A trigger for Tourette's syndrome.
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Amantadine↗
Biomedical subjects
G R Gaffney
Publications and source records attributed to G R Gaffney.
Somatic complaints in childhood tic disorders.
Twenty-six children diagnosed with chronic tic disorders (18 with Gilles de la Tourette syndrome and 8 with chronic motor tic disorder) were studied for unexplained physical complaints. Compared to normal controls, an excess of somatic complaints was found in the tic disorders group; this was similar to an excess of somatic complaints in a mixed psychiatric clinic group. Medication produced no significant effect on somatic complaints for patients in the tic and psychiatric clinic groups. Within the tic disorders group, no significant correlation was found between the increased somatic complaints and the severity of anxiety, dysphoria, or movement disorder.
Adolescent↗
Tc-99m HMPAO SPECT appearance of an atypical laminar heterotopia.
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Brain↗
Brain imaging: evoked potential, quantitative EEG and SPECT abnormalities in schizophrenia.
The case of a nineteen-year-old female with a three-year history of psychiatric symptomatology clinically consistent with the DSM-III-R diagnosis of schizophrenia is presented. Neurophysiologic assessment using topographic brain mapping demonstrated auditory evoked potential P300 asymmetry with left temporal inactivation and increased latency, while EEG frequency analysis was remarkable for left hemispheric slow wave predominance as well as increased left temporal beta activity. Single photon emission computed tomography (SPECT) using hexamethylpropyleneamine oxime (HMPAO) in the same patient revealed radionucleide uptake reductions in the frontotemporal cortical regions. The clinical presentation of schizophrenia in the context of these imaging correlations is reviewed.
Adult↗
Neuroimaging in child and adolescent psychiatry.
Although less well studied in child and adolescent psychiatry than in adult psychiatry, brain imaging has significantly altered psychiatric research and practice. This review focuses on the modalities that are used to image the brain. These include structural imaging techniques of computer tomography (CT) and magnetic resonance imaging (MRI), as well as functional imaging techniques of computed electroencephalography (CEEG), positron emission tomography (PET), and single photon emission computed tomography (SPECT). The technologies are reviewed, strengths and weaknesses of modalities discussed, and research progress reported.
Adolescent↗
MRI of brain abnormalities in Cockayne syndrome.
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Adolescent↗
Renal actions of oxyphenbutazone.
Oxyphenbutazone decreased the renal excretion of sodium and water in anesthetized dogs. As these excretions decreased, the drug also produced a decrease in renal blood flow and in the glomerular filtration rate. Blood pressure increased slightly. These changes are consistent with an inhibition of renal prostaglandin synthesis and could explain why oxyphenbutazone is reported to produce weight gain and edema when used clinically.
Animals↗
Effect of indomethacin and meclofenamate on canine mesenteric and celiac blood flow.
Two nonsteriodal antiinflammatory agents, indomethacin and meclofenamate, were found to produce a marked decrease in mesenteric blood flow, an increase in blood presure and no significant change in celiac blood flow. The initial effect of indomethacin on mesenteric blood flow differed from that seen with meclofenamate. Whereas meclofenamate induced a fall in mesenteric blood flow that was gradual in onset, indomethacin induced a marked vasoconstriction of the mesenteric bed that was immediate in onset and of short duration, which was followed by a decrease of slower onset similar to that seen with meclofenamate.
Animals↗
Effect of furosemide on canine splenic arterial blood flow.
Furosemide has been reported to cause pathological changes in the intestines as a consequence of the decrease in splanchnic blood flow that it produces. In view of the pancreatic toxicities of this diuretic, it was of interest to examine the effect of the agent on blood flow to this organ. An electromagnetic flow probe, was placed around the splenic artery, a vessel which supplies a major fraction of pancreatic blood flow. Within 60 min after furosemide (1 mg/kg, iv) administration, splenic blood flow (SBF) decreased by 20% and the decrease paralleled the drug-induced diuresis. When the diuresis was prevented, the agent failed to affect SBF. Thus, furosemide causes a reduction in SBF, which appears to involve a mechanism dependent upon the volume reduction produced by the drug-induced diuresis.
Animals↗
Decrease in hepatic blood flow during furosemide-induced diuresis.
The effect of furosemide on hepatic hemodynamics was investigated using electromagnetic flow probes positioned around the hepatic-portal vein and common hepatic artery of anesthetized dogs. Furosemide administration induced a vigorous diuresis and concomitantly decreased total hepatic blood flow. Hepatic arterial blood remained relatively stable. Thus, the decrease in total hepatic blood flow was due primarily to a decrease in portal blood flow. When furosemide was given to animals with ureters ligated to prevent extracellular volume contraction, the drug did not reduce total hepatic blood flow, portal blood flow or hepatic arterial blood flow. Thus, furosemide induces a decrease in total hepatic blood flow that appears to involve a mechanism dependent upon the volume contraction produced by the diuretic. The contraction causes a reduction in venous blood flow but not arterial blood flow to the liver.
Animals↗
Phenylbutazone-induced decrease in renal blood flow.
Phenylbutazone (Butazolidin), and anti-inflammatory agent, has been reported to decrease renal excretion of sodium and water. Whether or not an alteration in renal hemodynamics could be involved in producing these effects was tested in anesthetized dogs. Renal blood flow (RBF) was monitored with electromagnetic flow probes. After i.v. administration of phenylbutazone, 2 mg/kg, RBF fell by 20%. Glomerular filtration rate, sodium and water excretion were also decreased and blood pressure increased slightly. The reduction of RBF and glomerular filtration rate by phenylbutazone indicates that a hemodynamic mechanism could be involved in the retention of sodium and water induced by this agent. The decreased blood flow was correlated with a depressed renal secretion of prostaglandin E. Also, in animals pretreated with indomethacin, another inhibitor of prostaglandin synthesis, administration of phenylbutazone did not result in any additional changes in renal hemodynamics or excretion of sodium and water. In addition, phenylbutazone antagonized the ability of furosemide to increase RBF, an inhibition which has previously been shown to occur with indomethacin. Thus, phenylbutazone appears to alter renal mechanisms in a manner similar to indomethacin.
Animals↗
Effect of furosemide on mesenteric blood flow in the dog.
Diuretic therapy has been implicated as a possible inciting factor in nonocclusive mesenteric infarction. In view of this possibility, the effect of furosemide on superior mesenteric arterial blood flow (MBF) was investigated using electromagnetic flow probes in pentobarbital anesthetized dogs. After administration of furosemide, 1 mg/kg iv, MBF decreased by 44%. To assess the role of extracellular volume depletion induced by the diuresis in reducing MBF, volume depletion was prevented by infusing isotonic saline at a rate matching urine flow. In these experiments, MBF was not decreased by furosemide. Thus furosemide induces a marked decrease in mesenteric blood flow and this hemodynamic action involves a mechanism that is dependent upon the volume depletion induced by the drug.
Animals↗