ABSTRACT
BACKGROUND: Quantitative MRI techniques have demonstrated thalamocortical abnormalities in idiopathic generalized epilepsy (IGE). However, there are few studies examining IGE early in its course and the neurodevelopmental course of this region is not adequately defined. OBJECTIVE: We examined the 2-year developmental course of the thalamus and frontal lobes in pediatric new-onset IGE (i.e., within 12 months of diagnosis). METHODS: We performed whole-brain MRI in 22 patients with new-onset IGE and 36 age-matched healthy controls. MRI was repeated 24 months after baseline MRI. Quantitative volumetrics were used to examine thalamic and frontal lobe volumes. RESULTS: The IGE group showed significant differences in thalamic volume within 1 year of seizure onset (baseline) and went on to show thalamic volume loss at a significantly faster rate than healthy control children over the 2-year interval. The control group also showed a significantly greater increase in frontal white matter expansion than the IGE group. In contrast, frontal lobe gray matter volume differences were moderate at baseline and persisted over time, indicating similar developmental trajectories with differences early in the disease process that are maintained. CONCLUSIONS: Brain tissue abnormalities in thalamic and frontal regions can be identified very early in the course of IGE and an abnormal trajectory of growth continues over a 2-year interval.
Subject(s)
Epilepsy, Generalized/pathology , Epilepsy, Generalized/physiopathology , Frontal Lobe/pathology , Pediatrics , Thalamus/pathology , Adolescent , Analysis of Variance , Anticonvulsants/therapeutic use , Child , Epilepsy, Generalized/drug therapy , Female , Frontal Lobe/growth & development , Humans , Longitudinal Studies , Magnetic Resonance Imaging/methods , Male , Neural Pathways/growth & development , Neural Pathways/pathology , Statistics, Nonparametric , Thalamus/growth & development , Valproic Acid/therapeutic useABSTRACT
Carbon monoxide (CO) poisoning may result in focal and diffuse neuropathological changes, including basal ganglia lesions. The effect of CO poisoning on basal ganglia volumes over time is unclear. We assessed basal ganglia volumes longitudinally following CO poisoning. We prospectively enrolled 73 CO poisoned patients who underwent brain MR imaging on day 1 (baseline), 2 weeks, and 6 months post-CO poisoning. Basal ganglia volumes were obtained. One patient had bilateral globus pallidus lesions at two weeks and 6 months. Of the CO-poisoned patients 28% had volume reduction in at least one basal ganglia structure by 6 months, of which 21% had putamen, 15% had caudate, 15% had globus pallidus, and 16% had total basal ganglia volume reduction. Putamen volumes were significantly smaller from baseline to six months (p = 0.02). Verbal memory and mental processing speed correlated with smaller putamen and globus pallidus volumes. Carbon monoxide poisoning results in basal ganglia volume reduction 6 months post CO poisoning. Slow mental processing speed and impaired memory correlated with smaller putamen and globus pallidus volumes. Clinicians need to be aware of basal ganglia neuropathologic changes in the absence of observable lesions following CO poisoning.
