Neurological Symptoms of Lupus

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I got this information from the website below. I found it short and sweet. I have neurological minifestations from lupus and therefore this interests me. I thought maybe you all would like it too.

From: http://www.ninds.nih.gov/disorders/lupus/lupus.htm

What are Neurological Sequelae Of Lupus?

Lupus (also called systemic lupus erythematosus) is a disorder of the immune system. Normally, the immune system protects the body against invading infections and cancers. In lupus, the immune system is over-active and produces increased amounts of abnormal antibodies that attack the body’s tissues and organs. Lupus can affect many parts of the body, including the joints, skin, kidneys, lungs, heart, nervous system, and blood vessels. The signs and symptoms of lupus differ from person to person; the disease can range from mild to life threatening.

Initial symptoms of lupus may begin with a fever, vascular headaches, epilepsy, or psychoses. A striking feature of lupus is a butterfly shaped rash over the cheeks. In addition to headache, lupus can cause other neurological disorders, such as mild cognitive dysfunction, organic brain syndrome, peripheral neuropathies, sensory neuropathy, psychological problems (including personality changes, paranoia, mania, and schizophrenia), seizures, transverse myelitis, and paralysis and stroke.

Is there any treatment?

 

There is no cure for lupus. Treatment is symptomatic. With a combination of medication, rest, exercise, proper nutrition, and stress management, most individuals with lupus can often achieve remission or reduce their symptom levels. Medications used in the treatment of lupus may include aspirin and other nonsteroidal anti-inflammatory medications, antimalarials, corticosteroids, and immunosuppressive drugs.

What is the prognosis?

 

The prognosis for lupus varies widely depending on the organs involved and the intensity of the inflammatory reaction. The course of lupus is commonly chronic and relapsing, often with long periods of remission. Most individuals with lupus do not develop serious health problems and have a normal lifespan with periodic doctor visits and treatments with various drugs.

What research is being done?

 

Investigators researching lupus seek to increase scientific understanding of the disorder and to find ways to treat, prevent, and ultimately, cure it. Several components of the National Institutes of Health support research on lupus

Neurological Symptoms in Lupus

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I found this information at the webpage, asktheneurologist.com. It is something that interested me and I thought I would share it. Hope you all find it as interesting as I did!

Systemic Lupus Erythematosus (SLE or lupus for short) is disease of the immune system (autoimmune disease) affecting many different organ systems throughout the body.

Neurological and psychiatric symptoms occur in many patients due to the disease process itself however the issue is further complicated by the fact that drugs used in SLE and other “rheumatological” conditions may have a variety of neurological side effects. In addition neurological problems may result from damage to other organ systems such as the liver and kidneys.

Lupus Neurology:- Neurological features of SLE

 

SLE is characterized by the presence of circulating antibodies which attack the host (“autoantibodies”)

 lupus myelitis 

A wide variety of neurological symptoms may occur in patients previously diagnosed with SLE. However, patients ultimately diagnosed with SLE may initially present with neurological symptoms and have no obvious involvement of other organ systems on initial clinical evaluation. Therefore many patients originally going to a neurologist with neurological syndromes should be screened for clinical and laboratory features of SLE.

On the other hand, neurological evaluation of patients with established SLE may not be straightforward, as neurological problems may be a direct consequence of the disease, a result of other organ involvement or due to therapeutic interventions. The American College of Rheumatology defined 19 neuropsychiatric syndromes (NPS) occurring in SLE. These represent conditions directly associated with SLE and does not include conditions occurring because of other organ involvement or therapy.

The antiphospholipid antibody syndrome (APLAS) is a frequent accompaniment to SLE and the frequency of nervous system involvement is higher in SLE patients with antiphospholipid antibodies, particularly anticardiolipin antibodies. Furthermore, neuropsychiatric syndromes frequently occur in APLAS without SLE

 

Various neurological problems may be interrelated. For example, cerebrovascular disease or stroke may lead to “focal deficits” such as weakness of one side, cognitive problems, seizures and a movement disorder . Similarly, inflammation of the spinal cord (“myelitis”) may either be isolated, or reflect the co-existence of Neuromyelitis optica or Devic disease, or multiple sclerosis (MS) both of which which are sometimes an issue in “lupus neurology”.

A severe syndrome of short term memory loss due to bilateral hippocampal inflammation known as “limbic encephalitis” may occasionally occur.

Although headache is often considered to be one of the neurological manifestations of SLE the association is controversial. Headache is probably no more frequent in SLE when compared to the general population, while migraine with aura may be commoner in SLE sufferers especially with anticardiolipin antibodies. In children with SLE, headache may be associated with CNS involvement and may lead to referral for an MRI.

To summarize:- neurological dysfunction is an important cause of disability in SLE and many neurological disorders will prompt a neurologist to exclude the presence of a co-existing rheumatic condition such as SLE.

Antibodies Role in Neurological Symptoms of Lupus

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A friend of mine posted this on facebook and I thought it was an interesting article so I am reposting it here as well. This information came from the web page http://www.prweb.com/releases/neurological_symptoms/lupus_sle/prweb4748694.htm

Feel free to share your thoughts on this article int he comments section below…

How Antibodies Play a Role in Triggering Neurological Symptoms of Lupus

Betty Diamond, MD, head of the Center for Autoimmune and Musculoskeletal Disorders at the Feinstein Institute, has collaborated with colleagues at the Burke Cornell Medical Research Institute to identify two distinct mechanisms that explain the how lupus autoantibodies alter brain function and led to such a wide array of neuropsychiatric complaints.

Quote startWe think we understand why some manifestations are transient and some are not.Quote end

Manhasset, NY (Vocus) November 5, 2010

Many patients with systemic lupus erythematosus (SLE) suffer from a variety of neuropsychiatric problems and scientists at the Feinstein Institute for Medical Research have been trying to understanding the mechanism that underlies these devastating problems. Now, Betty Diamond, MD, head of the Center for Autoimmune and Musculoskeletal Disorders at the Feinstein Institute, has collaborated with colleagues at the Burke Cornell Medical Research Institute to identify two distinct mechanisms that explain the how lupus autoantibodies alter brain function and led to such a wide array of neuropsychiatric complaints.

Patients with lupus, an autoimmune disease that targets many different organs of the body, including the brain, generate autoantibodies that frequently bind double-stranded DNA and cross react with specific glutamate receptors that are toxic to brain cells. The autoantibodies can mediate the cognitive and emotional problems (depression, memory problems and confusion) that are common among lupus patients.

Patricio Huerta, PhD, and Bruce T. Volpe, MD, of the Burke Research Institute have worked with the Diamond lab at the Feinstein to figure out what is going at the level of the neuron that could help explain why the symptoms are so varied. They report in the latest issue of PNAS that the anti-DNA antibody binds to open receptors and that the antibody to the glutamate NMDA receptor only targets activated neurons. At low concentrations, the antibodies augment (NMDA) excitatory post synaptic potentials and at high concentrations they alter mitochondria permeability and cause cell death. This could explain, said Dr. Diamond, why the severity of the symptoms differs from patient to patient.

“This finding helps explain why some cognitive problems are transient and some are permanent,” she said. “Low concentrations of antibody cause transient problems and high concentrations (that lead to cell death) cause life-long problems.”

While this part of the research was conducted in lab dishes, they also studied cerebrospinal fluid samples from lupus patients and found that the levels from low to high concentrations are associated with their symptoms. “We think we understand why some manifestations are transient and some are not,” said Dr. Diamond.

The scientists have worked with medicinal chemists at the Feinstein Institute on the development of drugs that block the antibody from binding to the NMDA receptor. There is now work underway in laboratory models to test whether these can prevent the devastating neuropsychiatric symptoms of lupus.

About The Feinstein Institute for Medical Research

Headquartered in Manhasset, NY, The Feinstein Institute for Medical Research is home to international scientific leaders in cancer, leukemia, lymphoma, Parkinson’s disease, Alzheimer’s disease, psychiatric disorders, substance abuse, rheumatoid arthritis, lupus, sepsis, inflammatory bowel disease, diabetes, human genetics, neuroimmunology, and medicinal chemistry. Feinstein researchers are developing new drugs and drug targets, and producing results where science meets the patient, annually enrolling some 10,000 subjects into clinical research programs.

Lupus Neurology

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Once again, in researching some things about lupus, I found this interesting article discussing neurology and lupus. It is written by neurologists for neurologists but it is enlightening for patients as well. This information came fromt he website www.asktheneurologist.com.

Lupus Neurology


“Lupus neurology:- Here we deal with all the neurological manifestations of lupus including epilepsy, headache,and psychiatric problems

// //

Systemic Lupus Erythematosus (SLE or lupus for short) is disease of the immune system (autoimmune disease) affecting many different organ systems throughout the body.

Neurological and psychiatric symptoms occur in many patients due to the disease process itself however the issue is further complicated by the fact that drugs used in SLE and other “rheumatological” conditions may have a variety of neurological side effects. In addition neurological problems may result from damage to other organ systems such as the liver and kidneys.

Lupus Neurology:- Neurological features of SLE

 

SLE is characterized by the presence of circulating antibodies which attack the host (“autoantibodies”)

 

lupus myelitis 

A wide variety of neurological symptoms may occur in patients previously diagnosed with SLE. However, patients ultimately diagnosed with SLE may initially present with neurological symptoms and have no obvious involvement of other organ systems on initial clinical evaluation. Therefore many patients originally going to a neurologist with neurological syndromes should be screened for clinical and laboratory features of SLE.

On the other hand, neurological evaluation of patients with established SLE may not be straightforward, as neurological problems may be a direct consequence of the disease, a result of other organ involvement or due to therapeutic interventions. The American College of Rheumatology defined 19 neuropsychiatric syndromes (NPS) occurring in SLE. These represent conditions directly associated with SLE and does not include conditions occurring because of other organ involvement or therapy.

The antiphospholipid antibody syndrome (APLAS) is a frequent accompaniment to SLE and the frequency of nervous system involvement is higher in SLE patients with antiphospholipid antibodies, particularly anticardiolipin antibodies. Furthermore, neuropsychiatric syndromes frequently occur in APLAS without SLE

 

Various neurological problems may be interrelated. For example, cerebrovascular disease or stroke may lead to “focal deficits” such as weakness of one side, cognitive problems, seizures and a movement disorder . Similarly, inflammation of the spinal cord (“myelitis”) may either be isolated, or reflect the co-existence of Neuromyelitis optica or Devic disease, or multiple sclerosis (MS) both of which which are sometimes an issue in “lupus neurology”.

A severe syndrome of short term memory loss due to bilateral hippocampal inflammation known as “limbic encephalitis” may occasionally occur.

Although headache is often considered to be one of the neurological manifestations of SLE the association is controversial. Headache is probably no more frequent in SLE when compared to the general population, while migraine with aura may be commoner in SLE sufferers especially with anticardiolipin antibodies. In children with SLE, headache may be associated with CNS involvement and may lead to referral for an MRI.

To summarize:- neurological dysfunction is an important cause of disability in SLE and many neurological disorders will prompt a neurologist to exclude the presence of a co-existing rheumatic condition such as SLE.