Transverse myelitis has many potential etiologies, among which are demyelinating diseases, connective tissue disorders, infections, paraneoplastic syndromes, and drug/toxin-induced. An infectious etiology is frequently suspected, but the pathogenic agent is rarely identified. Enteroviruses are associated with different neurological syndromes, most commonly in children,Reference Ooi, Wong and Lewthwaite ¹ with transverse myelitis being a rare presentation particularly in the adult population.Reference Ooi, Wong and Lewthwaite ^{1 ,} Reference Cardosa, Farrar and Yeng ²

We describe a 23-year-old female who presented low back pain associated with lower limb numbness, urinary incontinence, and constipation. There was no viral prodromal illness, namely no respiratory or gastrointestinal symptoms. Two days later, she developed lower limb weakness. Neurological examination disclosed an asymmetric flaccid paraparesis with right predominance, brisk deep tendon reflexes, right Babinski sign, loss of pain sensation below T4 on the left and T8 on the right, decreased proprioception, and vibration sense on halluces with loss of ambulation. The patient had no skin rash. Brain magnetic resonance imaging (MRI) was normal, but the spinal cord MRI disclosed a long medullar hyperintensity (Figure 1). Cerebrospinal fluid (CSF) analysis revealed 112 leukocytes (108 monocytes), increased proteins and immunoglobulin G index, normal glucose, and a positive polymerase chain reaction for enterovirus. Oligoclonal bands were not identified and anti-aquaporin 4 antibodies were negative. The remaining CSF and serum studies, including blood count, biochemistry, serology, and immunology, were normal/negative. She was treated with bolus of intravenous methylprednisolone 1000 mg for 5 days followed by intravenous immunoglobulins 0.67 g/kg/day for 3 days, and presented immediate improvement. Control MRI, 9 months afterwards, also revealed signs of recovery (Figure 2). With 3 years of follow-up, she presented with minor right lower limb weakness with Babinski sign, decreased pain sensation below T8 on the right, and independent ambulation.

Figure 1 Admission MRI. A, B (axial and sagittal T2): C2-C7 enlargement and transverse medullar hyperintensity affecting more than two-thirds of cord diameter. C (sagittal T2): T3-T11 hyperintensity affecting the anterior cord half. D (sagittal T1): T1-T2 right anterolateral focal contrast enhancement.

Figure 2 Control MRI 9 months afterwards. A, B (sagittal T2): T1-T3 slight hyperintensity with minor cord atrophy.

We describe a patient with a typical presentation of an acute transverse myelitis (ATM), in whom neither the history, neurological examination, nor spinal MRI pointed to a specific etiology. In ATM, the thoracic cord is the most frequently involved site, with the triad of paraparesis, sensory impairment level, and sphincter dysfunction being the most common clinical signs. Up 40% of patients with ATM have no findings on MRI,Reference Scotti and Gerevini ³ with the remaining 60% presenting variable and nonspecific abnormalities. The lesion commonly extends through three to four spinal segmentsReference Desanto and Ross ⁴ and occupies more than two-thirds of the cross-sectional area of the cord,Reference Desanto and Ross ⁴ with variable enlargement that is frequently associated to oedema. A viral ATM has no specific imaging abnormalities. In our patient, where a viral prodrome was not present, neither were systemic symptoms, a viral etiology was suspected because of the presence of leukocytes on CSF and later confirmed by polymerase chain reaction.

Enterovirus’ tropism for the spinal cord is well-established, although pathophysiological mechanisms remain incompletely understood.Reference Cardosa, Farrar and Yeng ^{2 ,} Reference Teoh, Mohammad and Britton ⁵ Some authors suggest a direct role of the virus causing tissue destruction, whereas others propose an indirect mechanism caused by a cytokine-mediated small-vessel vasculitis.Reference McMinn, Stratov and Nagarajan ⁶ In the presented case, the major clinical improvement after corticosteroids and immunoglobulins supports an immuno-mediated mechanism and adds evidence to previous reported cases that also presented a favorable response to corticotherapy.Reference Nolan, Craig and Lahra ⁷