A 19‐year‐old man presented with several days of worsening fevers, severe headache, neck stiffness, and photophobia. He reported a sore throat, cough, and malaise 1 week earlier. He denied confusion, vision changes, dizziness, or weakness. He endorsed occasional nausea, vomiting, and mild lower abdominal pain. Previously healthy, he denied any sick contacts or recent outdoor, animal, or substance exposures. He had received the meningococcal vaccine 2 years prior. He was febrile with normal blood pressure and pulse. He was alert and oriented but ill‐appearing. Nuchal rigidity was present. Cranial nerve, strength, reflexes, and general sensation exams were normal. Suprapubic abdomen was tender to palpation. Cardiac, pulmonary, and skin exams were normal. White blood cell count was 14,800 with 80% neutrophils. HIV was negative. Sodium level was 128; the comprehensive metabolic panel was otherwise normal. Cerebrospinal fluid (CSF) contained 330 white blood cells with a lymphocytic predominance (86%), 159 red blood cells, with protein of 175 and glucose of 59. A bladder scan revealed a postvoid residual of 700 mL. The urinary retention was attributed to recent over‐the‐counter cold medications, and a Foley was inserted. Empiric meningitis coverage including dexamethasone was initiated, although steroids were stopped once gram stain was confirmed negative. The patient's symptoms drastically improved initially; however, on day 3, the patient's severe headache, malaise, and urinary retention returned. His neurologic exam otherwise remained normal. MRI revealed extensive T2 hyperintensity throughout the central spinal cord with multiple patchy, enhancing foci within the spinal cord, and diffuse leptomeningeal enhancement throughout the brain, consistent with acute disseminated encephalomyelitis (ADEM).
Recognition of ADEM by hospitalists is important because early diagnosis and treatment are essential in prevention of morbidity and mortality. Although historically more common in children, ADEM is increasingly identified in adults. ADEM is a demyelinating disease that generally occurs following a febrile illness or vaccination and is likely autoimmune in etiology. History often includes viral symptoms preceding the onset of encephalopathy or focal neurologic deficits. Meningismus and fever are common. CSF generally reveals lymphocytic pleocytosis, elevated protein, and normal glucose. ADEM may be suspected over meningitis when neurologic deficits are present. Focal deficits should prompt MRI. MRI reveals patchy areas of increased signal intensity in the white matter. Delay in diagnostic imaging may result in progressive neurologic damage or death. Steroids are the accepted first‐line therapy. Steroids were restarted in this patient with rapid and complete recovery.
This case demonstrates that significant demyelination associated with ADEM may be present with only subtle neurologic exam findings.
L.‐A. Wagner ‐ none