| 제목 |
Spinal cord infarction in young female with antiphospholipid syndrome |
| 소속 |
Dongguk University Ilsan Hospital, Department of Rehabilitation Medicine1, Dongguk University Gyeongju Hospital, Department of Rehabilitation Medicine2 |
| 저자 |
Ki Yeun Nam1†, Bum Sun Kwon1, Jin Woo Park1, Ho Jun Lee1, Jeong Hwan Lee2, Tae June Park1, Hee Jae Kim1, Tae Yeun Kim1, Sheng Shu Kim1, Yong Jin Cho1* |
Background :
Antiphospholipid syndrome(APS) is characterized by venous or arterial thrombosis in the presence of persistent laboratory evidence of antiphospholipid antibodies. APS is quite rare as an etiologic factor for spinal cord infarction (SCI).
Case Report :
This 37-year old woman was admitted to the emergency room with chest discomfort, cough and rhinorrhea on December 17, 2017. The patient had no past medical history that could cause coronary artery disease or pulmonary disease.
Immediately after arrival at the hospital, echocardiography and transthoracic echocardiography to evaluate for cardiac embolic source was normal. Chest CT was performed to rule out atypical pneumonia. Chest CT showed both lung pneumonia. The laboratory data showed WBC 14480, CRP 11.58, ESR 38, CK-MB 7.12 (0.0~3.61 ng/mL), Troponin T 0.490 (0~0.014), positive RSV B, lupus anticoagulant antibodies (1.32) and anti-cardiolipin IgM (18.9). Test for another lab was no specific sign. Antiphospholipid syndrome triggered by infection was suspected. On hospital 2days, the patient complained of both lower leg weakness and sensory loss below T8 dermatome. Immediate brain diffusion MRI was performed, there was no evidence of acute infarction or intracranial hemorrhagic lesion (Figure 1).
Physical examination showed incomplete motor and sensory impairment below the T8 level, including loss of deep tendon reflexes, and urinary retention.
Initial whole spine magnetic resonance imaging performed at hospital 3day after symptom onset didn’t show definite abnormal intramedullary SI or enhancing lesion in spinal cord. Enhance whole spine MRI showed degenerative changes with a herniated disc present at T2-3, T5-6 and T6-7 level pressuring the spinal sac without pressure on the cord (Figure 2).
Six days after clinical onset, electrical stimulation of the both median, ulnar, peroneal, tibial, sural nerves showed abnormal findings ; low amplitude on CMAP, of both common peroneal nerve. Somatosensory evoked potentials of lower limbs were no response.
Follow up MRI was performed on the 11 day after the first MRI. Enhance T-spine MRI was showed Long segmental intramedullary high SI at T5~conus medullaris. On axial image, the intramedullary high SI is noted at anterior part of spinal cord (Figure 3).
Treatment with anticoagulant therapy (warfarin 4mg daily) was given in order to prevent further ischemic attacks that might affect any other organs. The patient showed neurological improvement after rehabilitation.
Conclusions :
This is the first case of APS triggered upper respiratory infection with spinal cord infarction. The study indicated that APS should also be considered as an evaluation when a spinal cord infarction occurs without any specific cause. |
|
No evidence of acute infarction on DWI
T2-3, T5-6, T6-7 : mild central disc protrusion -> mild thecal sac indentation
Long segmental intramedullary high SI at T5~conus medullaris
|
