- As a physician specializing in the treatment of myasthenia gravis
(MG), a rare, debilitating neurological disorder, I witness on a daily
basis the adversities my patients face. Imagine being a hard-working,
active adult—a mom who drove her kids to school every day, who liked to
garden and exercise—suddenly faced with a disease that makes it
difficult to see, walk or even talk. This is the reality of MG. It
steals muscle strength to the point where those living with the disorder
can no longer do the things they love. But many fight back, and I am
consistently inspired by the strength and perseverance my patients
exhibit to overcome these challenges and to not let their disease define
them.
June is an important month for the MG community because it
marks Myasthenia Gravis Awareness Month—a time when the community can
come together, share experiences, and increase awareness for this rare,
debilitating disorder. For me, this month provides a key opportunity to
leverage my experiences seeing and treating patients with MG to elevate
the public’s understanding of the disease and call attention to the
special challenges faced by those living with it, including the need for
improved diagnostic approaches and new, effective treatment
options.Diagnosing and Treating MG
In the United States, a rare
disease is one that affects fewer than 200,000 patients.1 While the
number of patients affected may be small, the impact of rare diseases on
patients, their families, and society is profound.
Like other
rare diseases, people living with MG often face a long road to diagnosis
since many physicians are unfamiliar with the signs and symptoms of MG.
As a result, it may take patients several years before they are
accurately diagnosed with MG and can begin treatment.2
Even then,
there is no cure for MG, meaning people living with this disease cope
with it over the course of their lives. While there are treatment
options available that can help manage symptoms in many patients, some
patients find that their disease is not adequately controlled with
therapies. In fact, as many as 15 percent of MG patients have refractory
MG—meaning that despite current treatment, they continue to suffer from
debilitating muscle weakness that severely impairs their ability to
engage in simple daily activities.3Living with MG
Significant
muscle weakness is the hallmark symptom of MG, but no two people
experience MG exactly the same way. Basic functions that many take for
granted—like chewing, swallowing and walking —become difficult. Other
common symptoms include drooping eyelids, blurred vision, slurred
speech, and weakness in the arms and legs. Between 15 and 20 percent of
MG patients will experience a “myasthenic crisis”—difficulty breathing
that can require hospitalization and may be life-threatening.4
While
the physicality of this disorder is debilitating, the emotional strain
MG patients experience can be just as devastating. Many MG patients feel
isolated and worry they are losing their identity. Because of their
symptoms, many have had to give up their careers and may feel like a
burden to their families both financially and socially. Relationships
and friendships can suffer since any day can bring debilitating symptoms
that force patients to cancel plans. The ability to travel, or even
take a quick trip to the grocery store, may diminish, further
compounding feelings of isolation.What’s Next for MG
For MG
patients, learning to cope with a lifelong disease can be daunting, so
it’s important to focus on cultivating a support system to help overcome
challenges. Family, friends, fellow MG patients, and physicians all
play a role in helping patients get through difficult times and cheering
them on through the great times.
Today, I am optimistic about
what the future holds for people living with MG. Unlike some rare
diseases, MG is an active area of research, with new clinical trials
under way. I am especially hopeful that new research may benefit
patients with refractory MG—who continue to suffer without adequate
treatment options.
My hope for the MG community is that the
scientific advances over the past 30 years—and particularly today’s
research—will lead to a better quality of life for patients with this
disorder. Please join me today, and every day during the month of June,
in celebrating Myasthenia Gravis Awareness Month and spreading the word
about this rare disease.
For more information about MG, including
education, support, and resources for people living with MG and their
families, visit the Myasthenia Gravis Foundation of America website at www.myasthenia.org.
James
F. Howard Jr., M.D., is a Distinguished Professor of Neuromuscular
Disease and Professor of Neurology & Medicine at the University of
North Carolina at Chapel Hill School of Medicine.
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Friday, May 13, 2016
Friday, November 13, 2015
Myasthenia Gravis Fact Sheet October 11, 2015 Lussy williams
What is myasthenia gravis?
Myasthenia gravis is a chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body. The name myasthenia gravis, which is Latin and Greek in origin, literally means “grave muscle weakness.” With current therapies, however, most cases of myasthenia gravis are not as “grave” as the name implies. In fact, most individuals with myasthenia gravis have a normal life expectancy.The hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected.
What causes myasthenia gravis?
Myasthenia gravis is caused by a defect in the transmission of nerve
impulses to muscles. It occurs when normal communication between the
nerve and muscle is interrupted at the neuromuscular junction—the place
where nerve cells connect with the muscles they control. Normally when
impulses travel down the nerve, the nerve endings release a
neurotransmitter substance called acetylcholine. Acetylcholine travels
from the neuromuscular junction and binds to acetylcholine receptors
which are activated and generate a muscle contraction.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. These antibodies are produced by the body’s own immune system. Myasthenia gravis is an autoimmune disease because the immune system—which normally protects the body from foreign organisms—mistakenly attacks itself.
In myasthenia gravis, antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. These antibodies are produced by the body’s own immune system. Myasthenia gravis is an autoimmune disease because the immune system—which normally protects the body from foreign organisms—mistakenly attacks itself.
What is the role of the thymus gland in myasthenia gravis?
The thymus gland, which lies in the chest area beneath the
breastbone, plays an important role in the development of the immune
system in early life. Its cells form a part of the body’s normal immune
system. The gland is somewhat large in infants, grows gradually until
puberty, and then gets smaller and is replaced by fat with age. In
adults with myasthenia gravis, the thymus gland remains large and is
abnormal. It contains certain clusters of immune cells indicative of
lymphoid hyperplasia—a condition usually found only in the spleen and
lymph nodes during an active immune response. Some individuals with
myasthenia gravis develop thymomas (tumors of the thymus gland).
Thymomas are generally benign, but they can become malignant.
The relationship between the thymus gland and myasthenia gravis is not yet fully understood. Scientists believe the thymus gland may give incorrect instructions to developing immune cells, ultimately resulting in autoimmunity and the production of the acetylcholine receptor antibodies, thereby setting the stage for the attack on neuromuscular transmission.
The relationship between the thymus gland and myasthenia gravis is not yet fully understood. Scientists believe the thymus gland may give incorrect instructions to developing immune cells, ultimately resulting in autoimmunity and the production of the acetylcholine receptor antibodies, thereby setting the stage for the attack on neuromuscular transmission.
What are the symptoms of myasthenia gravis?
Although myasthenia gravis may affect any voluntary muscle, muscles
that control eye and eyelid movement, facial expression, and swallowing
are most frequently affected. The onset of the disorder may be sudden
and symptoms often are not immediately recognized as myasthenia gravis.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among individuals, ranging from a localized form limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles—sometimes including those that control breathing—are affected. Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, a change in facial expression, difficulty in swallowing, shortness of breath, impaired speech (dysarthria), and weakness in the arms, hands, fingers, legs, and neck.
In most cases, the first noticeable symptom is weakness of the eye muscles. In others, difficulty in swallowing and slurred speech may be the first signs. The degree of muscle weakness involved in myasthenia gravis varies greatly among individuals, ranging from a localized form limited to eye muscles (ocular myasthenia), to a severe or generalized form in which many muscles—sometimes including those that control breathing—are affected. Symptoms, which vary in type and severity, may include a drooping of one or both eyelids (ptosis), blurred or double vision (diplopia) due to weakness of the muscles that control eye movements, unstable or waddling gait, a change in facial expression, difficulty in swallowing, shortness of breath, impaired speech (dysarthria), and weakness in the arms, hands, fingers, legs, and neck.
Who gets myasthenia gravis?
Myasthenia gravis occurs in all ethnic groups and both genders. It
most commonly affects young adult women (under 40) and older men (over
60), but it can occur at any age.
In neonatal myasthenia, the fetus may acquire immune proteins (antibodies) from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia gravis are temporary and the child’s symptoms usually disappear within 2-3 months after birth. Other children develop myasthenia gravis indistinguishable from adults. Myasthenia gravis in juveniles is uncommon.
Myasthenia gravis is not directly inherited nor is it contagious. Occasionally, the disease may occur in more than one member of the same family.
Rarely, children may show signs of congenital myasthenia or congenital myasthenic syndrome. These are not autoimmune disorders, but are caused by defective genes that produce abnormal proteins instead of those which normally would produce acetylcholine, acetylcholinesterase (the enzyme that breaks down acetylcholine), or the acetylcholine receptor and other proteins present along the muscle membrane.
Because weakness is a common symptom of many other disorders, the
diagnosis of myasthenia gravis is often missed or delayed (sometimes up
to two years) in people who experience mild weakness or in those
individuals whose weakness is restricted to only a few muscles.
The first steps of diagnosing myasthenia gravis include a review of the individual’s medical history, and physical and neurological examinations. The physician looks for impairment of eye movements or muscle weakness without any changes in the individual’s ability to feel things. If the doctor suspects myasthenia gravis, several tests are available to confirm the diagnosis.
A special blood test can detect the presence of immune molecules or acetylcholine receptor antibodies. Most patients with myasthenia gravis have abnormally elevated levels of these antibodies. Recently, a second antibody—called the anti-MuSK antibody—has been found in about 30 to 40 percent of individuals with myasthenia gravis who do not have acetylcholine receptor antibodies. This antibody can also be tested for in the blood. However, neither of these antibodies is present in some individuals with myasthenia gravis, most often in those with ocular myasthenia gravis.
The edrophonium test uses intravenous administration of edrophonium chloride to very briefly relieve weakness in people with myasthenia gravis. The drug blocks the degradation (breakdown) of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. Other methods to confirm the diagnosis include a version of nerve conduction study which tests for specific muscle “fatigue” by repetitive nerve stimulation. This test records weakening muscle responses when the nerves are repetitively stimulated by small pulses of electricity. Repetitive stimulation of a nerve during a nerve conduction study may demonstrate gradual decreases of the muscle action potential due to impaired nerve-to-muscle transmission.
Single fiber electromyography (EMG) can also detect impaired nerve-to-muscle transmission. EMG measures the electrical potential of muscle cells when single muscle fibers are stimulated by electrical impulses. Muscle fibers in myasthenia gravis, as well as other neuromuscular disorders, do not respond as well to repeated electrical stimulation compared to muscles from normal individuals.
Diagnostic imaging of the chest, using computed tomography (CT) or magnetic resonance imaging (MRI), may be used to identify the presence of a thymoma.
Pulmonary function testing, which generally call for immediate medical attention—may be triggered by infection, fever, or an adverse reaction to medication.
In neonatal myasthenia, the fetus may acquire immune proteins (antibodies) from a mother affected with myasthenia gravis. Generally, cases of neonatal myasthenia gravis are temporary and the child’s symptoms usually disappear within 2-3 months after birth. Other children develop myasthenia gravis indistinguishable from adults. Myasthenia gravis in juveniles is uncommon.
Myasthenia gravis is not directly inherited nor is it contagious. Occasionally, the disease may occur in more than one member of the same family.
Rarely, children may show signs of congenital myasthenia or congenital myasthenic syndrome. These are not autoimmune disorders, but are caused by defective genes that produce abnormal proteins instead of those which normally would produce acetylcholine, acetylcholinesterase (the enzyme that breaks down acetylcholine), or the acetylcholine receptor and other proteins present along the muscle membrane.
How is myasthenia gravis diagnosed?
The first steps of diagnosing myasthenia gravis include a review of the individual’s medical history, and physical and neurological examinations. The physician looks for impairment of eye movements or muscle weakness without any changes in the individual’s ability to feel things. If the doctor suspects myasthenia gravis, several tests are available to confirm the diagnosis.
A special blood test can detect the presence of immune molecules or acetylcholine receptor antibodies. Most patients with myasthenia gravis have abnormally elevated levels of these antibodies. Recently, a second antibody—called the anti-MuSK antibody—has been found in about 30 to 40 percent of individuals with myasthenia gravis who do not have acetylcholine receptor antibodies. This antibody can also be tested for in the blood. However, neither of these antibodies is present in some individuals with myasthenia gravis, most often in those with ocular myasthenia gravis.
The edrophonium test uses intravenous administration of edrophonium chloride to very briefly relieve weakness in people with myasthenia gravis. The drug blocks the degradation (breakdown) of acetylcholine and temporarily increases the levels of acetylcholine at the neuromuscular junction. Other methods to confirm the diagnosis include a version of nerve conduction study which tests for specific muscle “fatigue” by repetitive nerve stimulation. This test records weakening muscle responses when the nerves are repetitively stimulated by small pulses of electricity. Repetitive stimulation of a nerve during a nerve conduction study may demonstrate gradual decreases of the muscle action potential due to impaired nerve-to-muscle transmission.
Single fiber electromyography (EMG) can also detect impaired nerve-to-muscle transmission. EMG measures the electrical potential of muscle cells when single muscle fibers are stimulated by electrical impulses. Muscle fibers in myasthenia gravis, as well as other neuromuscular disorders, do not respond as well to repeated electrical stimulation compared to muscles from normal individuals.
Diagnostic imaging of the chest, using computed tomography (CT) or magnetic resonance imaging (MRI), may be used to identify the presence of a thymoma.
Pulmonary function testing, which generally call for immediate medical attention—may be triggered by infection, fever, or an adverse reaction to medication.
What are myasthenic crises?
A myasthenic crisis occurs when the muscles that control breathing
weaken to the point that ventilation is inadequate, creating a medical
emergency and requiring a respirator for assisted ventilation. In
individuals whose respiratory muscles are weak, crises—which generally
call for immediate medical attention—may be triggered by infection,
fever, or an adverse reaction to medication.
h measures breathing strength, helps
to predict whether respiration may fail and lead to a myasthenic crisis.How is myasthenia gravis treated?
Today, myasthenia gravis can generally be controlled. There are
several therapies available to help reduce and improve muscle weakness.
Medications used to treat the disorder include anticholinesterase agents
such as neostigmine and pyridostigmine, which help improve
neuromuscular transmission and increase muscle strength.
Immunosuppressive drugs such as prednisone, azathioprine, cyclosporin,
mycophenolate mofetil, and tacrolimus may also be used. These
medications improve muscle strength by suppressing the production of
abnormal antibodies. Their use must be carefully monitored by a
physician because they may cause major side effects.
Thymectomy, the surgical removal of the thymus gland (which often is abnormal in individuals with myasthenia gravis), reduces symptoms in some individuals without thymoma and may cure some people, possibly by re-balancing the immune system. Thymectomy is recommended for individuals with thymoma. Other therapies used to treat myasthenia gravis include plasmapheresis, a procedure in which serum containing the abnormal antibodies is removed from the blood while cells are replaced, and high-dose intravenous immune globulin, which temporarily modifies the immune system by infusing antibodies from donated blood. These therapies may be used to help individuals during especially difficult periods of weakness. A neurologist will determine which treatment option is best for each individual depending on the severity of the weakness, which muscles are affected, and the individual’s age and other associated medical problems.
With treatment, most individuals with myasthenia can significantly
improve their muscle weakness and lead normal or nearly normal lives.
Some cases of myasthenia gravis may go into remission—either temporarily
or permanently—and muscle weakness may disappear completely so that
medications can be discontinued. Stable, long-lasting complete
remissions are the goal of thymectomy and may occur in about 50 percent
of individuals who undergo this procedure. In a few cases, the severe
weakness of myasthenia gravis may cause respiratory failure, which
requires immediate emergency medical care
Thymectomy, the surgical removal of the thymus gland (which often is abnormal in individuals with myasthenia gravis), reduces symptoms in some individuals without thymoma and may cure some people, possibly by re-balancing the immune system. Thymectomy is recommended for individuals with thymoma. Other therapies used to treat myasthenia gravis include plasmapheresis, a procedure in which serum containing the abnormal antibodies is removed from the blood while cells are replaced, and high-dose intravenous immune globulin, which temporarily modifies the immune system by infusing antibodies from donated blood. These therapies may be used to help individuals during especially difficult periods of weakness. A neurologist will determine which treatment option is best for each individual depending on the severity of the weakness, which muscles are affected, and the individual’s age and other associated medical problems.
What is the prognosis?
What research is being done?
Within the Federal government, the National Institute of Neurological
Disorders and Stroke (NINDS), one of the National Institutes of Health
(NIH), has primary responsibility for conducting and supporting research
on brain and nervous system disorders, including myasthenia gravis.
Much has been learned about myasthenia gravis in recent years. Technological advances have led to more timely and accurate diagnosis, and new and enhanced therapies have improved management of the disorder. There is a greater understanding about the structure and function of the neuromuscular junction, the fundamental aspects of the thymus gland and of autoimmunity, and the disorder itself. Despite these advances, however, there is still much to learn. Researchers are seeking to learn what causes the autoimmune response in myasthenia gravis, and to better define the relationship between the thymus gland and myasthenia gravis.
Different drugs are being tested, either alone or in combination with existing drug therapies, to see if they are effective in treating myasthenia gravis. One study is examining the use of methotrexate therapy in individuals who develop symptoms and signs of the disease while on prednisone therapy. The drug suppresses blood cell activity that causes inflammation. Another study is investigating the use of rituximab, a monoclonal antibody against B cells which make antibodies, to see if it decreases certain antibodies that cause the immune system to attack the nervous system. Investigators are also determining if eculizumab is safe and effective in treating individuals with generalized myasthenia gravis who also receive various immunosuppressant drugs.
Another study seeks further understanding of the molecular basis of synaptic transmission in the nervous system. The objective of this study is to expand current knowledge of the function of receptors and to apply this knowledge to the treatment of myasthenia gravis.
Thymectomy is also being studied in myasthenia gravis patients who do not have thymoma to assess long-term benefit the surgical procedure may have over medical therapy alone.
One study involves blood sampling to see if the immune system is making antibodies against components of the nerves and muscle. Researchers also hope to learn if these antibodies contribute to the development or worsening of myasthenia gravis and other illnesses of the nervous system.
Investigators are also examining the safety and efficacy of autologous hematopoietic stem cell transplantation to treat refractory and severe myasthenia gravis. Participants in this study will receive several days of treatment using the immumosuppressant drugs cyclophosphamide and antithymocyte globulin before having some of their peripheral blood cells harvested and frozen. The blood cells will later be thawed and infused intravenously into the respective individuals, whose symptoms will be monitored for five years.
Much has been learned about myasthenia gravis in recent years. Technological advances have led to more timely and accurate diagnosis, and new and enhanced therapies have improved management of the disorder. There is a greater understanding about the structure and function of the neuromuscular junction, the fundamental aspects of the thymus gland and of autoimmunity, and the disorder itself. Despite these advances, however, there is still much to learn. Researchers are seeking to learn what causes the autoimmune response in myasthenia gravis, and to better define the relationship between the thymus gland and myasthenia gravis.
Different drugs are being tested, either alone or in combination with existing drug therapies, to see if they are effective in treating myasthenia gravis. One study is examining the use of methotrexate therapy in individuals who develop symptoms and signs of the disease while on prednisone therapy. The drug suppresses blood cell activity that causes inflammation. Another study is investigating the use of rituximab, a monoclonal antibody against B cells which make antibodies, to see if it decreases certain antibodies that cause the immune system to attack the nervous system. Investigators are also determining if eculizumab is safe and effective in treating individuals with generalized myasthenia gravis who also receive various immunosuppressant drugs.
Another study seeks further understanding of the molecular basis of synaptic transmission in the nervous system. The objective of this study is to expand current knowledge of the function of receptors and to apply this knowledge to the treatment of myasthenia gravis.
Thymectomy is also being studied in myasthenia gravis patients who do not have thymoma to assess long-term benefit the surgical procedure may have over medical therapy alone.
One study involves blood sampling to see if the immune system is making antibodies against components of the nerves and muscle. Researchers also hope to learn if these antibodies contribute to the development or worsening of myasthenia gravis and other illnesses of the nervous system.
Investigators are also examining the safety and efficacy of autologous hematopoietic stem cell transplantation to treat refractory and severe myasthenia gravis. Participants in this study will receive several days of treatment using the immumosuppressant drugs cyclophosphamide and antithymocyte globulin before having some of their peripheral blood cells harvested and frozen. The blood cells will later be thawed and infused intravenously into the respective individuals, whose symptoms will be monitored for five years.
Thursday, October 22, 2015
What is it like to have Myasthenia Gravis?
What is Myasthenia Gravis?
Myasthenia gravis is a neuromuscular disorder characterized by variable
weakness of voluntary muscles, which often improves with rest and
worsens with activity. The condition is caused by an abnormal immune
response.
What is it like to have Myasthenia Gravis?
| Common symptoms | What people are taking for it | |
|---|---|---|
| Pain | Pregabalin, Hydrocodone-Acetaminophen, Codeine-Acetaminophen | |
| Insomnia | Zolpidem, Clonazepam, Gabapentin | |
| Fatigue | Amphetamine-Dextroamphetamine, Wheelchair (powered), Amantadine | |
| Anxious mood | Alprazolam, Paroxetine, Lorazepam | |
| Depressed mood | Bupropion, Diet and exercise, Escitalopram |
What do patients take to treat Myasthenia Gravis and its symptoms?
| Treatments reported by members | |||
|---|---|---|---|
Pyridostigmine
(Kalymin 60N, Mestinon)
|
|||
Prednisone
(Pulmison, Pronizon, Deltasone, Encorton)
|
|||
Intravenous Immuno Globulin IVIg
(Carimune, Privigen, Pentaglobin, Sandoglobuline)
|
|||
Azathioprine
(Imurek, Azasan, Azapress, Imurel)
|
|||
These charts show data from Myasthenia Gravis patients’ latest treatment evaluations
Last updated:
- Major
- Moderate
- Slight
- None
- Can't tell
- Severe
- Moderate
- Mild
- None
Who has Myasthenia Gravis on PatientsLikeMe?
- 266 patients have this condition
- 3 new patients joined this month
- 192 say Myasthenia Gravis is their primary condition
| Age | Proportion | # of patients |
|---|---|---|
| <20 | 3 | |
| 20s | 12 | |
| 30s | 36 | |
| 40s | 58 | |
| 50s | 75 | |
| 60s | 34 | |
| 70+ | 15 |
Gender
Distribution of females vs. males
| 74% | Females |
|---|---|
| 26% | Males |
| Age at first symptom | Proportion | # of patients |
|---|---|---|
| 0-19 years | 17 | |
| 20-29 |
Tuesday, February 11, 2014
WANTED AN ASSISTANT TO HELP WITH HEALTHCARE
I was not quit aware of have it was to have an illness. I not talking about just the symptoms and the medications. I am speaking about keeping up with the appointments. To truly be a full time patient takes work. First you are of course monitoring your self. Making sure you are eating the correct foods. As much as I would love to eating whole cakes and gallons of ice cream is not a good look. especially when you may already have deficiencies. So eating healthy would be the most logical thing to do. Then there is the medications.You must make sure you are update with refills.Get them rewritten at time of Doctor visit. If you are using mail order services. No how long they take to process orders and if you need a hard copy script versus e-script. Because without all his knowledge it can leave you with no medication. I have experienced this first hand.If you have a pharmacy plan no your co-pay. (For the sake of sanity I will not go into Medicare programs.)So while monitoring what yo put into your mouth. You must also monitoring how it effects your body. Side effects and the symptoms or action of drug. So yo must research. Research what side effects are for a particular drug. An report if you are experiencing any of the side effects. Are you experiencing some type of symptom. If so what is it? Is it apart of your illness? Or a result of a side effect?
Thursday, December 19, 2013
THE GOOD OLD DAYS
The Good old days for some might have been when you were a child. Under most circumstances I would agree. But for me the good old days are when I had the energy and the strength to do anything I wanted. For me that is my Pre-Mayasthenia days. I cannot speak for most people. But I feel I have had Myasthenia long before I was diagnosed. Although prior to diagnosis I lived my life like I thought it was normal. I made adjustments for my lack of energy. And supplemented with coffee when ever needed. But I was able to hold down 2 jobs and raise 4 children without the help of their father or Government assistance. The good old days! Now I long for the days when my butt seems NOT to be glued to the chair. And it appears I cannot seem to get going. I must admit that I do not have the energy lapse everyday. But on the days that I do. It frustrates me so when I can not physically perform the duties I want to do. It is when I really feel Handicapped. Wow I said handicapped. But that is how I feel when I can not accomplish a task. I continue to have the drive and desire to excel as always. But even when I am having a great day I pay for it later. So today is one of the payback days. I understand it,but I just don't agree with it.....lol.. But it prompted me to write this post..... I just had to share........Awwww...... THE GOOD OLD DAYS!
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