LED syndrome antiphospholipide and CNS

Davies J.

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LED syndrome antiphospholipide and CNS

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Abstract

The neurolupus represents the second leading cause of death in the LED. Although its incidence is high, it remains difficult to diagnose because of the diversity of events and the possible confusion with other brain diseases. In the absence of pathognomonic lesions, the diagnostic approach based on research criteria for an LED, the distinction between functional or organic etiologies and the exclusion of symptoms unrelated to the LED. The search for specific serological parameters, an analysis of the LCR, an EEG, a brain imaging psychomotor tests or brain biopsy, if necessary, will be carried out. If the CNS lesions are associated with a syndrome antiphospholipide, treatment is based on anticoagulation otherwise immunosuppression should be considered

Summary
Introduction
Neuropsychiatric manifestations and LED
Neurological manifestations of primary LED
Psychiatric manifestations of lupus primary brain
Diagnostic approach of neuropsychiatric manifestations of systemic lupus erythematosus
Brain imaging
Cytokines, polymorphisms and LED
HLA and cytokines
Conclusion
Bibliography

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Extract

[...] Neuropsychiatric manifestations and LED It should be a distinction between neuropsychiatric events by forming part of the basic disease and may possibly occur as initial symptoms of SLE, other complications secondary disease once established. Neuropsychiatric manifestations of LEDs can be classified into neurological and psychiatric manifestations primary and secondary events. Their presentation may be diffuse, in which case they are often transient, reversible treatment and association with a specific pathological finding; unlike focal manifestations, often presenting acute refractory to treatment and for which histological lesions are found at autopsy. [...]

[...] Anxiety in the setting of the diagnosis LED or during exacerbations of the disease is manifested by palpitations, diarrhea, sweating, hyperventilation, difficulty speaking, memory impairment, and headache. The risk of progression to obsessive compulsive behavior, phobias or hypochondriac disorders should be considered. Diagnostic approach of neuropsychiatric manifestations of systemic lupus erythematosus There is no specific test to establish to establish the diagnosis of lupus neuropsychia tion. The diagnosis is, therefore, to establish a first step in the diagnosis of systemic lupus erythematosus and then seeks to distinguish attacks organic functional brain damage, and to exclude symptoms not related to an LED. [...]

[...] Of lupus retinopathy is a marker of activity of the LED and brain damage. It is usually associated with a good visual prognosis, but a decrease in survival. Transverse myelitis was diagnosed in some patients presenting with an acute muscle weakness of lower limbs and loss of control of sphincters. This presentation coincides in principle with other signs of active lupus disease. Arteritis is suspected to cause ischemic necrosis of the spinal cord. The association with the presence of antiphospholipid antibodies was not demonstrated by all studies. [...]

[...] In the case of LEDs made with achieving the SN, and when the symptoms are not solely due to a syndrome antiphospholipide, an immunosuppressant cyclophosphamide (or azathioprine in patients of reproductive age) is required. Cytokines, polymorphisms and LED Many factors influence the genetic susceptibility to the LED and the development of disease. Among these, the polymorphisms identified in genes of different cytokines appear to play a role. Currently available data suggest small but significant correlations between gene polymorphisms associated with TNFa, IL-10, IL-1Ra and LEDs. [...]

[...] IL-4, IL-6, IFNGR: Some studies suggest that polymorphisms of other cytokines, particularly IL-4 and IL-6 could be involved in susceptibility to LED An association between LED and a polymorphism in the gene coding of the IFNg receptor (IFNGR1) was recently reported. Conclusion SLE is a disease involving multiple genes of MHC and multiple non-HLA genes that determine the emergence and activation of T cells and B self. The genetic complexity of SLE, like other autoimmune diseases polygenic, is associated with a low penetrance of each gene contributes to susceptibility and genetic heterogeneity in practice where the same phenotype results from the combined effect different genes or alleles. [...]

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