CNS lupus: Symptoms, Pathogenesis & Treatments
Symptoms
Neurologic and psychiatric symptoms are known to occur in 10 to 80% of SLE patients, and the patterns of these symptoms vary widely. Neurological symptoms in SLE patients are due to involvement of the nervous system at various levels, and therefore, even if they involve the nervous system in the same way, The symptoms may vary from person to person. One of the reasons for this involvement is vasculopathy in most SLE patients. Because vasculopathy causes a direct injury to the blood vessels, it also destroys the blood-brain barrier (BBB), which is thought to result in the autoantibody entering the CNS through the damaged BBB.
Pathogenesis
In addition, anti-neuronal Ab targeting human neuroblastoma cells is seen in 45% of patients with CNS lupus. Of course, 5% of SLE patients with anti-neuronal Ab are not associated with CNS lupus, but if this autoantibody is found, it is likely to show seizure or psychosis. Lymphocytotoxic Ab is associated with cognitive dysfunction, anti-phospholipid Ab increases the risk of stroke, and anti-ribosomal P Ab is associated with psychosis and depression. Psychosis can also occur secondary to infection, metabolic complication, and hypertension following immunosuppressive therapy.
Treatments
Because of this variety of clinical features, the treatment varies accordingly, and therefore, the treatment according to the symptoms of the individual. Cognitive dysfunction usually decreases memory, abstract thinking ability, and judgment, and is most effective when using steroids as a prevalent symptom in SLE patients. Patients with stroke syndrome who have antiphospholipid Ab should use anticoagulants chronically with warfarin or aspirin. In addition, seizure occurs in about 10-20% of SLE patients and is associated with anti-Sm and aPL. The most recommended therapy is to give glucocorticoids and gabapentin or low dose tricyclic antidepressant when pain, intolerable parasthesia and nerve conduction test are abnormal.
Neurologic and psychiatric symptoms are known to occur in 10 to 80% of SLE patients, and the patterns of these symptoms vary widely. Neurological symptoms in SLE patients are due to involvement of the nervous system at various levels, and therefore, even if they involve the nervous system in the same way, The symptoms may vary from person to person. One of the reasons for this involvement is vasculopathy in most SLE patients. Because vasculopathy causes a direct injury to the blood vessels, it also destroys the blood-brain barrier (BBB), which is thought to result in the autoantibody entering the CNS through the damaged BBB.
Pathogenesis
In addition, anti-neuronal Ab targeting human neuroblastoma cells is seen in 45% of patients with CNS lupus. Of course, 5% of SLE patients with anti-neuronal Ab are not associated with CNS lupus, but if this autoantibody is found, it is likely to show seizure or psychosis. Lymphocytotoxic Ab is associated with cognitive dysfunction, anti-phospholipid Ab increases the risk of stroke, and anti-ribosomal P Ab is associated with psychosis and depression. Psychosis can also occur secondary to infection, metabolic complication, and hypertension following immunosuppressive therapy.
Treatments
Because of this variety of clinical features, the treatment varies accordingly, and therefore, the treatment according to the symptoms of the individual. Cognitive dysfunction usually decreases memory, abstract thinking ability, and judgment, and is most effective when using steroids as a prevalent symptom in SLE patients. Patients with stroke syndrome who have antiphospholipid Ab should use anticoagulants chronically with warfarin or aspirin. In addition, seizure occurs in about 10-20% of SLE patients and is associated with anti-Sm and aPL. The most recommended therapy is to give glucocorticoids and gabapentin or low dose tricyclic antidepressant when pain, intolerable parasthesia and nerve conduction test are abnormal.
