AMYOTROPHIC

LATERAL
SCLEROSIS

INTRODUCTION
Motor neuron diseases (MND) include a heterogeneous spectrum of
inherited and sporadic (no family history) clinical disorders of the upper
motor neurons (UMNs), lower motor neurons (LMNs), or a combination of
both.
Subtype
Nervous System Pathology
Amyotrophic lateral
Sclerosis

Degeneration of the corticospinal tracts, neurons in

the motor cortex and brainstem, and anterior horn
cells in the spinal cord

Primary lateral
Sclerosis

Degeneration of upper motor neurons

Progressive bulbar
Palsy

Degeneration of motor neurons of cranial nerves IX to

XII

Progressive muscular
Atrophy

Loss or chromatolysis of motor neurons of the spinal

cord and brainstem

AMYOTROPHIC LATERAL
SCLEROSIS
ALS commonly known as Lou Gehrigs disease
It can be defined as a rapidly progressive neurodegenerative disease

characterized by weakness, spasticity, and muscular atrophy

subsequent respiratory compromise leading to premature death.

with

It is caused by the destruction of motor neurons in the primary motor

cortex, brain stem, and spinal cord.

Amyotrophy refers to muscular atrophy occurring from the degeneration

of anterior horn cells in the spinal cord with muscle fiber denervation.
Lateral sclerosis describes the resultant hardening of the anterior and

lateral corticospinal tracts caused by replacement of dying motor neurons

with subsequent gliosis.

EPIDEMIOLOGY
The prevalence of ALS has been reported to be 4 to 10 cases per 100,000.

(OSullivan, 2014)
It is estimated that 30,000 individuals in the US have ALS at any one time and 15 cases

are diagnosed every day.

ALS most often afflicts people between 40 and 60 years of age with a mean age of

onset of 58 years.
This disease affects men slightly more than women, with an approximate ratio of

1.7:1 (OSullivan) | 1.5:1 (Braddom)

The worldwide prevalence is 5 to 7/100,000, making ALS one of the most common

neuromuscular diseases in the world. (Braddom, 2011)

Three Classifications of ALS:
1.
2.
3.

Familial Amyotrophic Lateral Sclerosis

Juvenile Amyotrophic Lateral Sclerosis
Sporadic Amyotrophic Lateral Sclerosis

FAMILIAL ALS
Approximately 5% to 10% of all ALS cases, however, are familial

(FALS) and most commonly have an autosomal dominant inheritance

pattern.
The age of onset of FALS occurs a decade earlier than sporadic

cases, and progression of the disease is more rapid.

Males and females are equally affected.
About 20% of FALS cases result from a copperzinc superoxide

dismutase (SOD1) gene defect.

JUVENILE ALS
It is by definition presents before age 25.
It is a rarely occurring form of FALS.
The progression of the disease is typically much slower than adult-

onset ALS and can present initially with either UMN or LMN signs.
Two autosomal recessive (ALS5 and ALS2) and one autosomal

dominant (ALS4) form of juvenile ALS have been described:

a.

ALS5
The disease-causing mutation has been mapped to chromosome 15q.
It typically presents in the teenage years with progressive limb spasticity,

distal limb weakness, and muscle atrophy.

JUVENILE ALS
b.

ALS2
The disease-causing mutation has been linked to chromosome 2q33.
Disease onset typically begins before age 10.
Prominent symptoms include limb and facial spasticity accompanied by

pseudobulbar affect.
c.

ALS4
presents with severe distal muscle weakness and pyramidal signs in the

absence of bulbar and sensory abnormalities.

It is caused by a mutation in the senataxin gene found on chromosome 9q34.
The senataxin protein is known to have a role in RNA processing.

SPORADIC ALS
The etiology of sporadic ALS is unknown and likely multifactorial with a

complex interplay of pathogenic cellular mechanisms.

These mechanisms includes:
1.
2.
3.
4.
5.
6.
7.

Oxidative stress
Exogenous neurotoxicity
Glutamate Excitotoxicity
Impaired axonal transportation
Protein aggregation
Apoptosis (programmed cell death)
Lifestyle factors (e.g. cigarette smoking, alcohol intake, anthropometric
measures), may be responsible for neuron degeneration in ALS.

ETIOLOGY

ETIOLOGY

ANATOMICAL &
PHYSIOLOGICAL
BACKGROUND
Motor neurons are nerve cells

located in the brain, brain stem,

and spinal cord that serve as
controlling
units
and
vital
communication links between the
nervous system and the voluntary
muscles of the body.
Messages from motor neurons in

the brain
neurons)are
neurons
in
(calledlower
from them to

(calledupper motor
transmitted to motor
the
spinal
cord
motor neurons) and
particular muscles.

ANATOMICAL &
PHYSIOLOGICAL
BACKGROUND
UMN

The upper motor neurons are located on the surface of

the brain and exert control over the lower motor neurons,
which are in the brainstem and the spinal cord.

LMN
The lower motor neurons are directly attached to muscles

through wires called axons. Bundles of these axons

leave the spinal cord and extend out to the muscles.

Bulbar Motor Neuron

Those that control the muscles of speaking, swallowing

and facial expression are in the brainstem. Theyre

sometimes called bulbar motor neurons, because the part
of the brainstem that houses them has a bulblike shape.

PATHOLOGICAL
BACKGROUND
ALS is marked by progressive and highly selective degeneration and

loss of upper and lower motor neurons in the brain and spinal cord
leading to paralysis of voluntary muscles and loss of ability to swallow,
speak, and breathe.
As motor neurons degenerate, they can no longer control the muscle

fibers they innervate. Healthy, intact surrounding axons can sprout and
reinnervate the partially denervated muscles, in essence assuming the
role of the degenerated motor neuron and preserving strength and
function early in the disease; however, the surviving motor units
undergo enlargement. Reinnervation can compensate for the
progressive degeneration until motor unit loss is about 50%. As the
disease progresses reinnervation cannot compensate for the rate of

PATHOLOGICAL
BACKGROUND

When these cells gradually die in ALS, muscles

atrophy (shrink) and become progressively weaker

and eventually unable to contract, resulting in
paralysis.
When upper motor neurons are lost and lower

motor neurons remain, movements are still

possible but can become tight (spastic) and less
precise. In ALS, a combination of these effects is
usually seen because both upper and lower motor
neurons are dying. People with ALS can have weak
and atrophied muscles with tightness (spasticity).
Muscle twitches (called fasciculations) and
cramps are common; they occur because
degenerating nerves become irritable.

CLINICAL
MANIFESTATIONS
Clinical manifestations of ALS vary depending on the localization and extent
of motor neuron loss, the degree and combination of LMN and UMN loss,
pattern of onset and progression, body region(s) affected, and stage of the
disease. At onset, signs or symptoms are usually asymmetrical and focal.
Progression of the disease leads to increasing numbers and severity of
impairments.

SYMPTOMS
Early signs and symptoms of ALS include:
Difficulty walking, tripping or difficulty doing your normal daily activities
Weakness in your leg, feet or ankles
Hand weakness or clumsiness
Slurring of speech or trouble swallowing
Muscle cramps and twitching in your arms, shoulders and tongue
Difficulty holding your head up or keeping a good posture

The disease frequently begins in your hands, feet or limbs, and then spreads to other

parts of your body. As the disease advances, your muscles become progressively
weaker. This weakness eventually affects chewing, swallowing, speaking and breathing.
However, ALS doesn't usually affect your bowel or bladder control, your senses, or your

thinking ability. It's possible to remain actively involved with your family and friends.

COMMON IMPAIRMENTS
ASSOCIATED WITH ALS
Pathology

LMN
UMN

Impairments

Muscle weakness, hyporeflexia, hypotonicity, atrophy, muscle

cramps, fasciculations
Spasticity, pathological reflexes, hyperreflexia, muscle weakness

Bulbar

Bulbar muscle weakness,

pseudobulbar affect

dysphagia,

dysarthria,

sialorrhea,

Respirator
y

Respiratory muscle weakness (inspiratory and expiratory), dyspnea,

exertional dyspnea, nocturnal respiratory difficulty, orthopnea,
hypoventilation, secretion retention, ineffective cough

Others

Rare impairments: sensory impairments, bowel and bladder

dysfunction, ocular palsy
Indirect and composite impairments: Fatigue, weight loss, cachexia,
decreased ROM, tendon shortening, joint contracture, joint
subluxation, adhesive capsulitis, pain, balance and postural control
impairments, gait disturbances, deconditioning,depression, anxiety

IMPAIRMENTS RELATED
TO LMN PATHOLOGY
The most frequent presenting impairment, occurring in the majority of

patients, is focal, asymmetrical muscle weakness beginning in the lower

extremity (LE) or upper extremity (UE), or weakness of the bulbar muscles.
Muscle weakness is considered the cardinal sign of ALS and may be caused

by LMN or UMN loss.

Initial muscle weakness usually occurs in isolated muscles, most often

distally, and is followed by progressive weakness and activity limitations.

DIAGNOSIS
No definite diagnostic test
No diagnostic biological marker exists

For individual with clinical presentation:

Laboratory studies
EMG
Nerve Conduction Velocity studies
Muscle and nerve biopsies
Neuroimaging studies

DIAGNOSIS
Diagnosis of ALS requires the presence of
1.

LMN signs by
examination

clinical,

electrophysiological,

or

neuropathological

2.

UMN signs by clinical examination

3.

Progression of the disease within a region or to other regions by clinical

examination or via the medical history

.The absence of
1.

Electrophysiological and pathological evidence of other diseases that

may explain the UMN and LMN sign and

2.

Neuroimaging evidence of other disease processes that may explain the

observed clinical and electrophysiological signs are also evaluated

DISEASE COURSE
ALS has a progressive and deteriorating trajectory
Disease course varies among individuals
From time of onset to death ranging from several months to 20

years
Average duration of ALS between 27 months to 43 months
Median duration between 23 and 52 months
Five-year and ten-year survival rates range from 9% to 40%

and 8% to 16%
A 50% survival probability after the first symptom of ALS

appears is slightly greater that 3 years

In most patients, death occurs within 3 to 5 years after

PROGNOSIS
Age at time of onset has the strongest relationship to prognosis
Patients <35 to 40 years of age at onset had better 5-year survival rates that older individual
Individuals with limb-onset have a better prognosis that bulbar-onset
5-year survival rates were reported to be 37% and 44%, compared to survival rates of 9% to 16%

for patients with bulbar-onset ALS

Other factor affecting prognosis

Less sever involvement at the time of diagnosis
Longer interval between onset and diagnosis
No symptoms of dyspnea at onset
A study of 144 individuals with ALS found that those individuals with psychological well-being

had significantly longer survival times compared to those with psychological distress.

Mortality rates were found to be 6.8 times greater

MANAGEMENT
Disease-Modifying Agents
Currently, there is no cure for ALS, although a number of clinical drug trials are ongoing. In

1995, the FDA approved riluzole (Rilutek), a glutamate inhibitor, for the treatment of ALS.
The standard dose of riluzole is one 50 mg tablet two times a day, and side effects include
liver toxicity (which requires discontinuation), asthenia, nausea, vomiting, and dizziness.
Evidence suggests the effects of riluzole to be modest, extending survival for 2 to 3
months.
Symptomatic Management
Because the pathological process cannot be reversed and is progressive in nature, the

context of medical management for individuals with ALS may be considered palliative. As
defined by the WHO, palliative care is an approach that improves the quality of life of
patients and their families facing the problem associated with life-threatening illness,
through the prevention and relief of suffering by means of early identification and
impeccable assessment and treatment.

Management of Dysphagia
Speech-language pathologists conduct swallowing examinations such as video

fluoroscopy to determine the degree and nature of the swallowing impairment and
to assist in formulating a plan of care
Nutritionists provide counseling and diet management throughout the course of the

disease.
Management of Respiratory Impairments
Important

management considerations include (1) pneumococcal and yearly

influenza vaccinations;68 (2) prevention of aspiration; and (3) effective oral and
pulmonary secretion management.

supplemental oxygen is recommended only for individuals with concomitant

pulmonary disease or as a comfort measure for patients who decline ventilator

support.
When VC decreases to 50% of predicted, positivepressure noninvasive ventilation

(NIV) is recommended.

Management of Sialorrhea and Pseudobulbar Affect

Management of sialorrhea in people with ALS and other diseases is often directed

toward prescription of anticholinergic medications that decrease saliva production.

Examples include:
glycopyrrolate (Robinul) benztropine (Cogentin) transdermal hyoscine (scopolamine),

atropine and trihexyphenidyl hydrochloride (Artane).

For patients with associated thick mucus production
beta-blockers such as propranolol (Inderal) or metoprolol (Toprol) are often prescribed.

For patients with pseudobulbar affect,

tricyclic antidepressants, such as amitriptyline (Elavil), or selective serotonin reuptake

inhibitors (SSRIs), such as fluvoxamine (Luvox), are often prescribed

Management of Dysarthria
Dysarthria

impairments are managed primarily by a speech-language

pathologist. Initial speech changes are usually managed with intelligibility
strategies

Management of Muscle Cramps, Spasticity, Fasciculations, and Pain

Anticonvulsant medication such as phenytoin (Dilantin) and carbamazepine

(Atretol, Tegretol) may be prescribed for muscle cramps, if they are not
relieved with a program of muscle stretching and adequate hydration and
nutrition.
Management of Anxiety and Depression
Pharmacotherapy and psychological counseling are important management

strategies for addressing the anxiety and depression that can develop.
Individuals with depression may be prescribed an SSRI, such as fluoxetine
(Prozac) or sertraline (Zoloft).
Benzodiazepines, such as chlordiazepoxide (Librium), clorazepate,

diazepam, and flurazepam (Dalmane), may be prescribed for anxiety or for

patients with depression and insomnia.

COGNITION
No ALS-specific cognitive test or measure exists
If dementia or cognitive impairments are suspected, executive function,

language comprehension, memory, and abstract reasoning should be

examined.

The Mini-Mental State Examination has been used in clinical studies,

although it may not be sensitive to frontotemporal function impairments.

Referral for a neuropsychological evaluation may also be indicated to

identify specific cognitive impairments.

PSYCHOSOCIAL FUNCTION
As depression and anxiety are common in individuals with ALS, screening is important

and referral to a psychologist or psychiatrist for further evaluation may be indicated.

The Becks Depression Inventory,
The Center of Epidemiologic Study Depression Scale
The Hospital Anxiety and Depression Scale (HADS)
The State-Trait Anxiety Inventory

Pain
Pain is common in individuals with ALS and should be examined subjectively and

objectively, using a Visual Analogue Scale (VAS)

Joint Integrity, Range of Motion,

and Muscle Length
Functional ROM, active, active-assisted, and passive range ROM, muscle length, and

soft tissue flexibility and extensibility using standard methods

MUSCLE PERFORMANCE
Specific deficits of muscle strength, power and endurance, and muscle

performance during functional activities, can be measured through:

manual muscle testing (MMT),
Isokinetic muscle
strength testing
handheld dynamometry

Maximum voluntary isometric contraction (MVIC) using a strain gauge

tensiometer system. This eliminates muscle length and velocity

MVIC is considered the most direct technique for investigating motor unit

loss, and has been used extensively for examining muscle strength in
individuals with ALS for the past 10 years.

MOTOR FUNCTION
Impairments in dexterity, coordination of large movement patterns, as well

as gross and fine motor control may be evident owing to spasticity and
muscle weakness.

Hand function and initiation, modification, and control of movement

patterns

TONE AND REFLEXES

Muscle tone may be examined using the Modified Ashworth Scale.
Deep tendon and pathological reflexes should be tested to distinguish

between UMN and LMN involvement.

CRANIAL NERVE
INTEGRITY
The cranial nerves commonly affected by ALS include V, VII, IX, X, and XII.
Cranial nerves should be tested to determine the extent of bulbar

involvement.

Screening for oral motor function, phonation, and speech production can be

accomplished through the interview and observation.

Referral to a speech-language pathologist is recommended.

SENSATION
If the patient complains of sensory symptoms or if sensory involvement is

suspected, sensory testing should be completed.

POSTURAL ALIGNMENT,
CONTROL, AND BALANCE
Static and dynamic postural alignment and body mechanics during self-care,

functional mobility skills, functional activities, and work conditions and activities

Postural stability, reactive control, anticipatory control, and adaptive postural

control should also be determined.

No ALS-specific balance test or measure exists.

A variety of balance status measures, originally designed for use with other

patient populations, including:

the Tinetti Performance Oriented Mobility

Assessment (POMA)
The Berg Balance Scale
The Timed Up and Go Test (TUG)
The Functional Reach Test

GAIT
Documentation of gait within a particular time period (e.g., within 15

seconds) or over a certain distance (e.g., 10 feet [3 meters]) has been

measured in clinical trials.

Gait stability, safety, and endurance should be examined.

Energy expenditure, alignment, fit, practicality, safety, and ease of use of

orthotic and assistive devices should also be examined at regular intervals.

RESPIRATORY FUNCTION
Determination of respiratory status and function includes examination of

respiratory symptoms and muscle function, breathing pattern, chest

expansion, respiratory sounds, cough effectiveness, and VC or forced vital
capacity (FVC) using a handheld spirometer.

Aerobic capacity and cardiovascularpulmonary endurance may be tested

in the early stages of ALS using standardized, modified protocols to

evaluate and monitor responses to aerobic conditioning.

INTEGUMENT
Skin inspection should be used to examine contact points between the

body and assistive, adaptive, orthotic, protective, and supportive devices,

mobility devices, and the sleeping surface

Such inspection is especially important when the patients mobility

becomes increasingly more dependent.

If present, swelling should also be examined and monitored.

Swelling of the distal limb may develop owing to lack of muscle pumping

action in a weakened extremity.

FUNCTIONAL STATUS
Functional mobility skills, safety, and energy expenditure are important

considerations

The Functional Independence Measure (FIM) has been used to document

functional status in clinical trials.

The Schwab and England Activities of Daily Living Scale is an 11-point

global measure of functioning that asks the rater to report activities of daily
living (ADL) function from 100% (normal) to 0% (vegetative functions only),
and has been used to examine function in individuals with ALS

ENVIRONMENTAL
BARRIERS
The patients home and work environments should be examined for current

and potential barriers, access, and safety.

FATIGUE
Fatigue is very common in individuals with ALS. No
ALS-specific measures exist; the Fatigue Severity Scale has been used in

clinical trials.

DISEASE-SPECIFIC
MEASURES
The ALS Functional Rating Scale (ALSFRS) and the revised version, ALSFRS-

R examine the functional status of patients with ALS. The patient is asked
to rate his or her function using a scale from 4 (normal function) to 0
(unable to attempt the task).
The ALSFRS-R was expanded to include additional respiratory items, and

was found to have internal consistency and construct validity, and to have
retained the properties of the original scale.

Other disease-specific scales include the:

Appel ALS Scale (AALS),
ALS Severity Scale (ALSSS),
Norris Scale

QUALITY-OF-LIFE
MEASURES
The Amyotrophic Lateral Sclerosis Assessment Questionnaire (ALSAQ-40),

an ALS-specific quality of life measure, contains 40 items that represent

five distinct areas of health: mobility (10 items), ADL (10 items), eating and
drinking (3 items), communication (7 items), and emotional functioning (10
items)

The questions refer to the patients condition during the past 2 weeks and

responses are given on a five-point Likert scale.

The ALSAQ-40 measures health status in each domain using a summary

score from 0 (best health status) to 100 (worst health status).

PHYSICAL THERAPY
INTERVENTIONS
Restorative intervention
directed toward remediating or improving impairments and activity limitations.

Compensatory intervention
directed toward modifying activities, tasks, or the environment to minimize activity

limitations and participation restrictions.

Preventative intervention
is directed toward minimizing potential impairments such as loss of ROM, aerobic

capacity, or strength, preventing pneumonia or atelectasis, and activity limitations.

1. CERVICAL MUSCLE
WEAKNESS
Progressive cervical extensor weakness will cause the head to fall forward,

resulting in overstretching of the posterior musculature and soft tissues.

For mild to moderate cervical weakness, a soft foam collar may be worn

during specific activities. Soft collars are comfortable and usually well
tolerated.

For moderate to severe weakness, a semirigid or rigid collar is prescribed.

Usually

made of padded rigid plastic or leather and provide very firm support.

2. DYSARTHRIA AND
DYSPHAGIA
In collaboration with the SLP and nutritionist, the physical therapist can

play a role in managing dysarthria and dysphagia by addressing the

patients head and trunk control and position in sitting

Physical therapist can reinforce the use of strategies for eating and

swallowing (e.g., chin tuck), the use of prescribed communication devices,

and the need for food consistency modifications.

3. UE MUSCLE WEAKNESS
Weakness of the UEs greatly affects the patients ability to carry out ADL.
Splinting of the wrist or hand may be indicated to prevent contractures or

to improve the patients function, such as the ability to grasp.

4. SHOULDER PAIN
Individuals with ALS may develop shoulder pain and present with capsular

patterns of restriction caused by several factors: abnormal scapulohumeral

rhythm secondary to spasticity or weakness causing imbalance that may
lead to impingement; overuse of strong muscles; muscle strain; faulty
resting position; glenohumeral subluxation secondary to weakness; or a
fall.

Interventions may include modalities, ROM exercises, passive stretching,

joint mobilizations, and education about proper joint support and

protection.

Recommendations for managing the pain and decreased ROM included a

protocol of an intra-articular analgesic and anti-inflammatory cocktail

injection, followed by a course of aggressive ROM exercises.

5. RESPIRATORY MUSCLE
WEAKNESS
Patients and caregivers must be taught how to balance activity and rest and

educated about energy conservation techniques.

Patients and caregivers should also be educated about signs and symptoms of

aspiration; positioning to avoid aspiration, such as upper cervical spine flexion

during eating; causes and signs of respiratory infection; and strategies for managing
oral secretions (use of oral suction device) or choking episodes (Heimlich maneuver).

Specific breathing exercises and positioning to optimize ventilation/perfusion

matching may also be incorporated, although their effectiveness in ALS has not been
determined.

Airway clearance techniques may be necessary when conditions that cause

secretion retention, such as pneumonia or atelectasis, arise.

To compensate for a weakened cough, the patient and caregiver may be instructed

in the use of manually assisted coughing techniques

6. LE MUSCLE WEAKNESS
AND GAIT
IMPAIRMENTS

Orthoses may be recommended to improve function by offering support to weakened

muscles and the joints they surround, decrease the stress on remaining functioning or
compensatory muscles, conserve energy, or minimize local or general muscle fatigue.

Important thing to consider is the weight of the orthosis as individuals with ALS will

have energy expenditure issues, and it may be more fatiguing for the patient to
ambulate with a heavy orthosis than to ambulate without the impairment being
corrected.

The type of ambulatory assistive device prescribed is dependent on the degree of

proximal muscle strength or instability; function of the UEs; the pattern, extent, and
rate of disease progression; acceptance by the patient; and financial constraints.

Wheeled walkers, are usually recommended.

In general, individuals with ALS are rarely prescribed crutches. If crutches are

warranted, Loftstrand (Canadian) crutches are preferred.

7. ACTIVITIES OF DAILY
LIVING
As the disease progresses and proximal shoulder weakness increases, a

mobile arm support may be incorporated to allow the patient to maintain

independence in eating.

In the late stage of ALS when the patient is dependent on the caregiver for

eating, a long straw and straw holder may be recommended to assist the
caregiver with the activity.

A large variety of adaptive equipment is available to assist individuals with

muscle weakness perform everyday tasks.

8. DECREASED MOBILITY
Patients with LE weakness may have difficulty with sit-to-stand or car transfers.

Simple interventions includes:

placing a firm cushion 2 to 3 in (5 to 7.6 cm) thick under the buttocks in the chair or elevating

the chair by placing the legs in prefabricated blocks

Self-powered lifting cushions are relatively inexpensive and portable, but the individual needs
adequate trunk control and balance in order to use the device safely
Upholstered reclining chairs with powered seat lifts may also be recommended, but are more
expensive.

Transfer boards may be used for transfers once the individual is unable to

stand, either alone if the person has adequate arm strength and good sitting
balance, or the caregiver can be instructed in how to assist the patient.

In the early or early-middle stage of ALS a manual wheelchair, preferably

lightweight, may be used for traveling long distances as an energy conservation

technique.

9. MUSCLE CRAMPS AND

SPASTICITY
Cold can temporarily decrease spasticity.
Physical therapists can perform and instruct caregivers in slow prolonged

stretches and passive ROM exercises to address spasticity.

Postural and positioning techniques can be incorporated to decrease

spasticity and splinting may be necessary to prevent contractures.

10. PSYCHOSOCIAL
ISSUES
The emotional responses of the person experiencing the disease, family

members, and individuals caring for the patient are multifaceted and may
fluctuate throughout the stages of the disease.

The physical therapist must be able to recognize the patients ability to

cope and adapt, and his or her psychological reactions, level of

acceptance, and willingness and ability to integrate therapeutic
recommendations.

PATIENT AND
FAMILY/CAREGIVER
EDUCATION

Providing accurate, factual information about the disease process and clinical

manifestations, and their significance in terms of management. Give only as much

information as the patient, family, and caregivers need; information should be provided in
a manner appropriate to their understanding.

Instructing patients, family members, and caregivers regarding interventions that can be

carried out independently such as monitoring the effects and side effects of medications,
use of assistive devices and adaptive equipment, and preventing secondary
complications.

Advising the patient about methods to promote general health. Instruction regarding

energy conservation, balancing rest and activity, and relaxation techniques may be
beneficial in assisting the patient to cope with the daily constraints of the disease.

Counselling regarding care and life decisions, if the patient asks about these issues.
Referring patients to support groups or psychological counselling.
Providing information on health and available social and support services