scholarly journals Neuropsychiatric manifestation in patient having SLE

2014 ◽  
Vol 9 ◽  
pp. S41
Author(s):  
Kunjan Shah ◽  
Nikhil Shory ◽  
Mitali Rathod Santosh ◽  
J.D. Lakhani
Keyword(s):  
Neuropsychiatric Manifestation

Integrated Biomarkers for Depression in Alzheimer’s Disease: A Critical Review

2017 ◽  
Vol 14 (4) ◽  
pp. 441-452 ◽  
Author(s):  
Sofia Wenzler ◽  
Christian Knochel ◽  
Ceylan Balaban ◽  
Dominik Kraft ◽  
Juliane Kopf ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Affect Regulation ◽  
Current Evidence ◽  
Diagnostic Process ◽  
Neuropsychiatric Manifestation ◽  
The Brain ◽  
Control Functional

Depression is a common neuropsychiatric manifestation among Alzheimer’s disease (AD) patients. It may compromise everyday activities and lead to a faster cognitive decline as well as worse quality of life. The identification of promising biomarkers may therefore help to timely initiate and improve the treatment of preclinical and clinical states of AD, and to improve the long-term functional outcome. In this narrative review, we report studies that investigated biomarkers for AD-related depression. Genetic findings state AD-related depression as a rather complex, multifactorial trait with relevant environmental and inherited contributors. However, one specific set of genes, the brain derived neurotrophic factor (BDNF), specifically the Val66Met polymorphism, may play a crucial role in AD-related depression. Regarding neuroimaging markers, the most promising findings reveal structural impairments in the cortico-subcortical networks that are related to affect regulation and reward / aversion control. Functional imaging studies reveal abnormalities in predominantly frontal and temporal regions. Furthermore, CSF based biomarkers are seen as potentially promising for the diagnostic process showing abnormalities in metabolic pathways that contribute to AD-related depression. However, there is a need for standardization of methodological issues and for replication of current evidence with larger cohorts and prospective studies.

Rapid-Onset Weakness and Numbness in a Patient With Systemic Lupus Erythematosus

2021 ◽  
pp. 120-121
Author(s):  
Floranne C. Ernste
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Cerebrospinal Fluid ◽  
Lupus Erythematosus ◽  
White Blood Cells ◽  
Cauda Equina ◽  
Transverse Myelitis ◽  
Lower Extremities ◽  
Systemic Lupus ◽  
Neuropsychiatric Manifestation ◽  
Fluid Analysis

A 33-year-old woman with systemic lupus erythematosus, diagnosed 2 years prior and treated with hydroxychloroquine, sought care for a 4-week history of pain and paresthesias in her low back and lower extremities. She described a bandlike sensation of numbness starting in her midback which descended to both legs. Her symptoms progressed to constipation and inability to urinate adequately. She reported difficulty with ambulation. Over the course of 1 week of hospitalization, urinary and fecal incontinence developed. On examination, she was alert and appropriately oriented. She had a malar rash and swelling of the metacarpophalangeal joints consistent with bilateral hand synovitis. Neurologic examination indicated hyperreflexia with brisk patellar and Achilles tendon reflexes bilaterally. She had trace motor weakness of the hip flexors, quadriceps, and hamstrings. She had loss of pinprick and temperature sensation in the lower extremities, extending beyond the saddle area to the T12 dermatome. Vibration perception and proprioception were preserved. She had a positive Babinski sign in the left foot. Her cerebellar examination showed slowing of rapid alternating movements in the left hand. Magnetic resonance imaging of the lumbosacral spine indicated subtle T2 signal change of the intramedullary conus and enhancement of the cauda equina nerve roots. Cerebrospinal fluid analysis showed an increased protein concentration. Two white blood cells/µL were found in the cerebrospinal fluid. The serum antinuclear antibody was strongly positive, and the anti–double-stranded DNA antibody level was greater than 1,000 IU/mL. The serum complement levels were low. Lupus anticoagulant, beta-2 glycoprotein antibodies, and antiphospholipid antibodies were increased, at greater than twice the upper limits of normal. Electromyography indicated multiple sacral radiculopathies. The patient was diagnosed with autoimmune myeloradiculitis as a neuropsychiatric manifestation of systemic lupus erythematosus (neuropsychiatric systemic lupus erythematosus). The patient received methylprednisolone followed by prednisone, with a gradual taper. Her hospital course was complicated by the development of deep venous thromboses in the bilateral lower extremities. She was started on heparin and transitioned to warfarin therapy. She started mycophenolate mofetil. Hydroxychloroquine was continued. At a 24-month follow-up visit, the patient remained in neurologic remission. Neuropsychiatric systemic lupus erythematosus events consist of a heterogeneous array of neurologic and psychiatric disorders including intractable headaches, cognitive dysfunction, psychosis, seizure disorders, transverse myelitis, aseptic meningitis, cranial neuropathies, and acute inflammatory demyelinating polyneuropathy.

scholarly journals Fulminant Guillain-Barré syndrome in a patient with systemic lupus erythematosus

2019 ◽  
Vol 12 (1) ◽  
pp. bcr-2018-226634 ◽  
Author(s):  
Eric Anthony Coomes ◽  
Hourmazd Haghbayan ◽  
Jenna Spring ◽  
Sangeeta Mehta
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Axonal Neuropathy ◽  
Guillain Barre Syndrome ◽  
Systemic Lupus ◽  
Outward Appearance ◽  
Intravenous Immunoglobulin Therapy ◽  
Neuropsychiatric Manifestation ◽  
Guillain Barré Syndrome ◽  
Guillain Barré

A 45-year-old man with a history of systemic lupus erythematosus presented with progressive weakness and areflexia. Electromyogram revealed reduced motor and sensory amplitudes without demyelinating features. He was clinically diagnosed with the acute motor and sensory axonal neuropathy variant of Guillain-Barré syndrome. Despite intravenous immunoglobulin therapy, he deteriorated with loss of all voluntary motor function and cranial nerve reflexes. Concomitant investigations revealed class V lupus nephritis. Therapy was initiated with plasma exchange, glucocorticoids and further immunosuppression, with gradual neurological recovery. We present the first documented case of fulminant Guillain-Barré syndrome as a neuropsychiatric manifestation of systemic lupus erythematosus, highlighting how immune-mediated polyneuropathy via diffuse deafferentation may mimic the outward appearance of brain death. While glucocorticoids are not indicated in idiopathic Guillain-Barré, when this neurological disorder is a consequence of systemic lupus erythematosus, immunomodulatory treatment should be initiated to prevent neurological deterioration.

scholarly journals Two different cases of SLE with neuropsychiatric manifestation

2011 ◽  
Vol 9 (S1) ◽  
Author(s):  
V Panaviene ◽  
S Rusoniene ◽  
M Jakutovic
Keyword(s):  
Neuropsychiatric Manifestation

scholarly journals Lobe-specific neuropsychiatric manifestation of neurocysticercosis

2020 ◽  
Vol 21 (2) ◽  
pp. 116
Author(s):  
Arun Selvaraj ◽  
VinothKrishna Dass ◽  
Lakshmi Sanjay
Keyword(s):  
Neuropsychiatric Manifestation

scholarly journals Recent Topics on the Mechanisms of Immunosuppressive Therapy-Related Neurotoxicities

2019 ◽  
Author(s):  
Wei Zhang ◽  
Nobuaki Egashira ◽  
Satohiro Masuda
Keyword(s):  
Early Recognition ◽  
Immunosuppressive Agents ◽  
Calcineurin Inhibitors ◽  
Mtor Inhibitors ◽  
Immunosuppressive Drugs ◽  
Individual Therapy ◽  
Therapeutic Drug ◽  
Neuroprotective Effects ◽  
Neuropsychiatric Manifestation ◽  
Neuropsychiatric Complications

Although transplantation procedures have been developed for patients with end-stagec hepatic insufficiency or other diseases, allograft rejection still threatens patient health and lifespan. Over the last few decades, the emergence of immunosuppressive agents, such as calcineurin inhibitors (CNIs) and mammalian target of rapamycin (mTOR) inhibitors, have strikingly increased graft survival. Unfortunately, immunosuppressive agent-related neurotoxicity is commonly occurred in clinical situations, with the majority of neurotoxicity cases caused by CNIs. The possible mechanisms whereby CNIs cause neurotoxicity include: increasing the permeability or injury of the blood-brain barrier, alterations of mitochondrial function, and alterations in electrophysiological state. Other immunosuppressants can also induce neuropsychiatric complications. For example, mTOR inhibitors induce seizures; mycophenolate mofetil induces depression and headache; methotrexate affects the central nervous system; mouse monoclonal immunoglobulin G2 antibody against cluster of differentiation 3 also induces headache; and patients using corticosteroids usually experience cognitive alteration. Therapeutic drug monitoring, individual therapy based on pharmacogenetics, and early recognition of symptoms have greatly reduced neurotoxic events. Once neurotoxicity occurs, a reduction in the drug dosage, switching to other immunosuppressants, using drugs to treat the neuropsychiatric manifestation, or blood purification therapy have proven to be effective against neurotoxicity. In this review, we summarize the recent topics on the mechanisms of neurotoxicity of immunosuppressive drugs. In addition, some information about neuroprotective effects of several immunosuppressants are also discussed.

Posterior reversible encephalopathy syndrome: A neuropsychiatric manifestation of systemic lupus erythematosus

2020 ◽  
pp. 102739
Author(s):  
Martín Valdez-López ◽  
Eduardo Aguirre-Aguilar ◽  
Sergio Iván Valdés-Ferrer ◽  
Francisco M. Martínez-Carrillo ◽  
Antonio Arauz ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Posterior Reversible Encephalopathy Syndrome ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Posterior Reversible Encephalopathy ◽  
Neuropsychiatric Manifestation ◽  
Reversible Encephalopathy

scholarly journals Pearls & Oy-sters: An unusual neuropsychiatric manifestation of systemic lupus erythematosus

Neurology ◽  
2018 ◽  
Vol 90 (21) ◽  
pp. e1929-e1932
Author(s):  
David Dongkyung Kim ◽  
Charles Ho ◽  
Rebecca King ◽  
Sarah A. Morrow
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Systemic Lupus ◽  
Neuropsychiatric Manifestation

scholarly journals Idiopathic intracranial hypertension as a cause of severe intractable headache in a patient with Systemic Lupus Erythematosus: A case report from Eastern Nepal

2018 ◽  
Vol 7 (2) ◽  
pp. 40-42
Author(s):  
Bhupendra Shah ◽  
Mathew Ibrahim Amprayil ◽  
Rahul Taparia ◽  
Shailesh Mani Pokhrel
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Intracranial Hypertension ◽  
Lupus Erythematosus ◽  
Idiopathic Intracranial Hypertension ◽  
Female Gender ◽  
Systemic Lupus ◽  
Hypervitaminosis A ◽  
Neuropsychiatric Manifestation ◽  
History Of

Correction: Unfortunately, several authors on this paper were omitted. Therefore, on 15th April 2019 the following authors were added to the paper: Mathew Ibrahim Amprayil, Rahul Taparia and Shailesh Mani Pokhrel. The editorial board apologises for this error. The common risk factors for Idiopathic intracranial hypertension are obesity, female gender, hypervitaminosis A, and steroid withdrawal. Even though Idiopathic intracranial hypertension is considered as a neuropsychiatric manifestation of Systemic lupus erythematosus, it is often missed by the physician as a cause of a headache in a patient with Systemic lupus erythematosus. We report a case of 21-year-old female who presented in our outpatient department with a history of a severe intractable progressive headache for a duration of four weeks and blurring of vision for five days who was later diagnosed as a case of idiopathic intracranial hypertension with Systemic lupus erythematosus. She recovered dramatically with the institution of steroid and acetazolamide therapy.

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