Substantia nigra hyperechogenicity in depressive subjects relates to motor asymmetry and impaired word fluency
- First Online:
- Cite this article as:
- Hoeppner, J., Prudente-Morrissey, L., Herpertz, S.C. et al. Eur Arch Psychiatry Clin Neurosci (2009) 259: 92. doi:10.1007/s00406-008-0840-9
- 171 Views
Substantia nigra hyperechogenicity (SNH) is a characteristic transcranial sonography (TCS) finding in Parkinson’s disease (PD). SNH, found also in about 10% of healthy adults, was related to a subclinical malfunction of the nigrostriatal dopaminergic system on positron emission tomography studies. Both, liability for developing PD and frequency of SNH were found to be increased in depressed subjects. Here, we investigated whether SNH in depression is related to motor or cognitive abnormalities resembling early PD.
Fourty-one patients with major depressive disorder and 15 with adjustment disorder with depressed mood were studied clinically and with TCS.
Frequency of SNH was similar in both groups (39, 33%; Chi-square test, P = 0.70). Larger SN echogenic size correlated with larger right-to-left asymmetry of finger tapping (Spearman test, r = 0.37, P = 0.009) and lower verbal fluency (r = −0.35, P = 0.038). These correlations were stronger in patients at ages ≥ 50 years (r = 0.52, P = 0.007; r = −0.50, P = 0.020), and, independently from age, in patients with reduced echogenicity of brainstem raphe suggested to reflect alteration of the serotonergic system (r = 0.40, P = 0.045; r = −0.51, P = 0.044). Whereas bilateral sum score of finger tapping was negatively correlated with severity of depression on the beck depression inventory (r = −0.50, P = 0.001) and the Hamilton depression rating scale (r = −0.34, P = 0.019), no correlation was found between depression severity and tapping asymmetry, or between depression severity and verbal fluency.
Data suggest that TCS detects a subgroup of patients with depression characterized by symptoms of early parkinsonism who are possibly at an elevated risk of later developing definite PD.