Yeteri kadar kontrol edilmeyen diyabet bilişsel işlevlere zarar verebilir, fakat çözülmeli belirtilerle ilgili herhangi bir rapor bulunmamaktadır. Biz bu raporda, ikinci tip diyabeti olan yaşlı bir hastadaki hiperglisemi bağlantılı tekrar eden bir disosiyatif füg vakası sunacağız. Muhtemel nörobiyolojik mekanizmaların üzerinde de durulacaktır.

This case report highlights the role of hyperglycaemia in a dissociative syndrome that may be overlooked by physicians, until it results in significant consequences. Traditionally dissociation is considered as an escape from overwhelming distress with partial or complete loss of control on voluntary actions or alienation of oneself or external world [6]. Possible biological factors implicated in pathogenesis include reduced perfusion in inferior prefrontal and anterior temporal regions in the right hemisphere and abnormal functioning of the Hypothalamo-Pituitary-Adrenal dysfunction, Glutamate/N-Methyl-D-Aspartate (NMDA) receptor, Serotonin (5-HT2a, 5-HT2c), Gama-Amino Butyric Acid (GABA), and Opioid receptors[7, 8]. Though diabetes may impair attention, speed of information processing, motor skills, working memory, the mechanism involved in the occurrence of dissociative fugue is unknown [9]. NMDA receptor that plays important role in cognitive impairment in other disorder (e.g. Alzheimer dementia) appears to play a role in causation of dissociative symptoms. Diabetes can induce NMDA receptor subunit composition resulting in cognitive impairment, and NMDA-receptor antagonists have shown to improves cognitive in over activation [10,11].On other hand activation of NMDA receptors in the dorsal vagal complex lowers glucose production, and it involved in glucose stimulated insulin secretion from beta cells [12]. Role of GABA and 5HT2 is unclear. The activation of GABA (A) receptors decreased insulin secretion and GABA (B) receptor antagonist increase insulin release in islets type 2 diabetic[13] .GABA synthesis is impaired in hyperglycaemic state [14,7].GABA-A antagonism and 5-HT2a/2c agonism can induce dissociative-like symptoms [15]. 5-HT2A receptors are implicated in the molecular mechanisms of anti-diabetic medication16.Hyper activation of the HPA axis is also reported in diabetes [5].Thus in isolation or in combination of above pathophysiology, hyperglycaemic state may result in dissociative symptoms.