Haloperidol in barbiturate detoxification.
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Biomedical subjects
Publications and source records attributed to R Snyder.
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Four Navajo children had a mutilating neuropathy with severe motor involvement. The disorder appears to be recessively inherited and is present from the earliest observable age. Manifestations include severe anesthesia, corneal ulceration, painless fractures, acral mutilation, and weakness. Mental function is normal. Sural nerves are practically devoid of myelinated fibers that show no evidence of regeneration. Unmyelinated axons show degenerative and regenerative morphologic and histometric features. Onion bulb formation is absent. We believe this neuropathy is a distinct clinical entity.
A case of intramedullary sarcoidosis simulating a tumor of the cervical spinal cord is presented. Autopsy showed that the disease was limited to the cervical cord and hilar lymph nodes. The literature is reviewed and six cases of histologically documented spinal cord sarcoidosis are discussed.
In summary, the effects of dimethyl sulfoxide (DMSO) and its metabolites, dimethyl sulfone (DMSO2) and dimethyl sulfide (DMS), were studied in five selected systems in rats and mice. DMSO enhanced the taurine excretion and the lethality produced by such aromatic hydrocarbons as benzene and chlorobenzene in rats. In mice, DMSO decreased the toxicity such cholinesterase inhibitors as paraoxon and octamethyl pyrophosphoramide. DMSO also lowered the body temperture of rats and reduced the motor activity of mice. Although DMSO2, the major metabolite of DMSO, was not effective in increasing the lethality of solvent hydrocarbons, it seemed to be quite as effective with respect to the other effects. DMS, although quite potent with respect to lowering body temperature and reducing motor activity, was relatively ineffective otherwise. Thus each of the metabolites has a spectrum of activity different from the parent compound; DMSO has the widest spectrum and DMS the narrowest. It remains to be determined whether the therapeutic effects of DMSO are related to the experimental effects reported above in animals, and whether DMSO2 and DMS may share any of the therapeutic effects of DMSO.
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Urinary xanthurenic and kynurenic acid levels were measured in five patients while they were receiving 50 mg and 100 mg of pyridoxine. The levels of tryptophane metabolite decreased progressively as the dose was increased but remained above basal levels. There was marked clinical improvement in these patients while receiving the higher dose only. The double-blind study with 76 asthmatic children followed for five months indicated significant improvement in asthma following pyridoxine therapy (200 mg daily) and reduction in dosage of bronchodilators and cortisone. The data suggest that these children with severe bronchial asthma had a metabolic block in tryptophane metabolism, which was benefitted by long-term treatment with large doses of pyridoxine.
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Autonomic functions were studied in three patients with hydrencephalus and five with hydrocephalus. Autonomic failure of central origin was found in the patients with hydrencephalus; whereas, those suffering from hydrocephalus had essentially normal autonomic function. In two patients with hydrencephalus, the hypothalamus was markedly abnormal but the rest of the autonomic nervous system was histologically normal. From this it is concluded that in some patients with mental and motor retardation, autonomic failure may be of cerebral origin but that this is not a feature of patients with hydrocephalus.
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