Background
Cerebral venous sinus thrombosis (CVST) composes an uncommon subtype of stroke caused by thrombotic occlusion of the cerebral venous system and tends to occur in hypercoagulable states. Albeit exceedingly rare, autoimmune hyperthyroidism and COVID-19 has been implicated as rare risk factors for CVST. As both conditions are capable of inducing degrees of inflammation and hypercoagulability, we postulate that COVID-19 could trigger CVST by superimposing endotheliitis and inflammation on the hypercoagulable and hypofibrinolytic state of hyperthyroidism.
Case presentation
We report the case of an adult male with headache, fever, nausea, vomiting, and previously known autoimmune hyperthyroidism. Diagnostics revealed elevated inflammatory and hypercoagulability markers, free T4, low TSHs, and positive SARS-CoV-2 PCR. Neuroimaging demonstrated an acute intracerebral and subdural hemorrhage attributable to cerebral sinus thromboses. A diagnosis of CVST with associated COVID-19 and autoimmune hyperthyroidism was established, and anticoagulation therapy was initiated. Follow-up examination revealed complete symptomatic resolution and regression of thrombosis.
Conclusions
Clinicians should be aware that even mild COVID-19 could precipitate CVST, especially in presence of other risk factors. Further studies should be conducted to evaluate the effects of mild COVID-19 on existing prothrombic states, including autoimmune hyperthyroidism. Furthermore, a high index of suspicion towards a secondary cause must be maintained for headaches in COVID-19, as it may indicate a serious etiology, including CVST.
<p>The pathophysiology behind neuropsychiatric SLE (NPSLE) remains poorly understood and its clinical and radiological manifestations are highly varied. In this report, we present a complex case of an adolescent female patient with a three-week history of systemic symptoms (fever, nausea, vomiting, weight-loss, polyarticular joint pain), progressive motor weakness, tremor, and altered mental status. Physical examination was significant for oromandibular and cervical dystonia rigidity, and general weakness with imposed right-sided hemiparesis. A head MRI demonstrated bilateral hyperintense lesions of the basal ganglia and brainstem, SS without restricted diffusion. The patient was diagnosed with NPSLE, lupus nephritis, electrolyte imbalance, severe hypoalbuminemia, lupus cardiomyopathy, autoimmune hemolytic anemia, pulmonary tuberculosis, and sepsis. The patient was given treatment in the ICU with pulse dose corticosteroids, intravenous antibiotics, intravenous immunoglobulins (IVIg), and supportive treatment with correction of hematologic and electrolyte abnormalities. Her condition improved rapidly. Full alertness was regained, and symptoms of oromandibular dystonia, tremor, and weakness diminished significantly. A follow-up MRI three weeks later revealed complete disappearance of lesions, which we attribute to resolution of the inflammatory process in the brain.</p>
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