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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic lupus erythematosus &#40;SLE&#41; affects at least 0&#46;1&#37; of the global population<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>&#59; its neuropsychiatric expression has been compiled by the ACR into 19 syndrome that range from vascular headache and behavioral alterations to cognitive abnormalities and other severe&#44; disabling manifestations such as transverse myelitis&#44; which have a well defined physiopathogenic basis&#44; leading to a targeted treatment&#44; but represent both a diagnostic as well as therapeutic challenge&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The prevalence of neuropsychiatric lupus &#40;NP-SLE&#41; varies from 37&#37; to 95&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> depending upon the definition&#44; heterogeneous designs &#40;prospective or retrospective&#41;&#44; the population studied &#40;adult or pediatric&#41;&#44; ethnicity&#44; time since onset&#44; severity and follow-up&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The most prevalent manifestations include cognitive alterations &#40;55&#37;&#8211;80&#37;&#41;&#44; headache &#40;24&#37;&#8211;72&#37;&#41;&#44; mood disorders &#40;14&#37;&#8211;57&#37;&#41;&#44; stroke &#40;5&#37;&#8211;18&#37;&#41;&#44; convulsions &#40;6&#37;&#8211;51&#37;&#41;&#44; polyneuropathy &#40;3&#37;&#8211;28&#37;&#41;&#44; anxiety &#40;7&#37;&#8211;24&#37;&#41; and psychosis &#40;8&#37;&#41;&#46; The rest of the syndromes have a prevalence of &#8804;1&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Cognitive alterations are not related to the time since onset of the disease&#44; activity or treatment&#44; and the most common are a reduced attention&#44; memory &#40;particularly visospatial&#41; and executive dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> It may be variably associated to dementia in 25&#37; and most often improve with treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Of the psychiatric alterations&#44; depression&#44; auditory hallucinations and anxiety disorders predominatel&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Transverse myelitis &#40;TM&#41; is rare but severe&#59; its onset usually occurs in the first five years of disease&#46; 50&#37; of patients present it at disease onset and it recurs in 21&#37;&#8211;55&#37;&#59; A fifth &#40;21&#37;&#41; do not improve or worsen&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Convulsions frequently accompany other SLE manifestations&#44; but may occur as an isolated event&#44; most commonly in younger patients and are associated to antiphospholipid antibodies &#40;APL&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The diagnosis is clinical and is additionally supported by laboratory and imaging testing&#44; as well as neuropsychiatric evaluations&#46; It represents a therapeutic challenge because none of the syndromes are exclusive to SLE and up to 41&#37; is attributable to other causes&#59; it is specifically necessary to rule out central nervous system infection&#44; uremia&#44; thrombotic thrombocytopenic purpura&#44; reversible encephalopathy&#44; steroid induced psychosis and hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Magnetic resonance &#40;MR&#41; is the test of choice<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>&#59; it detects focal lesions in the subcortical and&#47;or periventricular white matter &#40;15&#37;&#8211;60&#37;&#41;&#44; hyperintensity in the gray matter &#40;24&#37;&#8211;30&#37;&#41;&#44; atrophy&#44; ventricular dilation and infarctions&#44; although 30&#37;&#8211;40&#37; of NP-SLE has a normal MR&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Positron emission tomography and single or unique photon emission computed tomography detect hypoperfused or hypermetabolic areas and have a better sensitivity than MR&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> In spite of advances&#44; imaging studies do not allow the differentiation of active from inactive disease&#44; and findings are not specific&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">In spite of the effort to understand the physiopathology of SLE and of specific therapeutic proposals&#44;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> because of the varied nature of the physiopathogenic mechanisms underlying NP-SLE&#44; which frequently participate in diffuse &#40;psychosis&#44; depression or cognitive alterations&#41; o focal processes &#40;TM or stroke&#41;&#44; we classify them as vasculopathy &#40;generally with small caliber vessel affection&#41;&#44; mediated by autoantibodies and inflammatory components&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Vasculitis rarely explains NP-SLE&#44; which is commonly related to vasculopathy&#44; which is characterized by a perivascular mononuclear infiltrate&#59; small subsequent infarctions may be observed due to luminal occlusion with fibrin&#44; platelets and intimal hyperplasia&#44; and consequently an increase in the blood&#8211;brain barrier &#40;BBB&#41; and in the extravasation of antibodies&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">APL are related to convulsions&#44; stroke&#44; transient ischemic attacks and transverse myelitis&#59; elevated IgG anticardiolipin titers &#40;IgG aCL&#41; lead to a sensitivity of 58&#37; and a specificity of 81&#37; for the diagnosis of ischemic NP-SLE manifestations&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;14</span></a> The accelerated atherosclerosis characteristically associated to SLE increases the risk &#40;5&#8211;10 times&#41; of coronary disease and stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In the MR&#44; hyperintensities are translated as vasculopathy&#59; they are attributed to demyelination&#44; gliosis and interstitial edema due to ischemia and lacunar infarctions&#59; extensive and confluent hyperintensities in the white matter indicate chronic hypoperfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Antiphospholipid antibodies occur in 60&#37; of patients with SLE&#44; of which 30&#37; have the antiphospholipid antibody syndrome&#59; they are related to focal dysfunction and cognitive deficit&#44; in particular when lupus anticoagulant is present&#46; There is an association of aCL with psychomotor&#44; learning&#44; verbal memory and execution reduction&#46; LA and aCL inhibit the proliferation of astrocytes and increase the synaptoneurosomal depolarization&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">TM is classically considered as an inflammation-mediated syndrome&#44; but its relationship with aCL also indicates a concurrent ischemic contribution&#44; with a very probable thrombosis of the thoracic spinal vessels&#44; and with anticoagulation associated with a better prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;16</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Humoral immunity is extensive against neuronal antigens&#44; ribosomes and phospholipids&#59; it has been implicated in the pathogenesis of NP-SLE&#44; with autoantibodies in the CSF and&#44; to a lesser extent&#44; in cerebral tissue &#40;in autopsy&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Antineuronal antibodies are seen in the CSF of NP-SLE cases with diffuse manifestations &#40;65&#37;&#41;&#59; there is experimental evidence of direct toxicity&#59; thus&#44; in NZM88 mice&#44; predisposed to lupus nephritis and behavioral alterations&#44; IgG vs cerebral antigens might be found&#46; These antibodies against diamin-1 &#40;a molecule involved in the endocytosis of synaptic vesicles&#41;&#44; when injected into healthy models&#44; reproduce the behavioral alterations&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Gangliosides&#44; components of the neuronal membrane&#44; are involved in signal transduction&#44; memory&#44; synaptic transmission and the muscle union&#59; anti-ganglioside IgG antibodies are associated to migraine&#44; dementia and peripheral neuropathy&#44; and IgM to depression&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> They are common in juvenile NP-SL &#40;83&#37;&#41; and associate to cognitive dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">There are reports of anti-protein 2 antibodies directed against microtubules&#44; glial fibrillar acidic protein and neurofilaments&#44; important in communication&#44; cell structure and integrity of the BBB&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Those directed against alphatubulin occur in 36&#37; of NP-SLE cases&#44; in 4&#37; of SLE and in no controls &#40;multiple sclerosis&#44; epilepsy&#44; healthy&#41;&#59; they are associated to psychomotor alterations&#44; obsessive&#8211;compulsive neurosis&#44; temporal epilepsy&#44; memory and concentration deficits&#44; depression and migraine&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">We know that antibodies against the N methyl D aspartate receptor &#40;NMDAR&#41; occur in 40&#37;&#8211;50&#37; of patients with SLE and cross-react with dsDNA&#46; NMDAR is composed of two units NR1&#44; which presents a binding site for glycine &#40;coagonist&#41;&#44; and NR2 &#40;with 4 subtypes A&#8211;D&#41; A and B&#44; present mainly in the hippocampus &#40;learning and memory&#41; and the amygdala &#40;fear&#41;&#46; They function as voltage regulated calcium channels&#46; After electrical stimulation&#44; glutamate and glycine bind to NR2 and NR1 and allow the passage of calcium into the cell&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> Anti-NMDAR antibodies are not limited to NP-SLE&#59; they may occur without underlying disease or be associated o other diseases such as neoplasia&#46; The experimental administration of anti-NMDAR &#40;R4A&#41; with lipopolysaccharide and epinephrine induce BBB dysfunction&#46; R4A binds to the DWEYS pentapeptide in NR2A and NR2B&#44; permitting an increase in cytosolic calcium&#44; especially mitochondrial&#44; and conditions the depolarization of the membrane potential&#44; a reduction in respiration and an increase in oxygen reactive species&#44; with the consequential increase in permeability and apoptosis&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> Anti-NMDAR in CSF and the brain correlates with convulsions&#44; delirium&#44; psychosis&#44; headache and stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Anti-endothelium antibodies generate endothelial dysfunction&#44; increase inflammatory markers&#44; adhesion molecules&#44; apoptosis&#44; BBB permeability and the flow of autoantibodies&#59; the activation of endothelial cells is carried out through NF-&#954;B by anti NR2 antibodies&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;22</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">There are other antibodies associated to psychiatric manifestations&#44; such as those against Nedd 5 &#40;27&#37; of NP-SLE&#41; and septin &#40;which belongs to the cytoskeleton GTPase family that intervenes in cytokinesis&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Triosaphosphate isomeraze &#40;TPI&#41; intervene in glucolysis and the production of erythrocyte and neuronal energy&#59; IgM vs TPI favor anemia and neurological abnormalitied<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a>&#59; a-TPI IgG with high specificity in NP-SLE &#40;94&#46;5&#37;&#41; favor the activation of complement and low serum levels of C3d&#44; but increased in the CSF&#44; indicating intratechal production&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Ribosomal P antibodies &#40;P0&#44; P1 and P2&#41; are associated LEG-NP &#40;45&#37;&#8211;88&#37; psychosis&#41;&#44; lupus nephritis&#44; and hepatitis&#44; and determine the alteration of protein synthesis&#44; dysfunction and neuronal apoptosis&#44; impaired memory&#44; cognition&#44; emotion&#44; depression and olfactory dysfunction&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12&#44;25</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Particular attention has been paid to IL-6 in the inflammation associated convulsion and IFN-&#945; has been associated to psychosis&#59; MMP-9&#44; macrophage&#44; T lymphocytes and endothelial cells and smooth muscle cell gelatinase are implicated in the plaque rupture and loss of the BBB&#44; promoting the migration of inflammatory cells&#46; They are associated to cognitive alterations and hyperintense lesions in MR T1 and T2&#59; some periventricular lesions resemble leukoaraiosis&#44; which is translated as a loss of the BBB&#46; There may be thalamic&#44; hippocampal&#44; corpus callosum&#44; cortical atrophy&#44; among others&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;9&#44;15</span></a> In the NZM88 mice model&#44; elevated hypothalamic concentrations of IL-6&#44; IL-10&#44; IL-12&#44; IL-16&#44; IFN-&#947; and tumor necrosis factor alpha are found&#44; in addition to microglial activation which&#44; along with autoantibodies&#44; increases the proinflammatory cytokines even more&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17&#44;26</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Therefore&#44; its evident that&#44; in the same patient&#44; different physiopathogenic mechanisms converge in NP-SLE&#44; making it necessary to use a combination of drugs for its management&#44; including &#8220;symptomatics&#8221; &#40;anticonvulsives&#44; antipsychotics&#44; antiplatelet&#44; anticoagulants&#41;&#44; high dose steroids &#40;pulse methylprednisolone&#41; and immunomodulators &#40;antimalarials&#44; statins&#44; cyclophosphamide&#44; azathioprine&#44; methotrexate&#44; mycophenolic acid&#41;&#46; Plasmapheresis may be useful&#44; in addition to IV immunoglobulin and rituximab&#44; particularly due to the diversity of potentially pathogenic autoantibodies&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Long term remission is plausible although symptoms persist in 3&#37;&#8211;20&#37;&#59; most require steroids and the recurrence rate is 21&#37;&#8211;47&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;26&#8211;28</span></a> Mortality can be high &#40;&#8805;18&#37;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a></p></span>"
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Editorial
Neuropsychiatric Manifestations in Systemic Lupus Erythematosus: Physiopathogenic and Therapeutic Basis
Manifestaciones neuropsiquiátricas en lupus eritematoso generalizado: bases fisiopatogénicas y terapéuticas
Georgina Aguilera-Pickens, Carlos Abud-Mendoza
Corresponding author
Unidad Regional de Reumatología y Osteoporosis, Hospital Central «Dr. Ignacio Morones Prieto», Facultad de Medicina, Universidad Autónoma de San Luis Potosí, San Luis Potosí, Mexico
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    "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Systemic lupus erythematosus &#40;SLE&#41; affects at least 0&#46;1&#37; of the global population<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a>&#59; its neuropsychiatric expression has been compiled by the ACR into 19 syndrome that range from vascular headache and behavioral alterations to cognitive abnormalities and other severe&#44; disabling manifestations such as transverse myelitis&#44; which have a well defined physiopathogenic basis&#44; leading to a targeted treatment&#44; but represent both a diagnostic as well as therapeutic challenge&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The prevalence of neuropsychiatric lupus &#40;NP-SLE&#41; varies from 37&#37; to 95&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a> depending upon the definition&#44; heterogeneous designs &#40;prospective or retrospective&#41;&#44; the population studied &#40;adult or pediatric&#41;&#44; ethnicity&#44; time since onset&#44; severity and follow-up&#46;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> The most prevalent manifestations include cognitive alterations &#40;55&#37;&#8211;80&#37;&#41;&#44; headache &#40;24&#37;&#8211;72&#37;&#41;&#44; mood disorders &#40;14&#37;&#8211;57&#37;&#41;&#44; stroke &#40;5&#37;&#8211;18&#37;&#41;&#44; convulsions &#40;6&#37;&#8211;51&#37;&#41;&#44; polyneuropathy &#40;3&#37;&#8211;28&#37;&#41;&#44; anxiety &#40;7&#37;&#8211;24&#37;&#41; and psychosis &#40;8&#37;&#41;&#46; The rest of the syndromes have a prevalence of &#8804;1&#37;&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a> Cognitive alterations are not related to the time since onset of the disease&#44; activity or treatment&#44; and the most common are a reduced attention&#44; memory &#40;particularly visospatial&#41; and executive dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> It may be variably associated to dementia in 25&#37; and most often improve with treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Of the psychiatric alterations&#44; depression&#44; auditory hallucinations and anxiety disorders predominatel&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> Transverse myelitis &#40;TM&#41; is rare but severe&#59; its onset usually occurs in the first five years of disease&#46; 50&#37; of patients present it at disease onset and it recurs in 21&#37;&#8211;55&#37;&#59; A fifth &#40;21&#37;&#41; do not improve or worsen&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> Convulsions frequently accompany other SLE manifestations&#44; but may occur as an isolated event&#44; most commonly in younger patients and are associated to antiphospholipid antibodies &#40;APL&#41;&#46;<a class="elsevierStyleCrossRefs" href="#bib0040"><span class="elsevierStyleSup">8&#44;9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">The diagnosis is clinical and is additionally supported by laboratory and imaging testing&#44; as well as neuropsychiatric evaluations&#46; It represents a therapeutic challenge because none of the syndromes are exclusive to SLE and up to 41&#37; is attributable to other causes&#59; it is specifically necessary to rule out central nervous system infection&#44; uremia&#44; thrombotic thrombocytopenic purpura&#44; reversible encephalopathy&#44; steroid induced psychosis and hypertension&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> Magnetic resonance &#40;MR&#41; is the test of choice<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a>&#59; it detects focal lesions in the subcortical and&#47;or periventricular white matter &#40;15&#37;&#8211;60&#37;&#41;&#44; hyperintensity in the gray matter &#40;24&#37;&#8211;30&#37;&#41;&#44; atrophy&#44; ventricular dilation and infarctions&#44; although 30&#37;&#8211;40&#37; of NP-SLE has a normal MR&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Positron emission tomography and single or unique photon emission computed tomography detect hypoperfused or hypermetabolic areas and have a better sensitivity than MR&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a> In spite of advances&#44; imaging studies do not allow the differentiation of active from inactive disease&#44; and findings are not specific&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">In spite of the effort to understand the physiopathology of SLE and of specific therapeutic proposals&#44;<a class="elsevierStyleCrossRef" href="#bib0020"><span class="elsevierStyleSup">4</span></a> because of the varied nature of the physiopathogenic mechanisms underlying NP-SLE&#44; which frequently participate in diffuse &#40;psychosis&#44; depression or cognitive alterations&#41; o focal processes &#40;TM or stroke&#41;&#44; we classify them as vasculopathy &#40;generally with small caliber vessel affection&#41;&#44; mediated by autoantibodies and inflammatory components&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Vasculitis rarely explains NP-SLE&#44; which is commonly related to vasculopathy&#44; which is characterized by a perivascular mononuclear infiltrate&#59; small subsequent infarctions may be observed due to luminal occlusion with fibrin&#44; platelets and intimal hyperplasia&#44; and consequently an increase in the blood&#8211;brain barrier &#40;BBB&#41; and in the extravasation of antibodies&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">APL are related to convulsions&#44; stroke&#44; transient ischemic attacks and transverse myelitis&#59; elevated IgG anticardiolipin titers &#40;IgG aCL&#41; lead to a sensitivity of 58&#37; and a specificity of 81&#37; for the diagnosis of ischemic NP-SLE manifestations&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;14</span></a> The accelerated atherosclerosis characteristically associated to SLE increases the risk &#40;5&#8211;10 times&#41; of coronary disease and stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In the MR&#44; hyperintensities are translated as vasculopathy&#59; they are attributed to demyelination&#44; gliosis and interstitial edema due to ischemia and lacunar infarctions&#59; extensive and confluent hyperintensities in the white matter indicate chronic hypoperfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Antiphospholipid antibodies occur in 60&#37; of patients with SLE&#44; of which 30&#37; have the antiphospholipid antibody syndrome&#59; they are related to focal dysfunction and cognitive deficit&#44; in particular when lupus anticoagulant is present&#46; There is an association of aCL with psychomotor&#44; learning&#44; verbal memory and execution reduction&#46; LA and aCL inhibit the proliferation of astrocytes and increase the synaptoneurosomal depolarization&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p><p id="par0035" class="elsevierStylePara elsevierViewall">TM is classically considered as an inflammation-mediated syndrome&#44; but its relationship with aCL also indicates a concurrent ischemic contribution&#44; with a very probable thrombosis of the thoracic spinal vessels&#44; and with anticoagulation associated with a better prognosis&#46;<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;16</span></a></p><p id="par0040" class="elsevierStylePara elsevierViewall">Humoral immunity is extensive against neuronal antigens&#44; ribosomes and phospholipids&#59; it has been implicated in the pathogenesis of NP-SLE&#44; with autoantibodies in the CSF and&#44; to a lesser extent&#44; in cerebral tissue &#40;in autopsy&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">Antineuronal antibodies are seen in the CSF of NP-SLE cases with diffuse manifestations &#40;65&#37;&#41;&#59; there is experimental evidence of direct toxicity&#59; thus&#44; in NZM88 mice&#44; predisposed to lupus nephritis and behavioral alterations&#44; IgG vs cerebral antigens might be found&#46; These antibodies against diamin-1 &#40;a molecule involved in the endocytosis of synaptic vesicles&#41;&#44; when injected into healthy models&#44; reproduce the behavioral alterations&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a></p><p id="par0050" class="elsevierStylePara elsevierViewall">Gangliosides&#44; components of the neuronal membrane&#44; are involved in signal transduction&#44; memory&#44; synaptic transmission and the muscle union&#59; anti-ganglioside IgG antibodies are associated to migraine&#44; dementia and peripheral neuropathy&#44; and IgM to depression&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> They are common in juvenile NP-SL &#40;83&#37;&#41; and associate to cognitive dysfunction&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0055" class="elsevierStylePara elsevierViewall">There are reports of anti-protein 2 antibodies directed against microtubules&#44; glial fibrillar acidic protein and neurofilaments&#44; important in communication&#44; cell structure and integrity of the BBB&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> Those directed against alphatubulin occur in 36&#37; of NP-SLE cases&#44; in 4&#37; of SLE and in no controls &#40;multiple sclerosis&#44; epilepsy&#44; healthy&#41;&#59; they are associated to psychomotor alterations&#44; obsessive&#8211;compulsive neurosis&#44; temporal epilepsy&#44; memory and concentration deficits&#44; depression and migraine&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a></p><p id="par0060" class="elsevierStylePara elsevierViewall">We know that antibodies against the N methyl D aspartate receptor &#40;NMDAR&#41; occur in 40&#37;&#8211;50&#37; of patients with SLE and cross-react with dsDNA&#46; NMDAR is composed of two units NR1&#44; which presents a binding site for glycine &#40;coagonist&#41;&#44; and NR2 &#40;with 4 subtypes A&#8211;D&#41; A and B&#44; present mainly in the hippocampus &#40;learning and memory&#41; and the amygdala &#40;fear&#41;&#46; They function as voltage regulated calcium channels&#46; After electrical stimulation&#44; glutamate and glycine bind to NR2 and NR1 and allow the passage of calcium into the cell&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> Anti-NMDAR antibodies are not limited to NP-SLE&#59; they may occur without underlying disease or be associated o other diseases such as neoplasia&#46; The experimental administration of anti-NMDAR &#40;R4A&#41; with lipopolysaccharide and epinephrine induce BBB dysfunction&#46; R4A binds to the DWEYS pentapeptide in NR2A and NR2B&#44; permitting an increase in cytosolic calcium&#44; especially mitochondrial&#44; and conditions the depolarization of the membrane potential&#44; a reduction in respiration and an increase in oxygen reactive species&#44; with the consequential increase in permeability and apoptosis&#46;<a class="elsevierStyleCrossRef" href="#bib0105"><span class="elsevierStyleSup">21</span></a> Anti-NMDAR in CSF and the brain correlates with convulsions&#44; delirium&#44; psychosis&#44; headache and stroke&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Anti-endothelium antibodies generate endothelial dysfunction&#44; increase inflammatory markers&#44; adhesion molecules&#44; apoptosis&#44; BBB permeability and the flow of autoantibodies&#59; the activation of endothelial cells is carried out through NF-&#954;B by anti NR2 antibodies&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;22</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">There are other antibodies associated to psychiatric manifestations&#44; such as those against Nedd 5 &#40;27&#37; of NP-SLE&#41; and septin &#40;which belongs to the cytoskeleton GTPase family that intervenes in cytokinesis&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">Triosaphosphate isomeraze &#40;TPI&#41; intervene in glucolysis and the production of erythrocyte and neuronal energy&#59; IgM vs TPI favor anemia and neurological abnormalitied<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a>&#59; a-TPI IgG with high specificity in NP-SLE &#40;94&#46;5&#37;&#41; favor the activation of complement and low serum levels of C3d&#44; but increased in the CSF&#44; indicating intratechal production&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Ribosomal P antibodies &#40;P0&#44; P1 and P2&#41; are associated LEG-NP &#40;45&#37;&#8211;88&#37; psychosis&#41;&#44; lupus nephritis&#44; and hepatitis&#44; and determine the alteration of protein synthesis&#44; dysfunction and neuronal apoptosis&#44; impaired memory&#44; cognition&#44; emotion&#44; depression and olfactory dysfunction&#46;<a class="elsevierStyleCrossRefs" href="#bib0060"><span class="elsevierStyleSup">12&#44;25</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Particular attention has been paid to IL-6 in the inflammation associated convulsion and IFN-&#945; has been associated to psychosis&#59; MMP-9&#44; macrophage&#44; T lymphocytes and endothelial cells and smooth muscle cell gelatinase are implicated in the plaque rupture and loss of the BBB&#44; promoting the migration of inflammatory cells&#46; They are associated to cognitive alterations and hyperintense lesions in MR T1 and T2&#59; some periventricular lesions resemble leukoaraiosis&#44; which is translated as a loss of the BBB&#46; There may be thalamic&#44; hippocampal&#44; corpus callosum&#44; cortical atrophy&#44; among others&#46;<a class="elsevierStyleCrossRefs" href="#bib0005"><span class="elsevierStyleSup">1&#44;9&#44;15</span></a> In the NZM88 mice model&#44; elevated hypothalamic concentrations of IL-6&#44; IL-10&#44; IL-12&#44; IL-16&#44; IFN-&#947; and tumor necrosis factor alpha are found&#44; in addition to microglial activation which&#44; along with autoantibodies&#44; increases the proinflammatory cytokines even more&#46;<a class="elsevierStyleCrossRefs" href="#bib0085"><span class="elsevierStyleSup">17&#44;26</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">Therefore&#44; its evident that&#44; in the same patient&#44; different physiopathogenic mechanisms converge in NP-SLE&#44; making it necessary to use a combination of drugs for its management&#44; including &#8220;symptomatics&#8221; &#40;anticonvulsives&#44; antipsychotics&#44; antiplatelet&#44; anticoagulants&#41;&#44; high dose steroids &#40;pulse methylprednisolone&#41; and immunomodulators &#40;antimalarials&#44; statins&#44; cyclophosphamide&#44; azathioprine&#44; methotrexate&#44; mycophenolic acid&#41;&#46; Plasmapheresis may be useful&#44; in addition to IV immunoglobulin and rituximab&#44; particularly due to the diversity of potentially pathogenic autoantibodies&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Long term remission is plausible although symptoms persist in 3&#37;&#8211;20&#37;&#59; most require steroids and the recurrence rate is 21&#37;&#8211;47&#37;&#46;<a class="elsevierStyleCrossRefs" href="#bib0030"><span class="elsevierStyleSup">6&#44;26&#8211;28</span></a> Mortality can be high &#40;&#8805;18&#37;&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a></p></span>"
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