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Archive for the ‘Genitourinary’ Category

Congenital Thymic Aplasia and Receiving Disability

Wednesday, February 15th, 2012

Congenital thymic aplasia is a rare congenital disease. What congenital means is that it is something that is present at birth, something that you were born with.

The severity of congenital thymic aplasia and the host of difficulties that it may bring about vary widely. Congenital thymic aplasia leads to the poor development of several of your body’s systems.

One of the bad things about congenital thymic aplasia is that there are several different medical problems that are connected with this disease. Some of these medical problems include:

  • A cleft palate
  • Poor function of your immune system
  • Behavioral disorders
  • Poor function of your parathyroid glands
  • Heart defects

Pediatric endocrinologist Angelo DiGeorge was the first to describe this disease. He described it in 1968.

Congenital thymic aplasia is referred to in other ways. It is also known as Strong syndrome, thymic hypoplasia, 22q11.2 deletion syndrome, Shprintzen syndrome, velo-cardio-facial syndrome,  DiGeorge syndrome and conotruncal anomaly face syndrome.

Thankfully, congenital thymic aplasia is a rare disease. It occurs in around 1 in every 4,000 live births in the United States.

As mentioned at the beginning, congenital thymic aplasia is a disease that you are born with (congenital). The disease is the result of the deletion of a part of chromosome 22. However, the cause of this deletion has not yet been discovered.

The area of chromosome 22 that is deleted is referred to as 22q11.2. Researchers think that the wide variance in the signs and symptoms that congenital thymic aplasia produces in people is a result of the amount of genetic material that is lost in the chromosomal 22 deletion.

The signs and symptoms that are the result of congenital thymic aplasia may vary greatly both in their type and in their severity. The significant thing about this is that this is true even in the case of members of the same family who are afflicted with congenital thymic aplasia.

If you are experiencing sign and symptoms of congenital thymic aplasia, you may qualify for social security disability benefits like SSI or SSDI. It is always a wise move to contact one of the experienced social security attorneys at socialsecurityhome.com to checkout the disability benefits options that are open to you. Possible signs and symptoms that you may experience with congenital thymic aplasia may involve some combination of these things:

  • A cleft palate (a gap in the roof of the mouth) or other problems with your palate
  • Spasms or twitching around your mouth, throat, hands or arms
  • Certain facial features, such as low-set ears, wide-set eyes or a narrow groove in your upper lip
  • Poor muscle tone
  • Delay in the development of your speech
  • A bluish appearance of your skin that results from the poor circulation of oxygen-rich blood
  • Delays or difficulties with learning
  • Infections that occur frequently
  • Failure to thrive
  • Weakness or getting tired easily
  • Failure to gain weight
  • Shortness of breath
  • Congenital heart disease
  • Renal (kidney) anomalies
  • Autoimmune disorders
  • Hypocalcaemia (low serum calcium levels in your blood)

Inflammatory Fibrous Hyperplasia and Getting SSI or SSDI

Thursday, December 29th, 2011

Inflammatory fibrous hyperplasia is a chronic (continuing, ongoing) bone disease that is evidenced by a part of your bone developing abnormally. Scar-like (fibrous) tissue starts to replace and take the position of normal bone tissue. With the growth of your bone, the softer fibrous tissue keeps expanding, which leads to your bone becoming weakened by this process.

Deformity may occur in your bone that is infected by inflammatory fibrous hyperplasia. If deformity does develop, it will then increase the possibility of a fracture (break) occurring in your bone that has been affected. Do you have a severe case of inflammatory fibrous hyperplasia. If this is the case, you may be eligible to receive some form of social security disability benefits like SSI or SSDI. A smart move on your part would be to get in touch with one of the social security attorneys at socialsecurityhome.com to check this out. The social security attorneys at socialsecurityhome.com stand ready to assist you in obtaining all of the disability benefits that are rightfully yours.

Inflammatory fibrous hyperplasia is believed to begin before you are born. However, you may not realize that you are affected by inflammatory fibrous hyperplasia until you reach childhood, adolescence or adulthood.

About 7% of all benign bone tumors are due to this type of  hyperplasia. Your upper arm bone, skull, thighbone, shinbone and pelvis are the areas of your body where the disease occurs most often, but inflammatory fibrous hyperplasia may take place in any bone in your body.

In most cases, inflammatory fibrous hyperplasia involves only one of your bones. In these instances, it is known as monostotic inflammatory fibrous hyperplasia. When the disease affects two or more of your bones, it is called polystotic inflammatory fibrous hyperplasia. This form of the disease may affect two of your bones in the same limb or  several bones throughout your skeleton.

Men and women are affected equally by this. It also seems to affect all races equally.

Inflammatory fibrous hyperplasia is caused by a faulty (mutated) gene that has to do with your cells that produce bone. However, what causes this gene to become faulty is unknown.

What science does know is that inflammatory fibrous hyperplasia is neither inherited or passed down from parent to child. There are also no known environmental or dietary factors that lead to inflammatory fibrous hyperplasia.

Inflammatory fibrous hyperplasia is a disease that has no known cause. It develops spontaneously. This means that it does not result from another condition nor is it related to another disorder.

You might not have any signs and symptoms at all if your inflammatory fibrous hyperplasia is mild. If the disease is severe, however, you may experience several signs and symptoms. Some of these are:

  • Bone deformities
  • Problems with being able to walk
  • Bone sores (lesions)
  • Bone pain that grows worse with any type of activity but gets better when you rest
  • Pigmentation (an unusual skin color)
  • Bone fractures (breaks)
  • Problems with your endocrine gland
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Mesoectodermal Dysplasia Dwarfism and Getting Disability

Saturday, December 17th, 2011
Mesoectodermal Dysplasia Dwarfism

Image via Wikipedia

What is Mesoectodermal dysplasia?

Mesoectodermal dysplasia is a rare genetic (inherited) condition that is marked by  ectodermal dysplasia (abnormal development of nails, teeth, skin, hair and sweat glands), a high frequency of congenital (present at birth) heart defects and postaxial polydactyly (duplication of the small finger).  Mesoectodermal dysplasia is a condition of dwarfism that may qualify you for SSI or SSDI disability benefits.

Mesoectodermal dysplasia is characterized by disproportionate dwarfism (extremely short stature). It is also evidenced by abnormalities of your nails and hair, especially short forearms and lower legs, extra toes and/or fingers and a small narrow chest with short ribs. Do you have mesoectodermal dysplasia? Dwarfism?  If so, you may be entitled to social security disability benefits like SSI or SSDI. The way to find out is by checking with one of the social security attorneys at socialsecurityhome.com. The social security attorneys at socialsecurityhome.com will advise you in regard to receiving disability benefits. Do not delay. Contact one of the social security attorneys at socialsecurityhome.com, at your earliest convenience.

Mesoectodermal dysplasia is referred to in other ways. It is also known as  chondroectodermal dysplasia and Ellis-van Creveld syndrome.

Mesoectodermal dysplasia is often the result of something that is referred to as “founder effects.” In population genetics, founder effects is a term that is used in reference to the loss of genetic variation, like dwarfism, that may take place when a new population is established by an extremely small number of people from a larger population. Some small island populations and the Amish are examples of founder effects.

Thankfully, mesoectodermal dysplasia is a relatively rare condition. However, the condition does occur with a higher rate of incidence inside of founder-effect populations. Again, this is due to a lack of genetic variability.

Mesoectodermal dysplasia is an inherited condition. This means that the condition is passed down from parent to child by way of a defective (faulty) gene.

The pattern in which mesoectodermal dysplasia is inherited is what is known as autosomal recessive. This means that both of your parents have to have the faulty gene in order for you to inherit this condition.

The signs and symptoms that are produced by mesoectodermal dysplasia are not the same in every person who is afflicted with the condition. In addition, the severity of mesoectodermal dysplasia varies greatly from person to person.

Signs and Symptoms of mesoectodermal dysplasia

There are several different signs and symptoms that may take place with mesoectodermal dysplasia. Some of these are:

  • Short arms and legs, especially your forearms and lower legs
  • Heart defects, such as a hole in your heart (atrial septal defect)
  • Short stature such as dwarfism that usually ranges anywhere from 31/2 to 5 feet tall
  • Your urethra does not develop into a full tube and urine goes out of your body from an abnormal location as a result (epispadias)
  • Tooth abnormalities that may include peg teeth and/or natal teeth (teeth that are present at birth), widely spaced teeth and delayed or missing teeth
  • Nail difficulties that may include missing or deformed nails
  • A cleft palate or lip
  • Polydactyly (extra fingers)
  • Undescended testicle (cryptorchidism)
  • Sparse, absent or fine textured hair
  • A limited range of motion.
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Osler’s Disease and Receiving Social Security Disability Benefits

Wednesday, November 9th, 2011

Osler’s disease is a disease that is characterized by the formation of multiple abnormalities in your blood vessels (veins and arteries). These abnormal blood vessels may occur in places like your mucous membranes, skin and often times in organs like your brain, lungs and liver.

When your circulatory system is working like it ought to, blood that is transporting oxygen is pumped by your heart out of your lungs at high pressure into your arteries. By the time this blood reaches your capillaries and then flows into your veins, the pressure has gotten much lower.

If you are suffering from Osler‘s disease, some of your arteries go directly into your veins rather than being buffered by your capillaries. The high pressure has a tendency to strain and enlarge your veins due to the fact that they are not as elastic and have thinner walls than your arteries do. This may bring about compression or irritation of your adjacent tissues and frequent episodes of severe bleeding (hemorrhage).

There are different kinds of Osler‘s disease. These include type 1, type 2 and type 3. There is a higher risk for blood vessel malformations in your lungs and brain when you are afflicted with type 1 of Osler‘s disease. You are at a greater risk for malformations in your liver if you are suffering from type 2 or type 3. Women are affected by blood vessel malformations in their liver and lungs with both type 1 and type 2 more often than men are.

Osler’s disease is known by other names. It is also referred to as hereditary hemorrhagic telangiectasia and Osler-Weber-Rendu disease.

Osler’s disease is brought about by a missing or mutated (defective) gene. Researchers have been able to identify some of the genes that are responsible for leading to Osler‘s disease, but they have not yet discovered the way in which these gene defects result in these blood vessel malformations.

Osler’s disease is a disease that is passed down to you by your parents. The pattern of inheritance is what is known as autosomal dominant. What this means is that you only have to inherit a defective (mutated) gene from one of your parents in order to have the possibility of getting Osler‘s disease.

There are several different signs and symptoms that you may experience, which may be an indication of Osler‘s disease. Some of these are:

  • Black, tar-like stools
  • Unexplained, small strokes
  • Vomiting, coughing up blood
  • Dizziness, drowsiness
  • Frequent, sudden nosebleeds
  • Breathing problems, blue lips, domed fingernails (drumstick fingers)
  • Occasional paralysis
  • Fatigue
  • A pale appearance
  • Seizures (epilepsy)
  • Brain aneurysms
  • Shortness of breath when exercising
  • Lesions in your mouth and on your skin that may bleed
  • Digestive tract lesions

If you are having signs and symptoms of Osler’s disease, you may be able to get social security disability benefits. Contact the social security attorneys at socialsecurityhome.com. The social security attorneys at socialsecurityhome.com will be on your side when it comes to getting disability benefits from the Social Security Administration.

Cerebellar Ectopia and Receiving Social Security Disability Benefits

Saturday, October 8th, 2011
Cerebellar Ectopia

Image via Wikipedia

Cerebellar ectopia is a brain condition where there are abnormalities to your cerebellum. This is the lower part of your brain.

Cerebellar ectopia is marked by the lobes at the base of your cerebellum pushing through the hole at the base of your skull. These lobes are referred to as the cerebral tonsils.

The hole at the base of your skull is known as the foramen magnum. The foramen magnum is the hole through which your spinal cord passes so that it can connect to your brain. It does this by merging with the lowermost section of your brain, which is the medulla oblongata.

When your cerebellar tonsils protrude through (herniate) your foramen magnum, you may have various medical problems and complications. These will vary in their severity. The thing that determines the severity is the extent of your protrusion.

When the extent of the protrusion is severe the condition is known as a Chiari malformation. This condition is named after Professor Hans Chiari, a German pathologist. He first described this malformation in the 1890’s.

When the extent of the protrusion does not meet the guidelines for a diagnosis of being a Chiari malformation, the condition is referred to as cerebellar ectopia. Even though cerebellar ectopia is not as serious as a Chiari malformation, it can still result in problems and complications that may lead to your disability and not being able to work.

Cerebellar ectopia is caused by the area of your skull that holds your cerebellum being too small or deformed. When this is true, it presses and crowds your brain. It forces your brain downward.

Cerebellar ectopia is a congenital birth defect. What this means is that it was present when you were born.

What causes this birth defect to occur has not yet been discovered. Researchers have theorized that a problem that takes place during development in the womb may be what causes the malformation to develop in your brain.

In some instances of cerebellar ectopia, you may not have any signs and symptoms of the condition until you reach adulthood. In other cases, you may have neurological difficulties that begin in your infancy. As time passes, these problems may become more visible and apparent.

The signs and symptoms that you experience with cerebellar ectopia may vary from person to person. These signs and symptoms may become worse with the passage of time as a result of buildups of pressure.

There are several different signs and symptoms that you may have with cerebellar ectopia. Some of these include:

Ÿ  Poor hand coordination

Ÿ  Stiffness or pain that occurs in the back of your neck or head

Ÿ  Dizziness

Ÿ  A decrease in the strength of your arms

Ÿ  Numbness and tingling that takes place in your hands and feet

Ÿ  Rapid eye movements that go back and forth

Ÿ  Difficulties with your balance

Ÿ  A double or blurred vision

Ÿ  Problems with your breathing

Ÿ  Delays that occur in your development

Ÿ  A slurring of your speech

Ÿ  Headaches

Ÿ  A decrease in sensation in your arms and legs.

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Chronic Vesicoureteric Reflux and Receiving Social Security Disability

Friday, October 7th, 2011

Chronic vesicoureteric reflux is an ailment that is characterized by the backward flow of urine into your kidney. This leads to damage to your kidneys.

Urine flows out of your kidneys by way of your ureters and into your bladder. Each one of your ureters has a one-way valve at the point where urine goes into your bladder. The purpose of this one-way valve is to keep urine from flowing back up through your ureter and into your kidney.

Chronic vesicoureteric reflux takes place when these valves do not function the way that they should. Urine is then permitted to flow back up into your kidney when this occurs. If your bladder is infected or your urine contains bacteria, your kidney is placed at risk for getting pyelonephritis (infection).

What the reflux of urine does is expose your kidney to unusually high pressure. The reason for this is because the pressure in your bladder is usually higher than the pressure in your kidney. With the passage of time, this increased pressure results in scarring (focal segmental glomerulosclerosis) and damage to your kidney.

Chronic vesicoureteric reflux is known by other names. It is also referred to as chronic atrophic pyelonephritis, reflux nephropathy, nephropathy – reflux and ureteral reflux.

It is estimated that about 4 out of every 1,000 people in the United States have chronic vesicoureteric reflux without having any signs or symptoms at all. Up to 50% of infants and children in the United States who have urinary tract infections, also have chronic vesicoureteric reflux.

Chronic vesicoureteric reflux may develop in people whose valves of their ureters do not function right or whose ureters do not attach the way that they should to their bladder. This can be the result of a birth defect.

There are other conditions that may lead to chronic vesicoureteric reflux. These include:

Ÿ  Neurogenic bladder

Ÿ  Bladder outlet obstruction

Ÿ  Bladder stones.

 

Chronic vesicoureteric reflux may also be caused by swelling of your ureters that takes place after some kind of trauma to your ureter or a kidney transplant.

As mentioned earlier, you may not experience any signs or symptoms with chronic vesicoureteric reflux. You also may not have any signs or symptoms if only one of your kidneys is affected by this ailment.

If you do have signs and symptoms with chronic vesicoureteric reflux, they may be like the signs and symptoms of a urinary tract infection, chronic kidney failure or nephrotic syndrome. Some of the possible signs and symptoms that you may have are:

Ÿ  Increased urination at night (nocturia)

Ÿ  The feeling that your bladder in not fully emptying when you urinate

Ÿ  Stinging or burning with urination

Ÿ  Repeated urinary tract infections in a female

Ÿ  A single urinary tract infection in a male

Ÿ  Urinal frequency/urgency

Ÿ  Dark or foamy urine

Ÿ  Blood in your urine (hematuria)

Ÿ  Back pain, abdominal pain or flank pain.

There are other possible signs and symptoms that you may experience with this ailment. These include:

Ÿ  Chills

Ÿ  Urinary hesitancy

Ÿ  Vomiting and nausea

Ÿ  Fever

Ÿ  Nail abnormalities.

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Barbeau’s Disease and Receiving Social Security Disability

Sunday, September 11th, 2011

Muscular dystrophy is a term that is used to designate a group of hereditary, genetic muscle diseases. These diseases lead to progressive muscle weakness in the muscles that enable you to move.

Muscular dystrophy means that you have missing or incorrect information in your genes. There are certain proteins that you need in order to have healthy muscles. Muscular dystrophy keeps these proteins from being produced. Muscular dystrophy is something that you inherit from your parents. It is not contagious. You cannot “catch it” from someone who has it.

Muscular dystrophy causes your muscles to get weak over time. People who are afflicted with muscular dystrophy may gradually lose the ability to do things that most of us take for granted like walking or sitting up. These problems that are caused by muscular dystrophy can begin at birth or shortly after. However, they can also take place later on in childhood, adolescence or adulthood.

There are several different forms of muscular dystrophy that affect different muscle groups in different ways. Barbeau’s disease is one of the kinds of muscular dystrophy.

Barbeau’s disease is usually an adult form of the disease. The onset of Barbeau’s disease is usually when you are in your 40s or 50s. It can even occur up to around the age of 70.

Little was known about what causes any kind of muscular dystrophy until the 1980s. Then, researchers found out that it is caused by a mutated (defective) gene. There is an insufficient amount of dystrophin because of the defective gene. Dystrophin is a protein that aids in keeping your muscle cells intact. In the case of Barbeau’s disease, there is a faulty gene that is believed to make extra chemical material that causes the development of clumps in your muscle cells.

Barbeau’s disease progresses slowly. The first sign or symptom of Barbeau’s disease is usually muscle weakness of your throat and eyelids. You may have difficulty swallowing. Your may have trouble keeping your eyes open or with drooping eyelids.

As Barbeau’s disease advances, you may have other signs and symptoms. Some of these include:

  • Characteristic face
  • Progressive muscle weakness in your limbs
  • Progressive weakness in your facial muscles
  • Progressive ptosis (drooping of your eyelids)
  • Weakness and wasting (loss of muscle tissue) of your tongue.

 

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Dystrophia Myotonica and Receiving Social Security Disability

Thursday, September 8th, 2011
Histopathology of gastrocnemius muscle from pa...

Image via Wikipedia

Muscular dystrophy refers to a group of genetic (hereditary) muscle diseases. Progressive muscle weakness in your muscles that enable your body to move is what characterizes these diseases.

Muscular dystrophy involves incorrect or missing information in your genes. Proteins are stopped from being produced that are needed for healthy muscles. Muscular dystrophy is a disease that is passed down to you from your parents. It is not something that you can catch from someone who has it. Muscular dystrophy is not contagious.

Muscular dystrophy weakens your muscles with the passage of time. You may gradually lose your ability to do things that most people do not even think about, like sitting up or walking. These difficulties may have originated when you were a baby, or they can start in childhood, adolescence or adulthood.

There are several different kinds of muscular dystrophy that affect different muscle groups in different ways. Dystrophia myotonica is one of the forms of this disease.

Dystrophia myotonica is the most common kind of muscular dystrophy that starts in adulthood. It usually develops between the ages of 20 and 40. However, there is an infantile form of dystrophia myotonica. In fact, this disease can begin at any age from birth to old age.

Until the 1980s, there was not much known about what causes any type of muscular dystrophy. Then, researchers discovered that muscular dystrophy is caused by a defective gene. Not enough dystrophin is made because of the faulty gene. Dystrophin is a protein that helps keep your muscle cells intact. In the case of dystrophia myotonica, there is a repeated section of DNA on either chromosome 3 or chromosome 19.

The progression of dystrophia myotonica is slow. The disease can span 50 to 60 years.

The first signs and symptoms of dystrophia myotonica are usually generalized weakness and loss of muscle tissue (muscle wasting) in your hands, forearms, lower legs, face and neck. This is in conjunction with difficulty relaxing muscles after contracting them. Other signs and symptoms that you may experience are:

  • Mild diabetes
  • Difficulty breathing and swallowing
  • Frontal balding in men
  • Dizziness or fainting
  • Inability to concentrate
  • Problems with your digestive tract like diarrhea and constipation
  • Daytime sleepiness
  • Difficulty sleeping well at night
  • Clouding of the lenses of your eyes (cataracts).

You or your loved one may have decided to apply for the financial help that you need from the Social Security Administration by applying for Social Security disability benefits or disability benefits because of the disability that has resulted from dystrophia myotonica and/or complications that have been brought about by it or other ailments that you have in conjunction with this disease. You may have already applied and been denied by the Social Security Administration.

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Syracuse-related study raises serious questions about fairness of SSA disability judges

Saturday, July 30th, 2011

TRAC finds wide disparity among ALJ  rulings

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No study about SSA Disability in recent memory deserves more attention than the one recently released (and subsequently pooh-poohed by the SSA) from Syracuse University’s Trans­ac­tional Records Access Clear­ing­house (TRAC), a non-profit research orga­ni­za­tion.

Don’t let the system beat you down

If you (or a family member or friend) are one of the unlucky minions to feel trapped and ignored by the federal government’s program to aid disabled persons, please don’t let the findings of this admittedly bleak report stop you from pressing forward with your claim. If anything, this report should legitimize the idea that disability judges can be arbitrary in their rulings and therefore a trained, experienced disability attorney could be your best ally in this notoriously time-consuming process.

Huge disparity among judges’ approval rates

The following is from a Baltimore news site called Baltimore City Paper Blogs; it begins with a district centered in San Antonio, Texas–but the grim numbers apparently apply across the nation:

In San Anto­nio, Texas, peo­ple hop­ing to get Social Secu­rity dis­abil­ity pay­ments could see their cases assigned to any of 17 judges. The luck of this draw mat­ters a lot. One of the judges grants ben­e­fits in just 14 per­cent of cases. Another judge hands over benefits—which range from about $700 per month to about twice that—92 per­cent of the time.

That 78 per­cent dis­par­ity rate makes San Anto­nio the sec­ond most lottery-like sys­tem in the Social Secu­rity Administration’s arch­i­pel­ago of hear­ing offices, accord­ing to a data analy­sis by the Trans­ac­tional Records Access Clear­ing­house, a non-profit research orga­ni­za­tion housed at Syra­cuse Uni­ver­sity. (Dal­las is num­ber one, with 83 per­cent disparity).

“To a sur­pris­ing extent the records on dis­abil­ity deci­sions show again and again that even within the indi­vid­ual offices there is not a clear con­sen­sus among the judges about which claims should be awarded ver­sus which should be denied,” the authors of the report , David Burn­ham and Sue Long, write. “The prob­lem today is some­what worse than it was four and a half years ago.”

This study is from a group aligned with Syracuse University

In case you missed the in-line link, here it is again, the link to the report summary by TRAC, the research outfit aligned with Syracuse University, which reports studying nearly two million claims filed with the Social Security Administration. The report starts thusly:

A court-by-court analysis of close to two million Social Security Administration (SSA) claims has documented extensive and hard-to-explain disparities in the way the administrative law judges (ALJs) within the agency’s separate hearing offices decide whether individuals will be granted or denied disability benefits.

These findings — discussed in detail below — suggest that in many SSA hearing offices today, the chance a disability claim is granted or denied is often determined more by the particular judge assigned to handle it than by the facts and circumstances presented in the case. The findings further document that the problem is not simply the result of a few judges whose decisions are far out of line with those of other judges on the bench. Rather, the agency’s own case-by-case evidence demonstrates that the problem is systemic. To a surprising extent the records on disability decisions show again and again that even within the individual offices there is not a clear consensus among the judges about which claims should be awarded versus which should be denied.

Systemic.

That doesn’t sound good, as anyone with a systemic disease knows and understands. That means whatever the problem is, it’s not localized but instead spread throughout the entire system.

USA Today reports on ‘disparity’

Following is an excerpt from a recent USA Today report, illustrative of the perception of the status quo in such matters:

Congress and the agency’s inspector general have begun looking at the disparity. Yet both Social Security officials and advocates for the disabled say they are reluctant to interfere with the judges’ independence.

“Congress has been pretty enthusiastic about the idea of ALJ independence,” said Social Security Commissioner Michael Astrue, adding that only “a handful” of judges have approval ratings above or below average.

“They can’t tell an ALJ how to decide cases, but they can make sure they follow the agency’s policies.” said Ethel Zelenske, government affairs director for the National Organization of Social Security Claimants’ Representatives.

The Social Security Administration reports about 8.4 million disabled workers nationwide get an average monthly benefit of $1,069. Another 8.1 million low-income disabled people with little work history get about $500 a month in Supplemental Security Income. More than 2.9 million people applied for disability-worker benefits in fiscal year 2010, up 38% over the past five years, agency figures show.

To cope with the increase, Social Security has added about 200 judges in the past five years and streamlined the process of reviewing claims. The average wait time for a decision has steadily dropped, from a peak of 532 days in August 2008 to 354 days last month, agency data show.

TRAC responds to SSA’s response

To be fair, the SSA did respond to TRAC’s study-report, and TRAC’s response to that can be found here.

Just remember, we can help connect you with a compatible, trained attorney who can help you with your case–if nothing else, it’s possible that an experienced attorney might be able to steer your case toward a more reasonable outcome.

 

 

Senior-Loken Syndrome and Receiving Social Security Disability

Tuesday, July 26th, 2011
Frontal section through the kidney

Image via Wikipedia

Your kidneys have a crucial part to play in the way your body works, not only by getting rid of waste products and filtering your blood, but also by controlling your blood pressure, stimulating the production of red blood cells and balancing levels of electrolytes in your body.

Your kidneys are situated in your abdomen near the back. When things are normal, one is located on each side of your spine. The blood supply to your kidneys is through the renal arteries that come directly from your aorta, and they carry blood back to your heart through the renal veins to the vena cava. (The term “renal” is derived from the Latin name for kidney.)

Sensors within your kidneys determine how much water to excrete as urine. These sensors also decide your concentration of electrolytes when blood flows to your kidneys. For example, if you are dehydrated from sickness or exercise, your kidneys retain as much water as possible. Your urine becomes extremely concentrated. When you have enough water in your body your urine becomes clear and much more dilute.

Senior-Loken syndrome is a rare genetic (inherited) disorder. It is a disorder that involves the formation of cysts in the center of each of your kidneys that gradually cause your kidneys to lose their ability to function. Senior-Loken syndrome is evidenced by progressive wasting of the filtering unit of your kidney and progressive eye disease.

Senior-Loken disease is inherited in a manner that is known as autosomal recessive. What this means is that you have to inherit a defective (faulty) gene from each one of your parents in order to have the possibility of getting this syndrome.

There are several different signs and symptoms that you may have that may be an indication of Senior-Loken syndrome. Some of these include:

 

  • Excessive urination (polyuria)
  • Inability to concentrate urine
  • Renal salt wasting
  • Thirst
  • Kidney failure
  • Arterial hypertension (high blood pressure)
  • Anemia
  • Metabolic acidosis
  • Thickening of kidney filtration tissues
  • Increased blood creatinine level
  • Increased blood urea nitrogen
  • Retinitis pigmentosa
  • Progressive vision loss
  • Blindness
  • Tubulointerstitial nephropathy
  • Tapetoretinal degeneration
  • Growth retardation
  • Mental retardation
  • Endstage kidney disease.
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