Serum sodium improvement: change in Comprehensive Geriatric Assessment parameters in geriatric patients with hyponatremia.

BACKGROUND: Hyponatremia presents with symptoms considered age-associated in the elderly. We assess the change in Comprehensive Geriatric Assessment (CGA) parameters after hyponatremia improvement in hospitalized geriatric patients. METHODS: We took 100 hyponatremic and same number of eunatremic geriatric patients (> 60 years) who were comorbidity, presenting-complaints, and age-matched. Four CGA parameters were utilized, the new Hindi Mental State Examination (HMSE), Barthel's index of activities of daily living (ADL), Timed up and go Test (TUG), and handgrip strength by hand dynamometer (HG). We analyzed these at admission and discharge, and their relationship with change in sodium levels. RESULTS: Average age was 68.1 ± 5.8 years, with males constituting 75%. The CGA parameters demonstrated worse values amongst the hyponatremia than the normonatremia group. Severe hyponatremia group showed worse CGA scores in comparison with moderate and mild. With improvement in sodium level, the improvements in ADL, TUG, and HMSE scores were greater in the hyponatremia group (8.8 ± 10.1, 2.2 ± 2.5, and 1.7 ± 2.3 respectively) in comparison to the normonatremia reference group (4.7 ± 9.0, 1 ± 2.0, and 0.7 ± 1.3 respectively, P < 0.05). CONCLUSION: Our study is the first utilizing HMSE to assess change in cognitive ability with improvement in serum sodium levels in the Indian elderly. Hyponatremic patients show worse baseline CGA parameters, and hyponatremia severity correlates with worse motor and cognitive function. Improvement in the serum sodium level improves the CGA parameters. Correction of hyponatremia in the geriatric age group significantly impacts life quality.

The autism and schizophrenia associated gene CYFIP1 is critical for the maintenance of dendritic complexity and the stabilization of mature spines.

Copy number variation (CNV) at the 15q11.2 region has been identified as a significant risk locus for neurological and neuropsychiatric conditions such as schizophrenia (SCZ) and autism spectrum disorder (ASD). However, the individual roles for genes at this locus in nervous system development, function and connectivity remain poorly understood. Haploinsufficiency of one gene in this region, Cyfip1, may provide a model for 15q11.2 CNV-associated neuropsychiatric phenotypes. Here we show that altering CYFIP1 expression levels in neurons both in vitro and in vivo influences dendritic complexity, spine morphology, spine actin dynamics and synaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor lateral diffusion. CYFIP1 is highly enriched at synapses and its overexpression in vitro leads to increased dendritic complexity. Neurons derived from Cyfip1 heterozygous animals on the other hand, possess reduced dendritic complexity, increased mobile F-actin and enhanced GluA2-containing AMPA receptor mobility at synapses. Interestingly, Cyfip1 overexpression or haploinsufficiency increased immature spine number, whereas activity-dependent changes in spine volume were occluded in Cyfip1 haploinsufficient neurons. In vivo, Cyfip1 heterozygous animals exhibited deficits in dendritic complexity as well as an altered ratio of immature-to-mature spines in hippocampal CA1 neurons. In summary, we provide evidence that dysregulation of CYFIP1 expression levels leads to pathological changes in CNS maturation and neuronal connectivity, both of which may contribute to the development of the neurological symptoms seen in ASD and SCZ.