Hemiplegia & Localization: A-Z Concepts

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Hemiplegia & Localization: A-Z Concepts

29 Oct, 1:30 PM

[Music] good evening everyone i welcome you all on behalf of netflix uh thanks a lot first of all the netflix the medical platform for giving me such an excellent opportunity to address medical students and doctors across the country today going on to the topic circle of village and stroke localization when the netflix prestigious metaphysics organization asked me to deliver a talk on a neurology topic a concept oriented topic i chose stroke localization because hemiplegia is such an important and common exam oriented topic not only for mbbs students but also for md general medicine pediatrics physiotherapy dental students including nursing so everyone has to know about stroke and amongst the stroke questions they commonly ask is stroke localization in fact stroke is one of the three leading causes of death the first being myocardial infarction or heart attack second stroke or brain attack followed by cancer so even seeing a disease which has got a huge mortality like stroke we need to understand it because of its of its impact on the disease and the death so today i'll be talking about circle of villus and stroke localization a to z concepts i'm dr srinivas neurologist from rajmandri andhra pradesh india my email address is 3k lpm gmail.com so if you have any suggestions or comments or questions or you want to get in touch with me you can always contact me on my email and as i said my youtube channel is dr srinivas medical concepts right neurology stroke especially for students quote neurology is learned stroke by stroke unquote charles miller fisher charles miller fisher said that entire neurology can be learned stroke by stroke so if a person learns stroke well all the different types of stroke he has learned the neurology well so neurology is learned stroke by stroke according to charles miller fisher which is very true charles miller fisher usually known as c miller fisher was a canadian neurologist whose notable contributions include lachner stroke transient ischemic attack and miller facial variant of gbs stroke the brain attack and hemiplegia so what exactly is stroke stroke is an acute that means sudden in onset focal brain dysfunction due to a vascular disease stroke is an acute focal brain dysfunction due to a vascular disease stroke is the second leading cause of death after myocardial infarction or heart attack stroke or brain attack is the second leading cause of death after myocardial infarction or heart attack basically there are two main types of stroke 85 percent are ischemic due to lack of blood flow and 15 percent are hemorrhagic due to bleeding so majority of the strokes are ischemic so if you are sitting in a primary health center without ct scan imaging or investigations and hundred percent with stroke come to you and you start treatment for as if it's an ischemic stroke 85 of the time you're right because 85 of the strokes are ischemic due to lack of blood flow and only 15 are hemorrhagic due to bleeding we have another condition known as transient ischemic attack and ischemic attack or deficit that results rapidly 24 hours but usually according to the latest literature is less than one hour without radiologic evidence of an infection which is termed as tia so transient ischemic attack is an ischemic deficit that revolves rapidly 24 hours or usually within one hour without radiologic evidence of an infection which is known as tia so how do we classify stroke so to approach a person who's got stroke we need to have a broad overview of the different types of stroke stroke arterial stroke is about 99 so 99 of strokes is because of arterial involvement only one percent is because of venous involvement so 99 of the strokes are due to arterial involvement and only one percent of stroke is due to venous involvement so we take the ischemic stroke of this 99 to 100 percent as i said earlier 85 percent are because of ischemic stroke and only 15 percent are because of hemorrhagic stroke so 85 percent are because of ischemic stroke and only 15 percent are because of hemorrhagic stroke in ischemic stroke again we have a large vessel stroke large vessels getting uh infection causing infarction to the brain uh cardioembolism from the heart which accounts for about 20 percent of ischemic stroke or small vessel disease that is a lack in our infection which is about another 20 percent and others unknown so we have the large vessel stroke cardio embolism about 20 percent small vessel stroke about 20 percent and others and unknown hemorrhagic stroke is about 15 and about 10 percent of hemorrhagic strokes are because of the intracerebral hemorrhage and about five percent is because of some arytenoid hemorrhage venous strokes we see it very rarely only one person and usually what we see is cortical vein thrombosis usually the presentation is women after delivery that is postpartum strokes presenting with severe headache and sieges always suspect a wiener stroke cortical vein thrombosis venous stroke is in a way very satisfying condition because when we give heparin and start on oral anticoagulants patients make a wonderful recovery even a person who is in an unconscious state makes a wonderful recovery if it is venous stroke and once we start giving heparin and oral anticoagulants uh i say oral anticoagulants you must have noticed it why am i saying oral anticoagulants for venous stroke because venous strokes are otherwise known as red thrombus venous strokes are otherwise known as red thrombus here platelets have got no role because there is no endothelial injury the venous stroke is because of the slow or sluggish blood flow according to the virtuose triad the three components which give rise to a thrombus formation are sluggish blood flow or vessel wall abnormalities or blood constituent abnormalities and therefore when there is sluggish blood flow it predisposes to thrombus and since there is no endothelial injury there is no platelet aggregation or agglutination and since there is no platelet agglutination or aggregation there is no role for anti-platelet therapy so a very important concept for venous strokes which is a red thrombus because of increased red blood corpuscles and since there are no platelets there is no rule for anti-platelet therapy so for venus strokes we give only anticoagulants we start with heparin and then continue with heparin for about five days along with it we start overall anticoagulants and then after five days we stop apparent and continue oral anticoagulants depending upon the upon the nature of the venous stroke so very important point for venous stroke we give oral anticoagulants for arterial strokes we give antiplatelets like aspirin or clopidogrel because in arterial stroke there is an endothelial injury when there is endothelial injury there is an increased platelet addition and platelet aggregation and therefore we give anti-platelet therapy it is otherwise known as white thrombus because there are no much red corpuscles it is because of platelets so very important arterial stroke which is a white thrombus which is because of endothelial injury platelet adhesion and aggregation we give anti-platelet drugs venous stroke where there is no endothelial injury which is because of sluggish blood flow and increased red blood corpuscles or red thrombus we give anticoagulants so for venous stroke we give anticoagulants for arterial strokes we give antiplatelets a very important clinical point right but to understand stroke and the different types of strokes basically we need to understand the blood supply of the brain which is known as circle of villus the main arterial supply of the brain comes from two systems one the anterior system or the carotid circulation which is about eighty percent and second is the posterior circulation or vertebral baseline circulation which is about twenty percent so anterior carotid circulation is about eighty percent that is the internal carotid artery the posterior or the vertebral based circulation is about 20 anterior circulation is through the internal carotid artery which supplies the anterior brain through the anterior and middle cerebral arteries and posterior circulation is through the vertebros restart system which supplies the posterior brain through the posterior cerebral arteries again the nature has been very kind to human beings by giving 80 percent of strokes due to anti-recirculation and 20 of the strokes only due to posterior circulation why is this important anti recirculation strokes are less dangerous as compared to posterior circulation strokes because anti-circulation strokes basically supply the cortex so they are not that dangerous but posterior circulation stroke basically supplies the brain stem medullo oblongata ponds and midbrain where we have the vital centers respiratory center cardiac center and therefore most of the time it results in mortality so posterior circulation strokes are more dangerous more most of the time it results in mortality and anti-recirculation stroke is less dangerous and most of the time patients recover so fortunately anterior circulation stroke or corrupted arterial circulation stroke is more common which is about 80 percent and posterior circulation stroke vertebrae based on circulation stroke is less common uh which is only 20 percent which is good for human beings because they are they cause less mortality so poetry circulation stroke is through the vertigo based on system which supplies the posterior brain to the posterior cerebral arteries right the anterior and middle cerebral arteries supply the frontal and parietal lobes while the posterior cerebral artery supplies the occipital lobe the vertebral and baseline arteries perfuse the brain stem midbrain and cerebellum we have an excellent communication going on between the various arteries supplying the brain we have an anterior communicating artery which connects both the sides of the brain the anterior cerebral arteries so until communicating arctic connects the both anterior cerebral arteries so both sides of the brain are connected and the posterior communicating artery which communicates the middle cerebral artery with the posterior cerebral artery that is the front anterior partial portion and the positive portion creating a protective anastomotic connections that is in the form of circulophilism so circle of bliss gives an excellent protection to the brain the left and the right sides of the brain are connected to the anterior communicating artery the anterior and the posterior parts of the brain are connected together through the posterior communicating artery so if there's a block in the anterior part blood comes the posterior part and tries to compensate there is a block on one side blood count tries to come to the other side and tries to compensate so the nature has given a wonderful protection to the brain in the form of circulation but despite this wonderful protection to the brain in the form of circle of village stroke or brain attack is the second leading cause of death imagine if the protective effect were not to be there perhaps stroke or brain attack would have been the leading cause of death despite this wonderful protection in the form of circle of village stroke or the brain attack is the second leading cause of death and therefore if this wonderful protection were not to be there perhaps stroke or brain attack would have been the most common cause of death so we have a very good protection to the brain in the form of circle of villus right so here the it has been depicted in the form of diagram you have the two posterior two vertebral arteries joining together to form the basilar artery we need to have an overview overview understanding of the blood supply of the different parts of the brain then only we can approach a person suffering from stroke confidently so we have two vertebral arteries coming together and joining as a basal artery so the lower most part that is the middle oblong data is supplied by the vertebral artery so medulla oblongata is supplied by the vertebral artery two vertebral arteries they join together to form basilar artery that means the pons is supplied by basilar artery the basilar artery divides into two posterior cerebral arteries that means the midbrain is supplied by the posterior cerebral artery the posterior cellulite winds around and then comes and supplies the occipital cortex back part so summarizing the medulla oblongata supplied by the vertebral artery pons is supplied to the basilar artery midbrain is supplied with the posterior circulatory which winds around and supplies the oxidative context so we need to know the different parts of the brain supplied by the different vessels this is about the posterior circulation stroke anterior circulation stroke it is supplied with the internal keratin artery we have the middle cerebral artery which supplies the entire cortex so internal characteristic middle circular treatment supply the entire cortex and anti-reserve lattice supplies a small anterior part of the brain which is joined together by the anterior communicating rt so the entire cortex lateral part of the cortex is supplied by the middle circular artery except the posterior part which is supply the oxford record which is supply the posterior circulatory and a small anterior part of the brain which is supplied the anterior cervical artery except that anti-cerebroblastic supply is a small anterior part and oxford cortex which is surrounding the posterior artery otherwise the entire cortex is supplied to the middle circular artery so a person develops a cortical stroke it is because of the middle circle artery again middle circularity divides into two divisions superior division and the inferior vein superior division supplies the broca's area and the inferior division supplies the vernix area we have the lenticlostriate artery coming from the middle cylinder which basically supplies the internal capsule so this is the broad overview of the circle of villus and this diagram is very very important in understanding in understanding the various pathophysiologic mechanisms of stroke yeah this is again another another diagram right so summarizing what all we've discussed so far in the form of diagram medulla oblongata is supplied by vertebral artery and a branch of vertebral artery known as spica posterior inferior cerebellar artery so if someone says person has got lateral medullary stroke or vallenberg stroke or medulla oblongata is affected we can be sure that it is the vertebral artery or a branch of vertebral artery that is a pica which is affected suppose a person develops pontine stroke that means it is the basilar artery which is involved suppose a person has got mid brain being involved it is a posterior cerebral artery the cerebellum is supplied by three arteries two arteries coming from the basilar artery that is the superior cerebellar artery anterior inferior cerebellar artery and the third artery is the pica posterior inferior cerebellar artery coming from the vertebral artery so cerebellum is supplied by three arteries one the superior cerebellar artery coming from the basilar artery second the anterior inferior cerebellar that is also coming from based on atp and third pica are posterior cerebellar coming from the vertebral artery the entire cortex the entire cortex other than the posterior and medial frontal cortex the entire cortex is supplied by the middle cerebral artery the occipital cortex is supply the posterior cerebral artery and the frontal cortex the medial part is supplied by the anterior cerebral artery so very important this is in nutshell the different parts of the brain supplied by the different vessels medulla oblongata by vertebral artery pons by basilar artery midbrain by posterior cerebral artery cerebellum by superior cerebellar artery anterior inferior cerebellar treatment cerebellar artery the entire cortex being supplied to the middle cerebral artery except the frontal part with the cellulite the ac anticipating and the oxygen context will supply the post central artery so this is a very very important diagram yeah now we are going to talk about the most important part of this lecture the internal capsule and its clinical significance so i need your attention because internal capsule lesions is the commonest case which is present which is kept for the exam especially for undergraduate exams for undergraduate exams usually the long case is neurology and in neurology usually the long case is stroke and in stroke it is usually because of the internal capsule lesion and therefore we need to understand the internal capsule in detail and have a clear understanding of internal capsule so internal capsule has basically got three parts anterior limb jeno and the posterior limb it has got three parts anterior limb genome and posterior lip for all practical purposes it is the posterior limb of the internal capsule which is very very important because all the mortar fibers cortico bulbar fibers and the corticospinal fibers lie in the posterior limb likewise the sensory fibers also lie in the posterior limb so the posterior limb gets affected person will have hemiplegia and hemisthesia very important is the posterior lip all the fibers come and condense in the posterior limb of the internal capsule then we have the genome where we have the cortical bulbar fibers and the anterior limb in the anterior limb basically we have a three important tract one is the paved circuit which is concerned with the memory second is the is a psychotic pathway frontal i feels area number weight which comes to the anterior limb of the internal capsule and goes to the pprf paramedic in quantum vertical formation and third is the frontal ponto cerebellar fibers coming to the anterior limb of the internal capsule going to the pawns and then finally cerebellum right this is about the important structures so the posterior limb is very very important which causes hemiplegia and hemisphere you can see the optic radiations lying just underneath and the auditory radiation is also going by and therefore if the posterior limb selector gets involved along with optic radiations patients will have hemiplegia hemisthesia and optic radiation being involved they'll have homonymous hemianopia right now another important point is the blood supply of the internal capsule the blood supply of the internal capsule is very very interesting because internal capsule is supplied by multiple vessels unlike cortex which is supplied by a single vessel either mca or ac or pca here the intel cache is supplied by the by multiple vessels and therefore when a vessel selectively affects a particular track we get a pure form of deficit like a pure motor hemiplegia a pure sensory hemisphere attacks here because all the parts are different parts of the internal capsule are supplied by different individual blood vessels and therefore a pure form is very common in internal capsule unlike in cortex for example the mortar part motor cortex and the sensory cortex both are supplied with the middle circular artery so they'll have hemiplegia and hemispheric combined form they'll not have pure monotony page or pure hemisphere unlike an internal capsule where they can have a pure mepj or whole pure hemisphere so what is the blood supply of the internal capsule internal capsule uh different books give blood supply in slightly different manner but very easy to remember is that the entire upper part we divide the internal capsule in upper part and the lower part the entire upper part is supplied by the middle cerebral artery so the entire upper part is supplied to the middle circularity the linty closed triad arteries of the middle circular artery and the lower part we divide it into three parts upper part middle part and the lower part of anterior middle and posterior one third the anterior one third is supplied by the anterior cerebral artery a branch of which is humorous artery the middle part is applied to the posterior communicating artery and finally the lower part is supplied by again ac anterior choroid artery which is a branch of internal carotid artery so easy to remember the lower part of the blood supply of the internal gases acpc ac ac is anterior circulatory a branch of which is humonous artery the middle part is the posterior communicating artery and the lower part or the posterior most part is the again the anterior coronal artery is a branch of internal carotid artery so in the anterior coral or a branch of indian carotid artery gets affected uh it basically affects the posterior limb of the internal capsule so it'll cause hemiplegia hemisthesia and visual radiations are also close by so it causes hormone seminar so passive got hemiplegia hemisphere and homonymous immunoglia it is because of the anterior coronal rt involvement which is a branch of the internal carotid artery again you have the anterior cervical artery the main anterior cervical artery supply is the medial part of the frontal lobe giving rise to leg involvement but a branch of the anterior circulatory humenus artery selectively affects the anterior part to some extent you know where the cortical bulbar fibers are placed so they'll have a facial brachial monoplegia so the person has got only face and hand involved it is because of the humerus arterial branch of the anti-cebular environment but if the main anticipation gets affected the leg area gets affected which can give rise to paraphrases so very important internal capsule so as i said the blood supply of the internal capsule the summary the and we divide the internal capsule into upper part and the lower part the entire upper part of the internal capsule is supplied by the lenticclose triad branches of the middle circular tree the lower part of the intel calcium is divided into three parts the first part anterior limb is supplied with the humerus artery a branch of the anterior circulatory the second part genus supply with the posterior communicating artery and the third part the posterior limb supplied by the anterior coral artery a branch of internal carotid artery which characteristically causes hemiplegia hemisthesia and homonymous semianoptia the internal capsule has got three divisions anterior limb genome and the posterior limb the posterior limb is very very important as it contains corticospinal tract and sensory fibers with nearby optic radiations causing then semiplega hemisphere homonymous hemianopia a lesion being anterior coronary environment here again one important point internal capsule lesion causes a dense semi pleasure because all the corticospinal fibers are so close together so hands and legs are equally affected when hands and legs are equally affected we call it as a density pleasure unlike anterior cervical artery or middle circular tree in anterior circulatory leg area is weaker than the hand whereas in middle circle artery hand is weaker than the leg so upper limb is weaker than the lower limb in a middle class environment whereas in anticipated environment lower limb is more weaker than the upper left but in internal capsule upper limb weakness and lower limb levels are equal because they are so close together which we call it as a dense hemiplegia so the genu has got cortico bulbar fibers and causes facial brachial hemi monoprint due to the humerus artery of the anticipated environment the anterior limb has got paper cerebellar fibers right as i said internal capsule uh very very important clinical signal because of multiple vessels supplying internal capsules there could be the following lachna syndromes we can get pure forms because a particular tract is supported as single vessel so we can get pure forms these vessels are commonly involved because they are end arteries if it causes lipo hypnolysis it causes infection if it causes charcot neutral aneurysm it causes hemorrhage so lipo hyaluronalysis because especially hypertension age causes lipoid noses in these end artists and causes infection these are known as lachma strokes because they are very small influx less than two centimeters less than one point five to two centimeters so what are the lachner syndromes we can have pure hemiplegia pure mortar any pleasure that is the corticospinal tract involved only because of the lenticuloside badges of the middle circulatory environment we have pure sensory anesthesia because sensory tract involvement because of the pecan artery or the posterior cellulite involvement we can have ataxic hemiparesis and lot of students fail to understand why internal capsulation produces ataxia because attacks is a manifestation of cerebellum internal capsule lesion produces ataxia because the of ponto cerebellar fibers goes to the anterior limb of the internal capsule and the corticospinal fibers go in the genome and the posterior limb so when there is a selective involvement there person can have attack say because the frontal ponto cerebellar involvement so they can have ataxic hemipares because of the frontal pontoo cerebellar and corticosterone and clumsy hand dysarthria syndrome because the corticospinal tract and frontal ponto cerebellar fiber involvement the venous circulation not very important or significant as arterial circulation like cyclophilus the venous collecting system is formed by a collection of sinuses over the surface of the brain which drains into the jugular veins the superior sagittal sinus thrombosis one of the common venous disorders encountered so this is the venous supply right right now we shall see the brain attack and humidity pathophysiology ischemic stroke blood supply to part of the brain is decreased leading to dysfunction of brain tissue in that area there are three types of ischemic stroke one thrombosis second embolism three systemic hypoperfusion because of the low flow strokes so thrombosis obstruction of a blood vessel by a blood clot formed locally it may be in a large vessel or a small visit like lachner infection whereas embolism is obstruction due to an embolus from elsewhere in the body like heart what we call as a cardio embolic stroke or from internal characterity what we call as an artery to embolism and third is the systemic hyperperfusion or low flow strokes they are occasionally seen with severe proximal stenosis and inadequate collaterals challenged by systemic hypotensive episodes so what is the systemic type of perfusion when there is systemic hyper perfusion imagine there is a middle circular artery and anticipate when there is systemic hypotension there is hyper perfusion so the proximal part of the artery gets good blood supply but as they go digitally the blood supply gets decreased decrease and then finally stops so between the anticipatory and medicinality the proximal parts get good blood supply but as they go digitally the blood flow stops so we call that as an anterior water zone in fact or anterior watershed infection which causes man in barrel syndrome especially the shoulders and the hip girdle gets affected so they be they they where the posts will be as if they are a man in a barrel like this mca and pc the proximal parts get good blood supply but as they go distally the blood supply gets decreased so this is posterior watershed infarction or posterior border zone infer characteristically causes balance syndrome because the oxygen cortex is involved they'll have lot of visual disturbances and balance syndrome is a triad of asymmetric nausea optic cortexia and oculomotor apraxia right this is about the ischemic stroke the pathophysiology now let's talk about the hemorrhagic stroke pathophysiology bleeding due to rupture of vessels there are two types of hemorrhagic strokes one is the intracerebral hemorrhage it is basically bleeding within the brain itself due to either intra parent chemical hemorrhage bleeding within the brain tissue or intraventricular hemorrhage bleeding within the brain's ventricular system and second we have the subarachnoid image which is basically bleeding that occurs outside the brain tissue but within the skull under the arachnoid matter here there's a very very important clinical point in subarachnoid hemorrhage subarachnoid image patients usually present with severe headache subarachnoid image and meningitis patient they usually present with severe headache whereas intracerebral hemorrhage or mcn fat they don't present with headache why because the brain is completely insensitive to pain there are no pain receptors in the brain you cut brain there is no pain it is only the coverings of the brain the meninges and the vessels in the meninges which are pain sensitive and therefore only when the meninges get affected patient will have severe pain and headache like sub-paragon hemorrhage where there's hemorrhage underneath the arachnoid membrane which is one of the membranes of the meninges or meningitis inflammation of the meninges it also produces severe headache so only when the meninges on the meningeal vessels get involved persons will have headache or pain brain parent chima per se does not produce pain you cut brain there is no pain only when the meninges are involved there is severe pain right what are the disease modifying factors we see so many stroke patients some do exceedingly well and they recover some they do not do well and they die in fact if you take an average of 100 stroke patients 25 percent of the stroke patients 25 percent of the stroke patients do extremely well even without giving much treatment they completely recover at the other end of the spectrum even whatever treatment we give 25 percent of the persons will die of the stroke patients will die in the rest 50 percent of the stroke patients 25 percent will have moderate disabilities and 25 percent will have severe disability so about 100 stroke patients if we see 25 patients completely recover 25 patients die or the 50 patients 25 percent have got mild deficit and 25 of the patients will have severe addiction so why is there variability what are the various disease modifying factors the variability in stroke recovery is influenced by collateral vessels as i said in the beginning of my lecture there are a lot of collaterals the both sides of the brain are connected by the anterior communicating artery the anterior and posterior part are coming are communicated by poster communicating artery so if one side of the brain gets affected the blood can come from the other side and compensate there's not going to be much they've said so if there's a good collaterals going good communication going between the ac mc and pca or between the internal carotid artery and the external carotid dirty or between the vertebral based system and the internal characteristic system if there are good collaterals new vessel formation opening up of the vessels person's deficit will be minimal so one of the most important disease modifying factors is collateral vessels second is the blood pressure if the good blood pressure is maintained obviously the deficit becomes less specific site as i said in the beginning of the lecture the cortex is not that much dangerous whereas brainstem is dangerous the pawns middle oblong and we have vital important cardiac centers respiratory centers and if those centers get affected the mortality will be high so specific site is important mechanism of vessel occlusion there's a certain block like an embolism there's a maximal deficit even at the start of the stroke whereas if it is slow formation thrombus formation slowly developing atherosclerosis there is a time for the collaterals to develop and therefore the deficit will be minimal so mechanism of vessel obstruction is also important so the important disease modifying risk factors are collateral vessels blood pressure specific site and mechanism of vessel occlusion if blood flow is restored prior to significant cell death the patient may experience only transient symptoms known as transient ischemic attack and one of the important manifestations of transient steaming attackers amorous has few gas when the internal carotid artery gets blocked the ophthalmic country gets affected the retina gets affected and person will have a visual loss on one side as if a curtain coming from upwards and going downwards if this is the kind of history you're getting you have to be really really careful because it is a sign of an impending stroke what we call as amorosis fugax autoregulation very important concept in health there are regulatory mechanisms which maintain a constant blood flow across a wide range of arterial blood pressures to meet the high resting metabolic activity of brain tissue cerebral blood vessels dilate when systemic blood pressure is lowered in health what happens brain tries to maintain a constant perfusion if there's a decrease in blood pressure vessels dilate so as to increase the blood flow to the brain if there is hypertension blood vessels constrict so that there is a decreased perfusion to the brain this is known as auto regulation but in stroke this autoregulatory system can be disrupted and can be disastrous so cerebral blood vessels dilate when systemic blood pressure is lowered several blood vessels constrict when systemic blood pressure is raised so here you can see in this diagram there is a constant perfusion of the blood flow but to certain limits but beyond these limits uh the the constant blood pressure blood flow changes so when the blood flow is decreased you can see the vessels dilating and the blood pressure is increased you can see the vessels constricting so there's a constant blood pressure constant perfusion across the a blood pressures [Music] clinical features and presenting problems most vascular lesions develop suddenly within a matter of minutes or hours and so it should be considered in the differential diagnosis of patient with any acute neurological presentation what are the usual clinical presentations of stroke usually they have urelatal weakness or hemiplegia which is a classic presentation of the stroke the weakness is sudden progresses rapidly and may improve the weaknesses of upper motor neuron type upper motor neuron of the phase seventh cranial nerve is often present motor deficit subtle parallel signs pronator drift clumsiness of finger moments you strongly suspect that the corticospinal tract is involved but you are not getting good signs like extensor plantar response or knee-jerking risk so what is the sign which you try to elicit so that you can pick up such a weakness and a subtle pyramidal cacti this is known as pronator drift generally corticospinal tract has got a predilection for certain muscles like supinators of the upper limb so when the supinators of the upper limb are weak the pronator takes over and person will have the pronator grip so you ask the person to extend his hand and if you see the person pronating a pronator a very classic sign of subtle uh corticospinal tract involvement and corticosteroid usually affects the distal muscles so they'll be having clumsiness of the finger moments so here you can see person has got the pronator drift so the weakness is not according to the quantity it is according to the quality uh the hand has got the highest representation you can see on the motor harmonically the hand has got the highest representation the phase has got the highest representation but the trunk and the lake has got a minimal representation so the fibers come the unit and the posterior limb of the entire capsule they go through the midbrain pawns where you'll cross over at the level of the medial object go to the opposite side goes to the anterior con cell here now i'm going to talk about a very very important concept what is upper motor neuron and lower motor neuron anything above the nucleus upper motor neuron anything below the nucleus is lower motor neuron so anything about the nucleus upper motor neuron there are two components one the corticobulbar fibers where the fibers go arise from the cortex and go for till the mortar part of the cranial non-nuclei second is the corticospinal fibers where it arises from the cortex and goes to the anterior ventrals of the spinal cord so upper motor neuron there are two commons one the cortical bulbar fibers second the corticospinal fibers again lower motor neuron anything below the nucleus is lower motor neuron so there are two components one coming from the motor part of the cranial nerve nucleus as cranial nose one coming from the anterior horn cells as the spinal nerves so these are all lower motor neuron why is it very important it is important to place the lesion and all the cranial nerve nuclei have got bilateral innervation one side cortical mark the other side corticobalabar fibers except seventh now seventh note has got a predominant supply only from the other side and therefore in a um lesion we see only the seventh in our normal environment not other cranial nerve involvement right now i've discussed so much of brain stem it may sound confusing i'll tell you a very easy method to remember all the important breaks and structures this is known as rule of four if you remember this rule of four we can remember all the important brainstem structures what does this rule of four say there are four cranial nodes in the medulla oblongata four cranial nerves in the palms four training nodes in the midbrain and above so the four cranial nerves in midbrain and above are the third and fourth in the midbrain first and second is above midbrain five six seven eight four cranial nerves in the pons nine ten eleven twelve fourth cranial nerves in the middle oblongata then we need to know what cranial nerves are placed medially and what cranial nerves are placed laterally all the cranial nerves which can divide twelve into equal parts are placed medially and all the cranial nerves which cannot divide 12 into equal parts are placed laterally like third now fourth note sixth note and twelfth note can divide twelve into equal parts so three and four are placed medially in mid brain six is spaced medial in pawns and twelfth now is placed immediately in the middle of the all the other cranial nerves which cannot divide 12 into equal parts are placed laterally second all the plaques which start with the letter m is placed immediately m for m example the the mortar track that is the corticospinal tract is placed immediately m m median longitudinal fascicles which connects third fourth sixth and eighth is placed immediately the medial lemniscus that is the posterior column is placed immediately the mortar part of the cranial nerves are spaced medially so all the structures which start with the letter m are placed medially m for m mortar track that is the corticospinal tract medial longitudinal fasciculus mlf medial lemniscus and the mortar part of the cranial nerve all these four m's are placed immediately all the structures which start with the letter s are placed sideways s for s the spino cerebellar tract the sympathetic tract the spinal tract of the trigeminal nerve so sympathetic tract spinal thalamic tract and the sensory tract of the trigeminal now which start with the letter s are placed laterally that's why in lateral medullary syndrome we have the spinocerebellar tract involvement having ataxia that is lateral part you have the sympathetic tract getting affected we have honest syndrome the spinal thalamic translating effect you have the pain and temperature loss and the spinal tract of the trigeminal nerve getting affected we have the facial sensors so four tracks we start with the letter s are placed four tracks which start with the letter m are placed immediately so if we remember this it becomes very very easy and then another important rule is the rule of 17 we have 12th now we have fifth note 10th now seventh note each now produces a different kind of manifestation some knows affect i pull the face to one side some moves will push the face to the opposite side how do we remember again very easy to remember by rule of 17 12 plus 5 is seventeen and ten plus seven is seventeen if tenth now and seventh now get affected the movement will be towards the healthiest side if twelfth nov and fifth now which pushes the face to the opposite side gets affected the movement will be towards the dc side so if 12th now and fifth number gets affected the movement will be towards the disease side 12 plus 5 is 17 if 10th now and 7th now gets affected the moment will be towards the healthier side 10 plus 7 is also 17. so if you remember these laws it becomes easy so here you can see the facial now seventh has got upper part and the lower part upper part has got bilateral innervation whereas the lower part has got innervation only from the opposite side so if there is an upper motor neuron lesion only the lower part on the opposite side gets affected lower part supply the lower part of the face so only the lower part of the face and the opposite side gets a fitted phase is deviated to the healthy side if there is an element lesion like belt's palsy both the upper part and the lower part on the same side gets affected so upper part and the lower part of the same thing gets affected they cannot close the eyelids and once they attempt to close the eyelids you can see the eyeball moving upwards it is known as bell's phenomenon so all cranial the cranial nerves do not get affected in a corticospinal attack lesion because all all traditionals have got bilateral inheritance except seventh note the lower part which gets innervation from the opposite side and therefore in a human lesion we only see the human seventh nepalese other cranial nerves do not get affected so these are the differences between the upper motor neuron and the lower motor neuron in the upper motor neuron there is less wasting the tone is plastic because it the tone is increased in anti-gravity muscles flexors of the upper limb and the extensors of the lower limb so they flex like this and they extend the lower limit and then they walk like this this is known as sub conduction gate subconduction gate nicely depicted in films also where you see a person having a flex portrait of the upper limb and extended posture of the lower limb it is because it increases the tone in anti-gravity muscles that is flexors of the upper limb and extensors of the lower limb which is known as plastic gate where you they have the characteristic subconduction gate the pattern of weakness it selectively affects the extensors of the upper limb uh and the flexors of the lower limb it affects the supinator and the deep tendon reflexes are increased and the plantar is extensor in a human lesion so they'll hide they can have the sensory disturbances they can have amorous fuel gas they can have speech disturbances as i said the upper part of the middle circular supply is the broadcast area and the the inferior division supplies the vernix area so broca's area is responsible for fluency and vernix area is responsible for comprehension so burning syria gets affected they cannot understand but they keep on speaking it is a fluent but a nonsense speech if broca's area gets affected they can understand but they cannot speak well it is a non-fluent but sensible speech so broca's aphasia vernix official and then we can have dysarthria if wealth now gets affected the tongue gets affected if seventh now gets affected the lips get affected if tenth note gets affected the palate gets affected so if a person has got difficulty in using the lips say for we have to use lips the person is not able to use ellipse that means orbicularis is affected that means seventh number is affected the person is not able to say to say they have to use tongue so if the person is not able to use tongue the lingual component is is affected that means the pelton is affected the person is able to not able to say they have to use palette that means strengthener is affected because tenderness supplies palettes so they cannot say car so ask him to say the person is able to say pa that means the lips are moving well the seventh nerve is intact the person is able to say that tongue is moving well the 12th nose is intact the person is able to say power will that means the paradise is working well that tenth now is working well if the brainstem is in all the way if c lateral cranial nerve pulses and contralateral hemiplegia for example midbrain is involved the third fourth is getting affected pawns five six seven eight middle obligated nineteen eleven two on one set and hemiplegia on the opposite side and the symptoms reflect the vascular territory involved so if the middle cerebral arteries involve they'll have hemiparesis because the mortal cortex is involved they'll have sensory deficit because the hemisensory is involved the superior region of the mca if it affects person will have broadcast aphasia that means a non-fluent but sensible speech the inferior division of the mca gets affected they'll have burning surface fluid but nonsense speech if the right side gets affected they'll have hemi neglect so much so that if they shave they shave only on one side they ask to wear a trouser they wear it on one side at the bedside you give them a clock and hasn't put all the 12 numbers they put only the 12 numbers on one side they completely neglect on the other side this is known as me neglect characteristic is seen in a non-dominant lesion pareto low so they'll completely neglect one side if you pick their hand they ask whose hand you're pinching it they'll ignore they'll completely deny the existence of one side of the body which you call as any neglect which you see in a non-dominant cortex dominant cottage is that cortex where the speech centers are situated so the dominant cottage gets affected they'll have all kinds of apraxia inability to perform a learned mortar act they'll have homonymous amino acid because the visual radiations get affected they'll have gase preference where the front line feels area number eight going to the pprf on the opposite side so the front cortex is stimulated the eyes go to the opposite side which is known as saccadic pathway so frontal cortex gets affected the eyes cannot move the opposite side so eyes will be looking to one side patient will have hemiplegia on the opposite side these the sternocleidomastoid has got a predominant ipsilateral innervation so cause the sternocleidomastoid on the same side gets affected so they cannot move the head to the opposite side they'll be moving ahead to one side so if the cortex gets affected the eyes cannot go to the opposite side eyes will be looking to the same side head dolls will be looking for the same set because of the fight because of the sternocleidomastoid environment and hemiplegia will be on the opposite side very classic and you say blood is involved that means the leg area gets affected so they'll have a paraphrase if both the legs are getting affected they'll have cortical sensory loss over the leg the bladder area is there so they'll have urinary incontinence gait gets affected gate apraxia they'll have the primitive reflexes getting affected if the posterior cervical artery gets affected basically the occipital cortex gets affected so they'll have a homonymous amino acid cortical blindness the temporal lobe is supplied by the pca so they can have memory deficits the thalamus can get depicted they can have spontaneous pain if the midbrain gets affected as i said third and fourth nose are in the mid brain so they'll have third knob pulse and contralateral hemiplegia you have basically two kinds of eye movement horizontal movement and vertical eye movement the vertical eye movement the center is in the mid brain so the vertical gaze gets affected especially the upgrades they'll have convergence retraction systems because convergence because the more the medial electric contract retraction because the super rectus and inferences contact at the same time it's a super nuclear type of policy so they have contraction convergence retraction nystagmus upgrades policy third no policy and contralateral hemiplegia if it responds we know that the sixth and seventh now gets affected so seven gets affected sixth now gets affected abduction gets affected horizontal eye movements pprf is responsible so they'll have conjugate gauge palacy uh pawns is supported by a single vista and therefore when it captures it affects both the sympathetic uh tracks so it can result in honor syndrome spinothalamic pact they'll have diminished pain and temperature sensation and the bulk of the pond you have the frontal ponto cerebellar fibers so they'll have ataxia if the medullas are affected the lateral medulla you remember the rule of four what i said the four structures which start with the letter s are placed sideways spinothalamic track so pain and temperature is affected on the opposite side the spinal tract of the trigeminal nose so pain and temperature loss is on the same side of the face the sympathetic track which results in harness syndrome and the spinal cerebel attack so they'll have attacks here so all these structures get affected so lateral medullary syndrome uh wallenberg syndrome you have these features very important point in valenburg syndrome or lateral medical symptoms that hemiplegia is not present because corticospinal attack is medially placed it's one of the important mcq questions the stroke symptoms we have the total anterior circulation syndrome partial anti-recirculation syndrome lachner syndrome and posterior circulation symptoms so the total anti-circulation system entire middle cerebral artery gets affected like you can have hemiparesis aphasia emissions loss or homonymous amino acid whereas if it is partial anti-recirculation syndrome only a branch of nca or aca gets occluded like isolated mortar loss isolated higher cervical function loss like aphasia if it is lactose syndrome as i said a small artery small place gets affected pure mortar hemi parasites pure sensory stroke because of thalamus atoxic chemicals because of internal capsule where we have the pontos uh cerebellar fibers frontal ponderable fibers or dysarthria clumsy hand syndrome posterior circulation stroke wember syndrome where the midbrain gets affected you have ipsilateral thermopylasy human seventh not palsy and contralateral hemipedia it spawns yeah cloth syndrome if the red nucleus is involved they'll have ipsilateral turn of palsy and contralateral cerebellar fibers and then you have parry knot syndrome also in midbrain where the update gets affected they cannot look upwards they'll be looking only downwards because the vertical centers are in the midbrain horizontal centers are in the palms so if the midbrain gets affected the vertical center gets affected in vertical central you have up gaze and down these upgrades fibers cross and then descend down guess fibers descend straight away so any lesion compressing on the top of the midbrain will affect the crossing of these fibers so they cannot look upwards they'll be looking downwards for example parry not syndrome calamine camera which goes and compares the top of the midbrain so eyes will be looking downwards hydrocephalus it goes and compares the top of the bit brain so eyes looking will be downwards you call that a sunset site so there are updates palacy and convergence retraction nystagmus you have the miliard kubler syndrome where you have the sixth and seventh opposite quadrilateral hemiplegia valenburg syndrome which i've already described ah yeah another important point is the cruciate hemiplegia very interesting general hemiplegia has one sided weakness upper limb low element say one side or this side upper limb lower limb but can you get upper limb weakness on one side and lower the weakness on the other side it is possible it is known as cruciate hemiplegia this can occur in medulla oblongata in medulla oblongata upper limb fibers cross above and the lower limb fibers cross below you can see in the diagram so you can have the crossed lower limb fibers and uncrossed you can have the uncrossed lower limb fibers and cross upper lip fibers you can see in the diagram so you can have a weakness of upper limb weakness of the lower limb same thing can happen the other side also so if there's a lesion here there's an uncrossed right lower limb and crossed left upper limb weakness there can be lesion here or when the both the upper limbs fibers if there's a region here there'll be upper limb fibers weakness only or when the lower limb fibers get weaker only the lower limb fibers get affected so you can have all kinds of permanent inflammation combinations in the middle of long term so up across upper lymph fibers or uncrossed lower limb fibers or both upper lip fibers or both lower lymphatics this you call it as cruciate immunity yeah again i thank once again for netflix for giving me such an excellent opportunity to give a very very important lecture on stroke especially for undergraduate students and perhaps for postgraduate students very important uh for exam point of view and even for practice point of view because stroke is the second leading cause of death after mi thank you so much sir so can we go through some questions yeah a few questions in the comment section you can read it out for me yes sir um so um dr ram murket is asking the target blood pressure in islamic stroke and second is hemorrhagic hemorrhagic stroke yeah a very good question i need to explain an important concept here we have an important concept known as monroe kelly hypothesis monroe kelly hypothesis says that there are three important components one is the brain second is the blood third is the cerebrospinal fluid so all these three components put together forms the intracranial space so if one space expands the other two has to has to come down in size so that the there is no intracranial pressure increased but for example if there is a space optimization like brain access or hematoma goes and compresses the brain so the intracranial pressure rises why the intracranial pressure rises why we don't say intra-abdominal pressure why we are talking only about interaction any pressure because there's an overlying skull bone it will not allow the brain to expand so when there is any mass in the brain it cannot expand because there's an overlying bone so the pressure in the brain rises in and it causes ammunition where brain from one compartment goes to the other compartment or because there is interact any pressure it will compress the vessels and causes ischemic stroke we do not have a raised intra-abdominal pressure because abdomen can expand there is no overlying bone so this raised intracranial pressure we let the csf into the peritoneal cavity so that to some extent we can compensate so we are worried about the raised intracranial pressure so when what happens we have another important thing the cerebral perfusion pressure is equal to mean arterial pressure minus intracranial pressure i repeat cerebral perfusion pressure is equal to mean arterial pressure minus intracranial pressure so when the cerebral perfusion is decreased we try to increase the mean arterial pressure to increase the cerebral perfusion pressure or decrease the intracranial pressure so to maintain cerebral perfusion pressure we either increase the mean arterial pressure or decrease the intracranial pressure we can decrease the intracranial pressure by doing you know by taking the flap out or by letting the csf from the brain into the abdominal cavity and we can increase the several perfusion pressure by increasing the mean arterial pressure so what happens is that i say as i said the auto regulation in my the beginning of my lecture so when there is good auto regulation going on brain tries to compensate so when there is ischemic stroke when the cerebral perfusion is decreased what brain does it tries to increase the mean arterial pressure so that the perfusion to the brain is increased so in the first one or two days we should not unduly lower the blood pressure because brain is trying to compensate the decreased cerebral perfusion by increasing the mean arterial pressure so as soon as possible for the first couple of days we should not unduly lower the blood pressure only after a couple of days we try to lower the blood pressure so the first two days generally we try to maintain the blood pressure by 185 to 100 that is the usual blood pressure a hemorrhagic stroke will slightly go down of the systolic and diastolic pressure we should not unduly lower the blood pressure so as not to try to decrease the compensatory mechanism of the brain which is trying to increase the mean arteries to maintain the several position pressure for a skipping stroke it'll be around say 180 by 110 and hemorrhagic stroke will be slightly lesser than that [Music] yeah so there is one more question oh can you explain how contralateral ataxia and claudia syndro dr guru prasad is asking about yeah yeah a very good question cerebellar ataxia a cerebellar science generally when one side cortex gets affected like corticospinal tract or spinal column intact environment we have the weakness on the opposite side we have the sensory involvement on the opposite side but cerebellum is peculiar when the cerebellum gets affected the cerebellum manifestations are on the same side why the cerebral manifestations are the same set because of the double crossing we have the track going from the cerebellum going and conveying the information to the brain frontal cortex this is known as dentato rubro thalamo cortical pack it goes for the dentitus for example on one side for the red nucleus thalamus and cortex on the opposite side finally everything has to take place the corticosteroid it distance and crosses the level of the middle orbit goes to the opposite side so one side cerebellum gets affected the manifestations are on the same side dentato root growth cortical factor but if the red nucleus is involved the this side it is already crossed so manifestations will be on the opposite side so if the red nucleus gets affected the manifestation will be on the opposite side but if cerebellum gets affected the manifestations will be on the same side yeah if you want further details this i gave an overview but if you want real details i made nearly 225 videos you can go back to my youtube channel doctors universe medical concepts where i've really discussed in depth so i think there are no more questions so thank you so much sir for a wonderful session and looking forward for your next session

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Dr. Sreenivas discusses the localization of lesions in hemiplegia in another engaging session in the 'Neurology Concepts' club. Join us to gain a thorough understanding of these concepts.

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