Clinicpathologic conference
Encephalitis and Status Epilepticus in a Patient With Systemic Lupus Erythematosus
Encefalitis con estatus convulsivo localizado en una paciente con lupus eritematoso sistémico
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Cullen, Santa Fe, Argentina" "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "aff0005" ] 1 => array:3 [ "entidad" => "Sección de Neurología, Hospital Iturraspe, Santa Fe, Argentina" "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "aff0010" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Encefalitis con estatus convulsivo localizado en una paciente con lupus eritematoso sistémico" ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 937 "Ancho" => 825 "Tamanyo" => 105915 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Central nervous system MR showing hyperintense lesions in T2 on the frontal, temporal and parietal right regions.</p>" ] ] ] "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Case Presentation (Dr. Emilio Benavente)</span><p id="par0005" class="elsevierStylePara elsevierViewall">The case is a 42-year-old female patient, diagnosed with SLE (ACR criteria 1997) 5 years ago, with joint and hematological involvement, immunological changes and low C3. Her disease was inactive for the past 3 years (SLEDAI 0) and she was being treated with hydroxychloroquine 200<span class="elsevierStyleHsp" style=""></span>mg/day.</p><p id="par0010" class="elsevierStylePara elsevierViewall">She had no family history of neurological or rheumatic disorders. She denied toxic habits, illicit drug use or a history of drug allergy. No history of surgery or trauma was present, with 3 daughters born at terms pregnancies without obstetric complications.</p><p id="par0015" class="elsevierStylePara elsevierViewall">She came spontaneously to the clinic on April 8, 2010 for involuntary movements of the foot and the left hand that had begun the day before, which determined her hospitalization.</p><p id="par0020" class="elsevierStylePara elsevierViewall">On physical examination there were no clinical signs of SLE activity or infectious diseases. Neurological examination revealed the presence of increased tendon reflexes on the left leg and a positive Babinski sign. Magnetic resonance imaging (MRI) showed T2 hyperintense lesions in the cortico-subcortical right frontal and parietal regions that stood out with gadolinium (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). The patient began treatment with oral prednisone 50<span class="elsevierStyleHsp" style=""></span>mg/day and was discharged from the hospital after 48<span class="elsevierStyleHsp" style=""></span>h.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0025" class="elsevierStylePara elsevierViewall">A week later (April 17), the patient reported a fall after loss of consciousness, for which she was readmitted to the hospital with the conclusion that she had a generalized seizure. On neurological examination she was found to have rhythmic movements, persistent hemiparesis of her left lower limb (foot) and positive Babinsky.</p><p id="par0030" class="elsevierStylePara elsevierViewall">During an electroencephalogram (EEG) she developed a tonic-clonic generalized seizure with loss of consciousness and postictal coma with ad integrum restitution. The EEG showed mild impairment of cortical bioelectrical activity, excess beta rhythms and parieto-temporal isolated sharp waves. On April 24, the patient developed a third generalized seizure.</p><p id="par0035" class="elsevierStylePara elsevierViewall">CT scans of the brain and chest were normal. The blood count, erythrocyte sedimentation rate, renal function, anticardiolipin antibodies, lupus anticoagulant, C3, C4, AAN, and anti-dsDNA antibodies were normal. The blood and urine cultures were negative. A lumbar puncture was performed, resulting in a cerebrospinal fluid (CSF) with a normal cytochemical analysis, with negative cultures (including fungi, bacteria, mycobacteria tuberculosis, Cryptococcus, Nocardia, and Listeria). We also performed polymerase chain reaction (PCR) for varicella zoster, herpes simplex, and Epstein-Barr virus, which was negative in all cases.</p><p id="par0040" class="elsevierStylePara elsevierViewall">Seizures located on the left foot continued despite treatment with immunosuppressive intravenous methylprednisolone (3 pulses of 1<span class="elsevierStyleHsp" style=""></span>g/day for 3 on consecutive days) and azathioprine 50<span class="elsevierStyleHsp" style=""></span>mg/day, and the additive treatment of antiepileptic drugs such as pregabalin, carbamazepine, phenytoin, and valproic acid. There was a hypersensitivity syndrome with skin reactions, fever, and elevated transaminase levels. Suspecting a skin drug reaction, these were suspended and a skin biopsy was performed. It reported erythema multiforme with negative cultures and therefore it was assumed as an adverse drug reaction. By suspending anticonvulsant drugs, clonazepam was employed at a dose of 2<span class="elsevierStyleHsp" style=""></span>g/day orally as well as IV immunoglobulin (2<span class="elsevierStyleHsp" style=""></span>g/kg for 5 consecutive days and then 4 monthly doses of 0.5<span class="elsevierStyleHsp" style=""></span>g/kg). The seizures stopped after a month of starting treatment.</p><p id="par0045" class="elsevierStylePara elsevierViewall">SLE remained inactive and the prednisone dose was gradually lowered. In March 2011 (after 10 months of being neurologically asymptomatic) she showed cognitive deterioration. A brain MRI revealed hyperintense lesions on T2 with the same features as above. We indicated a new pulse of 30<span class="elsevierStyleHsp" style=""></span>mg IV gamma globulin without improving the clinical response and with partial epilepsy still present, this time of the right leg. We performed a new brain MRI that showed lesions which had now become bilateral. We decided to perform a biopsy of the right frontal lobe brain which reported: cortical nervous parenchyma with increased cellularity at the expense of a reactive astrogliosis. No vasculitis or neoplastic proliferation was seen. Immunostaining: GFAP<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>CD68<span class="elsevierStyleHsp" style=""></span>+<span class="elsevierStyleHsp" style=""></span>NOGO A (−), P53 (−), IDH1 (−) (<a class="elsevierStyleCrossRef" href="#fig0010">Fig. 2</a>).</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Treatment was initiated with 1<span class="elsevierStyleHsp" style=""></span>g of IV cyclophosphamide, which resulted in restitution ad integrum of the lesions (<a class="elsevierStyleCrossRef" href="#fig0015">Fig. 3</a>) with clinical improvement after the first pulse.</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">At present, the patient has inactive SLE and is free of seizures while being treated with prednisone, hydroxychloroquine 200<span class="elsevierStyleHsp" style=""></span>mg/day, clonazepam 1<span class="elsevierStyleHsp" style=""></span>mg/day, and monthly pulse IV cyclophosphamide.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Differential Diagnosis (Dr. Sergio Paira)</span><p id="par0060" class="elsevierStylePara elsevierViewall">When faced with a patient with SLE presenting seizures, the first step in diagnostic reasoning should be to ask whether there is a secondary underlying pathology and concomitant conditions the treatment thereof.</p><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Seizures in Lupus Erythematosus</span><p id="par0065" class="elsevierStylePara elsevierViewall">Seizures are considered as an important manifestation of neuropsychiatric SLE.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> Between 10% and 20% of SLE patients develop epileptic seizures at some point in their illness. This means there is almost an 8 times higher prevalence of epilepsy than in the general population, therefore, it is much more common in SLE patients than expected. Between 5% and 10% of patients have mild seizures that can occur even years before the clinical onset of SLE.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Seizures have been reported in up to 24%–45% of patients with SLE with neurological involvement, but in the Hopkins lupus cohort only 10% were affected. Generally, seizures are produced in the context of an active systemic disease, but may be an isolated finding. Other possible causes of seizures are infections, uremia, hypertension or a previous stroke, so these conditions should always be excluded.<a class="elsevierStyleCrossRef" href="#bib0015"><span class="elsevierStyleSup">3</span></a></p><p id="par0075" class="elsevierStylePara elsevierViewall">About a quarter of seizures in patients with SLE are clinically detectable, with symptoms ranging from disturbances in sight to focal motor deficits or sensory focal seizures, and cannot be associated with focal brain<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> pathophysiological processes.</p><p id="par0080" class="elsevierStylePara elsevierViewall">The most direct cause of epilepsy in patients with SLE is the one associated with stroke. The most common seizure types in this group of patients are usually simple partial or complex seizures with or without secondary generalization. The main causes of focal brain lesions or thrombosis are cardiac embolism, both of large vessels and the microvasculature, or primary vasculitis but these are infrequent.<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0085" class="elsevierStylePara elsevierViewall">Liou et al. found that epilepsy was 3.7 times higher among patients with SLE who had anticardiolipin antibodies than among patients with SLE who did not have the antibodies.<a class="elsevierStyleCrossRefs" href="#bib0020"><span class="elsevierStyleSup">4,5</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Antiphospholipid Antibodies and Epilepsy</span><p id="par0090" class="elsevierStylePara elsevierViewall">Shoenfeld et al. concluded that epilepsy is common in APS and most of the risk appears to be related to extensive vascular disease manifested as central nervous system (CNS) disease, heart valve disease, livedo reticularis, and the presence of SLE.<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a></p><p id="par0095" class="elsevierStylePara elsevierViewall">The clinical, EEG or focused damage images in association with ANA, suggest that vascular occlusion of small cerebral vessels may be responsible for the occurrence of seizures in some patients with SLE.</p><p id="par0100" class="elsevierStylePara elsevierViewall">Inzelberg and Korczyn proposed that seizures in patients with APS are the expression of ischemic events that occur as a result of the hipercoagulability.<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a> In fact, seizures are a known symptom of cerebral ischemia and coexist with other vascular diseases in a high percentage (42.9%).<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0105" class="elsevierStylePara elsevierViewall">MELAS syndrome (mitochondrial encephalomyopathy with lactic acidosis and stroke-like syndrome)</p><p id="par0110" class="elsevierStylePara elsevierViewall">First described by Pavlakis et al. in 1984, mitochondrial encephalopathy with lactic acidosis and stroke-like syndrome (MELAS) is the convergence of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes. This is a genetic disease caused by mutations of the maternal mitochondrial genome, affecting the synthesis of adenosine triphosphate (ATP). The mutations are heteroplasmic in different tissues, which could involve especially those which are highly energy-dependent, such as muscles, brain, and CNS tissues. Neurologic manifestations include speech and visual disturbances, seizures and status epilepticus. MELAS may occur with continuous partial epilepsy. Seizures are often preceded by lengthy episodes of migraine. Partial focal seizures and stroke are, in many cases, originated in the occipital lobe. This condition should always be evaluated in patients under 40 years of age with stroke, regardless of whether they have a family history of disease.<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">Our patient was older than 40 years, had no family history and no lactic acidosis.</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Tropical Causes of Epilepsy</span><p id="par0120" class="elsevierStylePara elsevierViewall">There are several tropical parasitic diseases causing epilepsy.</p><p id="par0125" class="elsevierStylePara elsevierViewall">Neurocysticercosis is the main cause of focal epilepsy starting in adulthood in endemic areas (30%–50%). All phases of cysticerci (viable, transitional, and calcified) are associated with seizures. Specific treatment promotes faster disappearance of the cysticerci and reduces the risk of seizure recurrence in patients with viable cysts.</p><p id="par0130" class="elsevierStylePara elsevierViewall">Symptomatic epilepsy may be the first manifestation of neuroschistosomiasis in patients without systemic symptoms. The pseudotumoral form can lead to crises secondary to the presence of granulomas and edema of the cerebral cortex. Schistosoma japonicum eggs are smaller, and more easily reach the CNS and cause more frequent seizures.</p><p id="par0135" class="elsevierStylePara elsevierViewall">Both toxocariasis and sparganosis are helminthiasis that can cause symptomatic seizures. Similarly, cerebral malaria, particularly <span class="elsevierStyleItalic">Plasmodium falciparum</span>, can cause chronic epilepsy.</p><p id="par0140" class="elsevierStylePara elsevierViewall">About 20% of patients with cerebral infarction secondary to Chagas disease presented late vascular epilepsy as a complication. In this case we ruled out the presence of such pathogens.<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Vasculitis</span><p id="par0145" class="elsevierStylePara elsevierViewall">CNS vasculitis represents a heterogeneous group of inflammatory diseases that primarily affect small blood vessels and leptomeningeal cerebral<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> parenchyma. A variety of neurological insults can cause CNS vasculitis, including infection, cancer, ionizing radiation, cocaine use, and autoimmune<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> diseases.<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Among these, the primary CNS vasculitis, SLE, polyarteritis nodosa, giant<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a> cell arteritis, and Sjögren's syndrome are the main autoimmune diseases associated with CNS vasculitis.<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0150" class="elsevierStylePara elsevierViewall">While these disorders may present with generalized or focal seizures, our patients did not have signs of systemic vasculitis or morphological or histological evidence of cerebral vasculitis.</p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Neoplasms</span><p id="par0155" class="elsevierStylePara elsevierViewall">Brain tumors, whether benign or malignant, are a dreaded cause of seizures, but are rare. These may be primary, to be denominated according to the cell lineage (astrocytoma, oligodendroglioma, glioblastoma, etc.), or metastatic tumors from primary neoplasms located in some other place. Similarly, it may be malignant or benign by differentiation. Regardless of the oncological characteristics, they can cause seizures due to cerebral irritation or mass effect may present with seizures and partial localized continual epilepsy (EPC).</p><p id="par0160" class="elsevierStylePara elsevierViewall">While the tumors are causes of CLD in between 5% and 19% of cases, their presence was ruled out by morphological studies (MRI and brain biopsy).<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Rasmussen's Encephalitis</span><p id="par0165" class="elsevierStylePara elsevierViewall">Regarding the type of persistent movement disorder of the foot, we can define it as a focal status epilepticus, which is called EPC.</p><p id="par0170" class="elsevierStylePara elsevierViewall">EPC, originally described by Koshewnikow is a rare form of focal epilepsy, characterized by a localized somato-motor status epilepticus, i.e., regular or irregular muscle contractions and clonic seizures affecting a limited part of the body produced for a minimum of one hour intervals of no more than 10<span class="elsevierStyleHsp" style=""></span>s due to various injuries in a sector of the motor cortex.<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p><p id="par0175" class="elsevierStylePara elsevierViewall">Rasmussen encephalitis (RE), or chronic encephalitis and epilepsy, first described in 1958, is a rare clinical syndrome characterized by severe focal epilepsy (continuous partial epilepsy), usually accompanied by progressive hemiparesis and cognitive impairment, that develops in association with pathological features of chronic encephalitis.<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a></p><p id="par0180" class="elsevierStylePara elsevierViewall">Except for a few case reports, the frequency of association between Rasmussen's syndrome and autoimmune diseases (Sjögren's syndrome and SLE) remains uncertain.<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16,17</span></a></p></span></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Clinical Diagnosis (Dr. Sergio Paira)</span><p id="par0185" class="elsevierStylePara elsevierViewall">Our patient had clinical features of a continuous RE with intractable partial epilepsy and hemiparesis. Radiologically we found cortical–subcortical hyperintense lesions on T2, not highlighted with gadolinium, and histological evidence of brain swelling. Therefore, having ruled out other causes of CLD, I assume that the patient has an autoimmune disease associated to RE as the primary disease.</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Pathology Discussion (Dr. Susana Roverano–Dr. Gustavo Saredo)</span><p id="par0190" class="elsevierStylePara elsevierViewall">A brain biopsy is not necessary in all cases of RE, because other criteria may be sufficient to diagnose the disease, and this is reserved for cases of doubtful clinical diagnosis or atypical presentations of RE. It should be taken from an area where the T2/FLAIR signal is increased in the MR.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a> In cases in which MRI lesions are not clear, other studies such as PET or SPECT may be useful in determining the site of the biopsy.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a></p><p id="par0195" class="elsevierStylePara elsevierViewall">A German group described inflammatory cells and reactive astrocytes in brain samples obtained from regions with abnormalities on MRI. In areas where hyperintensity was observed, increased numbers of T cells, nodules of microglia and GFAP+ astrocytes are regarded as the chronically most affected areas.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p><p id="par0200" class="elsevierStylePara elsevierViewall">Another relevant diagnostic observation is that less than 5% of CD68+ cells had macrophage morphology; the vast majority had microglial<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a> morphology.</p><p id="par0205" class="elsevierStylePara elsevierViewall">These histopathological changes are similar to those observed in our patient, so the final diagnosis was that of RE in a patient with SLE.</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Final Results and Comments</span><p id="par0210" class="elsevierStylePara elsevierViewall">Although RE has long been considered a childhood disease (it has a more rapid and severe onset), adolescent and adult patients (with a more protracted and milder course, with a long and relatively nonspecific prodromal phase) have been described by several groups on the basis of the study of Hart et al., estimated at about 10% of cases of RE.<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21–24</span></a></p><p id="par0215" class="elsevierStylePara elsevierViewall">Clinically, RE is characterized by intractable focal seizures, called EPC, and cognitive impairment secondary to hemispheric involvement.<a class="elsevierStyleCrossRef" href="#bib0110"><span class="elsevierStyleSup">22</span></a></p><p id="par0220" class="elsevierStylePara elsevierViewall">There have been three special features of epilepsy in patients with RE: (a) the polymorphism of seizures in a given patient, (b) refractory to medical treatment of seizures, especially EPC, and (c) simple partial motor seizures involving one side of the body (77% of cases).</p><p id="par0225" class="elsevierStylePara elsevierViewall">One can also see secondarily generalized tonic-clonic seizures (42%), complex partial seizures (19% with generalized and 31% with subsequent unilateral motor), postural seizures probably originating in the supplementary motor area (24%) and somatosensory seizures (21%).<a class="elsevierStyleCrossRefs" href="#bib0110"><span class="elsevierStyleSup">22,24</span></a></p><p id="par0230" class="elsevierStylePara elsevierViewall">RE is an example of an autoimmune disease of the CNS. Serum samples from patients with this disease contain antibodies against glutamate receptors GluR3 and GluR (against the epsilon subunit 2). These patients may also have stimulated GluR epsilon 2T cells in peripheral blood, and it has also been shown that both cellular and humoral autoimmunity against GluR epsilon 2 may contribute to pathophysiological processes in RE. Their presence in other autoimmune disorders suggests similar pathological mechanisms, but not RE markers. The serum of some patients with RE also contain high levels of ‘classic’ autoimmune antibodies (glutamic acid decarboxylase, anti-cardiolipin, B2-glycoprotein I and SS-A, and RNP nuclear antigens).<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a></p><p id="par0235" class="elsevierStylePara elsevierViewall">The diagnosis of Rasmussen's report is based on clinical studies, electrophysiological (EEG) and morphological (MRI and, in some cases, histopathology) .<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a></p><p id="par0240" class="elsevierStylePara elsevierViewall">Our patient had two unusual features of RE, she was 42 years of age and had bilateral involvement.</p><p id="par0245" class="elsevierStylePara elsevierViewall">Bilateral RE is very rare. Some of the clinical and electrophysiological characteristics in typical unihemispheric cases or bilateral cerebral involvement have been suggested to be, for example, as a secondary spread of focal seizures in the contralateral side, intercritical epileptiform abnormalities on the contralateral side or contralateral mild atrophy.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> Therefore, the term ‘bilateral RE’ should be reserved for cases with inflammatory lesions in both hemispheres. Until 2005, about 200 cases were reported in the literature, with only 9<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> having bihemispheric involvement.</p><p id="par0250" class="elsevierStylePara elsevierViewall">There is now a wide range of available therapeutic strategies, such as bolus intravenous methylprednisolone, immunosuppressants, intravenous immunoglobulin (IVIG), plasmapheresis, cyclophosphamide, and rituximab. Surgical treatment is reserved for seizure control in refractory children and adults.<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">24,28</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Ethical disclosures</span><p id="par0260" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Protection of human and animal subjects.</span> The authors declare that no experiments were performed on humans or animals for this investigation.<span class="elsevierStyleVsp" style="height:0.5px"></span></p><p id="par0265" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Confidentiality of Data.</span> The authors declare that no patient data appears in this article.<span class="elsevierStyleVsp" style="height:0.5px"></span></p><p id="par0270" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleBold">Right to privacy and informed consent.</span> The authors have obtained the informed consent of the patients and /or subjects mentioned in the article. The author for correspondence is in possession of this document.</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle">Conflict of Interest</span><p id="par0255" class="elsevierStylePara elsevierViewall">The authors have no disclosures to make.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:12 [ 0 => array:2 [ "identificador" => "xres90919" "titulo" => "Abstract" ] 1 => array:2 [ "identificador" => "xpalclavsec78142" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres90918" "titulo" => "Resumen" ] 3 => array:2 [ "identificador" => "xpalclavsec78143" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Case Presentation (Dr. Emilio Benavente)" ] 5 => array:3 [ "identificador" => "sec0010" "titulo" => "Differential Diagnosis (Dr. Sergio Paira)" "secciones" => array:6 [ 0 => array:2 [ "identificador" => "sec0015" "titulo" => "Seizures in Lupus Erythematosus" ] 1 => array:2 [ "identificador" => "sec0020" "titulo" => "Antiphospholipid Antibodies and Epilepsy" ] 2 => array:2 [ "identificador" => "sec0025" "titulo" => "Tropical Causes of Epilepsy" ] 3 => array:2 [ "identificador" => "sec0030" "titulo" => "Vasculitis" ] 4 => array:2 [ "identificador" => "sec0035" "titulo" => "Neoplasms" ] 5 => array:2 [ "identificador" => "sec0040" "titulo" => "Rasmussen's Encephalitis" ] ] ] 6 => array:2 [ "identificador" => "sec0045" "titulo" => "Clinical Diagnosis (Dr. Sergio Paira)" ] 7 => array:2 [ "identificador" => "sec0050" "titulo" => "Pathology Discussion (Dr. Susana Roverano–Dr. Gustavo Saredo)" ] 8 => array:2 [ "identificador" => "sec0055" "titulo" => "Final Results and Comments" ] 9 => array:2 [ "identificador" => "sec0065" "titulo" => "Ethical disclosures" ] 10 => array:2 [ "identificador" => "sec0060" "titulo" => "Conflict of Interest" ] 11 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2012-02-02" "fechaAceptado" => "2012-05-09" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec78142" "palabras" => array:3 [ 0 => "Encephalitis" 1 => "Lupus erythematosus" 2 => "Status epilepticus" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec78143" "palabras" => array:3 [ 0 => "Encefalitis" 1 => "Lupus eritematoso" 2 => "Estatus convulsivo" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">We describe a 42-year-old woman with inactive systemic lupus erythematosus (SLE) at the time of her visit. She presented with an atypical movement disorder and partial continuous epilepsy. A brain biopsy excluded cerebral vasculitis and tumoral processes. We discuss the differential diagnosis of status epilepticus in a patient with SLE.</p>" ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "<p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Describimos a una paciente de 42 años de edad con diagnóstico de lupus eritematoso sistémico (LES) inactivo al momento de la visita. Se presentó con desórdenes del movimiento atípicos y epilepsia parcial continua (EPC). Una biopsia cerebral excluye procesos tumorales y vasculitis. Discutimos diagnósticos diferenciales de estatus epiléptico en una paciente con LES.</p>" ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "<p class="elsevierStyleNotepara">Please cite this article as: Benavente E, et al. Encefalitis con estatus convulsivo localizado en una paciente con lupus eritematoso sistémico. Reumatol Clin. 2012. <span class="elsevierStyleInterRef" href="doi:10.1016/j.reuma.2012.05.007">http://dx.doi.org/10.1016/j.reuma.2012.05.007</span>.</p>" ] ] "multimedia" => array:3 [ 0 => array:7 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 937 "Ancho" => 825 "Tamanyo" => 105915 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Central nervous system MR showing hyperintense lesions in T2 on the frontal, temporal and parietal right regions.</p>" ] ] 1 => array:7 [ "identificador" => "fig0010" "etiqueta" => "Fig. 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 614 "Ancho" => 1326 "Tamanyo" => 197325 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Diffuse astrogliosis of the cerebral cortex and GFAP+, CD68+ reactive astrocytes (Luxol Fast blue–hematoxylin–eosin).</p>" ] ] 2 => array:7 [ "identificador" => "fig0015" "etiqueta" => "Fig. 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr3.jpeg" "Alto" => 824 "Ancho" => 825 "Tamanyo" => 113223 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">Central nervous system MR after treatment with intravenous cyclophosphamide without evident lesions.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:28 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Evaluation and treatment of seizures in patients with systemic lupus erythematosus" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:2 [ 0 => "B. 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| Year/Month | Html | Total | |
|---|---|---|---|
| 2024 November | 15 | 16 | 31 |
| 2024 October | 100 | 43 | 143 |
| 2024 September | 112 | 25 | 137 |
| 2024 August | 110 | 42 | 152 |
| 2024 July | 117 | 34 | 151 |
| 2024 June | 101 | 41 | 142 |
| 2024 May | 131 | 48 | 179 |
| 2024 April | 112 | 22 | 134 |
| 2024 March | 86 | 28 | 114 |
| 2024 February | 85 | 31 | 116 |
| 2024 January | 69 | 28 | 97 |
| 2023 December | 78 | 34 | 112 |
| 2023 November | 100 | 42 | 142 |
| 2023 October | 132 | 53 | 185 |
| 2023 September | 152 | 48 | 200 |
| 2023 August | 75 | 20 | 95 |
| 2023 July | 96 | 33 | 129 |
| 2023 June | 63 | 22 | 85 |
| 2023 May | 64 | 12 | 76 |
| 2023 April | 72 | 10 | 82 |
| 2023 March | 151 | 46 | 197 |
| 2023 February | 128 | 28 | 156 |
| 2023 January | 130 | 23 | 153 |
| 2022 December | 141 | 60 | 201 |
| 2022 November | 169 | 24 | 193 |
| 2022 October | 144 | 82 | 226 |
| 2022 September | 149 | 66 | 215 |
| 2022 August | 181 | 43 | 224 |
| 2022 July | 142 | 48 | 190 |
| 2022 June | 123 | 52 | 175 |
| 2022 May | 128 | 46 | 174 |
| 2022 April | 157 | 59 | 216 |
| 2022 March | 163 | 45 | 208 |
| 2022 February | 175 | 52 | 227 |
| 2022 January | 157 | 46 | 203 |
| 2021 December | 121 | 49 | 170 |
| 2021 November | 105 | 43 | 148 |
| 2021 October | 100 | 69 | 169 |
| 2021 September | 93 | 50 | 143 |
| 2021 August | 79 | 45 | 124 |
| 2021 July | 74 | 39 | 113 |
| 2021 June | 87 | 32 | 119 |
| 2021 May | 97 | 36 | 133 |
| 2021 April | 276 | 120 | 396 |
| 2021 March | 145 | 35 | 180 |
| 2021 February | 66 | 23 | 89 |
| 2021 January | 79 | 23 | 102 |
| 2020 December | 68 | 26 | 94 |
| 2020 November | 63 | 25 | 88 |
| 2020 October | 72 | 25 | 97 |
| 2020 September | 170 | 35 | 205 |
| 2020 August | 51 | 39 | 90 |
| 2020 July | 29 | 31 | 60 |
| 2020 June | 37 | 31 | 68 |
| 2020 May | 76 | 15 | 91 |
| 2020 April | 57 | 19 | 76 |
| 2020 March | 14 | 6 | 20 |
| 2019 January | 1 | 0 | 1 |
| 2018 May | 13 | 0 | 13 |
| 2018 April | 132 | 11 | 143 |
| 2018 March | 166 | 10 | 176 |
| 2018 February | 106 | 2 | 108 |
| 2018 January | 111 | 4 | 115 |
| 2017 December | 124 | 12 | 136 |
| 2017 November | 158 | 8 | 166 |
| 2017 October | 123 | 6 | 129 |
| 2017 September | 128 | 11 | 139 |
| 2017 August | 116 | 4 | 120 |
| 2017 July | 98 | 11 | 109 |
| 2017 June | 126 | 7 | 133 |
| 2017 May | 136 | 17 | 153 |
| 2017 April | 113 | 12 | 125 |
| 2017 March | 110 | 23 | 133 |
| 2017 February | 96 | 7 | 103 |
| 2017 January | 80 | 12 | 92 |
| 2016 December | 155 | 22 | 177 |
| 2016 November | 170 | 12 | 182 |
| 2016 October | 195 | 21 | 216 |
| 2016 September | 286 | 8 | 294 |
| 2016 August | 229 | 7 | 236 |
| 2016 July | 93 | 9 | 102 |
| 2016 May | 1 | 15 | 16 |
| 2016 February | 1 | 20 | 21 |
| 2016 January | 3 | 17 | 20 |
| 2015 December | 2 | 0 | 2 |
| 2015 November | 1 | 0 | 1 |
| 2015 October | 2 | 29 | 31 |
| 2015 September | 1 | 0 | 1 |
| 2015 August | 1 | 0 | 1 |
| 2015 July | 116 | 9 | 125 |
| 2015 June | 128 | 5 | 133 |
| 2015 May | 168 | 13 | 181 |
| 2015 April | 182 | 12 | 194 |
| 2015 March | 192 | 6 | 198 |
| 2015 February | 204 | 7 | 211 |
| 2015 January | 149 | 9 | 158 |
| 2014 December | 162 | 10 | 172 |
| 2014 November | 190 | 9 | 199 |
| 2014 October | 185 | 13 | 198 |
| 2014 September | 146 | 11 | 157 |
| 2014 August | 135 | 13 | 148 |
| 2014 July | 175 | 18 | 193 |
| 2014 June | 184 | 11 | 195 |
| 2014 May | 136 | 21 | 157 |
| 2014 April | 164 | 14 | 178 |
| 2014 March | 153 | 17 | 170 |
| 2014 February | 121 | 12 | 133 |
| 2014 January | 97 | 9 | 106 |
| 2013 December | 85 | 12 | 97 |
| 2013 November | 78 | 9 | 87 |
| 2013 October | 110 | 10 | 120 |
| 2013 September | 90 | 14 | 104 |
| 2013 August | 95 | 20 | 115 |
| 2013 July | 70 | 11 | 81 |
| 2013 June | 74 | 19 | 93 |
| 2013 May | 104 | 35 | 139 |
| 2013 April | 30 | 13 | 43 |
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