As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors.

As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors receive adequate training in the management of acute stroke patients. In an important step towards achieving this goal, the Canadian Stroke Strategy and Heart and Stroke Foundation of Canada has developed an educational workshop and resource, Acute Stroke Management Resource, for healthcare professionals working with acute stroke survivors, focusing on the first 72 hours post stroke onset. Participants in this workshop will acquire knowledge and skills that can immediately be applied to their work with stroke survivors. This slide presentation, Overview of Canadian Stroke Best Practice Recommendations and Acute Stroke Management, is a part of the Acute Stroke Management Resource workshop.

Types of Stroke Objectives To review the two common types of stroke
To review the stroke mechanism for the two common types of stroke To review the etiology of the two types of stroke To describe common patient presentations of stroke mimics This section will begin with a review of the two common types of stroke, ischemic and hemorrhagic stroke. This section also reviews the stroke mechanism for ischemic and hemorrhagic strokes and the etiology of both types. This section will review the common patient presentation seen in stroke mimics.

Ischemic (80%) Hemorrhagic (20%)
Ischemic stroke, makes up 80% of all strokes and is caused by blockage of an artery resulting in diminished blood flow. This blockage is usually the result of a blood clot, which may be either thrombotic or embolic in nature. However, blockage may also occur because of progressive blood vessel occlusion, due to atherosclerosis, or because of local high pressure collapsing small blood vessels. Approximately 50% of all strokes are due to atheromatous vaso-occlusive disease of large and small vessels either occurring from thrombosis in situ or artery-artery emboli with distal occlusion. Of the 50% of these strokes, 30% are related to large-vessel disease, especially of the carotid, middle cerebral, or basilar arteries, and 20% are related to small vessel disease of the deep penetrating arteries, such as the lenticulostriate, basilar penetrating, and medullary arteries. These are known as lacunar infarcts. The remaining ischemic strokes are embolic and constitute 30% of all strokes. Hemorrhagic stroke is caused by arterial rupture. A hemorrhagic stroke is responsible for approximately 20% of all strokes. Hemorrhage can damage brain tissue not only in the area of the hemorrhage but also in areas distant from the hemorrhage, as a result of increased intracranial pressure and compression of brain tissue. Approximately 10% of strokes are due to intracerebral hemorrhage, including hypertensive intracerebral hemorrhage and lobar intracerebral hemorrhage, and 10% are due to subarachnoid hemorrhage or bleeding from an arteriovenous malformation.

Mechanism of Stroke Feature Hemorrhage Infarct Onset sedentary
With activity Nocturnal Hypertension present Usually present Often Clinical course static Rapidly progressive Stepwise or static Signs of ⁭ ICP Present Absent later CT scan changes Presence of blood Normal or subtle changes Signs and symptoms can be useful clues to the diagnosis but the confirmation of ischemic versus hemorrhagic stroke is via CT scan or MRI to rule out the presence of blood. Hemorrhagic stroke patients often appear sicker at the time of stroke onset and deteriorate more quickly than ischemic stroke patients. Hemorrhagic stroke is often fatal at onset and also has a higher mortality rate than ischemic stroke. Hemorrhagic stroke patients are more likely to be unconscious or semiconscious on arrival in ER Hemorrhagic strokes are not preceded by TIA and tend to occur during activity and in patients who have a history of hypertension. Hemorrhagic strokes tends to be rapidly progressive and signs of increased intracranial pressure can be present. CT scan of a patient that has experienced a hemorrhagic stroke reveals the presence of blood. Ischemic stroke is rarely fatal in the first hour but the patient’s condition may deteriorate during the first hours after the stroke onset. Patients with ischemic stroke may be drowsy but usually retain consciousness unless the infarcted area is very large. 30% of ischemic strokes are preceded by a TIA and tend to occur at night or when the person is inactive. The clinical course of ischemic stroke is generally stepwise or static Increased intracranial pressure is not usually present immediately after stroke but may develop within hours after symptom onset. The CT scan of patient with ischemic stroke may initially appear normal or display only subtle changes.

CT: Intracerebral Hemorrhage
This CT shows an intracerebral hemorrhage.

Ischemic Stroke: Hyperdense MCA Sign
Anatomy and Physiology of Acute Stroke Ischemic Stroke: Hyperdense MCA Sign Hyperdense MCA sign This CT scan shows a hyperdense left middle cerebral artery. The artery is visible due to the presence of an intra-arterial blood clot. A hyperdense middle cerebral artery sign which indicates an evolving large infarct involving the middle cerebral artery (MCA) and a poor prognosis, generally means that these patients are not good candidates for thrombolysis.

Ischemic Stroke: Early CT Signs
Anatomy and Physiology of Acute Stroke Ischemic Stroke: Early CT Signs Hyperdense middle cerebral artery sign Subtle decreased attenuation of grey matter Loss of grey-white differentiation Loss of cortical ribbon “Disappearing” basal ganglia Early mass effect Sulcal effacement Shift Only CT scanning can determine whether a stroke is ischemic or hemorrhagic. Most CT scans performed within the first few hours after ischemic stroke onset are normal but subtle signs may identify an early stroke. The CT scan shown here is normal. A hyperdense middle cerebral artery sign, the presence of increased density throughout the territory of the middle cerebral artery, indicates an evolving large infarct involving the middle cerebral artery (MCA) and a poor prognosis. Other early infarct signs involving the MCA territory, indicating poor prognosis include loss of the gray/white junction, loss of the insular ribbon and hypodensity in the lentiform nucleus. These signs may be seen by 6 hours after onset of symptoms in 82% of stroke patients with middle cerebral artery territory ischemia. Disappearing basal ganglia are caused by an increase in neuronal water content, resulting in a decreased and reduced visibility. Early mass effect may indicate a large infarct and the eventual development of massive cerebral edema. It may be manifested as sulcal effacement, resulting form intracellular fluid accumulation and swelling or by a shift of midline structures. Widespread signs of early infarction are associated with an increased risk of hemorrhagic transformation after thrombolytic therapy. However, early infarct signs on CT with an established stroke onset time less than 3 hours do not rule out tPA treatment or predict a poor outcome.

Ischemic Stroke: Etiology
Large Vessel Disease Cardioembolic Atherosclerosis Small Vessel Disease Lacunar Infarction Cryptogenic The cause of ischemic stroke can be classified as large vessel, small vessel and cryptogenic disease. Large vessel disease may be caused by cardioembolism, often a result of atrial fibrillation or left ventricular damage after myocardial infarction. Atherosclerosis may also contribute to ischemic stroke. Atherosclerosis causes a progressive narrowing of the blood vessel through deposit of plaque on the arterial wall. Small vessel disease, known as lacunar infarct, is thought to be the result of occlusion of single, small perforating arteries, located deep in the subcortical areas of the brain. Hypertension is thought to be a major risk factor associated with lacunar infarcts. Cryptogenic strokes are strokes with no identified cause or etiology. Cryptogenic strokes are more commonly found in younger population (<45years) (Ionita,et al, 2005) The classic risk factors for stroke are usually absent in cryptogenic stroke patients and cerebral angiography and TEE do not reveal the presence of large vessel disease or an embolic source. However, Ionita et al (2005) report that echocardiographic studies in these stroke patients showed an increase incidence of Patent Foramen Ovale (PFO) in up to 45% of cases.

Intracerebral Hemorrhage: Etiology
Secondary Vascular Malformations Aneurysms Tumors Hemorrhagic transformation of cerebral infarction Venous infarction with hemorrhage secondary to cerebral venous thrombosis Moya Moya disease Primary Chronic hypertension Cerebral amyloid angiopathy Anticoagulant/fibrinolytic use Antiplatelet use Drug use Other bleeding diathesis Hypertension is responsible for approximately 75% of all cases of primary Intracerebral Hemorrhage (ICH). Cerebral amyloid angiopathy (a disease of small blood vessels in the brain with deposits of amyloid protein which may lead to stroke, brain hemorrhage or dementia) is also a common cause of intracerebral hemorrhage. Underlying vascular abnormalities such as aneurysm, arteriovenous malformation are causes of secondary ICH, which makes up approximately 5 % of all ICH. The use of fibrinolytics and anticoagulants make up approximately 10% of all ICH. ( Manno et al, 2005) Drug abuse may cause sudden and severe elevations in blood pressure resulting in ICH. Hemorrhagic transformation is considered by some to be a natural evolution of a stroke and some studies suggest that almost all infarcts have some element of petechial hemorrhage. Hemorrhagic transformation may be influenced by the size, location and cause of the stroke. The use of antithrombotics including anticoagulants and thrombolytics increases the likelihood of hemorrhagic transformation.

Stroke Mimics The following four conditions represent 62% of stroke mimics Postictal deficit (unrecognized seizure) Systemic infection Tumour/abscess Toxic-metabolic disturbance Other mimics Bell’s palsy Peripheral nerve palsies Old stroke Confusion Head trauma Patients can present with focal neurological deficits that initially may resemble stroke deficits. Only proper history and examination, supplemented by imaging, can exclude stroke mimics, allowing the correct diagnosis to be made. Hand et al, 2006 state that a mimic was more likely if there was a known history of cognitive impairment, the patient lost consciousness or had a seizure at onset, the patient could still walk, there were no lateralizing signs and the examination revealed confusion, signs in other nonvascular systems and no neurological signs. A mimic was also more likely if the signs were inconsistent with the symptoms and did not conform to a vascular territory. A study of emergency room presentations with an initial diagnosis of stroke revealed that the following four conditions made up 62% of cases of stroke mimics: postictal deficit, systemic infection, tumour, and toxic-metabolic disturbance. The study also found that the likelihood of a stroke mimic increased in patients with a decreased level of consciousness and normal eye movements, and the likelihood of stroke increased in patients with signs of stroke and a history of angina. (Libman et al, 1995) Postictal deficit: Following a motor seizure, affected limbs may remain paretic for several hours. This sudden hemiparesis can be confused with stroke. It is important to question a family member about a history of seizure disorder and to review the patient’s medications. Systemic infection: May be differentiated from stroke by a careful history to identify a slower onset of symptoms and fever. Tumour: Sudden bleeding into a tumour or elevated intracranial pressure can produce a sudden onset of neurological deficits. Generally, the onset of neurological deficit with space-occupying lesions is gradual. Toxic or metabolic disturbance: Hypoglycemia is the most common toxic or metabolic stroke mimic. Capillary glucose should be performed as soon as possible. Drug overdose, especially cocaine, hyperglycemia and hepatic encephalopathy may also be confused with stroke. Bell’s palsy: Hemifacial paralysis caused by Bell’s palsy affects all facial muscles, whereas hemifacial paralysis associated with stroke affects the lower part of the face only. Peripheral nerve palsies: Radial nerve palsy can mimic stroke. Selective involvement of wrist and finger extensors with preserved flexors, plus reduced sensation in the radial territory, allows this condition to be differentiated from stroke. Old stroke: Careful history and physical examination will usually differentiate new stroke symptoms from those associated with an old stroke. Confusion: Stroke usually presents with features in addition to confusion, such as aphasia. Head trauma: Subdural or epidural hematoma, may resemble acute stroke.

Acute Stroke Management Resource
Anatomy and Physiology Review

Objectives Review the major blood vessels of the cerebral circulation
Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery Review the key functional areas of the brain List the common patient presentations related to carotid, vertebrobasilar and lacunar syndromes In order to understand why patients present with specific deficits a review of anatomy and physiology is important. This presentation will review the major blood vessels of the cerebral circulation: Anterior Cerebral Artery, Middle Cerebral Artery and Posterior Cerebral Artery This presentation will also review: Key functional areas of the brain Common patient presentation related to carotid, vertebrobasilar and lacunar syndromes

Cerebrum Largest portion Two hemispheres Joined by the corpus callosum
Dominance The cerebrum is the largest portion of the brain and contains 2 hemispheres. The left hemisphere controls the right side of the body and the right hemisphere controls the left side of the body. The two hemispheres are joined by the corpus callosum. In 97% of the population, the left hemisphere is the dominant hemisphere. This presentation will focus on this section of the population that are left hemisphere dominant.

Left and Right Hemisphere
Spatial-perceptual deficits Left sided weakness/sensory loss Neglect of the affected side Distractible Impulsive behavior Poor judgment Loss of flow of speech Defects in left visual field-homonymous hemianopsia Left Hemisphere Expressive aphasia Receptive aphasia Global aphasia Right sided weakness/sensory loss Intellectual impairment- alexia, agraphia, acalulia Slow and cautious behavior Defects in right visual field-homonymous hemianopsia A general review of the right and left hemispheres demonstrates the various functions of these hemispheres. These are a list of the more common functions and deficits that stroke survivors may present with.

Cerebral Cortex Divided into 4 lobes Frontal Parietal Temporal
Occipital The cerebral cortex is divided into 4 lobes: Frontal lobe Parietal lobe Temporal lobe Occipital lobe Two important structures are found in the frontal and parietal lobes. In the frontal lobe (posteriorly) the primary motor cortex can be found. This is also referred to as the motor strip and is involved in the ability of the body to move various body parts. Damage to parts of the motor strip may result in symptoms such as paralysis of the face, arm or leg or difficulty speaking. In the anterior part of the parietal lobe is the primary sensory cortex or sensory strip. It corresponds directly to the body part locations of the motor strip and is involved in the ability to feel or recognize textures.

Blood Supply to the Brain
Arterial supply from carotid and vertebral arteries which begin extracranially Internal carotid arteries supply anterior 2/3 of hemispheres Vertebral and basilar arteries supply posterior and medial regions of hemispheres, brainstem, diencephalon, cerebellum and cervical spinal cord This slide reviews the origins of the cerebral blood supply. Both the carotid (anterior) and vertebral (posterior) blood supply originates outside of the cranium from the internal carotid arteries. The carotid and vertebral arteries enter the cranial cavity via the internal carotid, which come off the common carotids and vertebral arteries which originate from the subclavian arteries. The internal carotid arteries and its branches supply 2/3 of the cerebral hemispheres. The anterior circulation major blood vessels are the anterior cerebral and the middle cerebral arteries. The posterior circulation’s major vessels are the vertebral, basilar and posterior cerebral arteries and supply the medial and posterior sections of the hemispheres, the brainstem, deep brain structures such as the diencephalon, the cerebellum and the cervical section of the spinal cord.

Circulation Review Circle of Willis Anterior Cerebral Artery (ACA)
Anterior Communicating Artery Middle Cerebral Artery (MCA) Posterior Communicating Artery Posterior Cerebral Artery (PCA) Anterior Circulation Posterior Circulation An important structure within the cerebral circulation is the Circle of Willis. The primary purpose of the Circle of Willis is to provide multiple paths of oxygenated blood to the brain. If any of the major vessels become occluded the various paths of the Circle of Willis attempt to ensure circulation. The Circle of Willis is comprised of the following vessels: Anterior Cerebral Artery Middle Cerebral Artery Posterior Cerebral Artery Posterior Communicating Artery Anterior Communicating Artery Some references do not include the Middle Cerebral Artery in the Circle of Willis, however, for this presentation it will be included. The Posterior and Anterior Communicating Arteries are responsible for connecting the right and left side blood vessels so that circulation is seamless.

Circle of Willis This is a picture of the Circle of Willis.

Anterior Cerebral Artery
Arises from internal carotid Supplies anterior portion of basal ganglia, corpus callosum, medial and superior portions of frontal lobe and anterior parietal lobe Key Functional Areas: Primary motor cortex for leg and foot areas, urinary bladder Motor planning in medial frontal lobe Middle and anterior corpus callosum- communication between hemispheres Legend for picture: Anterior Cerebral Artery- blue Middle Cerebral Artery- pink Posterior Cerebral Artery- green The Anterior Cerebral Artery originates from the internal carotid artery and supplies the anterior portion of the basal ganglia, the corpus callosum, the medial and superior portions of the frontal lobe and the anterior part of the parietal lobe. The key functional areas that receive blood supply from the anterior cerebral artery are: Primary motor cortex involving the leg and foot areas The centre for micturation found in the frontal lobe The motor planning centre found in the frontal lobe The anterior and middle portions of the corpus callosum A patient who has a stroke involving the anterior cerebral artery may experience weakness in the leg and foot, difficulties with micturation, difficulties with the ability to plan and carry out tasks such as dressing.

Anterior Cerebral Artery
This picture demonstrates the areas of the brain that are supplied with blood by the anterior cerebral artery.

Middle Cerebral Artery
Arises from the internal carotid Passes laterally under frontal lobe and between the temporal and frontal lobes M1 segment- lentriculostriate arteries supply basal ganglia and most of internal capsule Superior MCA branch- supplies lateral and inferior frontal lobe and anterior parts of parietal lobe Inferior MCA branch-supplies lateral temporal lobe, posterior parietal and lateral occipital lobe Legend for picture: Anterior cerebral artery-blue Middle cerebral artery- pink Posterior cerebral artery- green The middle cerebral artery is the largest of the major vessels and supplies blood to over 2/3 of the cerebrum. The MCA has 3 branches and passes laterally under the frontal lobe and between the temporal and frontal lobes. The M1 segment is also referred to as lentriculostriate arteries and are located in the deeper sections of the brain called the basal ganglia and most of the internal capsule. These lentriculostriate vessels are small vessels located deep in the brain and are also a common site for small vessel or lacunar strokes. The superior branch of the MCA supplies the lateral and inferior frontal lobe and anterior parts of the parietal lobe. The inferior branch of the MCA supplies the lateral temporal lobe, the posterior parietal lobe and the lateral occipital lobe.

Key Functional Areas Primary motor cortex for face, arm and leg Brocas language area (Superior MCA) Wernickes language area (Inferior MCA) Primary somatosensory cortex for face, arm, leg Parts of lateral frontal and parietal lobes used in 3D visual-spatial perceptions of own body, outside world and ability to interpret and/or express emotions The key functional areas of the brain that receive blood supply from the middle cerebral artery are: Primary motor cortex for the face, arm and leg. Broca’s language centre which receives its blood supply primarily from the Superior MCA branch. Wernickes language centre which receives its blood supply primarily from the Inferior MCA branch. Primary sensory cortex for the face, arm, leg Parts of the lateral frontal and parietal lobes that are involved in the visual-spatial perceptions of the patient’s own body, the outside world and the ability to interpret and /or express emotions Patients who have a stroke that involves the middle cerebral artery may present with symptoms such as motor and/or sensory loss of the face, arm or leg, difficulty understanding instructions, difficulty expressing themselves, problems with visual spatial perceptions of their body and the world around them. They may also have difficulty interpreting and/or expressing emotions.

This picture demonstrates the area of the cerebrum that receives its blood supply from the Middle Cerebral Artery.

Posterior Cerebral Artery
Blood supply for midbrain, hypothalamus and thalamus, posterior medial parietal lobe, corpus callosum, inferior and medial temporal lobe and inferior occipital lobe Key Functional Areas: Primary visual cortex 3rd nerve in midbrain Sensory control-temperature, pain, sleep, ADH Communication between hemispheres Legend: Anterior Cerebral Artery- blue Middle Cerebral Artery- pink Posterior Cerebral Artery- green The posterior cerebral artery is responsible for the blood supply to the midbrain portion of the brain stem, the hypothalamus and thalamus, the posterior medial portion of the parietal lobe, the corpus callosum, the inferior and medial portions of the temporal lobe and the inferior portions of the occipital lobe. The key functional areas of the brain that receive blood supply from the Posterior Cerebral Artery are: Primary visual cortex in the occipital lobe 3rd nerve in the midbrain Sensory control Hypothalamus-body temperature control, hunger, thirst, hormone release (Antidiuretic hormone) Thalamus-relaying messages to cortex, level of arousal, awareness, pain Communication between the hemispheres Patients who experience a stroke in the Posterior Cerebral Artery may present with symptoms such as problems with recognizing objects, visual disturbances, drooping eyelid, inability to move the eye in, up & out, down & out, difficulty maintaining body temperature, abnormal hormone responses, coma, hyperesthesia

Posterior Cerebral Artery
This picture demonstrates the area of brain that receives its blood supply from the posterior cerebral artery.

Vertebrobasilar Circulation
Arise from the subclavian arteries Run alongside the medulla Blood supply for brainstem and cerebellum Key Functional Areas: Spinal cord tracts-pyramidal and spinothalamic Cranial nerves 3-12 The vertebrobasilar circulation originates from the subclavian arteries and then run alongside the medulla. It also supplies blood to the brainstem and the cerebellum. The cerebellum arteries branch out to form the superior cerebellar, the anterior inferior cerebellar and the posterior inferior cerebellar arteries. The key functional areas that are supplied by the vertebrobasilar circulations are: The spinal cord tracts: pyramidal (motor) tracts and the spinothalamic (sensory) tracts The cranial nerves 3-12 originate in the brain stem 3- oculomotor 4-trochlear 5-trigeminal 6-abducens 7-facial 8-acoustic 9-glossopharyngeal 10-vagus 11-spinal accessory 12-hypoglossal

Vertebrobasilar Circulation
1- Posterior Cerebral 2- Superior Cerebellar 3- Pontine Branches of Basilar 4- Anterior Inferior Cerebellar 5- Internal Auditory 6- Vertebral 7- Posterior Inferior Cerebellar 8- Anterior Spinal 9- Basilar The vertebrobasilar circulation is comprised of the following vessels: Posterior cerebral artery Cerebellar arteries including: superior cerebellar, anterior inferior cerebellar and the posterior inferior cerebellar Basilar artery Vertebral arteries

Cerebellum Blood supply-own arteries from vertebrobasilar
Superior cerebellar Anterior Inferior Posterior Inferior Major Functions Control of fine motor movement Coordinates muscle groups Maintains balance, equilibrium The cerebellum has its own major blood vessels which originate from the vertebrobasilar vessels. The 3 cerebellar vessels are Superior Cerebellar, Anterior Inferior Cerebellar, Posterior Inferior. The major functions of the cerebellum are control of fine motor movement, coordination of muscle groups and maintaining balance and equilibrium. A patient who experiences a stroke in the cerebellar region may present with symptoms such as abnormal gait (walks like they are drunk), nausea and vomiting, headache. They may be alert initially, but often deteriorate in level of consciousness. Weakness may not be present at the time of onset but may present as the patient deteriorates. (Jensen,MB.(2005. Management of acute cerebellar stroke. Archives of Neurology,62(4), ) There are 2 syndromes often seen with cerebellar strokes: Lateral pontine syndrome Involves basilar and anterior inferior cerebellar artery Symptoms: ipsilateral ataxia of arm and leg, contralateral weakness of upper and lower extremities, contralateral hemisensory loss-pain and temperature Lateral Medullary Syndrome (Wallenberg Syndrome) Involves distal and superior medullary artery branches of vertebral artery and the posterior inferior cerebellar artery Symptoms: Ipsilateral sensory loss-face-pain and temperature Ipsilateral ataxia of arm and leg Gait ataxia Nystagmus Nausea and vomiting Vertigo Hoarseness Dysphagia Contrateral hemisensory loss-pain and temperature Horner syndrome( constricted pupil, partial ptosis,loss of hemifacial sweating Hiccoughs

Cerebellar Blood Supply
This slide demonstrates the cerebellar blood supply.

Brain Stem Blood supply: PCA & Vertebrobasilar
Major divisions: midbrain, pons, medulla Houses Cranial Nerves 3-12 Serves as a pathway Reticular Activating System The brain stem receives its blood supply from the posterior cerebral artery and the vertebrobasilar vessels. The brain stem is divided into 3 major sections: Midbrain: major functions include involvement in vision, hearing, eye movement and body movement Pons: involved in motor control and sensory analysis, level of consciousness, sleep Medulla: responsible for maintaining vital body functions such as breathing and heartrate One of the major structures housed in the brain stem are the cranial nerves. While there are 12 cranial nerves, Cranial nerves 1& ll originate in the frontal lobe and will not be discussed in this section. Cranial nerves lll-Xll originate in the brain stem. Patients that experience a stroke in the brain stem will present with symptoms that involve cranial nerve functions such as swallowing, eye movements, facial expression and tongue movements. The brain stem serves an important role as a pathway between the spinal cord and the brain. The afferent and efferent pathways run through the spinal cord and connect with brain centres for interpretation and response to stimuli. The Reticular Activating System originates in the brain stem and is responsible for our wakefulness and attention. It is a very sensitive system that spans the brain and reacts to interruptions in its ability to work. An expanding stroke will interrupt its ability to keep the patient awake, resulting in the patient presenting with a decreased level of consciousness. Patients who experience a brain stem stroke may present with any of the following: Decreased level of consciousness Ipsilateral lower motor neuron facial weakness or sensory loss Contralateral hemiparesis Pupillary changes Hiccoughs, vertigo Bilateral motor findings Diplopia, gaze palsies, intranuclear opthalmoplegia Dysphagia Dysarthria Ataxia

Cranial Nerves This slide demonstrates the location and functions of the cranial nerves.

Reticular Activating System
This slide demonstrates the location of the Reticular Activating System in the brain stem and the brain.

Collateral Circulation
Not all vessels have capability – lenticulostriate Common sites: External and internal carotid via opthalamic artery Intracranial vessels of the Circle of Willis Small cortical branches of ACA, MCA,PCA and cerebellar arteries Collateral circulation is an important feature of the brain and for stroke patients. Not all blood vessels have the capability to be able to create collateral circulation. Vessels such as the lenticulostriate vessels are terminal vessels which do not connect with other vessels. Therefore, vessels associated with the lenticulostriate vessels that become occluded will become ischemic. However, there are vessels that can connect or anastomose with other vessels to create collateral circulation. These vessels include: External and internal carotid via branches of the opthalmic artery Major intracranial vessels via the Circle of Willis Small cortical branches of the Anterior cerebral, middle cerebral and posterior cerebral and cerebellar arteries

Effectiveness depends on vessel size Effectiveness depends upon speed of occlusion Atherosclerosis Circle of Willis: vessels are often narrow and cannot adapt for sudden onset of blockage The effectiveness of collateral circulation depends on a few factors: Vessel size: the smaller the vessel diameter, the less likely its ability to carry enough blood to prevent infarction Speed of the occlusion: occlusion of a vessel as a result of lifelong atherosclerosis allows vessels to dilate to allow blood to flow Key point: The Circle of Willis anatomy suggests that it can support the shunting of blood from one side of the brain to another. However, sometimes one of these vessels may have become narrow and not able to carry sufficient blood for sudden abrupt blockages such as cardiac embolus. The Circle of Willis can compensate for slower developing occlusions such as athersclerosis.

Stroke Syndromes and Patient Presentations
Acute Stroke Management Resource Stroke Syndromes and Patient Presentations

Ischemic Stroke: Carotid Syndromes
Sensory/motor deficit Aphasia Cortical sensory loss Apraxia, neglect Retinal ischemia Visual field deficit The carotid arteries and their branches, the anterior and middle cerebral arteries, form the anterior circulation and the vertebral, basilar, posterior cerebral arteries and their branches form the posterior cerebral circulation. Clinical stroke syndromes depend on the area of the cerebral circulation disrupted. Typically, the anterior or carotid circulation stroke syndromes present with symptoms that include sensory or motor deficits, aphasia, cortical sensory loss, apraxia or neglect, visual field deficits or retinal ischemia.

Ischemic Stroke: Vertebrobasilar Syndrome
Diplopia Vertigo Coma at onset Crossed sensory loss Bilateral motor signs Isolated field defect Pure motor and sensory deficit Dysarthria Dysphagia Strokes affecting the posterior circulation or vertebrobasilar system, present with symptoms such as diplopia, vertigo, coma at onset, crossed sensory loss, bilateral motor signs, isolated field deficits, pure motor and sensory deficits, dysarthria and dysphagia. While each patient presentation is unique, depending on the blood vessel that is affected and the area of brain infarcted, these are a list of general symptoms in relation to anterior and posterior circulation.

Ischemic Stroke: Lacunar Syndromes
Makes up 25% of all ischemic strokes Presumed to be occlusion of single small perforating artery Predominantly in the deep white matter, basal ganglia, pons Blood vessel: lenticulostriate branches of the Anterior Cerebral and Middle Cerebral Arteries 30% of patients are left dependant and some long term data suggests up to 25% have a second stroke within 5 years (Wardlaw, 2007) 25 % of all ischemic strokes are lacunar strokes. These are small infarcts that involve the deep penetrating single vessels that branch off the anterior and middle cerebral arteries. The cause of these strokes remains under debate. Wardlaw, 2007 suggests that 30% of these patients are left dependant and some long term data suggests that up to 25% of patients will have a recurrence within 5 years. One study suggested that of the patients with lacunar stroke who had a stroke recurrence, 47% were lacunar. Hypertension and diabetes are believed to be strongly linked as risk factors. Hypertension is more common. It is also felt that 15-20% of patients that experience a lacunar stroke develop dementia due to the brain damage from the lacunar infarct. It has also be found that after a lacunar stroke, it is not uncommon for silent lacunar strokes to be found on imaging.

This CT Scan shows the presence of 3 possible lacunar infarcts.

Type of Syndrome Patient Presentation Pure motor hemiparesis Results from an infarct in the internal capsule or pons Contralateral Hemiparesis of face, arm and leg, dysarthria Contralateral motor hemiparesis with motor aphasia Results from an infarct of the left frontal area with cortical involvement Hemiparesis of face, arm and leg with inability to speak Lacunar infarction results from infarction of one of the lenticulostriate vessels, the penetrating branches of the circle of Willis, the MCA stem, or vertebral or basilar arteries. Kistler JP, Ropper AH, Martin JB. Cerebrovascular diseases. In: Isselbacher KJ, Braunwald E, Wilson JD, Martin JB, Fauci AS, Kasper DL, eds. Harrison’s Principles of Internal Medicine. 13th ed. New York: McGraw Hill;1994: Fisher,CM. (1991). Lacunar Syndromes,1, These next 2 slides review the common presentations of patients experiencing lacunar infarcts.

Type of Syndrome Patient Presentation Ataxic hemiparesis Results from an infarct in the pons Paresis of the contralateral leg and side of the face, ataxia of the contralateral leg and arm Dysarthria and clumsy hand syndrome Results from an infarct in the pons or internal capsule Dysarthria, dysphagia, contralateral facial and tongue weakness, paresis and clumsiness of the contralateral arm and hand Pure sensory stroke Results from an infarct in the thalamus Contralateral sensory loss to all modalities that usually affect the face, upper and lower extremities May be painful

Case Examples Add patient case examples of:
Anterior circulation strokes Posterior circulation strokes Lacunar Infarcts This next section will start to combine the information provided in the previous slides through the use of patient scenerios. Use this section to add and present local case studies of : Anterior circulation stroke Posterior circulation stroke Lacunar infarcts

Ischemic Stroke: Left (dominant) Hemisphere Stroke
Aphasia Right field defect Left gaze preference Right upper motor neuron facial weakness Right hemiparesis Right hemisensory loss The CT scan shows a large area of infarction in the territory of the left middle cerebral artery. The associated neurological signs and symptoms form a common pattern of stroke presentation involving the left, or dominant, hemisphere. Aphasia Right field defect Left gaze preference Right upper motor neuron facial weakness Right hemiparesis Right hemisensory loss

Ischemic Stroke: Right (non-dominant) Hemisphere Stroke
Left neglect, inattention Left field defect Right gaze preference Left upper motor neuron facial weakness Left hemiparesis Left hemisensory loss, sensory extinction The CT scan shows a large area of infarction in the territory of the right middle cerebral artery. The associated neurological signs and symptoms form a common pattern of stroke presentation involving the right, or non-dominant, hemisphere. Left neglect, inattention Left field defect Right gaze preference Left upper motor neuron facial weakness Left hemiparesis Left hemisensory loss, sensory extinction

Ischemic Stroke: Cerebellar Infarct
Headache, nausea/vomiting Vertigo, imbalance Normal tone, power, reflexes Inability to sit or stand Ataxia Late signs Decreasing level of consciousness Diplopia, gaze palsy Ipsilateral V,Vll impairment The MRI scan shows an area of ischemia in the left cerebellum. This stroke presentation should be considered a neurological emergency because of the possible risk of raised intracranial pressure due to compression of the fourth ventricle. The following associated signs and symptoms form a common pattern of stroke presentation involving the cerebellum. Headache, nausea/vomiting Vertigo, imbalance Normal tone, power, reflexes Inability to sit or stand Ataxia Late signs: Decreasing level of consciousness Diplopia, gaze palsy Ipsilateral V,Vll impairment

Ischemic Stroke: Brainstem Stroke
Decreased LOC Crossed findings Ipsilateral lower motor neuron facial weakness or sensory loss Contralateral hemiparesis Pupillary changes Hiccoughs, vertigo Bilateral motor findings Diplopia, gaze palsies, intranuclear opthalmoplegia Dysphagia Dysarthria Ataxia This MRI scan shows an area of ischemia in the right pons, in the brainstem. The following associated neurological signs and symptoms form a common pattern of stroke presentation involving the brainstem. Decreased LOC Crossed findings Ipsilateral lower motor neuron facial weakness or sensory loss Contralateral hemiparesis Pupillary changes Hiccoughs, vertigo Bilateral motor findings Diplopia, gaze palsies, intranuclear opthalmoplegia Dysphagia Dysarthria Ataxia

Conclusions Rapid assessment and triage key to optimal treatment
CT scan required to exclude hemorrhage Knowledge of typical stroke symptoms key Anatomical and etiological diagnosis necessary Exclusion of stroke mimics vital A good understanding of common stroke mechanisms and presentations assists in making a correct diagnosis quickly. This is critical, as rapid assessment and triage are key to optimal treatment. In addition, it is important to remember that a CT scan is mandatory to exclude hemorrhage, prior to initiating thrombolytic therapy. In making a diagnosis, knowledge of typical stroke symptoms may be useful. In addition, both to institute appropriate medical and possible surgical therapy and to prevent a second stroke, it is necessary to make an accurate anatomical and etiological diagnosis. Finally, stroke mimics must be excluded.

Resources American Association of Neuroscience Nurses
American Stroke Association Brain Attack Coalition Canadian Hypertension Education Program Canadian Stroke Strategy European Stroke Initiative

Resources Heart and Stroke Foundation Prof Ed
Heart and Stroke Foundation of Canada Internet Stroke Centre National Institute of Neurological Disorders and Stroke National Stroke Association Scottish Intercollegiate Guidelines Network StrokeEngine

CSS Acute Stroke Management
Heart and Stroke Foundation, 2008

As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors.

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Presentation on theme: "As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors."— Presentation transcript:

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As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors.

Similar presentations

Presentation on theme: "As new diagnostic techniques and treatments become available for acute stroke, it is essential that all healthcare professionals working with stroke survivors."— Presentation transcript:

Similar presentations

About project

Feedback