Cerebrovascular Accident (CVA)

Reported by: Lalin Fe P. Evangelista PT Intern 2012 UPH-DJGTMU

Table of Contents Anatomy Definition Epidemiology Classification Clinical key Risk Factors Pathophysiology Types Medical Management Rehabilitation Management

Fundamental Anatomy Arteries of the brain >Internal Carotid Artery -Opthalmic Artery, Post. Communicating artery, choroidal artery, ACA, MCA >Vertebral Artery -ascends in the neck by passing through upper 6 cervical vertebrae, at level of pons it unite to form basilar artery Branches: meningeal branches, ant. Spinal artery, posterior spinal artery, PICA, medullary arteries >Basilar Artery- at the upper border of pons, it divides into two PCA Branches: pontine arteries, labyrinthine artery, AICA, SCA, PCA Notes to Specific brain areas: >corpus striatum and internal capsule are supplied mainly by medial and lateral striate central branches of MCA >thalamus- supplied by branches of PCA, basilar and PCA >midbrain- PCA, superior cerebellar and basilar arteries >pons- supplied by basilar, anterior, inferior and superior cerebellar arteries, basilar arteries. >medulla oblongata- ant. And post spinal arteries >cerebellum- superior cerebellar, AICA, PICA

Christy Often Stays Frying For Ian Jay Howard (memonics) Blood Supply of the Brain

Anterior circulation controls most motor, activity, sensation, thought, speech, and emotion supplied by the carotid arteries Hallmark: Aphasia & monocular blindness Posterior circulation supplies the brainstem and the cerebellum, controlling the automatic parts of brain function and coordination supplied by the vertebrobasilar arteries Hallmark:
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CN affectation

Neurological Deficit by the artery involved: MCA- UE>LE, aphasia, visual agnosia ACA- LE>UE, apraxia, urinary incontinence, impaired judgement/ insight PCA- visual agnosia, alexia, memory impairments

Neurological deficit by laterality: (L) optimist aphasia Alexia without agraphia Visual agnosia (R) pessimist Auditory agnosia Music and art d/o Judgement Poor retention of new tasks Gait problem

CEREBROVASCULAR ACCIDENT Definition

sudden loss of neurological function caused by an interruption of blood flow to the brain (Sullivan)

A sudden onset of focal neurological deficits caused by a vascular lesion to the brain (Payton)

Rapidly developing clinical signs of a focal or global disturbance of cerebral function presumed to be of vascular origin and lasting for more than 24 hrs ( WHO)

Other Names: Stroke Apoplexy Cerebrovascular Occlusion Stroke Is clinical term implying a vascular pathogenesis Stroke is a non-traumatic brain injury caused by failure of transport of oxygen due to occlusion or rupture of cerebral vessel.

Epidemiology

3rd leading cause of death after heart disease and cancer

most common: a. serious neurologic disorder in the United States comprise half of all patients admitted to hospital for a neurologic disease b. cause of chronic disability among adults in the United States age related uncommon before age 50 Incidence doubles each decade after age 55 Gender: more common in men Race: African american 2x > Whites > Asians Mortality rate: hemorrhagic stroke account for the largest number of deaths Most common cause of disability >65 y/o
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Classifications of Stroke 1. Duration and severity of neurological signs TIA, RIND etc. 2. Etiology ischemia vs. hemorrhage 3. Specific location of vascular injury MCA, ACA, PCA etc. 4. Management categories dependent on early acute care management Initial management is an indicator for the progress of the px ex: Management for TIA is different from the management of mild stroke

Temporal Classification of Stroke

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1. TIA signs of focal neurological deficits lasting for a few a minutes to several hours but do not last > for 24 hrs.

A.K.A mini stroke

2. RIND (Reversible Ischemic Neurological Deficit) focal brain ischemia in which the neurological deficits may resolve spontaneously (generally within 3 weeks) i.e. as brain swelling or clot formation subsides, thus lessening neurological deficit this term is no longer used

3. RNI (Residual Neurological Impairment) neurological impairments that persist longer than 3 weeks and may lead to permanent disability the patient presents with fixed deficits due to cellular death and/or cerebral infarction can present in 3 forms: 1. stable
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 the neurological deficit is permanent and will not improve or deteriorate Completed stroke

2. improving return of previously lost neurological function over several days to weeks 3. progressing the neurological status continues to deteriorate following the initial onset of focal deficits may see a stabilization period, followed by further progression Stroke in evolution

Temporal Classification of Stroke

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 TIA- neurological deficits persist less than 24 hrs RIND- greater than 24 hrs but is resolved within 1 week Stroke in evolution- hallmark is increasing neurological deficit after 1 week Cresendo- series of sudden neurological deficit 1week up to 3 mos. Completed- stable neurolic deficit persistent throughout life

TIA episodes of a temporary reduction in perfusion to a focal region of the brain causes a short-lived/ temporary disturbance of function symptoms vary depending on the CNS anatomy involved, and may include: numbness of the hand, arm, or one side of the face or tongue weakness or paralysis of a limb slurred speech onset is rapid no neurological deficit remains after the attack may be the only warning of an impending stroke

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 one episode in a lifetime to > 20 in one day

Factors that may cause TIA: 1. occlusive episodes 2. emboli 3. reduction of cerebral perfusion arrhythmia (irregular breathing)

CO

Hypotension over medication with anti-HTN drugs Subclavian Steal Syndrome caused by excessive aerobic exercise of upper limb

due to obstruction of subclavian artery before the origin of cerebral artery

blood flow to vertebral artery goes in the subclavian artery 4. Cerebrovascular spasm

Etiological Classification of Stroke

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1. Ischemic Stroke caused by a decreased blood supply to the brain

result of a thrombus, embolus, or conditions that produce low systemic perfusion pressures Maybe 2 to cardiac failure or significant blood loss with resulting systemic hypotension

deprives the brain of needed oxygen and glucose, disrupts cellular metabolism, and leads to injury and death of tissues 2. Hemorrhagic Stroke Caused by large amounts of blood within a closed cranial cavity abnormal bleeding into the extravascular areas of the brain Due to a rupture of a cerebral vessel or trauma

Has a very sudden onset

Closely linked to chronic hypertension

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Classification of Ischemic Stroke Thrombotic Most common type of stroke Accounts for ~40% of all stroke

Has a gradual onset Occurs commonly at night during sleep or during periods of inactivity

due to development of a clot within the large cerebral arteries or their branches in with large infarctions, edema may be severe enough to cause brain displacement, herniation, and death

Embolic Accounts for 30% of all stroke Has an abrupt onset may arise from thrombi in the heart, or on heart valves or the large extracranial arteries

occlusion occurs in small cortical vessels Commonly in the middle cerebral artery

large vessel occlusions do occur may involve the carotid or vertebrobasilar circulation (rarely)
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 commonly affect the elderly

represent an important cause of stroke in younger adults Cortical deficit is the hallmark of embolic stroke & includes: Seizures Aphasia ( dominant hemisphere) Neglect (non dominant hemisphere)

emboli may consist of: fat (from fractured long bones)

air (in decompression sickness) venous clot that passes through a patent foramen ovale with shunt (paradoxical embolus)

Causes of cerebral embolism: 1. Cardiac Atrial fibrillation, other arrhythmias recent MI rheumatic heart disease (eg, mitral stenosis) cardiomyopathy Bacterial endocarditis Valve prosthesis
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 Nonbacterial valve vegetations Atrial myxoma 2. Large artery Atherosclerosis of aorta and carotid arteries 3. Paradoxical Peripheral venous embolism with R-to-L cardiac shunt

Lacunar constitute ~20% of all strokes

May be gradual or sudden in onset Affect small, deep penetrating branches of the large vessels which perfuse the subcortical structures i.e. lenticulostriate arteries (MCA)

Lacunae small, circumscribed lesions <1.5 cm in diameter seen in the putamen, pons, thalamus, caudate, and internal capsule More commonly seen in patients with hypertension and diabetes

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 Pathology is due to microatheroma with progressive vessel wall thickening and fibrinoid necrosis, microembolism, or rarely arteritis

Hallmark: pure motor or pure sensory stroke

(-) involvement of higher cortical function (language, praxis, nondominant hemisphere syndrome, vision)

Classification of Hemorrhagic Stroke Intracerebral hemorrhage

Has an abrupt onset

Linked to chronic hypertension Occurs due to rupture of microaneurysms (Charcot-Bouchard aneurysms) false aneurysms due to arterial wall dilations 2 to HTN > 1/3 occur in normotensives

commonly occurs at the site of small, deep, penetrating arteries weakened by atherosclerosis producing an aneurysm Locations include the putamen, thalamus, pons, cerebellum, and cerebrum Frequently extends to ventricular subarachnoid space

Symptoms: Sudden onset of headache and/or LOC

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Vomiting at onset in 2244%.

Seizures occur in 10% of cases (first few days after onset) Nuchal rigidity is common

Subarachnoid hemorrhage affects large blood vessels

Results from from rupture of an arterial aneurysm at the base of the brain with bleeding into the subarachnoid space saccular or berry aneurysm Arterial dilations found at bifurcations of larger arteries at the base of the brain 9095% of saccular aneurysms occur on the anterior part of the Circle of Willis

Rupture occurs usually when patient is active rather than during sleep (eg, straining, coitus)

Peak age for rupture is between 5th & 6th decade

usually asymptomatic prior to rupture

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Clinical key for diagnosis of hemorrhagic stroke: Increase in intracranial pressure headache Vomiting Decrease level of consciousness Patient may be lethargic or comatose

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Cause Large vessel occlusion/infarction Embolism Small vessel occlusion, lacunar Intracerebral hemorrhage Subarachnoid hemorrhage

% 32 32 18 11 7

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Pathophysiology Atherosclerosis, cerebral edema, bleeding Interruption/restricted supply of blood flow going to the brain Oxgen and/or nutrient deprivation cell damage impaired neurologic function

Sites of Predilection (of atherosclerotic plaque)

include bifurcations,constrictions, dilation, or angulations of arteries

The most common sites for lesions to occur are at the: 1. origin of the common carotid artery 2. transition of common carotid into the middle cerebral artery 3. at the main bifurcation of the middle cerebral artery 4. junction of the vertebral arteries with the basilar artery

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Risk Factors: Non-modifiable (Biological indicators)

1. Age the single most important risk factor for stroke worldwide After age 55, incidence increases for both males and females Risk more than doubles each decade after age 55 2. Sex male > female Acc. To Sullivan: Women has higher risk because they tend to live longer 3. Race African Americans 2 > whites > Asians 4. Family history of stroke

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Risk Factors: Modifiable

1. Hypertension (A) the most important modifiable risk factor Especially for subjects with BP levels higher than 160/95 mm Hg increases the risk of thrombotic, lacunar, and hemorrhagic stroke and increases the likelihood of subarachnoid hemorrhage 2. History of TIA/prior stroke (S) ~ 5% of patients with TIA will develop a completed stroke within 1 month if untreated ~ 14% of patients with TIA will develop a completed stroke within 1 year 3. Heart disease (A) Ischemic/ hypertensive

Congestive heart failure (CHF) and coronary artery disease (CAD) increase risk by twofold

Valvular heart disease and arrhythmias increase risk of embolic stroke

Atrial fibrillation is an independent risk factor

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 increased risk of stroke 5x 4. Diabetes (A) Independent risk factor increases the risk b y twofold Unfortunately, good blood sugar control has not been shown to alter the risk of stroke 5. Cigarette smoking (A) risk of ischemic stroke in smokers is about double that of nonsmokers 6. Hyperlipidemia (A) Elevated low-density lipoprotein (LDL) cholesterol is an important risk factor for ischemic heart disease small additional risk, mainly for individuals younger than age of 55 several clinical trials have shown a reduction in stroke with use of cholesterol-reducing agents (~ 30% reduction risk of stroke with use of HMG-CoA reductase inhibitors) 6. Carotid stenosis (and carotid bruit) risk of stroke decreases with carotid endarterectomy (CEA) on selected symptomatic patients (> 70% stenosis) 7. ETOH abuse/cocaine use < 2 drinks/day relative risk 0.51
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 > 7 drinks/day relative risk 2.96 (Sacco, 1999) 8. High-dose estrogens (birth control pills) considerable increased risk when linked with cigarette smoking 9. Systemic diseases associated with hypercoagulable states (A)

Result to generalized reduction of cerebral blood flow Elevated RBC count Elevated hematocrit Elevated fibrinogen are higher in individuals who smoke and have a high-cholesterol diet Protein S and C deficiencies Sickle-cell anemia Cancer

10. Migraine headaches 11. Sleep apnea 12. Patent foramen ovale (PFO) Note: Obesity/sedentary life style have no clear relationship with increased risk of stroke

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Other risk factors Geographical location: higher risk of stroke in the southeastern United States than in other areas

the so-called stroke belt states

Socioeconomic factors some evidence that strokes are more common in people with low income than among more affluent people

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Signs of Focal/ Neurological deficits changes in the level of consciousness sensory impairment on the side of the body opposite to the side of the lesion motor impairment on the side of the body opposite to the side of the lesion Hemiparesis or hemiplegia cognitive impairment perceptual impairment language impairment aphasia, dysarthria Note: to be classified as stroke, the above signs of focal deficits must be present for at least 24 hrs.

Determinants of Severity of Neurological deficits

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 Location of brain injury Extent of brain injury Amount of collateral blood flow Early acute care management important indicator for the progress of the patient

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DIFFERENTIAL DIAGNOSIS (according to De lisa) Symptoms seldom due to CVA Vertigo alone, Dizziness Dysarthria alone Dysphagia alone Displopia alone Headache Tremor Confusion Memory loss Delirium Coma Syncope (loss of consciousness) Incontinence (Inability to control excretory function) Tinnitus (Ringing of ear) Condition Most Frequency Mistaken Seizures Cerebral tremor Subdural hematoma Cerebral Abscess Peripheral neuropathy Multiple Sclerosis Encephalitis Psychogenic Migraine

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ACA Syndrome supplies the medial aspect of the cerebral hemisphere (frontal and parietal lobes) and subcortical structures, including: basal ganglia (anterior internal capsule, inferior caudate nucleus), anterior fornix anterior four fifths of the corpus callosum

Occlusion proximal to anterior communicating results in minimal deficit Because it allows perfusion on either side Lesions distal to AcomA produce more significant deficits Contralateral weakness and sensory loss, affecting mainly distal contralateral leg Mild or no involvement of upper extremity Head and eyes may be deviated toward side of lesion acutely (frontal gaze) Urinary incontinence with contralateral grasp reflex and paratonic rigidity may be present May produce transcortical motor aphasia if left side is affected ((loss of power to comprehend written or spoken words; patient can repeat)

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 Gait apraxia (if corpus callosum is affected) If both anterior cerebral territories are affected, profound mental symptoms may result (akinetic mutism)

MCA Syndrome Superior division supplies rolandic and prerolandic areas Most common cause of occlusion is an embolus S/sx: 1. Sensory and motor deficits on contralateral face and arm > leg 2. Head and eyes deviated toward side of infarct (frontal gaze) 3. Muscle tone usually decreased initially and gradually increases over days or weeks to spasticity 4. With left side lesion (dominant hemisphere) - global aphasia initially, then turns into Brocas aphasia (motor speech disorder) 5. Right side lesion (nondominant hemisphere) - deficits on spatial perception, hemineglect, constructional apraxia, dressing apraxia

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MCA Syndrome Inferior division blood supply to the lateral temporal and inferior parietal lobes Left side lesion Wernickes aphasia Right side lesion left visual neglect

PCA Syndrome supplies the corresponding occipital lobe and medial and inferior temporal lobe also supplies the upper brainstem, midbrain, and posterior diencephalon, including most of the thalamus Occlusion proximal to the posterior communicating artery results in minimal deficits owing to the collateral blood supply from the posterior communicating artery

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S/sx: 1. Occlusion of thalamic branches - may produce hemianesthesia (contralateral sensory loss) or central post-stroke (thalamic) pain 2. Occipital infarction homonymous hemianopsia, visual agnosia, prosopagnosia, or, if bilateral, cortical blindness (Anton syndrome), alexia (inability to read) 3. Temporal lobe ischemia amnesia (memory loss) 4. Cerebral peduncle Contralateral hemiplegia 5. Brainstem

Affectation of CN3 (oculomotor palsy) & CN4 (vertical gaze palsy)

Weber syndrome

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Vertebrobasilar Syndrome

Vertebral arteries supply: cerebellum (via posterior inferior cerebellar arteries) medulla (via the medullary arteries) Basilar artery supplies: pons (via pontine arteries) the internal ear (via labyrinthine arteries) cerebellum (via the anterior inferior and superior cerebellar arteries) Occlusions of the vertebrobasilar system can produce a wide variety of symptoms with both ipsilateral and contralateral sign Cerebellar and cranial nerve abnormalities also are present

There is absence of cortical signs (such as aphasias or cognitive deficits) that are

may present with any combination of the following signs/symptoms: Vertigo Nystagmus Abnormalities of motor function often bilaterally Ipsilateral cranial nerve dysfunction
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 Crossed signs: motor or sensory deficit on ipsilateral side of face and contralateral side of body; ataxia, dysphagia, dysarthria

Weber Syndrome (Base of Midbrain)

Obstruction of interpeduncular branches of posterior cerebral artery or posterior choroidal artery or both S/Sx: Ipsilateral CN3 paralysis Contralateral hemiplegia contralateral Parkinson signs
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 contralateral dystaxia (mild degree of ataxia) Benedikt Syndrome (Red Nucleus/Tegmentum of Midbrain)

Obstruction of interpeduncular branches of basilar or posterior cerebral artery, or both S/Sx: Ipsilateral CNIII nerve paralysis with mydriasis contralateral hypesthesia (medial lemniscus) hyperkinesia (ataxia, tremor, chorea, athetosis) due to damage to red nucleus

Locked-in syndrome (LIS)

occurs with basilar artery occlusion thrombosis and bilateral infarction of the ventral pons is a catastrophic event with sudden onset S/Sx: acute hemiparesis rapidly progressing to tetraplegia lower bulbar paralysis (CN V through XII) Initially the patient is dysarthric and dysphonic but rapidly
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 progresses to mutism (anarthria) preserved consciousness and sensation The patient cannot move or speak but remains alert and oriented Horizontal eye movements are impaired vertical eye movements and blinking remain intact Communication can be established via these eye movements

Millard-Gubler Syndrome (Base of Pons)

Obstruction of circumferential branches of basilar artery S/Sx: Ipsilateral abducens (CN6) and facial (CN7) palsies Contralateral hemiplegia, analgesia, hypoesthesia Extension to medial lemniscus = Raymond-Foville Syndrome (with gaze palsy to side of lesion)

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Lateral Medullary (Wallenberg) Syndrome

A.K.A PICA syndrome, and vertebral artery syndrome occurs due to occlusion of the following: 1. Vertebral arteries (involved in 8 out of 10 cases) 2. Posterior inferior cerebellar artery (PICA) 3. Superior lateral medullary artery 4. Middle lateral medullary artery 5. Inferior lateral medullary artery Signs and symptoms include the following: Ipsilateral side Horners syndrome (ptosis, anhydrosis, and miosis) Decrease in pain and temperature sensation on the ipsilateral face Cerebellar signs such as ataxia on ipsilateral extremities (patient falls to side of lesion) Contralateral side Decreased pain and temperature on contralateral body Dysphagia, dysarthria, hoarseness, paralysis of vocal cord Vertigo; nausea and vomiting Hiccups
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 Nystagmus, diplopia Note: No facial or extremity muscle weakness seen in this syndrome

ICA Syndrome

supplies both ACA & MCA Ocular infarction

Transient monocular blindness (amaurosis fugax) embolic occlusion of retinal branch of opthalmic artery occurs prior to onset of stroke in approximately 25% of cases of ICA occlusion.

Cerebral infarction variable presentation with complete ICA occlusion from no symptoms (if good collateral circulation exists) to severe, massive infarction in ACA and MCA distributions Patients will present with contralateral motor and/or sensory symptoms significant edema will lead to coma & eventually death (+) uncal herniation

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Gerstmann syndrome
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 Anatomy: cerebral hemispheredominant parietal lobe Artery: middle cerebral artery Symptoms: Agraphia acalculia Finger agnosia Right and left disorientation

Anton syndrome

Anatomy: cerebral hemispheresbilateral occipital lobes Artery: posterior cerebral artery (bilateral basilar artery) Symptoms: visual lossbilateral Unawareness or denial of blindness

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 Weber syndrome Anatomy: midbrainbase Artery: posterior ocerebral artery (penetrating branches t midbrain) Symptoms: contralateral hemiparesis Ipsilateral lateral gaze weakness DejerineRoussy syndrome Anatomy: thalamus Artery: posterior cerebral arterypenetrating branches to thalamus Symptoms: hemisensory lossall modalities Hemi-body pain

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Medical Management Goals

1. improve cerebral perfusion, re-establish circulation & O2 O2 via mask or nasal cannula coma assisted ventilation, suctioning, intubation 2. maintain adequate BP 3. maintain sufficient CO by meds 4. restoring fluid & electrolyte balances 5. maintain blood glucose level within (N) range 6. control seizures/ infection (common in ICA syndrome) 7. control ICP & herniation using anti edema agents if surgery ventriculostomy (drain & monitor ICP) 8. maintain bladder fxn. by catheterization 9. maintain jt. integrity coma, complete bed rest, paralysis - PROM 10. maintain skin integrity turning every 2 hrs. WC P relief should be done every 15 20 mins. or 10 15 mins. Pharmacological Management

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1. anti-coagulant therapy inhibits clotting factors Indicated for: 1. embolic strokes Not given for lacunar strokes and completed strokes 2. also prevent DVT and pulmonary embolism Heparin (through IV route) given for stroke in evolution Coumadin (Warfarin)- given orally; for short term

2. anti-platelet therapy Aspirin (ASA), Aspirin/Dipyridamole (Aggrenox), Clopidogrel (Plavix) indicated to reduce the risk of subsequent attacks after an initial TIA or other event indicating risk of future ischemic stroke Patients with non-cardioembolic ischemic stroke or TIA (for thrombotic, embolic, & lacunar stroke only)

Patients who are at risk of recurrent stroke and other cardiovascular events

Given orally (The daily dose given is 100 mg)

beneficial as secondary stroke prevention of presumed arterial origin

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 improves cerebral perfusion

platelet aggregation

long term, low dose = risk of recurrence of stroke

high dose = given to px with independent risk factor (Atrial fib)

3. anti-HTN agents indicated for acute stroke (especially hemorrhagic)

if acute myocardial infarction, aortic dissection, severe CHF or hypertensive encephalopathy are present

Diuretics, Beta blockers, ACE inhibitor blockers

, Ca channel

4. anti- spasticity drugs Diazepam/ Benzodiazepine (BNz) vs. baclofen & dantrolene sodium

Tests & Measures (Laboratory Tests)

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 Complete blood count (CBC) platelet count prothrombin time (PT) and partial thromboplastin time (PTT) electrolytes, calcium, glucose, blood urea nitrogen (BUN) creatinine chest x-ray electrocardiogram (EKG) sedimentation rate Lipid profile thyroid profile

In selected cases, antithrombin III, protein C and protein S

Tests & Measures (Imaging Studies)

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1. Non contrast CT Scan evaluates presence of blood (cerebral hemorrhage or hemorrhagic infarction) especially when thrombolysis is being considered

CT studies are often normal during the first few hours after brain infarction

2. MRI Scan More sensitive than CT scan in detecting ischemic infarcts (including small lacunes)

Can detect edema due to ischemia within a few hours of onset of infarct

3. Carotid Doppler/ultrasound can be useful in screening the extracranial internal carotid arteries for significant stenosis

4. Magnetic resonance angiography (MRA) may be used to evaluate the carotid circulation, the vertebral-basilar system, the circle of Willis, and the
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anterior, middle, and posterior cerebral arteries and their major branches Tends to overestimate the degree of stenosis compared with contrast angiography 5. Contrast cerebral angiography provides the most detailed and reliable information on the presence of carotid and intracranial disease In experienced hands, complications should result in less than 1% morbidity and mortality

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Factors influencing functional outcomes

Good functional outcome Hemiparesis no sensory loss (or pure motor stroke)

Absence of significant associated disease like DM, HPN, MI etc.

Young age signs of motor recovery of the hand by 4 weeks (full or good recovery of hand function) Fair functional Outcome (+) hemiplegia w/ moderate spasticity (+) expressive aphasia (+) intermittent incontinence at night
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 Mild sensory loss Poor functional Outcome Advanced age (old) 60 above Presence of global aphasia Continuing urinary and bowel incontinence Severe sensory loss No measurable grasp strength by 4 weeks Severe proximal spasticity Prolonged flaccidity period Complete arm paralysis at onset (poor prognosis of recovery of useful hand function) Late return of proprioceptive facilitation (tapping) response > 9 days Late return of proximal traction response (shoulder flexors/adductors) > 13 days

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OTHER RISK FACTORS FOR DISABILITY AFTER STROKE Global aphasia Severe neglect Sensory and visual deficits Impaired cognition Delay in medical care Delay in rehabilitation Bilateral lesions Previous stroke Previous functional disability Diabetes mellitus Cardiac disease Electrocardiograph abnormalities
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Negative Factors for Return to Work After a Stroke Low score on Barthel index at time of rehabilitation discharge Prolonged rehabilitation length of stay Aphasia Prior alcohol abuse

Impairments I. Sensory impaired but rarely absent on the hemiplegic side Type and extent of impairment is related to the location and size of the vascular lesion distribution of sensory loss face-UE-LE-pattern cortical lesions localized areas of dysfunction
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Involves complicated sensory processing such as two-point discrimination, accurate localisation of perceptions, stereognosis, and graphesthesia

subcortical lesion

diffuse involvement throughout one side of the (e.g. history of significant numbness or sensory loss)

involving the thalamus and adjacent structures

brainstem lesion crossed anesthesia ipsilateral facial impairment, contralateral arm & LE lesion

thalamic pain constant, severe burning pain with intermittent sharp pain exaggerated response to specific stimulus usually in the contralateral half of the body stimulus: touch, pain (pin prick), P, light (bright), sounds, T (hot or cold) prevents the patient from actively participating in rehabilitation

II. Motor

1. Weakness or paralysis
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2. tone alteration Flaccidity present immediately after stroke due to cerebral shock short lived tone (last for few days or wks.) occur to px with 1 motor cortex & cerebellar type of lesion (PCA) Spastic stage occurs in antigravity ms. UE: scapular retractors, shoulder adductors, depressors & IR, elbow flexors, forearm pronators, wrist & finger flexors LE: pelvic retractors, hip adductors, IR & extensors, knee extensors, ankle plantarflexors & supinators, toe flexors Trunk/ neck: lateral flexors of hemiplegic side2. tone 3. Abnormal Synergy emerge with spasticity can be elicited by: reflex, associated reaction, minimal voluntary movt.

III. Abnormal reflexes

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Occurs during recovery when spasticity and synergies are strong

ATNR if persists, may cause difficulty in rolling & midline hand play to promote midline hand play & promote self feeding, place px in sidelying postn. STNR if persist, may cause difficulty in assuming quadruped position Moro tested last coz it will result to crying Tonic labyrinthine reflex Tonic lumbar reflex

Rot. of trunk to one side : result in flex. of the UE and LE and vice versa

Galant stroke lumbar area on the , lateral flexion to the

Associated rxn

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 Consist of ab(N) automatic response of the involved limb, resulting from acton occurring in some part of the body by voluntary or reflex stimulation (yawning, sneezing, or coughing) SOUQUES PHENOMENON Elevation of the hemi. arm above the horizontal plane may elicit an extension and abd. response of the fingers RAIMESTES PHENOMENON Resistance to add. R abduction produce a like response in the opposite Limb HOMOLATERAL LIMB SYNKINESIS

Flex of the arm elicits flex. of the leg on the hemi. side.

IV. Posture & Balance

altered coordination

Result from cerebellar or basal ganglia involvement & proprioceptive losses or weakness

sensory ataxia (with PCA lesion involving basal ganglia) Motor ataxia (with cerebellar lesion)

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 apraxia (basal ganglia lesion or cerebellar lesion) Ipsilateral Pushing/ Pushers syndrome/ Controversive Syndrome unusual motor behavior characterized by active pushing of the stronger ms. esp. towards the weak side Results to listing towards the affected side results to fall caused by severe misperception of body orientation in relation to gravity Has a poor prognosis Typical arm posture Cortical thumb

V. Visual

Homonymous hemianopsia

lesion in the optic radiation in the internal capsule (if the MCA is affected) or the 1 Visual cortex (if PCA is affected)

Monocular blindness Visual neglect (visual inattention) Hemispheric lesion = visuospatial neglect
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 Forced gazed deviations Hemispheric lesion the pxs eye deviate away from hemiplegic side Brainstem lesion pxs eye deviate towards the hemiplegic side

VI. Speech, Language & Swallowing Aphasia an acquired communication disorder caused by brain damage characterized by an impairment of language comprehension, formulation, and use Dysarthria motor speech disorders caused by lesions in parts of the central or peripheral nervous system that mediate speech production lesion can be located in the primary motor cortex in the frontal lobe, the primary sensory cortex in the parietal lobe, or the cerebellum Dysphagia Difficulty in swallowing CN 9 & 10

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VII. Perception

Due to lesion of the parietal lobe of the non-dominant hemisphere 1. Spatial relations disorder a difficulty in perceiving the relationship between the self and two or more objects in the environment Pt. may not be able to judge distance, size, position, rate of movement, or the relation of parts to the whole figureground discrimination, form discrimination, spatial relations, position in space Pt. may consistently bump the W/C into the door frame and seem unable to get through the doorway 2. Body image / Body scheme disorder Body Image Visual and mental memory of the body parts Body Scheme Perception of precise location and relationship of body parts.
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 Simultagnosia or Autopagnosia impairment of body scheme Lack of awareness of the body structure and relation of body parts on ones self or on other Lesion site is the dominant parietal lobe or post. Temporal lobe

3. Topographic Disorientation Difficulty n understanding and remembering the relation of one place to another Lesion site : occipital- parietal lobe of the non dominant hemisphere 4. Agnosia inability to recognize incoming information despite intact sensory capacities can include visual object agnosia, auditory agnosia or tactile agnosia 5. Unilateral Neglect Pt. are unaware of what happens on the hemi. side. Inability to register and integrate stimuli and perceptions from one side of the body and the environment Lesion on (R) nondominant hemisphere parietal lobe.
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6. Apraxia Disorder of vol. learned movt. Inability to perform purposeful movt in the absence of paralysis/ impaired sensation Ideomotor Apraxia Ref. to breakdown bet. concept or performance Pt. is able to carry out habitual tasks automatically and describe how they are done but is unable to perform a task upon command and is unable to imitate gesture Lesion : Dominant supramarginal gyrus. Ideational Apraxia Failure in the conceptualization of the task. Inability to perform a purposeful motor act bec. pt. cant understand the overall concept of act, cant retain the idea of the task and cant formulate the motor pattern required. Lesion : dominant parietal lobe Constructional Apraxia Inability to prod. 2 or 3 dimensional forms by drawing constructing, or arranging blocks or obj. spontaneously or upon command. Lesion : either hemisphere.

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 Dressing Apraxia Inability to dress ones self properly owning to a disorder in the body scheme or spatial relationship.

Lesion site : nondominant occipital lobe.

VIII. Cognition

Attention disorder Memory disorder Perseveration continued repetition of words, thoughts, or acts not related to current context lesions in the premotor and/or prefrontal cortex lack of abstract thinking, impaired organization and sequencing (executive functions) Dementia delirium

IX. Emotional Status pseudobulbar affect (PBA) also known as emotional lability or emotional dysregulation syndrome
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 emotional outbursts of uncontrolled or exaggerated laughing or crying that are inconsistent with mood Depression Seen with lesions in the left frontal lobe (acute stage) and with lesions in the right parietal lobes (subacute stage) Occurs between 6 mos 2 years post CVA Apathy Euphoria

X. Bladder & Bowel

Urinary incontinence Common during acute phase may be caused by CNS damage, UTI, impaired ability to transfer to toilet or impaired mobility, confusion, communication disorder/aphasia, and cognitive perceptual deficits that result in lack of awareness of bladder fullness Persistent incontinence is associated with a poor long-term prognosis for functional recovery Treatments

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 Treat possible underlying causes (eg, UTI) Regulation of fluid intake Transfer and dressing-skill training Patient and family education Medications (if no improvement with conservative measures) Timed bladder-emptying program Remove indwelling catheter and perform postvoid residuals (PVRs) Intermittent catheterization (IC) Bowel incontinence may be associated with infection resulting in diarrhea, inability to transfer to toilet or to manage clothing, and communication impairment/ inability to express toileting needs Constipation Management: adequate fluid intake/hydration modify diet (eg, increase in dietary fiber) bowel management (stool softeners, stool stimulants, suppositories allow commode/ bathroom privileges
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 Physical activity is also helpful to improve these problems

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Rehab Management

Should begin early in the acute stage when the patients condition is stable Includes: 1. Traditional therapy positioning, ROM exercises, strengthening, mobilization, compensatory techniques, endurance training (eg, aerobics) 2. PNF (by Knott & Voss) 3. NDTs (Bobath) 4. Brunnstroms movement therapy 5. Roods tech. 6. Motor relearning (Carr and Shepard Approach) 7. FES, ES

Bobath Stage 1- Flaccidity Stage 2- Spasticity Stage 3- Relative Recovery

PNF
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 Indicated for patients with orthooedic and neurologic condition Can be use to assist problem with strength (recite components) BS, BA, BRCD,BRSD

BOBATH Principle: to inhibit spasticity and facilitate (N) movement Sequence: Normalization of tone Selective movement Practice using functional movement BRUNNSTOM Long duration of flaccidity and severe spasticity are poor prognosis Mirroring reflex ATNR UE flexor synergy elbow flexion and supination, sh adduction *first to appear and last to disappear Isolation and combination

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Factors that might influence the timing of rehabilitation effect include: 1. Medical stability 2. motivation 3. Patient endurance 4. stage of recovery 5. ability to learn

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