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Biomedical subjects

K Y Little

Publications and source records attributed to K Y Little.

43 records · Page 3Linked to original sources
PubMed1990

Brain markers and suicide: can a relationship be found?

Recent work suggests that some persons who commit suicide have altered neurochemistry in their brains. It remains unclear which of the many reported abnormalities are most reliably present and whether they reflect a specific psychiatric disorder or a disposition to violent impulsivity. A number of technical and interpretive problems must be clarified, but a postmortem test indicating that a subject was at high risk for suicide may eventually emerge. This approach would not be useful for ruling out suicide, since altered neurochemistry is not likely to be involved in every case.

Brain Chemistry↗
PubMed1989

Predictors of response to high dose antipsychotics in chronic schizophrenics.

Significant numbers of chronic schizophrenic patients do not experience sufficient symptom relief from usual doses of antipsychotic medication. Clinicians must decide if high doses of antipsychotics should be tried. In this study baseline symptoms, drug levels, and the symptomatic effects of an acute stimulant challenge were examined before 14 subjects received a 50% increase in their antipsychotic dosing. The group as a whole did not improve. Several individuals with lower drug levels, high baseline hallucinations, and stimulant-induced improvement in hallucinations improved mildly after 3 weeks on the higher antipsychotic dose.

Adult↗
PubMed1988

Lack of acute d-amphetamine effects on thyrotropin release.

Case reports have suggested that amphetamine abuse causes excessive secretion of thyrotropin (TSH) and thyroxine (T4). Such an amphetamine-induced effect might be noradrenergic-mediated in the hypothalamus. The current controlled study examined oral d-amphetamine effects on the hypothalamic-pituitary-thyroid axis in normal humans. No acute effects were seen on TSH, T3 or T4 levels. d-Amphetamine elevated cortisol levels at 180 min, as previously reported.

Adult↗
PubMed1988

Amphetamine, but not methylphenidate, predicts antidepressant efficacy.

Several researchers have explored the possibility that acute stimulant response may predict eventual improvement after specific antidepressants. This review analyzes the relationship between stimulant response and nonspecific antidepressant response. In five studies, amphetamine responders were found to eventually improve after antidepressant treatment in 85% of the cases, while nonresponders improved in 43% of the cases. In contrast, acute methylphenidate responders and nonresponders eventually improved on antidepressants at equivalent rates. Amphetamine sensitivity appears to be a trait (possibly pharmacodynamic) that is independent of depressive illness but predictive of tricyclic responsiveness. Other evidence has suggested that amphetamine and methylphenidate cause similar behavioral and symptomatic effects through distinct mechanisms of potential clinical relevance. The most effective method for administering an amphetamine challenge and its appropriate clinical use remain unclear.

Amphetamine↗