Cerebrovascular Accident (CVA)

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

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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

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-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

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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:

CN affectation

Neurological Deficit by the artery involved:

MCA- UE>LE, aphasia, visual agnosia

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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)

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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

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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

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

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◦ ex: Management for TIA is different from the management of mild stroke

Temporal Classification of Stroke

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

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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

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

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Temporal Classification of Stroke

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

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may be the only warning of an impending stroke

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

1. Ischemic Stroke

◦ caused by a decreased blood supply to the brain

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◦ 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

Classification of Ischemic StrokeThrombotic

Most common type of stroke

Accounts for ~40% of all stroke

Has a gradual onset

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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)

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:

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◦ 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

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

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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

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

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> 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

◦ Vomiting at onset in 22–44%.

◦ 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

90–95% 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)

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

usually asymptomatic prior to rupture

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 32

Embolism 32

Small vessel occlusion, lacunar 18

Intracerebral hemorrhage 11

Subarachnoid hemorrhage 7

Pathophysiology

Atherosclerosis, cerebral edema, bleeding

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↓

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

Risk Factors:Non-modifiable (Biological indicators)

1. Age

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◦ 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

Risk Factors:Modifiable

1. Hypertension (A)

◦ the most important modifiable risk factor

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◦ 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

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

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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

◦ > 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

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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

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.

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Determinants of Severity of Neurological deficits

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)

◦ Gait apraxia (if corpus callosum is affected)

If both anterior cerebral territories are affected, profound mental symptoms may result (akinetic mutism)

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MCA SyndromeSuperior 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 Broca’s aphasia (motor speech disorder)

5. Right side lesion (nondominant hemisphere)

- deficits on spatial perception, hemineglect, constructional apraxia, dressing apraxia

MCA SyndromeInferior division

blood supply to the lateral temporal and inferior parietal lobes

Left side lesion

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◦ Wernicke’s 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

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

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◦ amnesia (memory loss)

4. Cerebral peduncle

◦ Contralateral hemiplegia

5. Brainstem

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

◦ Weber syndrome

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)

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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

◦ Crossed signs: motor or sensory deficit on ipsilateral side of face and contralateral

◦ side of body; ataxia, dysphagia, dysarthria

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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

◦ 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

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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

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

◦ Horner’s 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

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◦ Vertigo; nausea and vomiting

◦ Hiccups

◦ 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 hemisphere—dominant parietal lobe

Artery: middle cerebral artery

Symptoms:

Agraphia

◦ acalculia

◦

◦ Finger agnosia

◦ Right and left disorientation

Anton syndrome

Anatomy: cerebral hemispheres—bilateral occipital lobes

Artery: posterior cerebral artery (bilateral basilar artery)

Symptoms: visual loss—bilateral

◦ Unawareness or denial of blindness

Weber syndrome

• Anatomy: midbrain–base

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• Artery: posterior ocerebral artery (penetrating branches t midbrain)

• Symptoms: contralateral hemiparesis

• Ipsilateral lateral gaze weakness

Dejerine–Roussy syndrome

• Anatomy: thalamus

• Artery: posterior cerebral artery—penetrating branches to thalamus

• Symptoms: hemisensory loss—all modalities

• Hemi-body pain

Medical ManagementGoals

1. improve cerebral perfusion, re-establish circulation & O2

◦ O2 via mask or nasal cannula

◦ coma – assisted ventilation, suctioning, intubation

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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 Pº relief should be done every 15 – 20 mins. or 10 – 15 mins.

Pharmacological Management

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

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◦ 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

◦ 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

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◦ Diuretics, Beta blockers, ACE inhibitor , Ca channel blockers

4. anti- spasticity drugs

◦ Diazepam/ Benzodiazepine (BNz) vs. baclofen & dantrolene sodium

Tests & Measures(Laboratory Tests)

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

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Tests & Measures(Imaging Studies)

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

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4. Magnetic resonance angiography (MRA)

◦ may be used to evaluate the carotid circulation, the vertebral-basilar system, the circle of Willis, and the 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

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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

◦ 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)

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◦ Late return of proprioceptive facilitation (tapping) response > 9 days

◦ Late return of proximal traction response (shoulder flexors/adductors) > 13 days

OTHER RISK FACTORS FOR DISABILITY AFTER STROKE

Global aphasia

Severe neglect

Sensory and visual deficits

Impaired cognition

Delay in medical care

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Delay in rehabilitation

Bilateral lesions

Previous stroke

Previous functional disability

Diabetes mellitus

Cardiac disease

Electrocardiograph abnormalities

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

ImpairmentsI. Sensory

impaired but rarely absent on the hemiplegic side

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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

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), Pº, light (bright), sounds, Tº (hot or cold)

◦ prevents the patient from actively participating in rehabilitation

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II. Motor

1. Weakness or paralysis

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 1º 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 mov’t.

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III. Abnormal reflexes

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

◦ Consist of ab(N) automatic response of the involved limb, resulting from acton occurring in some part of the

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body by voluntary or reflex stimulation (yawning, sneezing, or coughing)

◦ SOUQUE’S PHENOMENON

Elevation of the hemi. arm above the horizontal plane may elicit an extension and abd. response of the fingers

◦ RAIMESTE’S 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)

◦ apraxia (basal ganglia lesion or cerebellar lesion)

Ipsilateral Pushing/ Pusher’s syndrome/ Controversive Syndrome

◦ unusual motor behavior characterized by active pushing of the stronger ms. esp. towards the weak side

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◦ 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 1º Visual cortex (if PCA is affected)

Monocular blindness

Visual neglect (visual inattention)

◦ ® Hemispheric lesion = visuospatial neglect

Forced gazed deviations

◦ Hemispheric lesion

the px’s eye deviate away from hemiplegic side

◦ Brainstem lesion

px’s eye deviate towards the hemiplegic side

VI. Speech, Language & Swallowing

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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

VII. Perception

Due to lesion of the parietal lobe of the non-dominant hemisphere

1. Spatial relations disorder

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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

figure–ground 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.

◦ Simultagnosia or Autopagnosia

impairment of body scheme

Lack of awareness of the body structure and relation of body parts on one’s 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

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◦ 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.

6. Apraxia

◦ Disorder of vol. learned mov’t.

◦ Inability to perform purposeful mov’t 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.

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Inability to perform a purposeful motor act bec. pt. can’t understand the overall concept of act, can’t retain the idea of the task and can’t 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.

◦ Dressing Apraxia

Inability to dress one’s 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

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delirium

IX. Emotional Status

pseudobulbar affect (PBA)

◦ also known as emotional lability or emotional dysregulation syndrome

◦ 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

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◦ Persistent incontinence is associated with a poor long-term prognosis for functional recovery

◦ Treatments

◦ – 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. NDT’s (Bobath)

4. Brunnstrom’s movement therapy

5. Rood’s tech.

6. Motor relearning (Carr and Shepard Approach)

7. FES, ES

Bobath

◦ Stage 1- Flaccidity

◦ Stage 2- Spasticity

◦ Stage 3- Relative Recovery

PNF

Indicated for patients with orthooedic and neurologic condition

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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

Factors that might influence the timing of rehabilitation effect include:

1. Medical stability

2. motivation

3. Patient endurance

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4. stage of recovery

5. ability to learn

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