Cerebrovascular Accident (CVA) Notes

Cerebrovascular Accident (CVA)

• Prepared by Sherman Mercado, PT, DPT

Cerebrovascular Accident / Stroke

• Definition: Sudden loss of neurological function due to interruption of blood flow to the brain.
  • O'Sullivan: Sudden loss of neurological function caused by an interruption of blood flow to the brain.
  • Neurologic Interventions for PT: Sudden onset of neurologic signs and symptoms resulting from a disturbance of blood supply to the brain.
  • Temporary or permanent loss of function as a result of injury to cerebral tissue.
  • Cerebrovascular disease refers to any disorder involving the blood supply to the brain (Umphred).
• Classification as Stroke: Neurological deficits must persist for at least 24 hours.

Epidemiology

• Fifth leading cause of death in the United States.
• Leading cause of serious long-term disability in the United States.
• Estimated 7.6 million Americans older than 20 years of age have experienced a stroke.
• 795,000 new strokes occur annually; 610,000 are first attacks; 185,000 have sustained a previous stroke.
• Incidence:
  • Men < Women; Women > 85 years > Men
• Incidence increases dramatically with age, doubling in the decade after 65 years of age.

Etiology

• Two major types of strokes: ischemic and hemorrhagic.
  • 87% of all strokes are ischemic.
  • 13% of all strokes are hemorrhagic.
• Hemorrhagic strokes account for 30% of all stroke deaths.

Cerebral Blood Supply

• Key arteries:
  • Anterior cerebral artery
  • Middle cerebral artery
  • Posterior cerebral artery
  • Internal carotid artery
  • Vertebral artery
  • Basilar artery
  • Anterior communicating artery
  • Posterior communicating artery
  • Superior cerebellar artery
  • Anterior inferior cerebellar artery
  • Posterior inferior cerebellar artery
  • Anterior spinal artery
  • Internal auditory artery
  • Optic chiasm
  • Circle of Willis

Ischemic Strokes

• Ischemia: Hypoxia or decreased oxygenation to tissue and results from poor blood supply.
  • Lack of cerebral blood flow (CBF) deprives the brain of needed oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of tissues.
  • Brain has no mechanism to store metabolic reserves; requires adequate blood supply for glucose, oxygen, and nutrients.
• Two major categories of ischemic strokes:
  • Resulting from thrombosis.
  • Resulting from an embolus.

Thrombotic Strokes

• Most frequently a consequence of atherosclerosis.
• Thrombus results from platelet adhesion and aggregation on plaques.
• Cerebral thrombosis: Formation or development of a blood clot within the cerebral arteries or their branches.
• Atherosclerosis: Major contributory factor in cerebrovascular disease.
  • Characterized by plaque formation with an accumulation of lipids, fibrin, complex carbohydrates, and calcium deposits on arterial walls that leads to progressive narrowing of blood vessels.
  • Lumen (opening) of the artery decreases in size as plaque is deposited within the vessel walls.
  • Blood flow through the vessel is reduced or can be occluded.
• Common sites for lesions:
  • Origin of the common carotid artery or at its transition into the middle cerebral artery.
  • At the main bifurcation of the middle cerebral artery.
  • At the junction of the vertebral arteries with the basilar artery.
• Cerebral infarction or tissue death (atherothrombotic brain infarction).

Atherosclerosis Progression

• Initial Lesion: Histologically normal with endothelial dysfunction.
• Fatty Streak: Macrophage infiltration, isolated foam cells, mainly intracellular lipid accumulation; onset from the first decade; growth mainly by lipid addition; clinically silent.
• Intermediate Lesion: Intracellular lipid accumulation, small extracellular lipid pools; from the third decade; growth mainly by lipid addition; clinically silent or overt.
• Atheroma: Intracellular lipid accumulation, core of extracellular lipid; from the fourth decade; increased smooth muscle and collagen; clinically silent or overt.
• Fibroatheroma: Single or multiple lipid cores, fibrotic/calcific layers; from the fourth decade; thrombosis and/or hematoma.
• Complicated Lesion/Rupture: Surface defect, hematoma-hemorrhage, thrombosis; Thrombosis and/or hematoma; coronary artery plaque/thrombus.

Embolic Strokes

• Frequently associated with cardiovascular disease, specifically atrial fibrillation, myocardial infarction, or valvular disease.
• Blood clot breaks away from the intima (inner lining of the artery) and is carried to the brain.
• Embolus can lodge in a cerebral blood vessel, occlude it, and cause death or infarction of cerebral tissue.
• Most common source of cerebral embolus (CE) is disease of the cardiovascular system.

Cerebral Blood Flow

• Brain relies on constant blood perfusion to maintain neuronal function (~50 mL per 100 g of brain tissue per minute).
• Lower than 20 mL/100 mg of tissue per minute: disruption in neurologic functioning.
• Perfusion is less than 8 to 10 mL/100 mg: cell death occurs.
• Ischemic penumbra or transitional zone: area surrounding the infarcted cerebral tissue; cells may be damaged but preserved.
  • Cells in the area are vulnerable to injury because cerebral blood flow is diminished and, as a result, cannot support neuronal function.
  • Functionally impaired yet still viable tissue surrounding the ischemic core.
  • Includes ischemic areas that recover spontaneously (benign oligemia) and areas that progress to irreversible changes unless effective treatment is used (penumbra).

Neurotransmitters changes

• Changes to neurotransmitters are thought to cause further injury after the ischemic insult.
• Cells that control glutamate levels are compromised.
• Increase in glutamate in the extracellular space facilitates the entry of calcium ions into the cell; further propagate cellular destruction and death

Hemorrhagic Strokes

• Result from abnormal bleeding from rupture of a cerebral vessel.
  • Include intracerebral and subarachnoid hemorrhage and arteriovenous malformation (AVM).

Intracerebral Hemorrhage (ICH)

• Low among persons less than 45 years old and increases after age 65.
• Major cause of morbidity and death, accounting for 30% of all stroke deaths.
• Higher for blacks and individuals of Asian descent (30%) as compared with 10% to 15% in whites.
• Common causes of spontaneous ICH: Vessel malformation and changes in the integrity of cerebral vessels due to effects of hypertension and aging.
• Secondary causes of ICH: Trauma, exposure to toxins, impaired coagulation, or some type of lesion.

Subarachnoid Hemorrhages

• Consequence of bleeding into the subarachnoid space (located under the arachnoid membrane and above the pia mater).
• Primary causes:
  • Aneurysms (ballooning or outpouching of a vessel wall).
  • Vascular malformations.
  • 90% of subarachnoid hemorrhages: caused by berry aneurysms (congenital defect of a cerebral artery in which the vessel is abnormally dilated at a bifurcation).

Arteriovenous Malformation (AVMs)

• Congenital anomalies that affect the circulation in the brain.
• Characterized by a tortuous tangle of arteries and veins with agenesis of an interposing capillary system.
• Blood vessels become dilated and form masses within the brain; defects weaken the blood vessel walls, rupture, and cause a stroke.
• Hemorrhagic strokes in individuals younger than 40 are often caused by AVMs.

Transient Ischemic Attacks (TIAs)

• Frequently called mini-strokes, resemble a stroke in many ways.
• Blood supply to the brain is temporarily interrupted.
• Neurologic dysfunction, including loss of motor, sensory, or speech function; resolve within 24 hours.
• Usually, no residual brain damage or neurologic dysfunction.
• Serious warning sign of risk for a future stroke.
• 40% of individuals will have a stroke, and almost half of all strokes occur within a few days after a TIA.

Risk Factors and Stroke Prevention

• Major risk factors for stroke:
  • Hypertension, diabetes mellitus (DM), disorders of heart rhythm, high blood cholesterol and other lipids, smoking/tobacco use, and heart disease (HD).
  • Blood pressure (BP) is a powerful determinant of risk for both ischemic stroke and intracranial hemorrhage; BP less than 120/80 mm approximately half the lifetime risk of stroke of those with hypertension.
  • Marked elevations of hematocrit: increased risk of occlusive stroke due to a generalized reduction of CBF.
  • Atrial fibrillation, End-stage renal disease and chronic kidney disease, Sleep apnea.
• Medical risk factors: previous stroke, TIA, cardiac disease, diabetes, atrial fibrillation, and hypertension.
• Risk factors associated with lifestyle: smoking, obesity, alcohol and drug use, and inactivity.
• 80% of all strokes are preventable: changes in one’s lifestyle; following recommendations of your health care provider (CDC).
• Modifiable risk factors: cigarette smoking, physical inactivity, obesity, diet, and sleep.

Blood Pressure Categories (American Heart Association)

• Normal: Less than 120/80 mm Hg.
• Elevated: 120-129/Less than 80 mm Hg.
• High Blood Pressure (Hypertension) Stage 1: 130-139/80-89 mm Hg.
• High Blood Pressure (Hypertension) Stage 2: 140 or higher/90 or higher mm Hg.
• Hypertensive Crisis (consult your doctor immediately): Higher than 180/Higher than 120 mm Hg.

Early Warning Signs (F.A.S.T.)

• Face Drooping
• Arm Weakness
• Speech Difficulty
• Time to Call 911

Medical Intervention

• Hospitalization to determine the etiology of the infarct (physical examination to evaluate motor, sensory, speech, and reflex function; evaluation of the patient’s cardiac status).
• Neuroimaging: CT scan, MRI; determine whether the stroke is the result of ischemic or hemorrhagic injury, which guides medical treatment.
  • MRI can diagnose an ischemic event within 2 to 6 hours after the initial onset.

Acute Medical Management

• Monitoring the patient’s neurologic function and preventing the development of secondary complications.
• Regulation of the patient’s blood pressure, cerebral perfusion, and intracranial pressure.
• Pharmacologic interventions: manage hypertension, including diuretics, beta-blockers, and angiotensin-converting enzyme inhibitors.
• Thrombolytic agents: Recombinant tissue plasminogen activator (rt-PA) - dissolve blood clots, improve blood flow, and minimize tissue damage.
  • Must be administered within 4.5 hours of the event to maximize effectiveness.
  • Patients treated with rt-PA within 90 minutes of their first symptom are 25% less likely to die in the hospital, 28% less likely to sustain an intracranial hemorrhage, and 33% more likely to be discharged home.
• Tissue plasminogen activator (tPA) cannot be given to patients with hemorrhagic stroke or patients with active intracranial bleeding; contraindicated severe uncontrolled hypertension.
• Medications that modify or interfere with glutamate release or enhance recovery from calcium overload; continued clinical trials to determine effectiveness
• Surgical intervention: Endovascular thromboaspiration, carotid endarterectomy, sonothrombolysis, angioplasty, or stent placement.

Carotid Endarterectomy

• Plaque is removed to restore normal blood flow.

Sonothrombolysis

• Acoustic waves and microbubbles are used to enhance the effect of thrombolytic agents.

Stent Placement

• A stent is inserted and a balloon is inflated to open the artery.

Stroke Syndromes

Artery Distribution Patient Deficits

• Anterior cerebral:Supplies the superior border of the frontal and parietal lobes. Contralateral weakness and sensory loss primarily in the lower extremity, incontinence, aphasia, and apraxia.

• Middle cerebral Supplies the surface of the cerebral hemispheres and the deep frontal and parietal lobes. Contralateral sensory loss and weakness in the face and upper extremity, less involvement in the lower extremity, homonymous hemianopia, and aphasia.

• Vertebrobasilar: Supplies the brainstem and cerebellum. Cranial nerve involvement (diplopia, dysphagia, dysarthria, deafness, vertigo), ataxia, equilibrium disturbances, headaches, and dizziness.

• Posterior cerebral: Supplies the occipital and temporal lobes, thalamus, and upper brainstem.Abnormal perception of pain, temperature, touch and proprioception (proximal component of the artery). Contralateral sensory loss, pain, memory deficits, homonymous hemianopia, visual agnosia, and cortical blindness (posterior component of the artery).

Anterior Cerebral Artery Occlusion

• Blockage in the anterior cerebral artery is uncommon and is most frequently caused by an embolus.
• Anterior cerebral artery (ACA): supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobes) and subcortical structures, including the basal ganglia (anterior internal capsule, inferior caudate nucleus), anterior fornix, and anterior four-fifths of the corpus callosum.
• Contralateral hemiparesis and sensory loss with greater involvement of the lower extremity (LE) than the upper extremity (UE): somatotopic organization of the medial aspect of the cortex includes the functional area for the LE.

Clinical Manifestations of Anterior Cerebral Artery Syndrome

Middle Cerebral Artery Syndrome

• Most common type of stroke.
• Middle cerebral artery (MCA): most common site of occlusion in stroke; supplies the entire lateral aspect of the cerebral hemisphere (frontal, temporal, and parietal lobes) and subcortical structures, including the internal capsule (posterior portion), corona radiata, globus pallidus (outer part), most of the caudate nucleus, and the putamen.
• Occlusion of the proximal MCA: extensive neurological damage with significant cerebral edema; Increased ICP - loss of consciousness, brain herniation, and possibly death.
• Contralateral spastic hemiparesis and sensory loss of the face, UE, and LE, with the face and UE more involved than the LE.
• Lesions of the parieto-occipital cortex of the dominant hemisphere (usually the left hemisphere) typically produce aphasia.
• Lesions of the right parietal lobe of the nondominant hemisphere (usually the right hemisphere) typically produce perceptual deficits (e.g., unilateral neglect, anosognosia, apraxia, and spatial disorganization).
• Homonymous hemianopia (hemianopsia): defect or loss of vision in the temporal half of one visual field and the nasal portion of the other.

Clinical Manifestations of Middle Cerebral Artery Syndrome

Homonymous Hemianopia

• Left hemianopia is vision loss on the left half of each eye.
• Right hemianopia is vision loss on the right half of each eye.
• Crossing at the optic chiasm, all fibers recording the left visual field of both eyes project to the right hemisphere, fibers recording the right visual field project to the left hemisphere.

Vertebrobasilar Artery Occlusion

• Vertebral arteries supply the cerebellum (via posterior inferior cerebellar arteries) and the medulla (via the medullary arteries).
• Basilar artery supplies the pons (via pontine arteries), the internal ear (via labyrinthine arteries), and the cerebellum (via the anterior inferior and superior cerebellar arteries).
• Complete occlusion of the vertebrobasilar artery: often fatal.
  • If the patient survives, bilateral brainstem symptoms can be evident.
• Cranial nerve involvement including diplopia (double vision), dysphagia (difficulty in swallowing), dysarthria (difficulty in forming words secondary to weakness in the tongue and muscles of the face), deafness, and vertigo (dizziness).
• Ataxia (characterized by uncoordinated movement), equilibrium deficits, and headaches.
• Blockage of the basilar artery: locked-in syndrome.
  • Locked-in syndrome: patient is alert and oriented; unable to move or speak because of weakness in all muscle groups; Eye movements are the only type of active movement possible, becomes the patient’s primary means of communication.

Internal Carotid Artery Syndrome

• ICA supplies both the MCA and the ACA.
• Collateral circulation to the ACA from the circle of Willis is absent, extensive cerebral infarction in the areas of both the ACA and MCA can occur.
• Significant edema, possible uncal herniation, coma, and death (mass effect).

Posterior Cerebral Artery Syndrome

• Two posterior cerebral arteries (PCAs): supplies the corresponding occipital lobe and medial and inferior temporal lobe; supply the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus.
• Occlusion of thalamic branches: hemianesthesia (contralateral sensory loss) or central poststroke (thalamic) pain.
• Occipital infarction: homonymous hemianopsia, visual agnosia (a neurological condition where an individual can see objects clearly but is unable to recognize or name them), prosopagnosia (also known as face blindness, is a neurological disorder characterized by the inability to recognize faces, even familiar ones like family members or friends), if bilateral - cortical blindness.
• Temporal lobe infarction: amnesia (memory loss).

Thalamic Pain Syndrome

• Infarction or hemorrhage in the lateral thalamus, the posterior limb of the internal capsule, or the parietal lobe.
• Intolerable burning pain and sensory perseveration.

Pusher Syndrome

• Strokes in the right or left posterolateral thalamus may demonstrate pusher syndrome.
• Actively push and lean toward their hemiplegic side and are at increased risk for balance deficits and falls.
• Efforts to passively correct the patient’s posture are met with resistance.
• Experience a mismatch between their perception of vertical and the body’s orientation to the environment and gravity; report sitting or standing upright when, in fact, they are actually tilted approximately 18–20 degrees toward their hemiparetic side.

Lacunar Strokes

• Deep regions of the brain, including the internal capsule, thalamus, basal ganglia, and pons; named for their crescent-shaped appearance.
• Lacuna is used because a cystic cavity remains after the infarcted tissue is removed.
• Strongly associated with hypertensive hemorrhage and diabetic microvascular disease.
• Clinical findings: contralateral weakness and sensory loss, ataxia, and dysarthria.

Patient Impairments

Motor Impairments

• One of the primary and most prevalent of all clinical manifestations: spectrum of motor problems resulting from damage to the motor cortex.
• Characterized by paralysis (hemiplegia) or weakness (hemiparesis), typically on the side of the body opposite the side of the lesion.
• Approximately 70% of all patients with stroke experience persistent motor impairments.
• Initially: state of low muscle tone or flaccidity; transient, patient soon develops characteristic patterns of hypertonicity or spasticity.
• Spasticity: motor disorder characterized by exaggerated deep tendon reflexes (DTRs) and velocity-dependent increased muscle tone.

Spasticity Development

• Develop from abnormal processing of the afferent (sensory) input after the stimulus reaches the spinal cord.
• Defect in inhibitory modulation from higher cortical centers and spinal interneuron pathways leads to the presence of spasticity in many patients.

Modified Ashworth Scale for Grading Spasticity

Brunnstrom Stages of Motor Recovery

• Developed by Signe Brunnstrom.

• The patient experienced flaccidity in involved muscle groups.
• As the patient recovered, flaccidity was replaced by the development of spasticity.
• Spasticity increased and reached its peak in stage 3. At this time, the patient’s attempts at voluntary movements were limited to the flexion and extension synergies.
• Synergy: group of muscles that work together to provide patterns of movements initially occur in flexion and extension combinations; movements produced are stereotypical and primitive and can be elicited either as a reflexive or a volitional movement response.

Components of the Brunnstrom Synergy Patterns

Other Motor Impairments

• Muscle weakness or paresis.
• Difficulty in maintaining a constant level of force production to control movements of the extremities.
• Atrophy.
• Abnormal recruitment and timing of muscle activation.
• Stroke does not affect only one side of the body; muscles on the uninvolved side can also exhibit mild weakness.
• Motor planning deficits: patients with involvement of the left hemisphere (primary role in the sequencing of movements).
  • Apraxia: difficulty in performing purposeful movements, although no sensory or motor impairments are noted.
    • Example: the patient may have the ability to perform a specific movement combination such as a sit-to-stand transfer but is unable to determine or remember the steps necessary to achieve this movement goal; the patient may not remember how to don a piece of clothing or what to do with an item, such as a comb or a brush.

Sensory Impairments

• Tactile (touch) or proprioceptive capabilities.
• Visual–perceptual deficits: result of lesions in the right parietal cortex and are seen more with left hemiplegia than right; May include disorders of body scheme/body image, spatial relations, and agnosias.
  • Body scheme: postural model of the body, including the relationship of the body parts to each other and the relationship of the body to the environment.
  • Body image: visual and mental image of one’s body that includes feelings about one’s body.
  • Impairments of body scheme/body image include unilateral neglect, anosognosia (neurological condition characterized by a lack of awareness or insight into one's own disability, disease, or disorder, despite evidence of it), somatagnosia (awareness of one's own body and its parts), right–left discrimination, and finger agnosia.
• Spatial relations syndrome: difficulty in perceiving the relationship between the self and two or more objects in the environment; impairments in figure–ground discrimination, form discrimination, spatial relations, position in space, and topographical disorientation.
• Agnosia: inability to recognize incoming information despite intact sensory capacities; visual object agnosia, auditory agnosia, or tactile agnosia (astereognosis).

Communication Impairments

• 33% of all patients with strokes have some degree of language dysfunction.
• Aphasia: acquired communication disorder caused by brain damage; characterized by impairment of language comprehension, oral expression, and use of symbols to communicate ideas.
  • Global aphasia: severe expressive and receptive dysfunction. Do not comprehend spoken words and are unable to communicate their needs, and frequently they also have difficulties understanding gestures that have communicative meaning.
  • Broca vs. Wernicke aphasia (review p 355 Neurologic Interventions for Physical Therapy; p 603 Physical Rehabilitation).
• Orofacial deficits:
  • Facial asymmetries result from weakness in the facial muscles, muscles of the eye, and muscles around the mouth.
  • Inability to smile, frown, or show anger or displeasure affects a person’s ability to use body language as an adjunct to verbal communication.
  • Inadequate lip closure: problems with control of saliva and fluids during swallowing.
  • Drooping or ptosis of the eyelid; unable to close the eye to assist with lubrication.
• Dysarthria: difficulty articulating words due to weakness and inability to control the muscles associated with speech production.
• Emotional lability: right hemispheric infarcts; difficulties in controlling emotions; may cry or laugh inappropriately without cause.

Orofacial deficits Dysphagia

• Difficulty or inability to swallow foods and liquids.
• Acute phase, approximately 50% of patients experience dysphagia.
• Can result from muscle weakness, inadequate motor planning capabilities, and poor tongue control.
• Unable to move food from the front of the mouth to the sides for chewing and back to the midline for swallowing poor coordination between eating and breathing.
• Lead to poor nutrition and possible aspiration of food into the lungs.
• Aspiration: penetration of food, liquid, saliva, or gastric reflux into the airway; occurs in about one-third of patients with dysphagia.

Reflex Activity

• Primitive spinal and brainstem reflexes may appear (present at birth or during infancy and become integrated by the CNS as the child ages).

Spinal Reflexes

Brainstem Reflexes

Respiratory Impairments

• Decreased control of the muscles of respiration, specifically the diaphragm.
• Poor lung expansion: decrease vital capacity.
  • Vital capacity (VC): maximum amount of air a person can expel from the lungs after a maximum inhalation.
• Pneumonia.
• Atelectasis.
• Cough effectiveness may be impaired.
• Impairments in the neuromuscular, respiratory, and cardiovascular systems lead to a decreased tolerance to exercise.

Lung Volumes and Capacities

• Tidal Volume resting tidal volume (VT)
• Inspiratory Reserve Volume (IRV)
• Expiratory Reserve Volume (ERV)
• Residual Volume
• Inspiratory Capacity (VT+IRV)
• Functional Residual Capacity (FRC) (ERV + RV)
• Vital Capacity (ERV + VT+IRV)
• Total Lung Capacity (VC+RV)

Associated Reactions

• Automatic movements that occur as a result of active or resisted movement in another part of the body; can be misinterpreted as voluntary movement.

Cognitive Deficits

• Impairments in alertness, attention, orientation, memory, or executive functions.
• Disorientation: unable to provide information about self, time of day, physical or geographical location, or disability; lesions affecting the prefrontal cortex, limbic system, and limbic cortex.
• Executive functions: abilities that enable a person to engage in purposeful behaviors; include volition, planning, purposeful action, and effective performance.

Complications Following Stroke

Abnormal Posturing and Positioning

• Spasticity in specific muscle groups can lead to the development of contractures and deformities.
• Flexion contractures of the elbow, wrist, and fingers as a result of spasticity in the flexor muscle groups; hygiene and other self-care activities become extremely difficult.
• Plantar flexion contractures of the involved ankle; Ankle contractures make ambulation and transfers difficult by preventing the patient from bearing weight on a flat or plantigrade foot; impedes foot clearance