cerebrovascular accidents - types, causes and its management

This PowerPoint presentation provides in-depth knowledge regarding cerebrovascular accidents types, stages of management, medical management, surgical management, nursing management, complications and their management

1. Cerebrovascular accidents Medical-Surgical Nursing Viresh Sunil Mahajani M. Sc Medical Surgical Nursing (Cardiovascular and Thoracic Nursing) Institute of Nursing Education, Mumbai

2. Anatomical review Neurons Primary functional unit of nervous system. Three main characteristics Excitability Conductivity Influence Three main parts- Cell body Multiple dendrites An axon

3. Cell body contains nucleus and cytoplasm. It is the metabolic centre of neuron. Dendrites are the short processes that extends from cell body. They receive impulses or signals from other neurons. Axons are the long projections that extends from cell body. They carry impulses away from the cell body towards other neurons or end organs like smooth muscles, striated muscles and glands. These axons may be mylinated or unmylinated . Myline sheet is a white lipoprotein substance that acts as an insulator For conduction of impulses.

4. Glial cells/ Neuroglial cells Supporting cells of the Nervous system. Provide support, protection and nourishment to the neurons of the nervous system. Constitutes almost half of the mass of brain and spinal cord. Two types – Microglial cells and Macroglial cells.

5. Microglial cells – Microphage of nervous system. Capable of phygocytosis Mobile with in brain. Capable of multiplication when brain injury occurs. Macroglial cells – Three types- Astrocytes, oligodendrocytes, ependymal cells. Astrocytes – Found in gray matter Provide structural support to neurons Forms blood brain barrier along with endothelium of blood vessels Plays important role in synaptic transmissions.

6. Oligodendrocytes – Found in white matter Specialized cell that helps to produce myline sheet of nerve fibers in CNS. Schwann cells produce same action in peripheral nervous system.

7. Ependymal cells – Present along the lines of brain ventricles
Aids in secretion of cerebrospinal fluid.

8. Most of the primary CNS tumors are of glial cells. Primary malignancy of neurons are reare .

9. Brain

10. Brain has three major intracranial components – Cerebrum Cerebellum Brain stem

11. Cerebrum Cerebrum is divided into left and right hemisphere. Each hemisphere is divided into four lobes – frontal, parietal, temporal and occipital lobe. Frontal lobe controls higher cognitive function, memory, concentration, voluntary movement and motor functions. Frontal lobe contains broca’s area that controls speech production. Parietal lobe contains sensory cortex that interprets Spatial information Occipital lobe processes information related to sight Temporal lobe processes somatic, visual and auditory data.

12. Mid brain Med brain is located in the inner side of the cerebrum. It consists of basal ganglia, thalamus, hypothalamus and limbic system.

13. Basal ganglia Located centrally to cerebrum and mid brain. Responsible for initiation, execution and completion of voluntary movement, learning, emotional response and autonomic movements like salivation, blinking and swinging hands while walking. Thalamus Placed just above the brain stem. Major relay centre for sensory input from the body, face, Retina, cochlear and taste receptors. Motor relay centre that connects cerebellum and basal ganglia to frontal cortex. Hypothalamus Located inferior to thalamus, in front of midbrain. Exert direct influence on release of pituitary hormones.

14. Hypothalamus It also contains center for regulation of appetite, body temperature, water regulation, circadian rhythm and expression of emotions. Limbic system Located neart the inner surface of cerebral hemisphere Responsible for emotional responses, feeding behaviour, and sexual behaviour.

15. Brain stem

16. Brain stem It consists of midbrain, pons and medulla oblongata. It is the nuclei of cranial nerve III to nerve XII. Vital centre for respiratory, vasomotor and cardiac functions. Contains reticular system that facilitates communication among brain stem, reticular formation and cerebral cortex. Functions of reticular system is to relay sensory information, influence the excitatory and inhibitory control of spinal motor neurons amd controlling vasomotor and respiratory activity. Brain stem also contains center for regulating arousal and sleep wake transition. It also contains center for sneezing, coughing, hiccups, vomiting, sucking and swallowing.

17. It is located in posterior cranial fossa. It co-ordinates voluntary movements and maintaine trunk stability and equilibrium. It receives information from cerebral cortex, muscles, joints, and inner ear. It influences motor activity through axonal connection to thalamus, motor cortex and brain stem and descending pathways. Cerebellum

18. Ventricles and cerebrospinal fluid

19. Brain contains four interconnected fluid filled cavities called ventricles. This cavity extends centrally through the full length of the spinal cord. This cavity is filled with the fluid called as cerebrospinal fluid. Avarage volume of CSF is 150 ml. CSF is produced by chlorid plexuses located within fourth ventricle of the brain. Avarage rate of CSF production is 500 ml/day Absorption of CSF occurs through arachinoid villiv that are located within subarachnoid space.

20. Cerebral circulation

21. Blood supply to the brain is supplied by Internal carotid arteries Vertebral arteries Internal carotid artery on entering into cranial cavity splits into two branches –anterior cerebral artery and medial cerebral artery. Anterior cerebral artery supplies blood to the medial and frontal portion of frontal lobe. Mid cerebral artery supplies blood to the outer portion of frontal lobe, parietal lobe and superior temporal lobe. Two vertibral arteries join to form basilar artery. Basilar arteries are joined to left and right internal carotid arteries by posterior communicating arteries.

22. Both left and right internal carotid arteries are joined anteriorly by anterior communicating artery. From the posterior communicating arteries arises posterior cerebral arteries. Posterior cerebral arteries supplies blood to the medial portion of occipital lobe and inferior temporal lobe. The structure formed by internal carotid arteries, anterior and posterior communicating arteries and basilar artery resembles the circular structure. This structure is called as circle of Willis. This structure is considered as a safety valve for blood flow.

23. Meninges Meninges are the protective membranes that surrounds brain and spinal cord. There are three layers of meninges – Dura matter, Arachinoid matter and pia matter.

24. Dura matter is the thick outermost layer of meninges. The space between dura matter and arachinoid matter is called subdural space. Arachinoid layer is the fragile web like membrane that lies between dura matter and pia matter. It is vascular inner most layer of meninges. The space between arachinoid matter and pia matter is called as subarachnoid space. This space is filled with CSF. Pia matter is the innermost layer of the meninges.

25. Skull Skull is the protective compartment in which brain lies . Skull is made up of 8 cranial bones and 14 facial bones 8 cranial bones are- Frontal bones- 1 Parietal bones -2 Temporal bones-2 Occipital bone-1 Ethmoid bone-1 Sphenoid bone-1 Cranium is the safety Vault of the brain that protects brain from external injury.

26. Intracranial pressure Hydrostatic force measured in the brain CSF compartment is called Intracranial pressure. Normal Intracranial pressure ranges from 5 to 15 mm of Hg. ICP more than 20 mm 9f Hg is considered to be abnormal is needed to be treated. Normal ICP is maintained by balance among three components – Brain tissue Blood Cerebrospinal fluid. All these components are placed into the enclosed space of skull. Of the three components brain tissue along with intracellular and extracellular fluid constitute 78% of total intracranial volume, while blood in arteries, veins and capillaries makes 12% and remaining 10% is made up of CSF.

27. Normal Compensatory Adaptation Monro – Kelli in their hypothesis stated that under normal conditions, when skul is intact and closed, if volume of any one of the three components increases within the close cranial vault, the volume of the other component is displaced so that normal intracranial volume is maintained to be constant. Thus adapts to the volume changes within the skull in three different ways – Change in CSF volume – By altering CSF absorption or production or displacing CSF into spinal subarachnoid space. Change in intracranial blood volume – Regional cerebral vasoconstriction or dilation, changes in venous outflow, collapse of cerebral veins and sinuses. Changes in brain tissue volume – Distention of dura or compression of brain tissue.

28. Normal cerebral blood flow Amount of blood flowing through 100gm of brain in 1 min. Normal CBF is 50ml/100gm/1min i.e 750 to 1000ml / min. It is about 20% of total cardiac output. Factors affecting normal Cerebral blood flow – CO2 concentration O2 concentration Hydrogen ion concentration. Systemic blood pressure Cardiac output Blood viscosity If blood flow to the brain is interrupted for 30 sec it alters neurological metabolism, if upto 2 min neurological metabolism stops and if more than that cellular death occurs.

29. Stroke Cerebrovascular Accident

30. Cerebrovascular Accidents Cerebrovascular Accidents is an umbrella term used to describe the functional abnormalities of the central nervous system (especially brain) that usually occurs due to disruption of the blood supply to the brain.

31. Prevalence In India, prevalence rates of stroke ranges from 144 -922 cases per 1 lakhs of population. This data is not exact due to improper reporting and recoding facilities in India. Prevalence rates are high in urban area (334 – 424/ 100,000) as compared to urban areas (84 – 262/100,000) Prevalence rate is higher in women (564/100,000) as compared to mens (196/100,000). Stroke contributes 41% of cause of deaths and 72% for cause of permanent lifetime disabilities among the non- communicable diseases. Currently CVA / Stroke is the 15 th leading cause of death in India with 119 to 145 death per 100,000 population.

32. Risk factors of stroke Non modifiable Risk factors Age ( Age >60 years) Gender (Males are more prone to stroke, but women’s die more of stroke) Ethnicity Race Family history (Person with two first degree relative with the history of bleed or aneurysm are at risk of stroke) Heredity Modifiable Risk factors Hypertension Heart diseases Diabetes Mallitus Smoking Serum Cholesterol levels Obesity Sleep Apnea Metabolic syndrome Lack of physical exercise Poor diet Drugs Alcohol

33. Transient Ischemic Attack The transient episode of neurological dysfunction caused due to focal brain ischemia or spinal or retinal ischemia, but without acute infraction to the brain is referred as TIA. Clinical symptoms of TIA last for less than 1hour.

34. TIA mostly occurs due to formation of microembolies that mostly temporarily blocks the blood flow to any perticular part of the brain. Symptoms of TIA may depend on blood vessels that are involved and the area of brain that experience the ischemia. Signs of TIA may include temporary loss of vision, transient hemiparesis, numbness or loss of sensation, sudden inability to speak, vertigo, blurred vision, diplopia, dysphagia, ataxia,etc . TIA should be treated as medical emergency as it may proceed into ischemic stroke. One third of the individuals who experience TIA have chances to progress to stroke. ABCD2 score is used as a tool to predict the risk of stroke in a patient with TIA.

35. Types of Stroke Stroke or Cerebrovascular Accidents are majorly of two types – Ischemic Stroke Haemorrhagic stroke

36. Ischemic stroke Sudden loss of functions of brain due to disruption of blood supply to a part of brain is called as Ischemic stroke. Ischemic stroke can be of two main types – Thrombotic stroke Embolic stroke

37. Types of Ischemic stroke Thrombotic Stoke – Stroke that occurs due to formation of blood clot due to injury to the atherosclerotic blood vessels of the brain. Embolic stroked – Stroke that occurs when embolus lodge into and occludes the supply of the cerebral artery, resulting in to ischemic, infraction and cerebral edema is called as Embolic stroke.

38. Thrombotic stroke Normal cerebral blood flow 50 ml/100gm/min Atherosclerosis in blood vessels supplying to brain. Formation of thrombus in those atherosclerotic veins Decreased blood supply to brain (Less than 25ml/100gm/min)

39. Development of penumbra region (Region with decreased cerebral blood flow) Persistent decreased blood supply to brain Development of infraction along with more penumbral area Around the site of infraction. Extension of stroke A person experiencing strock looses 1.9 millions of neurons each minutes if not treated on time.

40. Thrombotic stroke can be of two types- Large artery thrombotic stroke Small artery thrombotic stroke Large artery thrombotic stroke – About 20% of all the patient with stroke are of large artery thrombotic stroke. It occurs due to thrombosis and occulsion of large blood vessels of the brain. As large artery supplies major part of brain, obstruction of those affectes major part of the brain.

41. Small artery thrombotic stroke – It mostly affect one or more small capillaries supplying to the brain. About 25% of person with stroke are of small artery thrombotic stroke. This type of stroke is also called as lacunar stroke as infraction causes cavity in the brain after the death of brain cells.

42. Most of thrombotic stroke are associated with the history of hypertension or diabetes mellitus or both, which accelerate the process of atherosclerosis. Most of the ischemic stroke are preceded by TIA. Patients with ischemic stroke may not have decreased level of consciousness in the first 24 hours. Manifestations of ischemic stroke may increase in mext 72 hours with further decrease in blood supply and increase in area of infraction along with increased cerebral edema .

43. Embolic stroke This type of stroke occurs mostly when an emboli that originated at some other site of the body, is carried away with the blood flow and gets logged into one of the blood vessels supplying to the brain. Embolism is the second most common cause of stroke. Most of the emboli originates from the heart and enters into the circulation. Heart conditions like atrial fibrillation, myocardial infraction, infective endocarditis, rheumatic heart diseases, valvular heart diseases and atrial septal defect cause Embolic stroke. Rheumatic valvular heart disease is most common cause of Embolic stroke in Young and middle aged adults. Atherosclerotic emboli are common in older adults. Air and fat emboli developed after long bone fracture are less common causes of Embolic stroke.

44. Pathophysiology of the Embolic stroke is same as that of thrombotic stroke after the occlusion of blood vessels. Clinical manifestations of embolic stroke are often sudden and sever. Thus it gives very little time to adapt to the occulsion by developing collateral blood flow. Patients with emboli stroke develops sever neurological deficit. Recurrence of Embolic stroke keeps on occuring unless the underlying cause of thrombus formation is aggressively treated.

45. Haemorrhagic stroke Death of brain tissue resulting from bleeding into brain tissue itself is called as haemorrhagic stroke . In haemorrhagic stroke bleeding may occur into intracerebral region or within subarachnoid space or within the ventricles. Depending upon the site of bleeding severity of the stroke may differ.

46. Intracerebral bleeding Bleeding that occurs inside the parenchyma of the brain due to rupture of blood vessels supplying to brain is called as intracerebral bleeding. Prognosis of patients with intracerebral bleed is very poor with almost 50% of death occuring in first 48 hours, if not upto 80% of mortality within 30 days of IC Bleed.

47. Causes / Risk factors Hypertension is the most common cause of intracerebral bleed. Other causes includes – Vascular malformations Coagulation disorders Anticoagulant and thrombolytic drugs Trauma Brain tumors Ruptured aneurysm

48. Clinical Manifestations Clinical manifestations of intracerebral bleed have sudden onset along with progression of symptoms every minute along with progression of ongoing bleed. Manifestations may include – Neurological deficit Headache Nausea and vomiting Decreased level of consciousness Hypertension Signs and symptoms may vary depending upon amount, location and duration of bleed.

49. Approximately half of the intracerebral bleed are found in the region of putamen, internal capsule, central white matter, thalamus, cerebral hemisphere and pons

50. Patients with putaminal bleeding and intracapsular bleed shows one side weeknedd in face, arms, and legs along with slured speech and deviation of eyes Patients with Thalamic hemorrhage results in hemiplegia with more sensory loss than motor loss Bleeding in subthalamic area of brain leads to problem with vision and eye movements. Cerebellar hemorrhage are characterized by sever headaches, vomiting, loss of ability to walk, dysphagia, dysarthria, and eye movements disturbances Haemorrhage in the pons is the kost serious because basic functions like respiration are rapidly affected. Haemorrhage in pons is characterized by hemiplegia leading to complete paralysis, coma, abnormal body posture, fixed pupils, hyperthermia and death

51. Subarachnoid haemorrhage Haemorrhage that occurs into the subarachnoid space is referred as subarachnoid haemorrhage. It mainly occurs due to rupture of cerebral aneurysm. Cerebral aneurysms are viewed as silent killer, as individuals may not get any warning signs or symptoms of an aneurysm until it is ruptured. Other causes of subarachnoid haemorrhage can be head trauma drugs like cocaine, etc.

52. Clinical manifestations of Stroke There is no significant difference between clinical manifestations of ischemic stroke and haemorrhagic stroke. As in both the situation there is destruction of nervous tissue results in to neurological dysfunction. Clinical manifestations of stroke may differ on the basis of location of the stroke. The functions affected are directly related to the artery involved and the area of brain that is supplied by the artery.

53. Artery involved Manifestations that may occur Anterior cerebral artery Motor and sensory deficit, suckling and rooting reflexes, gait problem, loss of propreciation , fine touch Mid cerebral artery Dominant side - Aphasia, motor and sensory deficit, hemianopsia . Nondominant – motor and sensory deficit. Posterior cerebral artery Hemianopsia , visual hallucinations, spontaneous pain, motor deficit Vertebral artery Cranial nerve deficit, diplopia, dizziness, naisea and vomiting, dysarthria, dysphagia, coma

54. Stroke affects body functions like – Motor functions Bladder and bowel elimination Intellectual functions Spatial and perceptual function Personality Affect Sensation Swallowing Communication

55. Motor functions Motor function deficit is the most obvious effect of any kind of stroke. Motor functions deficit mainly includes impairment of – Mobility Respiratory functions Swallowing and speech Gag reflex Self care abilities These symptoms are caused due to destruction of motor neurons in the pyramidal pathway Characteristic motor function deficit includew loss of skilled voluntary movement, impairment of integrated movements, alterations in muscle tone and alteration in reflexes.

56. Communication

57. Communication Left hemisphere of the brain is dominant for language skills in all right handed person and most of the left handed person. Patients with stroke in the dominant hemisphere may experience complaint of aphasia. Aphasia means difficulty in communication. Aphasia can be receptive aphasia i.e. Inability to understanding the language or expressive aphasia i.e. inability to produce language or global aphasia i.e. total inability to communicate. Aphasia can be No fluent (minimal speech with slow speech that requires obvious efforts) and fluent (speech production is present but with very little meaning. Patients with stroke may also experience dysphasia i.e difficulty in communication. Term aphasia is different that dysphasia. Dysphasia should not be confused with dysphaia as dysphagia is difficulty in swallowing.

58. Affect Affect is the immediate expression of emotions to any particular situation. Patients who experience a stroke may have difficulty in controlling their emotions. Patients with CVA may have exaggerated and unpredictable effects to the situation. It may be due to changed body image and loss of functions along with loss in ability to communicate.

59. Intellectual functions Stroke may affect the functions of memory and judgement of an individual. Person with left brain stroke are likely to get memory related problems Patients with left brain stroke get over cautious while making decisions, whereas persons with right side bleed tends to be very impulsive and more quick in making judgements.

60. perceptual alteration Perception is the ability to interpret the sensation Stroke may cause visual–perceptual dysfunction, disturbance in visual-spatial relation, and sensory loss. Visual perceptual dysfunction is caused due to disturbance in primary sensory pathways between the eyes and the visual cortex. Patients with stroke in the right side of the brain are more prone to have spatial perceptual dysfunction. Visual perception test Spatial perception test

61. Diagnostic investigation CT Scan – Rapid tool to rule out hemorrhage MRI – More effective in identifying ischemic stroke CT angiography – To visualize cerebral blood vessels. If the patient is suspected of embolic stroke, 2D Echo of the heart. Cerebral angiography – to identify cervical and cerebrovascular oclusion , atherosclerosis, plague formation, and malformation of blood vessels.

62. Management of stroke

63. Management of Tia Medical management of patients with TIA and risk of Ischemic stroke Warfarin or other anticoagulants if the stroke is thrombotic and the underline cause is cardiac. If anticoagulants are contraindicated, aspirin with clopidogrel. Statins to lower the levels of LDL and prevent the formation of atherosclerosis If a patient has a history of hypertension, antihypertensive drugs like ACE inhibitors along with diuretics are prescribed. Endovascular management of TIA If TIA is caused due to occlusion of the carotid artery (the most common cause found) carotid endarterectomy, transluminal angioplasty, and stenting are preferred.

64. Carotid endarterectomy is  a surgical procedure to remove a build-up of fatty deposits (plaque), which cause the narrowing of a carotid artery . 

65. Carotid angioplasty and stenting are  procedures that open clogged arteries to restore blood flow to the brain . They're often performed to treat or prevent strokes.

66. Medical management of patients with ischemic stroke Thrombolytic agents like t-PA (tissue plasminogen activators) are used in the treatment of patients with ischemic stroke. Most commonly used t-PA in India are Eminase ( Anistreplase ) Retavase ( Reteplase ) Streptase (Streptokinase) TNKase (Tenecteplase) Patient should be rapidly diagnosed and treated with these drugs within the period of 3 hours from the onset of the symptoms to decrease the size of the stroke and for overall functional improvement in the next 3 months after interventions. The goal should be to administer IV tPA within 60 min from the time patient is arrived in the emergency department. Delay makes the patient ineligible for therapy because revascularization of necrotic tissue after 3 hours increases the risk of cerebral edema.

67. Others medicine may include- If the patient is hypertensive (Systolic B.P > 200 mm of Hg, and diastolic > 120 mm of Hg) I.V. antihypertensive like Labetalol, are administered. As the administration of fibrinolytic therapy without settling BP is not possible, as it may lead to hemorrhage. If the patient has increased ICP, an osmotic diuretic like mannitol 20% is administered to relieve increased ICP. Fluid and electrolytic levels are maintained. Patient may get a seizure, so anticonvulsant drugs like phenotine , and fosphynotine , are administered. Patient may have inflammatory changes due to necrosis and ischemia of tissue, so corticosteroid drugs like dexamethasone are administered. Patient may have a fever, so antipyretic drugs are administered.

68. Nursing management

69. Nursing assessment History and data collection Description of current illness Previous history of such symptoms Medical, and surgical history with use of medications Family history Assessment Level of consciousness Presence or absence of voluntary movements GCS Vital signs Neurological assessment

70. Nursing Diagnosis Impaired respiratory pattern Impaired cerebral tissue perfusion Impaired physical mobility Impaired comfort Impaired elimination pattern Impaired communication Imbalanced nutrition Anxiety related to diseases condition Fear related to the prognosis of diseases Risk of impaired skin integrity

71. Nursing Interventions Positioning. Position to prevent contractures, relieve pressure, attain good body alignment, and prevent compressive neuropathies. Prevent flexion. Apply the splint at night to prevent flexion of the affected extremity. Prevent adduction. Prevent adduction of the affected shoulder with a pillow placed in the axilla. Prevent edema. Elevate affected arm to prevent edema and fibrosis. Full range of motion. Provide full range of motion four or five times a day to maintain joint mobility.

72. Nursing Interventions Prevent venous stasis. Exercise is helpful in preventing venous stasis, which may predispose the patient to thrombosis and pulmonary embolus. Regain balance. Teach patient to maintain balance in a sitting position, then to balance while standing and begin walking as soon as standing balance is achieved. Personal hygiene. Encourage personal hygiene activities as soon as the patient can sit up. Manage sensory difficulties. Approach patient with a decreased field of vision on the side where visual perception is intact.

73. Nursing Interventions 10. Visit a speech therapist. Consult with a speech therapist to evaluate gag reflexes and assist in teaching alternate swallowing techniques. 11. Voiding pattern. Analyze voiding pattern and offer urinal or bedpan on patient’s voiding schedule. 12. Be consistent in patient’s activities. Be consistent in the schedule, routines, and repetitions; a written schedule, checklists, and audiotapes may help with memory and concentration, and a communication board may be used. 13. Assess skin. Frequently assess skin for signs of breakdown, with emphasis on bony areas and dependent body parts

74. Recent Research on stroke Effectiveness of an educational program on improving healthcare providers’ knowledge of acute stroke: A randomized block design study Rababah J, Mohammed Al Hammouri , et al, 2021 conducted study to assess the effectiveness of educational program on improving the knowledge of health care provider regarding acute stroke. A randomized block designed method with only post test method was used for the study. Around 189 participants including physicians, staff nurses and paramedics participated in this study. A one session stroke educational program was conduycted on those health care workers and post test was conduted to assess the knowledge regarding stroke.

75. The study showed that physicians have higher mean score of stroke related knowledge when compared with nurses and other paramedics. Implementation of such education program can help to increase the level of knowledge among the healthcare workers. Utilization of this knowledge can be done in evidence-based assessment of patient with suspected stroke. This study concluded that implementation of educational program among health care workers can improve their knowledge regarding stroke

76. Bibliography 1.Lewis’s Medical-Surgical Nursing, Assessment, and Management of Clinical Problems, Volume -2, Fourth Edition, ELSEVIER Publication, Harding, Kwong, Robert, Hagler, Reinisch , Chintamani, Page No –1358-1370. 2. Brunner and Suddharths , Textbook of Medical-Surgical Nursing, Volume -2, Edition –Second, Wolters Kluwer Publication, Suresh K. Sharma, S. Madhavi, Page No –1645-1670. 3. Lippincott Manual of Nursing Practice, South Asian Edition, Sandra M. Nettinaand Suresh K Sharma, Wolters Kluwer Publication, page no-968 - 975.

77. 4.https://emedicine.medscape.com/article/248840-treatment#d9 5.https://my.clevelandclinic.org/health/diseases/21183-subdural-hematoma 6.https://www.mayo.edu/research/clinical-trials/cls-20192462 7. Rababah JA, Al- Hammouri MM, AlNsour E. Effectiveness of an educational program on improving healthcare providers' knowledge of acute stroke: A randomized block design study. World J Emerg Med. 2021;12(2):93-98. doi : 10.5847/wjem.j.1920-8642.2021.02.002. PMID: 33728000; PMCID: PMC7947558.