Study on the intervention effect of SMG health management in patients with ischemic stroke.

INTRODUCTION: The aim of the study was to explore the clinical effect of brain and heart health managers combined with the "SMG" health management mode on nursing intervention in ischemic stroke patients. MATERIAL AND METHODS: A total of 187 ischemic stroke patients divided into 96 patients in the observation group and 91 patients in the control group with the random number table method. The control group conducted the routine care intervention, and the observation group used the brain and heart health managers combined with the "SMG" health management model for the nursing intervention. The control of stroke risk factors was explored by comparing blood pressure, blood glucose and blood lipid and other indicators between the two groups before and after treatment. RESULTS: Compared with that before the intervention, the Stroke Self-Efficacy Questionnaire (SSEQ) score of both the observation group and the control group were significantly higher ( p < 0.05), and the Hamilton Anxiety Scale (HAMA), Hamilton Depression Scale (HAMD), National Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) scores were all decreased ( p < 0.05). The proportion of patients with treatment adherence did not differ significantly before and after the intervention in the control group ( p > 0.05), and it increased significantly in the observation group after the intervention ( p < 0.05). The observation group had higher SSEQ score and lower HAMA, HAMD, NIHSS, and mRS scores after the intervention compared with the control group, with statistically significant differences. CONCLUSIONS: The combination of brain and heart health managers and "SMG" is more conducive to improving the selfefficacy of ischemic stroke patients, alleviating patient anxiety and depression, improving patient treatment compliance, controlling stroke risk factors, and promoting neurological function recovery.

Progressive ataxia of cerebrotendinous xanthomatosis with a rare c.255+1G>T splice site mutation: A case report.

BACKGROUND: Cerebrotendinous xanthomatosis is an autosomal recessive disorder of lipid metabolism caused by the mutation of the CYP27A1 gene encoding sterol 27-hydroxylase, an essential enzyme for the conversion of cholesterol to chenodeoxycholic and cholic acids. Cerebrotendinous xanthomatosis is a rare neurological disease with a wide range of clinical symptoms that are easily misdiagnosed. CASE SUMMARY: Here we report the clinical, biochemical, and molecular characterization of a 33-year-old female patient with cerebrotendinous xanthomatosis. The patient developed ataxia and had the typical symptoms of juvenile cataracts, tendon xanthomata, and progressive nervous system dysfunction. Magnetic resonance imaging of the brain revealed bilateral dentate nucleus lesions and white matter abnormalities. This patient was misdiagnosed for 2 years resulting in severe neurological complications. After 2 years of chenodeoxycholic acid treatment, she still presented with ataxia and dysarthria. The pathogenic sites of CYP27A1 were identified as c.255+1G>T and c.1263+1G>T, which were both caused by shear denaturation. CONCLUSION: Cerebrotendinous xanthomatosis requires a multidisciplinary diagnosis that must be made early to avoid progressive neurological degeneration. c.1263+1G>T is a known mutation, but c.255+1G>T is a rare mutation site.