Several epidemiological studies have shown that Diabetes Mellitus (DM) or Insulin Resistance (IR) increases the risk of dementia. Besides, some authors suggested that poor glucose control to be associated with worse cognitive function. We aimed to assess cognitive functions and IR-degree over time in diabetic. We also evaluated whether a greater magnitude of cognitive decline could be related with their IR degree. We enrolled 335 diabetic patients and 142 non-diabetic subjects; participants were subdivided into three groups in accordance with their IRdegree assessed by Homa-Index (HI): Normal-HI (non-diabetic NHI < 2,6), Moderate-HI (MHI > 2,6 < 10) and High-HI (HHI > 10). Metabolic status and a comprehensive neuropsycological test battery (MMSE, ADAS-Cog, ACDS-ADL) were assessed at baseline and every 12-months during the follow-up (6,8 years). At the end of the study, the average MMSE decreased significantly in patients of HHI group (P = .001) compared to baseline. MMSE scores were also reduced both in MHI group and in controls, but the difference between two groups was not significant. In HHI group, similar effects were observed for the ADAS-Cog score compared to baseline (P = 0.001); instead, when ACDS-ADL was evaluated, no differences was observed among the three groups. These results remained unchanged also after adjustment for confounding variables (i.e. APOε-status, sex, BMI, education level, heart diseases and HbA1c). We suggest that higher IR-degree is associated with greater cognitive decline in diabetic patients; so we hypothesize that IR degree, more than IR status itself, could be related to the severity of cognitive impairment.
The results of this study illustrate that hippocampal sclerosis has offered a fertile substrate for intractable ADNFLE to develop. The present findings also highlight the importance of acquired factors that are directly relevant to the epilepsy phenotype and its severity even in monogenic epilepsies.
A 70-year-old woman presented with a 2-year history of progressive difficulty in walking with frequent falls. Neurologic examination showed postural instability with backward falls, vertical supranuclear gaze palsy with normal vestibular-ocular reflex, rigidity, and pyramidal signs in the right limbs. There was no clinical response to levodopa. Laboratory serologic tests had normal results. MRI displayed midbrain compression and dislocation caused by a large tumor in the left lateral ventricle (figure). Dopamine transporter SPECT showed normal striatal binding. The patient died before neurosurgery could be performed; there was no autopsy. Brain tumors should be considered in the diagnostic workup 1 of progressive supranuclear palsy-like phenotypes.
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