Clinical and Neuroimaging Profile of Children with Lesions in the Corpus Callosum
Corresponding Author
Chellamani Harini MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Chellamani Harini and Rohit R. Das contributed equally.
Correspondence: Address correspondence to Chellamani Harini, MD, Division of Epilepsy & Clinical Neurophysiology, Boston Children's Hospital, Harvard Medical School, Fegan 9, 300 Longwood Avenue, Boston, MA 02115. E-mail: [email protected]Search for more papers by this authorRohit R. Das MD, MPH
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Indiana State University, Indianapolis, IN
Chellamani Harini and Rohit R. Das contributed equally.
Search for more papers by this authorSanjay P. Prabhu MBBS
Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, Boston, MA
Search for more papers by this authorKanwaljit Singh MD, MPH
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, Boston, MA
Search for more papers by this authorAmit Haldar MD, DM
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorMasanori Takeoka MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorAnn M. Bergin MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorTobias Loddenkemper MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorSanjeev V. Kothare MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY
Search for more papers by this authorCorresponding Author
Chellamani Harini MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Chellamani Harini and Rohit R. Das contributed equally.
Correspondence: Address correspondence to Chellamani Harini, MD, Division of Epilepsy & Clinical Neurophysiology, Boston Children's Hospital, Harvard Medical School, Fegan 9, 300 Longwood Avenue, Boston, MA 02115. E-mail: [email protected]Search for more papers by this authorRohit R. Das MD, MPH
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Department of Neurology, Indiana State University, Indianapolis, IN
Chellamani Harini and Rohit R. Das contributed equally.
Search for more papers by this authorSanjay P. Prabhu MBBS
Department of Radiology, Boston Children's Hospital and Harvard Medical School, Harvard Medical School, Boston, MA
Search for more papers by this authorKanwaljit Singh MD, MPH
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Lurie Center, Massachusetts General Hospital for Children, Harvard Medical School, Boston, MA
Search for more papers by this authorAmit Haldar MD, DM
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorMasanori Takeoka MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorAnn M. Bergin MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorTobias Loddenkemper MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
Search for more papers by this authorSanjeev V. Kothare MD
Division of Clinical Neurophysiology, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA
New York University Medical Center, Comprehensive Epilepsy Center, Langone Medical School, NY
Search for more papers by this authorConflicts of Interest: None of the authors have any conflicts of interest to declare.
ABSTRACT
PURPOSE
T2-hyperintense signal changes in corpus callosum (CC) have been described in epilepsy and encephalitis/encephalopathy. Little is known about their pathophysiology. The aim of this study was to examine the clinical presentation and evolution of CC lesions and relationship to seizures.
METHODS
We identified 12 children among 29,634 patients from Radiology Database. We evaluated following characteristics: seizures and accompanying medical history, antiepileptic drug usage, presenting symptoms, and radiological evolution of lesions.
RESULTS
CC lesions were seen in patients with prior diagnosis of epilepsy (n = 5) or in those with new onset seizures (n = 3), or with encephalitis/encephalopathy without history of seizures (n = 4). Seizure clustering or disturbances of consciousness were the main presenting symptoms. No relationship was observed between CC lesion and AEDs. On imaging, ovoid lesions at presentation resolved on follow up imaging and linear lesions persisted. DTI showed that the fibers passing through splenial lesions originated from the posterior parietal cortex and occipital cortex bilaterally.
CONCLUSION
In patients with seizures, no clear relationship was demonstrated between seizure characteristics or AED use with CC lesions. Ovoid lesions resolved and may have different pathophysiologic mechanism when compared to linear lesions that persisted.
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