Cerebral
Palsy
Definition
While
cerebral palsy is a blanket term commonly described by loss or impairment of
motor function, cerebral palsy is actually caused by brain damage.
The brain
damage is caused by brain injury or abnormal development of the brain that
occurs while a child’s brain is still developing — before birth, during birth,
or immediately after.
Cerebral
palsy affects body movement, muscle control, muscle coordination, muscle tone,
reflex, posture and balance. It can also impact fine motor skills, gross motor
skills and oral motor functioning.
Those with
cerebral palsy are most likely born with the condition, although some acquire
the condition at birth or shortly thereafter depending on cause. Signs and
symptoms of cerebral palsy may not always be apparent at birth. The child will
likely experience a delay in development and growth milestones. (www.cerebralpalsy.org)
The term
cerebral palsy refers to any one of a number of neurological disorders that
appear in infancy or early childhood and permanently affect body movement and
muscle coordination but don’t worsen over time. Even though cerebral palsy
affects muscle movement, it isn’t caused by problems in the muscles or nerves.
It is caused by abnormalities in parts of the brain that control muscle
movements. The majority of children with cerebral palsy are born with it,
although it may not be detected until months or years later. The early signs of
cerebral palsy usually appear before a child reaches 3 years of age. The
most common are a lack of muscle coordination when performing voluntary
movements (ataxia); stiff or tight muscles and exaggerated reflexes
(spasticity); walking with one foot or leg dragging; walking on the toes, a
crouched gait, or a “scissored” gait; and muscle tone that is either too stiff
or too floppy. A small number of children have cerebral palsy as the
result of brain damage in the first few months or years of life, brain
infections such as bacterial meningitis or viral encephalitis, or head injury
from a motor vehicle accident, a fall, or child abuse. (http://www.ninds.nih.gov)
Types
Spastic
Cerebral Palsy- Spastic cerebral palsy is the most common type of cerebral palsy,
occurring in about 70%-80% of all cases.. The muscles of people with spastic
cerebral palsy appear stiff and their movements may look stiff and jerky.
Spasticity
is a form of hypertonia, or increased muscle tone. When people without cerebral
palsy perform a movement, some groups of muscles turn on and some groups of
muscles turn off. In people with spastic cerebral palsy, both groups of muscles
may become turned on at the same time. In some instances the wrong muscle
groups may turn on. This makes movement difficult or even impossible.
Spasticity is seen in a number of different
conditions including cerebral palsy, traumatic brain injury, spinal cord
injury, stroke and multiple sclerosis.People may have difficulty moving from
one position to another and controlling individual muscles or muscle groups
needed for performing certain tasks like handling objects or speaking
In cerebral palsy, spasticity is due to damage
to the motor cortex of the brain before, during or after birth. This part of
the brain is considered the supreme command centre for control of body
movements.
Dyskinetic Cerebral
Palsy-
People with dyskinetic forms of cerebral palsy have variable movement that is
involuntary (outside of their control). These involuntary movements are
especially noticeable when a person attempts to move.
Dyskinetic cerebral
palsy results from damage to the basal ganglia of the brain. The basal ganglia
is like the brain’s switchboard for interpreting messages between the movement
centre and the spinal cord – it is responsible for regulating voluntary movements.
The different forms of dyskinesia result from damage to slightly different
structures within the basal ganglia. This form of cerebral palsy occurs in
about 10% of all cases.
Ataxic-Ataxic cerebral palsy
affects coordinated movements. Balance and posture are involved. Walking gait
is often very wide and sometimes irregular. Control of eye movements and depth
perception can be impaired. Often, fine motor skills requiring coordination of
the eyes and hands, such as writing, are difficult.
Ataxia is the least
common form of cerebral palsy. Ataxia means ‘without order’ or ‘incoordination’.
It happens when there is damage to the cerebellum which helps with
coordination. Ataxic movements are characterised by clumsiness, imprecision, or
instability. Movements are not smooth and may appear disorganised or jerky.
The incoordination seen
with ataxia occurs when a person attempts to perform voluntary movements such
as walking or picking up objects. Ataxia causes an interruption of muscle
control in the arms and legs, resulting in a lack of balance and coordination.
Who
Cerebral Palsy can
affect any person, as it is neither genetic nor a disease. It is caused by
brain damage, usually because of so trauma or complication during pregnancy or
birth.
Symptoms
General
Symptoms
Signs of
cerebral palsy are different than symptoms of cerebral palsy.
Signs are
clinically identifiable effects of brain injury or malformation that cause
cerebral palsy. A doctor will discern signs of a health concern during exam and
testing.
Symptoms,
on the other hand, are effects the child feels or expresses; symptoms are not
necessarily visible.
Impairments
resulting from cerebral palsy range in severity, usually in correlation with
the degree of injury to the brain. Because cerebral palsy is a group of
conditions, signs and symptoms vary from one individual to the next.
The
primary effect of cerebral palsy is impairment of muscle tone, gross
and fine motor functions, balance, control, reflexes, and posture. Oral
motor dysfunction, such as swallowing and feeding difficulties, speech
impairment, and poor muscle tone in the face, can also indicate cerebral palsy.
Associative conditions, such as sensory impairment, seizures, and learning
disabilities that are not a result of the same brain injury, occur frequently
with cerebral palsy. When present, these associative conditions may contribute
to a clinical diagnosis of cerebral palsy.
The most
common early sign of cerebral palsy is developmental delay. Delay
in reaching key growth milestones, such as rolling over, sitting, crawling and
walking are cause for concern. Practitioners will also look for signs such as
abnormal muscle tone, unusual posture, persistent infant reflexes, and early
development of hand preference.
Many signs
and symptoms are not readily visible at birth, except in some severe cases, and
may appear within the first three to five years of life as the brain and child
develop.
If the
delivery was traumatic, or if significant risk factors were encountered during
pregnancy or birth, doctors may suspect cerebral palsy immediately and observe
the child carefully. In moderate to mild cases of cerebral palsy, parents are
often first to notice if the child doesn’t appear to be developing on schedule.
If parents do begin to suspect cerebral palsy, they will likely want to consult
their physician and ask about testing to begin ruling out or confirming
cerebral palsy or other conditions.
Most
experts agree; the earlier a cerebral palsy diagnosis can be made, the better.
However, some caution against making a diagnosis too early, and warn that other
conditions need to be ruled out first. Because cerebral palsy is the result of
brain injury, and because the brain continues to develop during the first years
of life, early tests may not detect the condition. Later, however, the same
test may, in fact, reveal the issue.
If a
diagnosis can be made early on, early intervention programs and treatment
protocols have shown benefit in management of cerebral palsy. Early diagnosis
also helps families qualify for government benefit programs and early
intervention.
Eight
Clinical signs of Cerebral Palsy:
Muscle
Tone
Movement
Coordination and Control
Reflexes
Posture
Balance
Fine Motor
Function
Gross
Motor Function
Oral Motor
Dysfunction
Type
Specific Symptoms
Spastic-Muscles appear stiff
because the messages to the muscles are sent incorrectly through the damaged
part of the brain.When a muscle is affected by spasticity, the faster the limb
is moved, the stiffer it seems.Spasticity arises as a result of damage to bundles
of neurons in the brain and spinal cord called the corticospinal tracts and
corticobulbar tracts.
The stress on the body
created by spasticity can result in associated conditions such as hip
dislocation, scoliosis, and limb deformities. One particular concern is
contracture, the constant contracting of muscles that results in painful joint
deformities.
Dyskinetic- Dyskinetic movements
can be:
- Twisting and repetitive movements – known as dystonia
- Slow, ‘stormy’ movements – known as athetosis
- Dance-like irregular, unpredictable movements – known
as chorea.
Dyskinetic cerebral
palsy is characterized by both hypertonia and hypotonia.
Dyskinetic cerebral
palsy results from damage to the basal ganglia of the brain. The basal ganglia
is like the brain’s switchboard for interpreting messages between the movement
centre and the spinal cord – it is responsible for regulating voluntary
movements. The different forms of dyskinesia result from damage to slightly
different structures within the basal ganglia.
Ataxic- People with ataxia may
have:
- Unsteady, shaky movements or tremor
- Difficulties maintaining balance
- People with ataxia appear very unsteady and shaky
because their sense of balance and depth perception is affected.
Ataxia results from
damage to the cerebellum. The cerebellum is the balance centre of the brain.
The cerebellum fine-tunes movement commands in order to compensate for whatever
posture is being used. It also accounts for the various forces being generated by
different parts of the body.
Diagnose
Diagnosing
cerebral palsy takes time. There is no test that confirms or rules out cerebral
palsy. In severe cases, the child may be diagnosed soon after birth, but for
the majority, diagnosis can be made in the first two years.
For those
with milder symptoms, a diagnosis may not be rendered until the brain is fully
developed at three to five years of age. For example, the average age of
diagnosis for a child with spastic diplegia, a very common form of cerebral palsy,
is 18 months.
This can
be a difficult time for parents who suspect something might be different about
their child. Often, parents are first to notice their child has missed one of
the age-appropriate developmental milestones.
If a
growth factor is delayed, parents may hope their child is just a slow starter
who will “catch up.” While this may be the case, parents should inform the
child’s doctor of concerns, nonetheless.
Confirming
cerebral palsy can involve many steps. The first is monitoring for key
indicators such as:
·
When does the child reach development milestones and growth chart
standards for height and weight?
·
How do the child’s reflexes react?
·
Does it seem as if the child is able to focus on and hear his or
her caregivers?
·
Does posture and movement seem abnormal?
Doctors
will test reflexes, muscle tone, posture, coordination and other factors, all
of which can develop over months or even years. Primary care physicians may
want to consult medical specialists, or order tests such as MRIs, cranial
ultrasounds, or CT scans to obtain an image of the brain. Even once a diagnosis
of cerebral palsy is made, parents may wish to seek a second opinion to rule
out misdiagnosis.
Treatments
Cerebral
palsy can’t be cured, but treatment will often improve an individual's
capabilities. In general, the earlier treatment begins the better chance
children have of overcoming developmental disabilities or learning new ways to
accomplish the tasks that challenge them. Treatment may include physical
and occupational therapy, speech therapy, drugs to control seizures, relax
muscle spasms, and alleviate pain; surgery to correct anatomical abnormalities
or release tight muscles; braces and other orthotic devices; wheelchairs and
rolling walkers; and communication aids such as computers with attached voice
synthesizers.
TR
Implications
Cerebral
palsy cannot be cured, so recreation therapy should work to treat symptoms and
adapt activities to the individual's abilities. This can be done by: goals
written to maintain functional ability, maintain range of motion and
socialization; objectives dynamic. Healing is paramount. Adaptive equipment,
universal design, supports and attitude makes life bearable.
Treatments
focused upon symptom reduction and management. The goal is to maximize the
individuals independent functioning and to maintain their mental well being.
Outcomes:
mastery, self-efficacy, self-discovery, self-control, stress management,
adjustment to disability, improved body image, sense of self.
Therapeutic
recreation is an important step in helping an individual with cerebral palsy
become a well-rounded individual afforded the benefits that physical, mental,
and social experiences provide. Recreation therapy focuses on inclusion, not
exclusion, by allowing the individual to participate and be an integral part of
activities they enjoy and learn from.
However,
recreation therapy also has another purpose – to enhance the ability of a child
with cerebral palsy to plan, strategize and perform tasks in an effort to
achieve improved physical functioning and encourage emotional well-being by
facilitating inclusion into activities they benefit by and enjoy. This provides
quality of life.
Recreation
therapy is a treatment that helps children with cerebral palsy develop and
expand physical and cognitive capabilities while participating in recreational
activities. Though a child may participate in other therapies that specifically
address physical function need, recreation therapy is specifically designed to
allow children to partake in leisure pursuits by eliminating the roadblocks
that impede the pursuit of sports, arts, crafts, games and other life-enhancing
activities.
‘Where
there is a will, there is a way’ montra applies to recreation therapy. When
children with impairment are presented with an obstacle to perform a
life-enhancing activity, recreation therapists work to identify the interest
level, capabilities, adaptive approaches, and in some cases modified processes
required to complete the activity successfully.
Recreation
opportunities have advanced through the years. Sports like rugby, soccer and
tennis have been modified for individuals in wheelchairs. Hockey can be played
using an innovative, custom-designed sled and extreme sports, such as modified
downhill bike racing, prove that those with impairment have more sporting
options – and fewer limits – than ever before.
Recreation
therapy also addresses arts and cultural pursuits. Children with compromised
fine motor hand strength can use softer than average clay to make ceramic pots.
Organized painting instruction using vibrant colors can help children build
crucial neurological connections. Artwork can be created by using specialized
applications and assistive equipment. Children are participating in dance
recitals using adaptive equipment, modified movements and accepted grace.
The goals
of recreation therapy include:
Determining
a child’s capacity for recreational performance
Minimizing
a child’s disability by teaching him or her adaptive strategies
Motivating
a child to take part in activities with encouragement and support
Modifying
process and procedures to enhance inclusion
Expanding
a child’s ability to socialize and make friends
Enhancing
a child’s self-concept and self-confidence
Helping a
child develop interests
Resources
Multiple
Sclerosis
Definition
Multiple sclerosis (or MS) is a chronic, often disabling disease that attacks the central nervous system (CNS), which is made up of the brain, spinal cord, and optic nerves.
As part of
the immune attack on the central nervous system, myelin (the fatty substance
that surrounds and protects the nerve fibers in the central nervous system) is
damaged, as well as the nerve fibers themselves. The damaged myelin forms scar
tissue (sclerosis), which gives the disease its name. When any part of the
myelin sheath or nerve fiber is damaged or destroyed, nerve impulses traveling
to and from the brain and spinal cord are distorted or interrupted, producing
the variety of symptoms that can occur. This process is called Demyelination.
Symptoms
may be mild, such as numbness in the limbs, or severe, such as paralysis or
loss of vision. The progress, severity, and specific symptoms of MS are
unpredictable and vary from one person to another. Most people with MS learn to
cope with the disease and continue to lead satisfying, productive lives. Today,
new treatments and advances in research are giving new hope to people affected
by the disease.
Types of Multiple
Sclerosis
People with MS can
typically experience one of four disease courses, each of which might be
mild, moderate, or severe. The Four Courses of MS are
1. Relapsing-Remitting
MS
People with this type of
MS experience clearly defined attacks of worsening neurologic function. These
attacks—which are called relapses, flare-ups, or exacerbations —are followed by
partial or complete recovery periods (remissions), during which no disease
progression occurs. Approximately 85% of people are initially diagnosed with
relapsing-remitting MS.
2. Primary-Progressive
MS
This disease course is
characterized by slowly worsening neurologic function from the beginning—with
no distinct relapses or remissions. The rate of progression may vary over time,
with occasional plateaus and temporary minor improvements. Approximately 10% of
people are diagnosed with primary-progressive MS.
3. Secondary-Progressive
MS
Following an initial
period of relapsing-remitting MS, many people develop a secondary-progressive
disease course in which the disease worsens more steadily, with or without
occasional flare-ups, minor recoveries (remissions), or plateaus. Before the
disease-modifying medications became available, approximately 50% of people
with relapsing-remitting MS developed this form of the disease within 10 years.
Long-term data are not yet available to determine if treatment significantly
delays this transition.
4. Progressive-Relapsing
MS
In this relatively rare
course of MS (5%), people experience steadily worsening disease from the
beginning, but with clear attacks of worsening neurologic function along the
way. They may or may not experience some recovery following these relapses, but
the disease continues to progress without remissions.
Causes of MS
While the cause of MS is
still not known, scientists believe that a combination of several factors may
be involved. Studies are ongoing in the areas of immunology (the science of the
body’s immune system), epidemiology (that looks at patterns of disease in the
population), and genetics in an effort to answer this important question.
Understanding what causes MS will be an important step toward finding more
effective ways to treat it and—ultimately—cure it, or even prevent it from
occurring in the first place.
The major scientific
theories about the causes of MS include the following:
1. Immunologic
It is now generally
accepted that MS involves an immune-mediated process—an abnormal response of
the body’s immune system that is directed against the myelin (the fatty sheath
that surrounds and insulates the nerve fibers) in the central nervous system
(CNS—the brain, spinal cord and optic nerves). The exact antigen, or target
that the immune cells are sensitized to attack, remains unknown -- which is why
MS is considered by most experts to be immune-mediated rather than autoimmune.
In recent years, however, researchers have been able to identify which immune
cells are mounting the attack, some of the factors that cause them to attack,
and some of the sites, or receptors, on the attacking cells that appear to be
attracted to the myelin to begin the destructive process.
2. Environmental
MS is known to occur
more frequently in areas that are farther from the equator.
Epidemiologists—scientists who study disease patterns—are looking at many
factors, including variations in geography, demographics (age, gender, and
ethnic background), genetics, infectious causes, and migration patterns, in an
effort to understand why. Studies of migration patterns have shown that people
born in an area of the world with a high risk of MS who then move to an area
with a lower risk before the age of 15, acquire the risk of their new area.
Such data suggest that exposure to some environmental agent that occurs before
puberty may predispose a person to develop MS later on.
Some scientists think
the reason may have something to do with vitamin D, which the human body
produces naturally when the skin is exposed to sunlight. People who live closer
to the equator are exposed to greater amounts of sunlight year-round. As a
result, they tend to have higher levels of naturally-produced vitamin D, which
is thought to have a beneficial impact on immune function and may help protect
against autoimmune diseases like MS.
Other scientists study
MS clusters—which are defined as higher-than-expected numbers of cases of MS
that have occurred over a specific time period and/or in a certain area. These
clusters are of interest because they may provide clues to environmental (such
as environmental and industrial toxins, diet, or trace metal exposures) factors
that might cause or trigger the disease. So far, cluster studies have not produced
clear evidence for the existence of any triggering factor or factors in MS.
3. Infectious
Since initial exposure
to numerous viruses, bacteria and other microbes occurs during childhood, and
since viruses are well recognized as causes of demyelination and inflammation,
it is possible that a virus or other infectious agent is the triggering factor
in MS. More than a dozen viruses and bacteria, including measles, canine
distemper, human herpes virus-6, Epstein-Barr, and Chlamydia pneumonia have been
or are being investigated to determine if they are involved in the development
of MS, but none have been definitively proven to trigger
4. Genetic
While MS is not
hereditary in a strict sense, having a first-degree relative such as a parent
or sibling with MS increases an individual's risk of developing the disease
several-fold above the risk for the general population. Studies have shown that
there is a higher prevalence of certain genes in populations with higher rates
of MS. Common genetic factors have also been found in some families where there
is more than one person with MS. Some researchers theorize that MS develops
because a person is born with a genetic predisposition to react to some
environmental agent that, upon exposure, triggers an autoimmune response.
Who Gets Multiple
Sclerosis?
MS is thought to affect
more than 2.3 million people worldwide. While the disease is not contagious or
directly inherited, epidemiologists—the scientists who study patterns of
disease—have identified factors in the distribution of MS around the world that
may eventually help determine what causes the disease. These factors include
gender, genetics, age, geography, and ethnic background.
Patterns in the Distribution of MS
MS is
significantly more common (at least 2-3 times) in women than men.
MS is not
directly inherited, but genetics play an important role
in who gets the disease. While the risk of developing MS in the general
population is 1/750, the risk rises to 1/40 in anyone who has a close relative
(parent, sibling, child) with the disease. In families in which several people
have been diagnosed with MS, the risk may be even higher. Even though identical
twins share the same genetic makeup, the risk for an identical twin is only
1/4—which means that some factor(s) other than genetics are involved.
While most
people are diagnosed between the ages of 20 and 50, MS can appear in young children and teens as well as much older
adults.
In all
parts of the world, MS is more common at northern latitudes that are farther
from the equator and less common in areas closer to the equator.
MS occurs
in most ethnic groups, including African-Americans, Asians and
Hispanics/Latinos, but is more common in Caucasians of northern European
ancestry. However some ethnic groups, such as the Inuit, Aborigines and Maoris,
have few if any documented cases of MS regardless of where they live. These
variations that occur even within geographic areas with the same climate
suggest that geography, ethnicity, and other factors interact in some complex
way.
Symptoms
Symptoms
of MS are caused by the disruption in nerve signaling from the central nervous
system (CNS) to other parts of the body as a result of damage to the myelin
(the protective coating around nerve cells) and the nerve cells. The course of
the disease, some symptoms will come and go, while others may be more lasting.
The more
common symptoms include:
- Fatigue- is one of the most
common symptoms of MS, occurring in about 80% of people. Fatigue can
significantly interfere with a person's ability to function at home and at
work, and may be the most prominent symptom in a person who otherwise has
minimal activity limitations.
- Numbness- of the face, body, or
extremities (arms and legs) is one of the most common symptoms of MS, and
is often the first symptom experienced by those eventually diagnosed as
having MS.
- Walking (Gait), Balance, &
Coordination Problems- Problems with gait (difficulty in walking) are
among the most common mobility limitations in MS. Gait problems are
related to several factors
- Bladder Dysfunction- Bladder
dysfunction, which occurs in at least 80% of people with MS, usually can
be managed quite successfully
- Bowel Dysfunction- Constipation
is a particular concern among people living with MS, as is loss of control
of the bowels. Diarrhea and other problems of the stomach and bowels also
can occur.
- Vision Problems- A vision
problem is the first symptom of MS for many people. The sudden onset of
double vision, poor contrast, eye pain, or heavy blurring is frankly
terrifying-and the knowledge that vision may be compromised can make
people with MS anxious about the future.
- Dizziness and Vertigo- People
with MS may feel off balance or lightheaded. Much less often, they have
the sensation that they or their surroundings are spinning, a condition
known as vertigo.
- Sexual Dysfunction- Sexual
problems are often experienced by people with MS, but they are very common
in the general population as well. Sexual arousal begins in the central
nervous system, as the brain sends messages to the sexual organs along
nerves running through the spinal cord. If MS damages these nerve
pathways, sexual response—including arousal and orgasm—can be directly
affected. Sexual problems also stem from MS symptoms such as fatigue or
spasticity, as well as from psychological factors relating to self-esteem
and mood changes.
- Cognitive Dysfunction-
Cognition refers to a range of high-level brain functions, including the
ability to learn and remember information: organize, plan, and
problem-solve; focus, maintain, and shift attention as necessary;
understand and use language; accurately perceive the environment, and
perform calculations. Cognitive changes are common in people with
MS—approximately 50% of people with MS will develop problems with
cognition.
- Emotional Changes- Emotional
changes are very common in MS—as a reaction to the stresses of living with
a chronic, unpredictable illness and because of neurologic and immune
changes caused by the disease. Bouts of severe depression (which is
different from the healthy grieving that needs to occur in the face of
losses and changes caused by MS), mood swings, irritability, and episodes
of uncontrollable laughing and crying (called pseudobulbar affect) pose
significant challenges for people with MS and their family members.
- Spasticity- Spasticity refers
to feelings of stiffness and a wide range of involuntary muscle spasms
(sustained muscle contractions or sudden movements). It is one of the more
common symptoms of MS. Spasticity may be as mild as the feeling of
tightness of muscles or may be so severe as to produce painful,
uncontrollable spasms of extremities, usually of the legs. Spasticity may
also produce feelings of pain or tightness in and around joints, and can
cause low back pain. Although spasticity can occur in any limb, it is much
more common in the legs.
Less
Common Symptoms
- Speech
Disorders
- Swallowing
Problems
- Headache
- Hearing
Loss
- Seizures
- Tremor
- Respiration
/ Breathing Problems
- Itching
Diagnosing
Multiple Sclerosis
At this
time, there are no symptoms, physical findings or laboratory tests that can, by
themselves, determine if a person has MS. The doctor uses several strategies to
determine if a person meets the long-established criteria for a diagnosis of MS
and to rule out other possible causes of whatever symptoms the person is
experiencing. These strategies include a careful medical history, a neurologic
exam and various tests, including magnetic resonance imaging (MRI), evoked
potentials (EP) and spinal fluid analysis.
Diagnosis
In order
to make a diagnosis of MS, the physician must:
- Find evidence
of damage in at least two separate areas of the central nervous system
(CNS), which includes the brain, spinal cord and optic nerves AND
- Find evidence
that the damage occurred at least one month apart AND
- Rule out all
other possible diagnoses
The Tools for Making a
Diagnosis
1. Medical History
and Neurologic Exam
The physician takes a
careful history to identify any past or present symptoms that might be caused
by MS and to gather information about birthplace, family history and places
traveled that might provide further clues. The physician also performs a
variety of tests to evaluate mental, emotional and language functions, movement
and coordination, balance, vision, and the other four
senses.
In many instances, the
person’s medical history and neurologic exam provide enough evidence to meet
the diagnostic criteria. Other tests are used to confirm the diagnosis or
provide additional evidence if it’s necessary.
2. MRI
MRI is the best imaging
technology for detecting the presence of MS plaques or scarring (also called
lesions) in different parts of the CNS. It can also differentiate old lesions
from those that are new or active.
The diagnosis of MS
cannot be made solely on the basis of MRI because there are other diseases that
cause lesions in the CNS that look like those caused by MS. And even people
without any disease — particularly the elderly — can have spots on the brain
that are similar to those seen in MS.
Although MRI is a very
useful diagnostic tool, a normal MRI of the brain does not rule out the
possibility of MS. About 5% of people who are confirmed to have MS do not
initially have brain lesions on MRI. However, the longer a person goes without
brain or spinal cord lesions on MRI, the more important it becomes to look for
other possible diagnoses.
3. Visual
Evoked Potential (VEP)
Evoked potential (EP) tests are recordings
of the nervous system's electrical response to the stimulation of specific
sensory pathways (e.g., visual, auditory, general sensory). Because damage to myelin (demyelination) results
in a slowing of response time, EPs can sometimes provide evidence of scarring
along nerve pathways that does not show up during the neurologic exam. Visual
evoked potentials are considered the most useful for confirming the MS
diagnosis.
4.
Cerebrospinal Fluid Analysis
Analysis of the
cerebrospinal fluid, which is sampled by a spinal tap, detects the levels of
certain immune system proteins and the presence of oligoclonal bands. These
bands, which indicate an immune response within the CNS, are found in the
spinal fluid of about 90-95% of people with MS. But because they are present in
other diseases as well, oligoclonal bands cannot be relied on as positive proof
of MS.
5. Blood
Tests
While there is no
definitive blood test for MS, blood tests canrule out other
conditions that cause symptoms similar to those of MS, including Lyme
disease, a group of diseases known as collagen-vascular diseases, certain rare
hereditary disorders, and AIDS.
Treatment
Although
there is still no cure for MS, effective strategies are available to modify the
disease course, treat exacerbations (also called attacks, relapses, or
flare-ups), manage symptoms, improve function and safety, and provide emotional
support. In combination, these treatments enhance the quality of life for
people living with MS.
Modifying
the Disease Course.
The following agents can reduce
disease activity and disease progression for many individuals with relapsing
forms of MS, including those with secondary progressive disease who continue to
have relapses. Aubagio (teriflunomide), Avonex (interferon beta-1a), Betaseron
(interferon beta-1b), Copaxone (glatiramer acetate), Extavia (interferon
beta-1b), Gilenya (fingolimod), Novantrone (mitoxantrone), Rebif (interferon
beta-1a), Tysabri (natalizumab)
Managing
Symptoms.
Symptoms of MS are highly variable
from person to person and from time to time in the same individual. While
symptoms can range from mild to severe, most can be successfully managed with
strategies that include medication, self-care techniques, rehabilitation (with
a physical or occupation therapist, speech/language pathologist, cognitive
remediation specialist, among others), and the use of assistive devices.
Promoting
Function through Rehabilitation.
Rehabilitation programs focus on
function—they are designed to help you improve or maintain your ability to
perform effectively and safely at home and at work. Rehabilitation
professionals focus on overall fitness and energy management, while addressing
problems with accessibility and mobility, speech and swallowing, and memory and
other cognitive functions.
Rehabilitation
is an important component of comprehensive, quality health care for people with
MS, at all stages of the disease. Rehabilitation programs include:
- Physical
Therapy
- Occupational
Therapy
- Therapy for
Speech and Swallowing Problems
- Cognitive
Rehabilitation
- Vocational
Rehabilitation
TR
Implications
Recreation
therapy professionals see very few cases where the MS actually patient
improves. This presents challenges: goals written to maintain functional
ability, maintain range of motion and socialization; goals modified continually
as the disease progresses; objectives dynamic. Healing is paramount. Adaptive
equipment, universal design, supports and attitude makes life bearable.
Treatments
focused upon symptom reduction and management. The goal is to maximize the
individuals independent functioning and to maintain as much of his or her
pre-illness lifestyle as possible.
Outcomes:
mastery, self-efficacy, self-discover, self-control, stress management,
adjustment to disability, improved body image, sense of self.
Resources
and Organizations
There are
several organizations that can help you find accurate and useful resources for
dealing with MS. Some of these organizations have local chapters, support
groups and events to help you connect with other people with MS. Other
organizations are more focused on research and medical news.
1.
National Multiple Sclerosis Society
The
National Multiple Sclerosis Society is the largest and most famous of MS
organizations with chapters in every state. The MS Society joins researchers
and celebrities to raise the awareness of MS nationwide. Whether you are
looking for a support group or trying to understanding the latest research, the
MS Society can help.
2.
MedlinePlus: MS Webpage
MedlinePlus
is a service of the National Library of Medicine that helps the average person
to understand many health conditions. MedlinePlus contains links to federal and
other organizations with information on the medical aspects of a wide range of
diseases and conditions. This is a good website to check for links on the
latest NIH research and patient information pages.
3.
National Institute of Neurological Disorders and Stroke (NIH-NINDS)
The
National Institute of Neurological Disorders and Stroke (NINDS) is the NIH
Institute that leads research on MS. NINDS occasionally publishes information
pages for non-medical professionals that will give an overview of MS. You can
also find lists of current research on MS, clinical trials and recent
scientific publications.
4.
Multiple Sclerosis International Federation (MSIF)
For a
global perspective on MS research, news and treatment, visit the Multiple
Sclerosis International Foundation's website. You will find an overview of MS,
a bibliography of MS research, news about international MS events, and
information about MS in other countries. The MSIF's Atlas of MS has a series of
interactive maps that provide data about MS rates throughout the world.
5.
National Multiple Sclerosis Foundation (MSF)
Founded in
1986, this Florida-based organization seeks to "ensure the best quality of
life for those coping with MS by providing comprehensive support and
educational programs." The MSF conducts fundraising for a number of
service and educational projects for people with MS.
6.
Multiple Sclerosis Association of America (MSAA)
Founded in
1970, the MSAA is a national organization that provides programs and services
for people affected by MS. The MSAA has regional offices and can help connect
you with MS resources in your area. The organization conducts fundraising,
educational and support events regularly.
7. Rocky
Mountain MS Center
The
for-fee informational website has one the most comprehensive information on
Complementary and Alternative Medicine (CAM) and MS. For a 20 dollar fee, a
person can have access to discussion boards, information pages and more. The
Rocky Mountain MS Center is a non-profit center focused on providing
information about CAM and MS. As always, check with your doctor before using
any CAM therapy.
8.
Consortium of Multiple Sclerosis Centers (CMSC)
This
organization is committed "To be the preeminent professional organization
for Multiple Sclerosis healthcare providers and researchers in North America,
and a valued partner in the global MS community. Our core purpose is to
maximize the ability of MS healthcare providers to impact care of people who
are affected by MS, thus improving their quality of life." The CMSC
website is a great place to learn about some of the latest developments in MS
research and treatment.
Sources
http://www.nationalmssociety.org/index.aspx
http://www.msconnections.org/multiple-sclerosis-information/1316/
http://www.va.gov/MS/multiple-sclerosis-symptom-management.asp
http://multiplesclerosis.com/us/
Muscular
Dystrophy
Definition
Muscular
dystrophy (MD) is a group of muscle diseases that weaken the musculoskeletal
system and hamper locomotion. Muscular dystrophies are characterized by
progressive skeletal muscle weakness, defects in muscle proteins, and the death
of muscle cells and tissue.
Types
Duchenne muscular
dystrophy (DMD) is a recessive X-linked form of muscular dystrophy, affecting
around 1 in 3,600 boys, which results in muscle degeneration and eventual
deathThe disorder is caused by a mutation in the dystrophin gene, the largest
gene located on the human X chromosome, which codes for the protein dystrophin,
an important structural component within muscle tissue that provides structural
stability to the dystroglycan complex (DGC) of the cell membrane. While both
sexes can carry the mutation, females rarely exhibit signs of the disease.
Symptoms usually appear
in male children before age 6 and may be visible in early infancy. Even though
symptoms do not appear until early infancy, laboratory testing can identify
children who carry the active mutation at birth. Progressive proximal muscle
weakness of the legs and pelvis associated with a loss of muscle mass is
observed first. Eventually this weakness spreads to the arms, neck, and other
areas. Early signs may include pseudohypertrophy (enlargement of calf and
deltoid muscles), low endurance, and difficulties in standing unaided or
inability to ascend staircases. As the condition progresses, muscle tissue
experiences wasting and is eventually replaced by fat and fibrotic tissue
(fibrosis). By age 10, braces may be required to aid in walking but most
patients are wheelchair dependent by age 12. Later symptoms may include
abnormal bone development that lead to skeletal deformities, including
curvature of the spine. Due to progressive deterioration of muscle, loss of
movement occurs, eventually leading to paralysis. Intellectual impairment may
or may not be present but if present, does not progressively worsen as the
child ages. The average life expectancy for patients afflicted with DMD is
around 25
Becker Muscular
Dystrophy-Becker
muscular dystrophy (BMD) is a less severe variant of Duchenne muscular
dystrophy and is caused by the production of a truncated, but partially
functional form of dystrophin. Survival is usually into old age. Affects only
boys (with extremely rare exceptions)
Cogenital
Muscular Dystrophy-Congenital muscular dystrophy (CMD) refers to a group of muscular
dystrophies that become apparent at or near birth. Muscular dystrophies in
general are genetic, degenerative diseases primarily affecting voluntary
muscles.
Age at
onset: birth; symptoms include general muscle weakness and possible joint
deformities; disease progresses slowly; shortened life span. Congenital muscular
dystrophy includes several disorders with a range of symptoms. Muscle
degeneration may be mild or severe. Problems may be restricted to skeletal
muscle, or muscle degeneration may be paired with effects on the brain and
other organ systems. A number of the forms of the congenital muscular
dystrophies are caused by defects in proteins that are thought to have some
relationship to the dystrophin-glycoprotein complex and to the connections
between muscle cells and their surrounding cellular structure. Some forms of
congenital muscular dystrophy show severe brain malformations, such as
lissencephaly and hydrocephalus.
Distal
Muscular Dystrophy-Distal Muscular Dystrophy(DD) is a class of muscular dystrophies
that primarily affect distal muscles, which are those of the lower arms, hands,
lower legs and feet. Muscular dystrophies in general are a group of genetic,
degenerative diseases primarily affecting voluntary muscles.
Types of
distal muscular dystrophy include: distal myopathy with vocal cord and pharyngeal
weakness; Finnish (tibial) distal myopathy; Gowers-Laing distal myopathy;
hereditary inclusion-body myositis type 1; Miyoshi distal myopathy; Nonaka
distal myopathy; Welander’s distal myopathy; and ZASP-related myopathy.
Distal
muscular dystrophy can lead to weakness and wasting of muscles of the hands,
forearms and lower legs. Distal muscular dystrophies' age at onset: 20 to 60
years.
Emery-Dreifuss
muscular dystrophy- Emery-Dreifuss muscular dystrophy (EDMD) is one of nine types of
muscular dystrophy, a group of genetic, degenerative diseases primarily
affecting voluntary muscles. It is named for Alan Emery and Fritz Dreifuss,
physicians who first described the disorder among a Virginia family in the
1960s.
EDMD
usually shows itself by age 10 and is characterized by wasting and weakness of
the muscles that make up the shoulders and upper arms and the calf muscles of
the legs. Another prominent aspect of EDMD is the appearance of contractures
(stiff joints) in the elbows, neck and heels very early in the course of the
disease.
Finally,
and very importantly, a type of heart problem called a conduction block is a
common feature of EDMD and requires monitoring
EDMD is
caused by mutations in the genes that produce proteins in the membrane
surrounding the nucleus of each muscle cell. EDMD can be inherited several
different ways, although symptoms are essentially the same for all inheritance
patterns. EDMD progresses slowly. Muscle weakness may not become a source of
difficulty until later in life, although cardiac problems are usually
detectable by age 20. Intellect isn’t affected.
Facioscapulohumeral
muscular dystrophy-Facioscapulohumeral muscular dystrophy (FSHD) is a genetic muscle
disorder in which the muscles of the face, shoulder blades and upper arms are
among the most affected.
The long
name comes from facies, the Latin word and medical term for face; scapula, the
Latin word and anatomical term for shoulder blade; and humerus, the Latin word
for upper arm and the anatomical term for the bone that goes from the shoulder
to the elbow.
The term
muscular dystrophy means progressive muscle degeneration, with increasing
weakness and atrophy (loss of bulk) of muscles. In FSHD, weakness first and
most seriously affects the face, shoulders and upper arms, but the disease
usually also causes weakness in other muscles.
FSHD
usually begins before age 20, with weakness and atrophy of the muscles around
the eyes and mouth, shoulders, upper arms and lower legs. Later, weakness can
spread to abdominal muscles and sometimes hip muscles.
Some
experts divide FSHD into adult-onset and infantile-onset forms. The adult-onset
(which includes FSHD that begins in adolescence) is far more common.
In either
type of FSHD, facial weakness can start in childhood. Occasionally, other FSHD
symptoms appear in early childhood. Infantile-onset FSHD generally runs a more
pronounced course with regard to muscle weakness and sometimes also affects
hearing and vision. Preliminary evidence suggests that the infantile-onset form
is associated with a larger piece of missing DNA.
FSHD may
be inherited through either the father or the mother, or it may occur without a
family history. It is almost always associated with a genetic flaw (mutation)
that leads to a shorter than usual segment of DNA on chromosome 4. The segment
isn’t part of any particular gene, but it nevertheless seems to interfere with
the correct processing of genetic material.
A small
number of people have a disorder that looks exactly like FSHD but don’t have
the short segment on chromosome 4. The genetic cause of their disorder has yet
to be identified.
FSHD
usually progresses very slowly and rarely affects the heart or respiratory
system. Most people with the disease have a normal life span.
Limb-girdle
muscular dystrophy-Limb-girdle muscular dystrophy (LGMD) isn’t really one disease.
It’s a group of disorders affecting voluntary muscles, mainly those around the
hips and shoulders. The shoulder girdle is the bony structure that surrounds
the shoulder area, and the pelvic girdle is the bony structure surrounding the
hips. Collectively, these are called the limb girdles, and it is the muscles
connected to the limb girdles that are the most affected in LGMD.
The term
proximal is also used to describe the muscles that are most affected in LGMD.
The proximal muscles are those closest to the center of the body; distal
muscles are farther away from the center (for example, in the hands and feet).
The distal muscles are affected late in LGMD, if at all.
As of late
2012, there are more than 20 different subtypes of LGMD, and this is a complex
and constantly evolving area of research
LGMD, like
other muscular dystrophies, is primarily a disorder of voluntary muscles. These
are the muscles you use to move the limbs, neck, trunk and other parts of the
body that are under voluntary control. Over time, muscle weakness and atrophy
can lead to limited mobility and an inability to raise the arms above the
shoulders.
The
involuntary muscles, except for the heart (which is a special type of
involuntary muscle), aren’t affected in LGMD. Digestion, bowel, bladder and
sexual function remain normal. The brain, intellect and senses also are
unaffected in LGMD. Cardiopulmonary complications sometimes occur in later
stages of the disease.
LGMD is
caused by a mutation in any of at least 15 different genes that affect proteins
necessary for muscle function. Some types are autosomal dominant, meaning LGMD
is inherited from one parent. Other types are autosomal recessive and occur
when a faulty gene is inherited from each parent.
At this
time, progression in each type of LGMD can’t be predicted with certainty,
although knowing the underlying genetic mutation can be helpful. Some forms of
the disorder progress to loss of walking ability within a few years and cause
serious disability, while others progress very slowly over many years and cause
minimal disability.
LGMD can
begin in childhood, adolescence, young adulthood or even later. Both genders
are affected equally.
When
limb-girdle muscular dystrophy begins in childhood, some physicians say, the
progression is usually faster and the disease more disabling. When the disorder
begins in adolescence or adulthood, they say, it’s generally not as severe and
progresses more slowly.
Myotonic
muscular dystrophy-Myotonic muscular dystrophy (MMD) is a form of muscular dystrophy
that affects muscles and many other organs in the body.
The word
myotonic is the adjective for the word myotonia, an inability to relax muscles
at will. The term muscular dystrophy means progressive muscle degeneration,
with weakness and shrinkage of the muscle tissue.
Myotonic
muscular dystrophy often is abbreviated as “DM” in reference to its Greek name,
dystrophia myotonica. Other names for this disorder include simply myotonic
dystrophy and, occasionally, Steinert disease, after the German doctor who
originally described the disorder in 1909.
MMD is
divided into two types.
Type 1 MMD
(MMD1) occurs when a gene on chromosome 19 called DMPK contains an abnormally
expanded section.
Type 2 MMD
(MMD2) is caused by an abnormally expanded section in a gene on chromosome 3
called ZNF9. MMD2 was originally called PROMM, for proximal myotonic myopathy,
a term that has remained in use but is somewhat less common than the term MMD2.
The expanded
sections of DNA in these two genes appear to have many complex effects on
various cellular processes.
MMD causes
weakness of the voluntary muscles, although the degree of weakness and the
muscles most affected vary greatly according to the type of MMD and the age of
the person with the disorder.
Myotonia,
the inability to relax muscles at will, is another feature of MMD. For example,
it may be difficult for someone with MMD to let go of someone's hand after
shaking it.
As the
disease progresses, the heart can develop an abnormal rhythm and the heart
muscle can weaken. The muscles used for breathing can weaken, causing
inadequate breathing, particularly during sleep.
In
addition, in type 1 MMD (see Types of MMD), the involuntary muscles, such as
those of the gastrointestinal tract, can be affected. Difficulty swallowing,
constipation and gallstones can occur. In females, the muscles of the uterus
can behave abnormally, leading to complications in pregnancy and labor.
The
development of cataracts (opaque spots in the lenses of the eyes) relatively
early in life is another characteristic of MMD, in both type 1 and type 2.
Overall
intelligence is usually normal in people with MMD, but learning disabilities
and an apathetic demeanor are common in the type 1 form. In congenital MMD1,
which affects children from the time of birth, there can be serious impairment
of cognitive functioning. These children also may have problems with speech,
hearing and vision.
Generally,
the earlier MMD1 begins, the more profound the symptoms tend to be. For more,
see Signs and Symptoms.
In
general, MMD2 has a better overall prognosis than MMD1. The symptoms are often
relatively mild and progress slowly. MMD2 rarely occurs during childhood, and
there is no known congenital-onset form.
The
progression of MMD varies greatly among individuals, but in general, symptoms
progress slowly.
The most
common type of MMD1 — the "adult-onset" form — begins in adolescence
or young adulthood, often with weakness in the muscles of the face, neck,
fingers and ankles. The weakness is slowly progressive for these and eventually
other muscles.
When MMD1
begins earlier in life than adolescence — the congenital-onset and
juvenile-onset forms of the disease — it may be quite different in progression
from the adult-onset type. Children with congenital-onset MMD1, once they
survive the crucial neonatal period of respiratory muscle weakness with the
help of assisted ventilation, usually show improvements in motor and breathing
functions over the first year or so. They may have cognitive impairment,
delayed speech, difficulty eating and drinking and various other developmental
delays. Most will learn to walk. As adolescence approaches, children begin to
show symptoms of the adult-onset form of MMD1 and follow its usual progression.
The
childhood-onset form of MMD1 — beginning after infancy but before adolescence —
is more often characterized by cognitive and behavioral abnormalities than by
physical disabilities. Eventually, muscle symptoms develop, to varying degrees.
MMD2 is,
in general, a milder disease than type 1. It does not appear to have a
congenital-onset form and rarely begins in childhood.
In
contrast to type 1 MMD, the muscles affected first in MMD2 are the proximal
muscles — those close to the center of the body — particularly those around the
hips. However, some finger weakness may be seen early as well. The disorder
progresses slowly, but mobility may be impaired early because of weakness of
the large, weight-bearing muscles.
MMD2 is
quite rare, except in Germany and in people of German descent. Not as much is
known about MMD2 as about MMD1.
Oculopharyngeal
muscular dystrophy-OPMD is one of nine types of muscular dystrophy, a group of
genetic, degenerative diseases primarily affecting voluntary muscles. Although
named for the muscles it affects first — the eyelids (oculo) and throat
(pharyngeal) — OPMD also can affect facial and limb muscles.
Difficulty
swallowing and keeping the eyes open are common with OPMD. Later on, some
people with OPMD may have mobility problems.
OPMD is
caused by a genetic defect leading to production of extra chemical material
that forms clumps in the muscle cells. It can be inherited from either one or
both parents, and affects men and women equally.
Symptoms
of OPMD usually do not appear until the 40s or 50s, and progression is slow.
Who
Muscular dystrophies are generally inherited, and the different muscular
dystrophies follow various inheritance patterns. Many, like Becker,Duchenne,
and Emery-Dreifuss only affect males as they are inherited on the X
chromosomes. Other forms of muscular dystrophy, like FSHD and cogential, can
affect both males and females.
Symptoms
Progressive
muscular wasting
Poor
balance
Drooping
eyelids
Atrophy
Scoliosis
(curvature of the spine and the back)
Inability
to walk
Frequent
falls
Waddling
gait
Calf
deformation
Limited
range of movement
Respiratory
difficulty
Joint
contractures
Cardiomyopathy
Arrhythmias
Muscle
spasms
Diagnose
The
diagnosis of muscular dystrophy is based on the results of muscle biopsy,
increased creatine phosphokinase (CpK3), electromyography, electrocardiography
and DNA analysis.
A physical
examination and the patient's medical history will help the doctor determine
the type of muscular dystrophy. Specific muscle groups are affected by
different types of muscular dystrophy.
Often,
there is a loss of muscle mass (wasting), which may be hard to see because some
types of muscular dystrophy cause a build up of fat and connective tissue that
makes the muscle appear larger. This is called pseudohypertrophy.
Specific
Needs for Muscular Dystrophy
Equipment
needed for someone with MD varies depending on the type and severity of the
disease. Some of the more common types of equipment include:
- Wheelchair
- Van lifts
- Shower chairs
- Specialized
driving equipment
- Ramps for home
- Specialized
clothing
Insurance
companies aren't very helpful in covered the costs of equipment so it is hard
for families. Due to this burden, many organizations exist to aid families in
obtaining equipment, as well as a support system for a family with a member who
has MD.
Treatments
There is
no known cure for muscular dystrophy. Physical therapy, occupational therapy,
orthotic intervention (e.g., ankle-foot orthosis), speech therapy and
orthopedic instruments (e.g., wheelchairs, standing frames and powered mobile
arm supports) may be helpful. Inactivity (such as bed rest, sitting for long
periods) and bodybuilding efforts to increase myofibrillar hypertrophy can
worsen the disease.
There is
no specific treatment for any of the forms of muscular dystrophy.
Physiotherapy, aerobic exercise, low intensity anabolic steroids, prednisone
supplements may help to prevent contractures and maintain muscle tone. Orthoses
(orthopedic appliances used for support) and corrective orthopedic surgery may
be needed to improve the quality of life in some cases. The cardiac problems that
occur with Emery-Dreifuss muscular dystrophy and myotonic muscular dystrophy
may require a pacemaker. The myotonia (delayed relaxation of a muscle after a
strong contraction) occurring in myotonic muscular dystrophy may be treated
with medications such as quinine, phenytoin, or mexiletine, but no actual long
term treatment has been found.
Occupational
therapy assists the individual with MD to engage in activities of daily living
(such as self-feeding and self-care activities) and leisure activities at the
most independent level possible. This may be achieved with use of adaptive
equipment or the use of energy conservation techniques. Occupational therapy
may implement changes to a person's environment, both at home or work, to
increase the individual's function and accessibility. Occupational therapists
also address psychosocial changes and cognitive decline which may accompany MD,
as well as provide support and education about the disease to the family and
individual.
High
dietary intake of lean meat, seafood, pulses, olive oil, antioxidants such as
leafy vegetables and bell peppers, and fruits like blueberry and cherry is
advised. Decreased intake of refined food, trans fats, and caffeinated and
alcoholic beverages is also advised, as is a check for any food allergies.
After
diagnosis, medical care may include services in neurology, nutrition,
gastroenterology, respiratory care, cardiac care, orthopedics, psychosocial,
rehabilitation, and oral care.
TR
Implications
Because muscular dystrophy is a degenerative disorder, it is important
for the CTRS to remember that their patient will lose most of their muscle
strength. Before this happens, it is key to keep the person moving and as
actively involved as possible. Inactivity progresses the inevitable disability
much quicker.
Different
types of TR activities will help such as encouraging individuals to do as much
as they can on their own, deep breathing exercises to maintain lung function,
writing or arts and crafts to retain fine motor skills, wheelchair sports,
aquatics to help in range of muscle and relaxation, as well as many different
MD riding lessons.
Treatment
can focus on dealing with symptoms or addressing other diagnoses that can come
along with these conditions, such as depression, anxiety, etc. Its important to
remember that most people with these disabilities will not get “cured.” As a
CTRS it’s critical to
- Be Patient
- Work on Range
of motion
- Use of Adaptive
Activities is important
- Adapt goals and
activities as condition progresses
Muscular
Dystrophy Resources
Parent
Project MD
This is a
specific resource for parents of children who have been diagnosed with Duchenne
MD. They have information regarding the diagnosis, care, and research that is
being done to help in the fight against Duchenne MD. They also have information
of advocation and donation to the cause. You can find them at
www.EndDuchenne.org
New
Horizons Un-Limited Inc.
This
organization is a general resource for those whose children have MD and given
information on national, community, and internet levels. You can find them at
www.new-horizons.org
Muscular
Dystrophy Family Fund
This
organization came about to help families gain access to special equipment for
their family member with MD as well as advocacy and support groups. They are
sponsored by many different companies and have helped many families across the
nation. You can find them at www.mdff.org
Muscular
Dystrophy Canada
This is a
Canadian organization to help families living with MD. This is an informational
resource about the diagnosis, how to live with it, as well as information on
conferences and workshops in Canada. You can find them at www.muscle.ca
Band Back
Together
This is an
important organization that helps those living with MD know that they are not
alone. They specialize in helping fight against abuse to those with MD as well
as depression of those who have MD. They offer information about the diagnosis
and other resources in the area. You can find them at www.bandbacktogether.com
Muscular
Dystrophy Association
The MDA is
a national resource that gives information you can find in each and every state
in the United States. You can find resources near you by going to
www.mdausa.org
Sources
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