Lupus

Saturday, September 1, 2012

CNS Lupus









There are many ways in which lupus can affect the nervous system, some are very dangerous and others can be mild.  When SLE causes what is called CNS lupus this is a very serious and potentially life threatening condition that needs swift medical attention. Inflammation of the brain tissue can cause seizures, high fevers, and coma. 


Cerebritis Symptoms And Treatment Alternatives

Cerebritis is a medical term referring to the inflammation of the brain tissue and as the swelling caused by the inflammation grows, the patient may experience different cerebritis symptoms. Cerebritis is caused by infections in the brain and it is mainly a symptom itself.
Although the main cause of cerebritis is infections, patients with lupus (an autoimmune inflammatory disorder) frequently develop a certain degree of inflammation of the brain tissue. Lupus can cause other symptoms such as red patches on the cheeks which may also extend to the rest of the face, neck and other parts of the body. Discoid lupus is a condition that only affects the skin. Systemic lupus on the other hand, is a condition that can cause sudden symptoms or symptoms that develop over months or years. Commonly, systemic lupus is signaled by chronic fatigue.
It is estimated that more than half of the patients with lupus from the United States suffer from a degree or another of lupus cerebritis.
An accurate lupus cerebritis diagnosis must be established prior to following a specific treatment plan. The lupus cerebritis diagnosis is quite difficult to make. The disease can result in mild to severe symptoms which include headaches, seizures, stroke, dementia, peripheral neuropathy, cerebellar ataxia (the inability to coordinate the muscles, usually on one side of the body), chorea (involuntary movements), psychosis, and others. However, laboratory tests and imaging tests can help in diagnosing the condition.
Before starting the cerebritis treatment, it is important to accurately establish what causes the inflammation in the first place. Cerebritis is not only a result of lupus but it can be caused by a wide range of infections that either start in the brain or travel to the brain through blood. Brain inflammation can be a result or either bacterial infection such as meningitis or fungal infections. The first is mainly treated with broad spectrum antibiotics while the latter is cured with antifungal medication. Cerebritis treatment varies based several factors including the age of the patient, the general health condition of the patient, the specific type of disease that is causing the inflammation and the severity of the disease. For example, cerebritis may lead to brain abscesses which are medical emergencies and which are treated with antibiotics or antifungal drugs or surgery. In this particular case, surgery may remove that abscess but only if it is not too deep in the brain and if it is not too large. Thus, so many factors must be taken under consideration when establishing a specific treatment schema for a patient wit cerebritis.
Cerebritis is however a severe medical condition. As the symptoms evolve and worsen, patients may develop severe and life-threatening conditions such as heart-related death-causing diseases or stroke or coma. It is recommended that patients who experience sudden symptoms of cerebritis are brought to the nearest hospital as soon as possible.
As a conclusion, cerebritis symptoms may develop gradually and that makes it difficult to recognize them in the first place but given the severity of the condition, anyone who is at risk of developing it must be aware of them.

Neurologic manifestations are among the features of systemic lupus erythematosus (SLE), a multisystem autoimmune connective tissue disorder with various clinical presentations. SLE affects many organ systems, including the central and peripheral nervous systems and muscles.[1]
Central nervous system (CNS) lupus is a serious but potentially treatable illness, which still presents very difficult diagnostic challenges (see the following image). This condition is in the differential diagnosis for many neurologic conditions. Thus, neurologists and other clinicians need to be aware of the various presentations and neurologic complications of SLE; patients with SLE often have neurologic symptoms, and SLE is sometimes diagnosed after patients present for treatment of a neurologic event.[2, 3]
This axial, T2-weighted brain magnetic resonance iThis axial, T2-weighted brain magnetic resonance image (MRI) demonstrates an area of ischemia in the right periventricular white matter of a 41-year-old woman with longstanding systemic lupus erythematosus (SLE). She presented with headache and subtle cognitive impairments but no motor deficits. Faintly increased signal intensity was also seen on T1-weighted images, with a trace of enhancement following gadolinium that is too subtle to show on reproduced images. The distribution of the abnormality is consistent with occlusion of deep penetrating branches, such as may result from local vasculopathy, with no clinical or laboratory evidence of lupus anticoagulant or anticardiolipin antibody. Cardiac embolus from covert Libman-Sacks endocarditis remains less likely due to the distribution.
The pathophysiology of SLE has not been defined fully, although many genes that affect immune function, particularly the human leukocyte antigen (HLA), may augment susceptibility to clinical disease. Most monozygotic (identical) twins are discordant for clinical SLE, strongly suggesting that additional factors, probably environmental, trigger the widespread development of autoimmunity in susceptible individuals.
Certain medications (eg, phenytoin, hydralazine, procainamide, and isoniazid) may produce drug-induced lupus, but this disorder differs from classic SLE in its autoantibody profile (eg, antihistone antibody positive) and in sparing the kidneys and CNS. Once triggered, SLE's autoimmune reaction affects many sites through multiple mechanisms such as deposition of immune complexes, effects of cytokines and other chemical neuromodulators, direct attack by autoantibodies or activated leukocytes, and others.
Non-neurologic sites of damage include the renal glomeruli, joints, pleural or pericardial serosa, integument, cardiac or vascular endothelium, cardiac valves, and the oral and conjunctival mucosa. Multiple sites may be involved within the nervous system.

1 comment:

  1. The very first symptom of possible CNS Lupus I had was sudden onset extremely stiff neck and severe headache. It lasted 2 weeks, and included two ER visits, in which I was turned away without diagnosis or treatment. I also have ocular migraine on occasion, loss of balance from ataxia with resulting falls. I still am undiagnosed, though my rheumatologist is suspicious. Thanks for this blog. I think it is pointing me in the right direction.

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