Medical Stroke - Clinical Neurosciences - PDF

Clinical Neurosciences MEDICAL STROKE Dr. Guillermo Manalo III – August 14, 2023 SEM 1 PRELIMS – TRANS 1 OUTLINE B. Lobes of the Brain I. Anatomy and Physiology a. Nervous System...

Clinical Neurosciences MEDICAL STROKE Dr. Guillermo Manalo III – August 14, 2023 SEM 1 PRELIMS – TRANS 1 OUTLINE B. Lobes of the Brain I. Anatomy and Physiology a. Nervous System b. Lobes of the Brain c. Protection of CNS d. Cerebral Circulatory System II. Etiopathogenesis a. Definition of Terms b. Facts about stroke c. Risk Factors d. Pathophysiology III. Classification of Stroke IV. Manifestations a. Ischemic vs. Hemorrhagic Stroke b. Anterior vs. Posterior Stroke c. Clinical Findings According to Arterial Involvement d. Lacunar Syndromes Figure 2. Brain Lobes (from Natured Trans) V. Diagnosis Frontal lobe a. Plain Cranial CT Scan o Personality, behavior, emotion b. Cranial MRI o Judgement, problem solving and planning VI. Management o Speech (Broca’s area) a. Key Actions to Achieve Better Stroke Management o Body movement concentration, and awareness b. Benefits of Advances in Stroke Management Temporal lobe c. Stroke Chain of Survival o Understanding language (Wernicke’s area) d. Early Specific Management of Hemorrhagic Stroke o Memory e. Early Specific Management of Ischemic Stroke o Hearing VII. Primary and Secondary Prevention of Stroke o Sequencing and organization VIII. Class Activity: Stroke Case (Naregget) Parietal lobe o Interpret language and words 1. Legends o Sense of touch, pain, and temperature [In dark blue color] From the book; Batch Naregget Lecture o Interpret signals from vision, hearing, motor, sensory notes; board-sensitive notes; other references and memory General info (from 2024 trans, Doc’s ppt) o Spatial and visual perception Occipital lobe o Interpret vision: colour, light, movement I. Anatomy And Physiology Brainstem A. Nervous System o Pons o Medulla o Midbrain C. Protection of the CNS Figure 3. Brain Meninges (from Natured Trans) Meninges Figure 1. Nervous System (from Natured Trans) o Dura matter Central Nervous System o Arachnoid o Brain o Pia matter o Spinal cord Cerebrospinal fluid Peripheral Nervous System o It flows around and within the brain and spinal cord o Cranial nerves – 12 pairs o It is produced inside the ventricles o Spinal nerves – 31 pairs o The CSF flows in the subarachnoid space to cushion the brain NEURO – Medical Stroke | TG3 1  D. Cerebral Circulatory System o (Lacerum) segment ▪ No branches o C4 (Cavernous) segment: complex course, runs anteriorly then cephalad, then posterolaterally through the carotid cave to pierce the dura ▪ Branches: meningohypophyseal trunk, inferolateral trunk (can provide collateral anastomotic flow from ECA in the setting of ICA stenosis) ▪ Meningohypophyseal trunk branches into inferior hypophyseal artery (which perfuses the pituitary gland), arteries of Bernasconi and Cassinari, and dorsal meningeal artery (perfuses abducens nerve) ▪ Cavernous sinus - Holds ICA as well as cranial nerves III, IV, V1, V2, and VI - Only CN VI lies within the sinus; the other cranial nerves are located in the lateral dural wall - Receives blood from ophthalmic veins; drains into petrosal sinuses - Exits cavernous sinus through a dural ring o C5 (Supraclinoid) segment: first subarachnoid portion ▪ Branches: ophthalmic, superior hypophyseal, Figure 4. Cerebral vasculature (from Natured Trans) posterior communicating, anterior choroidal Aorta ▪ Ophthalmic artery: first major intracranial ICA o Main source of cerebral blood supply branch o Brachiocephalic (innominate) artery: most proximal - Ophthalmic artery occlusion: monocular branch of aortic arch vision loss o Bifurcates into right common carotid and right ▪ Anterior choroidal artery: subclavian arteries - Originates from posterior aspect of ICA distal o Right vertebral artery originates from right subclavian to the posterior communicating artery artery (PCOM) ▪ Left common carotid artery: usually the second - Supplies internal segment of globus pallidus, main vessel off aortic arch part of posterior limb of internal capsule, part ▪ Left subclavian artery gives off left vertebral artery of geniculocalcarine tract, choroid plexus ▪ Subclavian arteries give off internal thoracic - Ends at middle cerebral/anterior cerebral arteries, thyrocervical and costocervical trunks artery bifurcation, also known as the “carotid ▪ Bovine aortic arch: normal variant with shared T” origin of brachiocephalic artery and left common - “T occlusions” are associated with extensive carotid artery (CCA) morbidity and mortality Common carotid artery (CCA) o Absent ICA: Congenital absence from agenesis, o Travels within carotid sheath with internal jugular vein, aplasia, hypoplasia can occur in less than 0.1 % vagus nerve, and ansa cervicalis ▪ Collateral flow will occur through ACOM and o Bifurcates into external carotid and internal carotid PCOM arteries between C3-C5 vertebral levels (most o Aberrant ICA: Involution of cervical portion of ICA leads commonly C4) to enlargement of inferior tympanic and o Bifurcation can be as high as C1 or as low as T2 caroticotympanic arteries for collateral flow (through Internal carotid artery (ICA) middle ear); This enlargement can be associated with o Commonly originates posterolaterally to external tinnitus carotid artery (ECA) o Carotid dissections most commonly start distal to the o Dilates at the origin to form ICA “bulb,” which is 1–2 cm origin and below the entry into the skull in length, then tapers External carotid artery (ECA) o C1 (Cervical) segment: ascends distally to penetrate o Differentiate from ICA by presence of cervical branches the skull base through carotid canal in the petrous o Superior thyroid artery: first branch, supplies larynx temporal bone and upper thyroid gland ▪ Branches: none o Ascending pharyngeal artery: supplies pharynx, o C2 (Petrous) segment: courses medially in the dura, lower cranial nerves horizontal plane, then cephalad to enter the posterior o Facial artery: supplies most of face, palate, lip/cheek cavernous sinus o Terminates as angular artery around the orbit, which ▪ Branches: caroticotympanic artery (middle, inner anastomoses with branches of ophthalmic artery from ear), vidian artery, periosteal branches ICA NEURO – Medical Stroke | TG3 2  Other branches include lingual, occipital, posterior o ▪ Atherothrombotic strokes (most) auricular, maxillary, and superficial temporal arteries ▪ Cardioembolism (commonly non- Circle of Willis (COW ) rheumatic atrial fibrillation) ▪ Artery-artery embolism o Network of anastomoses between the anterior and ▪ Lacunar infarcts posterior circulations that sits at the base of the brain o Cerebral blood flow: o Complete COW only seen in about 25 % of population ▪ Normal: 50 mL/100 g/min o Is formed at ICA terminus, marked by bifurcation into ▪ Ischemic penumbra: 18-35 mL/100 middle cerebral artery (MCA) and anterior cerebral g/min artery (ACA) branches ▪ Core infarct: Stroke or “brain attack” spontaneous rupture of small o Sudden onset of focal or global neurologic penetrating arteries of the Circle of deficit due to an underlying vascular pathology Willis (possibly from weakened o Stroke or cerebrovascular event is an acute vessel wall and formation of Charcot- heterogenous syndrome caused by several Bouchard aneurysms) disorders leading to an occlusion or rupture of o Most common sites: blood vessels supplying brain tissue. ▪ Basal ganglia, especially putamen o A stroke is caused by interruption of blood flow and internal capsule to the brain, which if left untreated, may lead to ▪ Thalamus permanent damage to the brain tissue ▪ Cerebellum Transient ischemic attack (TIA) ▪ Pons o Transient neurological dysfunction caused by ▪ Lobar areas focal brain, spinal or retinal ischemia without the evidence of infarction documented by a III. Classification of Stroke normal cranial imaging o Symptoms typically last less than an hour. Table 1. Basis of Classification of Stroke Basis Description F. Some Facts About Stroke Stroke is the leading cause of adult disability. More than Ischemic (80-85%) half of all stroke survivors are left dependent on others Etiology Hemorrhagic (10-15%) for everyday activities. The Stroke Alliance for Europe (S.A.F.E) states that in From the time of onset 2017 the total costs relating to strokes was 45 billion Hyperacute (0-6 hours) euros. Ictus Acute (6-72 hours) For every 1000 patients who receive thrombolysis, 80 Subacute (72 hours to 3 weeks) will live more independently. Chronic (>3 weeks) Based on National Institute of Health Stroke Scale G. Risk Factors (NIHSS) score Non-modifiable risk factors: Severity Mild (0-5 score) o Older age Moderate (6-21 score) o Male sex Severe (>22 score) o Ethnicity (non-white) o Family history of stroke Table 2. Common Classification Schemes for Stroke Modifiable risk factors: o Hypertension, diabetes, dyslipidemia, cardiac Basis Description diseases Oxfordshire Predicts stroke territory o Smoking, excess alcohol intake Community Stroke size, outcome, and o Physical inactivity, obesity, stress Project (OCSP) or severity o Extracranial and intracranial stenosis Bamford Classification Does not indicate the o Peripheral arterial disease pathophysiologic mechanism H. Pathophysiology Ischemic stroke Trial of ORG 10172 in Widest accepted o Acute occlusion of intracranial vess el leading Acute Stroke subtyping system based to reduction in blood flow to supplied brain Treatment (TOAST) on pathophysiologic regio mechanism o Causes: NEURO – Medical Stroke | TG3 3  Utilized in major stroke Cortical dysphonia, trials dysfunctions dizziness, diplopia Facial weakness Facial paralysis that spares the involving all STROKE CLASSIFICATION (Doc’s PPT 202) frontalis and muscles of facial 1. Transient Ischemic Attack corrugator muscles, expression The blood supply to an area of the brain is temporarily contralateral to the ipsilateral to the interrupted but is restored within 60 minutes and the lesion lesion patient returns to normal. Eye deviation Eye deviation 2. Ischemic Stroke looking away from looking toward the The blood supply to an area of the brain is completely the side of hemiparetic side blocked, causing tissue death and neurological hemiparesis (away from the damage. (towards the sign of side of the lesion) Commonest form of stroke (88%) the lesion) An untreated patient loses approximately 2 million neurons every minute in the ischemic area Prognosis Ischemic core – brain tissue destined to die Extensive ischemia of the More complete Penumbra - salvageable brain area brain results to less neurologic With a stroke, time lost is brain lost complete neurologic recovery for small 3. Hemorrhagic Stroke recovery infarcts Also known as intracerebral hemorrhage Large infarcts are Bleeding within the brain itself due to either often fatal because ○ INTRAPARENCHYMAL HEMORRHAGE – of vital centers bleeding within the brain tissue located in the ○ INTRAVENTRICULAR HEMORRHAGE – brainstem bleeding within the brain’s ventricular system IV. Manifestations * Ipsilateral manifestation of cerebellar lesions is because of the A. Ischemic vs Hemorrhagic Stroke double decussation of the frontopontocerebellodentatorubro Ischemic Stroke thalamocortical tract. o Deficit maximal at onset o Atherothrombotic stroke: occurs during sleep C. Clinical Findings According to Arterial Involvement o Cardioembolic stroke: sudden onset of Internal carotid artery (ICA) maximal deficit ( lower extremity weakness Hemorrhagic Stroke § Dominant hemisphere: aphasia o Headache, vomiting, SBP of >220 mmHg, (global, Broca’s, Wernicke’s) impaired consciousness and evolution of focal § Non-dominant hemisphere: neglect deficits over minutes to hours syndrome, topographical difficulty, o Hypertensive intracranial hemorrhage: constructional and dressing apraxia develops over 30-90 minutes o Anticoagulant-induced intracranial Anterior cerebral artery (ACA) hemorrhage: evolve as long as 24-48 hours o Lower extremity > upper extremity § Abulia, muteness, perseveration, disinhibition B. Anterior vs Posterior Stroke Table 3. Comparison of anterior and posterior circulation strokes Posterior cerebral artery (PCA), peripheral branches Anterior Circulation Stroke Posterior Circulation Stroke o Memory deficits § Cortical blindness, ocular apraxia, Incidence other visual deficits More frequent (80%) More frequent (80%) Posterior cerebral artery, central branches Site of Ischemia o Thalamic syndrome (aka Dejerine-Roussy Cerebral hemisphere Brainstem and cerebellum syndrome) Arteries Involved § Contralateral hemi-body pain Internal carotid Vertebrobasilar artery and § Contralateral hemisensory loss of all Middle cerebral its branches modalities Anterior cerebral o Cranial nerve deficits and other manifestations Anterior communicating of brainstem and diencephalic dysfunction Vertebrobasilar artery Laterality o Brainstem stroke syndromes Usually unilateral which is Bilateral signs § Crossed signs: contralateral long contralateral to the lesion frequently present tract signs with ipsilateral cranial Crossed signs nerve deficit seen in brainstem o Cerebellar manifestations lesions Cerebellar lesions D. Lacunar Syndromes manifest Small stroke at 75% of largest hematoma slice – counted as 1 slice least definite sign of hyperacute stroke and must therefore be o If 25-75% – count as 0.5 slice correlated clinically o If 180 mmHg b. Absence of ischemic penumbra allows for more aggressive BP treatment in intracranial hemorrhage Figure 11. Sulcal effacement: The cortical sulci are flattened at c. Acute lowering of SBP of 40 seconds injury involving >1/3 of the MCA § PT of >15 seconds territory o Active internal bleeding C. Dose of IV alteplase: 0.9 mg/kg o Arterial puncture at a non-compressible site a. Maximum dose of 90mg within 7 days b. Given over 60 minutes with initial 10% o Infective endocarditis given as IV bolus over 1 minute o Aortic arch dissection D. Patients who have elevated BP and are eligible o GI malignancy or recent GI bleed within 21 days for IV alteplase should have their BP carefully o Use of low molecular weight heparin within the lowered to 185 mmHg or d. Have NIHSS score of >6 DBP >110 mmHg despite aggressive treatment e. Have Alberta Stroke Program Early CT Relative contraindications: score of >6 o Mild ischemic stroke syndrome f. Can receive treatment (groin puncture) o Intracranial vascular malformation within 6 hours of symptom onset o Cerebral microbleeds on MRI g. Have large-vessel occlusion in the anterior o Extra-axial, intracranial neoplasm circulation o Procedural stroke B. Mechanical thrombectomy o Seizure at the onset of stroke symptom a. Recommended for selected patients with o Unruptured and unsecured intracranial acute ischemic stroke within 6-16 hours aneurysm of 130 mmHg reduction is more important than § Not more than 15% of baseline MAP the specific agent Secondary prevention: within 24 hours antihypertensive medications d. Use easily titratable or short acting recommended for all types of antihypertensive agents ischemic stroke and TIA patients i. Nicardipine beyond the hyperacute period ii. Alternatives: hydralazine, labetalol, esmolol e. Do not use rapid-acting sublingual agents Target HBA1c of 94% ischemic → because of increased b. Monitor: atherogenic risk, most especially i. Pulse oximetry the small cerebral vessels ii. ABG Stroke outcome if with poor C. Avoid Hypoglycemia and Hyperglycemia glycemic control: a. Target capillary blood glucose (CBG): 140-180 ○ Reduced survival mg/dL ○ Permanent neurologic and functional disability b. Use isotonic saline (0.9% NaCl) ○ Longer hospital stay c. Avoid glucose-containing (D5) fluids ○ Dementia Diabetes D. Avoid Hyperthermia Primary prevention Mellitus a. Target: normothermia ○ Aspirin is not b. Relative risk of death or disability increased recommended if with no two-fold for every 1o increase in body evidence of temperature atherosclerotic disease c. Treat fever with antipyretics and cooling ○ Delays onset and progression of blankets microvascular d. Work-up the source of fever complication E. Neuroleptic and Neurorestorative Drugs ○ If with intensive insulin a. Use remains a matter of preference of the therapy – may also attending physician protect from b. Examples: macrovascular complication i. Citicoline Secondary prevention: glucose ii. Cerebrolysin control, all ischemic stroke patients iii. NeuroAID and TIA should be screened for DM NEURO – Medical Stroke | TG3 9  HBA1c more accurate in the as identified via immediate post-event period Valvular heart TEE Pharmacologic management: disease ○ Drugs used ○ Metformin – decrease Warfarin stroke occurrence (Coumadin) ○ SU – decreased - microvascular events but Patientswithrheu may increase stroke maticmitralvalve incidence diseaseorprosth ○ Pioglitazone – decreased etic valve without MI, stroke, death prior stroke or ○ Aspirin – if with TIA atherosclerosis - Reasonable use in patients Target LDL level: 70-100 mg/dL with stroke of Primary prevention: statin TIA with therapy reduces all stroke types Secondary prevention: rheumatic heart ○ ≤75 years old with clinical disease with or Dyslipidemia ASCVD (including TIA without AF (INR and stroke): high target: 2.0- intensity statin therapy 3.0→average of (moderate if contraindicated) 2.5) ○ >75 years old with clinical Antiplatelet ASCVD: moderate or agents high intensity statin - Not added to therapy warfarin to avoid Statins additional ○ Simvastatin – reduction of bleeding risk stroke incidence -Aspirin ○ Atorvastatin – reduction of 80mg/day is recurrence suggested if recurrent embolism despite Atrial 4-5x higher risk of stroke warfarin therapy Fibrillation (regardless of whether paroxysmal (AF) or sustained) Mitral valve prolapse Oral anticoagulation for a patients ○ Most common form of with CHA2DS2-VASc= 1 → valve disease in adults ○ Increased risk for provided that the thromboembolic score is not because of a female phenomena gender ○ No particular anti- Aspirin monotherapy if unable to thrombotic therapy take anticoagulants ○ General stroke and TIA Drug of choice: warfarin (also guidelines in the use of used for cardiomyopathy and anti-platelets are ischemic heart recommended disease) Mitral annular calcification Target INR: 2.0-3.0 for at least 3 ○ Thrombus formations months up to 1 year seen on heavily calcified annular tissue on autopsy ○ Drugs: antiplatelets or All patients with mechanical heart warfarin therapy valves (with or without AF) require Aortic valve disease anticoagulation ○ Incidence of Rheumatic heart disease microthrombi or calcific ○ Increased risk of emboli recurrent embolism o ○ Antiplatelet therapy – Long-term anticoagulation ischemic stroke with TIA therapy but with no AF Reduce risk of Prosthetic heart valves systemic ○ Increased risk of embolism thromboembolism, May help in the especially if with AF disappearance ○ Oral anticoagulation with of LV thrombus or without ischemic stroke NEURO – Medical Stroke | TG3 10  or TIA maintaining I NR of 3.0 (range: 2.5-3.5) Smoking Smoking cessation for all current ○ Anticoagulants with smokers aspiring 75-100 mg/day if with ischemic stroke or TIA maintaining INR of Excessive Eliminate or reduce alcohol 3.0 (range: 2.5-3.5) alcohol consumption ○ Bioprosthetic heart Light to moderate intake of alcohol valves with ischemic ○ 1 drink per day for non- stroke or TIA – warfarin is pregnant women o 2 given with maintained INR 10 drinks per day for men of 2.0-3.0 Nutrition Limit sodium intake to