Cecilia Soavi

Age-related differences in plasma BDNF levels after prolonged bed rest

Brain-derived neurotrophic factor (BDNF) is a member of the family of neurotrophins and has been implicated in brain resistance to insults. Murine studies have demonstrated increased hippocampal concentration after acute immobilization and decreased concentration after chronic immobilization. In humans, chronic stress and sedentary lifestyle result in decreased plasma BDNF levels, but there no data exist regarding acute immobilization. The aim of our study was to evaluate age-related responses [comparing 7 younger subjects (age 23 ± 3 yr) and 8 older subjects (age 60 ± 4 yr)] of plasma BDNF before (baseline data collection, BDC) and after 14 days (BR14) of horizontal bed rest (BR). At BDC, BDNF levels were not different between the two groups (P = 0.101), although at BR14, BDNF levels were higher in older subjects (62.02 ± 18.31) than in younger subjects (34.36 ± 15.24 pg/ml) (P = 0.002). A general linear model for repeated measures showed a significant effect of BR on BDNF (P = 0.002). The BDC BDNF levels correlated with fat-free mass in both populations (ALL) (R = 0.628, P = 0.012), (older, R = 0.753, P = 0.031; younger, R = 0.772, P = 0.042), and with total cholesterol in ALL (R = 0.647, P = 0.009) and older study subjects (R = 0.805, P = 0.016). At BR14, BDNF correlated with total cholesterol (R = 0.579, P = 0.024) and age (R = 0.647, P = 0.009) in ALL. With an increase in age, the brain could become naturally less resistant to acute stressors, including the detrimental effects of prolonged bed rest, and thus the increase in BDNF in the older study group might reflect a protective overshooting of the brain to counteract the negative effects in such conditions.

Bilateral strio-pallido-dentate calcinosis (Fahr's disease): report of seven cases and revision of literature.

BackgroundFahr’s disease is rare a neurodegenerative idiopathic condition characterized by symmetric and bilateral calcifications of basal ganglia, usually associated with progressive neuropsychiatric dysfunctions and movement disorders. The term “Fahr’s syndrome” is used in presence of calcifications secondary to a specific cause, but the variability of etiology, pathogenesis, and clinical picture underlying this condition have raised the question of the real existence of a syndrome. Several classifications based on the etiology, the location of brain calcifications and the clinical presentation have been proposed. Here we describe seven clinical cases of basal ganglia calcifications, in order to search for pathognomonic features and correlations between clinical picture and imaging findings.Cases presentationThe patients came to our attention for different reasons (most of them for memory/behavior disturbances); all underwent neuro-psychologic evaluation and neuro-imaging. All patients showed variable degrees of deterioration in cognitive function; anxiety and depression were frequent too, and resistant to treatment in all cases. Less frequent, but severe if present, were psychotic symptoms, with different grade of structure and emotional involvement, and always resistant to treatment. We observed only few cases of extrapyramidal disorders related to the disease itself; anyway, mild extrapyramidal syndrome occurred quite frequently after treatment with antipsychotics.ConclusionBased on these findings we discourage the use of the term “Fahr’s syndrome”, and suggest to refer to Idiopathic or Secondary basal ganglia calcification. Unlike early onset forms (idiopathic or inherited), the clinical presentation of late onset form and Secondary basal ganglia calcification seems to be really heterogeneous. Case–control studies are necessary to determine the actual significance of basal ganglia calcification in the adult population and in the elderly, in cognitive, physical and emotional terms.

Eosinophilic Gastroenteritis Cured with Helicobacter pylori Eradication: Case Report and Review of Literature

To the Editor: Eosinophilic gastroenteritis is a rare disorder characterized by eosinophilic infiltration of the gastrointestinal mucosa, peripheral eosinophilia without other causes, and abdominal complaints including nausea, vomiting, diarrhea, and abdominal pain. The etiology of eosinophilic gastroenteritis remains unknown; although it has been associated with food allergy, the treatment with elimination diets gives poor results while steroid therapy is effective in 90% of patients [1]. We report a case of eosinophilic gastroenteritis resolved after eradication of Helicobacter pylori infection. A 21-year-old woman presented to our Department complaining nausea and postprandial vomiting lasting 6 months, with a weight loss of 10 kg. She had previously been treated with ursodeoxycholic acid for gallbladder microlithiasis, protonic pump inhibitors, and levosulpiride without any improvement; she was currently assuming prebiotics and oral contraceptives. Her anamnesis was positive for inhalant allergy (ragweed pollen rhinitis); she smoked 10 cigarettes/day and did not assume alcoholics nor other drugs. Clinical examination was unremarkable, with the exception of mild epigastric tenderness. Laboratory testing showed moderate eosinophilia (860 eosinophils/lL) with normal blood count. Renal, hepatic, and thyroid function, as well as inflammatory markers were normal. Serology for hepatitis viruses, research for parasites and their ova in stools, coproculture, and fecal occult blood were negative. Total IgE count (129 kU/L; normal value: <100) was slightly increased. Abdominal ultrasound showed moderate splenomegaly and confirmed gallbladder microlithiasis. The patient underwent chest X-rays and upper digestive tract X-rays (both normal). A gastroscopy showed erythematous mucosa with antral linear erosions. Histology from duodenal bulb and gastric antrum biopsies showed chronic superficial and deep gastritis with prevalent eosinophilic component, associated with Hp infection (Fig. 1). We counted 116 eosinophils per HPF (409) in the gastric antral and duodenal bulbar lamina propria. The patient was treated with amoxicillin 1 g bid, clarithromycin 500 g bid, pantoprazole 40 mg/day, and metoclopramide 10 mg tid, with rapid clinical improvement. The therapy was continued for a total of 2 weeks. Six weeks after the end of eradicating therapy, the patient reported the complete disappearance of symptoms and weight recovery. Eight weeks after the end of treatment, histology showed both Hp negativity and complete disappearance of gastric antral and duodenal bulbar eosinophilic infiltration. In the meantime, repeated laboratory testing showed normal eosinophilic count (350/ll). The patient did not complain of any relapse during the following 20 months and is currently undergoing follow-up as an outpatient. The only successful eradication therapy against Hp infection was able to resolve both Hp infection and eosinophilic gastroenteritis in our patient. Although eosinophilic gastroenteritis in H. pylori positive patients is a very rare finding, recent case reports seem to confirm the efficacy of Hp eradicating therapy in curing eosinophilic gastroenteritis [2,3]. Moreover, Moorchung et al. [4] showed a strong association between the density of eosinophils and of H. pylori in gastric biopsies, and a correlation between eosinophil score and severity of chronic gastritis. As we have previously showed that H. pylori presence is strongly associated with neutrophilic infiltration of the stomach [5], representing the Figure 1 Hematoxylin and eosin-stained preparation from gastric antral biopsy. Large numbers of eosinophils can be seen in the lamina propria.

Computerized cognitive training and brain derived neurotrophic factor during bed rest: Mechanisms to protect individual during acute stress

Acute stress, as bed rest, was shown to increase plasma level of the neurotrophin brain-derived neurotrophic factor (BDNF) in older, but not in young adults. This increase might represent a protective mechanism towards acute insults in aging subjects. Since computerized cognitive training (CCT) is known to protect brain, herein we evaluated the effect of CCT during bed rest on BDNF, muscle mass, neuromuscular function and metabolic parameters. The subjects that underwent CCT did not show an increase of BDNF after bed rest, and showed an anti-insular modification pattern in metabolism. Neuromuscular function parameters, already shown to beneficiate from CCT, negatively correlated with BDNF in research participants undergoing CCT, while positively correlated in the control group. In conclusion, BDNF increase can be interpreted as a standardized protective mechanism taking place whenever an insult occurs; it gives low, but consistent preservation of neuromuscular function. CCT, acting as an external protective mechanism, seems to modify this standardized response, avoiding BDNF increase or possibly modifying its time course. Our results suggest the possibility of differential neuroprotective mechanisms among ill and healthy individuals, and the importance of timing in determining the effects of protective mechanisms.

Diogenes syndrome or isolated syllogomania? Four heterogeneous clinical cases.

Diogenes syndrome (DS) is an acquired behavioural disturbance more often affecting elderly patients, but possible in all ages. It is characterised by social withdrawal, extreme self and house neglect, tendency to hoard any kind of objects/rubbish (syllogomania), and rejection against external help for lack of concern about one’s condition. It is considered infrequent, but with quite high mortality. DS might be divided into several forms including Active (the patient gathers objects outside and accumulates them inside his house), Passive (patient invaded by his own rubbish), “à deux” (DS sharing between two people), and “under-threshold” (DS “blocked” by precocious intervention). Four cases are here presented. In case 1 (passive DS) alcoholism and cognitive impairment could be trigger factors for DS, predisposed by a “personality alteration”. In case 2 (active, “à trois”) superimposed psychosis could be the trigger, borderline intelligence being the predisposing factor. In case 3 (active), fronto-parietal internal hyperostosis might support an organic aetiology. Finally, case 4 was an example of isolated syllogomania in patient with evolving Alzheimer’s dementia. Despite being heterogeneous, our casuistry suggest that DS can develop in both sexes, is prevalent in geriatric age and often associated with cognitive impairment/psychiatric disturbances, which are not specific, nor sufficient to justify DS. Isolated syllogomania only shares the characteristic hoarding with DS; although cognitive impairment might be present, the other DS typical aspects (social isolation, help refusal, characterial aspects, personal hygiene neglect) are absent.