Case Report: Stroke-like migraine attacks after radiation therapy syndrome: a rare complication 26 years after cranial radiotherapy.

Stroke-like migraine attacks after radiation therapy (SMART) syndrome is a rare delayed complication of cranial radiotherapy, that may present decades after brain irradiation. Here we present a case of 41-year old patient with a history of grade 3 oligodendroglioma, epilepsy and migraine, 26 years after brain radiation therapy, who was admitted with right hemicranial headache, nausea, left homonymous hemianopsia, weakness of the left arm and left-sided hemihypesthesia. After considering alternate diagnoses, we ultimately diagnosed SMART syndrome. Despite its rare occurrence and unknown pathophysiology, there are more case reports of SMART syndrome reported due to advancements in oncology treatment and increasing patients' survival rates. Therefore, diagnosis of SMART syndrome should always be considered in patients with a history of cranial radiation presenting with focal neurologic deficits and migraine, especially with a change in pattern of their usual migraine attack.

Huperzine aggravated neurochemical and volumetric changes induced by D-galactose in the model of neurodegeneration in rats.

The multimodal MRI and 1H MRS study was designed to provide a structural and neurochemical view of D-galactose induced rat brain degeneration and its treatment with huperzine A. The volume changes were captured using MRI focused on the hippocampal region and a neurochemical profile was obtained from the same area using in vivo localized 1H MRS, which was compared with in vitro1H MRS hippocampal spectra at the high field after the animals were culled. At the four week point, we observed a small decrease in N-acetylaspartate/creatine (NAA/tCr), myo-inositol/creatine (mIns/tCr) and glutamine/creatine (Gln/tCr) in the group in which neurodegeneration was induced. At the eight week point, we found only slight but statistically significant decreases in NAA/tCr, mIns/tCr and glutamate/creatine (Glu/tCr) in this group in vivo. However, in the treated group, the decrease in NAA/tCr and Glu/tCr was much more pronounced compared to the D-gal group. In vitro1H MRS analysis from rat hippocampal samples showed very similar changes in metabolites, which were also much more pronounced in the treated group. Neurodegeneration was also confirmed by a significant decrease in γ-aminobutyrate/creatine (GABA/tCr) observed only in the treated group, but not in the D-gal group. MRI image data and subsequent volumetric quantification showed mild hippocampal degeneration at the four week point in D-gal group. At the eight week point, we observed a decrease in hippocampal volume in both experimental groups, with a more pronounced decrease in the huperzine-treated group. In conclusion, in our experimental design huperzine A treatment worsened the neurodegeneration of the rat brain, which was supported by all of the used MRI and 1H MRS methods.

D-galactose-induced aging in rats - The effect of metformin on bioenergetics of brain, skeletal muscle and liver.

Chronic D-galactose administration induces accelerated aging in rodents. The aim of the study was to find by in vivo31P MRS suitable markers of early stages of brain degeneration on this metabolic model in rats. Additionally, we studied the therapeutic effect of antidiabetic drug metformin. The study has been extended by in vitro determination of mitochondrial function in brain, skeletal muscle and liver mitochondria, oxidative stress parameter thiobarbituric acid reactive substances (TBARS), and lipophilic antioxidants levels. In vivo31P MRS revealed lower intracellular pH (pHi) and lower inorganic phosphate to ATP ratio (Pi/ATP), with higher index of oxidative phosphorylation - phosphocreatine (PCr) to Pi ratio - in brain of rats chronically administered with D-galactose. The function of brain mitochondria was not affected. Administration of metformin diminished changes in brain pHi and plasma TBARS. The function of skeletal muscle mitochondria and their coenzyme Q (CoQ) content were considerably reduced after D-galactose administration. Metformin administered simultaneously with D-galactose did not prevent these changes. The results of in vivo31P MRS revealed evidence of early stage of neurodegeneration that may indicate pre-inflammation. Our data show different susceptibility of brain, skeletal muscle, and liver to the chronic exposure to D-galactose and metformin. The D-galactose model presented in the literature as a model for "age-related dementia" had much more devastating effects on skeletal muscle than on the brain.

Improved tissue integrity after alginate treatment in rat spinal cord injury: evidence from ex vivo diffusion tensor imaging.

Diffusion tensor imaging (DTI) is a magnetic resonance imaging technique used to characterize fibrous structures such as white matter in the central nervous system, including normal and spinal cord injury (SCI) conditions. Our aim was to evaluate the effect of alginate treatment in the rat SCI by DTI parametric measures. Ex vivo DTI data were collected by spin echo sequence with following parameters TR/TE: 2500 ms/32 ms and b-value of 1500 s/mm2. Main significant changes were found in fractional anisotropy (FA), and radial diffusivity (RD), between the saline- and alginatetreated group at the level of individual sections and whole spinal cord. Results indicate that ex vivo DTI can be used as a tool for tissue structure characterisation and both FA and RD as promising prognostic parameters of SCI treatment.