P300 and contingent negative variation in migraine

We reviewed P300 and contingent negative variation (CNV) studies performed in migraine in order to identify their relevance in migraine and the role of neurophysiology in migraine. Publications available to us were completed by a Medline search. There is experimental and clinical evidence for loss of cognitive habituation in migraine which may serve as a specific diagnostic tool; therefore, we reviewed studies on migraine that analyzed habituation and lack of habituation by P300 and CNV, performing short-term habituation (STH) and long-term habituation (LTH). Finally, we described the two components of P300 (a and b) and of CNV (early and late wave) and the two abnormalities reported from the majority of studies on event-related potential in migraine: increased amplitude of average event-related potential and lack of habituation. These abnormalities are especially related to the early component characterizing orienting activity.     

Induced hypoglycemia. A unusual case of child battering

We describe a case of Munchausen's syndrome by proxy in a 12 years old child. The administration of glibenclamide by the mother led to severe hypoglycemias in the child, who underwent various instrumental researches and a subtotal pancreatectomy before the final diagnosis could be reached. The diagnosis also was possible with the substantial help of an accurate psychological survey. The case solution, with disappearance of hypoglycemias, was made possible by the removal of the maternal presence settled by the juvenile court.     

Thyrotrophin-Releasing Hormone Raises Cytosolic Free Calcium Concentration in Human Adenomatous Somatotrophs and Corticotrophs; Comparison with in vivo Responsiveness to Thyrotrophin-Releasing Hormone in Patients with Acromegaly or Cushing's Disease

The effect of thyrotrophin-releasing hormone (TRH) on intracellular free Ca²⁺ concentration, [Ca²⁺)i, was investigated with the fluorescent dye fura-2 in cell suspensions obtained from 13 human growth hormone-secreting adenomas and 6 adrenocorticotrophin-secreting adenomas. Preoperatively, 9 out of 13 acromegalic patients showed a positive growth hormone response to TRH administration while none of the 6 patients with Cushing's disease had a plasma adrenocorticotrophin increase after TRH injection. In all the growth hormone-secreting adenomas the addition of TRH (100 nM) caused a significant rise in [Ca²⁺]i (from a resting level of 133±40 (±SD) to a value of 284±119 nM at 100 nM TRH, n = 42; P<0.001). The transient induced by TRH was found to have a dual origin, one due to Ca²⁺ mobilization from intracellular stores which was maintained in presence of EGTA (3mM) and verapamil (10 μM) and a plateau phase due to Ca²⁺ influx from the extracellular media. Somatostatin (0.1 μM) lowered both resting [Ca²⁺]i and TRH-induced transients. The effect of gonadotrophin-releasing hormone on [Ca²⁺]i was evaluated on cell suspensions obtained from 6 growth hormone-secreting adenomas. Gonadotrophin-releasing hormone (100 nM) caused a marked rise in [Ca²⁺]i (from 179±25 to 283±15nM) on the cell suspension obtained from the only in vivo responsive adenoma while it was ineffective in the remaining 5. Although TRH was ineffective in modifying plasma adrenocorticotrophin levels in all patients with Cushing's disease, in 5 out of 6 tumors the addition of 100 nM TRH caused a significant rise in [Ca²⁺]i (from 102.5 ± 36 to 163±66 nM, n = 22; P < 0.005). However, the effect of TRH on [Ca²⁺]i was significantly lower than that caused by arginine vasopressin, a physiological stimulator of adrenocorticotrophin release ([Ca²⁺]i values; 145±78 nM at 100 nM TRH versus 300±140 at 10 nM arginine vasopressin, n = 15; P<0.05). Moreover, the effect of arginine vasopressin on [Ca²⁺]i was detectable at concentrations as low as 0.1 nM while TRH was effective at concentrations higher than 1 nM. By contrast, gonadotrophin-releasing hormone was ineffective in increasing [Ca²]i in all the adrenocorticotrophin-secreting adenomas studied. Collectively, these data indicate that sensitivity to TRH is present in almost all the growth hormone- and adrenocorticotrophin-secreting adenomas independently of the responsiveness of the individual patients to the peptide.     

Effect of bezafibrate on low levels of high density lipoprotein cholesterol in normolipidemia. Study in coronary patients and their first degree relatives

A pharmacological study was carried out in a group of 20 subjects composed of 13 coronary patients and 7 normal close relatives (first degree) who were considered at a high risk for coronary heart disease (CHD) because of their low levels of high density lipoprotein cholesterol (HDLch) (mean +/- SD: 34.1 +/- 5.2 mg/dl) and their high total cholesterol/HDLch (Tch/HDLch) ratio (mean +/- SD:6.7 +/- 1.1), despite their normal serum lipid values. With the purpose of normalizing these parameters they were submitted to a 4-month treatment with bezafibrate, a hypolipidemic agent which has a known effect in increasing HDLch and in decreasing the Tch/HDLch ratio. At the end of the study total serum cholesterol and triglycerides decreased significantly by 10 and 30%, respectively (p less than 0.01). HDL increased in its cholesterol content by 33% reaching a value of 45.4 +/- 9.8 mg/dl (mean +/- SD, p less than 0.01) as well as in its apolipoprotein A1 (Apo A1) content (13%, p less than 0.02). HDL2 subfraction also rose in cholesterol and in Apo A1: by 90 and 38%, respectively (p less than 0.01). HDL3 subfraction rised only its cholesterol content by 24% (p less than 0.01). Tch/HDLch ratio was significantly reduced (p less than 0.01) to a value of 4.6 +/- 0.9 (mean +/- SD). Total serum Apo B diminished by 14% (p less than 0.01). No adverse effects were observed during the follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Asymmetric dimethyl-arginine (ADMA) response to inflammation in acute infections.

BACKGROUND AND METHODS: The endogenous inhibitor of nitric oxide synthase (NOs) asymmetrical dimethyl-arginine (ADMA) has been implicated as a possible modulator of inducible NOs during acute inflammation. We examined the evolution in the plasma concentration of ADMA measured at the clinical outset of acute inflammation and after its resolution in a series of 17 patients with acute bacterial infections. RESULTS: During the acute phase of inflammation/infection, patients displayed very high levels of C-reactive protein (CRP), interleukin-6 (IL-6), procalcitonin and nitrotyrosine. Simultaneous plasma ADMA concentration was similar to that in healthy subjects while symmetric dimethyl-arginine (SDMA) levels were substantially increased and directly related with creatinine. When infection resolved, ADMA rose from 0.62 +/- 0.23 to 0.80 +/- 0.18 micromol/l (+29%, P = 0.01) while SDMA remained unmodified. ADMA changes were independent on concomitant risk factor changes and inversely related with baseline systolic and diastolic pressure. Changes in the ADMA/SDMA ratio were compatible with the hypothesis that inflammatory cytokines activate ADMA degradation. CONCLUSIONS: Resolution of acute inflammation is characterized by an increase in the plasma concentration of ADMA. The results imply that ADMA suppression may actually serve to stimulate NO synthesis or that in this situation plasma ADMA levels may not reflect the inhibitory potential of this methylarginine at the cellular level.     

阶段性健康教育对老年食管癌患者术后配合行为的影响

目的探讨阶段性健康教育对老年食管癌患者术后配合行为的影响。方法将51例患者按入院先后分为观察组（26例）和对照组（25例）。观察组实施阶段性健康教育，即住院当日、术前1～3d、术后回病房、术后第1天、拔除胃管当日、出院前1d，由管床护士实施不同内容的健康教育；对照组实施传统健康教育。术后1周评价两组患者术后的配合行为及术后并发症的发生率。结果观察组术后配合行为显著优于对照组（均P〈0．01）；并发症发生率显著低于对照组（P〈0．05）。结论对老年食管癌手术患者实施阶段性健康教育，可提高患者的术后配合行为，降低并发症的发生。     

Buprenorphine in balanced anesthesia

Buprenorphine was administered for the balanced general anaesthesia in 300 patients during several operations. The results obtained, the good features of analgesia, morphine-like, the absence of cardiovascular and respiratory side effects are presented.     

Spatiotemporal modeling of cerebral evoked magnetic fields to median nerve stimulation.

We measured somatosensory evoked magnetic fields during median nerve stimulation in 6 normal subjects. We applied multiple dipole models to study the spatiotemporal structure of early somatosensory evoked magnetic fields (SEFs), as well as the number, 3-dimensional location and time activity of their underlying neuronal sources. Two dipole sources were necessary to model the first 40 msec of SEFs explaining 85% of the data variance. Source 1 was located deeper than source 2, showed primarily a tangential orientation, and accounted for a larger part of the variance; source 2 showed no consistent orientation across subjects. Both sources showed biphasic time activities corresponding to the previously described N20-P30 and P25-N35 components. Spatiotemporal modeling could identify sources which could not be modeled consistently above noise by single moving dipoles (P25 component), revealed small latency differences of the two sources in some subjects suggesting parallel activation of these sources, and allowed separation of sources overlapping considerably both in space and time. We conclude that spatiotemporal modeling of SEFs may be useful to study functional anatomy of human sensorimotor cortex non-invasively.