תוצאת חיפוש

Nutritional Status and Vitamin B⁶ Supplementation in the Institutionalized Elderly

Felicia Stern, Yitshal N. Berner, Zeev Polyak, Sophya Bernadiner, Margarita Komarnitsky, Ben Ami Sela, Ram Doolman, Yoseph Dror

Institute of Biochemistry, Food Science, and Nutrition, Hebrew University of Jerusalem; Subacute Dept. and Clinical Nutrition, Hartzfeld Geriatric Hospital, Kaplan Medical Center, Gedera; and Institute of Chemical Pathology, Sheba Medical Center, Tel Hashomer

Nutritional status and vitamin B⁶ status were assessed in 18 men and 32 women, average age 84, living in a home for the aged. Average proportion of energy derived from protein was higher than the recommended; fiber intake was very low. Also low were intakes of calcium, magnesium, zinc, copper, vitamins D and E, thiamin, folic acid and vitamin B⁶.

Supplementation with vitamin B⁶ (10mg/d) for 28 days in those with the lowest B⁶ status assessed by B⁶ intake, activation coefficient of aspartate transaminase and plasma pyridoxamine concentrations led to improved B⁶ status (marked decrease in activation coefficient) and increased synthesis and decreased degradation of many short-lived neutrophil proteins. Though our elderly enjoy a variety of foods, some have marginal deficiencies that can be improved. Therefore, in the institutionalized elderly, micronutrient supplementation should be administered at a level low enough to be safe (below recommended upper level of intake) but high enough to be effective.

Cerebellar Infarction: Clinical Presentation, Diagnosis and Treatment

Y. Skurnik, S. Brandiner, G. Gandelman, Z. Shtoeger

Medical Dept., Kaplan Medical Center, Rehovot (Affiliated with Hebrew University-Hadassah Medical School, Jerusalem) and Dept. H, Harzfeld Hospital, Gedera

Cerebellar infarction is relatively infrequent and accounts for about 2% of all strokes. Its clinical presentation and course are variable. It may resemble vestibulitis in mild cases, but the presentation may be more dramatic in other cases. Cerebellar infarction may cause life-threatening complications such as acute hydrocephalus or brain stem compression, resulting from their mass effect in the posterior fossa or extension of the infarct to the brain stem.

Clinical features alone are insufficient for the diagnosis and for follow-up of patients with cerebellar infarction. However the advent of CT and MRI and their availability enable early diagnosis of cerebellar infarction, and early recognition of the development of acute hydrocephalus or brain stem compression which require surgical decompression. The prognosis of most cases is good when treatment is appropriate.