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.