessive patterns where they skip generations of in a dominant pattern where they involve at least one member in every generation or when in a mitochondrial pattern where there is no male to male transmission then you must consider these possibilities also. Thank you Vinny with this we come to the end of the first part of this podcast which is comprehensively covered various aspects of stroke the remaining aspects shall be discussed in the part two of this podcast and we look forward to having you again with us Vinny to discuss these important issues. Thank you.