Case Presentation:
A 42-year-old male with no significant past medical history presented with approximately one year of progressive bilateral upper extremity numbness, tingling, and impaired gait. His symptoms started when he was rear-ended while driving his car a year prior. Approximately two weeks after the car accident, he began to notice numbness and tingling of his fingertips, progressing up his right upper extremity to the shoulder. He then experienced numbness and tingling of his left fingertips, which progressed proximally in a similar pattern. Subsequently, the symptoms involved his bilateral lower extremities. The lower extremity symptoms were associated with difficulty ambulating, especially lifting his left leg off the ground and occasional buckling of both knees causing him to fall. He also endorsed pain at both hips and over his neck musculature but denied pain elsewhere, including his back. With regards to sensation in his hands, only pressure sensation was spared. His only additional complaint was urge urinary incontinence. His slow gait exacerbated this problem. He had no issues with his bowel function.
Physical examination was notable for generalized hypertonia (Left > Right), spasticity, hyperreflexia in all four extremities, positive Hoffman sign in both hands, myoclonus in bilateral ankles, and loss of pinprick sensation in bilateral upper extremities.
Tests for Human Immunodeficiency Virus (HIV), Thyroid Stimulating Hormone (TSH), Erythrocyte Sedimentation Rate (ESR), Creatine Kinase (CK), and syphilis were all unremarkable. Computed Tomography (CT) of the cervical spine did not show any fracture or dislocation but did show left-sided foraminal stenosis at the C3-C4 level. Cervical MRI showed a long cord section of edema and a ”pancake enhancement ” pattern as illustrated in Figure 1 and Figure 2, corresponding to Spondylotic Myelopathy. Brain MRI was negative for areas of white matter enhancement, excluding Multiple Sclerosis and other demyelinating diseases such as Acute disseminated encephalomyelitis. Lumbar puncture was not performed as the risks given the cord edema outweighed the benefits.
Hence, due to signs of cord inflammation seen on MRI and the fact that steroids have been tried even in such cases that were compressive triggered pancake sign enhancement,2 and that there was no concern for an infective process, the decision was made to start an empiric steroid course with methylprednisolone 1 gram daily followed by high dose prednisone and taper. Neurosurgery was also consulted for possible surgical decompression. However, as per their assessment, decompression at the level C3-4 level would not be beneficial due to the minimal residual compression and the fact that underlying cord enhancement had not been clearly resolved with surgery in previously published literature.2 Thus, the patient was planned for a follow-up MRI of the cervical spine and aggressive rehabilitation to maintain strength.