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Abstract Details

Spinal Cord Infarction: A Diagnostic Challenge
Cerebrovascular Disease and Interventional Neurology
P4 - Poster Session 4 (5:30 PM-6:30 PM)
3-025

Spinal cord infarction is a rare form of myelopathy and often misdiagnosed due to diagnostic challenges.

A 17 year old girl presented to the emergency department after sudden onset of severe back pain after minor twisting movement developing bilateral lower extremity weakness within one minute.

Initial spinal cord MRI was negative. She had flaccid paraparesis with absence of lower extremity reflexes. Guillain Barré was suspected at initial facility and IVIG was given. On day six, repeat MRI showed T10 to T12 cord edema and enhancement with gadolinium isolated to the anterior cord with “owl eye” appearance on axial section. Transverse myelitis was subsequently suspected, and IV corticosteroids were given followed by plasmapheresis without improvement.

Cerebrospinal fluid studies were normal including cultures, oligoclonal bands, and infectious studies. Autoimmune, hypercoagulable, vitamin deficiencies, aquaporin 4 antibody, anti MOG antibody testing was negative.

Two months later when re-evaluated at subsequent facility, patient had a sensory level at T10 with preservation of vibration and proprioception and spastic paraparesis with lower extremity hyperreflexia and sustained clonus on the left.

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Spinal cord infarction is commonly misdiagnosed as an inflammatory myelopathy due to diagnostic challenges and rarity of the condition. Anterior spinal artery syndrome is the most common syndrome presenting classically with preservation of vibration and proprioception. Sudden back pain is a common initial symptom. T2 hyperintensities restricted to a particular vascular territory raises concern for vascular myelopathy as opposed to inflammatory myelopathies.

The most powerful tool for diagnosis is temporal evolution of symptoms. Diagnosis should be considered when there is sudden onset of symptoms with nadir reached within 12 hours, absence of cord compression, and typically absence of inflammatory changes in CSF. Importantly mild pleocytosis, elevated protein in CSF and gadolinium enhancement are potentially seen in spinal cord infarction and should not exclude this diagnosis.

Authors/Disclosures
Michlene Passeri, MD (UTMB)
PRESENTER
Dr. Passeri has nothing to disclose.
Ram N. Narayan, MD, FAAN (Barrow Neurological Institute) Dr. Narayan has nothing to disclose.