Stroke Rehabilitation

STROKE REHABILITATION   INTRODUCTION I. DEFINITION OF STROKE  Sudden occurrence of permanent damage to an area of brain caused by a blocked blood vessels bleeding within the brain.  Traumatic injury to the brain, demyelinating lesions, brain tumors, brain abscesses, & other stroke-like symptoms are not included in this definition. II. CLASSIFICATION  Ischemic – vascular occlusion  Hemorrhagic – bleeding within the parenchyma of the brain *Nonparanchynmal hemorrhage – Subarachnoid hemorrhage (SAH) due to a ruptured intracranial aneurysm. III. MANIFESTATION  Focal weakness – most common  Sensory loss  Speech  Language disturbance  Visual loss IV. OBJECTIVE OF STROKE REHABILITATION  Achieve max. level of functional independence  Facilitate neurological recovery  Successful reintegration back into home, family and community  Reestablish meaningful and gratifying life  Educating of the stroke survivor and his family regarding secondary stroke prevention V. EPIDEMIOLOGY  780,000 Americans suffer, of which 600,000 are an initial event.  Stroke remains 3rd leading cause of death in US, after heart disease and cancer.  Age related- uncommon before age 50, but doubling each decade after 55.  More common in men--young cohorts, but women for over age 85. VI. RISK FACTORS  Annual risk of 5% after initial stroke, 5-year cumulative risk of 25 %, or as high as 42%.  Hypertension, heart disease, DM

 Heavy alcohol consumption

VII.

TYPES OF STROKE 1. Transient Ischemic Attacks  Strokelike event that completely resolves within 24 hrs.  Symptoms occurs only a few seconds or minutes followed by apparent resolution.  Despite complete resolution – acute infarcts can be present in some MRI results – high risk for further vascular events.  TIA requires thorough investigations. 2. Cerebral Thrombosis  Thrombosis of large extracranial and intracranial vessels as the result of atherosclerotic CVD – approximately 30% of all cases of stroke.  Common in vessels of Neck and base of brain.  Occlusion of these vessels causes large infarction.  Risk factor of atherosclerosis: HPN, DM, smoking & hyperlipidemia.  It begins subtly and affected individual may have weakness or difficulty to walk or get out of bed.  It worsens over some hours or days, followed by stabilization and then gradual improvement.

3. Cerebral Embolism  Responsible for about 30% of all cases  SOURCES OF EMBOLI:  Cardiogenic – thrombus at a recent site of MI, area of myocardial hypokinesis, w/in left atrium in pts with atrial fibrillation, or on diseased or prosthetic valves.  Paradoxical embolism – DVT in the pelvis or leg.  Cerebral – blood flow and anatomy of the cerebral circulation favor passage in the middle cerebral artery.  Treatment:  Anticoagulants- for long term secondary prevention of recurrence, but immediate anticoagulation with heparin can increase risk of symptomatic hemorrhagic conversion. *That is why anticoagulation therapy is delayed from the acute onset for up to 2 weeks in individuals with large cardioembolic infarctions. 4. Lacunar Stroke  Approximately 20% of all strokes  Small, circumscribed lesions, 1.5 cm from occlusions in the deep penetrating branches of the large vessels of subcortical structures.  Highly asso. with HPN, microatheroma or lipohyalinosis.

5. Cerebral Hemorrhage  Approx. 11% of cases  HPN- most common cause- at the site of small, deep , penetrating arteries.  Occurs through rupture of microaneurysms (Charcot-bouchard aneurysms)  Majority of lesions occurs in the putamen or thalamus, and about 10% occurs in cerebellum.  Cerebral amyloid angiopathy- another cause of cerebral hemorrhage- about 520% cases.  Clinical onset is often dramatic with severe headache and rapidly progressive neurologic deficits.  Well-recognized complication of anticoagulant therapy  Other causes : trauma, vasculitis and bleeding into a tumor & pts with bleeding diasthesis.  Manifestations: sudden headache, inability to stand, n&v, and vertigo  Acute hydrocephalus- caused by large posterior fossa lesions in which edema and hematoma occludes the 4th ventricle.– requires immediate decompression 6. Subarachnoid Hemorrhage  Accounts for 7% of cases  Usually result from rupture of arterial aneurysm at the base of the brain with bleeding in the subarachnoid space.  Risk of aneurysm rupture increases as the size increases-- intervention is advised for asymptomatic aneurysm.  Signs and symptoms of rupture:  Sudden severe headache  Nausea and vomiting  Signs of meningeal irritation  Focal signs- complication of arterial vasospasm  Coma- 1/3 of patients die acutely.  Nimodipine- reduce likelihood or severity of vasospasm.  Complication:  Hydrocephalus – obstruction of ventricular system or arachnoiditis from blood in the CSF  SAH may also result from bleeding from an arteriovenous malformation (AVM) – a tangle of dilated blood vessels found on the surface of the brain parenchyma.  These are congenital abnormalities and tend to bleed in childhood and young adulthood.  S/sx- seizure or chronic headache  Treatment: surgical excision, proton beam therapy, or neurovascular ablation.

  STROKE SYNDROMES  Cluster of signs and symptoms produced due to the occlusion of an artery supplying a particular region of the brain Classification: 1. Large vessel Stroke within the Anterior Circulation 2. Large vessel Stroke within the Posterior Circulation 3. Small vessel Disease of either Vascular Bed CEREBRAL CIRCULATION

1. Anterior Circulation – MCA, ACA, and Anterior Choroidal Artery 2. Posterior Circulation – Vertebral Artery, Basilar Artery and Posterior Cerebral Artery STROKE WITHIN THE ANTERIOR CIRCULATION A. Middle cerebral artery, Anterior cerebral artery, Anterior choroidal artery B. Occlusion of the Internal Carotid Artery and its branches 1. Internal Carotid Artery Syndrome  no observable deficit to catastrophic  good collateral circulation  no neurological consequences  may occur with carotid occlusion 2. Middle cerebral artery is occluded at its origin  cerebral edema that usually accompanies such a large lesion with brain displacement  depressed consciousness  head and eyes deviated to the side of the lesion  Contralateralhemiplegia  decreased sensation  homonymous hemianopia  Dominant hemisphere is involved  aphasia is usually present without weakness, which may be severe if the entire territory of the MCA is infarcted  Nondominant hemisphere lesions, perceptual deficits and neglect  Patients who survive the acute lesion regain control of head and eye movements, and normal level of consciousness is restored. However, severe deficits involving motor, visuospatial, and language function usually persist.  Occlusion of the middle cerebral artery branches, except for the lenticulostriate -almost always embolic in origin, and the associated infarctions are smaller and more peripherally located than those seen after occlusion of the MCA trunk -dense sensory-motor deficit on the contralateral face, arm, and leg, with less involvement of the leg. Recovery:  The patient is usually able to walk with a spastic, hemiparetic gait  Little recovery occurs in motor function of the arm  Small focal infarctions from occlusions of branches of the superior division will produce more limited deficits -pure motor weakness of the contralateral arm and face, apraxia, or expressive aphasia. Lesions affecting the right hemisphere - Neglect of the left side of the body.

-Initially, the patient may completely ignore the affected side and even assert that his left upper extremity belongs to someone else. - Such severe neglect often gradually improves but may be followed by a variety of persisting impairments such as deficits in attention, constructional apraxia, dressing apraxia, perceptual deficits, and aprosodia. Lacunar strokes occur in the distributionof the lenticulostriate branches of MCA - Internal capsule (most common) - Causing a pure motor hemiplegia a. anterior lesion in the internal capsule may cause dysarthria with hand clumsiness b. lesion of the thalamus or adjacent internal capsule causes a contralateral sensory loss with or without weakness * The neurologic deficits in these lesions often show early and progressive recovery with good ultimate outcome. 3. Anterior Cerebral Artery Syndromes  Supplies the Median and paramedian regions of the frontal cortex and the strip of the lateral surface of the hemisphere along its superior border  Occlusions (uncommon) - contralateral hemiparesis with relative sparing of the hand and face and greater weakness of the leg  Lesions affecting the left side  Transcortical motor aphasia characterized by diminution of spontaneous speech but preserved ability to repeat words  Grasp reflex ,sucking reflex and paratonic rigidity (also known as gegenhalten—muscle hypertonia presenting as an involuntary variable resistance during passive movement of a limb)  Urinary incontinence is common  Large lesions of the frontal cortex -often produce behavioral changes -lack of spontaneity, distractibility, and tendency to perseverate.  Affected individuals may have diminished reasoning ability.  Bilateral anterior cerebral artery infarctions may cause severe abulia (lack of initiation)

STROKE WITHIN THE POSTERIOR CIRCULATION A. Paired Vertebral Arteries B. Basilar Artery C. Paired Posterior Cerebral Arteries 1. Vertebrobasilar Syndromes  The two vertebral arteries join at the junction of the medulla and pons to form the basilar artery.  They supply the brainstem by paramedian and short circumferential branches and supply the cerebellum by long circumferential branches  When motor impairments are present, they are often bilateral, with asymmetric corticospinal signs, and they are frequently accompanied by cerebellar signs  Cranial nerve lesions are very frequent and occur ipsilateral to the main lesion  There may be dissociated sensory loss (involvement of the spinothalamic pathway with preservation of the dorsal column pathway or vice versa), dysarthria, dysphagia, disequilibrium and vertigo, and Horner’s syndrome a. Lacunar infarcts  occlusion of small penetrating branches of the basilar artery or posterior cerebral artery b. Brainstem lacunes  symptomatic c. Pontine lacunar infarcts  pure motor hemiparesis d. Lateral medullary syndrome (Wallenberg’s syndrome)  infarction in the lateral wedge of the medulla  It may occur as an occlusion of the vertebral artery or the posterior inferior cerebellar artery e. Basilar Artery Occlusion  May result in severe deficit with complete motor and sensory loss and cranial nerve signs from which patients do not recover f. Locked-in syndrome  is an uncommon but devastating stroke syndrome involving the brainstem  affects the upper ventral pons, involving the bilateral corticospinal and corticobulbar pathways but sparing the reticular activating system and ascending sensory pathways g. Focal infarctions may occur in the midbrain and affect the descending corticospinal pathway  sometimes also involving the third cranial nerve nucleus (Weber’s syndrome)  resulting in ipsilateral third nerve palsy and paralysis of the contralateral arm and leg. h. Occipital lobe infarction

 partial or complete contralateral hemianopia, and when these visual deficits involve the dominant hemisphere, there may be associated difficulty in reading or in naming objects 2. Thalamus is involved  There is contralateral hemisensory loss o contralateral hemianesthesia and central pain (25 %) (brainstem and parietal lobe)  Thalamic syndrome o patients report unremitting, unpleasant, burning pain affecting the opposite side of the body Evaluation of the Stroke Etiology  Mostly, stroke represents only one facet of systemic atherosclerotic vascular disease - hypertension, diabetes, and smoking. Stroke, however, can occur in the absence of common risk factors or atherosclerosis  Basic evaluation of stroke cause -thorough physical and neurological examination -cerebral imaging (CT or preferably MRI) -an electrocardiogram - noninvasive carotid studies -echocardiogram  Possible cardiogenic embolism, a 24-hour Holter monitor is appropriate  CT or MR angiography  When concerns regarding large vessel occlusion, stenosis, or dissection are present  Conventional angiography – reserved for use during intravascular interventions. STROKE IN CHILDREN AND YOUNG ADULTS  40% to 50%, no obvious risk factors such as sources of cardiogenic emboli and atherosclerosis are found. Acute Stroke Management Goals : (a) to limit or reverse neurologic damage through thrombolysis or neuroprotection (b) to monitor and prevent secondary stroke complications such as elevated intracranial pressure a. Intravenous thrombolysis with recombinant tissue plasminogen activator -known to be effective when administered to appropriate individuals within 3 hours of symptom onset since the mid-1990s b. Thrombolysis (recent) -safe as late as 4.5 hourspoststroke in a selected population, it is clear that this interventionnis most effective when given as early as possible

c. Clot removal devices -e.g.Merci device, have been studied but are not yet in routine clinical use d. Control of blood pressure, fever, and hyperglycemia - improve outcome in acute stroke e. Brain cooling -remain under investigation Secondary Stroke Prevention -involves a multipronged effort at risk factor reduction, which may involve behavioral change -smoking cessation, aerobic exercise, and dietary modifications in addition to optimizing treatment of associated medical risk factors, such as hypertension and diabetes Specific Medications for Stroke Prevention A. Antiplatelet medications are appropriate for the majority of patients for secondary prevention of ischemic stroke 1. Aspirin 50 to 325 mg provides a reduction in stroke of approximately 25% S.E: Gastrointestinal toxicity & Allergy 2. Clopidogrel (more costly) same as Aspirin (efficacy) 3. Ticlopidine is a related drug, with similar efficacy. It has largely fallen out of use due to concerns regarding neutropenia 4. Dipyridamole, has some efficacy when taken alone but is generally prescribed as part of a fixed dose combination with aspirin (Aggrenox). 5. Warfarin use for stroke prevention is generally restricted to patients with atrial fibrillation or other known cardiac or other embolic source B. Carotid endarterectomy - reduces the risk of stroke in those patients with single or multiple TIAs and with 70% or greater stenosis of the ipsilateral internal carotid artery C. Carotid stenting -has been studied as an alternative to carotid endarterectomy, particularly in patients who may be at poor surgical risks

 REHABILITATION DURING ACUTE PHASE  In US, acute stroke care is often transitioned rapidly to rehab care, often within matter of days.  Should not be considered a separate phase of care, that only begins after acute medical intervention, rather it is integral part of medical management. FOCUS OF REHABILITIVE CARE Pressure Ulcers  among pts with hemiplegia, lethargy, and incontinent Management:  protection of skin from excessive moisture  use of heel –protecting splints  maintenance of proper position with frequent turning  Daily inspection  Routine cleaning Aspiration and Pneumonia • Among patients with dysphagia • Among able-bodied- aspiration usually results from vigorous coughing Management:  Avoiding oral feeding among patients who are not alert  Assessment of ability to swallow even in alert pts  Swallowing videofluoroscopy or flexible endoscopic evaluation of swallowing (FEES) may be performed  NGT feeding or gastrostomy may be necessary  Keep head of the bed elevated Impairment Of Bladder Control • Initially cause a hypotonic bladder with overflow incontinence • If indwelling catheter- should be removed as soon as possible– then reassessment. • Regular intermittent catheterization is preferable than indwelling catheter. Contractures  May result when spasticity is present Management: • Regular passive stretching • Moving the joints thru ROM Deep Vein Thrombosis  High especially in pts with hemiplegia Management: Mobilization  Useful to prevent:  DVT  Deconditioning  Gastrophageal regurgitation and aspiration pneumonia  Contracture formation

 Skin breakdown  Orthostatic intolerance o

Specific task: (gen. begins w/in 24-48 hrs)  Turning from side to side  Sitting up in bed  Transferring to a wheelchair  Standing and walking

Evaluation for Rehabilitation Program 1. Patients with premorbid conditions such as dementia- subacute rehabilitation program may be appropriate 2. Less intense rehab program with a lesser degree of medical supervision over a longer period of time. 3. Some individuals needs complete period of intensive “acute” rehabilitation followed by “subacute” rehabilitation, before returning home. 4. Outpatient basis and homecare agency- patients with partial aphasia, visual loss or monoparesis Criteria For Admission To A Comprehensive Rehab Program  Stable neurologic status  Significant persisting neuro deficit  Identified disability affecting atleast 2 of the ff: mobility, self care activities, communication, bowel or bladder control, or swallowing  Sufficient cognitive function to learn  Sufficient communicative ability to engage with the therapist  Physical ability to tolerate the active program (atleast 3hrs/day)  Achievable therapeutic goals Hemiparesis  Arm is more involved than leg  most importantly because greater number of stroke involves Middle cerebral artery than Anterior cerebral artery  Very distinct functional demands placed on upper limbs than lower limbs  Poor prognosis --complete arm paralysis at onset or no measurable grasp strength by 4 weeks.  For patients with motor recovery by 4 weeks– 70% will make a full or good recovery.  Poor prognosis– no initial motion w/in 3weeks or if motion in a second segment is not followed within a week. Aphasia  Time course of recovery is usually slower and more prolonged than motor abilities, with improvement continuing more than a year.  Broca’s (nonfluent) aphasia : a. With large lesions- little recovery b. Smaller lesions- milder aphasia with anomia and word-finding difficulty  Global aphasia-tend to progress slowly , with comprehension often improving more than expressive ability. Visual impairment

 Generally , visual improvement is modest, if the field defect persists beyond a few weeks, late recovery is less likely. Tools that can be used to assess mental status:  Mini-Mental State Examination (MMSE)- screens variety of mental demands and gives a well- validated of overall mental function.  NIH stroke scale(NIHSS)- includes some elements of cognitive and language ability. Specific Stroke Impairment & their rehabilitation  Dementia– usually there is premorbid cognitive decline already, undiagnosed  Delirium- early treatment of underlying cause such as F&E disturbances, infection, sleep disruption, or medication side effects.  Consciousness- stimulants ( dextroamphetamine or methylphenidate) as well as modafinil.  Visual neglect- letter cancellation tasks or line bisection  Hemispatial neglect- visual and/or verbal cuing or fresnel prism applied to eyeglasses.  Construction ability( unable to copy or draw simple figures)  Others impairment of preceptual function: failure to recognize palm writing ( graphestesia), unable to identify objects in hand(astereognosis), and extinction of simultaneous bilateral stimulation.  Anosognosia- inability to recognize disability  Apraxia- inability to execute an intended movement with motor ans sensory function  Behavioral changes- usually involves frontal lobe damage; apathy is common  Deficits in attention and executive function- commonly mistaken for memory impairment Emotional Lability  more common in right hemisphere lesions.  Unable to control or suppress emotional response to stimuli  May cry or laugh very easily– though they recognize it as inappropriate  Often mistaken for depression  May respond to TCA or SSRI antidepressants

 VISUAL DEFICITS, DYSPHAGIA, MOTOR IMPAIRMENT, SENSORY IMPAIRMENT AND CENTRAL PAIN VISUAL DEFICITS •

VISUAL FIELD DEFICITS • common among patients with strokes in the middle cerebral artery or posterior cerebral artery distributions. • Bedside testing of visual fields, including examination for extinction with simultaneous stimulation • More formal visual field testing • Patients with isolated visual field deficits, but without concomitant hemispatial neglect, generally learn to compensate effectively. • Improving size of visual fields: • therapist-directed and computer-based training (e.g., Vision Restoration Therapy, Novavision, Inc.)

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EXTRAOCULAR PALSIES AND ASSOCIATED DIPLOPIA • Stroke in the brainstem • Patching is often useful to prevent diplopia • alternated between eyes

DYSPHAGIA • • • • • •

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affect 40% of patients with a unilateral hemispheric stroke more severe and persistent in brainstem lesions or bilateral hemispheric strokes risk factor for pneumonitis and aspiration pneumonia. favorable prognosis may affect either or both the oral preparatory pharyngeal phases of swallowing Bedside evaluation: • observation of the function of the lips, tongue, cheeks, and jaw • elevation of the larynx during swallowing • vocal quality. • oral control, the timeliness of swallowing, presence or absence of a wet vocal quality, and the presence or absence of coughing • patient swallow a small amount of water (30–90 mL) at the bedside If initial screening examination suggests dysphagia • more extensive bedside evaluation by a speech and language pathologist • A videofluoroscopic swallowing study (VFSS) (also called a modified barium swallow) • Swallowing mechanism • Direct visualization of aspiration • FEES • More direct visualization of swallowing • Alternative to VFSS • Avoid radiation present with VFSS • Compensatory and recovery strategies are useful for dysphagia. • Modified food consistencies • pureed foods or thickened liquids • physical maneuvers • controlling food bolus size and pacing, or using a “chin tuck” or double swallow. • It appears likely that practicing swallowing over time improves performance and may enhance the process of spontaneous recovery. • nasogastric, gastrostomy, or jejunostomy tube • hemispheric stroke • patients who cannot swallow safely recover good swallowing • NGT – short term use function • Gastrostomy – Long term use • brainstem lesions or • Not entirely effective in preventing bilateral hemisphere aspiration pneumonia lesions progress more MALNUTRITION • Nutritional Supplementation is necessary • If ineffective – do tube feeding

slowly some require indefinite use of a feeding tube.

MOTOR IMPAIRMENT • •

Strength, power, motor control and coordination, muscle tone, and balance may all be affected by stroke MEDICAL RESEARCH COUNCIL’S (MRC) 6-POINT SCALE, 0 to 5

most widely used clinical scale often supplemented by qualifying descriptions (e.g., “elbow flexion is 4/5 on MRC scale in a flexion synergy pattern with moderately reduced motor control”). DYNAMOMETER – limited use BRUNNSTROM • movement patterns are evaluated and motor function is rated according to stages of motor recover • strength correlates with performance on functional tasks • •

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OTHER TESTS:for Research • FUGL-MEYER SCALE(Fugl-Meyer, et. al) • evaluates strength, reflexes, and coordination, and a composite score is derived on a scale of 0 to 100. • reliable, and repeat scores reflect motor recovery over time. • WOLF MOTOR FUNCTION TEST • MOTOR ACTIVITY LOG • ARM RESEARCH ACTION TEST SPASTICITY OR MUSCLE TONE • Abnormal increases in muscle tone are quite commonly seen in hemiparetic limbs, and patients with more severe spasticity tend to have less well-preserved motor control. • Factors such as posture and limb position can affect spasticity and must be considered when measuring muscle tone. • ASHWORTH SCALE - most widely used for measuring spasticity • MANAGEMENT: • conservatively with stretching and positioning. • injection therapy (principally botulinum toxin, but previously more commonly phenol or alcohol injection) MOTOR RECOVERY • Motor recovery may become evident within hours to days after a stroke • APPROACHES TO FACILITATE AND ENHANCE MOTOR RECOVERY: • Traditional approaches, such as the neurodevelopmental technique advocated by Bobath • little empiric evidence supporting the use of these techniques (NDT, Brunnstrom, Rood, PNF)

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functionally oriented exercise training (such as practicing transfers and early ambulation), • increasingly replaces traditional techniques repetitive task-oriented practice. Neurodevelopmental (NDT) exercises

NEW TECHNIQUES • Constraint-Induced Movement Training (CIMT) • intensive short course (generally 2 weeks) of upper limb training with repetitive task-oriented practice and behavioral shaping techniques to enhance not only motor control of the upper limb but also incorporation into behavioral repertoires. • MECHANISM: unknown; overcome “learned nonuse” of the weak limb • Robot-Aided Exercise • used by individuals with more severe paresis after stroke • Upper limb devices, such as the InMotion2 (Interactive Motion Technologies, Cambridge, MA), have been shown to provide benefit in both the acute and chronic phases of stroke . • Lower limb robotic systems have been developed for gait training • not proven superior to comparably dosed hands-on therapy • Electrical stimulation of the limb (sometimes termed therapeutic electrical stimulation or functional neuromuscular stimulation) • treatment for hemiparesis • may be beneficial in restoring motor use to some extent • Biofeedback using electromyogram (EMG) signals • used in an attempt to improve motor control poststroke. • Results of trials have been mixed

THERAPY FOR MOBILITY • HEMIPLEGIC PATIENTS • intensive gait training when therapy consists of walking on a treadmill with body weight partially supported (PBWSTT) with a harness • Robotic therapy • proposed as an alternative to PWBSTT training, • Lokomat (Hocoma, Inc.) and the ReoAmbulator (Motorika, Inc • therapist-assisted locomotor training with a treadmill is more effective

SENSORY IMPAIRMENT AND CENTRAL PAIN • •

Sensory impairment may occur with or without accompanying motor weakness following a stroke loss of proprioception generally results in reduced motor performance even in the absence of weakness

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CENTRAL PAIN SYNDROME • Lesions of the thalamus may cause severe contralesional sensory loss and result in a central pain syndrome • strokes involving the spino-thalamo-cortical pathway • begins a few weeks after stroke onset and becomes intractable to conventional medications • described as burning in character

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PERCEPTUAL IMPAIRMENT • often seen in parietal lobe lesions

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Manifestation: • inability to perceive stimulation of the affected side during simultaneous bilateral stimulation (extinction), • reduced two-point discrimination, • reduced object recognition (stereognosis), • impaired recognition of digits drawn in the palm (graphesthesia).

MANAGEMENT: • Sensory loss – few interventions • Central pain • PHARMACOLOGIC: • TRICYCLIC ANTIDEPRESSANTS • Some have inadequate response • Problematic Anticholinergic side effects (-) • Anticonvulsants(gabapentin or lamotrigine) • Some efficacy

 OUTCOME AND PROGNOSTICATION IN STROKE REHABILITATION Important elements of prognosis • Prospects of survival • Degree of recovery • Extent of possible residual disability

Developing accurate prognostic models • Complex functions of the brain • stroke lesion location and size • Limitation of assessment technique • Impact of baseline factors • Age • Comorbid conditions • Personality and coping abilities • Social factors

Predicting Survival  Coma following a stroke onset indicates a poor prognosis  when it occurs in relation to cerebral infarction, it reflects a large lesion with cerebral edema.  Early death following a stroke is usually related to the underlying pathology, the patient’s age, and to the severity of the lesion. First cerebral

Hemorrhagic stroke

infarction Ag e

Survival at 30 days 88%- 92%

62%- 63%

88%- 92%

55%

4564 65 I.

Predicting Disability and Functional Status key outcomes: 1. restoration of function 2. community reintegration

central purpose: lessen ultimate disability

prognosis for recovery from • lacunar lesions is usually excellent • large vessel infarctions is related to the volume of the lesion • 54% - 80% walk independently within the first 3 months post stroke • 80% independent in mobility • 47% and 76% of survivors achieve partial or total independence in ADLs The capacity of individuals to perform these activities is usually scored on ADL scales, such as the Functional Independent Measure (FIMR)  Other important variables include age and sitting balance  The effect of age on outcome may partly be related to more frequent comorbid diseases and functional impairments •

initial ADL assessment • (most commonly, the FIM score) • The single most useful predictor of functional outcome

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Post-Stroke Rehabilitation Outcomes Project • better outcomes if admitted into a rehabilitation program early • reduce the likelihood of secondary complications and help patient motivation

II. •

Social Variables long-term institutional care • need maximum physical assistance in ADLs • bowel or bladder incontinence

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prestroke family interaction and the presence of an able spouse The best estimate of prognosis can be made only after a thorough and comprehensive evaluation of the patient’s medical, neurologic, functional, and psychosocial statuses.

MEDICAL MANAGEMENT DURING REHABILITATION • There is a high incidence of comorbid medical disorders among patients recovering from stroke, reflecting the of the patient population and the fact cerebrovascular disease is often part generalized disease process • medical complications frequently occur during the postacute phase of rehabilitation I. Cardiac Disease  a stroke is an acute event in the course of a systemic disease

age that of a

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embolic stroke o Atherosclerosis o hypertensive vascular disease Common problems: o cardiac disease • Angina 75% evidence of coexisting cardiovascular disease • uncontrolled hypertension o hypertension (50% to 84%) • Hypotension o coronary artery disease (65%) • myocardial infarction cardiogenic cerebral embolism • congestive heart failure o atrial fibrillation • atrial fibrillation o arrhythmias from multiple causes • ventricular arrhythmias o valvular disease o cardiomyopathy o endocarditis o recent myocardial infarction Concomitant heart disease has a negative impact on short-term and long-term survival and probably on functional outcome of stroke patients Acute exacerbations of heart disease occur frequently during postacute stroke rehabilitation Congestive heart failure and angina decrease exercise tolerance

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Urinary Tract o Urinary function can be affected in • Acute management: ways by stroke, including urinary Catheterization infection, urinary retention, and urge • Anticholinergic incontinence. medications acute stroke • oxybutynin o urinary retention due to altered chloride status (Ditropan) o direct effects of the stroke on the • tolterodine neurological control of micturition (Detrol)  Men: Premorbid voiding dysfunction  Women: stress incontinence Disinhibition of the bladder detrusorà urinary frequency and urgency Noninvasive measurement of bladder volume using ultrasound

several

mental

MUSCULOSKELETAL PAIN AND COMPLEX REGIONAL PAIN SYNDROME • develop several weeks to 6 months postonset • more intensive and earlier rehabilitation programs incorporating range-of-motion exercises • pain in most patients with hemiplegia • glenohumeral subluxation *- most common cause Preventative measures for • spasticity shoulder pain • Contracture • Proper positioning • Supporting the arm VENUS THROMBOEMBOLISM • avoiding traction -All patients with significant immobility related to stroke should • Spasticity receive DVT prophylaxis • botulinum toxin • DVT prophylaxis • phenol injections • Low dose subcutaneous heparin • Low molecular weight heparin

• external pneumatic compression devices preventive measures for upper limb venous duplex ultrasound imaging newly diagnosed DVT should immediately receivecomplex regional pain syndrome • Frequent passive range of full-dose anticoagulation with low molecular weight motion heparin • desensitization with • therapeutic INR (between 2 and 3) massage • Acute DVT - bed rest for 24 hours • Inferior vena cava filter to prevent pulmonary embolism • active incorporation of the • cannot safely receive anticoagulation paretic upper limb DEPRESSION • relationship between left frontal or bifrontal lesions and major depression • Theories: • stroke may result in brain catecholamine depletion through lesion-induced damage to the frontal noradrenergic, dopaminergic, and serotonergic projections • •

• Active treatment reliable indicators: • standard • Persistently depressed antidepressant mood medications • loss of interest in • SSRIs socialization • stimulant medication • limited participation in the (methylphenidate) SEXUALITY rehabilitation program • sexual dysfunction • reductions both in libido and sexual performance • psychosocial and medical issues • Stroke is most common in • Older • Hypertension • Diabetics • Prevalence: 57% and 75% after stroke • Fears • most practitioners agree that resuming sexual activity is safe and appropriate after discharge from the hospital • 82% of those who experienced erectile dysfunction after stroke improved spontaneously within a few months • Iatrogenic • SSRI antidepressants (fluoxetine and paroxetine) • antihypertensives,(b-blockers) • Anticonvulsant • Management • Phosphodiesterase-5 inhibitors • (sildenafil (Viagra) • Late issues • tadalafil (Cialis) • Depression • counseling • Spasticity • Contracture Ongoing Care • Osteoporosis • continued improvement in motor function is • weight gain possible in stroke survivors even after years of • Deconditioning stable chronic deficits •

rehabilitation needs may extend for many years after the initial even periodic physiatric ass