Is it ever "too late" to treat my migraine?

The information provided in this handout does not necessarily reflect the views of the University of Minnesota Medical School physicians and faculty. These materials are provided for informational purposes only and are in no way intended to take the place of the advice and recommendations of your personal health care provider. You use the information provided in these handouts at your own risk.Migraines are very painful headaches with certain identifying features, such as unilaterality, throbbing, nausea and/or vomiting, and sensitivity to light and/or sound. Patients are generally advised to treat their migraine attacks early or they risk not achieving adequate pain relief. This pamphlet is designed to suggest that patients do have effective treatment options, even if they miss the opportunity to treat an attack early in its course

Depressive behavior and selective down-regulation of serotonin receptor expression after early-life seizures: reversal by environmental enrichment

Depression is the most common psychiatric comorbidity in epilepsy. To better understand the contribution of seizures versus environment to depression in epilepsy, we investigated differential gene expression using microarray and quantitative RT-PCR, and depressive behavior, in the Porsolt forced swim test in juvenile rats reared in different environments after kainic acid (KA)-induced seizures. We selected for genes significantly down-regulated by KA seizures and upregulated by environmental enrichment. This common gene selection process yielded one known gene involved in mood and affect: serotonin receptor 5B. The changes in serotonin receptor gene expression were paralleled by decreased mobility in the forced swim tests; depressive behavior exhibited after seizures was no longer evident in rats reared in environmental enrichment. Our results suggest that seizures lead to increased susceptibility to depression through transcriptional regulation while environment, in turn, can interact with gene expression to influence the behavioral outcome of epilepsy

Iron Is Essential for Neuron Development and Memory Function in Mouse Hippocampus1–3

Iron deficiency (ID) is the most prevalent micronutrient deficiency in the world and it affects neurobehavioral outcome. It is unclear whether the effect of dietary ID on the brain is due to the lack of neuronal iron or from other processes occurring in conjunction with ID (e.g. hypoxia due to anemia). We delineated the role of murine Slc11a2 [divalent metal ion transporter-1 (DMT-1)] in hippocampal neuronal iron uptake during development and memory formation. Camk2a gene promoter-driven cre recombinase (Cre) transgene (Camk2a-Cre) mice were mated with Slc11a2 flox/flox mice to obtain nonanemic Slc11a2hipp/hipp (double mutant, hippocampal neuron-specific knockout of Slc11a2hipp/hipp) mice, the first conditionally targeted model of iron uptake in the brain. Slc11a2hipp/hipp mice had lower hippocampal iron content; altered developmental expression of genes involved in iron homeostasis, energy metabolism, and dendrite morphogenesis; reductions in markers for energy metabolism and glutamatergic neurotransmission on magnetic resonance spectroscopy; and altered pyramidal neuron dendrite morphology in area 1 of Ammon's Horn in the hippocampus. Slc11a2hipp/hipp mice did not reach the criterion on a difficult spatial navigation test but were able to learn a spatial navigation task on an easier version of the Morris water maze (MWM). Learning of the visual cued task did not differ between the Slc11a2WT/WT and Slc11a2hipp/hipp mice. Slc11a2WT/WT mice had upregulation of genes involved in iron uptake and metabolism in response to MWM training, and Slc11a2hipp/hipp mice had differential expression of these genes compared with Slc11a2WT/WT mice. Neuronal iron uptake by DMT-1 is essential for normal hippocampal neuronal development and Slc11a2 expression is induced by spatial memory training. Deletion of Slc11a2 disrupts hippocampal neuronal development and spatial memory behavior