![]() T2-weighted whole spinal cord MRI showed a high-intensity lesion at cervical levels 3–6, with faint enhancement on gadolinium-enhanced T1-weighted imaging (Fig. On fluid-attenuated inversion recovery (FLAIR) brain magnetic resonance imaging (MRI), a high-intensity lesion was found in the dorsal part of the medulla oblongata without enhancement, but no lesion was found in the hypothalamic or supratentorial region. The IgG index was 0.47, and the myelin basic protein level was not elevated. CSF examination showed elevated protein levels with normal cell counts. The plasma glucose level was 137 mg/dL, HbA1c was 7.0%, the CK level was 25 U/L, and the BNP level was 131.9 pg/mL. Anti-nucleotide antibody, ACE, anti-SS-A antibody, anti-SS-B antibody, PR3-ANCA, MPO-ANCA and anti-TPO antibody were not elevated. The soluble interleukin 2 receptor level was 638 U/mL. On laboratory examination, serum anti-AQP4 antibody was positive. Electrocardiography revealed a pacemaker rhythm, and cardiac ultrasonography showed no abnormalities. Bladder and rectal disturbances were also noted. Thermal and pain sensations were impaired in the upper and lower extremities, and vibration sensation was impaired in both lower extremities. Tendon reflexes were diminished with no pathological reflexes. The patient had muscle weakness manual muscle testing revealed grade 4 in the upper extremities and grade 3 in the lower extremities. Her consciousness was intact, and there was no abnormality in the cranial nerves. She had 10-year history of type 2 diabetes mellitus, hypertension and dyslipidemia but had no history of cardiac disease before pacemaker implantation. Two months after the operation, she was referred to our hospital because of weakness of the upper and lower extremities and sensory impairment of the lower extremities, which progressed over a month. 1 ), and permanent pacemaker implantation was performed after the diagnosis of SSS. ![]() She showed several episodes of syncope, and electrocardiogram (ECG) monitoring indicated sinus pauses lasting five to six seconds (Fig. Conclusionsīecause SSS is a life-threatening complication, clinicians should be aware of the possibility that medullary lesions in NMOSD can cause SSS as the initial manifestation.Ī 77-year-old female was admitted to a previous hospital with refractory nausea and vomiting. Then, she was transferred to another hospital for rehabilitation. She was treated with two courses of an intravenous methylprednisolone pulse and one course of plasma exchange. Her serum was positive for antibodies against aquaporin 4, and a diagnosis of NMOSD was made. ![]() T2-weighted magnetic resonance imaging (MRI) showed high-intensity lesions in the dorsal part of the medulla oblongata and C3–6 cervical cord. Tendon reflexes were diminished, while no pathological reflexes were present. The patient was confirmed to have muscle weakness manual muscle testing revealed grade 4 in the upper extremities and grade 3 in the lower extremities. Two months later, she was referred to our hospital because of limb weakness and sensory impairment that progressed over a month. The patient was diagnosed with SSS because sinus pauses lasting five to six seconds were observed, and pacemaker implantation was performed. Case presentationĪ 77-year-old female developed refractory nausea and frequent episodes of syncope. We report a patient with NMOSD who developed refractory nausea, vomiting and SSS as the initial manifestation. Although medullary lesions have occurred in patients with neuromyelitis optica spectrum disorder (NMOSD), there are few reports of SSS associated with NMOSD. ![]() Sick sinus syndrome (SSS) is known to occur due to lesions in the medulla oblongata. ![]()
0 Comments
Leave a Reply. |
AuthorWrite something about yourself. No need to be fancy, just an overview. ArchivesCategories |