2. Definition Transient Ischaemic Attack (TIA) – an acute focal neurological deficit resulting from cerebrovascular disease with resolution of signs and symptoms within 24 hours. Reversible Ischaemic Neurological Deficit (RIND) – attack lasting longer than 24 hours but with complete clearance of signs and symptoms within 7 days. Completed Stroke – neurological deficit lasts longer than 7 days.
3. HOW YOU GIVE THE DIAGNOSIS? The diagnosis should provide answers to the following questions: 1. What is the neurological deficit? 2. Where is the lesion? 3. What is the lesion? 4. Why has the lesion occurred? 5. What are the potential complications and prognosis?
4. What Artery Involved? Aphasia (dominant hemisphere) Hemiparesis / plegia Hemisensoryloss/disturbance Homonymous hemianopia Parietal lobe dysfunction, e.g. astereognosis, agraphaesthesia, impaired two-point discrimination, sensory and visual inattention, left-right dissociation and acalculia
6. What Artery Involved? Homonymous hemianopia Cortical blindness Ataxia Dizziness or vertigo Dysarthria Diplopia Dysphagia Horner’s syndrome Hemiparesis or hemisensory loss contralateral to the cranial nerves palsy Cerebellar signs
8. Brain Blood Supply Features: High oxygen requirement. Brain 2% of body weight - 15% of cardiac output 20% of total body oxygen. Continuous oxygen requirement Few minutes of ischemia - irreversible injury. Neurons - Predominantly aerobic. Sensitive areas: Adults -Hippocampus, 3,5th & 6th layer of cortex, Purkinje cells. Border zone (watershed areas) Brain stem nuclei in infants.
11. Frontal[f*ck – motor] Lobe Functions: High level cognitive functions. i.e reasoning, abstraction, concentration Storage of information – memory Control of voluntary eye movement Motor control of speech in the dominant hemisphere. Motor Cortex – Motor control of the contralateral side of the body Urinary continence Emotion and personality
12. Parietal[p-sx – sensory] Lobe Functions: Sensory cortex – sensory input is interpreted to define size, weight, texture and consistency (contralateral) Sensation is localised, and modalities of touch, pressure and position are identified. Awareness of the parts of body Non-dominant – processes visuospatial information and controls spatial orientation Dominant is involved in ideomotor praxis (ability to perform learned motor tasks
13. Temporal[t-telinga] Lobe Functions: Primary auditory receptive areas In dominant ability to comprehend speech (wernicke’s) – reception Interpretive area – area at the junction of the temporal, parietal and occipital lobes. Plays an important role in visual, auditory and olfactory perception Important role in learning; memory and emotional affect.
14. Occipital[O-optic] Lobe Functions: Primary visual cortex Visual association areas Visual perception Some visual reflexes (i.e. visual fixation) Involuntary smooth eye movement
15. Diencephalon Functions: Brain Stem: Midbrain, Pons & Medulla 10 of the 12 ranial nerves arise from the brainstem (ipsilateral signs) Cortical pathway decussation contralateral signs. Some major functions: eye movement, swallowing, breathing, blood pressure, heat beat, consciousness Cerebellum: movement – Balance & coordination
24. Global Ischemia: Etiology: Impaired blood supply - Lung & Heart disorders. Impaired O2 carrying – Anemia/Blood dis. Impaired O2 utilization – Cyanide poisoning. Morphology: 3rd, 5th and 6th layers of the cortex, hippocampus and in the Purkinje cells in the cerebellum Laminar necrosis, Hippocampus, Purkinje cells. Border zone infarcts – “Watershed” Sickle shaped band of necrosis on cortex. ClinicalFeatures: Mild transient confusion state to Severe irreversible brain death. Flat EEG, Vegetative state. Coma.
25. Morphology in Global Ischemia Watershed zone (Acute - ACA-MCA) Laminar necrosis - (chronic- short penetrating arteries) Sommer sector of hippocampus. Purkinje cells of cerebellum.
32. Brain Stem Stroke: Common Pattern Pure Motor - Weakness of face and limbs on one side of the body without abnormalities of higher brain function, sensation, or vision (MCA/ACA) Pure Sensory - Decreased sensation of face and limbs on one side of the body without abnormalities of higher brain function, motor function, or vision (PCA).
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34. MCA [most common] Features: Paralysis of the contralateral face, arm and leg Sensory impairment over the contralateral face, arm & leg Homonymous hemi or quadrantonopia Paralysis of gaze to the opposite side Aphasia (dominant) and dysarthria [broca/wernicke] Penetrating - contralateral hemiplegia/paresis, slurred speech. Impaired spatial perception
39. ACA stroke. Paralysis of contralateral foot and leg Sensory loss over toes, foot and leg Impairment of gait and stance Abulia (slowness and prolonged delays to perform acts) Flat affect, lack of spontaneity, slowness, distractibility Cognitive impairment, such as perseveration and amnesia Urinary incontinence Wikipedia: GNU Free Documentation license
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41. PCA stroke. Peripheral (cortical) Homonymous hemianopia Memory deficits Perseveration Several visual deficits (cortical blindness, lack of depth perception, hallucinations) Central (penetrating) Thalamus - contralateral sensory loss, spontaneous pain, mild hemi Cerebral peduncle - CN III palsy with contralateral hemiplegia Brain stem - CN palsies, nystagmus, pupillary abnormalities Wikipedia: GNU Free Documentation license
42. Posterior Cerebral Artery Visual disturbances contralateral homonymous hemianopsia (central vision is often spared) L. Hemi: lesions alexia (with or without agraphia) Bilateral lesions: cortical blindness patients unaware they cannot see (Anton's syndrome) Memory impairment if temporal lobe is affected ~ Proximal occlusion contralateral hemisensory loss, spontaneous pain and dysesthesia if thalamus affected (thalamic pain syndrome) contralateral severe proximal chorea (hemiballism) ~
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45. Haemorrhagic - Arterial embolus Embolic stroke: sudden, pin point hemorrhages over a triangular area.
60. Left (Dominant) Hemisphere Stroke: Clinical Aphasia Righthemiparesis Right-sided sensory loss Right visual field defect Poor right conjugate gaze Dysarthria Difficulty reading, writing, or calculating L affect R Diagnosis: Recent cerebral infarction in left MCA distribution. Left cerebral hemisphere shows swelling with compression of the lateral ventricle mainly in the frontal area, due to recent infarct in the Middle Cerebral Artery (MCA) distribution. The brain in the MCA area shows discoloration of the cortex and also blurring between the cortex and white matter.
61. Right (Non-dominant) - Hemisphere Stroke: Defect of left visual field Extinction of left-sided stimuli Left hemiparesis Left-sided sensory loss Left visual field defect Poor left conjugate gaze Dysarthria Spatial disorientation R affect L
62. CNS AV Malformations: Many types: AV Malformation * Cavernous angioma Telangiectasia Venous angioma Cause of Seizure disorders & hemorrhage. Most common congenital vascular malformation. Typically located in the outer cerebral cortex underlying white matter.
68. Stroke – Signs and Symptoms Ischemic Vertebrobasilar Circulation Vertigo Visual disturbance Both eyes simultaneously Diplopia Ocular palsy – inability to move to one side Dysconjugate gaze – asynchronous movement Paralysis Numbness Dysarthria Ataxia
69. Stroke – Signs and Symptoms Hemorrhagic Subarachnoid hemorrhage Sudden severe HA Transient LOC Nausea/Vomiting Neck pain Intolerance of noise/light AMS Intracerebral hemorrhage Focal sx w/ LOC, N/V
70. History Detailed history from relative or friend or patient if he is able to speak. Rapidity of onset – sudden onset of a focal neurological deficit. Time course of symptoms – maximum deficit over seconds or minutes before starting to improve. Headache, coma at onset and vomiting at onset are more common in haemorrhage but also occur with infarction. Sudden onset of severe generalised headache associated with neck stiffness – subarachnoid haemorrhage. Specific record should be made about the presence of vascular risk factors.
71. Examination General Examination BP – should be taken in both arms. Stroke may cause an acute rise in BP and therefore hypertension should not be diagnosed in the first few days after a stroke unless left ventricular hypertrophy of fundal changes are present. Pulse – for arrhythmias particularly atrial fibrillation. Peripheral pulses. Auscultation for a carotid bruit. Heart – for valvular heart disease especially mitral stenosis. Neck stiffness – subarachnoid haemorrhage or meningitis. Identify the anatomical localization of the lesion and record the degree of disability.
80. Subarachnoid haemorrhage Initial headache or coma – sudden rise in intracranial pressure. Focal symptoms if aneurysm ruptures into underlying brain. Cerebral vasospasm causes delayed cerebral infarction 4-14 days after onset in 30% of patients. Recurrent haemorrhage and hydrocephalus are other complications.
81. Intracerebral Haemorrhage Sudden rupture of microaneurysms caused by hypertensive vascular disease. Characteristically occurs in the basal ganglia, pons and cerebellum. Elderly patients – cerebral amyloid angiopathy, a degenerative disorder affecting the walls of the artey – subcortical haematomas. Cryptic av malformations are suspect especially in younger patients < 40 yrs and when the haemotoma is Lobar (frontal, temporal, parieto-occipital).
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87. MRI Scan Posterior circulation strokes are more readily identified than by CT.
88. General Investigations identify conditions which may predispose towards premature cerebrovasculardisease. Full blood count – polycythemia, thrombocytopoenia. Blood glucose – diabetes mellitus. Serum lipids – hypercholesterolemia. Blood cultures – SBE.
89. General Investigations II HIV screen – AIDS. Syphilis serology – VDRL. Clotting Screen. Thrombophilia Screen – Protein C, Protein S, Antithrombin III. Anticardolipin antibodies – SLE. Lumbar Puncture – subarachnoid haemorrhage.
90. DD Stroke Differential Diagnosis of Stroke Head/Cervical trauma Meningitis/encephalitis Hypertensive encephalopathy Intracranial mass Tumor Sub/epi dural hematoma Todd’s paralysis Migraine w/ neuro sx Metabolic Hyper/hypo glycemia Post arrest ischemia Drug OD
91. Differential Diagnosis Space occupying lesion 5% of people with stroke like symptoms have a subdural haematoma, tumour or cerebral abscess. Distinction is readily made on CT or MRI. If there is any doubt repeat the scan after 6 weeks.
92. Differential Diagnosis II Multiple sclerosis May present with hemiparesis, sensory impairment or brainstem symptoms that mimic stroke. Symptoms occur gradually over a few days. Hypoglycaemia May cause hemiparesis. Migraine
93. Complications I Cerebral oedema Should be suspected in a patient with a large infarct or haemorrhage experiences a lucid interval of 24-48 hours and then shows a decline in consciousness.
94. Complication II Haemorrhagic transformation Can occur as a result of thrombolysis. Pneumonia In patients with swallowing difficulties as a result of aspiration. Pressure sores Develop rapidly and may be exacerbated because of incontinence. Oedema of Weak Limbs Is common and has a partially autonomic basis.
95. Complication III Anxiety and Depression Common reactions to stroke but depression may have an organic basis related to damage of the frontal and limbic systems. Emotional Lability Precipitated by minor emotional stimuli.
96. Management I Has the following aims Confirmation of the diagnosis, anatomical site of the lesion, pathology and aetiology. Acute care. Rehabilitation of persistent disability and handicap. Prevention of recurrence.
97. Management II Acute Care Treatment aims Prevent progression of present event. Prevent immediate complication. Prevent the development of subsequent events. To rehabilitate the patient.
98. Management III General Measures Around the edge of the infarct, ischaemic tissue is at risk, but is potentially recoverable. This must be protected by ensuring a good supply of glucose and oxygen. Maintain hydration, oxygenation and blood pressure.
99. Specific MeasuresMedical Treatment Anticoagulation Patient with high risk of developing deep vein thrombosis. Thromboembolic stroke - started as soon as possible, except in large infarcts where it may be wise to delay anticoagulation for 2 weeks. Stroke in a patient with myocardial infarct - due to mural thrombus. Stroke in evolution. Exclude a haemorrhage by doing a CT scan first.
100. Medical Treatment IIAntiplatelet Agents Especially in TIA. Thrombolysis I/V thrombolysis espcially recombinant tissue plasminogen activator rTPA to be given only within the first 3 hours after onset to those patients who have not developed CT abnormalities especially in patients with basilar artery occlusion. Risk – haemorrhage.
101. Hypertension Treated cautiously in acute stroke. A reduction in blood pressure may lower cerebral blood flow in the regions surrounding the infarct below a critical level at which further ischaemic brain damage will occur. Mild to moderate elevations in BP – no treatment unless they are maintained for several days after admission.
102. If stroke associated with hypertensive encephalopathy or if diastolic BP is persistently above 120 mm Hg. The BP should be lowered cautiously using oral agents. Sudden precipitious fall in BP should be avoided. Hypertension II
103. Medical TreatmentCalcium Antagonist Nimodipine prevents ischaemic brain damage and reduces the number of patients remaining disabled after subarachnoid haemorrhage. Prescribed as soon as diagnosis is made (within 12 hours).
104. Neurosurgery Should be considered in subaracnoid and intracerebral haemorrhage. Evacuation of cerebellar haematoma. Evacuation of supratentorial haematomas should only be considered in younger patients with superficial cortical haematomas causing mass effect with a deteriorating level of conciousness.
105. Nursing Care and Rehabilitation Physiotherapy, proper positioning and early mobilization – prevent pressure sores. Support stockings – prevent deep vein thrombosis and pulmonary embolism. Swallowing difficulties. Lead to silent aspiration – aspiration pneuomonia. Nasogastric tube feeding. Percutanious endoscopic gastrostomy.
106. Rehabilitation Physiotherapy, occupational therapy, speech therapy and psychology input – multidisciplinary stroke rehabilitation team. Home visit by occupational therapist to plan adaptations to home before discharge.
107. Secondary Preventation Control hypertension and diabetes mellitus. Correct lipid abnormality. Stop cigarette smoking. Stop thrombogenic drugs e.g. oral contraceptives.
108. Secondary Preventation II Give platlet antiaggregation drugs to reduce the rate of reinfarction. Low dose aspirin (75 mg – 150 mg), if patient allergic or has gastrointestinal side effects give ticlopidine. Regular blood tests because of a small risk of neutropoenia. Remove or treat embolic source (long term anticoagulation in atrial fibrillation). Treat inflammatory or vascular inflammatory diseases.
109. Secondary Preventation III Carotid Endarterectomy – preventing stroke in symptomatic patients with recent TIA and stroke and severe stenosis of the internal carotid artery (at least 70%).
110. Chain of Survival Stroke Stroke Chain of Survival Detection Early sx recognition Dispatch Prompt EMS response Delivery Transport, approp, prehospital care, prearrival notification Door ER Triage Data ER evaluation incl, CT, etc. Decision Appropriate therapies Drug/Therapy
111. Detect & Dispatch Detection: Early Recognition Public education of Stroke sx Early access to medical care Dispatch: Early EMS and PDI’s Caller triage EMD recognition of Stroke sx
112. How to detect? Delivery: Pre-hospital Transport and Management How we scale the pre-hospital management of the patient?
114. CINCINNATI STROKE SCALE Identifies patients with strokes. It evaluates three major physical findings. Facial droop Motor arm weakness Speech abnormalities
115. CSS - Facial Droop Have the patient show their teeth or smile. Normal – both sides of the face move equally well Abnormal – one side of the face does not move as well as the other side
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118. Arm Drift Have the patient close his/her eyes and hold both arms out. Normal – both arms move the same way, or both arms do not move at all. Abnormal – one arm does not move or one arm drifts down compared to the other arm. Other findings such as pronator grip, may be helpful
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121. Speech Have the patient say “You can’t teach an old dog new tricks.” – “Perlambagaan Malaysia” Normal – patient uses correct words with no slurring. Abnormal – patient slurs words, uses inappropriate words, or is unable to speak
124. Cincinnati PrehospitalStroke Scale Patients with 1 of these 3 findings -as a new event - have a 72% probability of an ischemic stroke. If all 3 findings are present the probability of an acute stroke is more than 85% Immediately contact medical control and the destination ED and provide prearrival notification.
125. Stroke – Management In Review: Prehospital Critical Actions Assess and support cardiorespiratory function Assess and support blood glucose Assess and support oxygenation and ventilation Assess neurologic function Determine precise time of symptom onset Determine essential medical information Provide rapid emergent transport to ED Notify ED that a possible stroke patient is en route
126. Stroke - Management Door: ER Triage Stroke evaluation targets for stroke patients who are thrombolytic candidates Door-to–doctor first sees patient…….………… 10 min Door-to–CT completed …….………………….. 25 min Door-to–CT read ...…………..………………… 45 min Door-to–fibrinolytic therapy starts …………….. 60 min Neurologic expertise available*…..…………… 15 min Neurosurgical expertise available* …………… 2 hours Admitted to monitored bed ..……...…………… 3 hours *By phone or in person
127. Stroke - Management Data: ER Evaluation and Management Assessment Goal: in first 10 minutes Assess ABCs, vital signs Provide oxygen by nasal cannula Obtain IV access; obtain blood samples (CBC, ’lytes, coagulation studies) Obtain 12-lead ECG, check rhythm, place on monitor Check blood sugar; treat if indicated Alert Stroke Team: neurologist, radiologist, CT technician Perform general neurologic screening assessment
128. Stroke - Management Assessment Goal: in first 25 minutes Review patient history Establish symptom onset (<6 hours required for fibrinolytics) Perform physical examination Perform neurologic exam Determine level of consciousness (Glasgow Coma Scale) Determine level of stroke severity (NIHSS or Hunt and Hess Scale) Order urgent non-contrast CT scan/angiogram if non-hemorrhage (door-to–CT scan performed: goal <25 min from arrival) Read CT scan (door-to–CT read: goal <45 min from arrival) Perform lateral cervical spine x-ray (if patient comatose/trauma history)
129. Stroke - Management ER Diagnostic Studies CT scan – done w/in 25 mins, read w/in 45 mins r/o hemorrhage Often normal early in ischemic stroke Lumbar puncture EKG Changes may be caused by or cause of stroke MRA (Magnetic Resonance Angiography) Cerebral Angiography
133. Acute subarachnoid hemorrhage Diffuse areas of white (hyperdense) images Blood visible in ventricles and multiple areas on surface of brain
134. Stroke - Management Decision: Specific Therapies General Care ABC’s, O2 IV w/ BSS Treat hypotension Avoid over-hydration Monitor input/output Normalize BGL Manage Elevated BP?
135. Stroke - Management Indications for Antihypertensive therapy In general: Consider: absolute level of BP? If BP: >185/>110 mm Hg = fibrinolytic therapy contraindicated Consider: other than BP, is patient candidate for fibrinolytics? If patient is candidate for fibrinolytics: treat initial BP >185/>110 mm Hg Consider: response to initial efforts to lower BP in ED? If treatment brings BP down to <185/110 mm Hg: give fibrinolytics Consider: ischemic vs hemorrhagic stroke? Treat BP in the 180-230/110-140 mm Hg range the same The obvious: no fibrinolytics for hemorrhagic stroke
136. Stroke - Management Decision: Specific Therapies (cont.) Management of Seizures Benzodiazepines Long-acting anticonvulsants Management of Increased ICP Maintain PaCO2 30mm Hg Mannitol/Diuretics Barbiturates Neurosurgical decompression
137. Stroke - Management Drugs: Thrombolytic Therapy Fibrinolytic Therapy Checklist Ischemic Stroke Candidates for Neurointerventional Therapy Age 18 years or older Acute signs and symptoms of CVA <6 hours onset. No contraindications.
138. Stroke - Management Contraindications for Interventional Therapy Absolute Evidence of intracranial hemorrhage on non-contrast head CT Patient with early infarct signs on CT scan. Relative Recent (w/in 2 mo’s) cranial or spinal surgery, trauma, or injury Known bleeding disorder and/or risk of bleeding including: - Current anticoagulant therapy, prothrombin time >15 sec. - Heparin within 48 hrs of admission, PTT elevated - Platelet count <100,000/mm Active internal bleeding w/in the previous 10 days Known or suspected pregnancy History of stroke w/in past 6 weeks
139. Stroke - Management Contraindications for Interventional Therapy (cont.) Relative Patient comatose >85 years old Diabetic hemorrhagic retinopathy or other opthalmic hemorrhagic disorder Advanced liver or kidney disease Other pathology with a propensity for bleeding Infectiouse endocarditis Severe EKG disturbance, uncontrolled angina or acute MI
193. ANSWER 9 CT or MRI of the head, looking for ischaemic infarcts, haemorrhage, or mass lesions
194. QUESTION 10 What investigations would you perform in a stroke patient? MAINLY TO FIND THE CAUSE OF STROKE
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196. If patient is in AF, ask for results of transoesophageal echo, looking for thrombus or spontaneous atheromatous plaques in ascending aorta and arch of aorta that may have contributed to stroke
