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Cerebrovascular Accident(Stroke)

JACQUELYN ARAO

I.Definition of Terms:

Cerebrovascular Accident

- Also know as stroke and brain attacks

-is a sudden loss of neurological function caused by an interruption of the blood flow to the brain

I. Definition of terms

-It is a non-traumatic brain injury caused by occlusion or rupture of cerebral blood vessel that results in sudden neurological deficit characterized by loss of motor control.

I. Definition of Terms

Aneurysm

-It is a localized dilatation or bulging of the blood vessels especially arteries

- It promotes rupture of the vessel as it continues to bulge.


APOPLEXY – sudden strike of paralysis, dumbness or fainting, from which victim is frequently failed to recover

o Atherosclerosis

-Formation of multiple plaques within the blood vessels.


Embolus

- an object that migrates from one part of the body to causes blockage or occlusion to another part of the body.

I. Definition of terms

Hematocrit

-Also know as Packed Cell Volume (PCV) or Erythrocyte Volume Fraction (EVF)

-is the proportion of the blood volume, which is occupied by red blood cell.


Hemorrhage

-Is the loss of blood at the circulatory system or excessive presence of blood outside the circulation

- Can be internally or externally.


Hypertension– Also referred to as high blood pressure (HTN or

HPN.) – It is a medical condition in which the blood

pressure is chronically elevated

Infarction

-A process of anoxic death of tissue due to loss of blood supply because of occlusion or blockage of the artery


Ischemic

-Insufficient blood flow to an organ cause by the blockage of the artery.

Transient Ischemic Attack

-(Mini Stroke) Caused by changes in blood supply in the brain produces same manifestation as stroke within 24 hours.


Thrombus

- Is the final product of the blood coagulation step in hemostasis It is achieved via the aggregation of platelets that form a platelet plug. It is physiologic in injury but pathologic in case of thrombosis

II. Epidemiology

Stroke is the third leading cause of death. The most common cause of disability among

adults at the United States It is approximately 700,000 individuals was

affected each year.

II. Epidemiology

About 500,000 are new strokes and 200,000 are recurrent strokes (Usually people older than 65 y/o).

In United States, in 1960’s 200 per 100,000 are affected by stroke and it was decreased as it reached to late 1960’s –1970’s.

II. Epidemiology

In 1980’s the stroke is flattened because of the improvement of cranial computed tomography (CT) and Magnetic Resonance imaging (MRI).

According to age, 28% higher possibilities in people older than 65 y/o than younger ones

II. Epidemiology

According to sex, having an incidence of stroke, Men are 19% higher rather than women.

According to race, Black Americans are more prone rather that White Americans.

Asian Countries are more prone having stroke compared to United States. (Cause by intracranial hemorrhage)

Causes Percentage

Large vessel occlusion/infarction

32

Embolism 32

Small vessel occlusion/ lacunar

18

Intracerebral hemorrhage 11

Subarachnoid hemorrhage 7

II. Epidemiology

Table 77-2 Causes of stroke (Delisa)

II. Epidemiology

Most of the patients who die from acute stroke succumb in the first 30 days.

Survival in the first 30 days of new stroke reported to be 70- 85% dependent on the stroke type.

II. Epidemiology

In Intracerebral Hemorrhage is only 20-50% , cause death usually occur in first 3 days.

In Cerebral infraction is 85%. After 30 days of survival, the death rate

declines.

III. Epidemiology

Stroke is most commonly cause of chronic disability.

Through the survivors, 1/3 of them are dependent on ADL, ambulation and speech.

II. Etiology

A. Atherosclerosis

-Major contributory factor of Cerebrovascular Accident.

-accumulation of lipids, fibrins, complex carbohydrates and calcium deposit on the arterial walls that leads to progressive narrowing of blood vessels.

Found in the bifurcations of MCA and origin of ICA.

II. Etiology

B. Ischemic Strokes

-Results from a thrombus, embolism or conditions that produce low systemic perfusions pressures.

II. Etiology

C. Cerebral Thrombosis– Refers to the formation of development of

a blood clot within the arteries and their branches.

– Moving thrombus is called embolus.

II. Etiology

Thrombosis Ischemia Infarction IntraCerebral Hemorrhage

– Is cause by the ruptured of cerebral vessel with subsequent bleeding to brain

Types of IntraCerebral Hemorrhage

II. Etiology

-Primary CEREBRAL Hemorrhage -occurs in small blood vessels

weakened by atherosclerosis produces aneurysm.-SUBARACHNOID hemorrhage

-hemorrhage occurs at the sub arachnid space typically from a saccular or berry aneurysm affecting primary vessels.

II. Etiology

E. Artriovenous malformation– Is a congenital defect that can cause

stroke.

-The arteries and veins are tortuous tangled with interposing capillaries system.

III. Risk Factors of Stroke

Hypertension- Is the most important risk factors– It is define as a blood pressure higher than

160/95 mmHg.– Among the survivors of stroke, 67% of them

have chronic hypertension– It gives risk in cerebral infarction,

thrombotic, lacunars and hemorrhagic stroke.


2. Heart disease– Is an important risk factor for stroke– Atrial fibrillation and valvular heart disease

increase the risk of cerebral infarction because of presence of cerebral emboli.


3.Diabetes Mellitus Independent risk factor that doubles

the risk of stroke. It increases the risk of ischemic stroke

to three to six times. The prevalence of diabetes among

stroke survivors is 20%.


4. Hyperlipidemia – Poses only small additional risk for strokes

mainly for individuals younger at age of 55.

– Increase in blood viscosity, hematocrit and serum fibrinogen have been implied the risk factor of stroke.

Risk Factors of stroke

Smoking– It is an important factor for cardiovascular

disease but influence for stroke is not cleared.

– The risk for heavy smokers (>40 cigarettes) is twice than light smokers (<10 cigarettes).

III. Risk Factors Of Stroke

- Some studies that smoking to an increased risk of hemorrhagic stroke in addition to ischemic cerebral infarction.

III. Risk factor of stroke

6. Transient Ischemic Attack

-Is another important risk factor.

- An About 10 % of individuals with TIA will go on to have a major stroke within 90 days and 5 % will have a major stroke within 2 days.

III. Risk Factors of stroke

7. Obesity– Hypertension and diabetes mellitus are in

common in obese and strong influences risk of stroke.

– Some studies says that weight loss has positive influences on blood pressure and diabetic control and also helps in reduction of risk of strokes.

IV. Stroke Prevention

Active promotions of lifestyle changes by physicians have the best potential to decrease the annual rate of new stroke occurrence.


To the individuals who have a stroke in the past history additional intervention and medication was given like:

-Antiplatelet therapy

- Anticoagulation

-Carotid Endarterectomy.


Antiplatelet Therapy

-Aspirin is the most frequently prescribe antiplatelet agent.

-Aspirin achieves a significant anti platelet effect at fairly low serum concentrations.


Anticoagulation

-The use of Warfarin anticoagulation for primary stroke prevention in non-valvular atrial fibrillation.

-Warfarin reduces relative stroke risk by 58%to 86%over that in control subjects.


Carotid Endarterectomy– Is a surgical procedure that use to correct

the carotid stenosis– It is the removal of material inside the

artery.

PRINCESS PUNO

PATHOPHYSIOLOGY

CEREBRAL BLOOD FLOW (CBF)

Controlled by auto-regulatory mechanism that modulates a constant rate of blood flow through the brain.

These mechanisms provide homeostatic balance.


Normal: 50-60 ml/100g/min Reversible: 20ml/100g/min Irreversible: 10ml/100g/min


Factors Affecting CBF: Chemical regulation of CBF occurs in response to

changes in blood concentration of CO2 or O2.

Increase or decrease blood pH Changes in blood viscosity or intracranial pressure (ICP)

– CEREBRAL EDEMA Changes in blood pressure produces minor alterations

of CBF

EXCITOTOXICITY

The pathological process by which nerve cells are damaged and killed by glutamate and similar substances.

ISCHEMIC CASCADE

Within seconds to minutes of the loss of perfusion to a portion of the brain, an ischemic cascade is unleashed.

CLASSIFICATIONS OF STROKE

• Ischemic Thrombus Embolism Lacunar

• Hemorrhagic Subarachnoid Intracerebral

ISCHEMIC STROKE

ThrombusDue to Atherosclerotic Plaque FormationOccurs frequently at major vascular branching

sites including COMMON CAROTID and VERTEBROBASILAR ARTERIES.

Occurs often in the presence of chronic hypertension.

ISCHEMIC STROKE

EmbolismMajor Source of cerebral emboli is the heart.

– Atrial fibrillation– Most emboli lodge in the middle cerebral

artery distribution because 80% of the blood carried by the large neck arteries flow through the middle cerebral arteries.

ISCHEMIC STROKE

Most Frequent Target:– Superficial branches of cerebral and

cerebellar arteries.

ISCHEMIC STROKE

ISCHEMIC STROKE

Lacunars InfarctLacunar infarcts occur as a result of an

occlusion of small, deep penetrating arteries known as Lenticulostriate Arteries branch from the MCA.

Occlusions of these vessels or penetrating branches of the circle of Willis, including vertebral or basilar arteries, are referred to as lacunar strokes.

ISCHEMIC STROKE

Small arteriole becomes torturous and develops subintimal dissection and micro-aneuryms rendering the arteriole susceptible to occlusion from micro-thrombi.

Fibrin Deposition

HEMORRHAGIC STROKE

Subarachnoid HemorrhageBleeding that occurs between the Dura

and Pia Mater.Commonly caused by:

1.ARTERIOVENOUS MALFORMATION (AVM)

1.ANEURYSMS

HEMORRHAGIC STROKE

1. AVM• Tangled, dilated blood vessels in which arteries flow

directly into veins.• Occur most often at the junction of cerebral arteries,

usually within the parenchyma of the frontal-parietal region, frontal lobe, lateral cerebellum, or overlying occipital lobe.

• Results to seizures.

HEMORRHAGIC STROKE

2. Aneurysms• Focal dilations in the artery• Found in the anterior region of the Circle of Willis,

particularly near branches of the Anterior Communicating Artery, ICA, MCA and junctions of almost any branch site.

• Contributing factors include atherosclerosis and hypertension.

HEMORRHAGIC STROKE

Intracerebral Hemorrhage Originates from deep penetrating vessels and causes

injury to the brain tissue by disrupting connecting pathways and causing localized pressure injury.

Bleeding in the surrounding brain tissue. Also caused by AVM and aneurysms.

OCCLUSIONS IN THE ARTERIES

• ANTERIOR CEREBRAL ARTERY (ACA) First of the two terminal branches of the internal carotid

artery (ICA). It supplies the medial aspect of the cerebral hemispheres (frontal and parietal) and subcortical structures, including basal ganglia.

Proximal occlusion results to minimal defects since the Anterior Communicating artery allows perfusion of the proximal ant. cerebral artery.

ACA occlusions are uncommon.ACA


• INTERNAL CAROTID ARTERY (ICA) There is a complete occlusion if ICA produces massive

infarction in both MCA and ACA territories. – Incomplete occlusions can produce mixture of MCA and

ACA symptoms. Extensive cerebral edema occurs and frequently leads

to coma and death.

ICA


• POSTERIOR CEREBRAL ARTERY (PCA) Two posterior arteries arise as terminal branches of the

basilar artery and each supplies corresponding occipital and temporal lobes.

Also supplies the brainstem, midbrain and posterior diencephalons, including most of the thalamus.

Occlusions proximal to the posterior communicating artery (PICA) typically results in minimal deficits owing to the collateral blood supply from the PICA.

PCA


• VERTEBROBASILAR ARTERYArise from the subclavian arteries and travel

into the brain along the medulla where they merge at the inferior border of the pons to form the basilar artery.

It supplies the pons, internal ear, and the cerebellum.

The basilar artery terminates at the upper border of the pons and gives rise to two PCA.

SIGN AND SYMPTOMS COMPLICATION

MARIVIC CALINGA

DEFINITION OF TERMS

DEEP VEIN THROMBOSIS(DVT)- is a blood clot (thrombus) in a deep vein, usually in the legs.

CARDIAC DECOMPENSATION- may refer to the failure of the heart to maintain adequate blood circulation, after long-standing (previously compensated) vascular disease.

PULMONARY ASPIRATION- the entry of secretions or foreign material into the trachea and lungs

DEFINITION OF TERMS

DYSPHAGIA- is the medical term for the symptom of difficulty in swallowing

HEMIPARESIS- is weakness on one side of the body.

ABULIA- refers to a lack of will or initiative. The patient is unable to act or make decisions independently. It may range in severity from subtle to overwhelming

DEFINITION OF TERMS

WEBER’S SYNDROME- (superior alternating hemiplegia) is characterized by the presence of an oculomotor nerve palsy and contralateral hemiparesis or hemiplegia.

MEDIAL MEDULLARY SYNDROME- also known as inferior alternating syndrome, hyploglossal alternating hemiplegia, or lower alternating hemiplegia, is a set of clinical features resulting from an infarct in the anterior spinal artery, which supplies the medial part of the medulla oblongata.

DEFINITION OF TERMS

LATERAL MEDULLARY SYNDROME- (also called Wallenberg's syndrome and posterior inferior cerebellar artery syndrome) is a disease in which the patient has difficulty with swallowing or speaking or both owing to one or more patches of dead tissue (known as an infarct) caused by interrupted blood supply to parts of the brain.

MEDIAL PONTINE SYNDROME- results from occlusion of paramedian branches of the basilar artery.

LATERAL PONTINE SYNDROME- It can be caused by an interruption to the blood supply of the anterior inferior cerebellar artery.

COMPLETE BASILAR SYNDROME- The cause of VD is atherosclerosis and vertebrobasilar insufficiency in the brain caused by blockage (occlusion).

SIGN AND SYMPTOMS

MARIVIC R. CALINGA

SIGN AND SYMPTOMS…

Symptoms of stroke depend on the type and which area of the brain is affected. Signs of ischemic stroke usually occur suddenly, and signs of hemorrhagic stroke usually develop gradually. Symptoms include the following:


Difficulty speaking or understanding speech (aphasia)

Difficulty walking Dizziness or lightheadedness (vertigo) Numbness, paralysis, or weakness, usually on

one side of the body Seizure (relatively rare) Severe headache with no known cause Sudden confusion


Sudden decrease in the level of consciousness

Sudden loss of balance or coordination Sudden vision problems (e.g., blurry vision,

blindness in one eye) Vomiting

Clinical Manifestations of Anterior Cerebral Syndrome

The most common characteristic of ACA syndrome is contralateral hemiparesis and sensory loss with greater involvement of the lower extremity because the somatotopic organization of the medial aspect of the cortex includes the functional area for the extremity.

Sign and Symptoms Structures involved

Contralateral hemiparesis involving mainly the LE

Primary Motor Area, medial aspect of cortex, internal capsule

Contralateral hemisensory loss involving mainly the LE

Primary Motor Area, medial aspect of cortex

Urinary Incontinence Posteromedial aspect of superior frontal gyrus

Problems with imitation and bimanual tasks, apraxia

corpus callosum


Abulia (akinetic mutism), slowness, delay, lack of spontaneity, motor inaction

Uncertain localization

Contralateral grasp reflex, sucking reflex Can be asymptomatic if circle of Willis is competent

Uncertain localization


Clinical Manifestations of Middle Cerebral Artery Syndrome

The most common characteristic of MCA syndrome are contralateral spastic hemiparesis and sensory loss of the face, upper extremity, and lower extremity, with the face and UE more involved than the LE. Lesions of the parieto-occipital cortex of the dominant hemisphere typically produced aphasia. Lesions of the right parietal lobe of the nondominant hemisphere typically produce perceptual deficits. Homonymous hemianopsia is also a common finding. The MCA is the most common site of occlusion in stroke.

Sign and Symptoms Structures Involved

Contralateral hemiparesis involving mainly the UE and face

Primary motor cortex and internal capsule

Contra;ateral hemisensory loss involving mainly the UE and face

Primary sensory cortex and internal capsule

Motor speech impairment: Wernicke’s or fluent aphasia with impaired auditory comprehension and fluent speech with normal rate and melody

Wernicke’s cortical area (posterior portion of the temporal gyrus)



Global Aphasia: nonfluent speech with poor comprehension

Both third convolution and posterior portion of the superior temporal gyrus

Perceptual deficits: unilateral neglect, depth perception, spatial relations, agnosia

Parietal sensory association, cortex in the nondominant hemisphere

Limb-kinetic apraxia Premotor or parietal cortex

Contralateral homonymous hemianopsia

Optic radiation in internal capsule

Loss of conjugate gaze to the opposite side

Frontal eye fields on their descending tracts


Ataxia of contralateral limb(s) (sensory ataxia)

Parietal lobe

Pure motor hemiplegia (lacunar stroke)

Upper portion of posterior limb of internal capsule

Clinical Manifestations of Posterior Cerebral Artery Syndrome

Occlusion of thalamic branches may produce hemianesthesia or central post-stroke pain. Occipital infarction produces homonymous hemianopsia, visual agnosia, prosopagnosia, or bilateral, cortical blindness. Temporal lobe ischemia results in amnesia. Contralateral hemiplegia occurs with involvement of the cerebral peduncle.


Sign and Symptoms Structures Involved

Peripheral territory

Contralateral homonymous hemianopsia

Primary visual cortex or optic radiation

Bilateral homonymous hemianopsia with some degree of macular sparing

Calcarine cortex (macular sparing is due to occipital pole receiving collateral blood supply from MCA)

Visual agnosia Left occipital lobe

Prosopagnosia (difficulty naming people on sight)

Visual association cortex

Dyslexia (difficulty reading) without agraphia (difficulty writing), color naming (anomia), and color discrimination problems.

Dominant calcarine lesion and posterior part of corpus callosum

Memory defect Lesion of inferomedial portions of temporal lobe bilaterally or on the dominant side only

Topographic disorientation Nondominant primary visual area, usually bilaterally



Central territory

Central post-stroke (thalamic) painSpontaneous pain and dysenthesias; sensory impairments (all modalities)

Ventral posterolateral nucleus of thalamus

Involuntary movements; choreoathetosis, intention tremor, hemiballismus

Subthalamic nucleus or its pallidal connections

Contralateral hemiplegia Cerebral peduncle of midbrain

Weber’s syndromeOculomotor nerve palsy and

contralateral hemiplegia

Third nerve and cerebral peduncle of midbrain

Paresis of vertical eye movements, slight miosis and ptosis, and sluggish papillary light response

Supranuclear fibers to third cranial nerve


Clinical Manifestations of Vertebrobasilar Artery Syndromes

Patient develops acute hemiparesis rapidly progressing to tetraplegia and lower bulbar paralysis. Initially the patient is dysarthric and dysphonic but rapidly progress to mutism. There is preserved consciousness and sensation. Thus the patient cannot move or speak but remains alert and oriented. Horizontal eye movements are impaired but vertical eye movements and blinking remain intact.


Signs and Symptoms Structure Involved

Medial medullary syndrome Occlusion vertebral artery, medullary branch

Ipsilateral to lesionParalysis with atrophy of half the tongue with deviation to the paralyzed side when tongue is protruded

CN XII, hypoglossal, or nucleus

Contralateral to lesionParalysis of UE and LE

Corticospinal tract

Impaired tactile and propricoceptive sense

Medial lemniscus


Lateral medullary (Wallenburg’s) syndrome

Occlusion of posterior inferior cerebellar artery or vertebral artery

Ipsilateral to lesionDecreased pain and temperature sensation in face

Descending tract and nucleus of CN V, Trigeminal

Cerebellar ataxia: gait and limbs ataxia

Cerebellum of inferior cerebellar peduncle

Vertigo, nausea, vomiting Vestibular nuclei and connections

Nystagmus Vestibular nuclei and connections

Horner’s syndrome: miosis, ptosis, decreased sweating

Descending sympathetic tract


Dysphagia and dysphonia: paralysis of palatal and laryngeal muscles, diminished gag reflex

CN IX, glossophraryngeal, and CN X, vargus, or nuclei

Sensory impairment of UE, trunk, or LE

Cuneate and gracile nuclei

Contralateral to lesionImpaired pain and thermal sense over 50% of body, sometimes face

Spinal lemniscus-spinothalamic tract

Complete basilar artery syndrome (locked-in syndrome)

Basilar artery, ventral pons


Tetraplegia (Quadriplegia) Corticospinal tracts bilaterally

Bilateral cranial nerve palsy: upward gazed spared

Long tracts to cranial nerve nuclei bilaterally

Coma Relicular activating system

Cognition spared

Medial Inferior pontine syndrome

Occlusion of paramedian branch of basilar artery

Ipsilateral to lesionParalysis of conjugate gaze to side of lesion (preservation of convergence)

Pontine center for lateral gaze paramedian pentine reticular formation (PPRF)


Nystagmus Vestibular nuclei and connections

Ataxia of limbs and gait Middle cerebellar peduncle

Diplopia on lateral gaze CN VI, abduncens, or nucleus

Contralateral to lesionParesis of face, UE, and LE

Corticobulbar and corticospinal tract in lower pons

Impaired tactile and proprioceptive sense over 50% of the body

Medial lemniscus



Lateral inferior pontine syndrome

Occlusion of the anterior inferior cerebellar artery, a branch of the basilar artery

Ipsilateral to lesionHorizontal and vertical nystagmus, vertigo, nausea, vomiting

CN VIII, vestibular, or nucleus

Facial paralysis CN VII, facial or nucleus

Paralysis of conjugate gaze to side of lesion

Pontine center of lateral gaze (PPRF)

Deafness, tinnitus CN VIII, cochlear, or nucleus


Ataxia Middle cerebellar peduncle amd cerebellar hemisphere

Impaired sensation over face Man sensory nucleus and descending tract of fifth nerve

Contralateral to lesionImpaired pain and thermal sense over half body (may include face)

Spinothalamic tract

Medial midpontine syndrome Occlusion of paramedian branch of mid-basilar artery

Ipsilateral lesionAtaxia of limbs and gait (more prominent in bilateral involvement)

Middle cerebellar peduncle


Contralateral lesionParalysis on face, UE and LE

Corticobulbar and corticospinal tract

Deviation of eyes PPRF

Lateral midpontine syndrome Occlusion of short circumferential artery

Ipsilateral lesionAtacia of limbs

Middle cerebellar peduncle

Paralysis of muscles on mastification

Motor fibers of nucleus of CN V, trigeminal

Impaired sensation over side of face

Sensory fibers or nucleus of CN V, trigeminal


Medial superior pontine syndrome

Occlusion of paramedian branches of upper basilar artery

Cerebellar ataxia Superior or middle cerebellar peduncle

Internuclear ophthalmoplegia Medial longitudinal fasciculus

Contralateral lesionParalysis of face, UE, and LE

Corticobulbar and corticospinal tract



Lateral superior pontine syndrome (occlusion of superior cerebellar artery, a branch of the basilar artery)

Ipsilateral lesionCerebellar ataxia of limbs and gait, falling aside of lesion

Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus

Dizziness, nausea, vomiting Vestibular nuclei

Horizontal nystagmus Vestibular nuclei

Paresis of conjugate gaze (ipsilateral)

Uncertain


Loss of optokenetic nystagmus Uncertain

Horner’s syndrome: miosis, ptosis, decreased sweating on opposite side face

Descending sympathetic fibers

Contralateral lesionImpaired pain and thermal sense of face, limbs, and trunk

Spinothalamic tract

Impared touch, vibration, and position sense, more in LE than UE (tendency to incongruity of pain and touch deficits)

Medial lemniscus (lateral portion)

COMPLICATION

COMPLICATION…

Complications may result from ischemic cascade or develop as a result of the patient becoming immobile or bedridden.

COMPLICATION…

Complications that may occur within 72 hours of stroke include the following:

Cerebral swelling (edema) Increased intracranial pressure (ICP) Intracerebral hemorrhage Seizures

COMPLICATION…

Complications that may develop gradually as a result of immobility include the following:

Bedsores Blood clots Fibrosis of connective tissue resulting in decreased

mobility Malnutrition Pneumonia Urinary tract infections (UTIs; if a catheter is required

MUSCULOSKELETAL

loss of voluntary movement and immobility result in loss of range of movement and contractures.

UE: limitations in shoulder motions of flexion, abduction, and external rotation

Contructure Disuse atrophy and muscle weakness Impairments in gait, balance, falls Osteoporosis

NEUROLOGICAL

SEIZURES- common right after stroke during the acute phase and late-onset seizures can also occur several month after stroke

Common in occlusive carotid disease (17%) HYDROCEPHALUS- may experience

headache, nausea, vomiting, ↑ lethargy, and ataxia.

CARDIOVASCULAR/PULMONARY

THROMBOPHLEBITIS/DVT -complication for all immobilized patientsDVT signs: - rapid onset of unilateral leg swelling

with dependent edema - tenderness, dull ache, or tight

feeling in calf; not severe pain


CARDIAC FUNCTION - impaired cardiac output - cardiac decompensation - serious rhythm disorders - directly alter cerebral perfusion and produce

additional focal signs - exhibit low work capacities result acute illness,

bedrest, and limited activities level. - ↓ activity levels may also related to depression


PULMONARY FUNCTION

- ↓lung volume

- ↓pulmonary perfusion

- ↓vital signs

- altered chest wall excursion

- ↑fatigue

- ↓endurance


ASPIRATION- more common during any phase of recovery and can occur during any phase of swallowing

DYSPHAGIA- lead to dehydration and compromised nutrition

INTEGUMENTARY

Ischemic damage and subsequent necrosis of the skin results in skin breakdown and decubitus ulcer

Skin breakdown typically over bony prominence from pressure, friction, shearing and/or maceration

INTEGUMENTARY

FRICTION- skin rubs or dragged against the supporting surface

SHEARING- sliding of adjacent structures in opposite directions

MACERATION- caused by excess moisture

Differential Diagnosis

KAREN BARRACA


Paralysis of one side of the body Hemiplegia Numbness Confusion Vision complications Fatigue Aphasia Vomiting Decrease level of consciousness


Lethargy Dizziness/Vertigo Slurred speech Loss of coordination Uncontrollable eye movements Behavioral changes


Disease

Hypoglycemia

Mass Lesions

History

Blood sugar is too low

Cerebral AbscessSubdural HematomaMetastatic Tumor

Distinguishing FeaturesHunger, Nervousness, Cold sweat, Convulsion

Progressive syndrome, Rigorous headache, Stiff/aching at the neck, shoulders and back


Disease

Multiple Sclerosis

Epilepsy

Encephalitis

History

Autoimmune disease that affects the CNS

Abnormal electrical activity in the brain

Inflammation in the brain

Distinguishing FeaturesDecrease attention span, urinary frequency, hearing loss

Electric shock feeling, drooling, twitching movements

Fever, , delirium, deafness, dementia

LABORATORY TEST AND DIAGNOSTIC TOOLS

NEEMA ESTORES

NEUROVASCULAR TEST

- Neck Flexion

- Palpation of arteries

- superficial and deep

- Auscultation of heart and blood vessel

-Ophthalmic pressure

TEST AND MEASURES

1. Urinalysis-Detects infection, diabetes, renal

failure, dehydration

-can reveal diseases that have gone unnoticed because they do not produce striking signs or symptoms.

TEST AND MEASURES

2. Blood analysis-Provides complete blood count, platelet count, prothrombin time, partial thromboplastin time, and erythrocyte sedimentation rate.

TEST AND MEASURES

3. Fasting blood glucose level-Is used to screen for and diagnose diabetes and pre-diabetes.-Collected after an 8 to 10 hr fast

4. Blood chemistry profile-Test measures the value of a different substance in the blood. These values provide information on the function of different organ systems (kidney, liver, etc.) or the risk for

TEST AND MEASURES

5. Blood cholesterol and lipid profile-Is a group of simple blood tests that

reveal important information about the types, amount and distribution of the various types of fats (lipids) in the bloodstream.

6. Thyroid function tests-A collective term for blood tests used to

check the function of the thyroid

TEST AND MEASURES

7. Full cardiac evaluation -Includes electrocardiograph to detect arrhythmias as source of emboli or coincidental heart disease.

8. Echocardiography -Also known as a cardiac ultrasound -It uses standard ultrasound techniques to image two-dimensional slices of the heart. The latest ultrasound systems now employ 3D real-time imaging.

TEST AND MEASURES

9. Lumbar puncture-diagnostic and at times therapeutic procedure that is performed in order to collect a sample of cerebrospinal fluid (CSF) for biochemical, microbiological, and cytological analysis, or occasionally as a treatment ("therapeutic lumbar puncture") to relieve increased

intracranial pressure.

IMAGING

1. Computerized Tomography -Commonly used imaging technique

-Allows identification of large arteries and vein, and venous sinuses

-Used to rule out other brain lesions

Hemorrhagic stroke Ischemic stroke

2. Magnetic Resonance Imaging-Measures nuclear particles as they interact with powerful magnetic field

IMAGING

IMAGING

3. Positron Emission Tomography-Allows imaging of regional blood flow and localized cerebral metabolism

4. Transcranial and Carotid Doppler-Used for noninvasive imaging of the neck and chest level.

Transcranial Doppler

IMAGING

5. Cerebral Angiography-Invasive and involves the injection of radiopaque dye into blood vessels with subsequent radiography

Cerebral Angiogram showing a transverse projection of vertebrobasilar and posterior cerebral circulation

PT Management

JENNYLYN C. PASSILAN

Recovery begins as people get better from the immediate effects of a stroke. Over months and even years, other areas of the brain might learn to take over from the dead areas.

Rehabilitation is the process of overcoming or learning to cope with the damage the stroke has caused.

Stroke can cause weakness or paralysis in one side of the body and problem with balance or coordination.

Helps regain as much mobility and muscle control as possible.

Assess the stroke survivor’s strength, endurance, ROM, gait abnormalities and sensory deficits to design individualized rehabilitation program.

Work at patient bedside assuring adequate ROM and teaching bed mobilities, rolling and sitting.

Helps survivors regain the use of stroke impaired limbs, teach compensatory strategies to reduce the effect of remaining deficits and establish ongoing program to help people retain their newly learned skills.

MENTAL STATUS EXAMINATION

LEVEL OF CONCIOUSNESSAlertness, response to stimulationAttentionMemory

Orientation, new learning, remote memoryCognition

Fund of knowledge, calculation, problem solving, Abstract thinking, judgmentPerception, Constructional Ability, ApraxiaAffect and Behavior

BEDSIDE TEST

Does the patient understand?Give verbal commands, ask patient to point objects

Is the patient able to talk?Ask the patient to name objects, describe them, and count. Listen for spontaneous speech.

Can the patient repeat?Ask the patient to repeat words.

BEDSIDE TEST

Can the patient read?Give commands in writing.

Can the patient write?Ask the patient to copy of to write dictated words.

Stage Characteristics

1 No activation of the Limb

2 Spasticity appears, and weak basic flexor and extensor synergies are present

3 Spasticity is prominent; the patient voluntarily moves the limb, but muscle activation is all within the synergy patterns

4 The patient begins to activate muscles selectively outside the flexor and extensor synergies

5 Spasticity decreases; most muscle activation is selective and independent from the limb synergies

6 Isolated movements are performed in smooth , phasic, well coordinated manner

Brunnstrom stages of Motor Recovery

Maintain ROM and prevent deformity

Promote awareness, AROM, and use of hemiplegic side

Improve trunk control, symmetry, and balance

Improve functional mobility

Initiate self care activities

Improve respiratory function

Monitor changes associated with recovery.

Positioning

The room should be arranged to maximize

patient awareness of the hemiplegic side.

Affected side should be towards the main part

of the room.

Since patient spends significant time on

bed, we have to prevent undesirable posture

which can lead to contractures or pressure

sores.

Passive Range of Motion Exercises

maintain good blood flow

keep the muscles and tendons flexible

preventing the joints from tightening

passive range of motion exercises are done for the shoulder, elbow, wrist, fingers, hip, knee, ankle, foot, and toes

Active Range of Motion Exercises

help to strengthen the muscles on the weak side,

but also should be done on the good side.

Balance and Transfer Exercises

The patient will practice moving from lying to

sitting position and then practice sitting balance.

Next they will learn to transfer from bed to

wheelchair and back to bed sometimes using a

sliding board if necessary.

Gait (Walking) Training Exercise

Starts practicing standing up in the parallel bars.

Next the patient learns to shift weight from one leg to

the other, shifting both from side to side and from front

to back. After this the patient walks a short distance

between the parallel bars using the bars for support.

Next, the patient will walk outside the bars using a

quad cane or walker

Bobath approach /neurodevelopmental technique (NDT)

The goal of NDT is to normalize tone, to inhibit primitive

patterns of movement, and to facilitate automatic,

voluntary reactions and subsequent normal movement

patterns.

inhibits abnormal patterns of movement

Brunnstrom approach/Movement therapy (Brunnstrom, 1970)

Uses primitive synergistic patterns in training in

attempting to improve motor control through central

facilitation

encourages the use of abnormal movements

Sensorimotor approach/Rood approach (Noll, Bender, and Nelson, 1996)

Facilitatory or inhibitory inputs through the use of

sensorimotor stimuli, including, quick stretch, icing,

fast brushing, slow stroking, tendon tapping,

vibration, and joint compression to promote

contraction of proximal muscles

Motor relearning program/Carr and Shepard approach (Carr et al., 1985)

Based on cognitive motor relearning theory and

influenced by Bobath's approach

Goal is for the patient to relearn how to move

functionally and how to problem solve during attempts

at new tasks

Proprioceptive (or peripheral) Neuromuscular Facilitation (PNF) (Knott and Voss, 1968)

Uses spiral and diagonal components of movement

rather than the traditional movements in cardinal

planes of motion with the goal of facilitating

movement patterns that will have more functional

relevance than the traditional technique of

strengthening individual group muscles

ADJUNCT THERAPIES

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS)

Encourages brain reorganization and recovery of function.

It involves using a small probe that generates an

electrical current to stimulate nerve activity in stroke-

impaired limbs. The mild electrical current generates heat

that serves to relieve stiffness, improve mobility, and

relieve pain.

ADJUNCT THERAPIES

TRANSCUTANEOUS ELECTRICAL NERVE STIMULATION (TENS)

ADJUNCT THERAPIESFUNCTIONAL ELECTRICAL STIMULATION (FES)

Used to promote and improve muscle function,

prevent atrophy, increase strength, maintain ROM

and increase circulation and blood flow to the

muscles

ADJUNCT THERAPIES

FUNCTIONAL ELECTRICAL STIMULATION (FES)

ADJUNCT THERAPIESELECTROMYOGRAPHIC BIOFEEDBACK

Another method designed to promote recovery and when

used along with FES can result in greater improvement.

EMG is the practice of measuring the electrical signal

produced by a contracting muscle.

ELECTROMYOGRAPHIC BIOFEEDBACK

BE PATIENT. REHABILITATION IS A SLOW

AND OFTEN FRUSTRATING PROCESS. DON’T

WORRY IF THERE ARE DAYS WHEN LITTLE

PROGRESS SEEMS TO BE MADE.

BE POSITIVE. CONSTANT

ENCOURAGEMENT AND PRAISE ARE

NEEDED TO KEEP UP EVRYONE’S

SPIRITS.

NO PROGRAM CAN SUCCEED WITHOUT

A STRONG DESIRE BY THE

PATIENT TO BE

INDEPENDENT.NEVERTHELESS;

FAMILY INVOLVEMENT IS ALSO A KEY

INGREDIENT IN A SUCCESSFUL

REHABILITATION PROGRAM.

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