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Patients with acute neurological changes, especially with focal neurological deficit, require images for its initial approach,generally skull tomography due to its availability.Here we report a case of an 80-year-old patient with altered state of consciousness and a seizure episode who was admitted on suspicion of cerebral hemorrhage. Her initial blood glucose was high and a hyperdense lesion was found in the right basal ganglion on brain computed tomography, laboratories in which no other metabolic alteration was identified apart from the acute decompensation of Diabetes, however, with a neuroradiology and clinical team, the diagnosis of diabetic striatopathy was made. The patient was treated with a fluid infusion, and serum glucose level was controlled with insulin. The patient gradually recovered consciousness and was alert to his baseline state within 24 hours,without neurological complications. Patients with risk factors and with findings suggesting stroke,the tomographic high densities,may suggest intracerebral hemorrhage;however,other metabolic and toxic pathologies may have similar tomographic changes. Our intention,is show to emergency physicians the presence of ganglio basal hyperintensities,mimics for gangliobasal hemorrhage should be studied according to history and clinical context and establish appropriate treatment in a timely manner.

Objectives To evaluate the effects of GH replacement therapy (GHR) for 3 years on glycated haemoglobin (HbA 1c ) and on the presence of dysglycaemia at any time during follow-up in Spanish adult patients with growth hormone deficiency (GHD). Study design A retrospective study of 41 patients with GHD was conducted using baseline and long-term data. Changes in HbA 1c values during the first 3 years of GHR were studied in both the overall population and patients with or without dysglycaemia during follow-up. Dysglycaemia was defined as FPG ≥ 100 mg/dl and/or HbA 1c ≥ 5.7%. Results Mean HbA 1c value (5.4 ± 0.4% at baseline) increased during the first and second years of GHR (HbA 1c 5.5 ± 0.4%, p = 0.05, and 5.5 ± 0.4%, p = 0.006 respectively). This increase was not maintained during the third year (HbA 1c 5.4 ± 0.3%, p = 0.107) of GHR. Twenty-eight patients (68.2%) had dysglycaemia during follow-up, 9 of them since baseline. In the 19 patients without baseline dysglycaemia, HbA 1c increased during the first year and remained stable in the next 2 years (mean HbA 1c 5.2 ± 0.4% at baseline; 5.5 ± 0.4% at 1 year, p p = 0.004, and 5.4 ± 0.4% at 3 years, p = 0.016). In the 9 patients with baseline dysglycaemia, HbA 1c did not significantly change during the 3 years of GHR therapy. Conclusions HbA 1c values increased during the first 2 years of GHR therapy. In patients with no dysglycaemia before treatment, HbA 1c steadily increased over the 3 years. However, it did not change in patients with baseline dysglycaemia.