# Neurologic Deterioration in Acute Traumatic Central Cord Syndrome Without Bone Injury Caused by Traumatic Cerebrospinal Fluid Rhinorrhea: A Case Report

## TL;DR

A case report shows that traumatic cerebrospinal fluid rhinorrhea may worsen spinal cord compression in a patient with no bone injury.

## Contribution

First report linking intracranial CSF leakage to cervical spinal cord compression in preexisting stenosis.

## Key findings

- Neurological deterioration occurred after traumatic CSF rhinorrhea in a patient with ATCCS and no bone injury.
- MRI findings were attributed to epidural venous plexus engorgement due to low CSF pressure.
- Neurological improvement followed surgery and CSF leak management.

## Abstract

Whether to perform surgery for acute traumatic central cord syndrome (ATCCS) without bone fracture or dislocation but with spinal cord compression due to preexisting cervical canal stenosis remains controversial. We present a case of ATCCS without bone injury in which neurologic deterioration was possibly caused by traumatic cerebrospinal fluid rhinorrhea (TCFR). An 82-year-old man with ATCCS (American Spinal Injury Association (ASIA) Impairment Scale (AIS) C) and an anterior skull base fracture was urgently transported to our hospital and was initially treated conservatively. However, on the day after admission, his quadriparesis worsened, and MRI showed high signal intensity in the epidural area on both T1-weighted and T2-weighted images, initially suggesting an epidural hematoma. In response to this neurological deterioration, we decided to perform urgent surgery aimed at spinal cord decompression. Although there was no obvious TCFR at admission, profuse TCFR was observed upon prone positioning for surgery. A lumbar CSF drain was inserted to control the CSF leak, but output remained negligible, consistent with marked intracranial hypotension. C3 laminectomy and C4-C6 laminoplasty were performed with the patient in the head-elevated position, leading to neurological improvement. No epidural hematoma was found intraoperatively. The abnormal MRI findings were presumed to be due to engorgement of the epidural venous plexus associated with low CSF pressure. Subdural hygroma was noted on head CT on postoperative day 7, which resolved spontaneously by day 14. To the best of our knowledge, there have been no previous reports describing exacerbation of cervical spinal cord compression due to intracranial CSF leakage in the setting of preexisting cervical stenosis. This report suggests that in patients with ATCCS and concomitant anterior skull base fracture, TCFR may contribute to neurological deterioration. Further accumulation of such cases is required to clarify this association.