Acute Hydrocephalus Following Cervical Spinal Cord Injury
A 75-year-old male patient was referred to our emergency department with a tetraparesis after a trivial fall at home. He had been intermittently admitted to our spine center due to cervical OPLL and diffuse idiopathic skeletal hypertrophy. There was no evidence of head injury and his mental status was alert. On neurological examination, his sensation was off below the C5 dermatome, with right side motor weakness of 0/V and left side motor weakness of II/V. In addition, we detected decreased anal tone, loss of urinary sense, and hypotonia of deep tendon reflex. He also exhibited signs of spinal shock, including hypotension and bradycardia.\nExcept for brain cortical atrophy, no abnormal findings were observed on brain computed tomography (CT). Plain cervical radiographs and CT showed diffuse, thick OPLL from level C1 to C4, which was slightly thickened, compared to a previous imaging study performed six years ago. Cervical magnetic resonance imaging showed severe spinal cord compression with signal change of the spinal cord from C1 to C4 (). In particular, heterogeneous signal change of the C1-2 level suggested acute intramedullary hemorrhage of the spinal cord.\nWe performed emergency cervical spine surgery. Decompressive total laminectomy from C1 to C5, and occipitocervical fusion from occiput to C5 were performed (). In the operation field, cord edema was severe and pulsation of the cord was weak. After the operation, his motor weakness showed slight improvement.\nTwo days after surgery, his mental status had deteriorated to drowsiness, with dilation of the right pupil of 4 mm. Findings on brain CT revealed acute hydrocephalus and subarachnoid hemorrhage (SAH) in the cerebellomedullary cistern (). Brain and carotid CT angiography showed no vascular abnormality. To alleviate symptoms, we performed lumbar cerebrospinal fluid (CSF) drainage. The pressure of lumbar drainage was as high as 26 cmH2O, and CSF was mixed with fresh blood. Despite lumbar drainage, his symptoms did not show improvement, therefore, extraventricular drainage (EVD) was performed. Two weeks after EVD, ventriculo-peritoneal shunt was performed, however, neurologic deterioration was not fully recovered. Three months after trauma, he eventually died due to heart failure.