Hearing disability in music and non-music students.
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Biomedical subjects
Publications and source records attributed to D R Hanson.
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BACKGROUND: Approximately 30% of schizophrenic patients defined as treatment refractory significantly improve with clozapine. However, clozapine produces agranulocytosis in approximately 1% to 2% of patients in the United States. The mechanism of clozapine-induced agranulocytosis has not been established, but evidence suggests an immune-mediated mechanism. METHOD: Human leukocyte antigen (HLA) typing was performed in a native American with clozapine-induced agranulocytosis. RESULTS: Our findings support previous observations of a role of the HLA-B16, DR4, DQw3 haplotype in predicting susceptibility to agranulocytosis in clozapine-treated patients. CONCLUSION: We suggest that HLA typing of clozapine candidates may be useful for predicting the risk for clozapine-induced agranulocytosis.
Foramen magnum tumours are rare. They may present with bizarre symptoms and mimic many conditions. We report a presentation with the sole complaint of hoarseness, never previously described in the literature. Voice returned to normal after surgical removal of the foramen magnum meningioma.
This evaluation of recent experience of hypoglossal-facial nerve anastomosis in ten patients who had undergone acoustic neuroma resection, indicates that this procedure may have a role to play in the treatment of this disfiguring condition. Facial symmetry at rest is satisfactory in the majority of patients, who suffered little long term deficit from the loss of their hypoglossal nerve. This procedure is ideally suited to otolaryngological practice.
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Thresholds of hearing of 76 subjects in the age range 18-24 years were measured using manual audiometers. Particular attention was paid to the otological selection of subjects. In spite of precautions the testers introduce some variation in results, and it is suggested that tester variation might account for differences between various manual audiometry studies and automatic audiometry studies. When tester variation is included there is no significant difference between results of this manual study and that undertaken with automatic audiometers by Robinson, Shipton, and Hinchcliffe, except that our average threshold is higher at 0.5 kHz. We support their main recommendation for adjustment of standards at 0.5 and 6 kHz.
The hormonal response to human skin fibroblasts after exposure to beta-adrenergic agonists, prostaglandin E1 (PGE1), and cholera toxin was monitored by intracellular cyclic AMP accumulation. Down syndrome (DS; trisomy 21) cells had an approximately 10-fold greater response to beta-adrenergic agonists than did either normal diploid skin fibroblasts or other aneusomic fibroblast strains (trisomy 13, 18, and 22). The altered response in DS fibroblasts was specific for beta-adrenergic agonists, because treatment of DS or control cells with PGE1 or cholera toxin resulted in the same degree of cyclic AMP accumulation. Experiments with 3-isobutyl-1-methylxanthine, a cyclic nucleotide phosphodiesterase inhibitor, indicated that the increased response of DS fibroblasts was not primarily a function of altered cyclic AMP degradation. Monosomy 21 cells responded less than normal diploid fibroblasts to stimulation by the beta-adrenergic agonist isoproterenol. These findings suggest that genetic information on chromosome 21 participates in regulating the beta-adrenergic response of human fibroblasts.
1 A procedure for examining the acquisition of a lever-pressing operant with conditioned reinforcement was used to compare the effects of three psychomotor stimulants. 2 Hungry rats were trained to associated and auditory tone (i.e., conditioned reinforcer) with food. Preference for the tone was then measured after treatment with pipradol (5, 10, 15 mg/kg), cocaine (1, 5, 10 mg/kg) or (+)-amphetamine (0.5, 1.5, 5.0 mg/kg). 3 In agreement with previous data, 10 mg/kg of pipradrol enhanced the effect of conditioned reinforcement whereas animals treated with any of the doses of (+)-amphetamine showed no effect. 4 Rats treated with cocaine (1 or 5 mg/kg) showed an effect of conditioned reinforcement but the effect was not significantly greater than in controls. 5 The present data suggest important differences in enhancement of responding for conditioned reinforcement by various drugs in the psychomotor stimulant class. These differences in turn may be related to the pharmacological actions of these compounds on release of catecholamines from different storage pools.
Previous studies have shown that pipradrol enhances the acquisition of responding with conditioned reinforcement. The present experiments replicated this finding and assessed the possible role of nonspecific stimulus change, feeding in the test environment and prior exposure to the conditioned stimulus. The test procedure consisted of three phases: Operant rates of pressing two levers, one of which produced a 3-s tone, were measured in the pre-exposure phase; the tone was paired with food in the four conditioning sessions; and conditioned reinforcement was demonstrated in the test phase by a relative increase in pressing the tone lever. A group (N = 8) receiving food but no tone during the conditioning phase also increased responding on the tone lever in the test phase and this effect was enhanced in a group (N = 8) receiving pipradrol prior to the test. A group (N = 8) receiving neither tones nor pellets during conditioning and pipradrol prior to test failed to show a change in lever bias, ruling out the possibility that pipradrol produced a nonspecific enhancement of responding for stimulus change. It was hypothesized that the conditioned reinforcement effect seen in the food-alone groups resulted from sensory preconditioning. According to this hypothesis, the tone was conditioned to environmental stimuli during the pre-exposure phase; subsequent presentation of pellets resulted in a learned association between environmental stimuli and food, leading to increased responding for the tone in the test phase. The results of two control experiments supported this view. One group (N = 8) received no tone in the pre-exposure phase, pellets alone in the conditioning phase and then pipradrol prior to test. The second group, but under altered environmental stimulus conditions, and then was given pipradrol prior to test. Neither group showed evidence of conditioned reinforcement. It was concluded that pipradrol enhanced acquisition of responding with conditioned reinforcement even if the conditioned reinforceing stimulus was established with sensory preconditioning procedures.
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Sensori-neural hearing loss after H. influenzae meningitis in children has been reported to occur more frequently after treatment with ampicillin than with chloramphenicol. In the present survey, hearing was assessed clinically and, in most cases, audiometrically in 47 children seen after H. influenzae meningitis. Three children were found to have some sensori-neural hearing loss. In no case was this severe or suspected prior to examination. One was among 27 children treated with ampicillin; one was among eight treated with ampicillin and chloramphenicol; and one was treated with chloramphenicol and streptomycin. Most of the children received ampicillin in a dose of 250mg/kg/day or less, but the two who were treated with ampicillin and developed hearing loss were among five children who received higher doses, suggesting that ampicillin may be ototoxic when given in very high doses.
A critical examination of the data for and against genetic factors in early infantile autism and childhood schizophrenia is presented. The extreme rareness of both disorders made analysis difficult. No strong evidence exists implicating genetics in the development of childhood psychoses that begin before the age of 5. Family pedigree data fail to support psychogenic transmission because very few siblings of early onset cases are affected. Biological but not genetic etiological agents are more likely. Genetic factors are implicated in the development of psychoses that begin near pubescence and such factors appear to overlap with those for adult schizophrenia. Reevaluation of the minimum age of onset for adult-type schizophrenia is suggested.
Prospective developmental data on 33 children of consensus diagnosed schizophrenic parents were compared to control samples of children of other psychiatric patients and children of normal parents. Contrary to several reports the children of schizophrenics, observed from birth to age seven, were remarkably normal on a host of pregnancy and delivery variables, neurological examinations, physical growth measures, and psychological tests. However, a combination of three indicators characterized five of the 116 children, and all five were offspring of schizophrenics (17 per cent of the high risk sample), thus matching the expected lifetime risk for schizophrenia previously observed in such samples. Case histories show that all five children have enduring patterns of maladjustment and exhibit behaviours often reported in the premorbid histories of schizophrenics. Most have family histories heavily loaded with schizophrenia. In terms of a diathesis-stress model, these five children appear especially vulnerable to future schizophrenia in the absence of rational methods of prevention.
An investigation by questionary, otological examination, and audiometry has been carried out on 505 students in higher education. Statistically significant hearing losses were found in the group that admitted frequent attendance at pop-music entertainment compared with a control group. Losses associated with vacation employment in loud noise or with gunfire exposure were also identified. Thses losses were unrecognised before investigation and indicate the need for preventive action.