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Quality of life in post stroke patients-role of nootorpil
 

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    Quality of life in post stroke patients-role of nootorpil Quality of life in post stroke patients-role of nootorpil Presentation Transcript

    • QUALITY OF LIFE IN POST-STROKE PATIENTS - ROLE OF NOOTORPIL Prof. A.V. SRINIVASAN 29th June 2003 Madras Medical College, Chennai-3
    • STROKE• Third cause of death after heart disease and cancer• Prevalence rates are around 500- 800 / 100,000• Enormous economic consequences A bad teacher complains; A good teacher explains; The best teacher inspires;
    • STROKE IN INDIA• A huge base of population• A prevalence rate of 900/ 100,000 can lead to an epidemic of stroke• 2% of all hospital admission, 4-5% of medical and 20% of neurological admission have CVD• Incidence of stroke in younger persons (<40years) is high (13-32%) as compared with western dataScience is below the mind; Spirituality is beyond the mind
    • Stroke - Risk factors• The risk factors for CVD and CAD are the same – hypertension – diabetes mellitus – stress – smoking• Crude prevalence rate for CVD in India is 90-222 per 100,000 Every thing should be made as simple as possible; but not simpler
    • Stroke• 85-90% of the total stroke are ischemic in origin while hemorrhagic stroke constitute only 10-15%• Main causes of ischemic stroke – thrombosis • atherosclerosis • vasculitis • arterial dissection • hematological disorders • drug absue – embolism – vasoconstriction
    • Stroke synonyms• Cerebrovascular accidents• Apoplexy• Cerebrovascular insufficiency Speak obligingly even if you cannot oblige
    • Stroke pathology• Disruption of blood supply to some part/s of the brain• Sudden onset of symptoms (paralysis, aphasia, temporary amnesia)• Symptoms due to damage to neurological functions / neurons (neurological deficit) Neuronal damage, including that of neuronal cell membrane
    • Neuronal damages types Ischemic neuronal damage begins a few minutes after disruption of the blood supply and not immediately, and therefore it is known as post- stroke sequel. Damage can be of 2 types• Zone of dead neurons - Core• Zone of damaged neurons - penumbra
    • Ischemic Neuronal injury• In the core region, failure of glucose and oxygen delivery leads to rapid depletion of energy stores and cell death• Cells remain viable for several hours within the penumbra region Develop the heart; art comes automatically
    • Damage to the cells(neurons) results indefectiveneurotransmission,resulting in the clinicalmanifestations of thepost-stroke sequlae
    • Clinical manifestation• Abrupt onset of focal neurologic deficits• manifestations can be in the form – TIA (transient ischemic attack) – RIND (reversible ischemic neurologic deficit) – Completed stroke – Progressing stroke / stroke in evolution Symptoms vary depending on the location of occlusion and the extent of the spared collateral flow
    • Post-stroke sequelae symptoms• Motor weakness• Paralysis – half side of the body (hemiplegia) – complete body (paraplegia)• Aphasia• Memory loss
    • Management• Recovery of neurological functions is the key goal in the management• Two ways of bringing about the above are – pharmacotherapy – rehabilitation Knowledge without action is useless; Action without knowledge is foolish
    • Pharmacotherapy• Drugs acting inside the vessel – Thrombolysis – Anti-platelet agents – Anti-coagulation therapy• Drug acting on the neuronal level – NootropilLet the wave of memory, the storm of desire, a fire of emotion pass through without affecting your equanimity
    • Money comes and goes, morality comes and grows Nootropil is approved for the management and early recovery of symptoms of post-stroke sequale of thrombotic originLove is selfishness and selfishness is lovelessness
    • Neuronal salvage• Collateral circulation tries to take over from the obstructed vessel to supply blood to neurons• Nootropil reaches the damaged neurons through these collateral circulation
    • Role of Nootropil• Crosses the blood brain barrier and binds to the neuronal cell membrane• Basic action of the drug is on the cell membrane specially that of the neurons• Helps to limit the damage in the penumbra region• Helps in the early recovery of neuronal function• No drug interactions with Thrombolytics and anti-
    • • The action of Nootropil on the neuronal cell membrane helps to improve its overall functioning
    • Nootropil mechanism of action• After binding to the neuronal cell membrane – improves the membrane fluidity – improves the uptake of glucose and oxygen in the neurons, thereby reducing the effects of hypoxia – improves the functioning of the receptors and neurotransmitters – improves intra-hemispheric transmission Helps to limit neuronal damage, and early restoration of neuronal function
    • Nootropil other actions• Nootropil also binds to the cell membranes of – RBC to improve its deformability resulting in better oxygen supply – Platelets to reduce hyper-aggregabilityTeachers are reservoirs from which, through the process of education, the students draw the water of life
    • Dose of Nootropil• Initiate therapy with IV bolus (60ml, 200mg/ml)to attain the desired levels through the collaterals (this will prevent progression of damage)• Follow-up with IV infusion for the next few days• Maintain therapy with Oral Nootropil 4.8gms per day for atleast 12 weeks for the optimum results It is not your position that makes you happy or unhappy It is your disposition
    • Injured Brain 25% men1. 45 85 yrs - Stroke occurs 20% women2. Guidelines for 24hrs: MandatoryLevel of Evidence Level A: Based on RCT or Meta analy. of RCT Level B: Based on Robust Experiment or Observation Studies Level C: Based on Expert opinion. A good teacher is a perpetual learner
    • According to WHODoctor assessment of Handicap may not coincide with PatientsAssessment. Neurologist depends on physiotherapy, occupationtherapy and speech therapy in rehabilitating the stroke patients.
    • NEUROLOGIC PREDICTORS.• Flaccid Paralysis for more than 96 hrs• When tendon reflexes recover without return of voluntary movement – prognosis poor• Recovery of sensory less in usual to a degree. Postion sense recovers but not pain and temperature• Recovery from Dysphasia is never complete• Dysarthria usual improves and Dysphagia never improves• Diplopia due to brain stem is usually permanent• Conjugate gaze – recovers• Vertigo improves but hearing loss is permanent• Pseudobulbar palsy permanent
    • 1. History And Examination a. Stroke clerking Performa (1994) R.C.P. 1. Improved patient Assessment 2. Improved Management - not clear 3. Improved outcome - not clear b. Examination 1. Secure Diag of Stroke 2. Specify Impairment 3. Identify sub type of Ischemic stroke Learn to adapt, adjust and accommodate Learn to give, not to take and learn to serve not to rule
    • Total anterior circulation syndromes :Implies a large cortical stroke in middle cerebral or middle and anterior cerebral artery territories. It is charecterised by• A combination of New higher cerebral dysfunction and homonymous visual field defect and an ipsilateral motor and/or sensory deficit involving at least two out of three areas of the face, arm or leg Hate screeches, fear squeals; conceits trumpets but love since lullabies
    • Partial anterior circulation syndrome• Implies a cortical stroke in middle or anterior cerebral arterial territory.• They are patients with two out of the three components of the TACS or new higher cerebral dysfunction alone or a motor/sensory deficit more restricted than those classified as a TACS.Reputation is made in a moment; character is built in a life time
    • Lacunar syndrome Implies a sub cortical stroke due to a small vessel disease• Pure motor stroke• Pure sensory stroke• Sensory motor stroke• Ataxic hemiparesisNB: Evidence of higher cortical dysfunction or disturbance of consciousness excludes a lacunar syndrome
    • Posterior circulation syndrome • Ipsilateral cranial nerve palsy with contralateral motor and or sensory deficit • Bilateral motor and/or sensory deficit • Disorder of conjugate eye movement • Cerebellar dysfunction without ipsilateral long tract involvement • Isolated homonymous visual field defectsCharacter gets you out of bed commitment moves you to action faith, hope and Discipline follow through to completion
    • Diagnostic evaluation of ischemic stroke The diagnostic evaluation should include parallel assessment of the following. 1. Imaging of the infarct 2. Vascular studies 3. Cardiac evaluation 4. Hematologic and other blood testingIt is the providence of the knowledge to speak and it is the privilege of the wisdom to listen - Hodly’s
    • • Guide: 3 (B) - CPR – Impaired Consciousness - From Stroke Resuscitation is rarely successful Schneider 1993• Guide: 4(B) Investigations:(Sagar 1995)- 435 PTS) – Chest x-ray 16% ABN – Only 4% change clinical management – Order x-ray chest if WT Loss or chest symptoms presentOpinion is ultimately determined by the feelings and not by the intellect
    • • Guide 5: (B) ECG: – Cardiac cause of Death (30 days) Ebrahim 1990. – All conscious patients to have ECG • Guide 6: (C) CT: – Routine CT Head is a Intell lazy approach – King’s fund forum(1988) gives useful framework – Weir 1994 Clinical scoring cannot distinguish Do CT if a) Uncertainty of Stroke b) If Anticoagulation or Anti Platelet treatment contemplatedA great many people think they are thinking when they are merely re arranging their prejudices W. James
    • • Guide 7:(B) M.R.I. – Moha 1995, - Unclear for Implications for clinical practice – No Routine MRI indication in Acute StrokeT T he ruth is fear and immorality are two of the greatest inhibitors of Performance to progress
    • CT versus MRI :1. Only a minority of infarction demonstrated within 24 hours. MRI document infarct as early as 6 hours.2. Anatomic extent and vascular distribution are better delineated in MRI. Small infarctions are easily seen.3. Posterior fossa infarctions are better visualised in MRI.4. MRI tends to demonstrate Prominent white matter abnormalities than CT which shows grey matter abnormalities.5. CT can distinguish between haemorrhage and infarction 95% cases. MRI demonstrates acute cerebral infarction earlier than CT.
    • • Guide 8: (B) ECHO no Routine – Echo in Acute Stroke – TOE Vs. TTE – Amer Heart Asson (1997) - same conclusion – Yield is very low. (Leung 1993; Chambors 1997) – Only when ABN ECGS - change clinical managementA true com itm is a heart felt prom to y m ent ise ourself fromwhich y will not back down - ou D. Mcnally
    • • Guide 9: (A) - Dopp scan for selected PTS: – 80% > more benefits from Endarterectomy – Minor stroke -No disability – Subst Storke -Good recovery do doppler – Medically fit Serious, sincere, systematic studies, surely secure supreme success
    • • Guide 10: (B) Management: – Fever (Worst Prog.) Reith 1996 – Hypoxia ( Moroney 1996) - Exac. by seizures Pneumonia and Arrythmias - Worst outcome – Hyperbaric O2 ineffective (Nighoghossaln 1995) – Haemodilut. Plasm Expanders; venesection – No evidence for efficacy (As plund - 1997) Check ABG only if Hypoxia suspected. Why is thought, being the secretion of the brain, more wonderful than gravity, a property of matter?
    • • Guide 11: (A) Steroids and Hyperosmolar agents Unproven treatment - should not be used – Tumor oedma responds but not cytotoxic stroke oedma qialbash 1997 - No effect on survival or improv. In funct. Outcome – Manntol - (Boysen 1997) - short term effective statistically in conclusive God is a comedian performing before an audience that is afraid to laugh
    • • Guide 12: (B) - Blood Pressure – Defer - acute reduction of BP - 10 days unless HT Encephalopathy or adrtic dissection present – Moris 1997 - Increase BP - falls in 10 days – UK - 5mm in D.B.P. 1/3 storke - Low BP prompt correct of hypovoll. and withdrawal of hypotonic drugs – Collins 1994 - HT - Prim. stroke prevent – Neal 1996 (Current RCT) - HTs in stroke survivors -study needed Man is made by his beliefs; as he beliefs, so he is
    • • Guide 13: (A/B) - AF – AF / ISCH Stroke/ Mild disability - warfarin after 48 Hrs (Longer for larger) – Aspirin for others • EAFT 1995 Less than 2 PT - No effect • SPAF 1996 > 5 - BleedingThe word shall perish not for lack of wonders but lack of wonder
    • • Guide 14:(B/C) - Blood sugar – Weir (1997) > 8 mm d/Lit - Poor outcome – Acute MI + 11 mm d/Lit - Intensive Insulin - improved (Malmberg 1997)• Guide 15: (A) Cholesterol – Prosp. Study collob.: 1993 - Epidem study do not support – Blaun 1997: Metranauetic - Chollest & statin 30% decrease - stroke in CAHD patients. – Sacks 1996 - Tot chol: decrease to 4.8 mmol/Lit benefits
    • • Guide 16: (A/C) Deep vein thrombosis – Kalra 1995 - 10 days - stroke Pts - 50% – Sandercock 1993 - Pul embol 6-16% only – Ist 1997 - 5000 IV or 12500 twice daily - Hemorrage greater – Gradual stocking value - useful in Surg - pts but its value not evaluated - (Wells 1994) – Use with caution - if periph artery insuf. is present hence do not use heparin on stockings. In any field, find the strangest thing and explore it
    • Indications for Carotid EndarterectomyDegree of Carotid Stenosis Recommendationby NASCET criteriaSymptomatic disease70% to 99% CEA50% to 69% CEA if in high risk group (men and patients with hemispherical TIAs or strokes)<50% Medical management (risk factor control + aspirin 50-325mg/day.Asymptomatic disease>60% Consider CEA
    • • Guide 17: (A/B) Pressure sure – Event health care (1995) specialised low pressure mattress systems to be used than stand Hospital - mattress• Manag of infarction – Guide 18: (A) • Aspirin 75 - 150 /Day • 3 yrs 40% reduces of vascular events in 1000 pts (APTC - 1994) • Stroke sub type value ? (TACI, PACI, LACI, POCI) • Dienners - 1996, synergy possibel with clopidogrel ticlopidine etc.
    • Anti Coagulation• Warfarin - AF – In sinus rhythm - uncertain – Spirit 1997 low dose ABP + Warfarin in TIA & Minorstorke - Stopped of HE – Heparin (IST 1997) - Signif. reduction in early death (12 fewor in 1000) not better than aspirin – So avoid Heparin (A) There are sixty trillion cells in the human body
    • • Thrombolysis (A)• Warlow 1997 - Uncertain clinical benefit at the expense of greater hazard avoid - thrombolysis “Men of Genius Adm ired: Men of W ealth envied wom of power feared but only en wom of character are trusted” en A- Friedman
    • Common Sites and their incidencePutaminal Haemorrhage - 35%.Lobar Haemorrhage - 25%Thalamic Haemorrhage - 10-15%Caudate Haemorrhage - 5%Pontine Haemorrhage- 5%Cerebellar Haemorrhage - 5-10%Baby hears 30,000 cycles / sec, teenage boy hears 20,000 and old hears 4,000 cycles / sec
    • • Guide 20: (I) Hemorrhage – Hankey and hon 1997: Supra tentorial evacuation for ICH is controversial - Avoid – Infra tentorial - Yes – Main Indication - Deteriorating or depressed consciousness “Motivation is the Spark that lights the Fire of Knowledge and fuels the engine of Accomplishment”
    • Causes of deterioration in stroke Neurological Non-NeurologicalProgression/completion of stroke InfectionsExtension/Early recurrence Metabolic derangementHaemorrhagic transformation of an DrugsinfarctDeveloping cerebral edema HypoxiaObstructive hydrocephalus HypercapniaEpileptic seizuresIncorrect diagnosis
    • 2 2 4 P ts Guide 21 : Ventilation 131 I n t u b a tio n 93 N o t In tu b -Decreased level of consciousness - increased 6 4 D is c h a r 6 7 D ie d mortality and poor final 3 4 R e d ta g 2 1 d is c h t o n ver h om e 8 D is c fo r p a llim a 1 D is c H om e outcome - Absent pupillary light 3 D ie d 7 D ie d 3 D ie d responses - poor prognosisIt is a great misfortune not to possess sufficient wit to speak well nor sufficient judgment to keep silent La Broyers character
    • Two diverging/converging pataways associated with VaDRisk factor CVD Ischemic Brain injury MRI lesion Clinical syndromeHTNArteriosclerosis 1. occlusion complete infarct lacune  lacunnar stateArteriosclerosis 2. Hypoperfusion incomplete infarct WHSM  Bingswanger syndrome “ He who cannot forgive others destroy the bridge s over which he him m pass” - Annoy self ust
    • Pathogenesis of dementia due to VaD 1. Lacunar hypothesis 2. Binswanger’s subtype of VaD 3. VaD with coexisting Alzheimer’s disease In all of us, even in good men, there is a wild - beast nature which peers out in sleep
    • Clinical syndromes1. Lacunar state --- 85%2. Strategic infarct dementia(e.g. thalamic dementia) --- unknown %3. Binswanger’s syndrome --- 10 – 15% “The True Art of Memory is The Art of Attention” - S.Johnson
    • Features suggestive of vascular dementiaFrom the history Onset associated with a stroke Improvement following acute event Abrupt onsetFrom the exam Findings typical of stroke e.g., hemiparesis, hemianopiaFrom imaging Infarct(s) above the tentorium
    • Patterns of blood supply to the cerebral hemispheres Vascular Arterial supply Collateral supply distributionCortex shorterCorpus callosum ShorterSub cortical U fibers Intermediate Inter digitatingExternal / extreme IntermediatecapsulesBasal Ganglia LongCentrum semiovale /PVWM Long
    • Categories of vascular Dementia Category Clinical presentationLacunar infarctions Progressive dementia, focal deficits, or apathetic, frontal-lobe-like syndrome, may have no stroke historySingle strategic infarctions Sudden onset aphasia, agnosia, anterograde amnesia, frontal lobe syndromeMultiple infarctions Step-wise appearance of cognitive & motor deficitsMixed AD – VaD Progressive dementia with remote or concurrent history of strokeWhite matter infarctions Dementia, apathy, agitation, bilateral cortico-(Binswanger’s disease) spinal/bulbar signs
    • Diagnosis Vascular Mechanism of Pathological distribution Brain injury phenotype “Infarct”Single artery Acute ischemia Multiple lacunarSmall arteriole infarctsSingle artery Acute ischemia Single strategically placed lacunar infarctBorder zone Chronic White matterSmall arteriole hypo perfusion demyelination and axonal loss
    • Diagnostic criteria1. Hachinski’s ischemic score2. DSM IV criteria3. ADDTC criteria4. NINDS – AIREN criteria5. Binswanger’s criteria Starving Emotion - Humor Less; Rigid; Stereotype Repressing Emotion - Literal; Holier than thou Encouraging Emotion - Performs in Life Discourage Emotion - Poison Life Juseph Colins. 1868
    • Short comings1. Not interchangeable hence four fold rise in frequency2. DSM IV R most liberal3. NINDS- AIREN criteria conservative4. Gold standard for VaD (pathological definition difficult)5. Most of the criteria failed to distinguish between small and large vessel subtypes Take time to think; it is the source of power Take time to read; it is the foundation of wisdom Take time to work; it is the price of success
    • Diagnosis of Dementia after stroke4 sets of criteria are used Sens Spec1.Hachinski ischemic score 89% 89%< 4 AD / 18, > 7 MID / 182. DSM IV 43% 95%3. NINDS – AIREN 50% 98%4. ADDTC criteria 50% 90% A (Neurologist’s) life is like a piece of paper on which everyone who passes by leaves an impression - Chinese proverb
    • Clinical characteristics of Neuro behavioral syndrome of VaD• Mental changes of dementia with single brain lesion• Sub cortical infarcts• Multi Infarct Dementia: -• Sub cortical arteriosclerotic leukoencephalopathy “ We Sometimes think we have forgotten something when in fact we never really learned it in the first place” Imp.Your Memory Skills
    • AD Vs VaD AD VaDNeuro transmitter defect Hemodynamic defectFemale predominance Male predominanceGradual onset Abrupt onsetSteady deterioration Stepwise deterioration, fluctuating courseBP normal HypertensionNo history of stroke History of strokeGlobal decline in cognitive function Focal neurological symptoms and signsUnlikely to respond to treatment May respond to a drug which modifies microcirculation and enhance cerebral tissue perfusion
    • Prognosis1. Risk factors• Advanced age• Education Develops dementia• Lacunar subtype following ischemic• Lt. Hemisphere CVA stroke• Non white Whatever the Mind can conceive and Believe, the mind can Achieve Napoleon Hill
    • Prognosis contd….2. In Lacunar stroke - Leukoariosis is a poor prognosis3. Recurrence of strokeHence• Atrophy• cognitive impairment• WMSH are inter related in VaD Many Ideas grow better when transplanted into another mind than in the one where they sprang UP O.W. Holmos
    • Prognosis contd..,Neuro imaging phenotype• CT lucency (lacunes and leukoariosis)• MRI hyper intensity (lacunes and WMSH) At twenty the will rules At thirty the intellect At forty the Judgment
    • Prevention and Treatment of vascular dementiaI. Brain at risk stage The aged Hypertensive Smokers Diabetics Atrial fibrillators Cardiac patients When they tell you to grow up, they mean stop growing P. Diccaso
    • II. Pre-dementia stage Patients with TIA Patients with stroke Patients with subtle cognitive infarctions Patients with silent cerebral infarctions Expert is one who think to his chosen mode of ignorance
    • III. Dementia stage Cardiac embolism Atherosclerotic cerebrovascular disease Hypertensive cerebrovascular disease Maintaining the right attitude is easier than regaining the right mental attitude
    • Potential therapies of vascular dementia1. Brain at risk stageSmoking cessationExercise (prevention and management of diabetes)Diet (control of diabetes, hyperlipidemias, obesity)Antihypertensives (ACE inhibitors and ca++ channel- blockers maybe particularly suitable)Lipid lowering agentsAnticoagulants (for atrial fibrillation)Aspirin (for selected patients at high risk)
    • 2. Pre-dementia stageCarotid endarterectomy (symptomatic patients with -carotid stenosis of 70-99%)AnticoagulantsAspirinTiclopidineAgents that interfere with amyloid deposition vesselsCa++ channel blockers (pre treatment to attenuate -effect of infarcts) NATURE, TIME AND PATIENCE are the 3 great physicians
    • 3. Dementia stage Antidepressents Antihypertensives – 6 mm of Hg reduction in systolic or diastolic BP -reduces the risk of stroke by 40% Cholinergics - Tacrine, Galantamine, rivastigmine, donepezil NMDA antagonist – Memantine Aspirin TiclopidineA woman’s desire for revenge outlasts all her other emotions
    • Prevention & TreatmentAnti dementia drug trials (not based on subtype of VaD)Alkaloid derivatives(hydergine or nicergoline)PentoxyfyllinePiracetam Modest benefitMemantineDonepezilGingko bilobaGive us the GR ACE to acce pt with se re nity the thing s that canno t bechang e d the COURAGE to chang e the thing s that sho uld be chang e d and the WISDOM to kno w the diffe re nce
    • Strategies to prevent – STROKE-TO-DEMENTIA TEN-STEP APPROACH1. Treat hypertension optimally2. Treat diabetes3. Control hyperlipidaemia, use dietary control for diabetes, obesity and hyperlipidaemia4. Persuade patients to cease smoking and decrease alcohol intake5. Prescribe anticoagulants for atrial fibrillation6. Provide antiplatelet therapy for high risk patients Thought is the labour of the intellect Reverie is its pleasure
    • Strategies to prevent – STROKE-TO-DEMENTIA contd…7. Perform carotid endarterectomy for severe (>70%) carotid stenosis8. Recommend lifestyle changes (e.g., weight loss, exercise, reduce stress, decrease salt intake)9. N-methyl-D-aspartate receptor antagonists, antioxidants)10. Intervene early for stroke and transient ischemic attacks with neuroprotective agents (e.g., propentofylline, calcium channel antagosists, - ? Rivastigmine
    • READ not to contradict or confute Nor to Believe and Take for Granted but TO WEIGH AND CONSIDERTHANK YOU“My Opinions are founded on knowledge but modified by experience”