Читать книгу Canine and Feline Epilepsy - Luisa De Risio - Страница 106

A presumptive diagnosis of thiamine (vitamin B1) deficiency is based on dietary history, clinical and MRI findings and response to therapy. MRI findings include bilaterally symmetrical hyperintensity on T2-weighted and FLAIR images localized to the red nuclei, caudal colliculi, vestibular nuclei and cerebellar nodulus in dogs (Figs 4.4a–e) (Garosi, 2003) and to the lateral geniculate nuclei, caudal colliculi, periaqueductal grey matter, medial vestibular nuclei, cerebellar nodulus and facial nuclei in cats (Fig. 4.5; plate 2) (Penderis et al., 2007; Palus et al., 2010). These MRI changes have been reported to resolve following thiamine supplementation (Garosi et al., 2003; Palus et al., 2010). Bilaterally symmetrical hyperintense lesions on T2-weighted and FLAIR images have been reported to affect also the cerebral cortex (parietal, occipital, hippocampal lobe) in cats with thiamine deficiency (Marks et al., 2011). Diagnosis can be confirmed by determining whole blood thiamine concentration by high-performance liquid chromatography. This test is now commercially available in many countries and has replaced the erythrocyte transketolase activity assay because of its superior sensitivity and specificity for thiamine status (Marks et al., 2011). Diet samples can also be submitted for thiamine analysis. Pathologic changes include bilaterally symmetrical spongiosis, necrosis and haemorrhage of upper brainstem nuclei including caudal colliculus, lateral geniculate (Plate 2), medial vestibular and oculomotor nuclei.