Effects of Type 2 Diabetes on the Neuropsychological Profile in Mild Cognitive Impairment.

Background: Diabetes is one of the main risk factors for developing mild cognitive impairment (MCI) and Alzheimer's disease. Most studies have demonstrated a worse performance in executive function, verbal fluency, and information processing speed in patients with diabetes. Objective: To assess the cognitive functioning of persons with type 2 diabetes and amnesic mild cognitive impairment (aMCI-T2DM) compared to persons with aMCI without diabetes and persons without diabetes or aMCI as controls, to understand the role of diabetes in the neuropsychological profile. Methods: Cross-sectional study involving a sample of 83 patients, ranging in age from 61 to 85 years and divided into three groups: aMCI-T2DM (27 patients), aMCI (29 patients), Controls (27 individuals). All the participants undertook an exhaustive neuropsychological assessment (auditory-verbal and visual memory, attention, information processing speed, language, executive function, and depression). Results: Both groups of aMCI patients performed significantly worse than the controls in all the neuropsychological tests. A significant linear tendency (p trend < 0.05) was found between groups, with the aMCI-T2DM group presenting worse results in global cognition assessed by the Mini-Mental State Examination and Montreal Cognitive Assessment; Rey-Osterrieth Complex Figure Test; Auditory Verbal Learning Test; Trail Making Test A and B, Verbal Fluency Test, and Hamilton Depression Rating Scale. Conclusions: aMCI patients with or without diabetes showed worse cognitive function compared to persons without diabetes or aMCI. Additionally, aMCI patients without T2DM presented a different cognitive profile than aMCI patients with T2DM, which tended towards presenting worse cognitive functions such as global cognition, memory, attention, executive function, and language.

Miastenia grave inducida por tratamiento con inhibidores del punto de control inmunológico: primer caso secundario a avelumab y revisión de casos previamente publicados / Myasthenia gravis induced by inmuno checkpoints inhibitors: first case report secondary to avelumab therapy and review of published cases

Introducción. Los fármacos inhibidores del punto de control inmunológico han supuesto una revolución en el tratamiento de varios procesos neoplásicos en estadio avanzado. Sin embargo, se han descrito numerosas complicaciones neurológicas, entre las que se encuentran polineuropatías, crisis epilépticas, radiculitis y miastenia grave. Caso clínico. Varón de 65 años con adenocarcinoma de pulmón en estadio IV en tratamiento con avelumab que desarrolla una miastenia grave ocular seropositiva, con buena respuesta a la piridostigmina y retirada de la medicación. Conclusiones. El mecanismo exacto por el cual el avelumab induce una miastenia grave aún se desconoce, y probablemente existe un proceso fisiopatológico diferente al de la miastenia grave idiopática. Un dato importante es la variabilidad en cuanto al tiempo de aparición de la miastenia grave después de iniciar el tratamiento con inhibidores del punto de control inmunológico. Desde el punto de vista clínico, la mayoría de los casos descritos comenzó con una forma de miastenia grave generalizada con afectación bulbar que posteriormente desarrolló oftalmoparesia y ptosis palpebral fluctuante. Este caso, así como la revisión de la bibliografía, puede ser útil para alertar al neurólogo clínico sobre la posibilidad del desarrollo de cuadros inmunomediados de esta naturaleza inducidos por el tratamiento con avelumab en la práctica clínica y para orientar sus características clínicas, pronósticas y de tratamiento

Introduction. The inmuno checkpoints inhibitors are new revolutionary treatment for many neoplastic diseases in advanced stadium. There are described several types of neurological complications induced by nivolumab: polyneuropathy, seizures, radiculitis and myasthenia gravis disease. Case report. A 65 years old man with metastatic lung adenocarcinoma who presented myasthenia gravis disease induced by avelumab therapy with good response to treatment with pyridostigmine and withdrawal of avelumab. Conclusions. The exact mechanism by which this drug induces myasthenia gravis is still unknown and there is probably a different pathophysiological process to idiopathic myasthenia gravis. An important fact is the variability in the time of onset of myasthenia gravis after initiating treatment with inmuno checkpoints inhibitors. From the clinical point of view, most of the reported cases appeared with a generalized form of myasthenia gravis with bulbar involvement and later developed ophthalmoparesis and fluctuating palpebral ptosis. Our case as well as the review of the previous literature can be useful to alert the clinical neurologist about the possibility of the development of immune-mediated cases of this nature induced by the treatment with avelumab in clinical practice as well as to guide its clinical, prognostic and clinical characteristics and treatment