A 23-year-old Brazilian man, a farmer in a rural area of Minas Gerais State, complained of an 8-month history of neck pain and upper-limb weakness. Flaccid tetraparesis, global hyperreflexia, and pyramidal signs were present. Cranial CT and brain MRI were normal. Spinal cord MRI showed an intramedullary tumoral lesion, extending from C3 to C5 vertebral bodies, with a cystic appearance (figure 1). With a presumptive diagnosis of spinal cord tumor, the lesion was completely removed. Microscopy revealed the diagnosis of neurocysticercosis (figure 2). The patient was started on corticosteroids and albendazole with good functional recovery after 4 months. MRI showed only residual alterations caused by the surgical procedure.CSF eosinophilia or a positive ELISA test to cysticerci are useful tools in the diagnosis of neurocysticercosis and unfortunately were not performed in our patient. Isolated cervical intramedullary spinal neurocysticercosis is extremely rare and not considered by most physicians.

Brain glucose hypometabolism and neuroinflammation are early pathogenic manifestations in neurological disorders. Neuroinflammation may also disrupt leptin signaling, an adipokine that centrally regulates appetite and energy balance by acting on the hypothalamus and exerting neuroprotection in the hippocampus. The Goto-Kakizaki (GK) rat is a non-obese type 2 diabetes mellitus (T2DM) animal model used to investigate diabetes-associated molecular mechanisms without obesity jeopardizing effects. Wistar and GK rats received the maintenance adult rodent diet. Also, an additional control group of Wistar rats received a high-fat and high-sugar diet (HFHS) provided by free consumption of condensed milk. All diets and water were provided ad libitum for eight weeks. Brain glucose uptake was evaluated by 2-deoxy-2-[fluorine-18] fluoro-D-glucose under basal (saline administration) or stimulated (CL316,243, a selective b3-AR agonist) conditions. The animals were fasted for 10-12 h, anesthetized, and euthanized. The brain was quickly dissected, and the hippocampal area was sectioned and stored at -80°C in different tubes for protein and RNA analyses on the same animal. GK rats exhibited attenuated brain glucose uptake compared to Wistar animals and the HFHS group under basal conditions. Also, the hippocampus of GK rats displayed upregulated leptin receptor, IL-1b, and IL-6 gene expression and IL-1b and the subunit of the transcription factor NF-kB (p-p65) protein expression. No significant alterations were detected in the hippocampus of HFHS rats. Our data indicated that a genetic predisposition to T2DM has significant brain deteriorating features, including brain glucose hypometabolism, neuroinflammation, and leptin signaling disruption in the hippocampal area.