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Consciousness and coma

Aug 31 | 1:30 PM

Level of conscious & coma are important stages to be evaluated cautiously in neurological examination of the patient. It is a very important prognostic marker in head injury, neurological infections & post-neurological surgical intervention. Also for evaluating brain dead for organ donation. join us for this interesting discussion.

[Music] good evening everyone welcome to the today's evening session on consciousness and coma i am dr lalit from andhra pradesh i was pleased to introduce our guest speaker dr sirikura shinwas who is currently working as a professor and consultant neurologist in gsl medical college rajamandri and he is also a consultant neurologist at sri padma madha euro super specialty hospital in rajamandur andhra pradesh sir has graduated from sri ram chandra medical college chennai and completed his master's in internal medicine from manipal academy of higher education which is a deemed university and completed his dm neurology from sri ram chandra medical college and research center from chennai which is also a deemed university sir is very passionate passionate teacher and is a resource person in various state and national conferences he published sneden syndrome in postgraduate medical journal in january 2000 he is also a medical author of the book focused neurology which has gone for repric within three years of publication by cbs publications which shows the popularity of the book among the undergraduates and postgraduates which make the difficult concepts of neurology very easy for them during this tough times of kovite 19 to help all the undergraduates and postgraduates to learn the concepts better he started his own youtube channel dr srinivas medical concepts which has more than 5000 subscribers and with more than 200 videos which makes the neurology learning the joy of neurology and is helping the undergraduates and postgraduates in this tough times now i would like to invite dr sirugur shinwasser to enlighten us with his lecture and would like to hand over to you sir thank you dr lalit for those wonderful words at the outset i would like to thank netflix for giving me such a wonderful opportunity to address an allied gathering of at national level coma is a deep sleep like state from which the patient cannot be aroused consciousness has basically two qualities arousal or alertness it's a primitive function sustained by brainstem second is the cognition or coherence of thought which requires an intact cerebral cortex the maintenance of consciousness is by a special thalamocortical alerting system termed as the reticular activating system ras which is diffusely located in the brainstem and projecting to the two cerebral cortexes this is a very very important concept so ras is the alerting system which makes us all to be in a conscious state which is present in the brainstem and goes to both the cortices and therefore if a person has to lose consciousness by affecting the ra system either the brain stem person should get affected or both the parties should get affected i repeat both the cortices should get affected if only one cortex gets affected person doesn't lose consciousness because there is other cortex which can compensate for it so ra is system to get affected either it should be the brainstem or both the cortexes that's why a very big mca fact which we see in now neurology watch those persons do not lose consciousness because it is restricted to one cortex only unless there is a massive edema which is going and compressing the other cortex or the brainstem whereas simple hypoglycemia affects the ra system in a diffuse manner and person loses consciousness so either the brainstorm should get affected or both the complexity should get affected for a person to lose consciousness right again here you can see a nice diagram depicting the ra system it is going through the brainstem and is going diffused into both the cortexes that's a very important and essential point right so how is coma produced now we have understood the physiology now let's try to understand the concepts of coma so how is coma pose produced coma can be produced by structural damage to both the cerebral hemispheres like a big mca in part causing massive videomic going and compressing the other cortex also or the brain stem like a pontine hemorrhage person loses consciousness not only structural causes not only structural causes even metabolic causes which impair the functioning of the ras can make a person to lose consciousness so suppression of the reticular cerebral function by drugs toxins metabolic derangements such as hypoglycemia anoxia uremia hepatic failure person loses consciousness because cerebral neurons and ras depend so much on glucose oxygen and sodium for its survival and therefore the moment the sodium level goes down or the oxygen level goes down or the glucose level goes down ras becomes dysfunctional and person loses consciousness so we have structural causes of coma we have metabolic cause of chroma the two broad approaches to coma and one important point to be noted that metabolic causes of coma are far more common than structural cause of coma so hypoglycemia hyponatremia causing coma are far more common like than tumors or any other structural abnormality causing coma right now let me talk about a very common common practice which we see in our day to day watts a common concept why antihistamines and anti-cholinergics produce sleep as side effects we give antihistamines for allergy we give anti-cholinergic drugs but then why should they produce sleep as side effect it is because the fibers in the reticular activating system are histaminergic cholinergic adrenergic dopaminergic and certain energy stimulation of the ras produces arousal and inhibition of the ras by antihistamines and antichrists therefore produce sleep as side effect so they inhibit histamine they inhibit acetylcholine and therefore they produce sleep as side effect right fine now a person has come in a state of coma she is in an unconscious state so what is the important history taking points we have to know from the patient's attendant so as to elucidate the cause of coma so history taking sudden onset if a person's attendant says that he was alright doctor suddenly he lost consciousness so a person suddenly loses consciousness it could be either subject not hemorrhage or seizure if there's a gradual or fluctuating onset it could be subdural hematoma in fact old persons might have had a trivial injury a venously blood might be slowly trickling down they might even have forgotten slowly they start losing consciousness in fact subdural hematoma is one of the treatable causes of dementia metabolic encephalopathy hypoglycemia hyponatremia it can be gradual or fluctuating nonsense if there are pre-monitored transient symptoms person may having may be having amorous few gas a loss of vision coming from from top and going downwards like a curtain amorous fuego it indicates that the octanic artery of the internal carotid artery there's a thrombus and therefore the vision is getting affected so such symptoms they are forthcoming that indicates as an imping that's hand that's an impending cause of stroke supreme transient symptoms such as transient ischemic attack if there are only focus and preceding loc we should think of structural causes like hematoma impart or tumor they'll produce only focal manifestations on the opposite side at the other end of the spectrum if it is metabolic cause like hypoglycemia hyponatema it will be diffuse and generalized presentation if there's a history of fever we have to think of infectious causes of coma if there is a history of fall we have to think of intra-cerebral hemorrhage the person has got confusion then we have to think of metabolic or toxic etiology and obviously history of trauma cardiac arrest and drug injection are obvious and we can easily get it from the patient's attendant right now having got important points in history now how are we going to go about and examine a person who is comatose so because systematically we can get to know lot of causes lot of points which is probably responsible for coma first we'll go step by step first pulse heart rate if a person has got bradycardia it could be heart diseases or increased intracranial pressure when there is increased intracranial pressure it goes and compresses the middle oblongata brainstem structures so body tries to increase the perfusion to the brain by producing hypertension bradycardia and irregular respiration so there is hypertension bradycardia and irregular respiration that is known as cushing's reflex and it suggests that the person is having raised ict intoxications if there is tachycardia there would be infections or as a compensatory feature of hypovolemia next blood pressure if there is hypotension it could be myocardial infarction intoxication due to ethyl alcohol or barbiturates or sepsis if there is hypertension it could be intracranial hemorrhage intra cervical hemorrhaging in fact intracerebral hemorrhage hypertension is one of the important causes if we see hemorrhage in putamen pons thalamus and cerebellum it is a hypertensive bleed and the bleeds in the brain usually do not produce headache unlike subarachnoid hemorrhage and meningitis which produce headache bleeds in the brain they do not produce a day why 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 structures and therefore only when meninges are affected like subarachnoid hemorrhage or meningitis it produces headache whereas intracerebral hemorrhage per se does not produce headache unless there is raised intracranial tension so increased icp renal diseases can cause hypertension respiration if a person's got breadth order acetone we have to suspect dka direct ketosis ethyl alcohol fetal hepatics or urine ferrous it could be urania garlic water it could be arsenic poison hyperventilation it could be hypoxia hypercapnia acidosis sepsis hyperventilation could be overdosed or hypothyroidism like mixed edema respiration again very very exciting and interesting concept if a person has got say hematoma coming from the cortex and then going to midbrain pons and medulla by just looking at the respiratory pattern we can say how the hematoma is coming from the rostral cordal direction for example if the cortex is involved person has got chain stroke respiration that means waxing and varying type of breathing then there's no build and then there's no breathing when it comes to mid brain it becomes central neurogenic hyperventilation they keep on hyperventilating but when it comes to pawns it becomes acne breathing they take a deep inspiration pause and then expiration deep inspiration pause and then expression and when it comes to medulla oblongata it totally becomes chaotic it is known as biots breathing so we see that change slopes breathing central neurogenic hyperventilation at music bearing and then bioxiding we know that the hematoma is descending from the cortex mid brain pons and middle up so just at the bedside by just observing the respiratory pattern we'll be able to find out how the descent of hematoma or whatever may be the reason is causing the coma yeah this is a nice diagram so it's showing the chain stroke respiration hyperventilation acne stick breathing a toxic breathing and finally the respiratory arrest temperature if there's fever it could be infection inflammation or hypothalamic lesion heat stroke thyroid storm or subarachnoid hemorrhage if there is hypothermia it could be sepsis shock mixed edema coma that is hypothyroidism or drug intoxications like barbiturates or hypoglycemia general examination fundus is very very important in for in in when we examine and evaluate a person having coma it gives a lot of information wealth of information increased icp can cause papillae demand sub background image can cause sub-bilot hemorrhage hypertensive encephalopathy can cause x-rates hemorrhages vessel crossing changes av nipping papilidema or diatic retinopathy so these are the changes on the fundus in hypertensive retinopathy exudates hemorrhages and av nipping these are the changes of infunders in direct retinopathy like microaneurysms and neovascularization right next we'll come to the examination of the headache if there's scalp laceration it could be drama battle sign achimosis over the mastoid raccoon send a chamois around the eyes both suggest basilar skull fracture and the person has got neck stiffness it could be sub not hemorrhage meningitis or cerebellar tonsillar herniation so here is a wonderful diagram showing the features of base of skull fracture science consider raccoon sign csf rhinoria how do we differentiate cs of rhinorrhea from the mucous secretion if there is sugar that means it is csf rinoria or it could be csf autoria battle sign echimosis or the mastoid hemo tympanum and there could be bump examination of the skin is also important if there is cyanosis it could be hypoxia cardiac disease cyanide or cherry red causes carbon monoxide intoxication causes cherry rate if there's jaundice we have to suspect hepatic encephalopathy and hemolysis if there is pallor it could be anemia shock hemorrhage if the speed decay and perpetuity crash it could be meningococcemia if they're sweating we have to always suspect hypoglycemia in fact hypoglycemia is one of the important and common causes of coma we should never miss out on hypoglycemia because it's a highly treatable condition the moment you give dextrose even before you complete giving the exposed person will sit and talk to you you feel so happy about it but why should there be sweating in hypoglycemia body always tries to maintain homeostasis so when the sugar increases insulin releases and sugar comes down when the sugar level comes down body tries to increase the sugar level by producing counter regulatory hormones like catecholamines and cortisol these catecholamines not only increase sugar level but produce other side effects of catecholamines like sweating and therefore a common toast patient having sweating always suspect hypoglycemia erythema it could be polycytin or alcohol bruises indicate trauma or coagulopathy heart if there is arrhythmia it could give rise to stroke cerebral embolism mohammad vallar heart disease gi tract hepatic encephalopathy or gi hemorrhage geo urinary incontinence seizures with positive commonly commonly seen urinary incontinence hematuria extremities very important you have to carefully look at the extremities if there is subtle pitching it could be something status because where we need to use eeg to pick up the convulsive non-conversive seizures posture very important and interesting question what is decorticate rigidity what does decelerate rigidity what is decorticated duty that is arms flexed and legs extended what is d celebrate rigidity that is extension posture of both arms and legs for this we need to understand important concepts there is red nucleus in the midbrain and vestibular nucleus in the medulla oblongata the trap coming from the red nucleus we called as a rubro spinal tract the tract coming from the vestibular nucleus we called as vestibulospinal tract the ruprospine and tract is responsible for flexion posture so when there's a lesion above midbrain above the red nucleus the ribrospinal tract functions effectively so person goes into a flexion posture called as decorticated rigidity so it implies that the lesion is above red nucleus suppose if there's a lesion between red nucleus and vestibular nucleus the rubrow spinal tract cannot function now because it is cut off now vestibular spinal will take over because hebrew spinal tract is not functioning vestibular spinal attack is responsible for extinction so a person will have decelerate posture so decorticate vegetative the lesion is above red nucleus her flexion posture d celebrate tragedy the lesions between the red nucleus and the vestibular nucleus so vestibular spinal tract will cause extinction which is known as deceleration so decorticated agility arms flexed and legs extended this is attributable to the intratrouble spinal pathways which enhance the exhaust tone for the upper extremities producing a flexed arm posture with an extended leg posture decelerate rigidity extension posture of both arms and legs with a lesion between red nucleus and vestibular spine vestibular nucleus the repro spinal tract ceases to function but the vegetable spinal tract remains intact frustrating extensor tone to all the four extremities so here you can see the d cortical gt the lesion being above red nucleus and decelerating dt the lesion being between the red nucleus and the vestibular nucleus this is a nice diagram depicting the decor to get entity and the d celebrate rich gt right now let's come to the neurological examination arousal tickling the nostril with the wisp of cotton pressure on the knuckles or bony prominences and pinprick stimulation are used to determine the threshold for arousal and the mortar response of each side of the body we have to carefully examine the brainstem reflexes if we go systematically it is very easy we need to examine the midbrain pons and middle oblongata how do we examine midbrain by pupillary reaction when we throw light on the pupil the pupil on the same side direct light reflect and the pupil on the opposite is constantly replaced both should constrict the pupil if the pupils are able to constrict when we throw light that means mid brain is functioning well then we have to check out on the pawns we do two we perform two important reflexes one the corneal reflex second is the ocr or clock catholic reflex how do we test corneal reflex with the wisp of cotton we touch the cornea once we touch the cornea ophthalmic division of the trigeminal nerve that is in the pons efferent is bilateral seventh row that is also the points both the eyelids close a very important clinical point perhaps nature wants the eye to be protected well and therefore there are no touch receptors on the cornea they are only pain receptors free nerve endings so the moment we touch it becomes a pain pain stimulation and person immediately closes the eyes because the nature wants to protect the eye well second is the oculopephalic reflex the vestibular reflex and the front line fields number eight connects to the pprf on the opposite side which pulls eyes towards each side by connecting sixth note on the same side and medial rectus through mlf on the opposite side so when the vestibular apparatus and the front life is area number eight estimated eyes will be pushed to the opposite side the vestibular apparatus pushes the eye slowly the front line feels area number eight will push the ice very fast so when i turn the head to the opposite side i am stimulating the vestibular apparatus or by putting the warm water and stimulating the vestibular apparatus so eyes will go to the opposite side so front like this area number eight will try to push the ice back to its normalcy so there will be nystagmus so easy to remember the acronym cows c o w s when you put warm water i will go to the opposite side but nystagmus will be to the same side when you put cold water you are inhibiting the vestibular apparatus the opposite festival or apartments will push the ice to this side and there will be nystagmus to the opposite side so cold opposite warm same and finally medulla oblongata is tested by the respiration pattern if there's no respiration that means the medulla is to function so this is how we test all these reflexes this is what we i just said warm water slow pace and then the nystagmus cold opposite patients with preserved brainstem reflexes typically have biohemistric localization to coma including toxic or drug intoxication so a person has taken toxic or drug intoxication resulted in coma brainstem reflexes will be intact that means both the cortices are affected if brain stem functions are affected brain stem persay is effected or both the cortices are coming in pinching on the brainstem so whereas patients with abnormal brainstem reflexes either have rds localization to their coma that is in the brainstem or are suffering from herniation syndrome impacting the brainstem remotely from a cerebral mass lesion pupillary signs very important the normal pupillary size is two point five to five millimeters pupillary dilatation more than six millimeters indicate that there's a compression of the third node simply a bit brain damage or anticholinergic drugs superficially on the third note so when when a hematoma or herniation or p-communication goes and impinges it is a pair of sympathy fibers which are superficial on the third not get affected first para simply causes constriction of the people since they are affected the ripu periodically so pupillary dilapidation indicates a third node damage or mid-brain damage whereas small people sympathetic causes directly to the people so the sympathetic tract gets affected like pontine hemorrhage there will be bilateral small pupil because pond is supplied by a single base directory and the basal artery ruptures the blood goes on both sides both the sympathetic tracts get affected so pupils can't dilate pupils will be small yeah ocular moments another important point is that in a comatose patient we look at the ocular movement the spontaneous eye movement means we don't even touch the patient we just look at the patient how the eye movements are the that is spontaneous second is we perform eye movements elicited eye moves and then see what's the response in spontaneous eye movements if the eye is looped to one side and hemiplegia is on the opposite side it's a frontal lobe lesion why frontal lobe pushes the eyes to the opposite side so there's a frontal lobe in past it cannot push the eyes to the opposite side so eyes will be on the same side but the particles will attract across the level of the middle and goes to the opposite side so hemiplegia will be on the opposite side so i is looking to one side and hemiplegia on the opposite side is a frontal lobe in part suppose if it is a pontine in part ppr will pull the eyes towards its side so the ponch is affected the eyes will go to the opposite side hemiplegia the particle spinal tract also crosses the level of the material and goes to the opposite side so eyes will be looking towards the side of hemiplegia very very interesting point eyes looking to one side hemiplegia on the opposite side is a frontal lobe lesion i is looking towards the side of him he plays as a pawn transition now spontaneous i want ocular bobbing and ocular dipping it has a brisk downward movement with a slow upward movement of the eyes associated with the loss of horizontal thigh movement that is bilateral content damage pons is concerned for all horizontal eye movements and mid brain is concerned with all vertical eye movements and therefore the pawns gets affected horizontal line movements get affected for example locked in syndrome when there's locked in syndrome there's an impact in the pons so all horizontal wounds get affected person cannot use upper limbs and the lowerings because corticobulbur corticospinal fibers are affected but since midbrain is intact he can move eyes up and down so locked in syndrome he cannot use eyes horizontally he cannot use upper limbs and lower limbs only thing is that he can move eyes up and down that is locked in syndrome so ocular bombing the horizontal movements get affected awkward dipping is just the opposite there's a slow downward movement followed by a fast upward moment with preserved horizontal moments so this is what cause i've already told this yeah herniation refers to the displacement of a brain tissue by an overlying or adjacent mass into a complete contiguous compartment that it normally does not occupy like we have the ankle herniation transfer hibernation where it goes into its continuous compartment very important as i have already mentioned caudal herniation if there's a rostral coral herniation coming from above and going downwards by looking at the breathing pattern and posture we can even make a diagnosis if it is the cerebral cortex there will change strokes breathing and decorticate rigidity if it is done in midbrain it will be central neurogenic hyperventilation and decelerate with ddt if it is in the pawns it will be acne stick breathing if it is the medullary biopsy breathing so we can see the descent of the herniation from the raw stroke coral direction by looking at the respiratory pattern and poster yeah these are the various comas you have ankle herniation sub pulsing herniation tonsillar herniation yeah so far i've been talking about the structural cause of coma now let me talk about the metabolic cause of coma many systemic metabolic abnormalities cause coma by interrupting the delivery of energy substrates like oxygen glucose sodium or by altering neuronal excitability like epilepsy anesthesia drugs and alcohol we give anesthesia anesthetic drugs person who says consciousness why it suppresses the reticular activating system after seizures person loses consciousness starts policy there'll be weakness sometimes a person loses consciousness why again the ra is suppressed in metabolic encephalopathy unlike structural encephalopathies there is a slow change from a complete conscious state to a complete comatose state so clouded consciousness confusion drowsiness trooper and then coma so they are in a continuum if it's in a continuum a granulon said it is metabolic encephalopathy so when a person comes in a comatose state the broad approaches whether it is a structural cause of coma metabolic or sarcoma very very important once a person comes into a coma the clinician should approach in this possible and this is the best possible way one whether it's a structural cause of common or two the metabolic cause of coma so how are we going to confirm whether the structural cause of coma or metabolic cause of coma structural cause of hormone like herniation usually produces focal side whereas metabolic causes usually produces generalized sign structural causes like like stroke tumor info will produce focus and it's on the opposite side pupils are due to effect because herniation goes and affects the mid brain so pupils are usually affected whereas in metabolic cause of coma pupils usually are not affected except drug overdose like opiate astrixis is not present in structural cause of coma whereas metabolic cause of coma especially hepatic encephalopathy there will be asterixes what is aspects is when you extend the hand and spread out the fingers and then dorsiflex it there will be fall and then the person tries to correct they'll be fall and then the person tries to correct so he's not able to maintain the position he tries to correct the position it is perhaps because of the neurotoxins affecting the posterior column at the level of the pareto cortex so a person's has got bilateral asterisks as he falls and tries to correct falls and tries to correct it is a sign of metabolic encephalopathy especially hepatic encephalopathy so in a drowsy and confused patient bilateral aspects is sign is a sign of metabolic encephalopathy or drug intoxication if it is structural cause of coma like hematoma tumor or infection ct and mri will be abnormal whereas it's a metabolic cause of coma like hypoglycemia hypoxia or hyponatremia ct and mri will be normal and the structural cause of coma blood investigations are normal but if it's a metabolic cause of coma blood investigations are usually abdominal like hypoglycemia hyponatremia or hypoxemia right now having made a good clinical evaluation of tomatoes patient what are the lab studies and imaging we do a chemical and toxicologic analysis of blood and urine to check out on glucose level sodium level and alcohol level we do arterial blood gas analysis to find out if there are lung disorders we do ct scan and mri to find out structural cause of hematoma structural cause of coma it could be extra dual hematoma subdural hematoma or stroke one important point here extra dural hematoma is dangerous because it's an arterial bleed middle meningeal artery rupture there'll be torrential bleed and immediately we need to call a neurosurgeon and take the hematoma out the person is going to die and once we take have taken the hematum out the person is going to survive and extra dual hematoma is above the meninges so the meninges will not allow it to expand so it will be it will come and be localized whereas subdural hematoma is underneath the dura so it'll be going from the right from the frontal cortex to the occipital cortex it's under the dura subdural hematoma is a venous bleed so blood will start slowly trickling and they can go on for a long time in fact one of the treatable causes of dementia as a subdued hematoma especially in old persons they might have even forgotten the injury the trivial injury they might have had a minor injury they would have forgotten venus extremely blood starts trickling the person starts losing consciousness i had a patient an old patient coming up with dementia i suspected subdue limitoma took a ct scan with subject limit called a neurosurgeon took the hematoma one person's memory caught back so dementia should never think that it's an irreversible process there are so many treatable cause of dementia one important treatable cause of dementia is the subdued hematoma the other important cause are vitamin deficiencies then we have to do eeg electro encephalum one important uh one important place of eeg one important use of eeg is non-conversation if a person has got conversation anyone can pick it up but person may have non-conversative seizures and in a comatose state then we'll be wondering what is the cause if we do eeg we can pick up the seizure pattern so very useful is non-conversation each is very useful cjd crude skull jacob disease they'll have periodic news coming up herpes simplex encephalitis there will be seizure focus in the temporal lobes why in the temporal lobe because the happiness where it goes to the nose and it affects the temporal lobes so if you see the spikes or sharp waves in the temporal lobe it is herpes simplex viral encephalitis and if it is hepatic encephalopathy we see the nice try basic waves and the person has taken lot of diazepam overdose benzodiazepine overdose there'll be a lot of beta activity and if we suspect infectious causes of coma we have to do csf analysis to rule out meningitis and encephalitis differential diagnosis of coma lot of students will keep on trying to memorize a different cause of coma i'll tell you the easy method of remembering the different cause of coma almost all causes of coma will fit into three categories almost all cause of coma will fit into three categories one coma without focal neurologic science like metabolic and toxic encephalopathy like hypoglycemia hyponatremia hypoxemia coma with prominent focal signs like stroke cerebral hemorrhage tumor coma with meningeal syndromes like meningitis meningoencephalitis characterized by fever or stiff neck with excess of spells in the spinal fluid like meningitis encephalitis and sh so we need not muck all the causes of coma almost all the cause of coma will fall into these three categories coma without focal neurologic signs like metabolic and toxic encephalopathies coma with prominent focal signs like stroke cerebral hemorrhage or coma with meningitis syndrome characterized by fever or stick stiff neck or excess of cells in the spinal fluid like meningitis encephalitis and sah right not only there are the different causes of coma even stroke different strokes can produce coma so how are we going to differentiate the various causes of cba causing coma for example basal ganglia and thalamic image can cause coma quantum image can cause coma cerebellar hemorrhage basalar artery thrombosis sah and nca stroke how are we going to differentiate if it is going to be basal ganglia communist site of hypertensive deed there will be hemiparesis and i is looking down and small pupils very important lot of students have asked me why in thalamic hemorrhage eyes look down and why there are smart cables very interesting question and we i have a very fantastic explanation for that the thalamus is very close to the mid brain the mid plane as i already said said is the center for vertical eye movements vertical eye movement there are two components up gaze and downgas upgrades fibers cross over and then descend whereas down gaze fibers descends straight away so when there's a thalamic hemorrhage it goes and impinges on the top of the midbrain because thalamus is very close to the midbrain and therefore the crossing up gas fibers get affected so person cannot look upwards they'll be looking downwards likewise parry knot syndrome pineal tumor it also goes and impinges on the top of midbrain so our case fibers get affected they cannot look upwards they'll be looking downwards again hydrocapilus it goes in pinches on the top of the midbrain the crossing up gas bibles get affected they cannot look upward they'll be looking downwards which is known as sunset sign and y eyes are small the sympathetic tracks originate from the hypothalamus which is very close to thalamus so hypothalamus causes directly to the people so when they get updated sympathetic get affected pupils are small so thalamic hemorrhage will produce small pupils and eyes looking downwards pontine hemorrhage produces pinpoint tuples on both sides why pontinium which is a small pupils on both sides because pond is supplied by a single baseline artery unlike medulla oblongata is supplied by two vertebral arteries and midbrain which is supported by the two posterior several arteries so in this rupture of the basilar artery in the palms since it's a single artery that goes diffuse it of both the sympathetic tracts and both the sympathetics get affected so it'll be like bilateral horns so pinpoint vehicles on both sides whereas if it is medulla oblongata only one vessel usually ruptures vertebral artery and the pupil on that side becomes small meiosis like valenburg syndrome the lateral medullary syndrome where the sympathetic class get affected very easy to remember some peop students get confused how to remember these sensory tracts motor tracks and cranial nerves just remember a simple rule which is known as rule of four there are four cranial nerves above mid brain and above four cranial nerves in the pons and four cranial nerves in the middle oblongata so the fourth cranial nose and midbrain above that is one two above midbrain three and four are in mid grade there are four cranial nerves in the pons five six seven eight there are four cranial nerves in the middle oblongata 9 10 11 12 so now we know how the cranial nerves are placed now another question comes what are the clinicians which are medially placed what are the cradial nerves which are laterally placed easy to remember the cranial nerves which divide 12 into equal parts are placed medially the cranial nerves which cannot divide 12 into equal parts are placed laterally for example third now and fourth nose divide 12 into equal parts 12 by 3 is 4 12 by 4 is three so three and four are placed medially the sixth canadian now divides twelve into two equal parts so six snow is placed immediately 12th in our device twelve into one equal parts so twelfth no space medially so three four six twelve are placed medially whereas other cranial nerves are placed laterally now about tracks the tracks which start with the letter m are placed medially m for m the track will start with the letter m are placed immediately the tracks which start with the letter s are placed sideways s for s the tracks which are placed immediately are more attack the corticospinal tract pyramidal tract that's why in medial medullary syndrome corticospinal cat gets affected 12th you know gets affected posterior column medial elements gets affected so medial lemniscus smart attack that is the corticospinal tract ml of medial longitudinal particles it connects third fourth sixth eighth and the motor part of the cranial nerves are placed immediately m for m s temperature that's when valenburg syndrome they get affected they place sideways sympathetic track causing horner's syndrome again valenburg syndrome they are placed sideways as far as and then finally spinal cerebellar tract which are pesticides so all these force tracks which start with the letter s and which are placed sides are affected in the lateral medullary syndrome valenburg syndrome because they are placed laterally easy to remember so pontine images produces bilateral pinpoint pupil cerebellar hemorrhage produces oxidative headache vomiting gas parasites and directing changing nystagmus if the vegetable gets affected it pushes the eyes to the opposite side nystagmus will be only in one side whereas if there's an instrument beating on one side coming to the center no changes direction starts beating on the other side it's a useless central cause of disciples like cerebellum so there's a direction changing hysteres we should always think of central cause of nystagmus like cerebellar hemorrhage basilar artery thrombosis bonds gets affected and then it causes diplopia and dysarthria again very important concepts for lot of arterial thrombosis which are known as white thrombosis because of endothelial injury platelet aggregation and agglutination we give antiplatelet agents anticoagulants have got no role but in basilar artery thrombosis we give anticoagulants in fact a lot of neurologists use heparin for baselayeratic thrombosis why in bristol artery thrombosis it's a red thrombus it is because of slow flow of blood like vircose triad workers triad says the three important causes which predispose for a person to develop thrombosis one slow blow flow of blood sluggish blood flow of blood or abnormality in the constituents of the blood or vessel wall abnormalities all these three causes predisposes to thrombosis so when there is a slower blood flow sluggish blood flow like basilar artery it causes red thrombus and then it causes thrombosis because of fibrin there's no role for platelets and therefore antiplatelets have got no role we give anticoagulants sub petrochromium is severe headache vomiting loc we think subarachnoid hemorrhage as i said the meninges have got pain sensitive structures brain does not have pain sensitive structures you cut brain there's no pain but meninges have got pain sensitive structures so if meninges get affected or meningeal vessels get affected they'll have severe pain like subarachnoid hemorrhage or meningitis mca stroke in the beginning of the class i emphasize re-emphasize that if only one side of the cortex gets affected person does not lose consciousness only both the cortisone loses consciousness so in mca stroke though it is the most common stroke it may not cause coma because it is restricted to one set unless there is a massive cerebral edema going and impinging on the opposite cortex or the brain stem yeah finally the treatment of coma we've been discussing so many cause of coma apart from the patient's point of view he wants to know the treatment of coma important causes hypoglycemia even if a person is diabetic always send the blood for analysis and immediately give insulin immediately start giving dextrose because hypoglycemia is one of the treatable causes of coma so even in a dietic person check the blood send the blood for evaluation but before even the result comes you can you have to keep text because hypoglycemia is killing the person it's more dangerous than hyperglycemia once the blood sugar level comes if you think it's on the higher side then you can always give insulin but hypoglycemia every second it is killing the person because ras and cerebral neurons depend so much on glucose sodium and oxygen for its survival and therefore hypoglycemia is one of the treatable conditions so always give dextrose even before you complete giving rise to a person sits and talks what more satisfaction you want but a word of caution a person with alcoholism is history of alcoholism and comes with hypoglycemia you should always give time in and then followed by dextrose why person is alcoholic it is his thyme and deprived vitamin d1 deficiency and on top of it if you give dextrose whatever little time is left out that'll be used for metabolism and you're frustrating the person to develop vernix encephalopathy so all hypoglycemics you give dextrose but with the history of alcoholism you first give thymine and then followed by glucose to avoid vernix encephalopathy narcotic overdose you have to give naloxone stroke cva you have to give thrombolysis and mechanical ambolectomy for diazepam overdose you have to give flumazinil and ethylene glycol you have to give form episode then sometimes we do not know the cause of coma and therefore we have to give coma cocktail which consists of dextrose flumas naloxone and thymine is sometimes used in the initial management of tomatoes patient which is known as coma cocktail prognosis metabolic cause of coma have got far more better produces than traumatic causes hypoglycemia you get dextrose percent recovers hyponatremia you give sodium person recovers the absence of cortical response of the somatosensory work potential has been shown to a strong indicator of poor outcome following hypoxic injury and then finally glasgow coma scale which is used in the evaluation of patients with impaired consciousness but particularly in head injury it depends on three components emv i response verbal response and motor response eye opening spontaneously you give there are 15 points the maximum of person can get is 15 points the least of person can get is three points not zero because even if there's no response we give one point so i opening i open spontaneously four points i opens only to verbal stimulate three points i opens only to paint two points never opens one point best verbal response oriented and converges five points disoriented confused four points in appropriate words three points incomprehensible sounds two points no verbal sounds one point best motor response obese command six points localizes pain five points withdraws to pain five points that is normal flexor response abnormal flexor that is decorticated three points extensor response decelerated these two points no more response one point the highest response as i said is 15 by 15 but the lowest response is not zero by 15 but three by 15 very important point this is the gcs depending on the eye opening verbal response and the motor response yeah as dr lalit said i started my own youtube channel dr srinivas medical concept you can see it on the screen dr sreenivas medical concepts i have nearly 5 000 subscribers 4.68 to be precise and i've uploaded nearly 210 neurology videos almost all topics of neurology i made it into video forms and uploaded for the benefit of students

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