Monthly Archives

May 2015

Leukemia

By Applying for disability benefits when you have:

Can I Get Social Security Disability Benefits for Leukemia?

  • How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Leukemia?
  • About Leukemia and Disability
  • Winning Social Security Disability Benefits for Leukemia by Meeting a Listing
  • Residual Functional Capacity Assessment for Leukemia
  • Getting Your Doctor’s Medical Opinion About What You Can Still Do

How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Leukemia?

If you have acute or chronic leukemia, Social Security disability benefits may be available. To determine whether you are disabled by leukemia, the Social Security Administration first considers whether your leukemia is severe enough to meet or equal a listing at Step 3 of the Sequential Evaluation Process. See Winning Social Security Disability Benefits for Leukemia by Meeting a Listing. If you meet or equal a listing because of leukemia, you are considered disabled. If your leukemia is not severe enough to equal or meet a listing, the Social Security Administration must assess your residual functional capacity (RFC) (the work you can still do, despite your leukemia), to determine whether you qualify for benefits at Step 4 and Step 5 of the Sequential Evaluation Process. See Residual Functional Capacity Assessment for Leukemia.

About Leukemia and Disability

What Is Leukemia?

Leukemia is a form of cancer arising in the bone marrow. Through a process known as hematopoiesis, the bone marrow produces the various types of cells that appear in the blood, including red blood cells (RBCs), platelets, and the various types of white blood cells (WBCs) (see Figure 1 below). In leukemia, the bone marrow produces excessive amounts of some type of white blood cell. The WBCs produced cannot carry out their normal functions because they are flawed.

During the process of hematopoiesis, white blood cells begin as blasts. Normally, the blasts then mature into more differentiated forms that carry out specific functions. For example, lymphoblasts eventually turn into mature lymphocytes; myeloblasts become granulocytes. In leukemia, the blasts do not mature properly.

Normal total white cell count in the blood is about 5,000 to 10,000/mm3. In leukemia, the WBC can rise into the 100,000/mm3 range or higher. Red blood cell production is decreased causing (often severe) anemia. Platelets may also be abnormal with high or low counts.

Composition of blood

Figure 1: The composition of blood, including white and red cells and platelets.

Symptoms of Leukemia

Symptoms of leukemia include fatigue and weakness. Patients are often pale from anemia and perhaps bleeding abnormally from some area in the body. Bleeding into the skin produces red-purple spots called petechiae.

Bone pain is common in acute leukemia. Involvement of the skin (leukemia cutis) may be present in a number of forms, such as ulcerations, blisters, raised, flat, or other lesions. Such involvement outside of the blood and bone marrow carries an even worse prognosis than acute leukemia.

Acute Leukemia

All cases of acute leukemia qualify for Social Security disability benefits based on the documented diagnosis. That diagnosis should come from a copy of the formal pathology report about the bone marrow biopsy. See Meeting Social Security Administration Listing 13.06A for Acute Leukemia.

In acute leukemia, the white cells involved are more immature and tend to be more toward the blastic end of development. These leukemias are more dangerous than the chronic forms involving more mature white cells. In adults, acute myelocytic leukemia (AML) is most frequently seen. There are other types of acute leukemia, such as acute monocytic leukemia or acute eosinophilic leukemia that involve different types of white cells. A rare form of hematologic (blood) cancer is hairy cell leukemia, which responds well to chemotherapy.

Over 10,000 new cases of AML are diagnosed yearly in the U.S. and about a third of these patients have a mutation in the FLT3 gene, which in turn produces an abnormal enzyme (tyrosine kinase) that drives the production of leukemic cells. Individuals with the FLT3 gene mutation have only a 10% to 20% cure rate, compared to individuals with other forms of AML who have a cure rate of 40% to 50%. In AML, patients under 60 years of age can expect a remission in 70% to 80% of cases with a 5-year survival of 40% to 50%; older patients only achieve complete remission in about 50% of cases with a 5-year survival of less than 10%.

Experimental drugs known as tyrosine kinase inhibitors are under development, and will probably greatly increase cures while eliminating the toxic side effects of the drugs usually required to treat acute leukemia. A different tyrosine kinase inhibitor used to treat chronic leukemia (Gleevec, imatinib) has been very effective, but is specific for chronic leukemia and will not work for acute leukemia. See Treatment of CML.

Treatment of Acute Leukemia

Chemotherapy is the treatment for acute leukemia, but in some instances a bone marrow or stem cell transplant is done. Some cases are incurable. A state in which there is no evidence of the leukemia after treatment is called remission, but it is not necessarily a cure because a relapse can occur. The longer a remission lasts, the more likely a cure has been achieved. To achieve a complete remission, which is the goal of treatment, there must be no detectable abnormal cells in peripheral blood or bone marrow aspirations.

If bone marrow transplantation is carried out at the time of the first relapse or second chemotherapy-induced remission, a cure can be achieved in about 30% of cases. That figure increases to 50 – 60% if the transplant is done during the first complete remission.

Chronic Leukemia

The chronic leukemias involve proliferation of white cells of a more mature and less cancerous variety than the acute leukemias. Chronic leukemias, while they are extremely serious diseases, do not tend to be quite as severe as the acute forms of leukemia. For that reason, a claimant is not automatically awarded Social Security disability benefits simply based on a diagnosis. See Meeting Social Security Administration Listing 13.06B for Chronic Leukemia.

Some people with chronic leukemia live for years with treatment. For example, some cases of chronic lymphocytic leukemia (CLL), which usually occurs in older people, require no treatment, or only modest treatment. Chronic myelogenous leukemia (CML) causes death in a substantial proportion of people within several years of diagnosis, even with treatment. Advances in treatment, including stem cell or bone transplantation and new drugs, continue to improve the prognosis.

Blastic Transformation of Chronic Leukemia into Acute Leukemia

The danger of a chronic leukemia, especially CML, is that it will change into an acute leukemia—acute myeloblastic leukemia (AML). The change of chronic to acute leukemia is known as a blastic transformation and is associated with an extremely high mortality, usually from infection. A blastic crisis means the majority of granulocyte white blood cells called myelocytes regress to a more immature stage of development in which they are both incapable of their normal specialized functions and are more aggressive as a blood cancer. So, a blastic transformation or crisis is the event most dreaded after diagnosis of CML.

Treatment of CML (Chronic Myelogenous Leukemia)

The transformation of normal myelocytic white blood cells into the cancerous cells of CML occurs by production of an abnormal protein known as BCR-ABL, which enables the cancer cells to live and proliferate. This protein is created by a specific enzyme known as tyrosine kinase.

Several different drugs inhibit tyrosine kinase so that the abnormal BCR-ABL protein cannot be created. Imatinib (Gleevec) is the first drug of its type to target a specific enzyme involved in the leukemic disease process. The side effects of imatinib are infrequent compared to conventional chemotherapeutic agents because it is not broadly toxic to cells like conventional chemotherapy. Nearly 25% of conventional chemotherapy patients will have severe side-effects and they will be much worse than with imatinib.

The overall 5-year survival with imatinib is about 83%, and about 63% remain in major cytogenetic (chromosomal) response after that amount of time. The best predictor for both overall and progression-free survival is a cytogenetic response at one year.

Imatinib can be toxic to the heart in patients with some conditions (hypereosinophlic syndrome and cardiac involvement, or chronic eosinophilic leukemia). These effects are generally controllable with corticosteroids. Older patients who have additional disorders may risk left ventricular dysfunction and congestive heart failure. See Can I Get Social Security Disability Benefits for Congestive (Chronic) Heart Failure? These serious side-effects are unusual; imatinib is usually well-tolerated.

In one study comparing Gleevec to standard chemotherapy with interferon and cytarabine, Gleevec was found to be about 10 times as effective in controlling CML. After 14 months, 68% of patients who received imatinib were completely free of leukemia, compared to only 7% of the interferon-cytarabine group. Furthermore, a much smaller number of patients in the Gleevec group progressed to more serious disease—blastic transformation. Unfortunately, if the patient has already entered a blastic crisis, Gleevec is much less effective, as are other medications. Once a blastic transformation occurs, Gleevec does not improve the very poor survival of standard chemotherapy when used alone. However, far fewer CML patients (1.5%) develop a blastic crisis than would otherwise be the case.

After 5 years of treatment, about 25% of patients taking imatinib discontinue it because of side effects or poor response.

Another tyrosine kinase inhibitor has been developed to be used as a second-line treatment of CML when imatinib fails. Dasatinib (Sprycel) is an oral drug that can be used in all phases of CML, including blastic transformation. A complete hematologic response has been seen with dasatinib in 92% of patients in the chronic phase of CML, and significant improvement in 70% of patients with accelerated CML, CML blast crisis, or Philadelphia chromosome positive acute lymphocytic leukemia (ALL). In one study, 85% of CML patients had achieved a complete hematologic response after 6 months of treatment with dasatinib.

Another tyrosine kinase inhibitor known as nilotinib (Tasigna) was FDA-approved in October 2007 for use in cases resistant to imatinib. A complete hematologic response with no evidence of leukemia has been achieved for at least 6 months using nilotinib. Its long-term effectiveness will require more time to determine. However, nilotinib appears to have more serious and diverse side-effects than imatinib, including thrombocytopenia, neutropenia, and cardiac toxicity, all of which carry a risk of death. Nilotinib can also be used in the accelerated phase of CML in which the disease is progressing with 10-19% blastic forms in peripheral blood. Still, chances of survival with nilotinib are far better than can be expected from untreated CML, which is certain death.

Regardless of the type of treatment, blastic transformation of either CML or CLL is associated with a survival of about 2 to 11 months, depending on the study. Those with lymphoid blastic transformation, as with conversion of chronic lymphocytic leukemia to acute lymphocytic leukemia (CLL to ALL), tend to live a few months longer than those who transform from chronic myelogenous leukemia to acute myelogenous leukemia (CML to AML). The worst prognosis is present when white cells are rapidly progressing to more immature forms and peripheral circulating blood has more than 50% of such blasts.

Continue to Winning Social Security Disability Benefits for Leukemia by Meeting a Listing.

Lupus

By Applying for disability benefits when you have:

Can I Get Social Security Disability Benefits for Lupus?

  • How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Lupus?
  • About Lupus and Disability
  • Winning Social Security Disability Benefits for Lupus by Meeting a Listing
  • Residual Functional Capacity Assessment for Lupus
  • Getting Your Doctor’s Medical Opinion About What You Can Still Do

How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Lupus?

If you have lupus, Social Security disability benefits may be available. To determine whether you are disabled by lupus, the Social Security Administration first considers whether your lupus is severe enough to meet or equal a listing at Step 3 of the Sequential Evaluation Process. See Winning Social Security Disability Benefits for Lupus by Meeting a Listing. If you meet or equal a listing because of lupus, you are considered disabled. If your lupus is not severe enough to equal or meet a listing, the Social Security Administration must assess your residual functional capacity (RFC) (the work you can still do, despite your lupus), to determine whether you qualify for disability benefits at Step 4 and Step 5 of the Sequential Evaluation Process. See Residual Functional Capacity Assessment for Lupus.

About Lupus and Disability

What Is Lupus?

Systemic lupus erythematosus (SLE) is a chronic inflammatory disease that can affect any organ or body system. It is frequently accompanied by severe fatigue, fever, malaise, and weight loss. SLE is much more common in women, who account for 85% to 90% of the cases.

SLE is a multisystem disease. The immune response against the body’s own tissues can affect any organ, with joint, muscle, ocular, respiratory, cardiovascular, digestive, renal, hematologic, skin, neurological, or mental involvement.

Cause of Lupus

Systemic lupus erythematosus (SLE) is an autoimmune disease. Its cause is not well understood, but it does have a genetic component. Numerous “lupus genes” that influence the probability of developing lupus have been identified. SLE probably appears when a person has a particular combination of genes. Due to the complexity of the disease, a cure for SLE is not likely in the near future.

Severity of Lupus

SLE is unpredictable; it is characterized by exacerbations and improvements. It may follow a benign course and be highly responsive to medication, or it may take a sudden severe course leading to early death despite therapy. Any combination of organ systems can be involved in a particular individual, in any degree of severity.

Effects of Lupus

Lupus may result in:

  • Inflammatory arthritis in the joints.
  • Muscle inflammation, pain and weakness.
  • Inflammation of the eye (uveitis), resulting in pain and blurry vision.
  • Respiratory (breathing) problems such as pleuritis, pneumonia, inflammation of the lungs (lupus pneumonitis), and bronchiectasis.
  • Heart problems, such as arrhythmias, murmurs, endocarditis, and cardiomyopathy with heart failure.
  • Digestive problems such as abnormal contractions of the esophagus (dysmotility) or inflammation of arteries (vasculitis) supplying organs of the gastrointestinal system, resulting in pancreatitis, intestinal obstruction, abdominal pain, ulcers, weight loss, or death of intestinal tissue (intestinal infarction) requiring surgical intervention.
  • Kidney problems such as chronic renal failure, which is a common cause of death in SLE.
  • Blood (hematologic) problems which can result in decreased platelets, decreased white cells, or decreased red cells (anemia). Decreased platelets increase susceptibility to bleeding. Decreased white cells increase susceptibility to infection. Anemia results in easy fatigability and weakness.
  • Skin problems leading to scarring, and the need to avoid direct sunlight (photosensitivity).
  • Nervous system involvement resulting in inflammation of the central nervous system—spinal cord and brain.
  • Mental disorders (e.g., psychosis, depression, and organic brain syndrome), which arises from nervous system inflammation.
  • Arterial inflammation (vasculitis) resulting in impaired blood flow to various organs. Impaired blood flow to the hands and feet can decrease tolerance to cold.

Additional possible abnormalities that may be associated with SLE include:

  • Muscle aches (myalgia).
  • Joint pain (arthralgia).
  • Hair loss (alopecia).
  • Fatigue.
  • Fever.
  • Enlarged lymph nodes (lymphadenopathy).
  • Enlarged spleen (splenomegaly).
  • Enlarged liver (hepatomegaly).
  • Sensitivity to cold (Raynaud’s phenomenon).
  • Hypertension.

Diagnostic Criteria Required by the Social Security Administration

There are no universally agreed-upon criteria for making a diagnosis of SLE. The table below shows the diagnostic criteria required by the Social Security Administration.

Criteria for Classification of Systemic Lupus Erythematosus
Criteria for Classification of Systemic Lupus Erythematosus
Criteria for Classification of Systemic Lupus Erythematosus

Treatment for Lupus

Since SLE is incurable, treatment is based on drug therapy that will control symptoms and progression of the disease. Kidney failure is a major cause of death and kidney function must be closely monitored.

Therapy for lupus is based on suppressing the immune system. Systemic corticostroid drugs like prednisone can be highly effective, but their use is limited by potential side-effects (e.g., hypertension, obesity, poor wound healing, osteoporosis, osteonecrosis, cataracts). Methotrexate is another immunosuppressive drug that is useful in treating SLE. The anti-malarial drug plaquenil is often capable of keeping SLE under control.

Specific medications may be required for particular problems like hypertension, depression, and skin lesions.

Every case is different. Some people respond rapidly to maintenance therapy with plaquenil and have minimal symptoms. Others are not so fortunate.

Continue to Winning Social Security Disability Benefits for Lupus by Meeting a Listing.

Multiple sclerosis

By Applying for disability benefits when you have:

Can I Get Social Security Disability Benefits for Multiple Sclerosis?

  • How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Multiple Sclerosis?
  • About Multiple Sclerosis and Disability
  • Winning Social Security Disability Benefits for Multiple Sclerosis by Meeting a Listing
  • Residual Functional Capacity Assessment for Multiple Sclerosis
  • Getting Your Doctor’s Medical Opinion About What You Can Still Do

How Does the Social Security Administration Decide if I Qualify for Disability Benefits for Multiple Sclerosis?

If you have multiple sclerosis (MS), Social Security disability benefits may be available. To determine whether you are disabled by MS, the Social Security Administration first considers whether your MS is severe enough to meet or equal a listing at Step 3 of the Sequential Evaluation Process. See Winning Social Security Disability Benefits for Multiple Sclerosis by Meeting a Listing. If you meet or equal a listing because of your MS, you are considered disabled. If your MS is not severe enough to equal or meet a listing, Social Security Administration must assess your residual functional capacity (RFC) (the work you can still do, despite your MS), to determine whether you qualify for disability benefits at Step 4 and Step 5 of the Sequential Evaluation Process. See Residual Functional Capacity Assessment for Multiple Sclerosis.

About Multiple Sclerosis and Disability

What Is Multiple Sclerosis?

Multiple sclerosis is a slowly progressive disease of the central nervous system (CNS), i.e., the spinal cord (see Figure 1 below) and brain. The incidence of multiple sclerosis in the U.S. is not reliably known—estimates vary between 250,000 to 350,000 people. In MS a substance known as myelin, which serves as the electrical insulating coating of nerve fiber tracts, is destroyed. Nerve tracts (bundles of communicating fibers) make up the “white matter” of the CNS. Therefore, white matter lesions (wounds or injuries) are characteristic of multiple sclerosis.

Interior view of the spinal cord

Figure 1: Interior view of the spinal cord.

The brain’s white matter lies beneath the brain’s outer cerebral cortex (see Figure 2 below), or “gray matter” that is composed of brain cells (neurons). Most of the volume of the brain is made up of cerebrospinal fluid-filled cavities and white matter. Since the white matter carries information to and from the cortical neurons composing the gray matter, the function of the gray matter can easily be affected by white matter abnormalities. For example, an impulse to move a leg that starts in the motor cortex of the brain could be disrupted when it enters the white matter for transmission to the spinal cord.

Outer cerebral cortex of the brain

Figure 2: Outer cerebral cortex of the brain.

The myelin destruction associated with multiple sclerosis is called demyelinization. MS is not the only disorder that can result in that abnormality. The white matter lesions of demyelinating disorders are called plaques. The plaques of MS occur in multiple and varied locations in the spinal cord and brain, particularly the brain (see Figure 3 below). Brain cells that make myelin are also damaged, but can regenerate to some extent to produce more myelin.

Most people with multiple sclerosis have a normal lifespan, so it is not known as a fatal disorder.

The base of the human brain

Figure 3: Base of the brain.

Cause of Multiple Sclerosis

The cause of MS is unknown. MS is more common in temperate than tropical areas, and moving between geographic regions at certain ages can affect the risk developing the disorder. Theories as to cause have considered a virus, brain trauma, or a problem in the immune system, but these are little more than speculation. Close relatives of people with multiple sclerosis have a higher incidence of the disorder, and this supports the possibility of a genetic contribution.

Genes on multiple chromosomes are suspected of playing some role in MS. People with multiple sclerosis are more likely to have abnormalities in human leukocyte antigens (HLA), proteins coded from chromosome 6 and important in the functioning of the immune system. If there is a genetic contribution to the development of MS, the path of “cause and effect” is not yet understood. There is no genetic test for multiple sclerosis, and even if there is a genetic contribution to cause, unknown environmental factors (such as a particular virus) may also play a role.

Although the primary cause of MS is not known, dysfunction in the immune system is the mechanism by which MS damages nerve tracts. Immune system cells called T lymphocytes (a type of white blood cell) attack the myelin of white matter nerve tracts while B lymphocytes damage the nerve fibers (axons) themselves. While demyelinated areas caused by T cell attack impair nerve impulse transmission, the B cell damage to axons themselves is more serious and slower to repair itself, if repair is possible.

This dual mechanism could explain the different types of MS discussed below. Relapse and remittance of MS may be caused by T cell activity and progression may be caused by B cell activity. All of the answers will have to await future research.

Types of Multiple Sclerosis

Several patterns are possible in the way MS first appears and the way it manifests over time (its clinical course). A typical exacerbation (worsening) of MS lasts 2 to 4 weeks, and takes several months to resolve or improve. However, this pattern is subject to considerable individual variation.

  • Relapsing-remitting MS is the most common type for which Social Security disability benefits are sought. In this form, MS first appears as a series of attacks interspersed with complete or partial improvement (remission), followed by some future relapse.
  • Primary-progressive MS is characterized by a slow progression in clinical severity, although there may be minor temporary stabilization or improvement.
  • Secondary-progressive MS begins as a relapsing-remitting form, then later becomes a primary-progressive form.
  • Progressive-relapsing MS is characterized by worsening, with additional acute exacerbations.

Patients with particularly severe MS might be described as having “malignant MS,” while those with minimal symptoms and limitations for extended periods of time are sometimes referred to as having “benign MS.”

The course of MS can vary significantly from person to person. The Social Security Administration needs detailed medical evidence about how your illness has progressed over time to make the best disability determination.

Diagnostic Categories of Multiple Sclerosis

MS affects women more frequently than men and most often first produces symptoms in the 20 to 40 age range. Disease appearing before age 10 or after age 55 is a strong argument for some other kind of disorder. The diagnosis of MS is still fundamentally clinical—a judgment based on your doctor’s evaluation of the history and physical examination, severity of signs and symptoms over time, and test evidence. The diagnosis cannot be made based on laboratory results alone, and there are no physical abnormalities unique to MS.

Diagnostic categories for multiple sclerosis

Signs and Symptoms of Multiple Sclerosis

There are a large number of possible signs and symptoms of MS. Some patients have no signs or symptoms. The major possibilities are as follows:

  • Muscle weakness sometime associated with muscle atrophy.
  • Spasticity (uncontrolled muscle contractions) – chronic spasticity can impair gait or use of arms; sudden spasms (paroxysmal dystonia) in arms or legs may occur with changes in posture or even certain kinds of sensation.
  • Impairment of pain, temperature, and touch senses – burning, itching, decreased sense of limb position, decreased touch or temperature sensation, etc.
  • Pain (moderate to severe) – sharp pains, including severe facial nerve pain (trigeminal neuralgia).
  • Ataxia – impaired ability to coordinate movement can range from mild to severe.
  • Impaired balance.
  • Tremors.
  • Decreased dexterity – impairment of fine manipulatory ability.
  • Speech disturbances – decreased clarity of articulation (dysarthria) caused by slurring, dyscoordinated speech (speech ataxia), “scanning,” i.e., with unnatural pauses and skipped sounds that result in a staccato-like delivery.
  • Aphasia – difficulty in instigating speech, understanding writing, understanding spoken words, etc.
  • Vision disturbances – paralysis of eye movement and pupillary function (internuclear ophthalmoplegia); double vision (diplopia), blurry vision (optic neuritis), abnormal eye movements (nystagmus); visual field loss is possible but unusual; color vision sensitivity may be decreased, Uhtoff’s phenomenon may occur (visual blurring after exertion or heat exposure).
  • Vertigo – dizziness may be intense, with associated nausea and vomiting; caused by inflammation of the vestibular nerve (vestibular neuronitis).
  • Bladder dysfunction – a common problem that may be urge incontinence, frequency, or decreased bladder sensation resulting in overflow incontinence.
  • Bowel dysfunction – constipation is common; loss of sensation near the anal sphincter may result in bowel incontinence.
  • Sexual dysfunction – frequently present as decreased libido in both sexes; erectile dysfunction in men; decreased vaginal lubrication in women.
  • Depression and anxiety – resulting from poor self-image, sexual dysfunction, worry about spousal rejection, and the debilitating nature of chronic disease.
  • Euphoria.
  • Seizures.
  • Cognitive (rational thinking) abnormalities – present in 40–70% of MS cases but profound mental impairment is uncommon.
  • Fatigue – easy fatigability is associated with both physical and mental activity, and not necessarily associated with obvious physical impairment or depression.
  • Exacerbation with exertion or exposure to heat.
  • Multiple sclerosis may produce findings of both upper and lower motor neuron syndrome, depending on location of the lesions.

Treatment of Signs and Symptoms of MS

Each of the signs and symptoms of MS may require separate treatment. For example, antiepileptic drugs (AEDs) would be required to control seizures and are also helpful in the treatment of the exquisitely painful disorder known as trigeminal neuralgia. Spasticity may be helped by muscle relaxants such as Baclofen (Lioresal), diazepam (Valium) and other drugs. Optic neuritis is treated with corticosteroids like prednisone or intravenous methylprednisolone. Pain may require analgesic or antidepressant medication. A number of different agents have been used to treat fatigue, such as amantadine (Symmetrel), pemoline (Cylert), and antidepressants. Self-injected papaverine in the corpus cavernosum of the penis can help temporarily reverse erectile dysfunction. There are also drugs that can help inhibit an over-active bladder, such as dantrolene (Dantrium).

In addition to drugs, physical therapy, occupational therapy, speech therapy, or psychiatric therapy may be needed in individual cases as appropriate.

Current Therapies for Multiple Sclerosis

Therapeutic Goals

The goals of therapy for MS are threefold: to improve recovery from attacks, to prevent or lessen the number of relapses, and to halt disease progression. Numerous therapies have been tried, but so far, treatment of multiple sclerosis designed to cure or stop disease progression has failed.

Therapies for MS under investigation include various treatments to alter or suppress the immune system, therapies to improve nerve impulse conduction, and therapies to reverse the damage to myelin and oligodendrocytes (the cells that make and maintain myelin in the central nervous system).

Many patients do well with no therapy, especially since many medications have serious side effects and some carry significant risks.

Steroids

Until recently, the principal medications used to treat MS were steroids possessing anti-inflammatory properties; these include adrenocorticotropic hormone (ACTH), prednisone, prednisolone, methylprednisolone, betamethasone, and dexamethasone. While steroids do not affect the course of MS over time, they can reduce the duration and severity of attacks in some patients. The mechanism behind this effect is not known. Because steroids can produce numerous adverse side effects (acne, weight gain, diabetes, seizures, hypertension, cataracts, osteoporosis, psychosis), they are not recommended for long-term use.

Interferons

One of the most promising MS research areas involves naturally occurring antiviral proteins known as interferons. Three forms of beta interferon (Avonex, Betaseron, and Rebif) have been approved by the Food and Drug Administration for treatment of relapsing-remitting MS. Beta interferon has been shown to reduce the number of exacerbations and may slow the progression of physical disability. When attacks do occur, they tend to be shorter and less severe. In addition, MRI scans suggest that beta interferon can decrease myelin destruction. However, if a patient develops neutralizing antibodies to a therapeutic drug then its effectiveness will be reduced. Once neutralizing antibodies have appeared, it does no good to switch to another type of beta interferon since the antibodies associated with the three different drugs cross-react. Common side effects of interferons include fever, chills, sweating, muscle aches, fatigue, depression, and injection site reactions.

Fingolimod

An immunomodulating agent known as fingolimod has much less prominent side effects than interferons and can be taken orally. Fingolimod is aimed at treating relapsing MS, and initial trials show a low relapse rate with continuous oral maintenance, decreased symptoms, and decreased number of lesions on magnetic resonance imaging of the brain. Fingolimod has not been approved by the FDA for human treatment outside of clinical trials. However, there is a good chance fingolimod will turn out to be a useful agent.

Natalizumab

A drug known as natalizumab was approved for treating multiple sclerosis in 2004. Natalizumab decreases the ability of white cells to enter the central nervous system. In 2005, use of the drug had to be suspended due to the risk of a rare but fatal disease known as progressive multifocal leukoencephalopathy (PML). Also, other serious problems such as hypersensitivity reactions can develop. In 2006, the drug was again approved, but only for restricted use in relapsing multiple sclerosis. Patients with progressive MS are not treatable with this drug at the present time. Treatment with natalizumab must be given intravenously on a monthly basis at a special infusion centers.

The significance of a person receiving natalizumab is two-fold for disability adjudication:

  1. The diagnosis must be very secure for the drug to be used; this should suggest to the adjudicator that the claimant has MS beyond any reasonable doubt.
  2. The drug is dangerous; it can be cleared for use only when severe relapsing MS has not responded to other treatments.

Therefore, if you are receiving this drug for treatment of MS, it should be a red flag to the Social Security Administration adjudicator to allow your case when the medical evidence is developed. If the medical evidence does not support an allowance, there is almost certainly a deficiency in the development of that evidence. Even if you have seemingly improved on natalizumab, exceptionally careful consideration of the evidence should be done before concluding that you have achieved a steady-state of improvement that would permit sustained substantial gainful activity.

Continue to Winning Social Security Disability Benefits for Multiple Sclerosis by Meeting a Listing.

Preguntas Luego de Ser Aprobado para Beneficios

By Spanish Blogs

¿Tengo que hacer algo en particular para comenzar a recibir mis beneficios?

los abogados de Lowell especialistas en los beneficios del Seguro SocialLuego de que usted reciba la notificación de que ha sido aprobado para recibir los beneficios del Seguro Social por Incapacidad, usted puede tener varias preguntas para los abogados de Lowell especialistas en el Seguro Social por Incapacidad. Aquí hay algunas preguntas comunes que nuestros abogados de Lowell especialistas en los beneficios del Seguro Social por Incapacidad contestaron.

Los abogados de Lowell especialistas en los beneficios del Seguro Social por Incapacidad pueden explicarle que usted no tiene que visitar ninguna oficina del Seguro Social o completar ningún tipo de formulario después de ser aprobado para recibir los beneficios. En su lugar, la Administración del Seguro Social comenzará a procesar sus beneficios de forma automática.

¿Cómo puedo obtener beneficios para mis hijos?

Si sus hijos son elegibles para recibir beneficios debido a su aprobación, usted tendrá que presentar una solicitud después de su fecha de autorización. Esto no afectará el procesamiento de sus propios beneficios.

¿Cuánto tiempo pasará antes de que comience a recibir mis beneficios?

Un abogado de Lowell especialista en los beneficios del Seguro Social por Incapacidad puede explicarle que, por lo general, pasarán uno o dos meses antes de que usted comience a recibir sus beneficios atrasados y sus beneficios mensuales. Si SSI está involucrado en el caso, es probable que tome mucho más tiempo. Algunos beneficiarios pueden recibir sus beneficios tres meses después de ser aprobados, mientras que otros pueden recibir los beneficios antes. Si pasan más de 90 días antes de que los beneficios sean procesados, es posible que usted tenga que ponerse en contacto con la Administración del Seguro Social para ver si hay un problema. Si usted no obtiene sus beneficios dentro de 90 días, su abogado de Lowell especialista en beneficios del Seguro Social puede ponerse en contacto con el centro de pago en su nombre.

Para más respuestas sobre sus beneficios del Seguro Social por incapacidad, comuníquese con Gerard A. Palma al 888-295-4955.

los abogados de Lowell especialistas en los beneficios del Seguro Social

Arthritis and Ineffective Ambulation

By English Blogs

Lawrence disability attorneyIf you suffer from arthritis or joint dysfunction, your Lawrence disability attorney may try to build your case by showing that your impairment prevents you from being able to ambulate effectively. By proving this, your Lawrence disability attorney can have your disability evaluated under the musculoskeletal listings.

Definitions

Your Lawrence Social Security disability attorney can explain that the lack of an ability to ambulate effectively is defined by the Social Security Administration as an extreme limitation on your ability to walk. This impairment must be one that interferes in a serious manner with your walking ability and ability to complete certain activities. This does not require you to be completely incapable of walking. Instead, your Lawrence Social Security disability attorney can explain that this means that you do not have sufficient functioning of your legs that allow you to walk without using a device to assist you.

Effective Ambulation

In contrast, effective ambulation consists of being able to sustain a reasonable walking pace over a specific distance that is correlated with your ability to complete daily living activities and to be able to travel without needing the assistance of a companion to school or work.

Examples

A few examples of ineffective ambulation include not being able to walk without a walker, two crutches or two canes, not being able to carry out basic activities, such as shopping or banking, not being able to use public transport and not being able to climb a few stairs without using a hand rail.

Talk to a Lawrence Social Security Disability Attorney

If you would like more information on this subject, contact Lawrence disability attorney Gerard A. Palma at 888-295-4955.