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Biomedical subjects

G Gerard

Publications and source records attributed to G Gerard.

At least 19 recordsLinked to original sources

Survey of migraineurs referred to headache specialists: care, satisfaction, and outcomes.

The authors report a survey of 281 migraineurs recently referred to headache specialists by primary care physicians. Compared with care before referral, specialists spent substantially more time with patients and were more likely to ask patients to take a prophylactic drug and to keep a headache diary, to discuss migraine triggers, and to prescribe 5-hydroxytryptamine1B/1D agonists (triptans). After referral, patients reported improved satisfaction with care and significant decreases in frequency, duration, and severity of attacks.

Adult↗

Postnatal catch-up growth induced by growth hormone and insulin-like growth factor-I in rats with intrauterine growth retardation caused by maternal protein malnutrition.

In this study, we examined the effects of exogenous IGF-I and GH on postnatal growth of rat pups with intrauterine growth retardation due to gestational protein restriction. From birth until weaning (d 23), pups born from dams fed ad libitum a low (5% casein; P5 pups) or a normal protein diet (20% casein; P20 controls) were cross-fostered to well nourished lactating dams. On d 2, the litters (n = 6/dietary group) were reduced in size to 6 pups, and littermates received, through postnatal d 23, two daily s.c. injections of bovine GH (2.5 microg/g of body weight (BW)/day), human IGF-I (1.8 microg/g of BW/day), or saline. At birth, BW and tail length (TL) of P5 pups were markedly decreased (to 72 and 70% of controls, respectively; p < 0.001). Despite food rehabilitation, stunting of body growth was still apparent on d 23 in the saline-injected P5 rats (BW and TL: 76 and 83% of age-matched saline-injected controls; p < 0.01). Serum IGF-I (-51%; p < 0.001) and weight of liver, heart, kidney, brain, and thymus (-13 to -35%; p < 0.01) were also reduced. Administration of GH in P5 rats raised their serum IGF-I (1-fold) to levels observed in saline-injected controls, and restored normal BW and TL (94 and 98% of controls, respectively), and organ weight (91-107% of those of controls). Injections of IGF-I in P5 rats increased after 1 h their serum IGF-I to levels 3 times greater than in saline-injected controls, and resulted in normalization of BW and TL (94 and 96% of controls), and organ weight (92-111% of controls). In P20 controls, 3-wk GH and IGF-I injections significantly increased serum IGF-I (0.6- and 2-fold increases, respectively), BW (14 and 11%), TL (12 and 11%), and organ weight (+10 to 30%) compared with saline-injected rats (p < 0.01). We conclude that under conditions of adequate nutrition, both GH and IGF-I may equally promote postnatal catch-up growth in rats with intrauterine growth retardation caused by gestational protein malnutrition.

Animal Feed↗

Zinc supplementation increases growth and circulating insulin-like growth factor I (IGF-I) in growth-retarded Vietnamese children.

To determine whether zinc deficiency might be involved in the failure to thrive observed in undernourished Vietnamese children, we assessed growth, incidence of infections, and circulating insulin-like growth factor I (IGF-I) concentrations in a double-blind study of zinc supplementation. Growth-retarded children (n=146) aged 4-36 mo were paired according to age, sex, commune, Z scores for weight (WAZ) and for height (HAZ), and number of siblings, and were randomly assigned to receive either 153 micromol (10 mg) Zn/d or a placebo for 5 mo. Weight, height, and episodes of infection were recorded each month and plasma IGF-I was measured 1 and 5 mo after the start of zinc supplementation. Multiple-linear-regression analysis for paired data showed that zinc supplementation increased weight (+0.5 +/- 0.1 kg; P<0.001) and height (+1.5+/-0.2 cm; P<0.001) after 5 mo compared with placebo treatment. The relative risk of infectious episodes in the zinc-treated subjects was reduced 3-fold for diarrhea (P=0.012) and 2.5-fold for respiratory infections (p=0.057). The probability of having at least two episodes of diarrhea or respiratory infection was 2.9- and 3.2-fold lower, respectively, in zinc-treated subjects between 1 and 5 mo (P=0.018), whereas they did not change in placebo-treated subjects (P-0.584). After 1 mo, IGF-I concentration (-x+/-SD) in zinc-treated subjects was 2.8+/-0.3 nmol/L compared with 1.9+/-0.2 nmol/L in placebo-treated subjects (P=0.021). After 5 mo, the values were 3.4+/-0.5 nmol/L (zinc-treated) and 2.0+/-0.3 nmol/L (placebo-treated; P=0.044). Our study suggests that zinc deficiency may limit growth in nutritionally deprived children. Because the increase in growth velocity resulting from zinc supplementation was associated with increased plasma IGF-I concentrations, we suggest that the growth-stimulating effect of zinc might be mediated through changes in circulating IGF-I.

Anthropometry↗

Central dizziness associated with cerebral blood flow disorders.

This retrospective study describes the use of transcranial Doppler (TCD) and history for further defining and diagnosing cerebral blood flow (CBF) disorders in patients with central dizziness. Central dizziness was defined as dizziness of nonlabyrinthine, non-peripheral causes. It was believed that at least some of the causes for central dizziness are not unknown but are associated with CBF disorders. Fifty patients who presented with central dizziness were examined and subsequently tested with TCD. In 33 of 50 cases (66%) a diagnosis could be assigned after TCD; whereas, on the basis of both history and TCD a diagnosis was assigned to 38 patients (76%).

Adolescent↗

Static stabilometry, transcranial Doppler, and single photon emission computed tomography in patients with central dizziness.

Previous studies have found that transcranial doppler (TCD) and single photon emission computed tomography (SPECT) are effective means of diagnosing cerebral blood flow disorders in patients with central dizziness whose etiology was unknown by standard audiologic and/or vestibular assessment techniques. Also, static stabilometry, which measures a person's standing center of pressure (COP) movements, has been used to distinguish between patients with central neurologic and peripheral vestibular disorders. The purpose of this retrospective study was to examine the relation between TCD, SPECT, and stabilometry in patients with central dizziness attributable to cerebral blood flow disorders. Stabilometry testing was conducted on 50 normal subjects and 31 subjects with dizziness, the latter group consisting of persons with cerebral dysautoregulation, migraines, and unknown etiology with negative or positive SPECT results. The results indicated that patients with cerebral dysautoregulation were not significantly different from normal subjects or the other three groups in their COP movements. The other three groups exhibited significantly higher COP movements than the normal subjects, particularly when visual inputs were compromised. Patients with negative SPECT results were significantly different in their COP movements from the other three groups of subjects with dizziness. These results suggest that the pattern of COP movements may be useful in identifying patients with postural dysfunctions whose etiology may then be detected by TCD and SPECT.

Adult↗

Syncope and seizures of psychogenic origin: identification with head-upright tilt table testing.

Psychogenic seizures and psychogenic syncope are common disorders but are difficult to identify. Head-upright tilt table testing has emerged as a promising means of evaluating vasovagally mediated syncope and convulsive syncope. Of a total of 42 patients evaluated by head-up tilt for recurrent syncope and 10 evaluated for recurrent idiopathic seizures, a total of 5 patients experienced syncope and 3 had tonic-clonic seizure activity unaccompanied by any significant changes in blood pressure, heart rate, transcranial Doppler cerebral blood flow velocity, and electroencephalographic monitoring. Psychiatric evaluation revealed that seven patients suffered from conversion reactions and one from probable malingering. We conclude that patients who pass out or convulse during head-upright tilt without any change in physiologic parameters can be presumed psychogenic in origin and may be referred for psychiatric evaluation without further expensive diagnostic studies.

Adolescent↗

Differentiation of convulsive syncope and epilepsy with head-up tilt testing.

OBJECTIVE: To evaluate the usefulness of head-upright tilt table testing in the differential diagnosis of convulsive syncope from epileptic seizures in patients with recurrent idiopathic seizure-like episodes. DESIGN: Prospective, nonrandomized study. SETTING: Electrophysiology laboratory of a university hospital. PATIENTS: Fifteen patients (8 men and 7 women patients; mean age, 29 +/- 20 years) with recurrent unexplained seizure-like episodes, unresponsive to antiseizure medication. MEASUREMENTS: Head-upright tilt table testing with or without isoproterenol infusion. Five patients who were initially tilt positive had a second tilt test with continuous electroencephalographic (EEG) recording. MAIN RESULTS: Syncope associated with tonic-clonic seizure-like activity occurred in six patients (40%) during the baseline tilt and in four patients (27%) during isoproterenol infusion (total positive tests, 67%). The EEG showed diffuse brain wave slowing (not typical of epileptic seizures) in five of five patients during the convulsive episode. All patients who had positive test results eventually become tilt table negative after therapy, and over a mean follow-up period of 21 +/- 2 months, no further seizure-like episodes have occurred. CONCLUSION: Upright tilt table testing combined with isoproterenol infusion may be useful to distinguish convulsive syncope from epileptic seizures.

Adolescent↗

Cerebral vasoconstriction during head-upright tilt-induced vasovagal syncope. A paradoxic and unexpected response.

BACKGROUND: To determine the effect of vasovagally mediated syncope on the cerebral circulation, transcranial Doppler sonography was used to assess changes in cerebral blood flow velocity during head-upright tilt-induced syncope. METHODS AND RESULTS: Thirty patients (17 men and 13 women; mean age, 43 +/- 22 years) with recurrent unexplained syncope were evaluated by use of an upright tilt-table test for 30 minutes, with or without an infusion of intravenous isoproterenol (1-4 micrograms/min), in an attempt to provoke bradycardia, hypotension, or both. Transcranial Doppler sonography was used to assess middle cerebral artery systolic velocity (Vs), diastolic velocity (Vd), ratio of systolic to diastolic velocities, pulsatility index (PI = Vs-Vd/Vmean), and resistance index (RI = Vs-Vd/Vs) before, during, and after tilt. Syncope occurred in six patients (20%) during the baseline tilt and 14 (46%) during isoproterenol infusion (total positives, 66%). In the tilt-positive patients, concomitant with the development of hypotension and bradycardia, transcranial Doppler sonography showed a 75 +/- 17% decrease in diastolic velocity, unchanged systolic velocity, a 46 +/- 17% decrease in mean velocity, a 295 +/- 227% increase in pulsatility index, and a 73 +/- 34% increase in resistance index. CONCLUSIONS: These findings reflect increased cerebrovascular resistance secondary to arteriolar vasoconstriction distal to the insonation point of the middle cerebral artery. This is paradoxic because the expected response of the cerebral circulation to hypotension is vasodilation. We conclude that abnormal baroreceptor responses triggered during vasovagal syncope result in a derangement of cerebral autoregulation with paradoxic vasoconstriction in the face of increasing hypotension.

Adult↗

Dysphagia as the sole manifestation of bilateral strokes.

Dysphagia can be caused by a host of factors, most of which are structural or functional. However, despite extensive evaluations, a certain number of patients have unexplained dysphagia. We present an extremely unusual case whereby a patient with an acute left hemispheric cerebral vascular accident presents with dysphagia as his sole complaint and after extensive neurological, gastroenterological, and radiographic examinations is found to have cricopharyngeal dysfunction. The etiology of this defect was not at all clinically apparent and, ultimately, magnetic resonance imaging (MRI) was performed which revealed a chronic infarction of the right frontal lobe and a smaller acute infarction in the same location of the left. This case demonstrates that swallowing disorders may be the sole presentation of stroke and that, if extensive evaluations of such patients fail to yield an etiology, one must strongly consider MRI as a tool for diagnosis, even if a CT scan is negative.

Aged↗

Reduction of serum insulin-like growth factor-I by dietary protein restriction is age dependent.

We have determined if dietary protein restriction for 1 wk has differential effects on growth, serum IGF-I, and liver growth hormone receptors at various stages of development. Female Wistar rats were fed a low (5%) protein diet for 7 d at 3, 4, 6, 8, and 12 wk of age, whereas controls were maintained on a normal (15%) protein diet. Body wt gain was impaired in the groups fed the low protein diet, despite normal energy intake, and the effect was attenuated with age. Liver cell number (DNA content) was reduced by low protein feeding in the 3-, 4-, and 6-wk age groups (p less than 0.01), but not in the older animals. Protein restriction caused a dramatic decrease in serum IGF-I in the younger animals (90 and 82% reduction versus normal fed age-matched controls, at 3 and 4 wk, respectively; p less than 0.001), and this effect was progressively attenuated with increasing age (49, 40, and 25% reductions of serum IGF-I at 6, 8, and 12 wk, respectively). Changes in serum IGF-I correlated with those of liver cell number (r = 0.80; p less than 0.001). Total and free liver growth hormone receptors were slightly decreased in the low protein diet groups at 4 (p less than 0.05) and 6 wk (total: p less than 0.001; free: p less than 0.01) but not in the other age groups. The occurrence of profound diet induced reductions in IGF-I without proportional reductions in liver GH receptors suggest that the apparent GH resistance occurs at a postreceptor level.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Dietary protein restriction decreases insulin-like growth factor I independent of insulin and liver growth hormone binding.

To determine the role of hypoinsulinemia and liver somatogenic (GH) receptors in growth retardation and decreased serum insulin-like growth factor I (IGF-I) levels during protein restriction, we have used a rat model where the effects of a low protein intake on body weight (BW), serum IGF-I concentration, and liver GH binding could be evaluated in the presence of low or high insulin concentrations. Two days after being made diabetic with streptozotocin (60 mg/kg BW), 6-week-old female rats (nine per group) were begun on a low (5%) or normal (15%) protein diet, without or with insulin supplementation (3 U lente daily). Nondiabetic rats fed both diets were used as controls (nine per group). In the nondiabetic animals, 7 days of protein restriction reduced BW gain by 50% (P less than 0.001), serum insulin by 44% (P less than 0.025), and serum IGF-I concentrations by 28% (P less than 0.001) without significantly changing liver GH binding. By day 9, BW was decreased in the diabetic animals by 12%, serum insulin by 80%, serum IGF-I by 55%, and liver GH binding by 62%; these effects were similar in the 5% and 15% protein-fed rats (P less than 0.001 vs. the corresponding controls). In the diabetes fed the normal diet, insulin treatment restored BW gain, serum IGF-I, and liver GH binding to normal values. In contrast, in the diabetics fed a protein-restricted diet and treated with insulin, BW gain and serum IGF-I concentrations remained low, similar to those in the malnourished controls. This diet-induced growth attenuation was observed despite high circulating insulin (2-3 times normal values), appropriate glucose control (63 +/- 9 mg/dl), and near restoration of liver GH binding. We conclude that while both protein restriction and diabetes attenuate growth and reduce IGF-I concentrations, the effects of protein restriction are independent of the effects of insulin and probably act by alteration of postreceptor mechanisms.

Animals↗

Early changes in serum concentrations of somatomedin-C induced by dietary protein deprivation in rats: contributions of growth hormone receptor and post-receptor defects.

To define the mechanism(s) for the decrease of somatomedin concentrations in acute protein malnutrition, we have assessed the relationships between serum immunoreactive somatomedin-C/insulin-like growth factor-I (Sm-C/IGF-I), serum immunoreactive GH and total (MgCl2-treated homogenates) as well as free (water-treated homogenates) liver somatogenic (GH) binding sites in growing rats fed a 5% protein diet for 12 or 24 h and given an s.c. injection(s) of rat GH (rGH) or saline. Control rats were fed a 15% protein diet and injected with rGH or saline. After 12 and 24 h of protein restriction, body weight was 6.9 and 8.2% below controls respectively (P less than 0.001), while Sm-C/IGF-I concentrations were reduced by 58 and 66% respectively (P less than 0.001 vs controls). Serum GH concentrations were not affected by the low protein intake. Furthermore, injection(s) of 50-100 micrograms rGH failed to raise serum Sm-C/IGF-I concentrations in the protein-deficient animals. The number of total and free GH-binding sites was modestly (15-20%) decreased at 12 and 24 h in the protein-restricted rats. Serum Sm-C/IGF-I concentrations correlated weakly with free and total binding sites (r = 0.48 and 0.38 respectively). Affinity constants of GH-binding sites were not changed by protein restriction. The profound reduction in Sm-C/IGF-I concentrations within a few hours of beginning protein restriction, and the discordance between this reduction and the small decline in somatogenic binding sites, suggests that, in addition to GH receptor loss, a postreceptor defect may participate in the GH resistance occurring in the early stages of protein deficiency.

Animals↗

MRI periventricular lesions in adults.

We studied MRI findings of a periventricular high-signal intensity pattern in 151 adults older than 50 years. Only 7.8% of patients who had no identified cerebrovascular risk factors and who reported no cerebrovascular symptoms had these MRI periventricular lesions; 78.5% of patients with a history of cerebrovascular risk factors and who had had cerebrovascular symptoms had periventricular patterns.

Age Factors↗

H-deficient blood groups of Reunion island. II. Differences between Indians (Bombay Phenotype) and whites (Reunion phenotype).

Two variants of recessive, H-deficient nonsecretor individuals (h/h, se/se) were identified on Reunion Island: (1) H-negative individuals corresponding to the classical Bombay phenotypes (OhO, OhA, OhB, OhAB) who lack completely the H antigen on their red cells; all of them were Indian and had strong anti-H antibodies reacting with normal O and Oh red cells from whites; and (2) H-weak individuals (Oh, Ah, Bh, ABh). This phenotype represented the majority (85%) of the H-deficient phenotypes on Reunion Island, and all of them were white. They had only a weak expression of the H antigen and showed small but detectable amounts of ABH antigens on their red cells. Their anti-H antibodies reacted with normal O erythrocytes, but failed to react with Oh red cells, regardless of the ethnic origin of the donor. They were all from the same geographical area on the Island (Cilaos) and showed homogeneous titers of anti-H antibodies in sera. We propose to call this particular variant of weak H phenotype, belonging to the so-called para-Bombay series, Reunion.

ABO Blood-Group System↗