Does age worsen EEG slowing and attention deficits in obstructive sleep apnea syndrome?

OBJECTIVE: The aim of this study was to determine whether EEG slowing is more pronounced in older than younger OSAS patients and to verify whether this cortical slowing is correlated to daytime performance, respiratory perturbation and sleep fragmentation. METHODS: Twelve young OSAS patients (mean age 38.2+/-2.0 y) and 13 older OSAS patients (mean age 62.2+/-1.9 y) along with 13 young controls (mean age 35.8+/-2.0 y) and 14 older controls (mean age 60.2+/-2.0 y) underwent a polysomnographic evaluation followed by a waking EEG recording. As a global index of cortical slowing, a ratio of slow-to-fast frequencies was calculated in all cortical regions. Daytime performance was assessed using the four choice reaction time test. RESULTS: Differences in waking EEG and in daytime performance were analyzed by ANOVAs with Group and Age as factors. Waking EEG did not yield a Group by Age interaction. OSAS patients had higher ratios across all regions than controls. Similarly, daytime performance revealed no Group by Age interaction. However, OSAS patients showed more lapses than controls and older subjects were slower than younger subjects. CONCLUSIONS: Our results indicate that age does not interact with OSAS to worsen the severity of cortical slowing, but age can add to the OSAS effect to worsen daytime performance deficits in OSAS patients. SIGNIFICANCE: The daytime performance deficits observed particularly in elderly OSAS patients warrant a careful clinical assessment of these patients to prevent accidents and injuries.     

Benign neonatal sleep myoclonus: case report and follow-up of four members of an affected family.

Benign neonatal sleep myoclonus (BNSM), characterized by myoclonic jerks of the extremities only in non-REM sleep, occurs in the first months of life with spontaneous disappearance within 3-4 months. We examined five siblings with typical BNSM, at the 3-10 years follow-up neurological examination. Psychomotor development, cognitive functions and EEG were completely normal. These cases confirm that BNSM is a self limited and nonepileptic disorder.     

Central sensory and motor conduction in vitamin B12 deficiency.

Four patients with subacute combined degeneration were studied through upper and lower limb SEPs recorded with a non-cephalic reference montage and through cortical and spinal magnetic stimulation. Clinical signs were confined to the lower limbs in 3 patients; the remaining patient presented only paraesthesiae in 4 limbs. Median nerve SEPs showed a normal cervical N13 response with a significant increase of central conduction time concerning exclusively the P9-P14 interpeak interval. Central motor conduction to upper and lower limb muscles was abnormal. Nerve conduction studies provided no evidence of peripheral nerve involvement. These electrophysiological findings suggest that in vitamin B12 deficiency the higher segments of the cervical cord are usually affected first and that central sensory and motor conduction studies are sensitive methods for detecting such damage.     

A neuroendocrinological approach to evidence an impairment of central cholinergic function in aging.

A hypothalamic pathogenesis for the reduced GH secretion in aging has been reported for both animal and man. To further address this issue we studied in 31 elderly normal subjects (6 males and 25 females, aged 66-90 yr) and in 22 young healthy controls (13 males and 9 females, aged 20-35 yr) the GH responses to GHRH test (GHRH29, 1 microgram/kg i.v. as a bolus at 0 min) alone and combined with pyridostigmine, a cholinesterase inhibitor (PD, 120 mg po 60 min before GHRH), or with arginine (ARG, 30 g in 100 ml infused from 0 to 30 min). Serum IGF-I levels were lower in elderly than in young subjects (mean +/- SE: 86.9 +/- 7.2 vs 288.7 +/- 22.1 micrograms/L, p < 0.01). The GHRH-induced GH increase was lower in elderly than in young subjects (p < 0.01). PD increased the GH response to GHRH in both groups (p < 0.001), but in elderly subjects this response persisted lower (p < 0.0001) than that observed in young adults. Also ARG coadministration potentiated the GHRH-induced GH release in both groups (p < 0.0001) but in this case the elderly's responses overlapped with the young's. The GH increase observed after combined administration of ARG and GHRH was higher (p < 0.0001) than that elicited by PD plus GHRH in elderly but not in young subjects. Analyzing individual GH responses, a GH peak below the limit of normality for young adults was observed in 19 (61.3%) elderly subjects after PD plus GHRH administration while ARG plus GHRH test elicited a normal GH peak in all but one.(ABSTRACT TRUNCATED AT 250 WORDS)     

Insulin resistance is associated with circulating fibrinogen levels in nondiabetic patients receiving peritoneal dialysis.

BACKGROUND: Insulin resistance (IR) and inflammation are associated with increased risk of cardiovascular disease in the general population. Continuous glucose absorption in peritoneal dialysis (PD) may induce hyperglycemia and hyperinsulinemia. METHODS: We evaluated IR in nondiabetic patients receiving PD, and analyzed the association between IR and systemic inflammation biomarkers by performing a cross-sectional study on ambulatory dialysis. A total of 25 nondiabetic patients receiving PD and 25 healthy individuals, matched for gender, age, and body mass index (BMI), were included. The PD group was composed of 11 men and 14 women, with a mean age of 47 +/- 14 years and mean BMI of 25.5 +/- 4.7 kg/m(2). The control group was composed of 10 men and 15 women, with a mean age of 45 +/- 12 years and BMI of 24.0 +/- 2.8 kg/m(2). RESULTS: IR was evaluated by the homeostasis model assessment method (HOMA-IR). Inflammation was assessed through high-sensitivity C-reactive protein (CRP) and fibrinogen. Body composition and truncal fat were evaluated by dual energy x-ray absorptiometry. HOMA-IR was significantly higher (P < .0001) in subjects receiving PD (4.9, range: 2.3-9.3 mmol/L x muU/mL) compared with healthy subjects (1.2, range: 0.4-4.8 mmol/L x muU/mL). As expected, compared with controls, patients receiving PD had significantly higher levels of insulin (26.5 +/- 7.5 muU/mL vs 6.3 +/- 3.4 muU/mL; P < .0001), CRP (6.3, range: 0.3-61.1 mg/L vs 2.4, range: 0.6-5.9 mg/L; P = .001), and fibrinogen (379 +/- 101 mg/dL vs 268 +/- 66 mg/dL; P < .0001). However, there were no significant differences in body and truncal fat mass between the groups. A significant correlation between HOMA-IR and fibrinogen (Rho = 0.48; P = .01) was observed. However, no correlation was found between HOMA-IR and CRP. Also, no significant correlations were found between HOMA-IR and body fat mass (Rho = 0.11), and between HOMA-IR and truncal fat mass (Rho = 0.19). CONCLUSIONS: Patients receiving PD demonstrate a state of IR that is associated with high circulating levels of fibrinogen. This suggests that hyperfibrinogenemia may be involved in the pathogenesis of IR in this setting.     

Meiotic recombination in the beta globin gene cluster causing an error in prenatal diagnosis of beta thalassaemia.

In the course of a prenatal diagnosis for beta thalassaemia by linkage analysis of restriction fragment length polymorphisms, a homozygous beta thalassaemia fetus was misdiagnosed as beta thalassaemia trait. Extensive studies of the polymorphic sites within the beta globin gene cluster in all the members of the family resulted in the conclusion that the paternal chromosome 11 of the newborn was different from that expected. Paternity was confirmed by HLA typing and blood group studies. The analysis of another polymorphic locus on chromosome 11 within the family was in agreement with the possibility of a crossing over between the two paternal chromosomes in a region 5' to the beta gene, previously indicated to contain a 'hot spot' area for recombination. This report underlines the risk of performing prenatal diagnosis using restriction polymorphisms 5' to the beta gene.     

Poly(Glu60Ala30Tyr10) (GAT)-induced IgG monoclonal antibodies cross-react with various self and non-self antigens through the complementarity determining regions. Comparison with IgM monoclonal polyreactive natural antibodies

Previous studies have shown that the antibodies of the preimmune repertoire are able to bind to various auto- and xenoantigens including chemical haptens. Sequence analysis of two such murine monoclonal IgM natural autoantibodies showed that they are encoded by unmutated germ-line variable regions of the light and heavy chain (V alpha and VH) genes which were also found in various murine immune responses, like phenyl-oxazolone, dinitrophenyl, arsonate, phosphorylcholine and influenza virus hemagglutinin. These data raised the question as to whether induced antibodies possessing germ-line sequence are also able to react with autoantigens. To study this problem, anti-poly(Glu60Ala30Tyr10) (GAT) and anti-alprenolol (Alp) monoclonal antibodies, carrying similar VH and V alpha genes and the same IgG1 isotype, were examined for their capacity to react with several self and non-self antigens. The results showed that: (a) the anti-GAT antibodies tested reacted with different autoantigens, such as murine tubulin, actin and myosin as well as trinitrophenyl (TNP) and bovine serum albumin. Similarly, one of the anti-Alp showed weak reactivities for myosin, DNA, actin and TNP; (b) in contrast two other anti-Alp antibodies did not react with any of the tested antigens. Since the major differences between the oligoreactive anti-GAT and the monoreactive anti-Alp antibodies are in the complementarity determining regions (CDR) our results suggest that the observed cross-reactions are mediated by hypervariable loops. Sequence comparison of these antibodies indicate a possible correlation between cross-reactivity and the presence of aromatic and charged amino acids in the CDR.     

Measurement of T-cell-derived antigen binding molecules and immunoglobulin G specific to Candida albicans mannan in sera of patients with recurrent vulvovaginal candidiasis

Immunoglobulin G (IgG) and T-cell-derived antigen binding molecules (TABM) specific to whole Candida extract and to Candida-derived mannans prepared by both the cetryltrimethylammonium bromide (CTAB) and alkaline degradation (PEAT) methods were measured in the sera of women with vulvovaginal candidiasis and controls. In the patients there were significantly higher levels of IgG to both CTAB and PEAT mannans and of TABM to CTAB mannan. TABM specific to CTAB mannan was purified from the serum of a patient with a high titer of this TABM. The purified TABM bound specifically to CTAB mannan and to other yeast and mold extracts. This TABM preparation was associated with transforming growth factor beta2 (TGF-beta2), and on specific binding to mannan there was a marked increase in the level of detectable TGF-beta2. This increase in TGF-beta2 level was critically dependent on the relative concentrations of the purified TABM and mannan, being smallest when either was in excess. The TABM specific to CTAB mannan was also shown to inhibit Candida-stimulated gamma interferon production. The results suggest that CTAB mannan-specific TABM may increase susceptibility to vulvovaginal candidiasis in association with a shift in the immune response to the Th2 type.