Growth hormone response in low-dose apomorphine test correlates with nigrostriatal dopamine transporter binding in patients with Parkinson’s disease

Abstract

Challenge with low-dose apomorphine causes a rise in growth hormone (GH) in patients with Parkinson's disease (PD). We studied 18 patients with early PD, who showed an increase of GH in the low-dose apomorphine test, by means of [(123)I] FP-CIT-SPECT. The mean specific dopamine transporter binding of the 18 patients was 1.50 +/- 0.56 in the striatum, 1.20 +/- 0.59 in the putamen, and 1.76 +/- 0.59 in the caudate nucleus. The increase of GH (1.05 +/- 1.01 ng/ml at baseline to 9.46 +/- 6.36 ng/ml 45 min after apomorphine injection; p < 0.001) was significant. There was a significant negative correlation of the increase of GH with the mean specific dopamine transporter binding in all three regions (r between -0.490 and -0.587; p between 0.04 and 0.01). Challenge with low-dose apomorphine may therefore be used as an indirect tool to measure the extent of nigrostriatal neurodegeneration in early PD.

Psychobiological risk factors for suicidal thoughts and behaviors in adolescence: a consideration of the role of puberty

“…Consequently, it is possible that adolescent-typical increases in testosterone during puberty, especially in boys, contribute to elevated STB risk through enhanced dopaminergic transmission. This is consistent with previous reports that, compared to depressed patients who did not die by suicide, depressed patients who die by suicide have lower growth hormone responses to apomorphine [ 102 , 107 ], which is an indication of higher dopamine transporter binding [ 108 ]. Nonetheless, it is important to note that some studies provide evidence of lower dopamine (measured by lower levels of homovanillic acid and total dopamine in urine) in patients who attempted suicide versus those who did not, see [ 103 ], or of no significant associations between dopamine levels/receptor binding and STBs [ 109 ].…”

Hypothalamic dopaminergic stimulation in cluster headache

“…Second, we did not control for a general decrease of dopaminergic neurons or dopamine receptors. In a consecutive study, it would be interesting to compare the stimulation results with the density of dopamine receptors as it has also been studied in Parkinson’s disease (22). It cannot be excluded, although it is unlikely from a clinical point of view, that cluster headache is associated with a degeneration of dopaminergic neurons, which would also explain our findings.…”