Stroke Pathophysiology, Types, and Management (PDF)

Stroke Pathophysiology, Types, management categories, and vascular syndromes Dr. Misbah Ghous DPT, MSNMPT Introduction  Stroke or Cerebrovascular Accident (CVA) or brain attack is the sudden loss of neurological function caused by an interruption of the blood flow to the brain. Risk Factors...

Stroke Pathophysiology, Types, management categories, and vascular syndromes Dr. Misbah Ghous DPT, MSNMPT Introduction  Stroke or Cerebrovascular Accident (CVA) or brain attack is the sudden loss of neurological function caused by an interruption of the blood flow to the brain. Risk Factors Nonmodifiable  Age  Gender (women more likely to die)  Race (African Americans)  Heredity Risk Factors Modifiable  Asymptomatic carotid stenosis  Diabetes mellitus  Heart disease, atrial fibrillation  Heavy alcohol consumption  Hypercoagulability  Hyperlipidemia  Hypertension  Obesity  Oral contraceptive use  Physical inactivity  Sickle cell disease  Smoking  Epidemiology  Stroke is the fourth leading cause of death and the leading cause of long-term disability among adults in the United States.  Incidence in Males >Females  The incidence of stroke increases dramatically with age, doubling in the decade after 65 years of age. Pathophysiology  Interruption of blood flow for only a few minutes sets in motion a series of pathological events.  Complete cerebral circulatory arrest results in irreversible cellular damage with a core area of focal infarction within minutes.  The transitional area surrounding the core is termed the ischemic penumbra and consists of viable but metabolically lethargic cells.  Ischemia triggers a number of damaging and potentially reversible events, termed ischemic cascade. Etiology and Pathophysiology  Brain requires continuous supply of O2 and glucose for neurons to function  If blood flow is interrupted  Neurologic metabolism is altered in 30 seconds  Metabolism stops in 2 minutes  Cell death occurs in 5 minutes  Cont..  Ischemic strokes produce cerebral edema, an accumulation of fluids within the brain that begins within minutes of the insult and reaches a maximum by 3 to 4 days.  It is the result of tissue necrosis and widespread rupture of cell membranes with movement of water from the blood into brain tissues.  The swelling gradually subsides and generally disappears by 2 to 3 weeks.  Significant edema can elevate intracranial pressures, leading to intracranial hypertension and neurological deterioration associated with contralateral and caudal shifts of brain structures (brainstem herniation). Types of Stroke  Classification based on underlying pathophysiologic findings  Ischemic  Thrombotic  Embolic  Hemorrhagic  Intracerebral haemorrhage  Subarachnoid haemorrhage Major Types of Stroke Fig. 56-3 Ischemic Stroke  Result of inadequate blood flow to brain due to partial or complete occlusion of an artery  Constitute 85% of all strokes  Most patients with ischemic stroke do not have a decreased level of consciousness in the first 24 hours  Symptoms often worsen during first 72 hours d/t cerebral edema Ischemic Stroke  1: Thrombotic stroke  Thrombosis occurs in relation to injury to a blood vessel wall → blood clot  Result of thrombosis or narrowing of the blood vessel  Two-thirds are associated with HTN and diabetes  Often preceded by a TIA  Most common cause of stroke  Ischemic Stroke  2: Embolic stroke  Embolus lodges in and occludes a cerebral artery  Results in infarction and edema of the area supplied by the vessel  Second most common cause of stroke  Majority of emboli originate in heart, with plaque breaking off from the endocardium and entering circulation  Associated with sudden, rapid occurrence of severe clinical symptoms  Patient usually remains conscious although may have a headache   Hemorrhagic Stroke  Account for approximately 15% of all strokes  Result from bleeding into the brain tissue itself or into the subarachnoid space or ventricles  Hemorrhagic Stroke Intracerebral hemorrhage  Bleeding within the brain caused by a rupture of a vessel  Hypertension is the most important cause  Commonly occurs during activity  Often a sudden onset of symptoms that progress over minutes to hours b/c of ongoing bleeding  Manifestations include neurologic deficits, headache, Nausea & Vomiting, decreased levels of consciousness, and HTN  Hemorrhagic Stroke  Subarachnoid hemorrhage  Bleeding into cerebrospinal space between the arachnoid and pia mater  Commonly caused by rupture of a cerebral aneurysm Management Categories  Transient ischemic attack (TIA); Temporary interruption of blood supply to the brain.  Major stroke; stable, usually severe, impairments  Deteriorating stroke; neurological status is deteriorating after admission to the hospital. This change in status may be due to cerebral or systemic causes (e.g., cerebral edema, progressing thrombosis).  Young stroke; persons younger than the age of 45 Transient ischemic attack (TIA)  Temporary interruption of blood supply to the brain.  Symptoms of focal neurological deficit may last for only a few minutes or for several hours, but do not last longer than 24 hours.  No residual brain damage or permanent neurological dysfunction.  TIAs may result from a number of different etiological factors including occlusive episodes, emboli, reduced cerebral perfusion (arrhythmias, decreased cardiac output, hypotension, overmedication with antihypertensive medications, ) or cerebrovascular spasm. NEUROLOGICAL COMPLICATIONS AND ASSOCIATED CONDITIONS IN STROKE  Altered Consciousness  Sensory deficits  Motor Deficits  Disorders of Speech and Language(dysarthria)  Dysphagia  Cognitive Dysfunction  Altered Emotional Status  Hemispheric Behavioral Differences  Perceptual Dysfunction  Seizures  Bladder and Bowel Dysfunction  Cardiovascular and Pulmonary  Dysfunction  Deep Venous Thrombosis and  Pulmonary Embolus  Osteoporosis and Fracture Risk Altered Consciousness  Coma, decreased arousal levels) may occur with extensive brain damage (e.g., large proximal MCA occlusion).  The Glasgow Coma Scale is the gold standard used to document level of coma  Three areas of function are examined:  eye opening,  best motor response,  verbal responses Cerebral Blood Flow (CBF)  Auto regulation  Normal flow of 50 to 60 ml/100 g of brain tissue per minute.  High energy requirements and very little metabolic reserves.  Brain requires a continuous, rich perfusion of blood to deliver oxygen and glucose to the tissues.  Cerebral flow represents approximately 17 percent of available cardiac output.  Anatomy of CBF (circle of Willis)  Internal carotid artery  Vertebral artery (entering through C6)  Basilar artery  Anterior cerebral artery  Middle cerebral artery  Posterior cerebral artery  Posterior communicating artery  Anterior communicating artery  Superior cerebellar artery  Inferior cerebellar artery  Anterior inferior cerebellar artery  Posterior inferior cerebellar artery Vascular Syndromes  Anterior cerebral artery syndrome  Middle cerebral artery syndrome  Posterior cerebral artery syndrome  Lacunar syndromes  Internal carotid artery syndrome Anterior Cerebral Artery Syndrome  It 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.  Because the anterior communicating artery allows perfusion of the proximal anterior cerebral artery from either side, occlusion proximal to this point results in minimal deficit.  The most common characteristic of ACA syndrome is contralateral hemiparesis and sensory loss with greater involvement of the lower extremity because the somatotopic organization of the medial aspect of the cortex includes the functional area for the lower extremity. Middle Cerebral Artery Syndrome  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 produces extensive neurological damage with significant cerebral edema.  Increased intracranial pressures typically lead to loss of consciousness, brain herniation, and possibly death.  Cont..  The most common characteristics of MCA syndrome are contralateral spastic hemiparesis and sensory loss of the face, upper extremity (UE), and lower extremity (LE), with the face and UE more involved than the LE.  aphasia… inability to speak   produce perceptual deficits (e.g., unilateral neglect, anosognosia, apraxia, and spatial disorganization).  Homonymous hemianopsia (a visual field defect) is also a common finding. The MCA is the most common site of occlusion in stroke. Posterior Cerebral Artery Syndrome  The two posterior cerebral arteries are terminal branches of the basilar artery and each supplies the corresponding occipital lobe and medial and inferior temporal lobe. It also supplies the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus.   Occlusion proximal to the posterior communicating artery typically results in minimal deficits owing to the collateral blood supply from the posterior communicating artery (similar to ACA syndrome). Cont..  Occlusion of thalamic branches may produce hemianesthesia (contralateral sensory loss) or central post- stroke (thalamic) pain.  Occipital infarction produces homonymous hemianopsia, visual agnosia, prosopagnosia, or, if bilateral, cortical blindness.  Temporal lobe ischemia results in amnesia (memory loss).  Internal Carotid Artery Syndrome  Occlusion of the internal carotid artery (ICA) typically produces massive infarction in the region of the brain supplied by the middle cerebral artery.  The ICA supplies both the MCA and the ACA.  If 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 is common with possible uncal herniation, coma, and death (mass effect). Vertebrobasilar Artery Syndrome  The vertebral arteries arise from the subclavian arteries and travel into the brain along the medulla where they merge at the inferior border of the pons to form the basilar artery.  The vertebral arteries supply the cerebellum (via posterior inferior cerebellar arteries) and the medulla (via the medullary arteries).  The 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).  The basilar artery then terminates at the upper border of the pons giving rise to the two posterior cerebral arteries Cont…  Occlusions of the vertebrobasilar system can produce a wide variety of symptoms with both ipsilateral and contralateral signs, because some of the tracts in the brainstem will have crossed and others will not.  Numerous cerebellar and cranial nerve abnormalities also are present.  Locked-in syndrome (LIS) occurs with basilar artery thrombosis and bilateral infarction of the ventral pons. LIS is a catastrophic event with sudden onset. Cont..  Patients develop acute hemiparesis rapidly progressing to tetraplegia and lower bulbar paralysis (CN V through XII are involved).  Initially the patient is dysarthric and dysphonic but rapidly progresses to mutism (anarthria).  consciousness and sensation is preserved thus the patient cannot move or speak but remains alert and oriented.   Horizontal eye movements are impaired but vertical eye movements and blinking remain intact. Communication can be established via these eye movements. Lacunar Syndromes  Caused by small vessel disease deep in the cerebral white mater (penetrating artery disease).  Associated with hypertensive hemorrhage and diabetic microvascular disease.  Consistent with specific anatomic sites.  Pure motor lacunar stroke is associated with involvement of the posterior limb of the internal capsule, pons, and pyramids.  Pure sensory lacunar stroke is associated with involvement of the ventrolateral thalamus or thalamocortical projections.  Cont..  Dysarthria/ clumsy hand syndrome (involving the base of the pons, genu of anterior limb or the internal capsule)  Ataxic hemiparesis  Deficits in consciousness,  language,  visual fields are not seen in lacunar strokes as the higher cortical areas are preserved. 7 stages of Stroke Recovery By Brunnstorms’ Approach…  Stage I : flaccidity  Stage II ; Spasticity Appears  Stage III: Spasticity Increases  Stage IV: Spasticity Declines  Stage V : Complex Movement Difficult  Stage VI : Spasticity Disappears  Stage VII: Normal Functions Returns  MEDICAL DIAGNOSIS OF STROKE  History and examination  Tests and measures  Use of NIHSS  Blood analysis  Imaging.. CT scan, MRI  Pharmacologic Management or surgical management…  Thrombolytics tPA.. Tissue plasminogen activator  Anticoagulants (e.g., warfarin [Coumadin], heparin, dabigatran etexilate [Pradaxa])  Antiplatelet therapy (e.g., acetylsalicylic acid [aspirin]; clopidogrel bisulfate [Plavix]; dabigatran etexilate [Pradaxa]; ticlopidine hydrochloride [Ticlid])  Antihypertensive agents (e.g., ACE inhibitors, alpha-blockers [Minipress], beta- blockers, calcium channel blockers, direct vasodilators, diuretics, postganglionic neuron inhibitors  Angiotensin II receptor antagonists (telmisartan [Micardis], losartan potassium [Cozaar])  Antispastics, anticonvulsants, antidepressants. Physical therapy Interventions in stroke patient  Strategies to Improve Motor Learning  Interventions to Improve Sensory Function  Interventions to Improve Hemianopsia and Unilateral Neglect  Interventions to Improve Flexibility and Joint Integrity  Interventions to Improve Strength  Interventions to Manage Spasticity  Interventions to Improve Movement Control  Strategies to Improve Upper Extremity Function  Strategies to Improve Lower Extremity Function  Interventions to Improve Functional Status  Interventions to Improve Postural Control and Balance  Interventions to Improve Gait and Locomotion  Interventions to Improve Aerobic Capacity and Endurance QUESTIONS ????  A TIA is characterised by a) Neurological symptoms lasting for less than 24 hours b) Neurological symptoms lasting for more than 24 hours but less than 1 week c) Neurological symptoms lasting for more than 1 week but less than 6 weeks d) Neurological symptoms lasting for more than 6 weeks Cont..  A 55 year old woman presents with contralateral spastic hemiparesis and sensory loss of the face, upper extremity (UE), and lower extremity (LE), with the face and UE more involved than the LE is characterized by the following vascular syndrome.  a) MCA  b) PCA  c)PCA  d) None of the above