ABSTRACT
A 71-year-old male with no previous medical history was admitted to our hospital for paralysis of the right upper extremity. Although DWI of the brain revealed high-intensity signals in the bilateral frontal and left parietal lobes, CT revealed a hyperdense spot in the anterior superior sagittal sinus (SSS). Because CT venography revealed SSS occlusion, he was diagnosed with cerebral venous thrombosis (CVT). In addition, laboratory findings, including free triiodothyronine, 8.85â pg/ml; thyroxine, 3.39â pg/dl, thyroid-stimulating hormone (TSH), < 0.02â µU/ml; and anti-TSH receptor antibody, 5.7â IU/l, led to the diagnosis of hyperthyroidism for the first time. Moreover, factor VIII procoagulant protein levels exhibited a marked increase (187.5%). Based on these findings, the patient was diagnosed with CVT due to Graves' disease.
Subject(s)
Graves Disease/complications , Graves Disease/diagnosis , Intracranial Thrombosis/diagnostic imaging , Intracranial Thrombosis/etiology , Aged , Antithyroid Agents/administration & dosage , Autoantibodies/blood , Factor VIII/metabolism , Graves Disease/blood , Graves Disease/drug therapy , Heparin/administration & dosage , Humans , Intracranial Thrombosis/blood , Intracranial Thrombosis/drug therapy , Levetiracetam/administration & dosage , Magnetic Resonance Imaging , Male , Methimazole/administration & dosage , Phlebography , Receptors, Thyrotropin/immunology , Tomography, X-Ray Computed , Treatment OutcomeABSTRACT
A 63-year-old woman presented to our hospital with sudden symptoms of unsteadiness while walking. Based on the neurological findings, i.e., ataxia and absence of tendon reflex in the extremities accompanied by antecedent infection at the time, she was tentatively diagnosed with Fisher syndrome. Following intravenous immunoglobulin (IVIg) therapy for 5 days, her ataxic symptoms improved. Laboratory data were negative for antiganglioside antibody against GQ1b in the IgG subclass. Six months after her first admission, cognitive impairment gradually developed. She was re-admitted owing to new onset of unsteadiness while walking 1.5 years after her first admission. Diffusion-weighted brain MRI (DWI) revealed linear high-intensity signals in the region of the corticomedullary junction. Cutaneous skin biopsy revealed intranuclear inclusion bodies in sweat gland cells. Considering her family history along with the examination results, we diagnosed with adult-onset sporadic neuronal intranuclear inclusion disease (NIID). Retrospective investigation of the previous DWI obtained at the first admission had also shown slight linear high-intensity areas, suggesting that a series of events, including repeated sudden-onset transient ataxia, resulted due to NIID.
