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Published on: February 19, 2021
Acute disseminated encephalomyelitis: an MRI/MRS longitudinal study
Lidia V Gabis1, David J Panasci, Mary R Andriola
1Department of Neurology, Stony Brook, New York, USA.
Insights
Acute disseminated encephalomyelitis (ADEM) in children can be diagnosed using neuroimaging. Magnetic resonance spectroscopy revealed specific metabolic changes indicating neuronal dysfunction and loss in ADEM.
Area of Science:
- Pediatric Neurology
- Neuroimaging
- Biochemistry
Background:
- Acute disseminated encephalomyelitis (ADEM) is an inflammatory demyelinating disease affecting the central nervous system.
- Diagnosis often relies on clinical presentation and neuroimaging findings.
Observation:
- Two children diagnosed with ADEM presented with distinct neurological symptoms and brain lesions.
- Neuroimaging, including MRI and 1H magnetic resonance spectroscopy, was used for evaluation.
- Patients were treated symptomatically and showed clinical recovery.
Findings:
- 1H magnetic resonance spectroscopy demonstrated abnormalities in N-acetyl-aspartate, choline, and lactate during the symptomatic phase.
- Persistent low N-acetyl-aspartate was observed during recovery, suggesting neuronal loss.
- Spectroscopic findings correlate with neuropathological evidence of neuronal dysfunction, inflammation, and metabolic stress.
Implications:
- 1H magnetic resonance spectroscopy can provide insights into the pathophysiology of ADEM.
- Spectroscopic changes may help differentiate ADEM from other neurological conditions.
- Understanding these metabolic alterations aids in assessing disease severity and recovery in pediatric ADEM.
Abstract:
A clinical and radiologic diagnosis of acute disseminated encephalomyelitis was made in two children: a 6-month-old female who presented with focal seizures and thalamic and cerebral white matter lesions, and a 4.5-year-old male who presented with tremor and dystonia and had bilateral basal ganglia lesions, without evidence of active brain infection. Serial clinical and laboratory evaluations were supplemented by neuroimaging including routine magnetic resonance imaging and (1)H magnetic resonance spectroscopy. They were treated symptomatically, without using steroids or intravenous immunoglobulin, and both children recovered. Single voxel (1)H magnetic resonance spectroscopy data were acquired from the involved areas and from normal-appearing white matter. Abnormalities in N-acetyl-aspartate, choline, and lactate peaks were evident during the symptomatic phase, and persistence of low N-acetyl-aspartate was observed during recovery. These spectroscopic findings are consistent with neuropathologic findings of neuronal dysfunction, cellular membrane turnover, cellular infiltration, and metabolic stress in the acute phase, and with neuronal loss in the chronic phase.

