CASE:  38 y/o female marathon runner with 2 weeks of gradual onset of diffuse, progressively worsening, sharp, midthoracic, right paraspinal back pain. She reported occasional subjective fevers, but no pleuritic chest pain, bowel/bladder incontinence, nausea, vomiting, or leg weakness. On exam, vitals were 98.6 deg, 58 bpm, 12 breaths/min, 99% RA. EKG demonstrated sinus bradycardia. No midline spinal tenderness. Straight leg testing negative, and ROM of back was painful, but within normal limits. Full neuro exam was normal except for a small band of decreased sensation along T5-T6 distribution (approximate site of pain), barely crossing the midline.


She returned 1 week later with excruciating thoracic and lower back pain that was keeping her awake at night. She was unable to walk comfortably. Exam changed to a widened area of decreased sensation to pinprick, light touch, and temperature. She also reported decreased sensation in her toes. Position, gait, and strength were all preserved. LP revealed clear CSF with 541 leukocytes per cubic millimeter (90% lymphocytes), normal glucose (51 mg/dL), and elevated CSF protein (171 mg/dL). Later, CSF was found to be positive for IgM and IgG to B burgdorferi and serum Lyme was positive by ELISA. Diagnosis?




ROLE IN THE ED:  TM is a diagnosis that may be made in the ED, although varied presentations are common. It should be in the differential for any patient with back pain and weakness. Classic presentation: rapidly evolving back pain (generally thoracic) and lower extremity weakness, similar to that of Guillain-Barre syndrome. Incontinence, ataxia, and leg weakness are also common. It is also possible (as in this patient) to have slowly progressive back pain with prominent sensory deficit and no other associated symptoms. It is important to remember that symptoms may evolve over hours, days, or weeks.

MRI is the imaging of choice. With rapid onset symptoms this may be easier to obtain given it may exclude cord compression as well. With slow onset symptoms, patient may be admitted to neurology service to rule out mimics such as MS, Guillain Barre syndrome, tick paralysis, or botulism.


THERAPY:  Most common therapy for TM is supportive (unless a treatable infection is diagnosed). The use of corticosteroids is controversial, and must be made on a patient to patient basis.


BACKGROUND:  TM is a rare syndrome characterized by focal inflammation within the spinal cord, and clinical manifestations are due to resultant neural dysfunction of motor, sensory, and autonomic pathways within and passing through the inflamed area.


Most patients have CSF pleocytosis and blood-brain barrier breakdown within a focal area of the spinal cord and conventional treatments are aimed at ameliorating immune activation (i.e., corticosteroids). In approximately 30% to 60% of idiopathic TM cases, there is an antecedent respiratory, GI, or systemic illness. Thus, a possible mechanism explaining TM may be molecular mimicry.

–Hammerstedt H, Edlow J, Cusick S. Emergency Department Presentations of Transverse Myelitis: 2 case reports. 2005; Volume 46(3); pp 256-259

–Kaplan A, Krishnan C, Deshpande D, et al. Diagnosis and Management of Acute Myelopathies. The Neurologist. 2005; Volume 11(1); pp 2-18.

June 2024